Love it or hate it, sleeping naked hits different. Not only is it less laundry to wash, but taking off those pajamas can do wonders for your health. While you may feel self-conscious at first, the openness of resting in the nude can actually boost your confidence and help you look your best self. 

There’s no right or wrong way to get ready for bed—it’s all a matter of preference. And while nakedness won’t miraculously cure all your sleep problems, experts say there are some modest benefits to going au naturel.

1. Younger-looking skin 

James Walker, a medical advisor for the healthcare platform Welzo, says sleeping without clothes gives your skin an opportunity to breathe, allowing for better airflow. He explains that clothes, especially tight-fitting ones, can restrict blood circulation, making it harder for your skin to receive vitamins and minerals needed for collagen production. Certain materials also might add to your discomfort in bed. Aditya Kashyap Mishra, a sex educator and relationship expert for Lustyboy, says synthetic fibers like spandex and nylon trap moisture in your skin—the added heat can make it hard to fall asleep. Other synthetic fabrics and pajamas with dyed cotton may cause skin irritation and acne from the fabric rubbing against you.

[Related: 5 surprising beauty benefits of running]

Tossing and turning from wearing the wrong clothing can affect your quality of sleep and your skin. The body makes collagen during sleep, which is essential for supple and younger-looking skin. Research shows that getting less than the recommended seven hours of sleep for adults increases skin aging and slows down recovery from sun damage.

2. A cooldown for your body

As you might expect, sleeping with your skin exposed helps regulate your temperature at night, says Walker. The drop in body temperature can prevent overheating—a real concern in summer and in places where winter is virtually non-existent. Research shows that feeling extremely hot at night increases wakefulness. Even if you manage to land some shut-eye, it will likely be less restorative with shorter cycles of slow-wave sleep and REM sleep. 

Feeling colder, on the other hand, can also help you fall asleep faster. Your body temperature is synced up with the light-dark cycles outside; it normally falls when the sun goes down. A lower body temperature from sleeping nude tells your biological clock it’s time to shut down.

3. Fewer fungal infections

Fungi and bacteria thrive in warm and damp areas like your nether regions. Mishra explains that trapped sweat from moisture-wicking clothing increases the risk of microorganisms building up, resulting in yeast infections and jock itch. Jock itch can also come from constant friction from clothes. Stripping down to nothing will allow more air circulation and keep your intimate parts from getting overheated.

4. Better emotional intimacy

Skin-to-skin contact between partners can strengthen your relationship. Research shows touching among consenting adults releases the “love hormone” called oxytocin. This chemical reduces stress and encourages openness and social bonding with others. One US marketing poll of more than 1,000 adults found that 57 percent of couples who regularly snoozed in the nude were happy in their relationship compared to 48 percent of pajama wearers. Getting used to baring it all in front of a partner can counteract self-consciousness of how you look in bed. Mishra says this openness is a huge stress reliever, and the added relaxation can help you sleep better.

What if you want to sleep in clothes?

If you’re still not convinced about sleeping naked, there are other ways to improve your slumber. Avoid tight or constricting apparel that would restrict your movement, irritate your skin, or otherwise cause discomfort. Walker recommends going to bed in loose-fitting and breathable fabrics like cotton or bamboo, or one simple layer like an oversized T-shirt and shorts to avoid overheating.

[Related: 11 ways to sleep better in unbearable heat]

There’s nothing wrong with slipping on a pair of socks before bed, Walker adds. Some people find it comforting and helpful in keeping their feet warm, especially during colder seasons. However, he warns against sleeping in socks that are too tight as they could restrict circulation. 

Whether you go to bed nude or in clothes, you should always remove your makeup and any heavy jewelry. Snoozing with makeup on can clog pores and lead to future breakouts. “It’s best to cleanse the face thoroughly before sleeping to allow the skin to breathe and regenerate,” advises Walker. Additionally, laying down in chunky necklaces, bangles, and other jewelry can be painful and might even leave abrasions on the skin.

“Ultimately, the key is to prioritize comfort and choose sleepwear that allows for optimal relaxation,” Walker says. “It’s always a good idea to listen to your body and make choices that help you feel comfortable and at ease during sleep.”

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What is life? It’s a fuzzy concept without a single answer. If you asked a philosopher, they might quote Plato and tell you it’s the ability to support yourself and reproduce, though that would make sterile donkeys non-living objects. Ask a biologist and they’ll likely hit you with a textbook definition of life as organized matter with genes—as diverse as a paramecium and an elephant.  

Oliver Trapp, a professor of chemistry at the Ludwig Maximilian University of Munich in Germany, offers a different description. He says life is a “self-sustainable reaction network,” in which organisms have the processes necessary to survive and adapt. This is in line with the definition NASA uses when looking for extraterrestrial life. Having a clear idea of what makes up life, and the conditions needed to sustain it, helps astronomers get a better picture of what to look for when searching for life on other planets. 

Specifically, they could look for the environments that have collected the essential ingredients. Prerequisites to making life, based on what happened during early Earth, are materials for organic chemical reactions. In a new study published today in Scientific Reports, Trapp and his colleagues simulated how our planet received the supplies for life-producing chemical reactions 4.4 billion years ago. They suggest that no special or lucky conditions were necessary. Instead, life on Earth was created from volcanic particles and iron-rich meteorites. These carried the building blocks essential to living things: amino acids, lipids, nucleosides, and sugars.

[Related: Here’s how life on Earth might have formed out of thin air and water]

“Understanding the origins of biology is one of the greatest unsolved scientific questions. It has important implications for understanding how common life may be beyond Earth and for understanding humanity’s place in the universe,” says Henderson (Jim) Cleaves, a chemistry professor at Tokyo Institute of Technology and president of the International Society for the Study of the Origins of Life, who was not involved in the study.

Previous theories suggested that Earth’s volcanoes were the starting points. Lava shaped the continents, and volcanic gases helped create oceans and atmosphere. Early Earth may have had another important boost, too, in the form of chemical-rich meteors falling from the sky. 

Trapp’s new study suggests it was the iron from fallen asteroids that helped convert atmospheric carbon dioxide into organic molecules such as hydrocarbons, aldehydes, and alcohol. “The meteorites entered the dense atmosphere, heated up and then you have this ablation of nanoparticles,” he explains. The natural minerals found on volcanoes would have helped support these chemical reactions.

To determine the interplay of space rocks and Earthly eruptions, the authors simulated the conditions of our young planet in the lab. They purchased chunks of two iron and stony meteorites and dissolved them in acid to create a solution, and soaked in crushed samples of volcanic ash and minerals assumed to have been present billions of years ago. The result was a model of meteorites crash landing on volcanic islands. The team also simulated atmospheric conditions on early Earth by combining carbon dioxide gas with hydrogen gas or water under a high-pressure and high-heat system. 

[Related: A new finding raises an old question: Where and when did life begin?]

Observing the reactions in this pressurized model, the team noticed an increase in the production of aldehydes, formaldehydes, alcohol, hydrocarbons, and acetaldehyde. These organic compounds would then be used in further chemical reactions to make amino acids, lipids, DNA, and RNA molecules. “Even at lower temperatures, the particles were highly reactive and quite robust,” Trapp says. The authors suggest that as Earth’s atmosphere cooled down and became more reactive, it was probably easier for iron to speed along the conversion of carbon dioxide into oxygen-containing organic compounds. 

“It is very interesting to see a demonstration of how micrometeorites could have contributed to prebiotic organic synthesis during their infall,” notes Cleaves. While he says the work provides ample evidence for this theory of how life first emerged, he warns this simulation is dependent on the composition of the early atmosphere. It’s unclear if those conditions existed exactly how the lab simulated them, he says.

Trapp says the findings are a start to uncover what makes up life. As long as the right materials are present, the conditions to sustain living things may not be unique to Earth. This could help space explorers decide if a planet is worth exploring. For example, inactive volcanoes have already been spotted in other places like Jupiter’s moon Io and Europa—a strong contender for extraterrestrial life since it holds a liquid water ocean underneath its icy surface.  

Alternatively, these simulations could rule out otherwise promising worlds. “If a planet is cooling down too quickly and no longer able to convert carbon dioxide into organic compounds, this process would completely stop and essentially cause life to die.” Even if we do stumble on a planet with the optimal environment for life, whether we actually find aliens is another matter entirely.

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Everyone has different perceptions of pain. Some can sit for hours getting tattooed for an arm sleeve, while others squirm at having their finger pricked. Because pain is subjective, doctors have a hard time evaluating and treating patients who are dealing with it chronically.

Now, neurologists have successfully used a person’s brain signals to predict how much pain they were feeling. The small but unprecedented study, published today in the journal Nature Neuroscience, identified hard clues in brainwaves that could objectively measure the intensity of chronic pain versus acute pain. 

The findings are part of a larger clinical trial aimed at creating a personalized brain stimulation therapy that could bring relief to the 51.6 million Americans living with chronic pain. Another recent study in the journal JAMA Network Open reported that the rate of chronic pain in the US was as high as other common health issues like diabetes, depression, and high blood pressure. 

“For the first time, the authors were able to understand and visualize the differences between the acute and chronic pain experience on a neural level,” says Akanksha Sharma, a neurologist at the Pacific Neuroscience Institute in California who was not involved in the research. “This is novel and important, learning how and where our brain perceives and processes acute and chronic pain and understanding how the individual brain rewires in response to chronic pain.”

[Related: Medical startup put useless plastic implants in chronic pain patients, says FBI]

The study authors invited four people with uncontrollable long-term pain—three recovering from strokes and one with phantom limb syndrome—to get implants that tracked neural activity. The patients had exhausted all their treatment options. “They tried medications, injections, and nothing was working. Brain surgery was the last resort,” says lead author Prasad Shirvalkar, a neurologist and pain medicine specialist at the University of California, San Francisco. 

Each participant underwent deep brain stimulation, a medical procedure that acts like a pacemaker for the cerebrum. The medical team implanted electrodes in specific areas to detect and record electrical activity from two brain regions associated with pain: the anterior cingulate cortex and the orbitofrontal cortex. The technique is commonly used for neurological conditions such as epilepsy and Parkinson’s, but has never been tested with chronic pain. 

For three to six months, the participants answered surveys about the severity and quality of their pain. Immediately after, they pressed a remote to let the electrode implants take a snapshot of their brain activity. A computer then used the recordings and survey responses to build models that calculated a pain severity score for each patient. Changes in the orbitofrontal cortex helped inform the personalized neural signatures more than any other brain region.

“This information can help drive more customized treatment options for patients,” Sharma says. “If we can objectively “see” the pain experience of a patient, then we can potentially modulate those areas of the brain with new interventions to alleviate or change the perception of pain.”

Brain activity recordings also showed a difference between chronic and acute pain. Signs of chronic pain were more strongly associated with changes in how neurons in the orbitofrontal cortex fired. According to Shirvalkar, this brain region is understudied in its role in shaping the pain experience. The anterior cingulate cortex, on the other hand, is better known for its role in perceiving and processing pain across the body. This brain region was found to be more associated with acute pain.

The team learned that they couldn’t apply the same kinds of brain activity used to chart acute pain in therapeutic research to chronic pain in the real world. “Chronic pain is not a more enduring version of acute pain—it’s fundamentally different in the brain with different circuits,” Shirvalkar explains.

Understanding the differences in how patients are neurologically wired for acute versus chronic pain can help further personalized brain stimulation therapies for the most severe forms of discomfort. Medhat Mikhael, a pain management specialist at the MemorialCare Orange Coast Medical Center in California who did not contribute to the research, says this would help treat the most difficult of chronic pain cases, especially those stemming from a stroke and traumatic brain injury.

[Related: The slow, but promising progress of electrode therapy for paralysis]

While Sharma finds the work fascinating, she warns people to exercise caution in interpreting the data and generalizing it to all neuropathic pain conditions, given that there were only four people in the trial. The study authors say their next goal is to recruit six patients and then move on to a phase two trial where the sample size would increase to 20 or 30 patients. There’s also a risk of life-altering complications with surgical implants in the brain. At the moment, Shirvalkar says noninvasive methods such as electroencephalography and functional MRIs would not be able to record for long periods of time. However, he hopes that one day tech companies can make small wearable devices that track brainwaves. 

“Treating pain relies on subjective reporting, or on how the person with pain communicates their pain to their provider. Not everyone’s pain is believed or treated equally,” Kate Nicholson, the executive director and founder of the National Pain Advocacy Center, wrote in an email to PopSci. “For these reasons, the search for phenotypes and objective measures for pain is the search for a holy grail in pain management. Objective measures [like the ones found through this study], if valid and validated, hold promise to transform pain’s assessment and treatment.”

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This year is going to be pretty unforgettable, and not in a good way. Climate scientists have predicted the arrival of El Niño, a climate pattern that temporarily warms up waters in the eastern Pacific Ocean and will change precipitation and temperature patterns around the world.. The last El Niño event took place from 2018 to 2019.

Each El Niño is unique in terms of how intense the warming effect gets, says Daniel Swain, a climate scientist at UCLA. This makes it harder for individual areas along the Pacific, like California and countries in Southeast Asia, to know how to properly prepare for upcoming storms or flooding. 

Past El Niño events can help areas get a broad sense of how strong the next one will be, but as time goes on, Swain says it is likely we will see an increase in extreme El Niño events because of climate change. This upcoming one is expected to make 2023 the hottest year in human history.

What is the forecast for El Niño 2023?

Climate scientists use a variety of tools to predict when and how hard El Niño will hit. Some examples include satellites to track wind and tropical rainfall patterns, ocean buoys to monitor sea surface temperatures, and mini radios strapped to weather balloons that measure air temperature, humidity, and pressure. 

David DeWitt, director of the Climate Prediction Center at the National Oceanic and Atmospheric Administration, forecasts an 82 percent chance of El Niño arriving between May and July. A weak El Niño is not out of the question, but the likelihood of a strong El Niño is about 55 percent. There’s also a 90 percent chance of El Niño persisting in the first few months of 2024.

How does El Niño warm the ocean?

During El Niño, weak winds coming from the east cause heat to build up along the equator in the eastern Pacific Ocean. As the waters warm up, they transfer heat to the atmosphere and create moisture-rich air that fuels rainstorms and floods.

One sign of an upcoming El Niño event to look out for is Kelvin waves in the Pacific. These aren’t your normal beach waves: They resemble the slow sloshing ones in your bathtub. The long movements pull expanding warm water to the ocean’s surface, which in turn, raises sea levels. They also strengthen El Niño by further reducing how much cold water is on the ocean’s surface. 

[Related: The jet stream is moving north. Here’s what that means for you.]

Recently, satellites orbiting Earth detected two- to four-inch-high Kelvin waves moving west to east along the equator. They also measured higher than average sea levels—another strong clue for El Niño. “If it’s a big one, the globe will see record warming,” NASA scientist Josh Willis said in a statement.

How will El Niño affect global weather patterns?

Brad Rippey, a meteorologist for the US Department of Agriculture, says El Niño is expected to cause flooding in some regions and droughts in others. During the Northern Hemisphere summer (June to August), El Niño will likely suppress Atlantic hurricanes and bring drought in regions such as Central America, the Caribbean Basin, and southern and southeastern Asia. During the Southern Hemisphere summer (December to February), areas like southern Africa, Australia, and the western Pacific Basin will experience more heat, droughts, and fires. 

Some regions of the world, however, will face wetter conditions. Rippey says that parts of South America, such as Argentina, have been reeling from drought because of the long-running La Niña that began in 2020. With El Niño, these areas would finally get doused with precipitation.

Is climate change making El Niño worse?

El Niño and its cooler counterpart La Niña are part of a natural cycle between warming and cooling of the Pacific Ocean that was first detected by South American fisherman in the 17th century. That said, climate change is interacting with this cycle and shaping a future with stronger El Niño episodes. “The Earth’s natural climate cycle and climate caused by humans are not independent of each other,” Swain explains. He adds that before global warming, the world’s temperature would reset after El Niño, but now it remains elevated.

The combination of human-caused global warming and short-term warming from El Niño could mean that the second half of 2023 or early 2024 will break global temperature records, Swain says.

Is the world prepared for the switch from La Niña to El Niño?

Yes and no. While most communities have experienced the upturns and downturns of El Niño before, each cycle is different. This upcoming one is no exception.

The level of preparation depends on the country and whether El Niño will trigger more heatwaves or flooding. Another factor is a country’s economy and whether they can afford to invest in protective measures.

[Related: This summer could push US energy grids to their limits]

“It’s usually the places that are most vulnerable that often have the least ability to shift things around to prepare,” says Swain. The 2015-2016 El Niño event, for example, caused heat stress, malnutrition, and disease outbreaks for more than 60 million people living in developing countries. But that doesn’t mean richer countries come out unscathed. For instance, El Niño events in the past 15 years cost the US economy $25 billion. A study published on May 18 in the journal Science estimates the average El Niño cost the global economy $3.4 trillion.

Being a few months away, Swain says it’s unlikely that a resource-poor region can change things around in a short time. “Now the question becomes, how much resilience do these places have to these kinds of natural hazards?”

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Humans are born with instincts for crying and smiling, but not for kissing. Sometime in the past, our ancestors had the idea to smack their mouths together and call it romantic. And though we may not know who gave the first smooch, ancient records of these steamy sessions are helping us piece together when people started locking lips. 

The generally accepted earliest evidence we have of making out is religious text written in India in 1500 BCE. And while there was no official word for kissing back then, sentences like “young lord of the house repeatedly licks the young woman” and lovers “setting mouth to mouth” implied more than platonic relationships. But whether this was when kissing all began is still up for debate. In fact, an overlooked collection of written texts from ancient Mesopotamia (modern-day Iraq and Syria) suggests people were kissing further in the past. 

Citing those texts, authors of a new perspective article published today in the journal Science argue romantic kissing occurred 1,000 years earlier than historians first predicted. And as kissing became more of the norm, old medical records reveal the widespread transmission of viruses that spread through lip-to-lip contact.

“Given what we know about the history of kissing in humans and the myriad of similar kissing-like behaviors observed around the animal kingdom, I’m not surprised by these findings,” says Sheril Kirshenbaum, the author of The Science of Kissing, who was not involved in the study. “Whether romantic or not, kissing influences our bodies and brains in so many meaningful ways by guiding our emotions and decisions.”

[Related: Scientists think they found a 2,000-year-old dildo in ancient Roman ruins]

Clay tablets left behind by ancient Mesopotamians in 2500 BCE describe two types of kissing. The first was the friendly-parental kiss. People kissed the feet of their elders or the ground as a sign of respect or submission. 

The second was the lip kiss with a more erotic and intimate overtone. However, there were a few cultural expectations when it came to this type of kissing. Romantic kissing was an action reserved for married couples, as people frowned upon any PDA in Mesopotamia. Kissing among unmarried folks was taboo, considered to be giving in to sexual temptation. People not meant to be sexually active, such as priestesses, were thought to lose their ability to speak if they kissed someone. “The need for such norms indicates that romantic kissing must have been practiced in society at large,” explains lead author Troels Pank Arbøll, an assyriologist (a person studying the language and civilization of ancient Mesopotamia) at the University of Copenhagen.

As more people adopted the practice of kissing on the lips, ancient medical texts described illnesses whose symptoms resemble viral infections spread through mouth-to-mouth contact. The authors note this aligns with DNA analysis from ancient human remains detecting viruses such as herpes simplex virus 1, Epstein-Barr virus, and human parvovirus. All three viruses transmit through saliva.

One example is a disease that the ancient Mesopotamians labeled bu’šānu. The infection involved boils in or around the mouth area. Its name also implies that the infected person might have stunk. While Arbøll says bu’šānu shares several symptoms with herpes, he warns people not to make any assumptions. “As with all ancient disease concepts, they do not match any modern diseases 1:1, and one should be very careful when applying these modern identifications. A disease concept like bu’šānu likely incorporated several modern diseases.”

Mesopotamians likely did not think infectious diseases were spread through kissing, since it is not listed anywhere in the medical texts. However, they had some religiously influenced ideas of contamination, which spurred some measures to avoid spreading the disease. For example, a letter from around 1775 BCE describes a woman in a palace harem with lesions all over her body. Assuming it was contagious, people avoided drinking from any cups she drank, sleeping in her bed, or sitting on her chair.

[Related: When you give octopus MDMA they hug it out]

The findings show that this form of kissing did not originate in a single place. Mesopotamia, India, and other societies separately learned to associate pecks on the lips as romantic. Arbøll says it’s possible other areas also learned about kissing but didn’t have the writing tools to record this behavior. This opens the question of how widely sexual kissing was practiced in the ancient world. 

Some experts are less convinced that kissing was a universal behavior. William Jankowiak, a professor of anthropology at the University of Nevada, Las Vegas, who was not involved in the study, points out that written records of kissing often occurred in complex societies and less so in people living in smaller foraging groups. It’s also difficult to know if romantic kissing was practiced in more than one class or reserved for elite groups in ancient civilizations. Additionally, other factors, such as living in tropical versus colder regions, could influence whether people wanted to lock lips. 

There’s still a long way to go in understanding the ancient history of kissing. But the study does clear up one thing—all the smooching our ancestors did is probably why oral herpes and other kiss-transmitted diseases are a global problem today.

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COVID-19 is no longer a public health emergency in the US. The Biden administration’s deadline follows the World Health Organization’s announcement last week that removed COVID’s status as a global health crisis.

Infectious disease experts tell Popular Science that it’s an encouraging step and a sign that we are in a very different place than where we were in 2020. And while the recent decisions in no way mean the virus is gone—it’s expected to be endemic like the flu—access to COVID testing, treatments such as Paxlovid, and the vaccines have put the US in a position to coexist with it.

That said, managing your safety will come at a higher cost now. In one of the biggest changes from ending the federal emergency response, insurances are no longer required to cover the costs of COVID testing or reimburse people if they bought an over-the-counter home COVID-19 test. The federal government is also ending its free COVID-test program over the mail. 

As the financial burden of testing shifts to families and individuals, knowing where and when to get tested will keep you protected as the country transitions into this new stage of the pandemic. “We’re still seeing up to 1,000 deaths a week in the US from COVID for people that are older and at risk,” warns Del DeHart, a medical director of the infectious diseases department at the University of Michigan Health-West. “For those people, COVID is still not over and so testing for early treatment is going to be critical.”

Where to get COVID tests

There are still options for getting free COVID tests around the US The last day to order four free at-home COVID tests from the government is May 31, but local community clinics can give away free COVID tests or at a lower cost until supplies run out. 

Access to free testing might also depend on where you live. David Souleles, the director of the COVID-Response Team at the University of California, Irvine, says some state governments are taking measures to avoid financial barriers with COVID testing. California, for example, issued a mandate for health insurances to continue providing reimbursement for eight monthly at-home tests. Check your state government’s website to see what policies are in place following the end of the public health emergency.

If you are uninsured, the US government will continue to provide access to swabs through the Increasing Community Access to Testing Program. This government program partners with specific healthcare sites such as Walgreens and Quest Diagnostics to provide no-cost COVID tests with priority for people with a known exposure to the virus or who are showing symptoms.

[Related: An at-home test for both COVID-19 and the flu gains approval]

At-home rapid tests and PCR laboratory testing will still be available at your local pharmacies and doctor’s office, but it’s up to your insurance company if they want to bear the cost or require a copayment. What’s more, insurance companies may charge different prices for COVID tests; if they cover the cost, they may set limits on how many tests they will cover per individual. 

Prices for COVID test kits in stores like CVS range from $9.99 to $28.99, meaning testing can quickly get expensive. DeHart is concerned that the prices will create a financial barrier that will deter people from getting tested. If affordability becomes a question, it’s important to make every COVID test you take count.

When it’s still important to get tested for COVID

While most COVID mandates have lifted around the country, some employers and places might require you to get tested. For instance, healthcare workers employed in facilities like nursing homes will likely continue routine COVID testing. And as of now, many hospitals still require routine COVID testing for admitted patients, though it remains unclear whether the hospitals will cover the cost or if the test will be added to a person’s medical bill.

For voluntary testing, it’s important to evaluate your risk of having a severe COVID infection. DeHart says individuals above the age of 65 and those with immunosuppressive conditions should get tested regularly, along with loved ones in close contact with those that fall under this category. Souleles also recommends taking a test before visiting a relative in assisted living or anyone who is considered at high-risk of exposure. 

Other scenarios may apply, too, Souleles adds. “We would still encourage people to test before and after travel and before and after gatherings if they have the ability to do so. Anytime that you have the ability to test before you’re going to be around lots of people is great, and anytime you have the ability to test three to five days after being around a lot of people, that’s also a good thing.”

[Related: Long COVID recovery is finally getting the attention it deserves in the US]

If you have COVID-like symptoms, get tested before going out in public, even if the side effects seem mild. Testing early will give you more chances to get Paxlovid, which is most effective when taken within the first five days of seeing symptoms, and potentially avoid life-threatening complications. 

If you need to purchase a COVID test, treat it like you would any other over-the-counter goods. This includes checking the expiration dates to avoid a false positive or false negative result. You will also want to throw out any recalled COVID tests. If purchased for a later date, keep COVID tests at room temperature and away from the hands of pets and young children.

What to do if you test positive for COVID

If the test comes out positive, follow the Centers for Disease Control and Prevention’s (CDC) guidelines. Stay home and isolate yourself from others in the household for five days. People experiencing moderate symptoms like difficulty breathing should isolate for 10 days. Monitor your condition and go to the hospital if there are any severe or life-threatening complications. 

If you must go outside, wear a high-quality mask and avoid going to places where you would have to take it off. Also contact your doctor to see if you are eligible for any COVID-19 treatments and start those as soon as possible.

You can stop isolating after five days if you have no symptoms. If you continue to show symptoms, the CDC says you should stay put until your symptoms improve or you are fever-free for 24 hours without using medication.

[Related: Getting COVID more than once might be even worse than we thought]

Keep in mind that COVID tests are only one of the many tools available to reduce your risk of severe infection and death. Both DeHart and Souleles strongly urge people to get vaccinated and get their booster shot when eligible. Insurers will still be expected to cover the bivalent COVID vaccine as a routine immunization, and the Biden administration’s Bridge Access Program for COVID-19 Vaccines and Treatments will continue to provide vaccines free-of-charge to the uninsured.

“Stay up to date with your vaccines,” says Souleles. “It’s still the most important tool that we have right now.”

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When the Human Genome Project launched in 1990, it was hailed as one of the greatest scientific endeavors of all time. The 13-year project identified about 20,000 genes and gave researchers a genetic blueprint to transform modern medicine. Doctors can now use genetic information to better diagnose diseases and debilitating conditions, such as linking a rare case of leg pain to a single mutation. The research also ushered in hope for an age of precision medicine, where every treatment would be tailored to the individual. There was only one problem—the work wasn’t really finished.

That’s because humans are 99.9 percent identical. But the 0.1 percent in genetic differences explains our uniqueness, and can also account for why some people are more susceptible to disease. Having one map of a single genome, which the 90s-era project produced, does not adequately represent the breadth of the human population.

An international study published today in Nature is filling in these gaps by analyzing a much more diverse set of genetic sequences. “We’re retooling the foundation of genomics to create a diverse and inclusive representation of human variation as the fundamental reference structure,” says senior study author Benedict Paten, an associate director at the University of California, Santa Cruz Genomics Institute. 

[Related: The benchmark for human diversity is based on one man’s genome. A new tool could change that.]

By eliminating bias and analyzing more inclusive genomic data, geneticists will have a better understanding of how mutations affect a person’s genes and move us closer to a future with equitable healthcare. 

What is a pangenome?

The research focused on creating a pangenome—a collection of DNA sequences within a single species. Past work focused on a reference genome, built from a few individuals, that was supposed to represent a broader set of genes. A pangenome, on the other hand, is created from multiple people worldwide to more accurately reflect our genetic diversity. 

It’s not as though past geneticists did not want to sequence more genetic variations—they just couldn’t. Erich Jarvis, a genetic professor at Rockefeller University Howard Hughes Medical Institute and a co-author of the study, says technology in the 90s and early 2000s did not allow researchers to see large variations between haplotypes—groups of genes inherited together from a single parent—within and across individuals. 

The focus of a pangenome is to study the genetic differences among individuals from across the world. Jarvis says knowing about genomic variations is important, because some mutations are associated with different traits and diseases. For example, the lipoprotein (a) gene has a complex structure that has not been sequenced in humans. But variations in the gene are known to be associated with an increased risk of heart disease among Black people. By sequencing the entire gene and understanding its variations, doctors may be able to revisit and treat previously unexplained cases of coronary heart disease.

“This paper helps us to understand that DNA [is] more than a sequence of letters; DNA is structurally organized, and human variation that structure is important for genomic function and trait diversity,” says Sarah Fong, a postdoctoral scholar studying human population variation at the University of California, San Francisco who was not involved in the study.

What does the first draft reveal?

The authors collected data on 47 genetically diverse individuals. About half came from Africa, with the others representing four other continents (excluding Australia and Antarctica). The genomic information added information on 119 million base pairs and 1,115 duplications—mutations where a portion of DNA on a gene is repeated. As expected, more than 99 percent of the genetic sequences were similar across individuals. But by including the less than one percent of variations in this new pangenome draft, the authors found that structural changes to genes explained 90 million of the identified base pairs. 

[Related: What we might learn about embryos and evolution from the most complete human genome map yet]

“By moving beyond a single, arbitrary, and linear representation of the genome, the work by the Pangenome Reference Consortium more accurately describes the diversity that exists in our species,” says Rajiv McCoy, an assistant professor of biology at Johns Hopkins University who was not involved in the current study but was recently involved in the first complete sequencing of the human genome.

With the latest pangenome model, it may become easier for geneticists to detect and characterize hard-to-find genetic mutations. When the authors analyzed a separate set of genetic information using the pangenome draft as a reference, they detected 104 percent more structural variants. They also improved the accuracy of the comparison sequence, reducing the  variant error rate by 34 percent.

Still a work in progress

Creating the first draft of the pangenome is only phase one of this two-part project. The second phase will take a couple of years, as the authors build collaborations among other international researchers and perform community outreach in areas where there is less genomic data, such as including members of indigenous cultures.

It might take decades before we see the drafts finalized into a complete picture of the human genome. There are several challenges to address, Fong says, such as the development of an efficient strategy to compare multiple human genomes and a concrete plan for testing for genetic variations in the medical field.

Still, Fong says the benefits will be worth the effort. Having complete, diverse human genomes will advance the way genetics is studied, and create a future where people’s genes are more fully considered when treating diseases.

The post What is a pangenome? Scientists just released their first draft. appeared first on Popular Science.

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Here’s some good news: Cigarette smoking hit record lows in the US, according to a new Centers for Disease Control and Prevention survey. An estimated 11.1 percent of American adults were regular cigarette users in 2022—a drop from the 14.4 percent reported in 2019.

The decline in smoking did not happen overnight. Since the 1960s, public health experts have been fighting against the glamorization of cigarettes to raise awareness of the danger they pose on human health. Cigarettes continue to be the leading cause of preventable death in the US with one in five deaths are related to a person’s smoking history. And while the recent news is a victory towards a healthier nation, e-cigarettes and other vaping products could make this a short-lived triumph.

What’s causing smoking rates to decrease?

Public health awareness

The decline first began in 1964 when the Surgeon General released a report linking cigarette smoking to a number of health problems, including a 70-percent increased risk of premature death and a nine- to tenfold risk of lung cancers compared to non-smokers. Since then, there has been a push for educational campaigns to teach people about the dangers of smoking to your health. 

Social stigma

For decades, the media glamorized smokers as cool, rebellious, or fashionable. (Holly’s cigarette holder from Breakfast at Tiffany’s has even become an iconic accessory.) Even in real life, there were social repercussions when people went out for smoking breaks or smoked in a restaurant. 

Again, the public perception of smoking started to shift after the Surgeon General’s report. The Food and Drug Administration (FDA) made companies print medical warnings of the dangers of smoking on every cigarette pack. In 1971, TV and radio channels banned cigarette ads and showed more anti-cigarette ads that would scare people with graphic images of the effects of tobacco, like people with permanent holes in their neck after contracting smoke-related throat cancer. Medical research on tobacco continued to link cigarette smoking to several preventable diseases and health problems. Lawmakers passed stricter regulations on cigarettes, including a ban on smoking at work and in most public areas. 

Nowadays, most indoor spaces like hotels and theaters don’t allow smoking; instead, people tend to slip out to take a quick cigarette break and spray their clothes down to hide the smell of cigarettes. Vincent Mase, a thoracic surgeon at Yale University School of Medicine in Connecticut, says smoking cigarettes has been more socially unacceptable among younger generations. He says tobacco smoke has become more taboo, too, because of how it affects a person’s hygiene with increased sweating, yellow teeth, and of course, the smell. 

Higher taxes

Smoking is expensive. While varying by state, the average cost for a pack in the US is $8. New York, for example, is the most expensive state to buy cigarettes at $11.96 while Missouri is the cheapest at $6.11. The varying prices come from a combination of state taxes and a federal tax. Increasing the price of cigarettes has helped deter young adults between 18 to 24 years old from pursuing the costly habit. It has also been an effective tactic in getting current smokers to quit, especially Black and Hispanic individuals. “if you look at an area like New York where the cigarette tax is very high, the smoking rate is very low. Compare that to a state like Kentucky, where the tax rate on cigarettes is low and smoking is relatively high,” explains Norman Edelman, a pulmonologist at Stony Brook University in New York. “Although it is falling everywhere, as people realize the deleterious effects of smoking.”

How to drive smoking rates down further

While it’s unlikely we’ll ever have a cigarette-free society, there are ways of pushing the rates as close to zero as possible. 

Banning menthol

Menthol is a chemical found in peppermint that changes how the brain processes taste and pain. It leaves a cool sensation in the throat and airways that acts as a local anesthetic and can mask the irritation cigarette smoke causes to the lungs. Because menthol makes the smoke less harsh, it encourages users to inhale more deeply and might increase exposure to other toxins such as carbon monoxide. While almost all cigarettes sold in the US have menthol, those with higher quantities are marketed as menthol-flavored.

Another concern with menthol is that it can increase cigarette addiction. Several studies found menthol stops the breakdown of nicotine, letting the stimulant exert its effects for longer. Enhancing the addictive effects of nicotine makes it harder for people who use menthol-flavored cigarettes to quit. In 2022, the FDA proposed a nation-wide ban on menthol-flavored cigarettes to curb its appeal—the decision is expected to be handed down later this year. 

[Related: The environmental argument for banning menthol cigarettes]

Edelman says there’s no question that menthol should be banned—but he’s not sure how much it would help curb smoking rates across the US. Canada’s experience in banning menthol-flavored cigarettes from 2015 to 2018 may provide some idea on what to expect. A 2022 study in The BMJ found that after the ban, chronic menthol smokers were more likely to stop smoking daily than non-menthol smokers. The authors estimate a similar prohibition in the US would help 789,724 daily smokers break the habit.

Increase on federal taxes

The current federal tax on cigarettes is $1.01 per pack. This reflects the latest increase in 2009 where federal taxes were raised to 62 cents a pack. The American Lung Association has advocated matching federal taxes to the rate of a state’s cigarettes tax to not only make cigarettes less affordable, but also increase funding for tobacco prevention efforts. 

Less smoking, but more vaping

The same CDC survey reporting a decline in smokers has also found a rise in e-cigarette users. In 2022, 6 percent of people in the US use an electronic cigarette or other electronic vaping product—a 1.6 percent jump from 2019.

The first e-cigarette was invented in 2003 as a less harmful and smelly alternative to traditional cigarettes. These battery-operated devices have since grown in popularity, especially among older kids. Not only are they more affordable than cigarettes—the average cost for a disposable e-cigarette is $8.01 and e-liquid cartridges are $6.83—but they come in appetizing flavors like mint, strawberry, cotton candy, bubblegum. Like menthol, the different flavors mask the harsh taste of smoke, which allows users to take more puffs. 

Mase says younger crowds prefer the product because of several common misconceptions surrounding e-cigarettes. A 2017 study surveyed adolescents on their attitudes towards vaping. About 19 percent of high schoolers believed e-cigarette smoke is water, 23 percent though e-cigarettes was not a tobacco product, and 43 percent thought they were safer than cigarettes. Mase warns that a number of short-term studies have linked vaping to respiratory symptoms and lung damage in adolescents. Last month, several state attorney generals reached a $462 million settlement with top e-cigarette brand JUUL for advertising to teens and making false claims that its products were harmless. The FDA also recently ordered the removal of JUUL products from the US market, citing health concerns and insufficient data on the toxicity of the vapes.

[Related: A $25 whistle-like tool could be a game changer for COPD patients]

Unlike regular cigarettes, there are no blanket regulations against vaping products in the US, so users can’t be completely sure of what they’re breathing in. “Every so often we get a rash of people getting sick because they’ve been inhaling something they shouldn’t inhale,” says Edelman. In 2018, there was an outbreak of vaping-related lung injuries and deaths: The culprit was vitamin E acetate being added to e-cigarettes and other vaping products that contained THC. While vitamin E is safe to consume and apply topically, it can affect a person’s lung function when smoked.

The lungs are one of the few organs in the body that makes contact with the outside environment, says Edelman. Just as shades protect the eyes and sunscreen protects the skin, not smoking is one way to keep lungs healthy and functioning for years to come.

Correction (May 9, 2023): The story previously stated that vitamin E acetate had been added to some cigarettes, leading to lung injuries and deaths in users. The vitamin E acetate was specifically added to THC-containing e-cigarettes and other vaping products.

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A rose by any other name would smell as sweet, as Shakespeare wrote, but erase just one little molecule in their flowers and you’d be lucky to catch a whiff of anything at all. In recent decades, commercial gardeners have bred roses that grow in different colors, are more insect-resistant, and have a longer vase life. But that manipulation has a trade-off: more visually appealing flowers often lose their strong aromatic fragrances. 

What do roses need to make their pleasant odors, and more importantly, how do we get them back? A new study published Monday in PNAS identified a key enzyme called farnesyl diphosphate (FPP) synthase, crucial for driving the reaction that creates a rose’s fresh and floral scent. The findings could help with finding a way to create more mesmerizing and beautiful roses. 

A chemical called geraniol is responsible for the sweet scent we associate with roses. Roses make the compound through a chemical reaction that involves FPP synthase plus several other enzymes. The process involves NUDX1 hydrolase, an enzyme found in the liquid interior of plant cells, or cytosol, that make up the rose petals. To create a strong and sweet aroma, flowers need a ton of NUDX1 hydrolase activity. This is only possible when there is enough of a binding molecule called geranyl diphosphate (GPP). GPP glues to the enzyme and propels it into action. 

[Related: 7 edible flowers and how to use them]

But in order for this process to work, the binding molecule needs to be nearby. This isn’t the case for roses. Senior author Benoît Boachon, a plant biochemist at the French National Centre for Scientific Research, says most plants keep GGP and NUDX1 hydrolase in another area called the plastids. These organelles act as key sites for photosynthesis. This motivated Boachon and his colleagues to figure out where roses get the GPP to make geraniol. He hypothesizes that GPP could have some mechanism transporting it from the plasmid to the cytosol, or there’s another pathway for the flower to generate its own supply of GPP. 

To solve the plant mystery, the study authors studied the biochemical reactions that take place in a variety of pink roses called Old Blush. They isolated different plant parts and shut down chemical pathways involved with the creation or release of geraniol. If the altered roses no longer made geraniol, or the plants produced it in low amounts, that was a major clue to the scientists—they’d found a pathway that plays a role in supplying GPP. On the other hand, the team could rule out a process if geraniol continued to be made at normal levels. 

Their search led them to a particular pathway in plant cytosol–where they took interest in a second, unknown role of the FPP synthase protein. When inhibitors blocked the plant’s ability to express this enzyme, it decreased geraniol levels.  

[Related: How to preserve flowers in 4 easy ways]

The enzyme was found to create two chemical compounds. Plant scientists have known that it makes a chemical related to GPP, called farnesyl diphosphate, which contributes to a rose’s sweet smell. But the study’s biochemical analysis reveals the enzyme is capable of producing GPP as well. Natalia Dudareva, the director of the Center for Plant Biology at Purdue University and one of the coauthors of the study, says that roses must have evolved FPP synthase long ago to produce more readily available GPP. Protein sequencing of the enzyme revealed two amino acids that may have mutated to allow it to produce GPP instead of converting all the GPP to farnesyl diphosphate.

The next step was to see if the FPP synthase enzyme produced similar effects inside a plant in real time. They engineered tobacco leaves to express this enzyme and the chemical pathway used for making geraniol. As they expected, the tobacco leaves where they found the enzyme produced both GPP and farnesyl diphosphate.  

Understanding the essential players involved in fragrance-making could restore the aroma of commercially grown roses. And by isolating the enzyme, Boachon says one potential application is to metabolically reintroduce the sweet fragrance into roses that have lost their iconic smell over time.

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Three years ago, Nancy Klimas sat in an auditorium waiting to discuss her latest research progress. The audience was made up of the usual suspects at a scientific conference: doctors, scientists, and other academic colleagues. But this group was a bit different. The room was also packed to the brim with retired US veterans, all waiting to hear about any new developments over a “moonshot” idea that could be the closest attempt to a cure for Gulf War illness. 

Klimas, who serves as the director for the Institute for Neuro-Immune Medicine at Nova Southeastern University in Florida, has been studying this debilitating condition for three decades. The strange sickness affects 175,000 to 250,000 soldiers who were deployed in the 1990-1991 Persian Gulf War. For those veterans, nearly half of who are pushing 50 or above, life has been an uphill battle. There is currently no cure for Gulf War illness, and because it involves a cluster of symptoms—fatigue, joint pain, diarrhea, memory loss—attempts to treat it have come up short. “These people served our country and put themselves in harm’s way,” says Klimas. “Now they’re sick with a chronic illness that ruined their quality of life and ability to work for more than 30 years.” Exhausting her options, Klimas came up with a rather unconventional idea: use a well-established abortion drug to reset the body’s overwhelming response to chronic illness.

[Related: The PACT Act will take the burden of proof off US veterans exposed to burn pits]

Mifepristone, more widely known as the abortion pill, is capable of treating multiple illnesses. At low doses and when paired with another pill, misoprostol, the synthetic steroid binds to a protein in the uterus and stops the release of progesterone and other hormones needed to sustain pregnancy. But the drug has another effect, which Klimas is looking to tap. When taken at higher doses, mifepristone also blocks hormone receptors in the adrenal gland, which regulates the body’s stress response. The drug has already proven capable of doing this, and is currently approved as a treatment for the metabolic disorder Cushing’s syndrome. 

Based on that evidence, Klimas wondered if the medication could temporarily block the adrenal gland and rebalance the hormone signals that are blunted with Gulf War illness. Repurposing the FDA-approved drug would also save the 10 to 15 years it would take to develop and test a brand-new drug. Klimas is halfway through her phase 1 trial testing the safety of the drug at different dosages on veterans, and is making plans for the second phase of the study. 

The recent legal mess surrounding mifepristone access threw a wrench in Klimas’s plans, along with those of other researchers using mifepristone in their work. In early April, a federal circuit judge in Texas overturned the FDA’s 23-year-long approval of mifepristone, citing claims that the drug is unsafe for public use because abortion is now illegal in some states. And while the Supreme Court blocked the ruling that would have suspended mifepristone access across clinics, pharmacies, and mail orders, the future of the treatment remains uncertain in the US. “Obviously, we’re very concerned,” says Klimas, adding that mifepristone was already hard to get for research purposes. “Attempts to limit access to this drug has already had a splashback on the veteran population in these trials, as we’re delayed in rolling things out. How long will they have to wait for an effective therapy?”

Further constraints on mifepristone could impact medical progress on many other diseases and conditions as well. The medication is being studied as a potential treatment for diabetes in people without Cushing’s syndrome. It has also shown some potential in preventing weight gain caused by antipsychotic medication. Some ongoing clinical trials have found that mifepristone can be effective in slowing down the spread of breast cancer: The drug blocks progesterone receptors from releasing the hormone, which would normally stimulate tumor cell growth. And at different dosages, the pill can improve the quality of life of people dealing with painful uterine growths.

[Related: Abortion bans are impeding access to ulcer, arthritis, and cancer medications]

Banning mifepristone goes beyond stalling research—it puts any FDA-approved treatment at risk of being recalled. “You have a medication with an excellent track record of safety, efficacy, and high patient satisfaction,” says Carrie Cwiak, an OB-GYN at Emory Healthcare in Georgia. “The idea that the entire process for approving medication can be overturned [in court] is earth-shattering.” She says that restricting mifepristone opens a dangerous door to having people with legal power make treatment decisions based on their opinion and ideology rather than medical evidence. 

If the courts decide to bar or limit mifepristone use down the line, it would discourage pharmaceutical companies from spending money on producing new drugs that appear controversial. That could include contraceptives, hormone blockers, or treatments completely unrelated to reproductive issues. “If you were a pharmaceutical company and it was going to cost you $20 million to move a pipeline drug all the way up through phase three [clinical trials], would you want to invest the money for it if it’s possible the bench could reverse the authority of the FDA?” Klimas asks. 

Despite the setbacks on mifepristone access and potential legal battles, Klimas is optimistic that the research she is doing will help give veterans their long and overdue treatment. Her team is hoping to start their phase 2 trial soon and get as many results before politics interferes in science again. 

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Humans and chimpanzees share a common ancestor, but 4 to 6 million years ago they split off on different evolutionary paths. Chimps continued to walk on all fours and live in trees, while we lost our fur and grew past the need for a tail. But it was our large brains that set us the most apart from our closest relatives. The human brain (about the size of 10 tennis balls) is three times bigger than a chimp’s.

There are multiple theories for why we evolved large and complex brains. Some evolutionary biologists think humans developed bigger bodies as a response to environmental pressures such as living in open, unforested habitats that required more cooperation and thinking to catch prey. Others speculate our brains needed to grow to handle the information needed to manage social relationships. And in a new study published in Science today, geneticists offer a third explanation: We just got lucky.

Lead author Katie Pollard, the director of the Gladstone Institute of Data Science and Biotechnology in California, likes to think of it as rolling dice. Every time another member of a species is born, there’s a chance that mutations will spring up in their genome. Each new generation gets more opportunities to score big with tweaks in the gene pool that increase the odds of survival. These beneficial mutations are more likely to stick around as organisms thrive and pass them on to offspring. In the case of humans and brain size, eventually, the buildup of mutations would be reflected in changes in the overall genome, Pollard says.

These random mutations could have contributed to the 49 short DNA sequences in our genome called human accelerated regions (HARs). Pollard and her team were the first to find these segments back in 2006 when comparing the genomes of humans to chimpanzees. HARs work as gene enhancers, controlling which genes are turned up or down during embryonic development, especially for brain formation. 

[Related: Eating meat may not have been as crucial to human evolution as we thought]

HARs in humans are very similar in each individual but vary when compared to accelerated regions in other vertebrates like chimps, frogs, and chickens. Since the initial discovery, research has found a connection between HARs and multiple traits that make our species distinct. And while Pollard has spent a lot of time understanding how HARs helped humans evolve, the current study focuses on why HARs emerged in the first place. 

The team collected data from 241 mammalian genomes (in concert with the larger Zoonomia project) and identified 312 accelerated regions across all of them. Most of the accelerated regions identified acted as neurodevelopmental enhancers, indicating a connection to brain development. But when comparing human and chimp DNA sequences, 30 percent of HARs were in areas of the genome where the DNA was folded differently. This suggests the structural variations in the human genome likely came from a random mutation during reproduction. “Mutations happen all the time and everytime sperm and eggs get made, there are some mistakes that cause cuts, deletions, and other edits to the DNA,” explains Pollard. “Many of the mutations don’t make any difference, but now and then some have a positive effect and that’s actually very rare.” 

In this case, scrunching and folding up DNA in different ways seemed to help with fitting a copy of the genome in every cell of the body. “It’s a big surprise that genome folding is involved since it hadn’t been on anyone’s radar when studying human accelerated regions,” says Pollard. “We had been thinking of DNA as a text file in a big folder full of A, C, T, and G’s, and looking for patterns as you move linearly through the sequence.”

The folding change would have affected how enhancers regulated gene activity in early humans. Depending on how the DNA was folded, enhancers could have been situated near new sequences, giving them different genes to target and boost. In humans, it just so happened that most of the adjacent genes were involved in brain development. In other words, we won the mutation lottery.

“The main achievement of this study is the discovery that the evolutionary history of HARs is connected in some way with the complex dynamics of structural configurations of the human genome,” says Anastasia Levchenko, a genetic researcher for the Institute of Translational Biomedicine at Saint Petersburg State University in Russia who has previously studied HARs’s role in brain development. However, she would like to see more research on the sequence of events in the evolution of the human genome. For example, it’s possible that HARs appeared way earlier than the changes in our DNA folds, or that DNA folding is only one factor contributing to the creation of HARs.

[Related: This is the most complete map we have of the human genome]

What’s more, humans might have used other genetic pathways to develop different features from other animals. Pollard’s study is one of 11 papers published in Science today as part of the Zoonomia Project, an international collaboration that aims to understand the codes behind shared and specialized traits across hundreds of mammalian species. For example, Zoonomia researchers identified the distinct parts of Balto’s genome that helped the sled dog deliver a serum to a remote Alaskan village, as well as genetic variants in early humans that could play a role in modern-day diseases. Another paper focuses on using information from DNA to predict which species are more likely to face extinction. All together, identifying the different genomes will open the door to understanding mammalian evolution and what exactly makes us uniquely human. 

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Ozone is like Earth’s natural sunscreen, protecting living things from the sun’s harsh UV rays. But this sunscreen is running out. Greenhouse gases are thinning out the ozone layer, and our skin is starting to pay the price. According to the World Health Organization, losing an extra 10 percent of ozone levels will cause an additional 300,000 non-melanoma and 4,500 skin cancer cases.

With skin cancer as the most diagnosed cancer in America, the US Preventative Services Task Force (USPSTF) updated their screening recommendations earlier this month, emphasizing the need for people to get moles and other spots checked early for potential tumors. 

The quicker skin cancer is caught, the better your chances of recovering from it. And recent technological advances in skin cancer research is transforming the way doctors and patients approach this deadly disease. Here are five tech tools to keep an eye on.

Therapeutic skin cancer vaccine

As multiple companies experiment with cancer vaccines, Merck and Moderna are focusing theirs on melanoma. Their phase II clinical trial results, shared last week, showed a 44 percent decrease in risk of death or a melanoma relapse when pairing the vaccine with the immunotherapy Keytruda. Additionally, about 79 percent of people who took the vaccine plus immunotherapy stayed cancer-free for 18 months compared to the 62 percent who just took immunotherapy. The data shows enough promise for the companies to start a Phase 3 trial in adjuvant melanoma this year, and could compel them to rapidly expand the vaccine to other tumor types, including non-small cell lung cancer, Eric Rubin, a senior vice president at Merck, wrote in an email.

[Related: A vaccine trial targeting the most lethal breast cancer just took its next step]

The vaccine isn’t a preventative treatment, but is instead given to melanoma patients early in recovery. The researchers take tumor samples from biopsies and identify which proteins are most likely to be recognized by the human immune system. They then make a personalized mRNA vaccine (adapted from the technology behind Moderna’s COVID jab) using a certain number of these abnormal genes to boost an individual’s adaptive immunity. If the rest of the trials go as planned, the vaccine could be available as soon as 2025 or early 2026, says Eric Whitman, the medical director of Atlantic Health System’s oncology service line.

Genetic tests and personal risk scores

Precision prevention is when doctors use multiple tools to map out a person’s risk of cancer and use that assessment to tailor their treatment and risk-reduction strategy. Instead of following a standard guideline like an annual dermal exam, a person who is considered high-risk (like someone with a history of skin cancer) may need more frequent screenings and extra body imaging, says Meredith McKean, the director of melanoma & skin cancer research at the Sarah Cannon Research Institute in Tennessee. People with very low risk, on the other hand, may be encouraged to learn how to do their own self-checks at home. McKean adds that it’s really helpful “to stratify patients and really help them do the best that we can to prevent another melanoma or skin cancer [case].”

Genetic tests can also be used to identify people with a predisposition to skin cancer. A 2022 study in the journal Cancer Research Communications found that people who were told they had a MC1R mutation, which carries a higher risk for melanoma, made more of an effort to protect themselves against the sun and get regular skin checks. Some doctors even use AI technology to a personalized risk score for individuals based on photos of skin lesions and moles.

Melanoma sticker

The Dermtech SmartSticker is an easy precursor for checking suspicious moles for melanoma. A dermatologist places four skin patches on the potential tumor for less than five seconds, and ships the sample to a Dermtech lab in San Diego, California. The lab then tests for DNA from cancerous cells. If the results come back positive, the dermatologist would follow up with a biopsy. If not, this painful step can be avoided and the doctor would just continue clinically monitoring the patient. 

“It’s a very good test. If it comes up negative, there is a greater than 99-percent reliability that the mole is not melanoma,” says Emily Wood, a dermatologist at Westlake Dermatology & Cosmetic Surgery in Texas. She adds that patients in her clinic favor the stickers over biopsies because they’re painless, cost-effective, and quick. “We’re going to save lives in catching melanoma earlier. I think this will make a dramatic impact for patients long-term.” While the studies are ongoing, there is research suggesting the tool could extend to detecting non-melanoma skin cancer. 

Artificial intelligence apps

Medical researchers are now training computers to recognize patterns and atypical features associated with skin cancer. “AI picks up a lot more subtle changes than the naked eye,” says Trevan Fischer, a surgical oncologist at Providence Saint John’s Health Center. The high accuracy in AI deep learning can help doctors determine whether a mole is malignant and worth biopsying—saving patients from some unneeded discomfort.

The beauty of AI is that you can do a full home skin exam with a press of a few buttons. Popular smartphone apps like MoleMapper lets users upload a picture and have it analyzed for potential skin lesions. They also let you store photos to show your doctor and keep track of any changes to your mole. (Wood warns that a smartphone app is not meant to substitute in-person skin check-ups with your doctor.)

While these apps are useful, there’s always room for improvement. For example, the AI’s accuracy goes down when the view of the mole has shadowing, blurriness, hair, or if the image is rotated. There’s also been research showing that AI databases lack images of darker skin types that would teach the system to better detect skin cancer from people of color. If anything, Wood says the apps can encourage people to submit photos of suspicious moles and start the conversation early with their doctor. 

Millimeter wave imaging 

The same technology used in airport security scanners is getting revamped and used to detect skin tumors. Millimeter wave imaging is a non-invasive method and a low-cost alternative to biopsies that works by scanning a person’s skin for any biochemical and molecular changes related to a disease or disorder. The radio waves reflect differently when looking at benign versus cancerous moles. 

[Related: Everything you need to know about UPF sun protection]

While the approach is not yet available for clinical practice, there is evidence backing up the proof of concept. A 2017 study in IEEE Transactions on Biomedical Engineering found considerable differences when looking back at the scans of healthy skin and those for two common skin cancer types: squamous cell carcinoma and basal cell carcinoma. The study authors could see detailed changes in water molecules, glucose concentrations, and protein levels. A 2018 study in the same journal used ultra-high resolution millimeter wave imaging to identify early-stage skin cancer. Most recently, the diagnostic tool was studied on 136 people suspected of skin cancer. Ultimately, it found malignant tumors from various types of skin cancer on 71 patients, giving the tech a “high diagnostic accuracy.” 

“We’re really trying to leverage all the different ways that advanced technology can help us diagnose and treat skin cancer like melanoma,” Whitman from Atlantic Health Systems says. He emphasizes that most of these strategies weren’t imaginable 10 years ago. Using data to improve on existing AI technology and create new models for personalized medicine, he notes, “can really make a difference for people and their lives.”

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Northern elephant seals are challenging the world record for the mammal that sleeps the fewest hours a day. The current record holder is the African elephant, who rests a measly two hours daily. Now scientists report that elephant seals also sleep an average of two hours a day when they’re out at sea and do this by splitting their slumber into a series of nap-like “sleeping dives.” 

These findings were published today in the journal Science. 

Elephant seals divide their time between land and sea, though it’s unequal. They spend an average of seven months out of the year in the open ocean and only resurface to breed, molt, and rest. Because they spend so much time in open waters, scientists figured these marine mammals must have developed some way of getting the sleep they need while avoiding detection from predators like the orca whales and great white sharks. But exactly how they do this has been poorly understood.

[Related: Take the best naps, with science]

One challenge in understanding the sleep behavior of elephant seals is finding a device that’s both waterproof and can handle deep-sea pressure. To overcome this, the study team created a flexible head cap that can respond to seals’ twisting and flexing motions. It’s also made up of a synthetic rubber called neoprene, the same material found in wetsuits. The scientists used this cap to monitor the seals’ brain activity, heart rate, and three-dimensional spatial movement.

Scientists outfitted 13 wild seals with the cap. Five were kept in a lab, while the other eight could freely roam around Monterey Bay, California. The EEG recordings collected from the head cap represented brain activity during different sleep stages. 

“We can take the data and use it to recreate what the sleeping dives look like, and also what’s happening within the animal brain, how fast its heart is beating, etcetera,” says lead study author Jessica Kendall-Bar, a Scripps postdoc scholar at the University of California, San Diego.

How do seals sleep in the ocean?

The collected data indicates elephant seals sleep about two hours a day while at sea, though not all at once. When it was time to get a little shut-eye, seals dove hundreds of meters below the surface—the maximum depth was about 1,200 feet—where they would take quick naps lasting less than 20 minutes. 

Kendall-Bar says this “degree of flexibility and sleep duration has really only been demonstrated in birds and is pretty much unprecedented in mammals.”

Dive naps likely evolved as a way for seals to avoid getting attacked since their natural predators lurk near the surface, explains Kendall-Bar. They are also more vulnerable than other marine mammals when resting because they undergo bilateral sleep. This means both halves of the elephant seal’s brain rest when they sleep. Human beings also experience bilateral sleep. 

Meanwhile, fur seals and sea lions experience unihemispheric sleep—one brain hemisphere rests while the other stays awake and monitors for predators.

Different stages of underwater sleep

The study data suggests seals go through one complete sleep cycle during each nap-like “sleeping dive.” When these brief sleep cycles end, the seals return to the surface. This process allows them to rest at depths with lower predation risk while staying vigilant in more dangerous waters. 

During nap dives, the seals entered slow-wave sleep while maintaining an upright posture. They then turned upside down while their sleep cycle transitioned from slow-wave sleep to rapid eye movement (REM) sleep. 

“The sleep state of the animal is actually reflected in its movement through the water,” explains Kendall-Bar. 

Once the cycle was complete, the seals immediately woke up and returned to the surface to find food.

[Related: Pendulums under ocean waves could prevent beach erosion]

Since muscle paralysis from REM sleep leaves seals exposed and defenseless, they took the shortest naps possible and compensated for the lack of sleep after reaching land again. As a result, the seals slept five times longer ashore than they did in the water. Some seals even slept up to 14 hours a day on land.

“What really stood out for me is the fine-scale analysis the researchers did to identify the different sleep states and how they were able to translate this analysis to estimate sleep patterns in seals at sea,” says Cassondra Williams, a comparative physiologist at the National Marine Mammal Foundation who was not involved in the study. “This will be an important tool for future behavior studies of pinnipeds freely diving at sea.”

Most diving naps took place just near the shore. While northern elephant seals are not currently endangered (in the 1800s, they were almost hunted to extinction), Kendall-Bar and her team are concerned that shipping traffic and traps on the seafloor may be disturbing their habitats. Understanding when and where seals slumber could help conservation efforts and ensure seals get all two hours of their beauty sleep.

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In early April, Cook Children’s Medical Center in Texas sounded the alarm on a possible surge in infant deaths. Since January 2022, the hospital reported 30 mortalities stemming from unsafe sleeping situations. And while the cause of death may not have been the same for every baby, most involved sharing a bed with a caregiver.

“We’re doing a better job at identifying what the causes are,” says Susan Katz, a nurse practitioner and the infant apnea program coordinator at Stony Brook Medicine in New York, about the report. In regards to bed-sharing, she and other experts say that though there are many reasons why parents might end up sleeping with their newborn, it’s never recommended. “The scream of a mom or dad who’s lost their baby because of something like bed-sharing outweigh any benefits,” adds Gina Posner, a pediatrician at MemorialCare Orange Coast Medical Center in California.

[Related: How to get your kids on a healthy sleep schedule]

About 3,500 babies in the US die each year from sleep-related incidents, including from suffocation and sudden infant death syndrome (SIDS). Bed-sharing increases the chance for these fatal events. And while the number of sleep-related infant deaths has gone down since the 1990s, reports like the one from Cook Children’s Medical Center are a reminder that there’s still work to do in preventing these accidents. 

Why is sleeping in a bed with a baby dangerous?

First off, babies need to lie on firm surfaces, like a crib pad, says Posner. A soft adult mattress can be harmful because it conforms to the shape of the baby’s head, creating pockets of space that can cover their nose and mouth if they turn over in their sleep. A 2019 study published in the journal Pediatrics reported 14 percent of SIDS cases were from suffocation. Of these, 69 percent of the suffocations were from regular mattresses.

Bed sharing also exposes infants to other soft materials like pillows and blankets that can easily smother children, explains Posner. What’s more, pillows that are slightly elevated can force a baby’s head down so their chin rests on their chest. This position can block the baby’s tiny airways and make it hard for them to breathe. The American Academy of Pediatrics warns that any surface inclining over 10 degrees is not safe for a baby.

Another danger is the adult itself. A lot of accidental deaths happen when a caregiver rolls over on a baby, pins the baby down under blankets, or traps the baby between a wall and a bed. “I’ve seen even the best of parents who are just exhausted accidentally suffocate their child,” says Posner.

Is there any way to make bed-sharing safer?

There are multiple reasons why people might want to sleep in the same bed as their child. For example, some caregivers find that infants sleep better when next to them. “Sometimes [the babies] really do,” explains Posner. “They were inside you for nine months and it can be a hard transition to be outside.” Other parents might do it for the convenience of breastfeeding and immediately getting to go back to sleep. For sleep-deprived adults, a few extra minutes of sleep matter.

But both Katz and Posner say there’s no way to keep your infant completely safe when bed-sharing and caution against it, at least until the child turns one. The American Academy of Pediatrics also doesn’t recommend bed-sharing with infants “under any circumstance,” and recommends other alternatives.

How to practice safe sleep

Instead of bed-sharing, Katz advises caregivers to keep the baby’s crib or bassinet in the room that they’re sleeping in. Room-sharing might make it easier to breastfeed; if you prefer to do it in bed, Katz says there should be another support person awake and keeping eyes on the baby to make sure no one accidentally falls asleep.

One downside to room-sharing is that babies—and by extension, caregivers—don’t sleep well. A 2017 study in the journal Pediatrics found that infants who slept in separate rooms from their parents before the age of four months rested longer than those who shared a room (and got fed more throughout the night). The solo-napping babies also slept up to 100 minutes longer at the age of nine months. 

[Related: Improving your baby’s bone health starts in the womb]

The idea of losing a few winks might make room-sharing an unappealing option. However, waking up from your baby’s cries could be a way of making sure they’re protected against SIDS. A 2014 study in the journal Acta Neuropathologica found that nearly 42 percent of infants who died from SIDS—which includes causes beyond bedsharing—had brain abnormalities that affected the hippocampus, an area in charge of controlling breathing and heart rate during sleep. Spending the night in the same room but in different sleeping areas gives adults the opportunity to check on babies and ensure there are no hazards nearby that would compromise their breathing. 

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Sitting for too long is harmful to your health—even if you don’t feel it at the moment, your body will remember. Staying motionless for at least four hours has been linked to an increased risk of blood clotting in humans. 

But there are some exceptions. People with permanent paralysis don’t show an elevated risk for blood clotting while those who are temporarily immobile—like being stuck in a hospital bed or in a cramped airplane seat—are more susceptible to clot formation. 

A new study published today in the journal Science probes this blood-circulation question in brown bears, a species known to withdraw in their dens for five to eight months out of the year and emerge clot-free. Hibernating bears avoided blood clots by reducing a protein in their body that triggers the blood clotting process. Humans also have this protein, it turns out, and can regulate it under certain circumstances.

[Related: Scientists stuck grizzly bears on treadmills and confirmed they hate hills as much as we do]

“I would have never thought to go to bears, but it’s an excellent idea to turn to nature for studying human biology,” says Mirta Schattner, the director of the Instituto de Medicina Experimental del CONICET in Argentina who wrote an accompanying perspective piece on the study, but wasn’t involved in the research. 

An international team led by scientists from Ludwig-Maximilians-University of Munich ran tests on brown bears and people who have long-term mobility issues to compare anti-clotting strategies. They collected blood samples from 13 free-ranging brown bears during hibernation and again when they were awake during spring. When analyzing the contents of the blood samples, the authors noticed hibernating bears showed more signs of an anti-clotting mechanism. It worked by lowering several protein levels, including heat shock protein 47 (HSP47), which regulates immune responses. Reducing HSP47 tamps down inflammation that would have otherwise started the process of blood clotting.

To see if chronically immobilized humans have a similarly helpful reaction, the authors extracted blood from 23 people with spinal cord injuries and compared it to the blood of 23 able-bodied adults. Just like with the hibernating bears, people with spinal cord injuries showed a decrease in HSP47 levels and fewer clumped platelets that form clots. 

The similar process in bears and humans suggests prolonged immobility is the trigger that switches on the anti-clotting strategy. In situations where you might be bedridden for only a couple of days, Schattner says the inflammatory proteins are more powerful than this protective mechanism. “It would be interesting to know if it’s worth blocking the clotting mechanism in patients with acute immobilization,” she theorizes. “It’s a new pharmacological target to access.”

[Related: Heart disease-related deaths rise in extreme heat and extreme cold]

Anti-clotting mechanisms are one of many adaptations biologists can study from bear hibernation. The ursine body has developed different tactics to remain dormant throughout the winter without waking up to a horde of health problems. For example, bears use their fat to break down energy without reducing their muscle mass. They also limited the renewal of damaged bone cells to prevent osteoporosis in their sleep. Another feature includes changing biological processes like heart rate when entering hibernation. Studying how bears lower their heart rate for months at a time could help doctors better understand the mechanisms that drive cardiac diseases in humans.

But the opportunity to look at these body-regulating strategies might be short-lived. Warmer temperatures and shorter winters from climate change are affecting bear hibernation patterns, says Heather Johnson, a wildlife biologist for the United States Geological Survey Alaska Science Center who was not involved in the study. “We’re seeing that bears are hibernating for a shorter period and having longer active periods.” The warmer winters signal to bears that there is less of a need to sleep when the conditions are fine to go foraging for food. 

There have also been a few anecdotal observations of bears not needing to hibernate at all, for example, because they have access to human food all winter. Johnson says that while it’s too soon to predict how climate change will affect bear survival, we are already seeing indirect effects by having more bears awake during open hunting season and getting into more conflicts with humans. As bears adjust to the changing climate, there’s no telling how their bodies will adapt. The anti-blood-clotting mechanisms they have today may be gone tomorrow—a disadvantage for the animals and a loss for potential thrombosis treatments.

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Picture this: You’re at your desk working on a project when your phone chimes. A quick glance tells you a friend sent over a video on TikTok. Convinced you’re due for a break, you click the link to find a new dance video from Charli D’Amelio. Fast forward an hour later, and you’re still on your phone, except now you’ve gone from viral dances to animal videos to fitness gurus raving about a weight loss hack. 

If this scenario hits too close to home, you’re not alone. Most people on social media check it daily, and younger people are likelier to return to their favorite platforms multiple times a day. TikTok is especially popular with teenagers: A 2022 survey from the Pew Research Center suggests 67 percent of teens use it, while 16 percent use it almost constantly. 

So why do people spend so much time online? One underlying reason is that platforms like TikTok promote infinite scrolling. You might start off in one video only for the page to continuously load a never-ending stream of content. Absent-mindedly scrolling through content might seem like an innocent activity and a great excuse to waste time. However, research suggests it can negatively influence the brain and mental health.

Anyone can fall prey to mindless scrolling. Younger people are especially vulnerable since the brain is not fully developed until age 25, says Lisa Pion-Berlin, a psychologist and president of Parents Anonymous, a child abuse prevention nonprofit. While limiting access to social media (like this Utah bill requiring parental permission is trying to do) is one option, learning how to be a more active user can help anyone stop infinite scrolling and still enjoy social media.

Why infinite scrolling is bad for you

Social media platforms like TikTok are not comprehensively bad for you. Several studies suggest social media can prompt feelings of connectedness and positive well-being. Further, they allow for personal expression, which fosters positive mental health.

Ultimately, how social media makes people feel depends on how they use it. For example, excess social media use is associated with feeling more anxious, lonely, and generally bad about yourself. 

“The more attached we are to our devices, the more problematic it becomes,” says Lisa Strohman, a psychologist and the founder of Digital Citizen Academy, an education program that teaches children and teens how to have a healthy relationship with technology. 

[Related: Do you never feel FOMO? Time to meet its twin, JOMO.]

Moreover, Strohman says watching pictures and videos of everyone living their best life might make you worried or sad that you’re missing out. Some research suggests that comparing yourself to others on social media can result in aggression and anxiety, while other studies suggest a link between negative comparisons on social media and suicidal ideation.

Meanwhile, mindless scrolling can result in a state of mind similar to being in a trance state, says Pion-Berlin. She’s concerned that “mindless scrolling is a way to tune out” or dissociate from reality. Some research suggests that overuse of social media can result in negative psychological impacts: A 2023 study in the journal JAMA Pediatrics found that middle schoolers who constantly checked their social media feeds showed changes in how their brains responded to feedback and criticism from peers.   

Infinite scrolling can also lead to disrupted sleep patterns in adolescents and adults. The screen’s blue light can make it difficult to fall asleep, and the constant content prevents your brain from shutting down for the night. 

When we sleep, the brain sorts through and categorizes the information from the day and commits the vital stuff into long-term memory, explains Strohman. But mindless social media surfing before bedtime keeps giving it more data for the brain to process throughout the night, “and that’s what tends to lead to that insomnia,” she explains.

How infinite scrolling can hijack the brain

Mindless scrolling helps make social media an addicting habit because it takes advantage of the brain’s reward system, says Strohman.

An enjoyable TikTok, for example, can trigger the brain’s reward pathway. Subsequently, this causes the brain to release a chemical called dopamine, which Strohman describes “as a hit or a high” for the brain. The dopamine surge tells the brain that scrolling through social media is pleasurable and that we should do it again. Because another attention-grabbing Tiktok plays immediately when the first is over, this process starts all over again immediately. 

“The brain is rewarded every time because of how the feeds and algorithms are set up so that anytime we’re not on the app, we think we’re missing something,” explains Strohman. “That makes us want to go back on it again.:

The same process applies to adolescents—possibly to a more significant effect. Pion-Berlin explains that because the prefrontal cortex is one of the last brain areas to mature fully, younger people are more impulsive and have less self-control than adults. With less self-control, it may be easier for teens to fall into this rabbit hole of social media content, she says. In addition, the limbic system—a part of the brain involved in behavioral and emotional responses—is also more sensitive during our teenage years, which makes them likelier to prioritize pleasurable and desirable activities.

What are some ways to stop infinite scrolling?

While infinite scrolling isn’t great, that does not mean you need to quit social media altogether. On the contrary, there are some benefits to staying on the apps, such as building communities among people with a shared hobby or interest, maintaining relationships with family who live miles away, raising awareness for a particular cause, and learning from credible experts.

[Related: All the ways you can reduce screen time across your devices]

To make the most of your time, you’ll want to become an active rather than a passive user. Active users interact with others— in practice, this could look like commenting on posts or creating content. The high engagement gives you a specific purpose for being on the app, allows you to nurture and maintain online friendships, and is associated with improved well-being. 

Meanwhile, infinite scrolling is a passive activity because you’re socially disconnected from others and lurking in the background. Of course, sometimes you just want to take a break from life and watch some mind-numbing videos. In these situations, you’ll want to set a timer to limit the time you spend online and know when it’s time to log off, Strohman says. 

Another suggestion from Strohman is turning off notifications. People often fall into mindless surfing when notified or tagged in something. And while you might start out looking at the relevant post, you can easily find yourself lost in a comment thread or other recommended videos. 

“Have a clear purpose when accessing social media,” Strohman says. If a friend shares a post, tell yourself you will only watch this one video and not spend the next two hours on TikTok. 

“The more you scroll, the less settled you’ll be,” advises Strohman. “Be mindful, recognize your part in it, and try to do what you can to manage yourself in those online worlds.”

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When it comes to tackling the opioid crisis in America, there is no single solution. Public health officials have taken measures to prevent future overdoses by reducing the number of opioid prescriptions, curbing the flow of illicit drug trafficking, and raising awareness of the dangers of opioids. But for the three million people already addicted to this class of drugs, the emphasis has turned to a quick-working treatment: naloxone.

It’s possible to reverse an opioid overdose with an injectable or single-dose nasal spray called naloxone (also known by the brand name Narcan). Street drugs and prescription painkillers like heroin, morphine, and codeine target opioid receptors in the brain to induce a pleasurable high. But they can also affect neurons that control respiration, causing a person to stop breathing if they overdose. Naloxone blocks the brain receptors so that the drugs can’t reach them, preventing this deadly side effect. “There are very few things I would call a perfect antidote, but, in this case, Narcan is one of them,” says Ryan Marino, a medical toxicologist and addiction medicine specialist at the Case Western Reserve University School of Medicine. He adds that naloxone works against synthetic opioids like fentanyl.

[Related: At-home test strips for fentanyl are just the first step to preventing overdoses]

In response to the growing number of opioid overdose deaths—75 percent of drug overdose deaths in the US in 2020 involved an opioid—the Food and Drug Administration (FDA) approved an over-the-counter version of naloxone. The decision makes the drug more accessible: People will be able to buy the nasal spray at places like their local pharmacy or gas station without a prescription. But while medical experts have lauded the FDA’s ruling, not everyone is happy with the news. There have been some concerns from the public about distributing naloxone and whether it encourages more drug use. PopSci spoke with medical experts on common misconceptions surrounding naloxone and its safety.

Myth 1: Naloxone encourages people to do more drugs

A common objection to expanding naloxone access is that it acts as a safety net for people with addiction to continue their drug habits with few repercussions. But Kathryn Cunningham, director of the Center of Addiction Research at the University of Texas Medical Branch, says research has shown no evidence that naloxone leads to more drug use. 

A well-known 2013 study in The BMJ journal found the number of opioid-related hospital visits did not increase in communities with programs distributing naloxone and those with less access to the nasal spray. Instead, naloxone helped in reducing the amount of risky drug activity in 19 communities that distributed it to residents.

Myth 2: Naloxone prevents users from getting treated for addiction

Think of naloxone as a fire extinguisher in your house, Marino says. You’ll likely use it if there’s a small blaze. But if you have repeated incidents or if your house becomes engulfed in flames, the fire extinguisher can only help so much. Eventually, you’ll have to call the fire department for help. Simply put, naloxone may actually convince people to find professional help because it gives them more opportunities to seek treatment and rehabilitation later in life. “You can’t seek medical services if you’re dead,” Cunningham explains. 

If there’s any deterrent to getting treatment, it’s the stigma surrounding substance use disorders. Research suggests laws hampering access to care and discrimination from medical professionals against patients with a history of drug use may discourage people from opening up about their addiction. Even when they seek out help, patients have reported being treated as if they were untrustworthy, intimidating, and immoral.

Myth 3: Only medical professionals can use naloxone safely

You do not need medical training to give naloxone to someone who’s overdosed. Marino says the over-the-counter nasal spray that the FDA approved was designed to be easy enough to be used by a child as young as 6. The box also has step-by-step instructions printed on the side. “It comes with this little nasal atomizer,” Marino adds. “You just take it out of the package, put it in someone’s nose, and press the pointer. That’s all there is to it.” If a person accidentally applies naloxone to someone who hasn’t overdosed, it will be benign.

[Related: How to break free of the bystander effect and help someone in trouble]

There is no age limit for being treated with naloxone. You can use it on a newborn with opioids in their system or even a toddler who’s exposed to fentanyl patches. The nasal spray expires after three years, and should be stored in temperatures between 77 and 104 degrees Fahrenheit. Naloxone freezes at temperatures below 5 degrees Fahrenheit, making it unusable until it thaws out.

Myth 4: Naloxone makes users violent

It’s been rumored that the sudden onslaught of withdrawal symptoms caused by naloxone might cause a person to become aggressive or lash out when they gain consciousness. That’s not typically the case. Cunningham says common side effects after treatment include headaches, disorientation, vomiting, and nausea—all of which are temporary, because it’s a short-acting drug. “Withdrawal is not life-threatening,” Cunningham notes. “Not breathing because of an opiate is life-threatening.”

Fact: Naloxone could save many lives if more people have it

The FDA’s decision (which doesn’t mention exact rollout dates) makes it so that anyone can be ready to jump in and prevent deaths from opioid overdoses. Marino says it’s best to think of naloxone as another item in your first aid kit in case of emergencies. “We might tell ourselves that no one in our life is using drugs or going to overdose, but you never want to have a situation where you need it and not have it.”

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IN 1989, Albert Wood and Peter Dunn thought they had unlocked a critical chemical door to treating hypertension and recurring chest pain. The two British Pfizer scientists reportedly created a new drug, named sildenafil, that reacts with a specific protein in muscle cells to allow for increased blood flow to the heart. 

But a few years later, human clinical trials revealed the drug was only effective when given multiple times a day and had a poor reaction with other existing cardiac treatments. What’s more, the blood rush was going to unexpected places in the body in addition to the heart. In one study, a nurse observed that most of the male volunteers were lying on their stomachs in embarrassment. The reason? Erections. Wood and Dunn had inadvertently stumbled upon the medicine that became Viagra. The small blue pill treats millions of people each year with erectile dysfunction, and further research suggests it may prove helpful for nonsexual problems such as pulmonary hypertension and altitude sickness.

Sidenafil is one of many prescriptions that treat multiple unrelated illnesses. How a drug becomes a medicinal Swiss Army knife depends on its chemical makeup. Each dose contains compounds that lock onto specific receptors, but that could also have the ability to create or suppress other reactions in the body.

“When somebody takes a medicine, it doesn’t necessarily go to the exact organ they are trying to target,” says Evelyn Huang, an emergency medicine resident physician at Northwestern Memorial Hospital. “The drug circulates through the entire body, so if there are certain receptors found in different parts, it would also affect that organ.” With sidenafil, the drug enlarges blood vessels generally and happens to prep the penis for action specifically. 

Another pill with the potential to tackle multiple conditions is mifepristone. This medicine is approved by the US Food and Drug Administration for medically induced abortions up to 70 days after a person’s last menstrual cycle starts. It works by blocking the effects of progesterone, which is needed to prepare and sustain pregnancy. (An ongoing lawsuit in a US district court in Texas could restrict its availability in pharmacies, doctor’s offices, and more.) Completely tamping down the hormone could also help prevent pancreatic cancer and melanomas, some early research shows. Additionally, at high doses, mifepristone aids in managing a condition called Cushing’s syndrome—characterized by extremely high levels of cortisol—by plugging the receptor that stimulates the production of sex and stress hormones. 

Dosage also matters in producing different drug responses. For example, barbiturates are a type of sedative prescribed in different amounts for a range of conditions from anxiety to seizures. This class of medications enhances the activity of GABA, a neurotransmitter that can slow down brain activity. At smaller doses, barbiturates can make someone feel drowsy and relaxed. But at higher amounts, they can be used as an anesthetic for rapid loss of consciousness. 

Because of the many ways a drug can affect the body, Huang warns against off-label use—taking a prescription for a condition other than the one it’s designed for. In any case, she recommends going over proper dosing, side effects, and other safety precautions with your healthcare provider. With more clinical and real-world research, it’s possible that off-label medications will be approved to target new health issues, producing formulas that pack more than one punch. Sidenafil, with its exciting possibilities, is at the top of that list.

Read more PopSci+ stories.

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Adulting is hard. On top of paying your bills and rent on time, you also have to factor in childcare, insurance, and student loan repayments, which are set to resume later this year. With inflation raising the cost of living, mass job layoffs, and the threat of a recession, it’s understandable if you feel like you’re spreading your money a bit too thin.

Everyone worries about money—and the lack of it—every once in a while. But constantly stressing out about your finances can manifest into a more debilitating mental health condition called financial anxiety.

 “It’s a fear-driven attitude towards money whether that’s money management or talking about money,” says Megan Ford, a financial therapist, and advisor for the financial wellness app Stackin. Fortunately, there are ways to change your relationship with cash and healthy ways to cope when thinking about personal finances.

About 23 percent of Americans have experienced financial stress at levels that meet the criteria for post-traumatic stress disorder, explains Joyce Marter, a psychotherapist, and author of The Financial Mindset Fix: A Mental Fitness Program for an Abundant Life. The number is even higher among millennials, where it goes up to 36 percent. “It’s very common for people to have symptoms of trauma while dealing with financial stress,” she says.

[Related: How to spend your money for maximum happiness]

Like any mental health disorder, financial anxiety affects your well-being. This condition can leave you feeling overwhelmed and in a state of self-imposed helplessness, here you feel like your actions won’t change the outcome so you give up and avoid it. With your mind preoccupied with money, there is only so much mental space for you to focus on other matters. A September 2022 study published in the Journal of Vocational Behavior showed that people suffering from financial anxiety have lower work performance as they tend to get distracted more easily, and emotionally exhausted from constantly worrying. 

This level of stress can also manifest itself in physical health problems. Research has previously linked financial anxiety to trouble sleeping, a greater risk of heart disease, and increased inflammation, which is associated with multiple health conditions: from gastrointestinal disorders to depression. Financial anxiety also has social repercussions with negative emotional consequences, especially when people choose to isolate themselves from loved ones only to avoid spending money, Marter says. 

Some might address their financial anxiety with unhealthy coping mechanisms, like totally refusing to look at their bank accounts, overspending and hoarding, or even avoiding spending money on things they actually need. The answer to overcoming this kind of stress lies somewhere in between splurging and extreme frugality and comes from nurturing your financial education.

“The more information you have, the more empowered and capable you’re going to feel in correcting your financial situation,” says Marter.

This doesn’t mean you have to spend thousands of dollars on a financial literacy college class. Marter says reading books on the topic, listening to money podcasts, and following money experts on social media, all help in learning how to best manage your personal finances. Following this approach also lets you digest small nuggets of information instead of trying to cram everything about money management from a single crash course. 

Just make sure the advice you’re getting is coming from a reputable source. Marter recommends financial experts such as Dave Ramsey and Suze Orman who offer online personal finance classes for under $100.

The first step is having a record of your income and setting a budget of how much you’re willing to spend each month. A popular method is to split your money by the 50/30/20 rule, which states that you should distribute your funds according to your needs, wants, and savings. 

First, about 50 percent of your finances should go towards your needs—this includes items such as your rent, insurance, and loan payments. These costs are often fixed expenses, which means that they tend to stay the same month over month, making it easier to plan ahead. Other essentials like groceries and utilities also fall into this category, but they provide more wiggle room for savings. For example, you can always opt for more store brands versus name brands when it comes to foods, or turn off the heat at home before leaving for work.

The next 30 percent of your income should go towards your wants—this is everything that’s optional, like dining out, movie tickets, and shopping. This is the area where you can cut back the most on your spending because they are variable expenses. Even though their price doesn’t change from month to month, subscriptions such as streaming services and gym memberships, also fall under this category, as they are optional.

The last 20 percent of your income should go to your savings. This will help with setting money aside in case of emergencies such as unexpected medical bills, or cushioning periods in between jobs. Unforeseen expenses may prevent you from putting this 20 percent straight into your savings account, but that’s ok. Just try to get this area of your budget back into shape as soon as you can. And even in the tightest of months, make the effort to save some money—experts say that even one percent can help you keep the habit. 

It’s also important to set up a budget that allows you to spend on the items that matter most to you. For example, some people may not think twice about cutting out rock climbing classes in favor of a lower-priced gym. But for someone else with a passion for the sport, there might be other budget areas they’re willing to modify to afford this activity. 

Everyone’s budget will look different. If you’re having trouble coming up with a plan, Marter recommends seeking support from organizations like the Consumer Credit Counseling Foundation which provides free assistance with creating a budget. Your bank or credit union may also have someone you can talk to in person for budgeting advice as well.

Your money buddy should be someone who can provide some tough love if and when you go over budget. Some people might choose their spouse or best friend as their accountability partner. If you don’t feel comfortable sharing your finances with your friends or family, Ford says you might want to consider seeing a financial therapist.

Marter says the best way to shift your mindset is through cognitive behavioral therapy. The approach teaches you to restructure your negative and irrational thoughts around money into more neutral or positive ones. An effective technique is thought-stopping. “When you have money anxiety and are worried about being homeless or some other catastrophic fear, literally say to yourself: stop. Then reroute your attention to a positive thought,” explains Marter. The latter could involve practicing gratitude and thinking about the all good things in your life—not just the material ones. 

You could also try calming techniques when you feel yourself spiraling. Mindfulness practices like deep breathing and meditation act as a reboot for the mind and shifts the focus to the present moment, helping you let go of negative thoughts. Marter recommends a deep breathing technique called square breathing, where you inhale through your nose, hold your breath, and exhale through your mouth all in counts of four. 

Ultimately, tuning into any shifts in your mind and body when talking and thinking about money, can better equip you for sticking to a budget strategy. “Turning up your awareness of your financial landscape is an important aspect of managing financial anxiety, but also a good money management habit in general,” Ford says. Because when it comes to your spending habits, the saying still rings true: knowledge is power. 

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The waste honeybees discard in their hives could hold valuable insight into the public health of our cities. In a study published this week in the journal Environmental Microbiome, scientists shared a new method for collecting microbial information from the environment using honeybee debris. Identifying germs in a city gives researchers a snapshot of the diversity of a city’s microbiome, which could lead to better health outcomes. The technique might also help in surveilling illness-causing bacteria and viruses among bees and humans. 

While we can’t see microorganisms, they play a critical behind-the-scenes role in shaping our survival. For example, microbes in the human gut support digestion, help keep our immune system healthy, and are the first line of defense from “bad” bacteria that cause food poisoning and other infections. Typically, the more diverse a person microbiome, the greater their health and well-being. One way to increase said variety is interacting with outside surroundings.

[Related: A link to depression might be in your gut bacteria]

“A lot of [microbes] are beneficial to human health,” says lead study author Elizabeth Hénaff, an assistant professor at the center for urban science and progress at New York University. “The goal of this study is understanding the whole breadth of diversity of microbiomes and the ones we’re interacting with in urban environments.” 

Hénaff and her colleagues knew they wanted to create microbial maps of different cities to get a better sense of  the diversity in each area. However, they weren’t sure what was the best way to move forward. One idea was swabbing noses, but it would be impractical to swab everyone in a broad and diverse area. The urban microbiomes might also differ from block to block, requiring extensive swabbing. Another option was wastewater surveillance, but the researchers wanted to look at everything urbanites came into contact with—not just what they digested. Then came the aha moment: they could study bee hives.

Because honeybees constantly interact with the environment when they forage for nectar, and they often carry back some bacteria, fungi, and other microorganisms from their travels  when they return to the hive. “As bees are foraging, they’re traversing all of these microbial clouds related to other aspects of the built environment,” explains Hénaff. “They’ve traversed the microbial cloud of a pond, a body of water, and groups of human beings if they happen to be in the same park where they’re going.”

The scientists used a technique called metagenomic sequencing to study all the genes found in a single environmental sample. This allowed them to match genes to different microbial species related to hive health and, in turn, learn the health status of the bees. But first they had to figure out what sample should be collected from the hive.  

In a pilot project in Brooklyn, New York, the scientists worked with local beekeepers. They took swab samples of honey, propolis (a resin-like material used to cover the inside of hives), debris, and bee carcasses—anything that could provide the most information on microorganisms.

Subsequently, they discovered that the microbes found in honey and propolis were similar across hives. “Bees are really good at controlling the microbial environment of their own beehives,” adds Hénaff. The only material that differed from hive to hive was the debris left at the bottom of the hive, and this became the source they collected in the next set of experiments.

To profile urban microbiomes, the team took samples of debris from 17 tended hives from four cities across the world: Sydney and Melbourne in Australia, Tokyo, and Venice. The DNA extracted from the bee debris contained material from different sources, including plants, mammals, insects, bacteria, and fungi in the area. 

Each city carried a unique microbial profile that gave a snapshot of how life is like there. The single Venice hive used in the study was filled with wood-rotting fungi. Hénaff says the findings makes sense since most buildings are built on submerged wood pilings. In Australia, the two Melbourne hives had large amounts of eucalyptus DNA, while Sydney’s revealed high levels of a bacterium called Gordonia polyisoprenivorans, that breaks down rubber. Tokyo’s dozen hives displayed genetic hints of lotus and wild soybean—a common plant found in Eastern Asia. There were also high levels of a soy sauce fermenting yeast called Zygosaccharomyces rouxii. 

“Most interesting to me was that [the results] didn’t feel like a disjoint metric from all the other things we know about these cities and their culture, but it actually felt like a puzzle piece we didn’t know existed that fit into our general understanding of these cities,” says Hénaff.

The debris were also helpful in identifying microbes involved in bee health. The team found three honeybee crop microbial species—Lactobacillus kunkeii, Saccharibacter sp. AM169, and Frishella perrara—along with five species related to the insects’ gut health. Three honeybee pathogens were also identified across cities. 

Next, the study identified the human pathogens bees could pick up when venturing outside. The researchers focused on the hive information collected in Tokyo because it had more hives than the other cities, and so had more data for DNA sequencing. They detected two bacteria: one that could cause bacillary dysentery and another involved in cat scratch fever. They then took the pathogen behind cat scratch fever, Rickettsia felis, and reconstructed the genome. Doing so allowed them to not only confirm the species was in the city, but that it had the bacteria-associated molecules to allow it to spread disease. 

[Related: 5 ways to keep bees buzzing that don’t require a hive]

Profiling the microbiome of different cities may be an additional tool for detecting potentially harmful pathogens in humans, says Hénaff. It could also open up new ways of surveying airborne pathogens—a growing interest since the recent arrival of SARS-CoV-2.

Jay Evans, a research entomologist at the US Department of Agriculture who was not involved in the study, says the new approach is “fine” and can help in identifying at least the microorganisms found in urban floral environments. However, he expressed reservations about overvaluing some results. Evans notes that one of the species genome-mapping algorithms used in the study is known to be “a bit greedy,” matching the best microorganism available at the moment. This suggests some genetic matchups to bacteria may not actually be the right fit, and that further tests would be needed to confirm their presence. Because bees can pick up non-living hitchhikers like pesticides, Evans also says it would be nice for the researchers to contrast these biological results with pesticide-specific studies and how that affects hive microbiomes.

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In the 10th century, or so the story goes, seven Persian princes fled their homeland and traveled on seven ships, eventually landing on the shores of East Africa. Each prince founded a town across this stretch of land known as the Swahili Coast. Today, people who identify as Swahili view this legend as an origin story that explains their diverse heritage. 

But there’s also debate over how real this legend is. Now, a team of scientists argue that this challenged history has caused us to overlook a critical cultural connection between two continents. 

A new analysis of ancient DNA reveals this connection between Africa and Asia is very real. In a study published today in the journal Nature, scientists show that people living more than 800 years ago on the Swahili coast had an intertwined African and Asian ancestry. This suggests a multiracial identity shaped early Swahili culture and brings a new understanding of the past to the people who are Swahili today.

In regards to understanding exactly how Swahili culture was formed, “they are a people without a history,” says Chapurukha Kusimba, a professor of anthropology at the University of South Florida and senior author of the study. “We have partially resolved the issue of who were the ancestors of the Swahili people and who built this great African civilization.”

One reason why this Africa-Asia connection was originally doubted is that the tale of the seven Persian princes was not recorded until the early 1500s. There are various versions of the story, and research suggests it’s possible that these contain the storytellers’ biases. Additionally, some Eurocentric archaeologists doubted Africans transformed the Swahili coast into vibrant port cities, and their prejudice caused them to venture that the cities were built by Europeans. Lastly, other African natives have accused wealthier Africans of exaggerating or lying about their connections to Asia to elevate their social status, says Kusimba.

[Related: Crystals and eggshells tell a 105,000-year-old story of humans in the Kalahari Desert]

To come to this conclusion, the study team received permission from local Swahili people to excavate cemeteries along the coast of East Africa where the first Swahilis lived. The team took DNA samples from the skeletal remains of 80 individuals estimated to have lived between 1250 and 1800 CE. They then compared the DNA sequences to the DNA of present-day coastal Swahili speakers and to a database containing the genetics of other Eurasian and Eastern African  groups. The bodies were then reburied in their respective burial sites.

The genetic analysis of the ancient DNA revealed a mixture of both African and Asian populations. About 80 to 90 percent of Asian DNA could be linked to Persia. The remaining 10 percent came from Indian ancestors. This suggests that intermarrying was happening by at least 1,000 CE, long after Africans first built the port towns where merchant trades took place. 

At this point in history, intermingling with other cultures was not an isolated event—it was happening in multiple locations across Eastern Africa. The study team also analyzed the DNA of modern people living in Kenya and Tanzania, and found that they also showed evidence of both African and Asian ancestry. This discovery made sense to the researchers, who expected that people of mixed Indian and Persian ancestry traveled beyond the coast and formed relationships with other local African groups. 

“We could see that there was this mixture between Africans and Asians happening at least two locations along the coast and possibly even more,” says lead author Esther Brielle, a postdoctoral fellow in the genetics and genomics department at Harvard University. 

Brielle says they had ample DNA samples to compare the genetics of people living in present-day Kenya and Tanzania. The genetic findings showed similar results of Asians having relations with local African groups. 

Overall, most of the DNA coming from Asian ancestry was inherited from men, while the African ancestry stemmed primarily from women. Brielle says the findings make sense because Swahili society was heavily involved in the Indian Ocean trading network, causing them to have a constant foreign presence on the coastline. Back in those days, traveling merchants were predominately male.

The study authors note that while in other parts of the world, similar genetic signatures suggest that men forcibly married local women, they don’t think this is what happened here. A hallmark of Swahili culture is following a matriarchal society and Persian men likely married into local trading families and adopted their customs. Kusimba thinks women had some choice over who they married, and it was appealing to marry these wealthy men from abroad. 

“While archaeologists, historians, and linguists have long suspected such intermarriages took place, this is the first time well-dated data, in the form of ancient DNA signatures, have been assembled the necessary empirical support for these suppositions,” says Paul Lane, an archaeologist at the University of Cambridge who was not affiliated with the study.

[Related: Eastern Africa’s oldest human fossils are more ancient than we realized]

However, interactions with foreigners may have differed depending on an ancient person’s social status. Matthew Pawlowicz, an archaeologist at Virginia Commonwealth University who was not a part of the study, points out that most of the samples of ancient DNA came from elite Muslim cemeteries. A broader socioeconomic sample would have helped with understanding the diversity of medieval Swahili people who may have lived outside of stone houses or who did not directly engage with merchants in the Indian Ocean trade network. 

Kusimba tells PopSci he plans to excavate other burial sites to provide a more diverse genetic picture of ancient Swahili people and understand why most of these cities collapsed around the 16th century. Ultimately, this work shows us the value of immigration and how refugees can contribute to the cultural diversity of a country.

“You have African communities welcoming people who are in need, giving them a place to live, and intermarrying with no problems,” says Kusimba. “These people are African people, but can trace their ancestry to many parts of the world.”

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Tick season is not only starting sooner—it’s becoming a year-round event. While April through September are usually the most active months, the pesky eight-legged parasites are biting people and animals much earlier in the year than expected. The increasing tick bites are leading to a rise in a variety of tick-borne diseases, including some that were previously uncommon.

One reason for the hike in tick-transmitted diseases like Lyme disease and babesiosis is because humans are expanding towns and cities into previously forested areas. Andrew Handel, a pediatric infectious disease specialist in Stony Brook Medicine, says cutting down forests creates an edge habitat—when one habitat type meets another—which presents more opportunity for common tick hosts such as deer and mice to interact with humans. 

[Related: A guide to the tick species every American should know]

Climate change is another culprit. Changes in rain and temperature have morphed regions with low rates of tick-borne diseases into a more palatable place for the parasites to live. What’s more, warmer conditions are getting ticks to wake up earlier from their winter sleep and have more time to bite nearby mammals. “As we see more mild winters, we’re absolutely going to see more tick-borne diseases,” says Handel.

The best thing to do is to stay aware of how ticks are circulating in your area. Even if you don’t live in the Northeast, you may be at risk for other tick-borne diseases. Knowing what to watch out for in spring, summer, and even other seasons can help treat and potentially prevent future tick bites—and the diseases that follow.

Babesiosis

Babesiosis is a parasitic infection transmitted by the bite of deer ticks (also known as black-legged ticks). These ticks are about the size of a poppy seed and found on small mammals like the white-footed mice living in the Northeast and upper Midwest. Minnesota and Wisconsin are two Midwestern states with endemic transmission of babesiosis.

Once the Babesia parasite enters the human body, it targets red blood cells. The parasites infect and destroy red blood cells by forcing their cell membrane to break open. A tremendous loss of red blood cells can, over time, cause hemolytic anemia. “It’s actually the same way that malaria works, and is why it’s called ‘the malaria of the Northeast,’” says Handel.

Babesiosis is treatable. Your doctor would prescribe a seven- to 10-day course of antibiotics if you are severely ill. Some people are at a higher risk of complications from anemia—people who are immunocompromised, those without a spleen, and newborn babies—and may need to get blood transfusions or other supportive care.

Lyme disease

Lyme disease is also spread through deer ticks. “These ticks carry and spread multiple diseases,” explains Chad Cross, a researcher at the University of Nevada, Las Vegas who studies parasites and vector-borne diseases. “If you are bitten by one, there’s always the possibility of being infected by more than one disease agent at the same time.”

While the CDC estimate shows 476,000 Lyme disease cases in the US each year, Cross states there are “at least 10 times more cases of Lyme disease than are actually reported” to the department. One reason for the discrepancy is that most cases are asymptomatic. When people do show symptoms, the fatigue and chills they exhibit can be mistaken for another condition. If left untreated, there is a risk of developing neurological problems such as facial paralysis and nerve damage to the limbs. Chronic lyme can lead to a host of persistent issues, too, many of which are still less understood. 

Most early Lyme disease cases are curable with a two- to four-week regimen of oral antibiotics such as doxycycline and amoxicillin. However, some patients may continue to experience pain, fatigue, and concentration issues six months after treatment. 

Anaplasmosis

Anaplasmosis manifests as a flu-like illness in humans. The bacterium is present in deer ticks in the Northeast and Midwestern US. The Western blacklegged tick, most prevalent around the coast of California, Oregon, and Washington, can also spread the pathogen. There has been an upward trend of anaplasmosis cases from 348 cases in 2000 to 5,655 cases in 2019.

Similar to Lyme disease, people who develop anaplasmosis develop nonspecific symptoms such as fever and muscle aches. If left untreated, it may turn fatal with some developing severe bleeding problems and organ failure. Handel says doxycycline is the most effective treatment option.

Powassan virus infection

Three tick species carry the Powassan virus: the groundhog tick, the squirrel tick, and the deer tick. Of those, the deer tick is the one that often bites and infects humans. Nearly all cases of this rare virus have occurred in the Northeast and Great Lakes region.

The virus causes mild symptoms such as headache, vomiting, and fever. By the time a diagnosis is made, Handel says about half of the patients present some type of neurologic deficit. People may also continue to show neurological problems, such as chronic headaches and memory problems after recovery.

Because there are only about 20 to 30 cases a year, Handel says there’s not a lot of medical research on how to treat it. There is no cure or antivirals to treat Powassan virus. Instead, infected individuals are given fluids, over-the-counter medications, and other supportive care to ease symptoms while the immune system fights off the infection.

Rocky Mountain spotted fever

There are two main ticks responsible for spreading rocky mountain spotted fever: the Rocky Mountain wood tick and the American dog tick. Cross says the American dog tick is very common out East while the Rocky Mountain wood tick is found in the West. Despite its name, Cross says Rocky Mountain spotted fever is being found more in the East and South than in the actual Rocky Mountain region. The less-common brown dog tick has also caused several cases along the US-Mexico border. The disease is part of a larger class of illnesses that strike thousands of people in the states each year.

The most noticeable sign is a rash that looks like red splotches or pinpoint dots in the first three days after getting bit. If treated with either doxycycline or an antibacterial agent within the first one to four days, the symptoms won’t worsen. Otherwise, the disease can be fatal. After a week, Cross says that people can develop swelling in the brain, life-threatening respiratory problems, and a coma-like state. Those who recover from severe illness may be left with permanent disability, such as paralysis or amputation of limbs.

Alpha-gal syndrome

A bite from the lone star tick can make you allergic to red meat for life. The unusual condition takes root when someone becomes highly sensitive to a sugar molecule called alpha-gal that’s found in most mammals. People who develop the allergy cannot eat red meat (fish and birds are safe to consume) or mammal-based products like dairy and gelatin. They may also be restricted in using certain medication such as heparin, which uses pig intestines. An allergic reaction can range from hives and nausea to more life-threatening reactions like anaphylactic shock.

Alpha-gal syndrome has been a rare but increasing tick-borne condition. In 2009, there were only 24 alpha-gal cases reported in the US. By 2021, the number was estimated to be around 34,000. While saliva from the lone star tick seems to trigger the mammalian allergy, deer tick bites are suspected of also causing it. According to the CDC, lone star ticks have concentrated in large numbers across the country. They are found in the southeastern, eastern, and south-central US states extending from Maine to central Texas and Oklahoma. 

There is no cure for alpha-gal syndrome. Instead, people need to learn to avoid certain foods and mammal-based products. Symptoms are managed using antihistamines and corticosteroids.

Reduce your chances of tick infections

These days, ticks are a threat across most of the US and in practically every season. Experts warn that cases will only continue to rise as ticks expand to previously uninhabitable areas. 

[Related: Climate change could introduce humans to thousands of new viruses]

Your best bet at avoiding tick-borne diseases is to keep the pests off your body. Rather than staying indoors for the rest of your life, both experts recommend spraying tick and mosquito repellant. “DEET is what we usually recommend at 20 to 30 percent,” says Handel. If you’re going to be hiking or spending a lot of time outside, learn how to handle an insecticide called permethrin. Handel advises leaving your clothes overnight in the solution to kill any insect on contact. The repellency lasts for up to 10 washes. But make sure to only use it on your clothes or gear—it’s not meant to be sprayed directly on human skin.

Remember, you can pick up ticks even if you’re not an avid hiker or camper. Ticks tend to live on tall grass, meaning they might climb on you at the park or even on your own property. Avoid rubbing up on any tall grass and keep to the middle when walking down a path. Wearing long sleeves and tucking your pants inside your socks further prevents any openings for the pests to crawl into if they latch on your clothes. 

Once you get home, immediately wash your clothes in high heat and perform a tick check for any stragglers. If you take your pet outdoors (even if it’s just the yard), you’ll want to check them daily for ticks as well. There are also topical medications that you or a vet can apply to your pet to control for any external parasites. If you or any members of your household are feeling unwell, always let your doctor know that you’ve been in wooded areas or places with high tick circulation.

“These tick-borne diseases have been around for a long time and they’re going to become more common over time,” says Handel. “But by following these steps you can keep yourself safe and still enjoying the outdoors without having to have too much anxiety about catching one of these infections.”

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One of the greatest inventions humans ever made was by accident. It was 1942, and the US had just entered World War II after the bombing in Pearl Harbor. As Americans enlisted to fight, companies were scrambling for ways to help with the war effort. At the time, the Eastman Kodak Company in Rochester, New York, came up with the idea of a plastic gun sight that would boost the aim of Allied soldiers. In trying to make the piece, chemist Henry Coover discovered the sticky properties of a compound called ethyl cyanoacrylate, which eventually became Super Glue.

Coover abandoned his efforts at converting ethyl cyanoacrylate into a plastic and instead focused on developing the product as an instant adhesive. But the potential is still there. Super Glue has the chemical monomer needed to create plastic—someone just needs to figure out how to keep it from instantly bonding with other surfaces. Now, a study published in the journal Science Advances details a new method for easily converting Super Glue into a plastic that can be recycled repeatedly. And while it might have the potential to replace nonbiodegradable plastics, some polymers experts warn that it could introduce different kinds of pollution in the manufacturing process.

[Related: Recycling one of the planet’s trickiest plastics just got a little easier]

Super Glue reacts with a lot of different materials, says Allison Christy, a graduate research assistant at Boise State University in Idaho and lead author of the new study. This is ideal if you’re creating an adhesive because it would produce short polymers that increase elasticity. For plastic-making, however, you need long polymers to maintain durability. 

The first challenge with Super Glue is stretching out its reaction time. To create long polymers, you need a longer reaction time. The authors screened for weakly bonding substances (known as initiators in chemistry) and co-reactants that would not produce a new compound once it made contact with Super Glue. They ultimately settled on acetone as their initiator with a small amount of dimethyl sulfoxide (DMSO), a colorless liquid that dissolves most organic and inorganic compounds. 

Another issue the team needed to address was where to set off the reaction. Because Super Glue sticks to mostly everything, they needed a container that would not react with ethyl cyanoacrylate and let them get the plastic out without sticking to the walls. The solution: Tupperware. “Super Glue doesn’t stick well to things like polypropylene and polyethylene,” which are the main plastics in Tupperware, says Scott Phillips, a professor of materials science and engineering at Boise State University and author on the study.

Next, the team came up with a reaction that slowed down the reactivity of Super Glue, lengthened the bonding time between molecules, and created longer polymers. Once they had their resulting plastic—polyethyl cyanoacrylate or PECA—they had to work on strengthening it. Christy did this by annealing the substance, or heating it for 20 to 30 minutes to improve its mechanical properties. The thermal properties of PECA also allowed the researchers to mold the plastic into different shapes, such as a bowl. 

The final step focused on sustainability. The researchers wanted to design a plastic that could be converted back to the raw materials, creating a closed-loop system that reduces waste. To do so, they heated the PECA to 410 degrees Fahrenheit to break the bonds holding the polymer together, along with a dehydrating agent called phosphorous pentoxide to remove any accidentally formed water. 

The process provided a 93-percent yield of the original monomers—a “pretty shocking” result, Phillips says. “The Superglue monomer is just so reactive and I assumed it would react with everything. But it’s also volatile, so under these conditions of heating, it evaporated and that immediately separates it from all the stuff that it would normally react with.” Because materials like acetone and DMSO are cheap and readily available, Christy expects the yield to be even higher if done in an industrial setting.

“This is an interesting paper reporting on synthesizing new polymers, and may provide useful properties for use in plastics applications,” says Ramani Narayan, a professor of chemical engineering and materials science at Michigan State University and expert in bioplastics, who was not involved in the study. However, he cautions that PECA could have the same issue as other non-degradable plastics and potentially shed microplastics that would accumulate in the environment.

That’s not the only pollution concern Narayan has. He says one of the reaction steps involves evaporating chemicals like acetone, which in turn allows residual solvents to be emitted into the air. This could be an issue in manufacturing plants that carry strict guidelines for volatile organic compound emissions. Additionally, Narayan notes that two of the ingredients needed to make ethyl cyanoacrylate are chloroacetic acid and sodium cyanide, and are “not generally considered safe [for human health] or environmentally responsible.”

[Related: How companies greenwash their plastic pollution]

The study does bring up an important question: What’s the best way to deal with plastics? There are an estimated 8.3 billion tons of plastic in the world today. While green efforts encourage people to reduce, reuse, and recycle, about 79 percent of plastic sit in landfills because they are unrecyclable. For example, polystyrene is a petroleum-based plastic that is difficult to break down. Yet, it’s a common and versatile plastic that’s used in everyday products such as yogurt cups and single-use spoons. The study authors note that it makes up six percent of total plastic waste. “If people could use [PECA] instead of the polystyrene for various applications, in theory, it should reduce that six percent because we’d be able to recycle [the plastic] back to starting material again,” explains Phillips.

“We can’t get rid of plastic entirely. It’s impossible. It’s one of the most valuable materials to society,” adds Christy. “If we can use creative approaches and rethink plastic and some of the other materials around us, there are solutions out there worth pursuing.”

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Deep in the South American rainforest lives one of the brightest colored amphibians in the world: the poison dart frog. But don’t take their dazzling appearance as an invitation to come closer. These hues are a warning that they are not worth attacking. Touching the skin of a poison dart frog—among the most toxic animals in the world—can induce nausea, swelling, and paralysis, even in humans. 

Predators to these frogs have learned to see bright shades as poisonous or unappetizing. But associating color with danger takes time, leaving evolutionary biologists with a paradoxical problem. How did prey species survive long enough to evolve colors as warning signals while living among predators who can better spot them and had not yet learned to avoid them?

[Related: These buff frogs never skip arm day]

One theory is that colorful warning signals, also known as aposematism, evolved indirectly and through gradual stages. A study published today in the journal Science suggests some creatures permanently adapted to vivid skins, by first using hidden signals to give predators plenty of time to learn that these colors should be treated with caution. These colors were often concealed in their bellies or undersides.

“If you’re the first conspicuous individual in a chemically defended lineage, it will be very difficult for that mutation to take hold in the population, because predators have no way of knowing your coloration is associated with chemical defense,” says Changku Kang, an assistant professor at Seoul National University in South Korea and study coauthor.

To study how colors evolved in animals, the study authors ranked over 1,000 species of frogs and salamanders into five groups. Most studies on the evolution of animal coloration try to place animals in one of two categories—either conspicuous or camouflaged—which limits the complex understanding of animal coloration, says Karl Loeffler-Henry, a postdoctoral fellow at Carleton University in Canada who served as lead study author. 

Instead, this research looked at those two extremes as well as other adaptations animals could have developed. Animals with colors that make them stand out like reds, yellows, and bright blue skins were classified as conspicuous. Animals that developed colors meant to camouflage into the environment were cryptic. Partially conspicuous animals were those with colors that were somewhat hidden in limbs and other body areas. Fully conspicuous critters had bright colors fully tucked away in their underbellies and other hidden regions. Amphibians with both cryptic and conspicuous forms were placed under the polymorphism category.

The biologists then tested nine different evolutionary models to reconstruct the evolutionary pathways their ancestors took, including when they developed both aposematism and toxicity as a defense strategy. 

The path to aposematism was not a straight line. Instead of evolving directly from a camouflage strategy, aposematism had an important transitional state. “The conditions favoring the evolution of this type of coloration are likely to be much less restrictive, and yet they provide a clear pathway to the evolution of overall bright coloration,” says Kyle Summers, an evolutionary biologist at East Carolina University who was not involved in the study. When animals first developed vivid pigments, they initially concealed them in body parts such as the limbs or the underbelly. 

[Related: Could reptiles and amphibians hold the key to the fountain of youth?]

If threatened, these animals would lift up their limbs or bodies to expose the colors that eventually served as warnings to predators who naively ate these creatures. “Aposematism has evolved independently many times in separate lineages of amphibians,” explains Loeffler-Henry. “Hidden signals give an answer to how this is happening and unravel a fascinating story of how the evolutionary process took place.”

“The study offers a novel solution to the long-standing paradox of evolution of conspicuous antipredator warning signals,” adds Alice Exnerová, an assistant professor of zoology at Charles University in Prague who was also not affiliated with the research. What’s more, she says the findings show the value of exploring alternative and overlooked evolutionary strategies, which can advance our understanding of diverse antipredator defense strategies in the natural world.

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Air pollution is messing with the love lives of fruit flies, warns a new study published on March 14 in the journal Nature Communications. Male common fruit flies had trouble in recognizing their female counterparts after breathing in toxic gas, causing them to make a move on another male. 

Though there’s been some research hinting at bisexuality among fruit flies, the current results suggest it has to do more with ozone pollution. Even brief exposure to O₃ was enough to alter the chemical makeup of pheromones, a unique trails insects use to detect and attract mates. Increasing levels of air pollutants from cars, power plants, and industrial boilers around the world could stop common fruit flies from reproducing, causing a dramatic decline in the insect species.

[Related: Almost everyone in the world breathes unhealthy air]

The chemical ecologists placed 50 male flies into a tube and exposed them to 100 parts per billion (ppb) of ozone—global ozone levels range from 12 ppb to 67 ppb—for two hours. After two hours, fruit flies showed reduced amounts of a pheromone called cis-Vaccenyl Acetate (cVA) in compounds involved in reproductive behavior.

A closer look revealed that ozone seems to have changed the chemical structure of pheromones. Most insect pheromones have carbon double bonds, explains Markus Knaden, a group leader for insect behavior at the Max Planck Institute of Chemical Ecology in Germany and study author. Whenever a compound has carbon double bonds, it becomes highly sensitive to oxidization by ozone or nitric oxide and starts to separate. The explanation is in line with their findings of high amounts of the liquid heptanal in the flies, a product that emerges after cVA breaks down. 

Did the altered pheromones affect a male’s chances at finding a partner? It appears so. A separate experiment exposed male flies to 30 minutes of either ozone ranging from 50 to 200 ppb or regular air with a much lower amount ozone before being placed them with female fruit flies. While males from both groups wasted no time in trying to court females, ozone-exposed fruit flies had more trouble getting a mate. 

“The male advertises himself with pheromones. The more he produces, the more attractive he becomes to the female,” says Knaden. Losing the chemical aphrodisiac made ozone-exposed males a less desirable option to females, who took nearly twice as much time choosing from the corrupted bachelors than the clean ones.

Not only is ozone pollution hampering the males’ ability to get female attention, it’s also affecting how they identify other individuals. Knaden says his team expected the altered pheromones to affect the ability for male fruit flies to distinguish between a male and a female, but what they didn’t expect were males to jump on each other. “In the beginning, it was a very funny observation to see really long chains where one male was courting the next and then the next down the line,” he describes. With the altered pheromones, “the male basically jumps on everything that is small and moves a little bit like a fly, regardless of what it is.”

“Very little is known about how air pollution interferes with insect sex pheromone signaling, so it is great to see this work underway,” says James Ryalls, a research fellow in the Center for Agri-environmental Research at the University of Reading in England, who was not affiliated with the research. “The study demonstrates how disruptive air pollution can be to insect communication, with potential ecological ramifications such as reduced biodiversity.”

[Related: Flies evolved before dinosaurs—and survived an apocalyptic world]

Getting rid of the buggers that crowd your bananas and melons might seem like a good idea at first glance. However, Ryalls warns that these agricultural pests contribute greatly to the world’s ecosystem. As nature’s clean-up crew, fruit flies help decompose rotting fruit, releasing nutrients for plants, bacteria, and fungi to use. They also serve as food for other animals like birds and spiders. Lastly, they are a common insect model used in biomedical research and have contributed to countless neuroscience and genetic discoveries.

Fruit flies are not the only ones feeling the effects of air pollution. Knaden says he has seen dangerous ozone levels affecting flower volatile compounds, which are used as cues for pollinators. His 2020 study found moths were less attracted to flower odors from plants exposed to the gas, resulting in less pollination. 

“Insects are on the decline, and we thought it was from pesticides and habitat loss,” says Knaden. “It seems there are more screws we have to turn, one of them being air pollutants.”

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The number of colorectal cancer diagnoses has nearly doubled in people younger than 55, a recent report from the American Cancer Society (ACS) warns. 

Colon cancer cases rose across the country from 11 percent in 1995 to 20 percent in 2019 people younger than 55.  There was an 8-percent jump in advanced cases across all ages since the mid-2000s. Most young people who were diagnosed had late-stage tumors. 

While the statistics are alarming, it doesn’t come as a surprise to doctors in the field who’ve noticed a trend in younger patients over the past few years. “This data is confirmation of that clinical observation,” says Deborah Nagle, the chief of colon and rectal surgery at Stony Brook Medicine in New York. 

Colonoscopies remain the gold standard for screening colorectal cancer. However, some might find the preparation, recovery, and procedure itself uncomfortable and time-consuming. Fortunately, there are other less invasive tools for detecting colon cancer, some of which you can access in the comfort of your own home. 

The reasons behind rising colon cancer rates

Why do some people get colon cancer over others? There’s “no smoking gun,” says Samir Gupta, a gastroenterologist and professor of medicine at the University of California, San Diego. Several causes factor into an individual’s overall risk.

One is antibiotics: The drugs might contribute to colorectal cancer by changing the composition of the gut microbiome that allows “bad” bacteria—those that lower a person’s immunity, create cancer-promoting metabolites, and damage DNA—to flourish. A 2021 study in Sweden found adults treated with antibiotics had a 17 percent risk of cancer in the ascending colon. The more antibiotics people took, the greater the risk. Gupta says there could also be a potential link between antibiotic exposure during infancy and future colorectal cancer. 

Obesity is another contributor for different kinds of cancers, including early-stage colorectal. Nagle says the obesity rate has significantly increased in the US in the past few decades. Nearly 42 percent of Americans have a BMI of or above 30. Excess body fat promotes inflammation and drives up the production of insulin and hormones, and in turn, can increase the number of cells that can lead to cancer. Additionally, inflammation from fat itself sometimes damages healthy cells and leads to cancerous mutations in cellular DNA.

While less studied in humans, chemicals put in food have also been seen as a potential cancer contributor. Dietary emulsifiers, which are usually added to processed foods to increase their shelf life, have been linked to colon cancer through animal research. In one 2022 study, titanium dioxide, a common food coloring in candies and baking products, helped promote colorectal tumor development in lab mice.

[Related: Two decades-long studies link ultra-processed foods to cancer and premature death]

Oncology researchers are also interested in looking at how big of a role genetics play in colorectal cancer formation. One in five people diagnosed with colorectal cancer carry a genetic mutation associated with tumor development.

Prevention is possible, however. At 91 percent, colorectal cancer has one of the highest five-year survival rates. The key is catching it in time. Both Gupta and Nagle recommend getting a colonoscopy screening to detect any early signs of cancer. A follow-up study in Europe last year showed that people who got a colonoscopy reduced their risk of colorectal cancer by 31 percent and the risk of dying from said disease by 50 percent.

When to get a colonoscopy

While there are standard guidelines for when you should get a colonoscopy, both experts urge anyone who experiences persistent rectal bleeding and changes in bowel habits to get immediate medical attention.

If you have no symptoms and no family history of colorectal cancer, the ACS recommends routine screenings starting at age 45. Those considered at high risk of colorectal cancer—family history of disease, history of radiation in the abdomen area to treat prior cancer, inflammatory bowel syndrome—are encouraged to get a screening before 45. 

People with Lynch syndrome, a hereditary condition that genetically predisposes a person to multiple types of cancer, are strongly urged to get a colonoscopy every one to two years starting in their early 20s or 2 to 5 years before the youngest case in the family.

Test your options

While colonoscopies are the go-to tool for colorectal screenings, says Nagle, they’re not all too popular among patients. The prep required for a colonoscopy—taking a laxative and adjusting your diet a few days before —can deter people. The procedure and recovery also takes up a huge chunk of time, which may not be doable for those who can’t take time off work. 

Stool-based tests like Cologuard offer an easier, at-home alternative. There’s no prep needed, and the results are generally accurate, though not on par with a colonoscopy. There are also fecal immunochemical tests (FIT) that look for hidden blood in your stool. This annual test can be done at home, though it is less accurate at detecting polyps smaller than 6 millimeters than colonoscopies.

A less invasive method some oncologists are turning to virtual colonoscopies. The procedure uses CT scans to create images of your large intestine to look for ulcers, polyps, and tumors.

[Related: First study of cancer-detecting blood test shows hopeful results]

There is ongoing research looking to improve screening results using a combination of these methods. Some involve using a person’s gut microbiome composition to identify the loss of certain “good” bacteria to predict their risk of precancerous tumors. Others include a multi-step screening process that still includes the recommended colonoscopy. A study from last spring suggests getting a colonoscopy after an at-home stool test; those who did not follow up were twice as likely to die from colorectal cancer.

“We have an opportunity to prevent some cancers from happening by doing the screenings,” says Gupta. “When people are diagnosed early, it’s more treatable.”

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For more than 50 years, Latin American countries have been culling vampire bats to limit the spread of rabies. These flying bloodsuckers are common hosts for the virus that causes the disease, which kills hundreds of cattle each year and costs an estimated $170,000 annually in losses to local farmers in southern Peru.

Wildlife culling uses vampiricide, a lethal poison that spreads to up to 15 bats per every animal treated. But there’s one issue humans did not account for—bats aren’t going to hang around and let themselves get poisoned. 

“The intervention had good intentions in trying to manage an infectious disease, but it had counterproductive effects because we didn’t understand how animals were going to respond,” says Daniel Streicker, a professor of viral ecology at the University of Glasgow and senior author of a new study published today in Science Advances. Instead of slowing down rabies, culling in areas with high-circulating virus caused bats to fly more frequently across the landscape, accelerating the disease’s spread. 

It’s all about timing

The study authors first studied how culling affected bat population size, and in turn, the risk of transmitting rabies to livestock living in a large area of southern Peru. While culling reduced the bat population, it did not completely stop the hungry biters. About 59 percent of farms in the area reported having at least one animal bitten by a vampire bat three months after culling.

The team also looked at how culling could affect the circulation of rabies virus. By sequencing viral genomes sequences, they reconstructed how the virus has spread across the landscape through space and time. 

Culling affected the speed of viral spread. If a culling took place in an area with active viral circulation, then the viruses seem to spread faster. Bats are social creatures, Streicker explains, and watching their group members die of poison likely caused them to fly away to avoid death. This increases the chances that bats will carry the virus across longer distances. 

In areas without recent rabies outbreaks, though, the virus takes more time to spread. The findings suggest it’s all about context. If cullings are done proactively in areas before the virus arrives, they might slow down the spread into new areas, letting areas stay rabies-free longer. “We can’t say that rabies would never happen, just perhaps that it would happen more slowly,” Streicker says.

Is culling the only strategy?

Vaccination is an alternative method to curb rabies, but Streicker says people in Latin America have historically been vaccine-hesitant. People often got the rabies vaccine after being exposed to the virus, which is less effective. Another issue is that some remote areas in Latin America make it difficult to deliver vaccines. 

Vaccinating livestock is another option to control rabies transmission. But immunizing every animal is costly for farmers, especially those that live in areas that have had little to no problem with rabies.

Some locals have tried to take matters into their own hands, by burning the roosts where bats live, or cutting trees down that may house other rabies-infected creatures. However, researchers do not recommend these methods because they can harm animals not affected by the virus.

Other ways to slow rabies 

Vampire bats aren’t the only bat species that carries rabies, but they’re likely the main spreaders. These bloodsuckers need to feed almost every night, which has a high risk of exposing their victims to rabies. And herding cattle and other livestock has given bats a nearly unlimited food source, Streicker says. 

Instead of vaccinating humans and cattle, one approach is looking into vaccines for vampire bats. The bats aren’t easy to vaccinate—they are reclusive wild animals, and it would be nearly impossible to catch each one. A successful rabies vaccine requires a delivery technology to reach a sufficient number of wild animals. Streicker and his team are currently working on a self-disseminating vaccine that they would administer to one bat. From there, the vaccine would be capable of spreading to other bats by itself.

Another approach is reproductive suppression, in which bats consume blood containing coumestrol, an organic compound that acts as a bat birth control. Ongoing research suggests that coumestrol affects the fertility of male and female vampire bats, reducing  their population. Ultimately, Streicker says limiting rabies in bats will require some type of population management. If vaccination and reproductive suppression tools become available to the public, there may not be a need for culling at all. 

Correction March 13, 2023: The article previously said roosters would be burned in an attempt to slow the spread of rabies. What are actually set on fire are bat roosts, though scientists do not recommend this.

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As a New Yorker, there’s a difference in whether it’s cold or “brick” outside. Cold weather is when you throw on a sweater before heading out. When it’s brick, you try to stay home as much as possible to avoid ending up like a human glacier. But the local lingo didn’t apply much this winter, with record-low snowfall and above-average temperatures across New York City.

A warm winter is more than just losing a few snow days. It’s knowing that the world will be dealing with more scorching heat waves and droughts, and natural disasters like the deadly flooding caused by Hurricane Ian in Florida and Cuba last year.

Climate change is only one of humanity’s long list of problems. This month we mark the third anniversary of the COVID pandemic, a disease that has killed millions worldwide and is becoming more chronic like the flu. On top of that, Turkey and Syria are still facing the aftershocks of a historically deadly earthquake, and soaring food prices from Russia’s invasion of Ukraine could worsen global hunger for years to come. 

[Related: How to manage your mental health as traumatic events pile up]

There seems to be no shortage of community-wide tragedies. Likewise, these events are taking a toll on people’s psyches. Whether conscious or subconscious, you might mourn a loss of safety and security, on top of the more obvious layers of sorrow. But these feelings can also help you be the change you need to move forward in this ever-evolving world.

Collective grief is both a shared and unique experience

Some tragedies, like a mass shooting or police brutality, resonate among an entire group of people. “Grief is a normal reaction to loss,” says Kriss Kevorkian, a thanatologist and founder of the counseling service, A Grieving World. “When it’s collective grief, we’re experiencing that on a larger scale with more people.”

Collective grief can take hold even if you don’t personally know the people directly affected. When the Uvlade school shooting occurred, there was a nationwide outpouring of anger and sorrow over the murders of the teachers and children. Violent events like these force you to rethink life and the safety of your family, says Kevorkian.

Younger generations have become the most vulnerable to collective grief, especially with environmental anxiety. Kevorkian says that government failure to stop climate change has caused children to become more helpless and apathetic. When young people like Greta Thunberg do speak out on climate change, they are mocked and subject to verbal abuse.

Your brain and body on grief

Grief doesn’t stay in one corner of your body—it consumes your entire being. You might feel more tired than usual from tossing and turning all night. Maybe you’ve lost your appetite or have trouble keeping food down. Research shows that the first few months of grief can affect your body’s immune system activity and increase your risk of blood clots.

When your mind is weighed down by sadness, anger, and loneliness, there is little space to focus on other matters. Having “grief brain” can make it feel like you’re in a fog. Everyday tasks such as watering the plants or taking out the trash become really challenging. As you try to process your loss, you might forget things like where you placed your keys or an important doctor’s appointment. 

Grief brain happens because your mind recognizes the stress and emotional trauma as a threat, triggering the entire body’s fight-or-flight response. Brain regions like the amygdala signal the alarm through stress hormones that elevate your heart rate and increase your blood pressure, upping your anxiety and panic to keep tabs on the stressor. 

When you don’t deal with the heavy emotion, your brain protects itself by going into constant survival mode. Believing it’s in danger, it allocates more energy and resources to fear centers like the amygdala. Your brain might also decide to escape the stressor by metaphorically running away. It might dissociate from daily happenings, for example, to give you a mental break from negative emotions. “Deciding how to approach your grief can foster healing as opposed to delaying it when we try to ignore or deny reality,” says Jasmine Cobb, a social worker specializing in grief and trauma at Visual Healing Therapeutic Services in Texas.

Consume your grief before it consumes you

The good news is that grief-related stress on the brain is reversible. Meditation and mindfulness can train you to focus on the present moment instead of reliving the past or dissociating from future threats. Going outside for a 30-minute walk instead of doom-scrolling or watching the news can help clear and calm the mind. Crying can also be a healthy release of stress as it releases feel-good hormones such as oxytocin and endorphins. 

There is no normal amount of time you’re supposed to grieve. You can spend months or years mourning, only for a news story or movie to trigger your pain all over again. “There are three words I really can’t stand, ‘get over it,’” says Kevorkian. “Grief never ends.” 

While time can help with the grieving process, it’s important that you’re actively working on your emotions and any unresolved issues related to the loss. Cobb says speaking with someone you can confide in is important, whether it’s a family friend, therapist, or a spiritual leader. There is also power in shared grief. People who have gone through a similar experience can help provide support in overcoming your grief. “Find your community who can hold a torch for you when you’re unable to do that for yourself,” advises Cobb.

Turning collective grief into collective action

Grief is one of life’s greatest teachers, says Kevorkian. It shows you how to live in the present and appreciate all that you have right now. Beyond acceptance, taking action can help you wrestle with some of the hopelessness you might feel when dealing with events out of your control, Kevorkian explains.

[Related: The biggest tool we have to fight climate anxiety is community]

One example of a group turning pain into lasting change is Mothers Against Drunk Driving (MADD). In 1980, 13-year-old Cari Lightner was killed by a drunk driver—a man who had just gotten out of jail two days after his fourth DUI arrest. For the next few years, Cari’s mother, Candace, used her daughter’s photo and story of her accident to raise awareness and change California traffic safety laws. Candace went on to form MADD, a political-advocacy group that gives other grieving parents the opportunity to feel like their tragedy was not in vain. 

“It’s easy for us to stay in bed under the covers and wallow in despair,” says Kevorkian. But finding the courage to take action can help you get out of your head and connect with others sharing similar distress. Hopefully, with time and work, the world will seem a little less bleak.

The post How to cope with collective grief—and even turn it into action appeared first on Popular Science.

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For as long as people have been telling stories, fables and legends have been used to explain the forces of nature. The Greeks made up tales of gods and heroes to teach why we have changing seasons or why misery and evil exist in the world. Medieval folktales rattled on about unicorns and men with dog heads. Norse mythology talked about giant sea monsters lurking in the ocean, ready to devour fish and ships that dared cross their path.

As far-fetched as these stories were, many hold a grain of truth, or were at least inspired by real encounters. Famed traveler Marco Polo, for example, believed he saw the first unicorn when he first laid eyes on an Indian rhinoceros. The latest example of animal mix-ups could explain a giant, mythical ocean beast, called the hafgufa, of Norse sagas. A study published Tuesday in Marine Mammal Science found that the feeding behavior in whales is similar to ancient Scandinavian texts describing the monstrous animal. 

The hafgufa,  a sea creature first mentioned in the 13th century in Old Norse mythology, was believed to have roamed Icelandic waters. It would lie in wait on the ocean’s surface, emitting a perfume that would lure fish into its wide-open mouth. Though described in several Norwegian tales, scholars were mystified about its origins. Some postmedieval historians have argued it was a derivative of other mythical creatures, such as mermaids or the Kraken. Other texts referred to it as a type of whale-fish. 

[Related: Siberian unicorns lived alongside humans, and they were so much cooler than the mythical version]

John McCarthy, a maritime archaeologist at Flinders University in Australia and lead author of the new report, learned of the hafgufa when he was studying a hunting strategy of certain baleen whales: The behavior, called trap-feeding, involves whales lying motionless in a vertical position with their mouths open at the surface. The whales keep the corners of their mouths partially below the surface, letting water pool into their mouths. Whales use their jaws to create a current in their mouths to lure panicked fish into what the prey mistakenly believes is a safe space. 

McCarthy caught a BBC documentary describing the mythical sea creature, which sounded a lot like what he’d observed in his whale research. Curious about the similarities, he spoke with some professors of medieval studies at his university who pointed him to some historical literature on Norse sea monsters. “The story just kept getting more interesting,” he recalls. 

Old Norse text from Konungs skuggsjá, or (The King’s Mirror, described trap-feeding activity that McCarthy and his colleagues say is similar to Eden’s whales hunting off the gulf of Thailand, as captured on video. The early Greek text of Physiologus also illustrated the trap-feeding behavior of hafgufa and another giant mythical creature, known as aspidochelone —think of a large sea turtle with an island on its back—that ate in the same way. 

[Related: A group of humpback whales is choosing violence]

As the unknown author of Physiologus wrote: “When it is hungry it opens its mouth and exhales a certain kind of good-smelling odor from its mouth, the smell of which, once the smaller fish have perceived it, they gather themselves in its mouth. But when his mouth is filled with diverse little fish, he suddenly closes his mouth and swallows them.” 

Trap-feeding behavior is a food strategy discovered in 2011 and documented on video. So how did Scandinavians observe this action 2,000 years ago? “It can be easy to forget that people in the medieval past were just as discerning as we are today,” says Lauren Poyer, an assistant teaching professor of Scandinavian studies at the University of Washington who was not involved in the study. “Their cultural knowledge and traditions were just as rich, and potentially even more valuable, than our knowledge today when it comes to surviving and thriving in their unique landscapes.”

McCarthy speculates the trap-feeding behavior was likely more visible because more whales existed then compared with today’s population, which has been decimated by commercial whaling. “It makes perfect sense to me that the Konungs skuggsjá and Ǫrvar-Odds saga authors would have knowledge and possibly direct observation of a fairly rare feeding behavior, as this article suggests,” adds Seth Koproski, an English doctoral candidate at Cornell University who has studied Physiologus and other ancient texts, and who was not affiliated with the new report. He says the Norse were expert seafarers who explored the northern Atlantic Ocean and they likely would’ve had consistent, direct contact with a large and diverse population of whales.

[Related: These now-extinct whales were kind of like manatees]

The hafgufa used to be an allegory for the devil, Koproski says, and its trap-feeding behavior symbolized deceitful snares that caught fish “of small faith” lured in by attractive odors. “These kinds of allegorical understandings were common in medieval Europe and the concept of nature,” he explains.

There may be other real-life inspirations for fictional creatures lurking out there, too.  A popular theory is that the one-eyed cyclops was inspired by elephant skulls, because the holes from their trunks could resemble giant eye sockets. And another suggests dinosaur fossils may have encouraged tales about dragons. With more research, the hunt for mythical beasts continues.

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Nearly a month after a train derailment in Ohio caused a toxic chemicals spill, the roughly 5,000 residents of East Palestine are worried about whether the air is safe to breathe. Since the accident, locals have complained of headaches, rashes, and a lingering smell in the air resembling “hair perming solution,” along with respiratory issues like chronic coughing, wheezing, and acute bronchitis, possibly from chemical irritants inflaming their airways. And now the concern has spread to people in other states.

Social media users living hundreds of miles away are posting videos showing alleged signs of acid rain and attributing it to air pollutants traveling from Ohio. There are also videos of individuals in other states saying they’re experiencing nausea and a burning sensation in their throats and noses due to a strong chemical odor in the rain. Some TikTokers have also attempted to explain how vinyl chloride, one of the main chemicals in the spill, is causing acid rain outside of East Palestine.

[Related on PopSci+: Dust clouds are killing people out West—and the dangers could spread]

Are their fears of traveling toxins justified? “Given the [high] amount of chemicals that were involved and the controlled conversion, I don’t think it’s a major issue for [people living] long-distance,” says Oladele Ogunseitan, a professor of population health and disease prevention at the University of California, Irvine. “I’m not saying it’s an absolute no because we don’t fully understand all the moving parts, but it’s just an infinitesimal chance.” 

First, what is acid rain?

Acid rain is any form of precipitation where water and oxygen react with nitrogen oxide and sulfur dioxide to form acidic compounds. While natural causes such as volcanic eruptions can release these chemicals, most acid rain events result from human activity, such as burning coal and other sulfur-containing compounds. 

Pure water has a neutral pH of 7, with regular rainfall being slightly more acidic with a pH of less than 6. Acid rain, however, usually falls between a range of 5 to 5.5 on the pH scale, meaning it’s more corrosive. 

Though making contact with acid rain won’t burn your skin off, you might experience irritation in your eyes, throat, and nose. The bigger issue is inhaling the chemical compounds in acid rain. The longer you spend time in acid rain, the likelier it is that pollutants will enter your lungs. Depending on how long you’re exposed and how many particles you inhale, acid rain can cause several long-term health problems, ranging from asthma and chronic bronchitis to heart attacks if you have a history of cardiac issues.

Can vinyl chloride cause acid rain?

In Ohio, officials decided on a “controlled release” after a temperature change in the five derailed train cars carrying vinyl chloride prompted worry about a possible larger explosion. Vinyl chloride—a synthetic, carcinogenic chemical used to make plastic for pipes, wire coatings, and car parts—was released in liquid form before being set ablaze for days in a barricaded area. Burning it breaks it down into hydrogen chloride, carbon monoxide, carbon dioxide, and a toxic gas called phosphene. 

And while burning vinyl chloride can also produce hydrochloric acid, a component of acid rain, it would have been immediately seen at the site at the time of the controlled chemical release. Right now there are some “pretty bad smells” in East Palestine, says Peter DeCarlo, an associate professor of environmental health and engineering at Johns Hopkins University, but not as much air pollution as there was on the first day. If the derailment was causing widespread acid rain, locals would experience it first.

What’s the current air pollution forecast in East Palestine?

After screening 578 homes in East Palestine over the past few weeks, the Environmental Protection Agency reported that outdoor air quality in the residential area was normal and continued to assert that there are no health risks. Some environmental scientists, however, are skeptical of the clean-cut assessment. 

“What would prove if the place is habitable is if nobody gets sick, but we know people are having symptoms,” says Ogunseitan. A separate group of environmental researchers at Texas A&M University conducted their own air sample analysis in the town’s streets. In a Twitter thread posted last Friday, they shared that nine of the 50 chemicals identified by the EPA are at higher-than-normal levels. 

[Related: Breathe easier during wildfires with a DIY air purifier]

While the research is ongoing, the Texas A&M team warns of a potential health concern if levels of chemicals such as acrolein stay elevated. Acrolein can cause irritation in the skin, eyes, and mucous membranes. When inhaled, the suffocating odor may trigger respiratory distress and dizziness. 

Ogunseitan doesn’t think locals need to evacuate again based on this initial study, but does say it should raise the alarm for continuous air monitoring and health screenings for residents. He points out that some people might be more sensitive to even the smallest amount of exposure to toxic chemicals, so solution is to “identify those who are particularly vulnerable to these levels of chemicals and have them temporarily move.”

Is there any chance the chemicals will reach other states?

Based on the EPA’s air emission models on wind direction, rainfall, and the natural settling of dust and smoke from the derailment site, Ogunseitan says the data doesn’t support pollutants traveling as far as the East and West Coasts. When an incident like this happens, he notes there’s always a level of mass hysteria that has people blaming the incident for something unrelated. 

On the very slim possibility of pollutants wafting outside the East Palestine area, DeCarlo says his biggest concern would be for anyone living just across the border in Pennsylvania because of close proximity to the accident. “As you move away from the site, the emissions from the fire become diluted and less concentrated,” he explains. “For people living several states away, this will not be the same type of issue as those in the immediate area.”

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For a long time, people have been trying not to get pregnant. In 500-100 CE, European women tied weasel testicles around their legs during sex to prevent pregnancy. Ancient Egyptians stuck a honey and crocodile dung mix up their vaginas to block sperm from entering. And in imperial China, sex workers were encouraged to drink liquid mercury (which might have stopped them from getting pregnant, but often killed them, too). Despite the obviously high demand for contraceptive options, it would take another couple of centuries until humans got their hands on a safe and effective birth control method. 

Nowadays, there are several female contraceptives to choose from, including the widely popular “pill”. But for people who might desire a hormone-free option for medical or religious reasons, the pickings are slim. “Birth control development is a prime symbol of the lack of innovation in women’s health,” says Kelly Culwell, an OB-GYN and head of Research and Development, Women’s Health for Sebela Pharmaceuticals.

With recent research making strides toward hormone-free birth control for men, why do female contraceptives feel so outdated? Here are three reasons.

The effectiveness of hormonal birth control

One of the big reasons why female contraceptives skew toward hormonal drugs is because of their proven effectiveness. Jill Purdie, an OB/GYN and the medical director at Pediatrix Medical Group, says there’s not much motivation for industries to invent a non-hormonal safeguard when they have repeatedly been less protective than hormonal birth control. “When you look at non-hormonal options, they are around the 80 to 89 percent range while your hormonal options are all going to be 95 percent or better.” The one exception is the non-hormonal copper IUD, which is 99 percent effective for up to 12 years after being implanted.

Costs of testing contraceptives

In the 1970s and ‘80s, Culwell says a lot of attention was focused on making lower doses of hormonal birth control pills to lower the risk of severe side effects such as dizziness and vomiting. Doing so was thought to be more cost-effective than starting from scratch. Even in the ‘90s and early 2000s, she says there weren’t many changes to the birth control method. While female birth control was designed in different forms, like rings, IUDs, and patches, Culwell says it still followed the same process of using synthetic versions of estrogen and progesterone hormones to prevent ovulation. “It’s really a capitalistic process for private companies,” she explains. “There’s a lot of research development going on in ‘big money categories’ like in the fields of cancer and neurology. Birth control doesn’t tend to bring the same level of monetary return.”

Sexism in research

Like many corners of innovation, medical research on contraceptives has a deep-seated gender gap problem. In the 1900s women were often excluded from participating in clinical trials or experiments, making it difficult to understand how birth control affected the female body. Culwell says scientists were concerned about enrolling women because there was a risk of getting pregnant, opting to use animal models like rats and rabbits instead. When women were involved in birth control trials, it was through unethical methods such as enrolling individuals hospitalized in mental institutions or recruiting poor Puerto Rican women without telling them what the medications did. It was not until 1994 that the Food and Drug Administration (FDA) made policy changes requiring all drug trials to enroll women in their studies.

Future birth control options

Both experts say there’s been a massive push for more effective non-hormonal contraceptives in the past decade. The overturning of Roe v. Wade has made Americans more vocal in having more options to prevent unwanted pregnancies.

Ironically, research on male contraceptives is helping to widen the field. Culwell says some of the hormonal side effects participants faced during a 2016 trial for shots that lowered sperm counts brought more attention to pursuing non-hormonal contraceptive choices. In response, the National Institute of Health has provided more grants towards research on new types of hormone-free birth control for both sexes, which Culwell says helps to fund innovations pharmaceutical companies initially passed on.

[Related: Everything you need to know about male hormonal birth control]

There are some new non-hormonal options already available and some currently in development. The FDA approved the vaginal gel Phexxi in May 2020. The contraceptive works by changing the pH of the vagina to stop sperm from moving around and reaching an egg. A phase 3 clinical trial with more than 1,300 individuals estimated Phexxi to be 86-percent effective in preventing pregnancy. For comparison, the hormonal pill is 99-percent effective when used properly.

Sebela Pharmaceuticals is also in phase 3 clinical trials of a new version of the copper IUD. It would be smaller, flexible, with half the amount of copper than the current copper IUD on the market. Culwell says that if the FDA approves the product, it could be on the market as early as next year. If so, “it would be the first new non-hormonal IUD in 40 years,” she explains.

While still years away from hitting pharmacy shelves, there is potential for a non-hormonal contraceptive that releases antibodies targeting sperm. Deborah Anderson, a professor of medicine at Boston University who is leading the research on this product, says it’s a topical film that can be inserted in the vagina before intercourse. Seconds after dissolving, it releases antibodies that bind and cause sperm to stick together until they can no longer move. The proteins then trap the bound sperm in the cervical mucus, the gatekeeper standing in the way of the ovaries. With more trials underway and a long FDA-approval process, Anderson gives a rough estimate of 10 years before you see these in the shelves of your local pharmacy.

“The field is getting back in gear as the NIH is putting a lot of money into it and looking for industry engagement again,” says Anderson. “[We] should look forward to more contraceptive productions in the future.”

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The death of Tyre Nichols at the hands of Memphis police earlier this year has set off new questions about what public safety really means in America. While the five former officers are being charged for Nichol’s murder, there’s been scrutiny over how EMS responders handled the victim’s injuries after arriving on the scene.

On the night of January 7, paramedics responded to a call of a person being pepper sprayed. Despite the man laying bloody and in distress against a police vehicle, they failed to make their own assessment of the patient beyond what the officers told them. It took another 19 minutes for the EMTs to bring a stretcher out for him. 

The mistreatment Nichols endured from people trained to save lives is a grave reminder that America is built on a system designed to treat minority communities differently. One in every 1,000 Black men in the US will be killed by law enforcement, estimates a 2019 criminal justice study. Among young Black men between 25 and 29, police brutality ranks as the sixth leading cause of death. And more than half of police brutality cases go unreported, especially when they involve Black people. 

[Related: Racism is undeniably a public health issue]

In the wake of Nichols’s murder, medical organizations like the Association of American Medical Colleges released statements condemning the violence. But they didn’t address the fact that fear of being harmed by figures of authority can also carry over to medical institutions and personnel. Sirry Alang, an associate professor of Black Communities & the Social Determinants of Health at the University of Pittsburgh School of Education, says police brutality must be considered a public health crisis. “Police brutality literally kills people. It causes death and disability and it shifts relationships with healthcare providers that make people less likely to seek care.”

The roots of medical mistrust

Medical mistrust is the belief that people working in the medical field want to harm you or don’t have your best interests at heart. Alang says it tends to come from the concern of being treated differently because you are affiliated with a specific racial or gender group. 

Medical mistrust has been justified through American history. From the 1930s to the 1970s, public health researchers with the Tuskegee syphilis study infected hundreds of healthy Black men and intentionally withheld treatment when penicillin became available. What’s more, the bogus science of eugenics promoted the forced sterilization of thousands of people of color in the 20th century. 

Mistrust has also arisen, in part, because of the prejudices workers at medical institutions hold against certain groups of people. For example, Black patients are less likely to be prescribed pain medication than white patients, even if they are experiencing the same level of pain, because of a deep-rooted stereotype that they have “thicker skin.” The US mortality rate among Black mothers from complications during pregnancy is also three times higher than that of white mothers, in part because of the failure of doctors to understand the pain of Black women.

“People don’t seek healthcare as individuals,” explains Alang—their choices are shaped by personal experience and the experiences of others in their community. “One bad experience can influence the expectations of others in that network and make it easy for medical distrust to spread.”

Cycles of violence, trauma, and more mistrust 

Experiencing police brutality creates traumatic racial experiences that can subvert a person’s belief on what to expect when dealing with a figure of authority. Think about the end of an abusive romantic relationship. Even if you moved on, you might always be wary of your new partner and whether they’ll behave just as badly. Similarly, a traumatic experience with the police keeps you on edge of being mistreated in other areas. 

“If people in authoritative roles have showed they don’t respect you, you’ll be more suspicious of other authority figures like healthcare providers,” says Georges Benjamin, the executive director for the American Public Health Association. What’s more, exposure to police violence can force survivors to develop feelings of hopelessness and worthlessness and further convince them to avoid care—even when they need it.

[Related: Teen girls and queer youth are facing a crisis of hopelessness]

Another issue is that healthcare institutions support a broken public-safety system that often works against those who need it. Take emergency medical dispatches, for example. First responders tend to talk to the officer at the scene first instead of speaking with the harmed individual to figure out what happened. “They then come to you like an object it has to fix instead of a person,” says Alang. 

Crumbling police-community relations

The stress and trauma that comes from the threat of police brutality can cause long-term stress that wears down the body over time. For example, a 2016 study of Black residents living in highly policed areas of New York City found they were more likely to have poor health outcomes such as high blood pressure, regardless of whether or not officers stopped them. Benjamin says that the perception that law enforcement is not actually there to protect you can create community stress that keeps your body in a constant fight-or-flight mode.

Constant stress contributes to a higher risk of heart disease, stroke, and diabetes, along with a number of mental health conditions. But when people are apprehensive about how they will be treated for “overreacting” to the constant threat of police brutality, Alang says they are more likely to skip out on seeing or talking to their doctor about the source of their stress and trauma. They might also be less likely to adhere to medication or treatment plan. “The relationship between a healthcare provider and a patient is one of fundamental trust,” Benjamin explains. “If you don’t trust that individual, you might have some suspicions on their advice or you may not believe what they told you.”

Building a safer public health system

Reducing police violence is just one part of fixing medical mistrust; hospital, EMS groups, and public health organizations need to actively build rapport with communities grieving the loss of their members. Alang says putting out anti-racist press statements after a violent incident does little to reassure the public. Instead, both she and Benjamin advise medical institutions to take action in ways that make people feel heard or supported. 

This can come from changes like hiring a healthcare workforce that represents the patient population it’s treating, and setting up accessible mental health programs focused on addressing trauma and stress. Benjamin adds that medical institutions can work with law enforcement to build out community-based policing, including teaching them how to interact with people under stress. “Public health is not going to [completely] solve this police violence problem,” he says. “But we are part of the solution.”

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Holding hands isn’t just for human sweethearts. Chimps often clutch each other’s palms while grooming in a behavior known as handclasping. Handclasping is common among chimpanzees, and this endearing act is a social custom passed on through generations, as a study published today in Science Advances reports. What’s more, a chimp will mimic the handclasp style of the most influential members of the group, the primatologists discovered. 

“This study is fascinating because it captures the nuance of social transmission of customs among chimpanzees,” says Mary Lee Jensvold, a primate communication scientist at the Fauna Foundation and senior lecturer at Central Washington University who was not affiliated with the study. “As someone who has known this in my interactions and relationships with captive chimpanzees, it’s great to see the data to support that.”

Behavioral scientists previously thought that mirroring others of a higher social status was something unique to humans. Consider the influential power of celebrities such as Michael Jordan. People who wanted to “Be like Mike,” as the classic Gatorade ad broadcasted, imitated the way he dressed and bought products that he used. Jensvold says that “in human culture we wouldn’t question that we adapt the customs of high-ranking and prestigious individuals, and this study provides preliminary evidence of the same methods in chimpanzees.”

[Related: Adolescent chimpanzees might be less impulsive than human teens]

Handclasp grooming was discovered in 1978, one of the first times researchers observed social customs in chimps. Though like a human handshake, there’s more than one way for a chimp to grip the other’s hand, observed Edwin van Leeuwen, an assistant professor of animal behavior and cognition at Utrecht University in the Netherlands and lead study author. Some chimps like to press their palms together. Others prefer grasping another’s wrist and elbow. Chimps seem to try out different handclasp styles throughout the years before adopting the one most used in their group. 

In humans, there are multiple driving forces—peer pressure, desire to be accepted by others, fear of being frozen out—that explain conformity in groups. In the current study, the authors wanted to figure out why chimps ended up following the most popular handclasp behavior in their group, too. Their hypothesis was that chimps learn to conform from similar social pressures as people do.

From 2007 to 2019, the team looked for two types of social-learning biases in two groups of 71 semi-wild chimpanzees living in the Chimfunshi Wildlife Orphanage Trust in Zambia. The first was majority bias, when a person or animal adapts its behavior to be like most of the group. The second was dominance and prestige-based bias, in which individuals imitate others with a higher social status.

Within a group, chimps showed signs of majority bias as most showed similar hand-holding methods. One explanation, the authors propose, is that following the majority may help with gaining support in times of conflict or if there is a need for cooperation. 

Mothers play a huge role in shaping the actions of chimps, exposing infants to the grooming technique they will use throughout their life. “The young ones in these groups grow up not knowing any better that this handclasp behavior is part of chimp life,” van Leeuwen says.

The authors also found clear signs of dominance and prestige-based bias. Young and lower-ranked chimps were more likely to adopt handclasp styles to match those of higher-ranked apes. 

One observation the team noticed is that the grooming handclasp does not seem to provide any survival benefit. Instead, adopting a certain handclasp style appears to be more of a social perk in some chimp communities. Chimps may have evolved to follow others in higher positions because they’re assumed to have a certain level of expertise or wisdom, write the authors. They may also mirror a higher-ranking chimp’s gestures as a way to increase their own status. “Adopting the styles of older and dominant individuals is a way to gain social acceptance, and with the increased rapport perhaps it garners increased dominance,” Jensvold says.

[Related: By combining screams, chimps seem to know 400 ‘words’]

Does this mean individuality is discouraged among chimps? Not necessarily. There is no body of evidence showing animals discourage or punish others for not adhering to social norms, says van Leeuwen. In fact, when there was some resistance to conform, van Leeuwen noticed some chimps would participate in “negotiations” between two partners who used different handclasp grooming preferences. However, he adds, “this has never resulted in any conflicts or agitations.”

Handclasping during grooming isn’t the only example of cultural transmission in the social lives of primates—tool use is a common one, but other, more difficult-to-detect behaviors probably exist, too. Expanding on the current findings, van Leeuwen is looking for evidence of other aspects of social learning in chimps’ everyday life. His theory is that cultural processes influence the social lives of animals more than we expect.

The findings could also give evolutionary biologists more insight into how our own social norms, such as mimicking the behaviors of influential individuals, could have contributed to our species’s success. Frans de Waal, a primatologist at the Emory National Primate Research Center in Atlanta who was also not a part of the study, says that “the more we learn about the cultural practices of other species, especially other primates, the more we learn that some of the cultural tendencies observed in human society are very ancient indeed.”

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The crafty cockatoos have done it again. A new study published today in the journal Current Biology found that Goffin’s cockatoos, a bird native to Indonesia, carry multiple tools and customize their kits to whatever complex problem they are facing. “They are super flexible,” says Antonio Osuna-Mascaró, an evolutionary biologist at the University of Veterinary Medicine Vienna in Austria and lead author of the research study. “They can learn how to use tools by themselves, innovate the tool sets, and transport what they [specifically] need from them.” The findings cement Goffin’s cockatoos as one of the smartest creatures on Earth.

Goffin’s cockatoos have caught the eye of animal biologists for some time. These small white parrots are capable of delayed gratification, resisting the temptation of snacking if they know they’ll get a better reward for waiting. Captive and wild individuals show similar problem-solving behaviors and can assess a situation through different means. For example, Goffin’s cockatoos know whether an object is heavy or light just by looking at it. More recently, animal biologists have discovered that these birds can learn to create complex and multipurpose tool sets.

[Related: Adolescent chimpanzees might be less impulsive than human teens]

While Goffin’s cockatoos use clubs, picks, and other DIY instruments, they are not the first animals to do this. Elephants, sea otters, and gorillas use tools for several purposes such as to get food or create shelter. Chimpanzees, humanity’s closest living relative, go one step further. Osuna-Mascaró explains that chimpanzees use two different tools to go termite fishing: a thick and short one to open a hole in the termite mound and then a flexible one to collect the insects. The primates have also adapted their hardware to their situation. Sometimes they may only bring the probe to fish for termites because the mound already had punctured holes. 

To see if Goffin’s cockatoos could also be flexible in their tool use, the study authors created three scenarios similar to how chimpanzees wield multiple strategies for termite fishing.

1. Can cockatoos learn to use new tools?

The first experiment tested 10 captive cockatoos on their ability to innovate their tool set. They were given one sharp and pointy stick that would need to be used first to tear open a transparent paper membrane hiding a cashew, and then one long and flexible object that with a wagging motion could reach the nut behind the ruptured barrier. The study authors note this is the first time the individual birds had a tool with a function to puncture objects, so they would need time to explore the implement and then figure out how to use it.

The cockatoos had 10 minutes to figure out the solution. If they failed, they could try again the next day. A successful session was defined by the bird being able to reach the cashews in three consecutive days. 

Out of the group of 10, six cockatoos successfully got the nutty prize in three back-to-back sessions. Certain members caught on quicker than others. “Figaro is probably the most famous cockatoo in the world because he was the one who showed us in past research that cockatoos are able to make, modify, and use their own tools,” explains Osuna-Mascaró. “I was suspecting Figaro to struggle a little, so I was super surprised to see him solving the experiment in 31 seconds.” The highest socially ranked female in the group, Fini, was a close second. She finished the task in 34 seconds. 

2. Can cockatoos fits their tools to the situation?

Five cockatoos who passed the first task then moved on to the second experiment. This task tested the birds’ ability to use the tool set in different ways. The researchers randomly alternated the subjects between two boxes with two different courses of action. The first box had a membrane in which the cockatoos would need two tools to break open and retrieve the cashew. The second box had a membrane with holes already in it, so they would only need to use the long and flexible probe. 

The team kept track of which tool the birds wielded first and when they used it correctly. They found that cockatoos gradually learned and got better at choosing the correct instrument in every passing session. One reason for the birds’ high performance is because of their switching behavior between the tools, observes Osuna-Mascaró. When the parrots had to choose between the two objects, the study authors noticed a pattern where they would pick up one tool, release it, and then pick up the second tool before releasing it as well. This behavior was also seen in the first experiment, but it increased significantly in the second. 

Cockatoos who engaged in switching behavior were more likely to do better in selecting the correct tool option for the box they were in. Osuna-Mascaró’s team suggests several explanations. Moving between the two choices could help with the thought process when mulling over the best decision. Holding the tools could also help the birds recognize their functional properties and whether these features would help with the task at hand.

3. Can cockatoos tell when they need a whole toolkit?

The third experiment tested how flexible the species was at transporting the toolset. The task involved a platform holding two randomized two boxes (membrane or no membrane) containing the cashew. In the first phase, the cockatoos needed to either climb up or fly horizontally to a table holding the implements before flying vertically to reach the box. The study authors looked to see if the birds would consider these new circumstances and decide to carry along the tools together as a set in their beaks or talons. Bringing both objects at once would be energetically cheaper than having to fly back and forth.

What’s more, it provides a huge advantage in solving trickier problems, says Elizabeth Hobson, an assistant professor of biological sciences at the University of Cincinnati, who was not affiliated with the research. She says that a cockatoo having multiple tools on the go is like a human having an Allen key prepared in their pockets.

[Related: 7 creatures with skills that easily beat humans]

Out of the five cockatoos, four transported tools across the platforms and three did it consistently (Figaro included). The fifth bird never carried both tools together, though Osuna-Mascaró says this is likely because he is the strongest bird in the flock, so flying back and forth was probably not seen as labor intensive for him. 

“A tool set is more than the sum of its parts.” says Osuna-Mascaró. “Now we can argue that cockatoos have a mental representation of the needs the tool set has for them.”

Overall, Hobson think the experiments offer clearer details on Goff’s cockatoos’ cognitive prowess. “There are a couple things in this study that stand out,” she says. “It fleshes out more details about what the cockatoos are capable of in terms of tool use, and builds on recent documentation of tool use in this species in the wild.”

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County prosecutors charged former labor and delivery nurse Lindsay Clancy with first-degree murder and three counts of strangulation on Tuesday, after the alleged killing of her three children in Duxbury, Massachusetts. Clancy, who has pleaded not guilty, underwent a psychiatric evaluation before her arraignment. Clancy’s lawyer is arguing that the mother was not in the right state of mind at the time of the killing, citing “overmedication” for issues with maternal mental health.

Although there has been no official diagnosis yet, her defense attorney has suggested Clancy has a rare disorder called postpartum psychosis. A major symptom of the condition, which occurs once or twice among every 1,000 people who give birth, is that a person loses their sense of reality after pregnancy. 

People may develop postpartum psychosis quickly, immediately following the delivery or within the first week following birth, says Ariadna Forray, an expert in postpartum maternal mental health psychiatry at Yale School of Medicine. Although it can cause severe mental illness that, if left untreated, could potentially bring harm to the individual and others, Forray says “it’s rare for women to develop postpartum psychosis, and it’s even rarer to have women act out on their symptoms.” And while Clancy was reportedly taking treatments for postpartum depression, which is far more common, months before the killing, the condition itself is very different from postpartum psychosis.

What are the signs of postpartum psychosis?

People with the disorder show sudden mood fluctuations. One moment, they might feel jittery and highly energetic, and then the next moment, they may seem sluggish and more irritable than usual. “It’s your brain’s extreme reaction to having a baby,” explains Allison Lieberman, a marriage and family therapist who specializes in postpartum depression and psychosis at the online mental health platform Choosing Therapy. Chemical and hormonal shifts from childbirth, along with the stress of being a parent, can trigger a mother’s brain to have a “survival reaction,” she says.

Postpartum psychosis can be hard to recognize at first, because a mother’s physical and emotional changes often result from typical tasks like caring for a newborn baby. Parents rarely get much sleep in the first few months and often show dips in energy and appetite. 

[Related: Meditation isn’t always calming. For a select few, it may lead to psychosis.]

Specific risk factors associated with the condition are not well understood, because it’s so rare. But the most important symptoms to watch out for are confusion and disoriented thoughts that signal a loss of touch with reality. For example, parents may create delusions about the baby being sick when the child is perfectly healthy. They could convince themselves that the only way to help is to harm. “It’s the difference between knowing the intrusive thoughts are real versus not real,” says Lieberman. “Even if you think ‘I’m going to throw my baby down the stairs,’ that’s not necessarily psychosis if it disturbs you.”

However, both Lieberman and Forray stress that having postpartum psychosis does not automatically make you a violent person. In Lindsay Clancy’s case, the defense team is arguing she killed her children because a voice compelled her to do it. 

Is postpartum psychosis a symptom of postpartum depression?

No, they are unrelated to each other. The only connection is that both conditions occur after delivery. 

Postpartum depression is a medical condition where people who give birth experience intense feelings of sadness, hopelessness, and low mood within the first four weeks after delivery. Lieberman says it’s a longer and more intense version of the :baby blues,: because the condition interferes with a mother’s ability to care for themselves. “There’s this extra level of guilt that’s associated with not being able to be the parent you want to be and not enjoying parenthood,” Lieberman says. 

[Related: We don’t really know how many pregnant people are dying in the US]

Postpartum depression is common. It affects one in seven people who give birth, though many cases go undiagnosed because of the stigma and fear of being judged. Lindsay Clancy allegedly was taking 12 prescription drugs for multiple mood disorders, including postpartum depression. However, both Lieberman and Forray say it is not possible for postpartum depression to manifest into postpartum psychosis. 

While depression may cause new mothers to exhibit mood swings, postpartum psychosis is considered a type of bipolar disorder. “An estimated 70 to 80 percent of cases are related to bipolar disorder,” Forray says. Research suggests that having a history of the manic illness puts someone at a higher risk of developing postpartum psychosis after giving birth.

How is postpartum psychosis treated?

While delusions and hallucinations can take on many forms, the majority do not cause an individual to become violent. If there is evidence of postpartum psychosis in a patient, the best plan is to prevent the condition from worsening and avoiding escalation to acting out on these delusional thoughts. 

People with suspected postpartum psychosis need to be admitted to a psychiatric hospitalization where they can be assessed by a mental health expert, Forray says. Depending on the symptoms, they might then be prescribed medications such as a mood stabilizer or an antipsychotic. Another modern-day and safe alternative is electroconvulsive therapy. Research has shown the therapy helps to improve the severity of symptoms. “There’s a whole host of treatments that can be very effective,” Forray says. “And women start doing better as soon as treatment starts.”

With immediate medical intervention and the right support, it is possible to recover from postpartum psychosis. If you or someone you know is experiencing a mental health crisis, consider texting HOME to 741741 to reach the National Crisis Text Line or dialing 988 to the National Suicide Prevention Hotline. The services are free, confidential, and equipped with staff trained to get you the help you need.

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It’s Super Bowl LVII time, and this year the Philadelphia Eagles are squaring off against the Kansas City Chiefs for the championship title. While the Chiefs are returning for their third final in four years, bets are slightly favored towards the Eagles as they’ve kept a strong and consistent offensive line all season, led by quarterback Jalen Hurts. But the Chiefs could defy the odds if quarterback Patrick Mahomes fully recovers from an ankle sprain he sustained more than a week ago against the Cincinnati Bengals. 

[Related: We calculated how much sweat will come out of the Super Bowl]

Ultimately, the game could come down to every single throw. Mahomes has already proven he can hit his mark in most circumstances: His football spirals are the “closest we’ll see to breaking the law of physics,” says Chad Orzel, an associate professor of physics and astronomy at Union College in New York. “He manages to make some amazing passes from bizarre positions that wouldn’t look like they would produce anything good.” Hurts has also been leveled up his game this season through “meteoric improvements” in his throws.

Throwing the perfect football spiral might seem like something reserved for Super Bowl quarterbacks. But with some practice and science know-how, you too can chuck up the perfect spiral.

Why do football players throw spirals?

Unlike baseball or basketball, the American football relies on a spiral rotation because of its prolate spheroid shape. If you make the ball spin fast enough, it will stay in the same axis it’s pointing towards and hit the intended target straight-on, Orzel says. This follows the conservation of angular momentum: an object preserves its rotational speed if no external force is acting on it. 

Think of a spinning top. When you twist the toy and release, it will rotate in the same direction that you wound it up in, and will continue to stay upright in that angle until another external force (like your hand) causes it to stop. “It’s the same idea with football,” explains Orzel. “If you get the ball spinning rapidly around its axis, it’s a little more likely to hold its orientation and fly through [the air] in an aerodynamic shape.” 

[Related: Hitting a baseball is the hardest skill to pull off in sports. Here’s why.]

In a game where you have seconds to pass before you get tackled or intercepted, the biggest priority is to flick the ball with its nose pointed toward you. This confers less air resistance, meaning the ball can travel farther in a straight path (as long as it doesn’t meet outside forces like strong winds), explains John Eric Goff, a professor of physics at the University of Lynchburg in Virginia and author of Gold Medal Physics: The Science of Sports. A wobbly pass will result in more air drag and take longer to reach its destination, he adds. If you have to duck a defender and then pass the ball off quickly, you will get erratic air drag, which also hurts the accuracy of the throw.

How to throw a football spiral

To get a great spiral, you need to master angular momentum, which involves a few key physical factors. First, a person’s grip on the laces of the ball acts as torque—a measure of force applied to an object to rotate on its axis. In other words, the friction from the fingers gives the ball traction to spin. 

Second, you need to perfectly balance the frictional force on the ball and the forward force needed to give the ball velocity. This requires strong core muscles to rotate the body all the way through the shoulder and increase throwing power. “Tom Brady used to practice drills where he would rotate his torso quickly to help develop fast-twitching muscles in his core,” says Goff. 

Third, the hand must also be on the back of the ball to give it forward velocity, but not too far back to prevent the necessary torque for the spin. “A typical NFL spiral rotates at around 600 rotations per minute, which is the low end of a washing machine’s rotational rate and about 30 percent greater rotation rate than that of a helicopter’s rotor blades,” adds Goff. “Pass speeds are typically in the range 45 to 60 mph—the same range for cars entering and driving on highways.” For maximum force, pull the ball back to your ear just above your armpit, then release it with your elbow fully extended. Your wrist should point down at the end of the pass.

Knowing the physics behind a football spiral is only half of the battle. Both physicists emphasize the importance of practice. Practice can be as simple as watching videos of pro footballers, studying their technique using computer simulations, and playing a game of catch at the park with friends. 

Achieving a perfect spiral is challenging but doable. Even your favorite NFL quarterback might have started with a clumsy first toss. But with practice, they’ve become the ideal throwing machines we cheer for every year. 

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One of humanity’s greatest traditions is honoring the dead. Vikings burned the deceased in boats to grant safe passage into the afterlife. Ancient Tibetans practiced sky burials where corpses were devoured by vultures to cleanse the sins of the departed and allow for a peaceful ascension into heaven. But one of the most well-known burial practices in living history is mummification. Ancient Egyptians began mummifying the dead as early as 3,500 B.C.E to keep the body intact as the soul transformed from an earthly entity to a celestial being. 

Mummies serve as a glimpse into humankind’s past, including what society looked like. But despite autopsies or X-ray scans, archaeologists are stumped on how ancient Egyptians actually mummified humans. A new study published today in the journal Nature provides an answer for how they mastered this complex process. By studying the residues left on a set of embalming pots, a team of archaeologists identified chemical mixtures used to preserve the dead.

Artificial preservation is a complex process. Ancient embalmers were challenged to remove organs like the brain (they used hooked instruments to remove chunks of brain tissue through the nose) without causing physical damage or alterations to the body. Defying natural decomposition meant that they also had to be masters of chemistry. They created concoctions that would stop the body from decaying. Archaeologists studying mummies have tried to identify the unique chemical recipes, but some labels inscribed on embalming containers have been lost in translation. 

In the current study, the authors studied the contents of ceramic vessels from an embalming workshop in Saqqara, Egypt. “This archaeological site in Saqqara is the only mummification workshop ever discovered in Egypt,” says Sahar Saleem, a mummy expert and radiology professor at Cairo University who was not involved in the study. She says this discovery was a rare opportunity to investigate embalming materials and methods the Egyptians likely meant to keep secret.

Found a few meters south of the pyramid of King Unas, the underground workshop is dated around 664-525 B.C.E. The team found 121 beakers and bowls marked with embalming instructions, such as for preparing linen bandages or for specific body parts. “The findings give us a unique understanding on the actual technical steps the embalmer took based on the instructions written on the pots: how to treat the head, the order of using different mixtures,” says Saleem.

[Related: A dried-up arm of the Nile provides another clue to how Egyptians built the pyramids]

The authors studied the chemical makeup from residues left on nine beakers and 22 red bowls. They identified a large diversity of natural substances from plant oils and bitumens (natural petroleum) to resins and animal fats. Sixty percent of the vessels contained remnants of juniper or cypress. The second most commonly found product was cedar oil or tar, which were found in over half of the pots. 

Some ceramics contained blends of different chemicals. For example, one container had ricinoleic acid (a type of fatty acid used in soap) mixed with oleic acid (fatty acid found in animal and vegetable fats and oils) and possibly castor oil. The authors suggest that this combination of ingredients was used as an antiseptic and antifungal agent to preserve human tissue and reduce unpleasant smells. Bitumens, tars, resins, and beeswax have hydrophobic and adhesive properties that when made into balms could be applied onto bandages to seal skin pores and remove moisture.

“I was fascinated with this chemical knowledge of ancient Egyptians,” says Phillip Stockhammer, a professor of prehistoric archaeology at the Max Planck Institute for Evolutionary Anthropology in Germany and senior study author. He says if the ancient Egyptians ever moved the body, it could become contaminated with microbes that would try to eat up the skin. “They knew immediately they needed antibacterial, antifungal substances to keep the skin preserved, and this is without having any microbiology background.” 

[Related on PopSci+: Inside the project to bring ‘self-healing’ Roman concrete to American shorelines]

The bowls were engraved with instructions for specific steps in the embalming process. Eight were designated for head treatment and, to the authors’ knowledge, this was the first time elemi oil or tar of juniper-cypress was found as ingredients for embalming the head. Some bowls contained markers of oil or tar of conifer to ‘to wash’ the body while another bowl labeled ‘to make his odor pleasant’ showed signs of animal fat and degraded resin. To preserve the skin, ancient Egyptians used a bowl of animal fat mixed with heated beeswax as a kind of moisturizing ointment.

The researchers also found that most of the embalming ingredients were imported from other lands, suggesting Egyptians were heavily involved in the international economy. They likely traded for bitumen in communities surrounding the Dead Sea. Others seemed to have made the long trek to the Mediterranean, tropical Africa, and southeast Asian woods to find resin and elemi. “The industry of embalming was driving forward early globalization because they were transporting these materials over large distances from across Southeast Asia to Egypt,” says Stockhammer. The expansive network of trade and exquisitely refined process gives a new glimpse at how embalmers were master specialists of their craft.

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Men taking erectile dysfunction pills may be adding years to their life, suggests a sweeping observational study published in early January. The research, published on January 13 in The Journal of Sexual Medicine, reported cardioprotective effects from sildenafil, the generic name for Viagra and Revatio. Sildenafil was originally developed as a heart medication before eventually becoming approved for ED. The findings support earlier claims during the drug’s development that it possesses cardiac benefits.

“In general, these drugs appear to be safe in regards to major adverse cardiovascular events,” says lead study author Robert Kloner, a professor of medicine at Keck School of Medicine at the University of Southern California, chief science officer at Huntington Medical Research Institutes, and lead author of the study. However, he cautions that the study only showed an association, not a causal relationship, between the drug and lowered risk of heart problems and mortality. The research was partially funded by Sanofi, a pharmaceutical company that produces the erectile dysfunction medication Cialis.

[Related: Viagra could have been a groundbreaking cure for period cramps]

Sildenafil is a phosphodiesterase type 5 (PDE5) inhibitor. It works by blocking an enzyme in the walls of blood vessels, which allows them to relax and widen, increasing blood flow, most notably in the penis. But it can also improve blood flow to other areas of the body and is currently approved as a treatment for pulmonary hypertension for both men and women in the US. Decades of research in men taking PDE5 inhibitors for erectile dysfunction suggests that the drug could also help treat other heart problems, although most of these studies lacked control groups and involved small sample sizes. Kloner and his colleagues were interested in studying other health benefits the drug provides in a much larger pool that would be more likely to use it—men with ED living in the US.

The study authors analyzed 14 years of medical records of men 18 years and older diagnosed with erectile dysfunction for at least one year. The patients were classified into two groups: The first group included more than 23,000 men who spent one or more years using PDE5 inhibitors like sildenafil, and the second group was made up of more than 48,000 men with no record of ever using these drugs.

Men who had taken PDE5 inhibitors showed a 13-percent lower chance of future heart problems that involve reduced blood flow to the cardiac muscle, such as a heart attack, stroke, or chest pain, versus men who have never taken the medications. What’s more, PDE5 users were 39 percent less likely to die from a cardiovascular-related death, and 25 percent less likely to die from any cause compared to the non-exposed group. 

The amount of pills they took also mattered. Men with ED prescribed the most PD5 inhibitors (an average of 191.2 tablets) showed the most reduced risk of heart issues (55 percent) and premature death (49 percent) than those given the lowest amount of pills (an average of 5.5 tablets). “The encouraging aspect of the study was that nearly all the endpoints were improved in the same direction that is in favor of PDE-5 inhibitor exposure. This finding was consistent across the study,” says Kloner.

At first glance, the positive results might make it seem like everyone should take ED treatments to stay heart-healthy. But that’s not the case, as the observational study design makes it difficult to rule out any other explanations. For one, it only measured the number of pills given to patients, not the number actually taken, says Rigved Tadwalkar, a cardiologist at Providence Saint John’s Health Center in California who was not involved in the research. “Filling a medication does not necessarily equal taking the medication.”

Men who chose to take Viagra could have also been heart-healthier from the start. A doctor may feel hesitant to prescribe the drug to someone with a history of poor cardiovascular health, says Rena Malik, a urologist and associate professor of surgery at the University of Maryland School of Medicine who also was not involved in the study. “When does sex become risky? It’s usually when you have really poor cardiac health, and that’s when you shouldn’t be having much sex.” What’s more, for those engaging in between-the-sheets activity, it may be the exertion itself that’s providing cardiovascular benefits. People who often have sex may already be fitter than someone who is not, Malik explains. “It’s possible they have less chronic pain, are more mobile, and are flexible.” Additionally, being intimate with someone could imply that they’re less lonely than someone without a partner. “We know loneliness is associated with mortality and poor heart health outcomes” Malik notes, all of which could contribute to a higher risk of cardiac-related mortalities.

But both Tadwalkar and Malik agree that the study findings shouldn’t be dismissed, even if there are several confounding variables. “There are many factors that could play a role, but PD5 inhibitors are vasodilators that allow for blood flow, so it makes sense that these could also be protective,” says Malik. She and Tadwalkar further noted that the study was well-executed and adds a lot of value to what we already know about PD5 inhibitors. Tadwalkar underscores that doctors may be more willing to use these drugs in patients with cardiovascular problems who want to take Viagra if there are no significant and harmful reactions to the drug. 

[Related: Research on aphrodisiacs is kind of unsatisfying]

PD5 inhibitors could also be prescribed to protect the heart health of women. While female patients were not part of the study, Kloner says the drugs have the capability of relaxing blood vessels and reducing mortality for them, too. A randomized, placebo-controlled clinical trial will be needed, however, to expand the findings to other populations and make more conclusive recommendations around PD5 inhibitors and any potential cardiac benefits.

“The issue is who is going to pay for a [clinical trial],” says Kloner. Because the drugs are generic, he says there has been low interest from pharmaceutical companies and the government to support a large erectile dysfunction-related analysis that isn’t based on preexisting data. “But perhaps with our study, there will be renewed interest in funding such a study,” he states, “[and possibly] allow for new indications for these drugs for the practice of preventative cardiology.”

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Cats are weird. You’ll buy the best toys on the market, and they’ll respond by spending all their time playing in the shipping box. They’ll also randomly get short bursts of energy that have them bouncing up and down the walls, and it always seems to happen at 3 a.m. And when playing with other cats from the same household, they’ll act like Jekyl and Hyde: They can be cuddled up one moment like the best of friends, and the next minute, they’re wrestling like UFC champions.

Playtime and socialization are important for feline health, but sometimes it’s hard to tell whether cats are tussling or actually fighting. In a new study published today in the journal Scientific Reports, cat behavioral researchers identified specific interactions that would show whether your pets were being playful, aggressive, or a mixture of both (with the potential to escalate into a full-out brawl). Understanding the behavioral differences can help cat owners manage any troubling relationships in the household and, hopefully, stop Fluffy from being a bully. 

[Related: Despite appearances, your cat does love you]

The findings would not surprise professionals who work with kitties, says Mikel Delgado, an animal behaviorist and cat behavior consultant with the pet sitter company Rover, who was not involved in the study. But it confirms the current expert opinion on what’s considered playing versus fighting, and gives new insights to anyone who just loves cats.

Noema Gajdoš Kmecová, lead study author and a researcher at the University of Veterinary Medicine and Pharmacy in Slovakia, and her colleagues watched 105 videos posted on YouTube or directly submitted by people around the world to break down the antics of 210 cats. The videos included both indoor and outdoor felines, but all were considered domestic. “Within domestic cats, we have a spectrum of lifestyles living in different types of environments,” she explains. Pet owners or passersby captured videos of fights and play out on the streets in human-populated areas, as well as indoors. 

The team looked for the following behaviors: wrestling, chasing, vocalization, inactive body posture (sitting, crouching, or lying down), other interactive activities (arched back, avoidance, belly-up, stalking, or something else), and non-interactive activities involving the little beasts or an inanimate object (self-licking, walking, or drinking). The researchers focused on overt behavioral changes rather than subtle body language, like prolonged staring or ear and tail movements associated with aggression, because they may be harder for the average cat owner to spot. They also excluded any cat videos whose behaviors (mounting or biting of the neck) might have been more sexual than playful or aggressive. 

After the first run-through of footage, four of the authors rated the behavior as either playful, intermediate, or agnostic. Emma Grigg, an animal behaviorist and research associate at the University of California, Davis, who was not associated with the study, says she appreciates the inclusion of an intermediate category, as it can seem overly simplistic to treat social interactions between cats as strictly positive or negative. For example, she notes that one important gray area is when an interaction starts as a mutual play, but shifts when one cat from the pair wishes to stop playing and the other doesn’t.

More than half of the cats in the candid clips showed playful behavior. Nearly 29 percent displayed aggressive tendencies toward other felines. Finally, about 15 percent showed behaviors falling in between play and fighting. 

Wrestling was commonly associated with being playful, though it has the potential to turn aggressive. But cats that use only their paws, have no pain-related sounds, and alternate positions are signs that they are fooling around. “These cats are very familiar with each other and can afford this type of close contact,” Gajdoš Kmecová explains.

Meanwhile, vocalizing (growls, hisses, snarls, gurgles, or yowls) and chasing were strongly tied to aggression. Chasing, however, can also be considered play if both animals take turns being the pursuer. “Their discussion of the importance of looking for signs of reciprocal play was great,” Grigg says. “This is something I often hear recommended for dogs but is less commonly emphasized for cats in my experience.” Gajdoš Kmecová says that her team is working towards studying subtypes of behavior to better understand interactive behaviors beyond labeling them as wrestling and chasing. Different types of wrestling positions, for example, involve a variety of interactive behaviors and ear and tail positions.

Several other behaviors could be considered a mix of play and fighting. Cats in the intermediate group often spent a good chunk of time laying on their back with their belly up, pouncing, stalking, and grooming the other cat. According to the authors, feline interactions vary day by day, which is why they show such range in play-fighting. Like with any family member, you’re bound to have some petty squabbles, then make up by hugging or goofing off a little. A kitty showing slightly more aggressive behavior toward their housemate could just be a brief argument, and not the two drifting apart. 

[Related on PopSci+: Do cats bond with humans like dogs?]

Grigg says that any single event can not predict a relationship between felines. Rather, “patterns of behavior over longer periods of time likely reflect whether the cats are true friends or incompatible roommates,” she explains. Delgado, for her part, thinks the creatures either have conflicted relationships or that there’s still much we don’t know about these clawed assassins.

Gajdoš Kmecová recommends taking a few minutes each day to observe your cat’s interactions. Once you get a sense of their behaviors, you can evaluate and put into context how these actions shape their relationships with others of their kind—and even yourself. This gives curious cat lovers more reason to watch, film, and obsess over their pets … for science.

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In the two years since the COVID vaccines became available to the public, they have become a popular target for misinformation. Anti-vaccine activists have made some wild claims—the vaccines alter DNA, cause infertility, and implant magnetic devices for the government to track your every move—with no credible scientific evidence. But they have managed to accomplish one goal: More Americans than ever are hesitant about getting a vaccine.

So whenever a person has a rare side effect from the COVID vaccines, news spreads rapidly. For example, Florida’s surgeon general recommended boys between 18 to 39 should not get the mRNA shots, citing a questionable state analysis that claimed the risk of cardiac death jumped up by 84 percent after immunization. More recently, people were quick to blame Buffalo Bills player Damar Hamlin’s sudden cardiac arrest in early January on the NFL’s mandatory COVID vaccine requirement. Cardiologists, however, were just as quick to debunk the notion with more realistic medical explanations.

Infectious disease experts have been investigating the risk of myocarditis since the beginning of the pandemic. Thousands of studies have been published on COVID, and some have found a connection between myocarditis with both the virus and the vaccines. Here are the answers we have so far.

What is myocarditis?

Myocarditis is a disease that causes inflammation in a middle layer of the heart muscle called the myocardium. The inflammation affects muscle cell function and the heart’s electrical system, causing irregular heart beats and interfering with pumping blood to and from the body. The inflammation results from your body’s immune response overreacting to an infection it’s currently fighting. Viruses are the common cause of most myocarditis infections and are responsible for 1.5 million cases every year.

A majority of myocarditis cases are mild and self-resolving, says Keren Hasbani, a pediatric cardiologist at Pediatrix Pediatric and Congenital Cardiology Associates of Texas. Most go away in less than two weeks without complications or need to go to the hospital. 

[Related: A good night’s sleep can boost cardiac health]

Myocarditis persisting for longer than two weeks is considered chronic and can create severe complications. The longer inflammation stays in the heart, the weaker the muscle becomes. Continued injuries to heart cells can lead to permanent scarring of cardiac tissue, which can cause the condition to come back and increase the risk of stroke, heart attack, heart failure, or death.

Myocarditis can strike anyone, at any age. However, the heart condition appears to occur at twice the rate in young men than women.

What does myocarditis feel like?

In some myocarditis cases, it is possible for a person to go about their day without knowing that their heart is inflamed. When there are symptoms, they could mimic those of a viral infection, including fever, vomiting, headaches, and a sore throat. 

The most common presenting sign of the condition is a discomfort or a feeling of tightening in the chest area. Hasbani says the pain can happen anywhere between your left side to the chest bone area. Rather than the soreness you feel when you pull a pectoral muscle, Hasbani says myocarditis chest pain is often described as aches originating from a place much deeper inside the body. “People usually say it’s different from any kind of chest pain they’ve felt before.”

Individuals with myocarditis also tend to describe rapid or abnormal heart beats because the inflammation affects the heart’s electrical system. Since the organ is not functioning to its full potential, blood is not being properly distributed to other parts of the body. This can lead to symptoms such as shortness of breath, especially as the chest pain makes it difficult to take big deep breaths. The lack of oxygen can then spur on lightheadedness and fainting spells. Less common symptoms include swelling in the legs, ankles, and feet from the lack of blood distribution.

While Hasbani says it’s extremely rare, myocarditis can be life-threatening when the weakened heart cannot meet the demands of the body. In these scenarios, a person would need to be hospitalized and given medication such as adrenaline to keep the heart pumping. Doctors may also have to provide a life support machine to oxygenate and pump the blood. This allows the heart to rest and recover from the damage myocarditis inflicted. 

Is there a relationship between myocarditis and COVID?

COVID infections can cause severe and life-threatening cases of myocarditis, but the overlap is still slim. Forty out of every 1 million people are estimated to develop myocarditis 28 days after testing positive. The chances of inflammation increases among people with severe COVID illness that requires hospitalization and people with preexisting health conditions such as high blood pressure and obesity.

A 2021 study from the Centers for Disease Control and Prevention (CDC) found the risk of myocarditis is 16 times higher among unvaccinated people with COVID than unvaccinated people who have never had the disease. It also found that men and adults 50 years and older are more vulnerable to the condition. Among unvaccinated children under 16, myocarditis risk was 37 times higher in those with COVID infection than their healthy peers. 

[Related: What patients find at long COVID clinics: rejection, outdated therapies, and unanswered questions]

Hasbani says the reason why people with myocarditis from a COVID infection have more serious complications is because the body is already overworked from dealing with the extensive damage the virus is causing to other organs like the lungs, kidneys, and GI tract. Inflammation in the heart may take a backseat to all the other ongoing bodily issues and take longer to resolve. In children under 16, the CDC speculates that COVID-induced myocarditis might actually be a sign of multisystem inflammatory syndrome, which is a potentially deadly condition associated with the coronavirus. 

Can COVID vaccines cause myocarditis?

Yes, but the chances are extremely rare. One August 2022 study in England calculated the rate of hospitalizations and deaths related to myocarditis in more than 42 million people 13 and older. The subjects consisted of two different groups: individuals fully vaccinated with either the AstraZeneca, Moderna, or Pfizer-BioNTech vaccines, and unvaccinated individuals who tested positive for COVID. The researchers found a 0.007-percent chance—that’s 2,681 out of 43 million vaccinated adultsof being hospitalized or dying from vaccine-related myocarditis. Only 0.001 percent occurred within 28 days of receiving a COVID vaccine or booster. A separate study from October 2022 estimated that the myocarditis risk is seven times greater in unvaccinated versus vaccinated individuals. 

So far only the mRNA vaccines have been associated with myocarditis. The risk appears to be higher in people with a second dose of the Moderna shot than the Pfizer-BioNTech one, says Jayne Morgan, a cardiologist and clinical director of the COVID task force at Piedmont Hospital in Atlanta. The large-scale study done in England last year showed more overlap of myocarditis cases with a second Moderna dose. Meanwhile, another 2022 study measured a two- to threefold higher chance of developing myocarditis after a second Moderna vaccine, with the association being the strongest among men and people between 18 to 39. Still, Morgan warns that the rate is small compared to that of unvaccinated populations with COVID.

[Related: The truth about COVID, vaccines, ED, and infertility]

Though incidence is low, research points to young men under 40 having the highest risk of developing myocarditis, says Morgan. A September 2022 study in Israel reported 28 mild cases of myocarditis after a the Pfizer-BioNTech booster shot—out of nearly four million adults. The results showed that men between the ages of 16 to 19 had the highest risk of myocarditis (a 1 in 15,000 chance), followed by men between the ages of 20 to 24. All individuals made a full recovery after spending an average of 3.5 days in the hospital.

There is no official explanation for why young men have a greater risk of myocarditis. Some COVID researchers have hypothesized that the SARS-CoV-2 spike protein that the mRNA vaccines were designed from might trigger an overly active immune response that causes inflammation in the heart. That doesn’t mean the vaccine causes the infection, warns Hasbani: Instead, the immune system is responding to the vaccine in a way that also happens to react with heart cells in the myocardium. The effect is nearly always temporary.

Myocarditis existed well before COVID vaccines

Hasbani says any medical treatment, including vaccines, has side effects, including ones that involve the heart. The smallpox vaccine, for example, helped eliminate smallpox worldwide in 1980, but was later found to have a 10-percent risk of mild myocarditis.

One likely reason we know more about the risks of myocarditis for the COVID vaccine is that “we haven’t vaccinated this amount of people this quickly for one specific illness, and followed a large population this closely,” Hasbani explains.

With all the facts, both experts stress that the small risk of myocarditis does not outweigh the severe complications you can get from a SARS-CoV-2 infection. For instance, long COVID remains an issue for millions of patients and has been associated with far more persisting heart problems. “Giving you and your family a vaccine is much safer than taking your chance on COVID,” Hasbani adds.

If the vaccine does cause cardiac inflammation in someone, there is little chance the condition would cause a heart failure. A January 2022 analysis of more than 17 million people found just 627 cases (or 0.0035 percent) of COVID vaccine-related myocarditis. Of those, 626 individuals fully recovered and one individual died. To put that into perspective, the National Institute of Health website states: “Your chance of getting myocarditis after getting a COVID vaccine is less than the chance of being struck by lightning during your lifetime.”

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Access to gender-affirming hormones significantly improves the mental health and overall life satisfaction of transgender and nonbinary teens, finds a new study published January 18 in The New England Journal of Medicine. In one of the longest and largest studies looking at psychological outcomes, the authors’ conclusions further support the idea of gender-affirming care as a life-saving treatment.

“The authors provide a compelling defense for maintaining access to gender-affirming care for adolescents,” says Melina Wald, a child and adolescent psychologist and clinical director of the gender identity program at Columbia University Medical Center who was not affiliated with the study. For instance, the team found teens felt more comfortable in their bodies, who they are as it relates to their gender, and their mental state when they took therapeutic hormones. 

A June 2022 report estimates 1.6 million people over the age of 13 identify as transgender in the US. Among the 13- to 17-year-olds identifying as transgender or nonbinary, the number has nearly doubled from previous estimates in 2017. A common experience transgender youth wrestle with is gender dysphoria—a feeling of discomfort and distress when your sex assigned at birth does not match your gender identity. Left untreated, gender dysphoria is associated with an increase in suicide attempts and self-harm among trans teens. A branch of the National Institute of Health, the Eunice Kennedy Shriver National Institute of Child Health and Human Development, funded the latest study to try to address the issue.

“There has been a lack of awareness in the past about the unique health needs and research opportunities for transgender and gender diverse populations,” a representative of the institute told Popular Science in an email. “Research in this area is important for expanding the evidence currently guiding the clinical care of transgender and nonbinary youth.”

One of the most effective ways to combat gender dysphoria is to make a person’s physical appearance more in line with their gender identity, and hormone therapy can help. Gender-affirming hormones—such as estrogen, testosterone blockers, progesterones—are a common medical path for transgender individuals to develop feminine or masculine features that help them feel more like their authentic selves. However, one long-standing complaint from critics against gender-affirming care is that it can cause “psychological mutilation” with some arguing hormone therapy “indoctrinates” children to continue treatment as adults, speculating that they would have been happier to not. The misinformation surrounding the dangers of gender-affirming care have fueled transphobic legislation that withholds medical care from adolescents.

[Related: Exploring the common misconceptions regarding trans and non-binary identities]

“Gender-affirmative care is safe, effective, and even lifesaving,” argues Michelle Forcier, a professor of pediatrics specializing in gender, sexual and reproductive health at Brown University not involved in the study. “Children should not be pawns of politicians [who hold] safe, effective healthcare hostage for political and personal goals. Most legislators are not qualified as medical experts in gender-affirming care and have no business inserting themselves in the clinical setting.” 

Forcier says that a patient’s decision to start and participate in gender-affirmative care is a personal and private one that should only be discussed with the child, caregivers, and their medical team. Popular Science reached out to multiple study authors for comment, but they had either declined or did not respond in time of publication.

The current study recruited 315 transgender and nonbinary youth between 12 to 20 undergoing gender-affirming hormone therapy from clinical sites in Chicago, Boston, San Francisco, and Los Angeles. About 60.3 percent of participants were transmasculine and 58.7 percent were non-Latinx white. The teens started gender affirming hormones at different stages of development, with 25 already on puberty blockers before the study. From July 2016 to June 2019, psychologists used several psychosocial tests from the National Institute of Health to track any depression or anxiety symptoms the teens experienced, as well as positive effects from treatment and their life satisfaction every six months.

During the two-year study period, teens who felt their appearance reflecting more of their gender identity after gender-affirming care reported more propensity towards positive emotions  and greater life satisfaction. Youths that initiated gender-affirming care earlier already came in with lower baseline levels of depression and anxiety than those who started hormone therapy in late puberty. 

[Related: LGBTQ+ health networks helped make urban neighborhoods more resilient against COVID]

Regarding race, non-Latinx white youth showed a more significant decrease in depressive symptoms than other ethnicities and mixed race groups. However, the results may not be generalized to reflect the Black community, as there was an underrepresentation of Black participants in the study. In addition, Wald says that tracking and comparing the outcomes of youth who did not pursue hormone therapy at the study clinics would help inform any differences across transgender youth who do not have access to this type of care.

One notable observation was that transmasculine, but not transfeminine teens, showed a significant reduction in symptoms related to anxiety and depression. The differences may lie in the hormones they are receiving. Gina Sequeira, the co-director of the Seattle Children’s Gender Clinic who was not involved in the study, says patients taking testosterone see physical changes congruent with their gender identity at a faster rate than people taking estrogen. Estrogen takes longer to reduce testosterone’s masculinizing effects on the body and develop feminine features. 

“A patient on testosterone, for example, would start noticing a deepening of the voice usually within the first six months,” describes Sequeira. “For estrogen, changes like breast development take years and my suspicion is that patients may not have achieved the breasts they wanted at the two-year mark.” 

Despite all the benefits observed with gender-affirming hormone therapy, it is not a cure-all for gender dysphoria. In the study, 11 participants disclosed that they experienced suicidal ideation and two had died by suicide during the two-year period. All experts say the findings emphasize the need for a multifaceted approach to care. 

“Gender-affirmative hormones offer some benefit and relief, but youth are still navigating a potentially hostile world around them,” says Forcier, who adds that after the treatment, people may still experience a body that is not aligned with their gender identity. 

Having support at home and in the local community “can’t be understated,” says Sequeira. She adds that the more spaces a young person is affirmed in their gender identity—in healthcare settings, school, sports—the better their mental health.

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Running does wonders for your body—it lowers your risk of heart disease, boosts brainpower, helps with weight loss, to name a few. But one lesser known benefit is what running does for your looks. Not only does running have you looking your physical best, but it gives you soft and beautiful skin that may fool people into thinking you’ve shaved off a few years.

[Related: Science helped me run my first marathon in 3 hours and 21 minutes]

You don’t need to zoom like a marathon runner or buy the latest athletic wear to start running. Erin Beck, a personal trainer and the director of training and experience at STRIDE Fitness based in California, says a 30-minute run at least three times a week is enough to notice results on your appearance. If that sounds too much for you, Beck recommends starting with a slower workout like a walk or brisk jog that still gets your heart pumping. “You can absolutely still get the benefits even if you’re at a lower intensity.” The key is to remain consistent and eventually challenge yourself to run longer or at a faster pace to see results sooner. Your hard work could pay off with a major glow-up. 

1. Rejuvenate dull skin

As you run, your heart rate increases compared to when you’re sitting. Exercising places stress on your muscles, and that requires having enough oxygen to keep them moving. Your cardiovascular and respiratory system responds to the increased demand in oxygen by pumping more blood through the body and at a quicker pace. Blood vessels in the muscles then enlarge to receive more of the oxygen-rich blood. Beck says that as your body pumps more blood, it’s simultaneously flushing out toxins from your bloodstream when you sweat. “It’s great for your veins, your arteries, and especially your capillaries,” says Beck.

Capillaries are small blood vessels that carry blood all over the body. Some run right underneath the skin and help with regulating body temperature by expanding or contracting when exposed to heat or cold. Dilated vessels cool the body down by increasing blood flow to the skin surface, which allows heat to escape into the environment. Beck says the increased blood circulation during a run gives the skin more opportunity to get nutrients from oxygen-rich blood. Better oxygenation of the skin helps with the regeneration of new skin cells, leaving behind supple and glowing skin.

2. Channel luscious locks

That increased blood circulation in your skin during a run also helps with the appearance and growth of your hair roots. Lindsey Bordone, a dermatologist and assistant professor at Columbia University Irving Medical Center, says running works similar to a regularly prescribed hair growth medicine called minoxidil. They both dilate blood vessels so that when blood is delivered to the tiny vessels in your scalp, there is more oxygen-rich blood making its way to feed hair follicles.

[Related: Rosemary is the secret to long and healthy hair. Here’s how to use it to grow luscious locks.]

3. Tone down acne and breakouts

Bordone says running can help lower hormones that cause acne. The secretion of “stress hormone” cortisol and testosterone increases oil production in skin glands, making you prone to clogged pores and acne breakouts. Running long distances can help with reducing cortisol levels and as you lose weight, you’ll reduce the risk for conditions that cause imbalances in testosterone levels, such as polycystic ovary syndrome.

Another obvious benefit to running: sweating. Sweating opens up clogged pores and flushes out acne-causing bacteria and dirt. Though Beck warns that if you’re not washing your face before and after workouts, the dirt and sweat lingering on your skin can dry it out and create more opportunities for acne breakouts. 

In general, your post-workout routine is also important. An indirect benefit of running is that your brain makes healthier decisions after your workout: Running increases brain flow to brain areas involved in emotions and higher thinking—and that includes choosing what you eat. “Typically, when you’re treating your body in a healthy manner, your body reacts by craving healthy things,” says Beck. “Those urges to get more sleep, drink more water, and eat less unhealthy meals will help with clearing up acne.”

4. Reduce the appearance of cellulite

Cellulite occurs when fat attaches beneath the skin. The more fat cells you have in your body, the more likely cellulite will appear. This is because as fat cells accumulate, it pushes up on the skin before being pulled back down by tough connecting cords between your outer layer of skin and the fat underneath. 

“Think about it like bubble wrap,” says Beck. “Those connectors surround air pockets in between your skin and the fat cells. When those connectors pull too tight they create that bubbly-looking effect on your skin the same way bubble wrap has a bubbly texture on top.” 

[Related: Pilates can improve your posture and balance. The killer body is just a bonus.]

Once you create a fat cell, it cannot be destroyed. But with exercise, fat cells shrink and your skin tightens. Cellulite, in turn, becomes less visible.

5. Give your face a lift

The increased blood flow and oxygen to your face help with cell turnover, nourishing healthy skin cells and regenerating new ones. The blood circulation flushes out free radicals as well—unstable molecules accidentally made during cell metabolism that damage cells and contribute to skin aging. 

A run can also decrease cortisol levels and increase the production of endorphins, which help relax the face. “Having tension in our jawlines, for example, can lead to wrinkles,” explains Beck. “But with running, you’ll have less tension in your face and that can prevent you from deepening out those wrinkles.”

However, outdoor runners should be aware of repeated exposure to UV sun radiation. Without taking precautions like using sunscreen or wearing hats, UV rays damage the DNA in skin cells and make them unable to carry out their jobs. Damage to the skin can lead to premature aging, such as wrinkling and leathery skin.

But no matter whether you enjoy running in the park or on a treadmill, both experts agree the best thing is to get your heart pumping. Even if it’s a short run around the block, over time your small efforts will make a big difference in your health. 

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WHEN FORMER Google executive Alan Eustace dove more than 135,000 feet through the air, it was the culmination of three years of work: parachute and balloon design, test falls from 57,000 and 105,000 feet up, and flight simulations. On October 24, 2014, Eustace donned a custom high-pressure spacesuit and strapped himself into a helium balloon. He focused on his breath as he made his ascent, and calmed his nerves by thinking of his practice runs. Then he made skydiving history. The plunge from the stratosphere was 1.5 miles longer than the previous record, making Eustace the current record holder for the highest-altitude free-fall jump.

Few would have the stomach to drop at speeds hitting 822 mph from the top of Earth’s ozone layer with nothing but a parachute on their back. If you have an extreme fear of heights, just the thought may be enough to make your legs feel like jelly. But, as Eustace’s preparation showed, there are ways to gird yourself physically and mentally for that dread.

Dreading lofty elevations is a universal feeling—even daredevils occasionally get uneasy in such settings. Elizabeth McMahon, a San Francisco–based psychologist specializing in treating phobias, says Homo sapiens evolved this way to avoid perils from an early age. In a 1960 experiment, psychologists placed crawling babies on a table with a clear plastic panel at the end, which they called a “visual cliff.” The extension gave the illusion the infants would fall if they tried to reach for their mothers on the other side. Almost all of the subjects refused to crawl over the plastic.

A fear of heights, which in extreme cases is called acrophobia, most likely helped our ancestors avoid falling from life-threatening ledges, according to McMahon. The apprehension is hard-wired into human brains. When you are faced with a long drop, there is a strong response in the amygdala, a primordial brain structure. This almond-shaped region activates additional parts of the limbic system like the hypothalamus, which triggers the fight-flight-or-freeze response by signaling glands to release adrenaline and cortisol. The hormones act as a distress call to the body, causing physical changes like increased blood pressure, breathing rate, and heart rate.

Because these areas are so highly stimulated at the sight of a potential threat, brain activity elsewhere is dampened. One important area in particular becomes impaired: the more recently evolved cerebral cortex, which is involved in logic and reasoning. This makes it harder to think and make rational decisions, McMahon says.

Understanding what’s causing you to feel lightheaded and anxious is the first step toward overcoming a fear of heights. The next is to practice relaxation techniques such as deep-breathing or mindfulness exercises when doing an activity far off the ground. The first sends oxygen to the brain, indicating that you’re not in danger. The reassuring effect then activates the parasympathetic nervous system, which relaxes your muscles and instills widespread feelings of calm.

The final step is slowly exposing yourself to the source of trepidation. A psychologist specializing in phobias can use a technique called exposure therapy to help you teach your brain that heights aren’t a guaranteed death sentence. This research-based method brings you in repeated contact with the source of your fear, and your therapist will teach you how to manage your anxiety as you gradually encounter greater increases in elevation. McMahon also recommends combining exposure therapy with virtual reality programs, where you can start with something as small as simulated walks up a 20-floor staircase and eventually work toward more extreme scenarios, like being perched on top of a skyscraper.

“In my experience, five to eight virtual reality sessions have often helped people get over their fear of heights,” McMahon says. “They don’t even have to travel to the Grand Canyon.”

This story originally appeared in the High Issue of Popular Science. Read more PopSci+ stories.

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The lifespan of humans has grown in the past two centuries from an average of 30 to 72 years old. Despite this impressive change in health, our longevity pales in comparison to the rockfish. Rockfish can live over 100 years on the seafloor of shallow waters, spending most of their days hiding under rocks. (Some have been reported to live over 200 years). The secret to rockfish longevity is more complex than stumbling on an underwater fountain of youth. Geneticists at Harvard propose that the answer could lie with how they control their genes.

A new study published today in Science Advances found that rockfishes have a complex genetic network that likely influences the species’ length of life. These same genes also seem to be found in humans. “The way fish are regulating traits like longevity is actually very similar to how mammals are regulating longevity,” says lead study author Stephen Treaster, a postdoctoral research scientist at Boston Children’s Hospital and Harvard Medical School. Understanding these genetic variations involved in longevity in animals like a rockfish could one day help with treating age-related diseases in humans. 

“It’s exciting to see rockfish genomics in the spotlight,” says Joseph Heras, an assistant professor of biology at California State University, San Bernardino, who was not involved in the study. “For many years, there have been many speculations around rockfish longevity, but now with modern genomic techniques, studies like this one provide more insight into the topic.”

[Related: Could reptiles and amphibians hold the key to the fountain of youth?]

While the rockfish is considered one of the longest-lived fishes, they have a wide range in lifespan. But the exact genetic mechanism that determines how long or short a rockfish will live remained a mystery. The study authors unraveled the genetic code of 23 different rockfish species that live from 22 to 108 years. Across all tissue samples, the team found a common network of genes involved with insulin signaling—a well-known regulator of aging that may have evolved as a survival tactic to better conserve energy. A 2021 study found that the longest-lived rockfish were more likely to express three types of genes, including those influencing the insulin signaling pathway. The new findings bring more evidence that insulin-regulating genes are a main contributor to rockfish longevity.

“The authors were able to confirm and extend on many of the observations we recently made in our sequencing of rockfish genomes, including the increased constraint on pathways associated with insulin signaling,” says Peter Sudmant, an assistant professor of integrative biology at the University of California, Berkeley, and senior investigator of the 2021 study.

But there was an additional result that was unexpected, says Treaster. The team identified another set of genes found across all rockfish that were involved in flavonoid metabolism. Flavonoids are chemicals produced in plants with anti-inflammatory, antimutagenic, and anticancer properties. Since they are known to be associated with modulating several cellular signaling and enzymatic pathways, the authors suggest flavonoid metabolism could induce anti-aging effects. According to Sudmant, the authors’ emphasis that flavonoid metabolism could play an important role in extending lifespan is a “very interesting and novel pathway to follow up on.” 

After identifying two potential genetic contributors to rockfish longevity, the team searched for any similar connections in human genes. They found the flavonoid metabolism genes are not only found in humans but are significantly linked to survival. “We have these two completely different vertebrate models, humans and rockfish, and both of them have the same pathway associated with longevity,” Treaster says.

[On PopSci+: Has the fountain of youth been in our blood all along?]

Rockfishes are not the oldest living vertebrates (a 392-year-old Greenland shark nabbed the title in 2016) and are not a typical animal model to study aging. While short-lived invertebrates such as fruit flies and roundworms are more likely to be selected to study changes in lifespan, they may not apply to vertebrates like humans who live an average of 70 to 75 years. 

Unlike other long-lived species, the shift in rockfish longevity was not a one-off event. Treaster says different lineages of rockfish evolved independently to have a lengthy lifespan. “This magnitude of change is unheard of, especially in vertebrates,” he says. This gave scientists an opportunity to “wash out unrelated changes” and hone in on relevant longevity contributors that are shared by the whole species.

While Treaster is excited about identifying an association between longevity and genes in the flavonoid metabolism pathway, he knows there’s a long way to go to understand how those genes/the link help with survival. Next, his team plans to genetically modify the genes involved in insulin and flavonoid metabolism in zebrafish to see if they could reverse signs of aging. Understanding exactly what these genes are doing—and if they can be manipulated—to extend lifespan can be valuable information for slowing down the aging process in humans. “The end goal of all this research is to intervene or prevent all these age-related diseases—cancer, Alzheimer’s, heart disease—that we have a difficult time solving with modern medicine,” says Treaster. 

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Every new year, many people vow to lose weight—and 2023 is no different.  Pledging to eat healthy or hit up the gym are two of the top resolutions among Americans this year. If you’ve been scrolling through TikTok, however, you might have seen a third option for your weight loss goals: several TikTokers are injecting themselves weekly with a Type 2 diabetes drug called Ozempic, claiming it can help quickly trim your tummy. Kim Kardashian is rumored to have used the drug to fit into Marilyn Monroe’s dress for the Met Gala (though she has denied this) and Elon Musk has tweeted that he’s a fan.

Now, Ozempic’s newfound status as a weight loss hack has infiltrated TikTok, which is causing the drug to fly off the shelves. But the increased demand for the injection has also sparked a drug shortage worldwide, leaving people with diabetes without a means to get their prescribed medication. As the trend takes off, multiple health professionals are questioning the safety of using an off-label drug and its long-term effectiveness for keeping the weight off.  

For people just looking to get skinny, quick, “it’s not meant to be a short-term solution to weight loss, and it’s very expensive with people paying close to $1,000 [if not covered by insurance],” explains Rose Lin, an endocrinologist at Providence Saint John’s Health Center in Santa Monica. Lin advises the drug is not medically necessary for people without diabetes or obesity when diet and exercise can give better results for your overall health. 

[Related: ‘Hormone diets’ might work—but not for the reason you think]

Ozempic is the brand name for a drug called semaglutide. It’s approved by the Food and Drug Administration (FDA) as a once-weekly injection to control blood sugar levels in people with Type 2 diabetes. It is also approved as a treatment to reduce the risk of heart problems for people with Type 2 diabetes and known heart disease.

Semaglutide mimics a hormone called glucagon-like peptide-1 (GLP-1) that binds to GLP-1 receptors. The activated receptors stimulate the pancreas to release insulin when blood sugar levels rise. GLP-1 also has a secondary role in appetite control. Like GLP-1 hormone, semaglutide slows down the digestive process so food sits in the stomach for longer periods of time, giving you the sensation of feeling full. This feeling of satiety sends a message to the brain which blocks the release of hunger hormones that cause food cravings. 

Weight loss is a known side effect of diabetic patients who are on semaglutide drugs. However, Ozempic, in particular, is not prescribed for weight loss purposes. There is another version of semaglutide called Wegovy that was FDA approved in 2021 as a weight management injection for adults with obesity. “Generally this would be for people carrying excessive weight,” explains Lin. People who are prescribed Wegovy are considered obese (a BMI of 30 or higher) or overweight (BMI of 27 or higher) with a secondary condition or disease that may cause obesity. A 68-week clinical trial found that middle-aged adults with obesity who took weekly injections of Wegovy lost an average of 35 pounds, while participants in the control group only lost an average of 6 pounds.

Semaglutide is an effective weight loss mitigation strategy for people with obesity, but experts warn that being skinny does not equate to being healthy. “There are no easy fixes for weight loss,” says Silvana Obici, chief of endocrinology and metabolism at Stony Brook Medicine. 

[Related: Why most diets don’t work—and what to try instead]

If you don’t need to be on the medication to manage diabetes, you probably shouldn’t be using it as semaglutide does pose some safety risks. One common side effect of semaglutide is nausea from having food stay in your stomach for long periods of time. “I’ve had patients have nausea to the point of vomiting or dry heaving,” describes Lin. Other common side effects of semaglutide drugs include stomach pain, diarrhea, and constipation. While rare, there is a possibility of developing thyroid tumors, as a past study in rodents found them after semaglutide injections. Carcinogenic effects in humans remain under dispute. There have also been reports of gallbladder problems in people taking semaglutide with symptoms ranging from yellowing of the skin or eyes, upper stomach pain, and fever.

Obici also warns that Ozempic is not very effective for sustaining long-term weight loss. People using the drug will not be able to maintain the weight loss without a healthy diet and regular exercise. “An unhealthy lifestyle when taking Ozempic might obliterate the beneficial [weight loss] effects of the drug,” she says. A 2021 clinical trial found people regained most of the weight they lost after discontinuing semaglutide injections. 

Due to this temporary weight loss, it may cause people to continue to use semaglutide drugs like Ozempic for extended periods of time. Obici and Lin are concerned that long-term reliance on Ozempic for weight loss will exacerbate the global drug shortage. It’s a serious problem for diabetic patients who are struggling to access the drug. “We’ve had people over the past month or two calling in and telling us they cannot get the drug for their diabetes,” says Lin. “We’re giving them samples when we can, but a lot of times there’s just no supply.”

There are alternative drugs that people with diabetes can take instead, but the shortage of Ozempic is causing a ripple effect with other injectable GLP-1 agonist drugs. The FDA has reported a shortage of other diabetic drugs such as Tirzepatide and several doses of Trulicity. Novo Nordisk, the pharmaceutical company that manufactures both Ozempic and Wegovy, announced they have Wegovy back in stock and are working to resolve the Ozempic shortage by early 2023.

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Buffalo Bills safety player Damar Hamlin collapsed on the field during Monday night’s football game versus the Cincinnati Bengals after a blow to the chest. Hamlin immediately became unresponsive, falling into cardiac arrest and prompting medical staff to start life-resuscitating measures. On Thursday, the Bills reported that the football star has woken up and is “neurologically intact.” Hamlin remains in critical condition and on a ventilator, but his doctors have said he can communicate via writing with his first words asking who won the game. 

As of this reporting, there is no official diagnosis or explanation of what triggered Hamlin’s cardiac arrest. Hamlin’s condition has been called an “unprecedented situation” and something people haven’t “ever seen before” in the professional football community. It has not only shaken the National Football League (NFL) but has shone a light on having medical resources available to make sure contact sports are as safe as possible. 

While there’s always a risk of injury during contact sports, medical research on football has often focused on head trauma such as concussions. Cardiac injuries, on the other hand, are less common. “Think about how many blows to the chest are delivered every week in hockey, lacrosse, basketball, and baseball with no lasting trauma,” says Hal Andrew Skopicki, the chief of cardiology at Stony Brook Medicine in New York who was watching the Bills and Bengals game live. One 2013 study on 107 cases of sudden cardiac arrest found only 20.5 percent of footballers survived and with a little more than half having an on-site defibrillator—a device that shocks the heart to restore a normal heartbeat. However, while these sports-related cardiac injuries are incredibly rare, they can be fatal, Skopicki cautions.  

What happens to your heart during cardiac arrest?

Our hearts beat around 100,000 times a day to pump blood throughout the body, explains Skopicki. Hearts use electricity to create a heartbeat. A group of heart cells work together as a pacemaker to create electricity, which transmits through the heart and gets it to contract and relax. The group of heart cells are “like an on-off switch that shoots electricity in the heart which tells it when to squeeze,” explains Shephal Doshi, director of cardiac electrophysiology and pacing at Providence Saint John’s Health Center. 

Cardiac arrest occurs when the heart’s electrical system malfunctions. A misconnection or over-connection, for instance, can short-circuit the electrical system and cause the heart to stop squeezing, meaning no blood is getting pumped out into the body, including the brain. Heart attacks, a common cause of sudden cardiac arrest, obstruct blood flow to the heart. The blockage deprives heart cells of oxygen, which affects their electrical impulses, resulting in an abnormal heart rhythm.

[Related: CPR can save lives. Here’s how (and when) to do it.]

Muscle problems can also cause electrical instability. People who fall into this category often have a type of heart defect. Hypertrophic cardiomyopathy is one condition where the heart muscle thickens, causing scarring that may not allow the electrical system to function correctly. Dilated cardiomyopathy is another heart muscle disease where the left ventricle is stretched out, making it difficult for the organ to pump blood.

What do we know about Damar Hamlin’s collapse?

The Bills and medical officials have not disclosed Hamlin’s health history to the public, and it’s not known whether he has a preexisting condition that could have triggered cardiac arrest. However, professional athletes undergo rigorous screenings to detect health conditions like hypertrophic cardiomyopathy or a congenital heart defect ahead of time, says Liz Gardner, a sports medicine orthopedic surgeon for Yale Medicine. (The NFL is often selective when sharing player injury and health information with the public.)

Some medical experts have speculated that Hamlin’s collapse may have to do with a condition called commotio cordis. This is a rare situation where a strike to the chest occurs during a certain point in the heartbeat cycle. The heartbeat cycle consists of different electrical waves that mechanically stimulate the heart. The T wave is a vulnerable 20-millisecond interval when the heart rests before it begins the next beat. A blunt impact to the chest in this short time period can reset the heart inappropriately and change its rhythm, leading to cardiac arrest. Hamlin’s cardiac arrest “it’s most likely not a genetic abnormality or a weak heart, but really just a case of bad luck and unfortunate timing,” says Matthew Martinez, director of sports cardiology at Morristown Medical Center. 

Commotio cordis could happen to anyone with a healthy heart. Because the condition is based on the timing of the blow to the chest, there are no screenings or medical tests to predict it. While the condition is often seen in athletes between the ages of 8 and 18, Martinez says it’s unlikely Hamlin’s age, 24, had anything to do with it. Commotio cordis can be life-threatening. Experts say the decisive factor is the time between when the heart stops beating and resuscitation. That timing also impacts the likelihood of long-term damage to organs, including the brain.

Skopicki says Hamlin fell backwards without trying to break his fall, which usually happens when the brain shuts off. “When you see a person go down like that, the thought immediately turns to whether or not the heart is pumping blood out to the brain,” he explains. “Your brain cells can only go about five minutes without oxygen.”

What are the chances of a full recovery from sudden cardiac arrest?

Sudden cardiac arrest has only happened a handful of times in the sports world. Danish soccer player Christian Eriksen experienced cardiac arrest during a Euro 2020 match against Finland. Eriksen made a full recovery and was later fitted with an implantable cardioverter defibrillator, a type of pacemaker that releases a small jolt to stabilize an irregular heart rhythm. He resumed playing 8 months later. Others have not been so lucky. St. Louis Blues defense player Jay Bouwmeester went into cardiac arrest and collapsed on the bench during a 2020 hockey game. He recovered three days later but had to retire from professional play. In a 2017 soccer match, former Dutch midfielder Abdelhak Nouri experienced cardiac arrest, which left him  in a coma for 13 months. He later woke up with permanent brain damage.

For Hamlin, there is some good news. Gardner told Popular Science the football star has the best chance for recovery, considering the rapid response of the medical team. Medical personnel took 10 seconds to reach Hamlin and started resuscitation, which went on for nine minutes. The athlete was also intubated by the time the ambulance arrived on the field.

“Not only was he in a setting where a defibrillator was immediately available, but CPR was provided right away.” Only 12 percent of people with cardiac arrest survive, although giving CPR can triple a person’s survival chances. 

[Related: We have no idea how dangerous football really is]

Without more details on his condition, it’s too soon to predict when Hamlin will walk out the hospital, much less play football again. Doshi says that considering the extent of the injury, it’s going to be a tough road to recovery and could be some time before he could be ready to play again on a competitive level. “But I’m sure many would agree that sports is secondary to being alive,” he says.

The incident is a grave reminder that football can be a dangerous sport that goes beyond entertainment. Gardner says it’s wonderful that the NFL had first responders who quickly rushed to the scene to perform CPR, but that’s not always the case with nonprofessional sports. High school football, for example, is one area where on-site medical care is virtually nonexistent. She says if high schools are slashing budgets, there’s a possibility that medical resources needed in case of cardiac events or concussions could be downsized. “If we are going to support and sponsor contact sports, there is a level of responsibility to do that safely.”

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Now that the new year is upon us, it’s a good time to do a self-audit of the things that went wrong, right, or what you want to change in life. One common New Year’s resolution is to get healthier. For some that might mean showing up to the gym or cutting back on the carbs. But if you’re constantly looking down at your phone or slouching, a healthy goal could be to improve your posture and balance. 

Enter Pilates, a low-intensity and beginner-friendly workout intended to build strength and flexibility to support every body muscle. You can go to a class, take one-on-one lessons with a certified instructor, or follow instructional videos at home. Lauren Vestal, a certified Pilates, yoga, and breathwork instructor based in Tennessee, says that if you’re hunched over a computer all day, Pilates can help spread the collarbones wider, pull the shoulder down and back, and focus on smaller movements to keep you stable. “You’ll see yourself standing up taller and straighter over time,” she notes. With enough repitition and effort, Pilates can have a lasting impact on your health, while improving your relationship to your body.

How does Pilates help with posture and balance?

While Pilates is a full-body workout, there are targeted exercises for improving balance and posture. Much of the practice focuses on strengthening your core—the pelvis, lower back, hips, and abs—and teaching it how to work in harmony as one unit. “If your hips are uneven, you may feel a bit wobbly in the knees or ankles,” explains Vestal. “Pilates is awesome because you can target specific muscles, small or big, which will allow for greater stability throughout the body.” A stabilized trunk gives your body better support to maintain an upright and erect position, whether you’re playing sports or lugging groceries around.

Building a strong core improves balance as well. Think of standing on one leg, which most humans aren’t accustomed to doing. Chances are you might feel wobbly and possibly tumble after a few seconds in that stance. But, Vestal says that the more consistent you are, the more you’ll build up the smaller stabilizing muscles and joints to keep the core tight and engaged. “That will keep you centered and balanced.”

[Related: Working from home can ravage your spine, but good posture can help fix it]

Pilates benefits all ages. A 2018 study in 17- to 22-year-old dancers showed improved body posture after taking classes twice a week for 14 weeks. This included fixing forward head postures, hyper-extended knees, and foot movements that can cause injury. Another study in older adults who do Pilates regularly showed a significant improvement in their balance and decreased risk of falling.

One of the best starting points for posture and balance is an exercise called bird dog, says Vanessa Johnson, the director of instructor training for Club Pilates in Hawaii. Other good moves to start with are planks and swans. 

What’s the best way to do Pilates?

Compared to standard gym routines, Pilates requires little gear and offers plenty of online resources. You can start at home with a yoga mat following along with an instructor online. For those looking to make more of an investment, a Pilates reformer machine could be a supportive tool for your training. This bed-like platform uses the spring and levers to create resistance for a more intense workout.

Johnson recommends trying an introductory class at a studio to see whether Pilates is a good fit. One benefit of training with a professional is they can guide you as you learn the practice. Not only can they provide easier or more challenging adjustments to a workout, but they can fix your form if it’s incorrect. “Oftentimes people don’t realize their posture is wrong or that they need to activate a particular area of your body at home unless somebody’s checking in on them,” Johnson says. 

Another perk of attending in-person classes is that you’re leveling up your commitment—about 43 percent of individuals give up their New Year’s resolutions after a month. When people buy a package or membership, Johnson says she sees them “sticking with it and meeting their goals more often.”

How long does it take to see results from Pilates?

There’s no magic number when it comes to Pilates, but there are some baselines for how much time and effort you should put in.

All experts recommend a minimum of two workouts a week to see progress. “If I see people in the studio twice a week, I would say you’ll see results in about two months,” Johnson says. She explains you’ll start feeling differences in your posture and balance at first. After 16 to 20 sessions, you can expect other people to notice changes in your body. And after 60 sessions, she says “your body is just a different body.”

[Related: A beginner’s guide to becoming buff]

Jaclyn Forrester, a Pilates instructor and the owner of Niche Pilates in Virginia, says it’s ideal to attend an hour-long class twice a week—but admits that’s not always possible. She recommends people “mix it up” by coming to a full class and doing a 10 to 30-minute class online. You can also supplement your workout by doing other activities such as cardio. 

Forrester also stresses that the exercises are not a cure-all for bad posture and other physical issues. “What are you doing all the other hours you’re not doing Pilates?” she asks. Continuing bad habits like slouching or eating fast food, for example, can mean it will take longer to see results. “You have to really be mindful of everything else that you’re doing in your life,” Forrester says. 

Don’t feel discouraged if you don’t see results right away. “It doesn’t have to be your best workout, and your practice will not look like the person next to you in class,” advises Vestal. “But getting yourself out there and putting in the work will eventually lead to more mobility, flexibility, and strength so you can live fully.”

The post Pilates can improve your posture and balance. The killer body is just a bonus. appeared first on Popular Science.

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If you feel like everyone’s getting sick right now, you’re not wrong. Seasonal illnesses—including the flu, RSV, and COVID—are surging strongly and leaving families scrambling to stock up on medicine. A recent children’s Tylenol and ibuprofen shortage has left shelves empty and added to the stress of caring for a sick child. The pharmacies that do have some children’s pain relief medication available are limiting purchases. With a lack of options, one alternative parents and caregivers might think of doing is giving adult cold medication.

But this is the wrong move. Medical experts say that under no circumstance should parents give adult doses or cut up adult medications to give to children. “Adult medicine has not been necessarily tested or approved for use in kids, so you’re putting your own child at risk for more complications,” says William Chu, pediatrician and medical director at Pediatrix Primary + Urgent Care of Texas. Not only is it ineffective but if administered incorrectly, it could be fatal. 

No meds is better than the wrong meds 

Depending on the age, children have no need to take over-the-counter (OTC) meds when they are sick. According to the American Academy of Pediatrics, children less than 4 years old shouldn’t be given cough and cold medication. Most cases resolve on their own, plus these medicines are not very effective for this age group. “The research doesn’t show that there’s a lot of benefit to giving cough and cold medicines to kids,” says Chu. “Most of the time it’s more risky to give, and by giving adult medicines you’re only increasing the risk with none of the benefit.” If your kid is between 4 to 6, Chu advises exercising extreme caution on using OTC pain relievers and consulting a doctor first.

[Related: Is it flu or RSV? It can be tough to tell.]

Younger kids, for instance, are unable to swallow pills, so giving them a Tylenol pill to swallow could be a choking hazard. Additionally, giving adult medications incurs serious side effects, including nausea, stomach pain, and even death. “Very high doses of these cough and cold medications can be fatal for children,” says Norma Perez, a pediatrician with AltaMed Health Services based in California.

The extensive list of side effects stems from the ingredients in medicine. Decongestants, for example, are stimulatory and a high dose of it could increase blood pressure and cause seizures. Dextromethorphan, a common cough suppressant, can slow breathing, increase heart rate, and induce a coma if an excess is ingested. Acetaminophen and ibuprofen are safe at normal doses, but large amounts could lead to severe liver damage, drowsiness, and abdominal pain. 

Medication doses are intentionally different for adults and children 

Most medicines have overlapping ingredients to treat multiple symptoms, which could increase the risk of an overdose. And the chances of a child overdosing on adult pain relievers is very high because of body size. Drugs like “acetaminophen and ibuprofen are not based on age but weight,” says Perez. “Depending on how much they weigh, that’s what we calculate for what’s an appropriate dose for children.” The one or two pills recommended on the bottle have been calculated for an adult weight, and that dose could be higher than normal for a child. One exception is if a child weighs over 95 pounds or who is over the age of 12. Chu says it’s generally safe for teenagers to have adult doses of OTC medicines.

Cutting up a pill or tablet won’t help lower the dose, warns both experts. “A lot of these medications are not designed to be effective when you break it up,” says Perez. What’s more, you’re still providing a “guesstimate” of an appropriate dose; there’s no way of knowing whether you’re providing too much or too little to your child. Crushing up medicine could also make it harder for a child to ingest. Chu says “it may be difficult to swallow a jagged pill or if it’s ground and mixed with something there is going to be a taste issue.”

[Related: Here are the cold and flu remedies that actually work]

What’s a caregiver to do?

If you’re still having trouble finding children’s pain relievers, there is some good news. A lot of home remedies are helpful for relieving flu, RSV, and COVID symptoms. Honey soothes sore throats and is possibly better than usual treatment of care such as OTC cold medication and antibiotics. It also helps with cough suppression, including coughs produced by post nasal drip. “The thickness coats and protects the throat, giving you relief,” explains Perez. Honey also has antimicrobial properties that can destroy pathogens responsible for upper respiratory tract infections. She recommends giving half to a full teaspoon of honey to kids older than one year of age. 

To help with nasal congestion, a humidifier or a steamy shower could alleviate that stuffiness, especially if done right before bed. The hot steam helps to thin out mucus allowing for clearer lung and nasal airways. The relief provided from steam inhalation will help kids breathe more comfortably, and in turn, sleep more comfortably. Another way to help with a stuffy nose is by using OTC nasal sprays every two to three hours, though both experts warn not to make your own at home. You can buy nasal saline sprays at your local pharmacy and depending on the symptoms.

With all these respiratory viruses, Chu says caregivers have a right to be worried. The best course of action is to manage your child’s symptoms and keep them comfortable. If there’s any lingering concerns, see your pediatrician or take your child to urgent care.

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Chestnuts roasting on an open fire and the smell of cookies wafting through the air can only mean one thing—the holidays are here. For many, this is a time to see family and get some much needed R&R. But for people with diabetes, the food-filled celebrations can be a bittersweet reminder of what you can and can’t eat.

Having Type 1 or Type 2 diabetes doesn’t mean you have to miss out on all the goodies, however. Popular Science spoke with diabetes experts who agree that you can treat yourself this season—as long as you do it in moderation. “It’s okay to indulge on the holidays. They’re special,” says Carolyn Maxwell, an endocrinologist at Stony Brook Medicine in New York.

[Related: FDA approves first drug that can delay onset of Type I diabetes]

Read on for the diabetes do’s and don’ts of navigating merry feasts and festivities. 

Do plan ahead

If you’re going over to a friend’s or family’s holiday dinner, there are several ways to prepare. For example, you can snack throughout the day so you’re not starving when it comes time for the big meal: Having something in your system makes you less likely to binge eat unhealthy foods, says Melissa Gaynor, a dietitian at the Pediatric Diabetes Center at NYU Langone’s Hassenfeld Children’s Hospital. You’ll also want to avoid an excess amount of carbohydrates in your main course. Holiday dinners often have turkey, stuffing, and mashed potatoes in their lineups—all of which are high in glucose-producing molecules. Gaynor says that eating a large amount of these savory dishes at one time can make it tricky to control blood sugar levels, even if you’re regularly taking insulin. 

While a few carb-loaded bites won’t severely harm your health, says Gaynor, you might want to ask the host for the recipes in advance so you can keep track of what you’re eating. “There are so many websites and apps where you can type in the ingredients of a recipe and it will tell you the nutritional content and the carbs so you don’t have to guess,” she adds. Foods with a low glycemic index—a measure of how quickly they affect your blood glucose levels—are typically healthy for diabetes.

If you want more options at a communal meal, Gaynor recommends making your own dish. Not only would you have something you can definitely eat, but you’ll also know the nutritional contents without extra research. Consider bringing a veggie platter or a side such as roasted cauliflower to the party. 

Don’t drink sugary cocktails

For those who want to fully get into the holiday spirit, having two or three glasses of alcohol at a party is not too bad for your diabetes, says Maxwell. Imbibing too much, however, can lower your inhibitions and make you more likely to indulge in food.

[Related: The best non-alcoholic drinks to sip soberly this holiday]

If you do decide to stir up a drink, skip the cocktails: They’re chock-full of liquid carbs from added juice and syrup, which can spike your blood sugar. Instead, Gaynor recommends making a mixed drink using diet or zero-calorie soda, ginger ale, or seltzer. Be sure to stay hydrated in between drinks—water and other unsweetened beverages can dilute the amount of sugar circulating in your bloodstream, keeping your glucose levels in a healthy range. 

Do eat protein and fiber-rich foods

While both experts say it’s okay to have some carbs, you’ll want most of your plate made up of protein, vegetables, and high-fiber foods that “are going to have less of an effect on blood sugar,” explains Gaynor.

Fibrous fare like artichoke hearts and beans will satisfy your hunger faster, and slow down any spikes in blood sugar because the body can’t break the plant-based nutrients down. Proteins are also super filling and have a minimal effect on raising blood sugar. You can find tasty protein-rich foods in the cheeses of a charcuterie board, olives, and deviled eggs, to name a few. 

Don’t go overboard with dessert

When it comes to sweet treats, it’s all about portion control. If you’re going to gift yourself a small slice of cake, Maxwell recommends pairing it with fresh fruit. “There is sugar in fruit, but it’s almost always going to be better for you than everything else on the dessert table,” she notes.

[Related: How to avoid added sugars]

For heavy dishes like pie, it’s tricky to know how many carbs you’ll end up consuming. Gaynor says this is when it’s important to talk to the host about nutritional details. Even if you cut yourself a piece, be mindful of the serving size, she adds. And remember, you can bring your own dessert, too. Opt for something made with ingredients that have a low glycemic index, like almond or whole grain flour. “You’ll know exactly what ingredients went into that dish,” Gaynor says, “and you can pre-slice it so the portions are set.”

Do take a walk after dinner

Both experts recommend getting some light exercise after a meal at the end of the day. Not only would it help with digesting a big feast, but being active helps with lowering glucose spikes. That doesn’t mean you have to leave the party to hit up the gym: Research shows just a two- to five-minute walk around the block can make a noticeable difference in your blood sugar levels.

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Walking on the moon is hailed as one of the greatest human achievements, but if you talk to any biological anthropologist, they’d probably say it’s the ability to walk upright on two legs in the first place. But the exact driving force that shifted locomotor behavior in our early human ancestors has largely remained a mystery. A new study published today in Science Advances makes the case that our ancestors transitioned to two-footed movement to better forage for food on tree branches. The research findings could potentially revise a long-standing theory of human bipedalism.

“Bipedalism is a defining feature of the human lineage and is the first thing to separate our fossil ancestors from other apes. Understanding why it evolved is thus key to understanding what made us human,” says Rhianna Drummond-Clarke, the study’s lead author and a biological anthropology Ph.D. student at the University of Kent in the United Kingdom.

If something jeopardized a basic need—food, water, air, and shelter—the evolutionary pressure to survive would have forced our early ancestors to adapt, the authors explain. The prevailing explanation supported by anthropologists is the “savanna hypothesis,” in which our ancestors began walking on two feet in response to changing environments. About 10 to 2.5 million years ago, tropical forests began shifting into dry and open savannas. Losing trees restricted the number of food options available, pushing human ancestors to move from foraging in trees to gathering down on the ground. This habitat transition is theorized to have been the driving force behind bipedalism.

However, some anthropologists have been skeptical of this explanation. A dwindling forest likely influenced but did not necessarily drive us toward two-legged walking, explains Alexander Piel, a biological anthropologist at the University College London and senior study author. 

One reason there hasn’t been a clear-cut answer is that there are limited fossil records of our ancestors during the timeframe that human bipedalism is thought to have emerged. What’s more, the evidence that does exist, doesn’t seem to align with the savanna hypothesis. For instance, past research reconstructing ancient habitats during that time period has suggested that fossils are not in open grasslands but found in wooded areas. What’s more, the hominin fossils that are available show signs of ape-like forelimbs that would have helped swing and climb trees. That’s why Piel leans towards an “arboreal hypothesis,” where humans evolved to walk upright as a way of better foraging for food in the trees.

[Related: Shifting ancient climates shaped human evolution]

For the current study, the authors spent 15 months studying the behavior of 13 chimpanzees in the savannas of Issa, Tanzania. The team chose the Issa community because it’s a closely related ape that lives in a habitat resembling the one from a million years ago, Piel says. “What better place to investigate some of the key features—and the pressures on their evolution—that define our own species?”

The Issa chimpanzees are a primate species that spend about half of their life in trees, with the rest of the time on the ground. The study authors wanted to test whether living in a savanna increased their time on land compared to living in a forested habitat. Results showed that Issa chimpanzees spent the same time in trees regardless of whether they were in a forest or savanna setting. Additionally, locomotion data of other chimpanzee groups from past research revealed that the Issa chimpanzees spent more time in the trees than those that primarily live in forested habitats. In fact, their behavior most closely resembled Kibale chimpanzees which reside in forests.

When it comes to walking upright, the researchers noticed something interesting in the chimps. Issa chimpanzees were seen walking with two feet when up on the trees more frequently than on the ground. Bipedal movement often happened when searching for food in the forest. The results suggest that bipedalism may have emerged as a way to spend more time thoroughly searching for food in trees that were still available in the savanna. 

Scott Williams, an evolutionary morphologist and paleoanthropologist at New York University who was not affiliated with the study, says this research is a “fantastic” contribution of locomotion data. However, he maintains that bipedalism primarily evolved because of savannas. He says the data showing savanna Issa chimps engaging in bipedal locomotion 4 to 25 times more than those in forests could actually be interpreted differently. “To me, this suggests almost the opposite of what the authors interpret—that savanna habitats selected for bipedal locomotion in early hominins.” Alternatively, Williams says chimps may have spent more time up in the trees because searching for food in higher locations may have been safer and made them less exposed to predators than foraging on the ground in an open savanna environment.

Some anthropologists, on the other hand, are open to the idea that bipedalism arose from something more than changing landscapes. Alyssa Crittenden, an anthropology professor at the University of Nevada, Las Vegas, says the study provides strong evidence towards the arboreal hypothesis, especially because of where the research took place. “While savanna ecologies are often centered in conversations on bipedalism, rarely do we have the opportunity to learn from chimpanzees living in such habitats,” she wrote in an email to PopSci. “This important study provides support for the hypothesis that hominin bipedalism likely evolved within an arboreal context and persisted long after hominids began living in and utilizing more open landscapes with less vegetation.”

[Related: Our long childhoods could be linked to food-gathering skills]

Despite the unique location that closely resembles the prehistoric landscape, Williams points out that one flaw to the arboreal hypothesis is that it does not explain how non-tree dwellers—think of kangaroos, hopping mice, and even cockroaches—also evolved to have bipedal movements as well.

“The traits we identify in hominins like Ardipithecus, Australopithecus, and Homo are clearly related to terrestrial, not arboreal, bipedalism,” Williams says. “Although many species seem to have retained [other] adaptations to arboreality, which is a useful thing when food is in the trees and predators are on the ground.”

The next step the authors are taking in their research is studying the resources available to Issa chimpanzees. Doing so will help to answer how our ancestors spent so much time in trees, given the sparse supply in savannas.

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It sounds like a page ripped out of a zombie apocalypse movie script, but biologists have managed to bring the dead back to life. In a study published without expert review online in November, environmental virologists resuscitated 13 amoeba-infecting pathogens trapped under several spans of permafrost in Siberia. The ancient viruses had laid dormant in ice for thousands of years: The youngest virus was estimated to be 27,000 years old and the oldest 48,500 years old, making it the most ancient virus to ever be reanimated. 

This isn’t the first time scientists messed with bygone nature. We’ve heard comeback stories of 32,000-year-old fruit to 101.5 million-year old bacteria found at the bottom of the ocean. “I thought, if they can revive a plant, we should be able to revive a virus [because] virus particles are inert,” says Jean Michel Claverie, a professor of genomic and bioinformatics at Aix-Marseille University in France, who was the senior author of the early research. The Arctic, specifically, is thought to have a reservoir of viruses locked in its many layers of ice.

[Related: Inside a frozen tunnel hiding the galaxy’s biggest secrets]

Claverie and his team have unthawed ancient amoeba-infecting viruses before by isolating them from permafrost core samples in the lab. But with climate change on their minds, they wanted to show that there’s a realistic chance of pre-ice age infections returning in a much hotter world. (Before this study, there were only two reports of frozen viruses, the pithovirus and mollivirus, remaining infectious after 30,000 years).

The authors successfully resuscitated 13 undocumented viruses taken from seven different permafrost samples in Siberia. The oldest was found at the bottom of a frozen lake, while others were buried in places like the stomach of a woolly mammoth and the intestines of the now-extinct dire wolf. The viruses came from amoeba-infecting families such as the pithovirus, pandoravirus, megavirus, and pacmanviruses. The researchers tested the pathogens’ infectious potential by exposing them to amoeba as bait, and found that they were still virulent. 

While the study only tested the infectiousness of amoeba-infecting viruses, Claverie infers that they’ve only scratched the surface on the number of contagious agents stuck in permafrost, including those that could target animals and humans. “Perhaps the most interesting finding is that if you try to revive ancient viruses from the melting permafrost, you can do it more easily than previously anticipated,” says Paulo Verardi, the department head of virology and vaccinology at the University of Connecticut, who was not a part of the experiment.

Of course, freeing a frozen pathogenic virus that might infect humans is a legitimate concern. One reason is because of the melting Arctic. The top “active” layer of permafrost briefly thaws in the summer, regularly releasing underground microbes back into our world. However, Claverie says the chances of ancient viruses encountering a proper host is small because they decay just as quickly as they’re let out when faced with heat, UV light, and oxygen. Climate change has accelerated the timeline of permafrost thawing, allowing deeper sections of ice to dissipate and potentially for more ancient viruses to be released. 

Rising temperatures have also made it easier for people to reside on the tundra. Siberia, a land rich in oil, is under constant mining and drilling, which has the potential to release these ancient viruses. With more people inhabiting these areas, there is a greater risk of a potentially dangerous virus, explains Claverie. For example, in 2016, a 12-year-old boy died from an anthrax outbreak in the Arctic Circle, which Russian authorities attributed to the release of centenarian spores being released from a warmed-up reindeer carcasses.

With the world still reeling from the COVID-19 pandemic, people are, understandably, on edge. In response to news on the paper, Twitter users expressed fear of another deadly pandemic and potentially something worse than H1N1 and SARS-CoV-2. However, “nothing in the study suggests that these viruses are capable of infecting humans,” says Michael Buchmeier, a professor emeritus of infectious diseases at the University of California, Irvine, School of Medicine, who was not affiliated with the research. He says that it’s “very unlikely” for a future pandemic to be caused by one of the revived pathogens in the study—with the worst-case scenario being that the amoeba-infecting viruses infect other protozoans.

For Veradi, the probability of an ancient Arctic virus re-emerging and causing problems to humans is very low, but not zero. However, he warns “it seems inevitable” that we’ll see a revival of a few of these organisms.

[Related: Can viruses be good for us?]

The idea of global warming thawing out deeper permafrost layers has drawn worry from other virologists as well. Mohamed Kamel, an assistant professor in medicine and infectious diseases at Cairo University in Egypt who has conducted his own research on climate change’s effects on infectious agents, argues that any possibility of millennia-old pathogens waking from their icy slumber should be a pressing matter. “This is definitely an issue worth worrying about, as it could result in major epidemics or even pandemics if not carefully monitored and contained,” he explains. One reason is the potential for novel microbial species to present unknown genotypes that we have no available vaccines for. Ancient strains that have been preserved for thousands of years could have also gained extremely robust characteristics as a way of surviving extreme elements. 

For now, rest assured that no sci-fi-like Siberian virus is infecting animals or humans. Nor are people turning into zombies, which one news outlet erroneously inferred from the study’s findings. If anything, the threat of another pandemic—no matter how small—may encourage virologists to invest more time into tracking viruses emerging from permafrost, as well as the living ones hanging out in other hidden reservoirs. 

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Of the trillions of microorganisms that call your gut home, 13 bacterial species may contribute to depression. A pair of studies published on December 6 in the journal Nature Communications identified bacteria linked to depression and a possible explanation for how they’re promoting depressive episodes. 

Depression is one of the leading causes of disability worldwide. About five percent of adults live with the condition. If left untreated, a depressive episode can significantly impair your life, from constant hopelessness to a loss of interest in day-to-day activities. Understanding just how these microbes contribute to our mental health could shape gut-driven approaches for managing the condition.

Certain gut bacteria could be causing a chemical imbalance in the brain 

In one of the studies, the authors examined the microbiome composition of 1,539 adults in the Netherlands. “Our biggest surprise was the strength of the relationship between gut bacteria and depression,” Robert Kraaij, a senior research scientist at Erasmus Medical Center Rotterdam in the Netherlands and study coauthor, wrote in an email to PopSci. Of the 13 microbial taxa linked to depression, people with a higher abundance of Sellimonas, Eggerthella, Lachnoclostridium, and Hungatella reported more depressive symptoms. 

The 13 microbial species help produce chemical messengers—glutamate, butyrate, serotonin, and gamma amino butyric acid (GABA)—which the levels are typically altered during the depression. The findings from the current study could help identify people who are most at risk for depression, explains Najaf Amin, a senior researcher at Oxford University and senior study author. 

In the future, Amin plans to study the levels of the four chemical messengers in the blood of people with and without depression to see how they compare. Doing so may help get a better sense of how gut bacteria influence a person’s brain chemistry and how the brain regulates mood.

[Related: Magic mushrooms help cancer patients deal with depression]

Differences across ethnicities in the gut microbiomes of people with depression

The second study investigated fecal samples of 3,211 individuals who resided in urban Amsterdam. The participants belonged to one of six different ethnic groups—Dutch, South-Asian Surinamese, African Surinamese, Ghanaian, Turkish, and Moroccan. The microbiome assessments showed changes in bacterial species associated with depressive symptoms, including those species from the Christensenellaceae, Lachnospiraceae, and Ruminococcaceae families. One interesting observation, however, was that not everyone with depression had the same amounts of each microbial species. About 18 to 29 percent of differences in depression-related bacteria was due to ethnic differences.

“This is pivotal research with interesting data on gut-brain [interactions], a burgeoning area of science and medicine now,” says Harvey Hamilton Allen Jr., chief gastroenterologist at Mohawk Valley Endoscopy Center at St. Luke’s Hospital, who was not involved in either of the studies.

What we know about the gut’s involvement in depression

One of the reasons depression is difficult to treat is that there seems to be no single cause. Prior research has linked depression to stressful or traumatic life events, while others have observed depression manifesting after chronic substance abuse. Genetic factors might also be at play, as people with a family history of depression are three times more likely to have it too. The gut microbiome might be another contributor at play. 

While the idea had been tossed around for centuries, biologists have only recently unearthed physical evidence of a gut-brain connection in the past couple of decades. The theory goes that humans have a “bidirectional” line of communication between the emotional and cognitive centers of the brain, explains Hamilton Allen Jr. Imagine a telephone wire running from your central brain to your enteric nervous system—a collection of neurons in the wall of the GI tract that controls your digestive system. The enteric nervous system is often called the “second brain” for its influence on the rest of the body. 

One important piece of evidence that the gut likely plays a role in depression is that about 95 percent of serotonin—often labeled the “happy hormone” for its mood-regulating effects—is made from gut bacteria. Paxil and Zoloft, two commonly prescribed medications for depression, block the body from reabsorbing serotonin to avoid the hormone’s levels from falling too low. 

Treating depression through the microbiome

A deep understanding of the ins and outs of the gut microbiome could revolutionize how we approach medicine, including how we treat depression. “If certain bacteria are part of the cause of depression, we can design treatments to modulate these bacteria,” says Kraaij.

One potential approach is through fecal transplants. While such a treatment might seem ripe for bacterial infections, it could help promote healthy gut bacteria in people who are unable to produce them on their own (there have been reported deaths from fecal transplants among immunocompromised people). Transporting the poop from a person with a healthy gut microbiota to someone with  an unhealthy gut has already become the standard of care for treating Clostridioides difficile infections. The procedure restores healthy bacteria back into the lower intestines. Just last week on December 2, the FDA approved the first pharmaceutical-grade fecal transplant to treat difficult intestinal infections.

[Related: Autism shapes the gut microbiome, scientists report, not the other way around]

There is also some growing evidence that fecal transplants could help with depression. In a small case study published in February 2022, two people with major depressive disorder underwent poop transplants in addition to their current treatment plan. Both showed a reduction in depressive-live behavior four weeks after the procedure. One of the patients continued to show improvement in their depressive symptoms for up to eight weeks after treatment, along with improvement in other GI problems. 

The two studies could make the fecal transplant process more efficient by knowing which of the 13 bacteria species need to be transferred to make the gut healthy again. What’s more, Hamilton Allen Jr. speculates the findings could even help fecal transplants to be more personalized to different ethnicities in the future. 

Still, gut microbes are one of many factors linked to depression, Hamilton Allen Jr. says. Without an experiment that could manipulate the microbiome to see how people fared with and without these microbes, scientists cannot definitively say a gut imbalance is a primary cause of depression. But he says, “this is definitely one of the new treatment modalities, and as we learn more about this organ, we are going to see more research going into treating the microbiome.”

Correction (December 12, 2022): This story has updated the genus name Clostridium difficile to Clostridioides difficile to reflect changes in taxonomic classification of the bacteria.

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The World Cup is in full swing, with countries duking it out on the soccer field for the championship and, of course, bragging rights. This World Cup has been anything but predictable. Fans were in uproar after Saudi Arabia beat out Argentina’s powerhouse team—the kingdom held a national holiday the day after to celebrate the win—while German fans were in disbelief after losing to Japan. And in a major upset, Mexico’s team was eliminated from the group stage, a first since 1978.

Whether or not you’re a soccer enthusiast, it’s hard to deny the excitement of seeing your home country move closer to the gold. And while not everyone can travel thousands of miles to the games held this year in Qatar, psychologists say there’s good reason to tune into a match. PopSci asked experts about the top five health benefits that come from rooting for a team, even if you’re just on the couch.

[Related: All the ways you can tune in to the 2022 Soccer World Cup]

You feel less lonely

Humans are, by nature, social creatures. This makes the world’s most popular sport a great opportunity to bond with others and find community. Carrie Wyland, a social psychologist at Tulane University in New Orleans, says there are two main reasons why. The first reason is that cheering for a team allows you to feel connected to something bigger than yourself. “Cheering for our favorite teams gives us a sense of identity,” she explains. This social identity is built on the small groups you’ve formed or connected with throughout your life. When you are deeply bonded with a group, your personal self shifts to a greater whole, creating a deeper sense of connectedness with others, explains Wyland. 

The second reason is collective joy. Whether you watch with family or go solo to a bar, your body experiences high arousal emotions, such as happiness and excitement, when you witness an event like your team scoring a goal. “When we experience and share these positive feelings with other people also watching the game, that actually allows us to enhance those emotions and have a greater emotional experience.”

And this social bond is felt through ups and downs—triumph and defeat. When your team loses, you might feel down for a few days, but there is an upside. Wyland says losing a game is still a collective experience and can continue to foster stronger bonds with others—whether in person, through a group chat, or even on social media—as you lament the loss together and figure out what went wrong.

You have higher self-esteem

A 2019 study in the journal Communication and Sport found that fans of winning sports teams reported higher self-esteem two days after the game. While more research is needed to confirm this link, Wyland says the boost in self-esteem after spectating a game may be from a psychological concept called “basking in reflected glory.” It’s when you associate another person’s wins with your own because of your close ties with this group. This can also be seen in fans who rejoice when their favorite music artist wins a Grammy or in supporters of a political party when their preferred candidate gets elected. In this case, a fan’s social identity in soccer may make them feel like they’re part of the team. So when fans cheer or perform rituals like wearing “lucky” socks, they feel like their support aided in the team’s victory.

You increase your life expectancy

There is some indirect support that cheering could help increase your lifespan. But this depends on how you cheer. Are you glued to the couch passively watching or are you physically getting up to jump and down or wave your hands when cheering? While it’s not near an actual physical workout, Wyland says small movements and gestures matter because it gets your body moving.

[Related: How to work out for your mental health] 

Socializing also positively impacts longevity. Social relationships—building friendships or feeling part of a community through sports—have been long associated with good physical and mental health. Regularly watching sports has even been linked to fewer depressive symptoms, which has been previously associated with a 10 to 12-year shorter lifespan in older adults. When you have that social support, there is evidence of a decreased risk of early death.

You relieve stress 

Getting swept away in the action of a game can help immerse yourself in the moment, especially in times of celebration, like when team USA’s Christian Pulisic scored that final goal against Iran to advance the team to the knockout rounds. 

“Sports are a celebration of life, and you are totally in the present—away from the regrets of the past or the anxieties of the future,” explains Eric Zillmer, a neuropsychologist and former director of athletics at Drexel University in Philadelphia. 

Watching and celebrating sports teams allows for a temporary escape from present reality. Zillmer says a game like soccer has rules and boundaries that can be therapeutic and easy to digest for people dealing with the unpredictability of life. Sports can also have people return to a simpler view of life: a triumphant comeback of the underdogs or the fairy tale moment of a superstar player carrying their team to the finals. 

“We know from studies on mindfulness and yoga that living your life in the present is very therapeutic for your health,” Zillmer says. “Sports make us feel alive, and it can be a catalyst for finding things that we hope to find in ourselves.” Sports are all about overcoming obstacles, he says; if those beating challenges exist in sports, they could exist in real life. 

[Related: The complex physics behind bending it like a World Cup player]

You are more motivated to exercise

Wyland says that seeing players zoom across the field and launch soccer balls into the air could inspire kids to get out and play the sport as well. Children may be energized after an exciting game and may want to play outside and emulate their favorite players like Argentina’s Lionel Messi or France’s Kylian Mbappé.

Adults can get in on the action, too, by channeling their excitement from watching the World Cup into their next workout. Zillmer advises linking high-probability behaviors (activities you like or enjoy doing) with low-probability behaviors (things you don’t want to do and may actively avoid). So if you’ve been meaning to exercise but can’t find the motivation to do it, think about your next session as a means to a reward. For example, if there’s a good chance you’re going to watch the USA versus Netherlands game (a high-probability behavior), then force yourself to engage in a low-probability behavior such as a walk around the block as a way of “earning it.” 

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There is no official cause for irritable bowel syndrome (IBS), but for one gastroenterologist, the answer has been right under our noses. A review published today in The American Journal of Gastroenterology posits that the all-too-common ailment is caused by the forces of gravity. The unconventional hypothesis suggests the human body has evolved to live with this universal force, and when our ability to manage gravity falters, it can have dire ramifications on our health.

“Our relationship to gravity is a little bit like a fish’s relationship to water,” says Brennan Spiegel, a gastroenterologist at Cedars-Sinai Medical Center in Los Angeles and author of the new paper. “The fish evolved to have a body that survives and thrives in water, even if it may not know it’s in water to begin with.” Similarly, Spiegel explains that while we aren’t always conscious of gravity, it’s a constant influence on our lives. For example, our early human ancestors evolved to become bipedal organisms, spending two-thirds of their lives in an upright position. But standing erect would cause gravity to constantly pull our body system down toward the ground, meaning organs and other bodily systems must have a plan in place to manage and resist gravitational forces. (For example, mammalian brains have evolved ways to sense altered gravity conditions.)

[Related: What to do when you’re trying not to poop]

Spiegel says he thought about the gravity hypothesis in relation to IBS when visiting a sick family member at an assisted living center. Lying in bed for most of the day, he noticed an increase in GI problems during her stay, including constipation, bloating, and abdominal pain, making him evaluate whether lying down all day changes a person’s relationship to the force of gravity. “Why is it that she’s not able to move her intestines as well as she could before,” he first questioned. 

Think of the GI tract as a sack of potatoes. Humans internally lug around this sack their whole lives, though Spiegel argues that some people’s body compositions are better suited to carry that sack around better than others. But according to Newton’s Third Law (for every force in nature there is an equal and opposite reaction), because gravity is pulling our body down, our body’s must have “antigravity” mechanisms in place to stabilize organs. This support comes from musculoskeletal structures like the spine and mesentery that works as an internal suspension system to hold the intestines in place. What’s more, the rib cage along with the spine helps to secure the position of the diaphragm, which acts as a ceiling mount to suspend organs in the upright abdominal cavity. All together, these structures work as a crane to stabilize and keep the organs in place.

But what happens when the antigravity mechanisms in our body fail? You’ll see symptoms very similar to those who have IBS, according to the research paper. When the musculoskeletal system is not aligned with gravity, it’s not capable of completely resisting this force of attraction. The mismatched strain between attractive and repulsive forces would theoretically cause tension in the body, resulting in muscle cramping and pain from being unable to properly support the contents in the abdomen. Additionally, excess pressure on the spine from trying to stabilize sagging structures would cause intense back pain. Finally, if the abdominal crane starts to sag and loosens its hold, the pull of gravity would cause the organ to move out of place, pushing the GI tract forward and giving little space for food to move in and out of the tract. All of these changes may compound in IBS symptoms.

One point Spiegel emphasizes is that the gravity hypothesis is not meant to disprove other ideas—two popular ones being that IBS is caused by changes in the gut microbiome or from elevated serotonin levels—but rather, a way to tie in all them into a concise explanation. 

“Intestines fall under the force of gravity, and they can develop a problem where they kink up almost like a twisted garden hose that makes it hard for water to get through,” Spiegel says. “As a result, they get bacterial overgrowth, and they get abdominal pain and gassiness.”

[Related: What happens if you get diarrhea in space?]

Julie Khlevner, a gastroenterologist at the NewYork-Presbyterian Morgan Stanley Children’s Hospital who was not affiliated with the research, says that while the gravity hypothesis is less conventional than other prevailing theories for IBS, it has been previously used to explain other diseases like amyotrophic lateral sclerosis. “Although [it’s] thought provoking and theoretically compatible with the clinical manifestations of IBS, it remains in its hypothetical stage and requires further research,” she cautions. “For now, the currently accepted concepts in pathophysiology of IBS [alterations in the bidirectional brain-gut-microbiome interaction] will remain the pillars for development of targeted therapies.”

If Spigel is right about his rationale, he could be onto something bigger. Understanding how gravity alters our bodily functions could help find answers on why certain exercises, such as yoga and tai chi, can relieve GI symptoms by strengthening musculoskeletal muscles and the anterior abdominal wall. Or why people experience more stomach problems at high altitudes like when climbing up mountains, or more generally, why women are disproportionately affected by IBS. Spiegel already has an explanation for the last issue (he says women have more elastic internal structures than men, including floppier and longer colons that are more susceptible to the pull of gravity), but he’s hoping others will pursue the same line of work and help bring relief to the millions of people living with IBS everyday.

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At most family gatherings, a Thanksgiving meal is not complete without the turkey. As the popular centerpiece is carved and served, chances are you’ll be asked: Would you like white or dark meat? And people have some strong preferences for specific slices of the giant bird. Dark meat devotees swear by the juicy tenderness of a plump thigh while white meat lovers will be quick to point out the healthiness in a lean turkey breast. From taste to nutrition, many have debated over which color meat is better.

Turns out, there is no right answer. “White or dark poultry meat, there’s not much of a difference [in terms of health],” says Dong Ahn, a poultry researcher and professor in the department of animal science at Iowa State University. “A lot of people in the US like white meat better than dark meat [in all poultry] because people are afraid of fat and try to avoid fats at all costs. But in other parts of the world, they prefer dark meat because it’s more flavorful.”

Fat vs. flavor

When people say white meat is better than dark meat, chances are they’re referring to saturated fat. “The saturated fat for the dark meat is a little bit higher than white meat,” explains Joan Salge Blake, a nutritionist and professor at Boston University. But, she adds that the difference in fat between white and dark meat can be really small. For example, a three-ounce serving (about the size of your palm) of white meat without the skin is about 125 calories and with less than two grams of fat, Blake says. In contrast, three ounces of dark meat without any skin has 147 calories and five grams of fat—just three more grams of fat from white meat.

[Related: Prep your organs to eat as much food as possible on Thanksgiving]

Dark meat may have increased fat content, but that’s often why people find it more flavorful, says Blake. As fatty acids are exposed to high oven temperatures, the heat oxidizes them into new volatile compounds that enhance meat flavor. Plus, while dark meat is a bit more caloric and fatty, it’s packed with helpful nutrients. The red meat also has a lot more vitamins and minerals—iron, vitamin B-12, vitamin A, and zinc—than lighter, leaner meat. 

Why does turkey have white and dark meat?

Regardless of color, all turkey meat is equally healthy. So why does white and dark meat look so different? That boils down to the muscle activity of the gobbler. Dark meat is typically found in the thighs and legs of the bird. Turkeys spend a lot of time on their gams, standing and walking around. This causes their muscle fibers in these areas to be typically larger and require a constant energy source, Ahn says. Energy is produced using muscle fat and oxygen taken from myoglobin, which are proteins found in muscle cells that capture oxygen from your blood and supply them to working muscles. Myoglobin naturally has a red pigment, and the more active the muscles are in the thighs and legs, the more myoglobin accumulates in the area.

[Related: 5 main dishes to serve up as alternatives to turkey at Thanksgiving]

White meat, on the other hand, comes from the wings and breasts of the turkey. Ahn says white meat has a lighter shade because the structure and muscle composition in these regions are different from dark meat. Turkeys do not normally fly unless startled or in danger—even then it’s only at a short distance and not very high from the ground. Because these muscles are not used often, there is less muscle fiber and, therefore, less demand to make constant energy from muscle fat. As a result, there is less of a  need for myoglobin to shuttle oxygen to these muscle groups. 

If you’re one of the few who hasn’t pledged loyalty to either color of meat, Blake says you can’t really go wrong with any part of the turkey. When cooked properly, the whole turkey is a rich protein powerhouse, she says. “It’s a bird that keeps on giving and giving.”

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Few openly admit it, but everyone picks their nose. Whether you’re digging for treasure, out of irritation, boredom or habit, it’s natural to indulge once in a while. Most start sticking their fingers up their schnozes as toddlers, and continue the occasional pick and flick as adults. But nose picking recently flooded headlines in a rather alarming—and misleading—way.

An Alzheimer’s study published in the journal Scientific Reports this February has generated a lot of buzz over the past week after Griffith University in Australia published a press release that linked nose-picking to a risk factor of late-onset Alzheimer’s disease.The reason, both the writeup and one of the study authors suggested, is that a harmful bacteria Chlamydia pneumoniae could travel up the nose and into the brain where it could create signatures of Alzheimer’s disease. (Popular Science reached out to the same study author for comment, but did not get a response.) 

Days after the initial press release, some news outlets ran fear-mongering headlines like “Picking Your Nose May Cause Dementia!” and “How picking your nose could increase risk of Alzheimer’s and dementia.” But there’s one problem—the study never showed that nose-picking causes future neurodegenerative disease. Instead, it describes a map of how outside pathogens might enter and infect the brain. “The study was very well done, but it’s important not to take it out of context,” says James Giordano, professor of neurology and biochemistry at Georgetown University Medical Center, who did not participate in the research. “Never did they say in the findings if you pick your nose, you’re going to get Alzheimer’s.” Here’s what the study really found. 

What was the “nose-picking” Alzheimer’s study about?

Alzheimer’s, the most common form of dementia in the US, impairs parts of the brain that control memory often in adults older than 65. But researchers are still trying to fully understand the exact mechanisms that trigger the disease. Past studies have suggested that certain bacteria and infections could be involved in damaging the same brain areas and functions commonly associated with Alzheimer’s. But evidence has remained unclear. 

[Related: One big reason why Alzheimer’s might be going undetected in the US]

In the February study, the authors found a potential nasal route for bacteria to reach the brain. When the olfactory mucosa, a membrane found in the upper region of the nose, is damaged, it gives the invading bacteria entry to an area heavily innervated with endings from the olfactory nerve. The olfactory nerve controls a person’s sense of smell and is one of the shortest cranial nerves as it starts at the brain to the upper roof of your nose. If bacteria bypasses the olfactory mucosa, it can travel directly into the brain. Giordano describes the journey as a “minimum toll road” to the brain, with the nasal mucosa being the only area where you’re forced to stop.

“If the nasal mucosa tollbooth is down, you can get right on the olfactory nerve superhighway and move up the brain.”

The connection to Alzheimer’s is the bacterial species used in the study. Chlamydia pneumoniae, which is not the same species behind the STI, is a bacterium that causes pneumonia and has been looked at as a possible contributor to Alzheimer’s. Past research has found a large presence of Chlamydia pneumoniae in people with Alzheimer’s brains. However, few studies have shown direct evidence of the bacterium causing neurodegenerative disease. 

The team observed signs of the brain fighting an infection days after the olfactory mucosa was injured. Additionally, they noticed increased Chlamydia pneumoniae levels, a buildup of beta-amyloid plaques (clumps of proteins that may block cell signaling at synapses) in the brain, and altered genes related to Alzheimer’s. The authors speculate the bacterium infected and hid inside glial cells, or non-neuronal cells, giving it time to clone itself and spread to other parts of the brain. 

While not studied directly, Giordano theorizes the bacterium could influence the development of Alzheimer’s by extending the time the brain is in a proinflammatory state. As the brain increases inflammatory responses to fight the bacterial infection, it could lead to a rise in chemicals called superoxides. Superoxides alter the metabolism of brain cells, which can then produce abnormal structural and functional proteins such as beta-amyloid and tau—fibers that can tangle and slow down memory recall. 

Can nose-picking damage your nose and trigger Alzheimer’s?

Extremely unlikely. As Giordano points out, the Scientific Reports study never set out to find whether Chlamydia pneumoniae leads to Alzheimer’s or dementia. Instead, it aimed to determine the probability that repeated intrusion of the nasal mucosa would give infectious agents the means to reach the brain through the olfactory nerve, which is a few degrees away from developing the actual condition. 

“What they’re suggesting is that individuals with repeated violations of the nasal mucosa have a high enough probability of bacteria and viruses migrating to the brain and potentially activating a proinflammatory state, which then has the potential for inducing neurodegeneration.” In other words, the study lays out theoretical scenarios explaining how bacteria could trigger Alzheimer’s, though it doesn’t answer whether nose picking can be a cause.

[Related: We have now seen our sense of smell in action]

Giordano notes three other issues with drawing conclusions from this type of research. First, it only included mice. While the species is usually an excellent model for studying Alzheimer’s and other diseases, at minimum, it would take 3,000 times more infectious agent to damage the olfactory mucosa in a larger subject. The second issue is that the study does not address whether the human immune system is more capable of responding to airborne or environmental agents that cause disease. This would mitigate any damage pathogens would have in the nose. Lastly, the neuroscientists involved in the research were not watching mice for hours until they picked their noses. Their experimental model involved inserting enough bacteria into the mice’s noses to break the nasal mucosa, which is not how people naturally encounter foreign pathogens.

Does this mean you can go back to nose-picking to your heart’s content?

Yes, but you still want to be cautious. Picking your nose doesn’t make the list of things that can cause severe injury to the nasal mucosa—you could cause more damage clipping your nose hairs or getting a foreign object stuck up there. Still, there’s a huge difference between someone who picks their nose every once in a while and someone who’s probing their schnoz all the time. 

If you aggressively pick your nose or do it with a dirty finger, you may get nosebleeds from scratching your insides. What’s more, frequent nose-picking increases the probability of introducing or spreading other types of bacteria or viruses that may try to invade your cerebrum. This has been a concern with SARS-CoV-2, in that it could directly infect the olfactory epithelium and affect a person’s sense of smell, Giordano explains. “That’s why the study is very good. It’s asking whether other infectious agents use similar vectors to access the brain.”

It’s a valid question to ask, and could maybe lead to more specific research on devastating diseases like Alzheimer’s. But the leap from picking your nose to Alzheimer’s is too far. So, for now, it’s better not to spread any scary assumptions. 

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Earlier this week, Brazilians elected Luiz Inácio Lula da Silva (popularly known as Lula) as their new leader over right-wing President Jair Bolsonaro. Lula’s victory is a historic comeback after he served 19 months in prison for bribery charges. But the real winner of the election? The Amazon rainforest. Lula, who had previously been the president of Brazil from 2003 to 2010, has made pledges for new climate policies, including reducing the amount of deforestation that was largely ignored under Bolsonaro’s presidency. And a win for the Amazon is a win for the planet in its fight against climate change.

“Everybody in the world can breathe a sigh of relief since the Brazilian Amazon is important in regulating the world climate,” explains Philip Stouffer, a conservation biologist and professor at Louisiana State University who has been researching the rainforest since 1991. “Our world battle against climate is maintaining the carbon in rainforests, and this election result moves the needle in a positive direction for maintaining that carbon.”

The Amazon rainforest has shrunk significantly in the last few decades. Since 1988, about 10,000 acres (nearly the size of California) of the Amazon has been destroyed everyday. The chief causes can be traced back to the impacts from climate change and human activity, explains Chris Boulton, an associate research fellow at the University of Exeter’s geography department. On one hand, weather changes in temperatures and rainfall patterns have contributed to Amazonian destruction. For example, longer dry seasons and frequent “100-year droughts” have made it harder for the rainforest to recover, making it less capable of absorbing carbon. “The Amazon is usually called the lungs of the Earth because it takes carbon dioxide from the atmosphere,” explains Boulton. 

On average, the Amazon rainforest absorbs about 123 billion tons of carbon. But deforestation and other human activity is helping to turn this carbon sink into a carbon source. Destroyed trees release carbon dioxide and other greenhouse gases back into the atmosphere. Under Bolsonaro’s rule in 2019 to 2022, the Amazon rainforest lost 4.8 million acres in just 2021 alone. Deforestation also reached its highest levels in 15 years as of 2021. What’s more, Boulton says that taking away trees breaks down the Amazon’s water recycling network—the forest needs about 80 percent of its trees to maintain it—making it harder to sustain itself during a drought.

[Related: The Amazon is on the brink of a climate change tipping point]

Boulton studies climate tipping points, when the accumulation of small changes cause large and irreversible climate conditions. He says the Amazon is getting closer to reaching that point of no return. “Our work earlier this year shows that around 75 percent of the forest is showing early signals where you’re moving towards a tipping point,” he explains. “It’s only in those areas where you’re getting a lot of rainfall that you don’t see an approach towards a tipping point.”

The Amazon is on its way to the tipping point, at an estimated 20 to 25 percent. Once that threshold is passed, researchers project the lush rainforest would collapse and become a dry savannah. One geographer studying land changes in the Amazon forecasts that the tipping point will be reached by 2064. Stouffer warns that a transition to savannah would have catastrophic effects on the global climate. As carbon would go back to the atmosphere, the trapped greenhouse gases would speed up global warming. The warmer temperatures would cause frequent flooding, fires, and the extinction of animals who live exclusively in rainforests.

“That’s why there’s a lot of optimism because Lula had a good track record at slowing deforestation when he was president before [in 2003 to 2011],” says Stouffer. 

[Related: Brazil’s president Bolsonaro plans to plunder the Amazon, which is bad news for all of us]

One of Lula’s proposed policies highlighted in his victory speech is zero deforestation, which entails increased surveillance of the Amazon and promoting sustainable development. He also plans to reignite talks for global cooperation on rainforest conservation—a welcoming development to countries such as Norway who stopped sending rainforest protection funds to Brazil in 2019 during Bolsonaro’s presidency. The Nordic country announced on Monday it will resume subsidies.

Stopping deforestation will be an uphill battle for the new administration as Bolsonaro leaves an office that crippled environmental agencies and dismantled dozens of environmental laws, such as those that imposed harsh fines for illegal deforestation, promoted biodiesel production, and limited mining permits. But if all goes well, one analysis predicts that Lula could reduce 89 percent of deforestation in the Amazon over the next decade, cementing his once-tarnished legacy into one as a formidable global environmental leader. Lula will officially take office as the 39th president of Brazil on January 1, 2023.

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No one enjoys tossing and turning through a nightmare, and now, sleep scientists from the University of Geneva in Switzerland may have found a way to make sure your rest stays peaceful and undisturbed. A new study published today in the journal Current Biology found that combining a cognitive technique called imagery rehearsal therapy with targeted memory reactivation during the REM stage of sleep reduces the number of nightmares a person experiences each night. The research included 36 people with moderate to severe nightmare disorder (having more than one episode a week)—a condition that affects 4 percent of adults around the world. 

“The study demonstrates again that imagery rehearsal therapy alone works to improve the nightmare disorder,” says Thomas Kilkenny, the director of the Institute Sleep Medicine at Northwell Health in New York City, who was not affiliated with the study. “But the new twist is that the addition of targeted memory reactivation to the imagery rehearsal therapy not only improves the nightmare disorder, but also increases the amount of positive dream experiences.” 

Individuals with nightmare disorder face more than the occasional bad dream. This rare type of sleep disorder causes people to have frequent nightmares, often causing problems falling and staying asleep. One reason sleep experts have trouble banishing nightmares for good is because they still don’t know why the phenomenon happens in the first place. There is no universally agreed upon reason why we dream, much less have nightmares, explains Kilkenny. He says one common belief behind dreaming is that they help store important memories, get rid of unimportant ones, and sort out complicated thoughts and feelings. Severe nightmares, in turn, are hypothesized to be dreams connected to unresolved anxiety and trauma.

[Related: For better sleep, borrow the bedtime routine of a toddler]

Imagery rehearsal therapy is already a commonly used tool for people who experience frequent nightmares. A psychologist will ask the individual to describe a recurring nightmare while awake and identify possible triggers for the experience. Afterward they work with the patient to “rewrite” a new ending to the dream with a more pleasant outcome. For example, if the nightmare involves someone chasing you down a dark alley, you may try to imagine a passerby you can flag down for help or visualize holding a weapon you can use to take down the assailant. The goal of rehearsing the ending is to change the nightmare to something less frightening and more peaceful.

The recent study hopes to enhance the success rate of imagery rehearsal therapy with another cognitive tool, which uses different external stimuli as a cue to reactivate more pleasant memories from earlier in the day. The authors used targeted memory reactivation to play a sound associated with a positive experience. Re-exposing those associations would, in theory, make the mind focus on consolidating them into long-term memory rather than a negatively charged memory fueling nightmares.

In the experiment, 36 people with nightmare disorder underwent an imagery rehearsal therapy session where they brainstormed alternative endings to their bad episodes. In addition, half of the patients were asked to complete an additional task: create a resolution to their nightmare and associate the happier ending with a sound. “The important point is to have the external stimuli be able to be associated with the thoughts one wishes to remember,” Kilkenny explains. In this instance, the sound was a one-second piano key that played every 10 seconds through headphones as patients imagined their positive endings over a five-minute period. For the next two weeks, the subjects practiced imagery rehearsal therapy every evening before bed while listening to the same sound. When they fell into slumber, a wireless headband would detect when they entered REM sleep—the stage for vivid dreams and nightmares. The headband would then transmit the piano note repeatedly while the person was in this particular sleep phase. 

The imagery rehearsal therapy helped reduce the number of nightmares for both groups. However, people with the additional targeted memory reactivation during REM sleep had the greatest reduction in weekly nightmares and were more likely to create dreams from positive memories. Those who went through the targeted memory reactivation continued to show a decrease in nightmares after three months. 

[Related: How lucid dreaming may help treat PTSD]

“We observed a fast decrease of nightmares, together with dreams becoming emotionally more positive,” said Lampros Perogamvros, a psychiatrist at the Sleep Laboratory of the Geneva University Hospitals and senior author of the study, in a press release. “For us researchers and clinicians, these findings are very promising both for the study of emotional processing during sleep and for the development of new therapies.”

The benefits of using targeted memory reactivation may go beyond nightmare disorder. The study authors note in their paper the combined therapy could prove effective for survivors with PTSD, anxiety disorders, and mood disorders who routinely experience insomnia and emotionally charged dreams.

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The US is seeing a spike in respiratory syncytial virus (RSV) infections, and it’s taking a toll on pediatric hospitals. Beds at these medical centers are filling up, and the limited capacity has prompted drastic measures. Last week, Connecticut Children’s hospital contacted the National Guard to help set up tents in its parking lot to serve as temporary units. At Rainbow Babies & Children’s Hospital in Ohio, staff are turning away emergency room visits that required hospitalization as they reached bed capacity.

RSV, a seasonal respiratory virus that causes cold-like symptoms, has been around for centuries. Today, it is the leading cause of severe respiratory illness in babies and infants. What makes the current outbreak so alarming is that most hospitalized children are older than 2. 

[Related: Flu and RSV hybrid virus studied in a lab for the first time]

“We’re seeing a tidal wave of RSV,” says Sharon Nachman, chief of the division of pediatric infectious diseases at Stony Brook Children’s Hospital. “And we’re not seeing it just in those first two years of life that we typically expect but in school-aged children who should have already had their RSV exposure.” Pediatric experts warn that pandemic disruptions have led to a brutal flu and RSV season.

Why is RSV season so bad this year?

Blame the pandemic. Daniel Ganjian, a pediatrician at Providence Saint John’s Health Center, explains that RSV exposure early in life is critical to training the immune system. Most RSV infections happen in babies whose immune systems are still developing. Infected infants may wheeze and cough for two weeks, but most make a full recovery. RSV was estimated to cause 7 percent of infant deaths, with most happening among those younger than 3. 

Having a memory of the virus allows the immune system to build up the necessary defenses to immediately destroy the pathogen the next time they cross paths. But in early 2020, children did not attend daycare or in-person school, lowering the chance of infection and the creation of an appropriate immune defense. “They have zero antibodies because these kids, who were 1 and 2 during the pandemic, were not exposed to RSV,” Ganjian says. “Now they’re getting it for the first time and they’re getting severe reactions,” he says.

[Related: The US may be in for a brutal flu season]

But what about the kids exposed to the virus in the past and are getting severely ill now? Nachman says that’s because our immune response to the virus is short-lived and easily forgettable. It’s only with repeated exposure that the immune response will get a “kick-start” to remember the virus, Nachman says. But, she adds, since these kids did not get exposed to the virus in the past few years, “their body really forgot how to make an immune response to RSV.” 

Is the RSV outbreak related to the flu?

Flu does not cause RSV infections—different viruses are responsible for the different illnesses. But having both circulating at the same time is a recipe for trouble. While your immune system is busy fighting off one virus, another can sneak in and cause infection. “We have families coming concerned their kid has been sick all month with the flu and that’s not true,” Nachman explains. It’s possible for children to appear sick for a month, but it’s likely they had one virus at a time. Even if there was just a small gap between symptoms, “they might have been infected with a second virus, making it seem like they never got better.”

Historically, flu and RSV season rarely overlapped. Before the pandemic, RSV season occurred from late October to December while flu season peaked in December and ended February. However, since most respiratory viruses took a backseat to COVID-19, there have been disruptions to their seasonal circulation. Now, Nachman says, “these viruses never left”: With many people going back to school and the office, there’s more opportunity for the viruses to spread from person to person.

How can you tell the difference between the flu and RSV?

You can’t tell the difference between the flu and RSV just by looking at someone. Adults and older children can get RSV, too, but in healthy individuals signs of infection are often mild. Both viruses cause similar symptoms such as congestion, cough, and runny noses. In RSV, though, not all symptoms appear at once, and very young infants may experience issues with breathing and irritability. “If your child is having difficulty speaking or you see they’re breathing faster, wheezing with a whistling sound, then you have to go to the pediatrics office to get tested,” says Ganjian. 

If you suspect RSV, you can take a rapid RSV antigen test at a pediatric office or urgent care site. The RSV antigen test detects active viral proteins using a nasal swab, with results provided to you in minutes. 

There is no specific medication or treatment for an RSV infection—although there are clinical trials underway for an RSV vaccine. However, there are ways to relieve symptoms. Since babies are mostly “nose breathers,” Ganjian recommends using a saline vaporize or a nasal suction to remove mucus and relieve nasal congestion. You will also want to keep your child hydrated and use acetaminophen and ibuprofen (never aspirin) to manage any fever or pain. 

How can you protect your family from RSV?

To avoid respiratory infections this fall and winter, experts recommend having children practice good hygiene such as washing their hands before they eat or after being outside, as well as showering and changing clothes once they get home from school. You also want to keep your child’s immune system strong—that requires getting enough sleep and making sure they’re eating foods such as broccoli and sweet potatoes.

[Related: Even dinosaurs couldn’t escape the sniffles]

If your child is showing signs of being sick, doctors recommend keeping them at home and avoiding crowded areas. Not only are you helping to contain viral spread, but you’re reducing the risk of your child getting a second infection. Since babies and toddlers under 2 cannot wear face masks, Nachman recommends that parents wear masks when outside to avoid bringing any viruses home.

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The world’s first insect vaccine is here, and it could help with stopping a fatal bacterial disease in honeybees. A study published on October 17 in the journal Frontiers in Veterinary Science found honeybees born from vaccinated queens were more resistant to American Foulbrood (AFB) infection than hives with unvaccinated queens. Not only would the vaccine help in improving colony health, but it might increase commercial beekeeping to make products, such as honey and medical wax.

Several factors have contributed to declining honeybee populations—higher temperatures from climate change, pesticides, and drought to name a few. “Bee health is a multifaceted problem and many factors play into the survival or perishing of a beehive,” says Dalial Freitak, associate professor at the University of Graz in Austria and senior author of the study. “As in any organism, diseases can cause havoc, especially if other stressors are at play.” The current vaccine tackles AFB, a devastating disease that’s caused early outbreaks in US beehives since the early 1900s. 

AFB is caused by the spores of the larva of the bacteria Paenibacillus. Young honeybees ingest the spores in their foods and in one to two days, the spores take root in their gut, sprouting out rod structures. Like an aggressive cancer tumor, the rods quickly multiply before invading the blood and body tissues and killing the young insect larva from the inside. By the time they die, new spores have formed to infect the bees that come in to clean up the honeycomb cells where the deceased laid. Beekeepers may also accidentally spread the disease by exposing contaminated honey or equipment to other bees. Freitak estimates at least 50 percent of beehives globally have AFB. While cultivators may not see any noticeable symptoms of the disease at first, it can feel like a ticking “time bomb” with an outbreak potentially happening at any moment, she says.

The recent study tests the safety and effectiveness of an oral breeder vaccine—an immunization that’s passed down from parents—to increase resistance against Paenibacillus larva. The oral vaccine is mixed into a new queen’s food which she ingests before being introduced into the hive. Once digested, the vaccine contents are transferred into the fat body, the storage organ in insects. Vitellogenin, or the yolk proteins that provide nutrients for growing embryos, bind to pieces of the vaccine and deliver it to eggs in the ovaries. “A little piece of vaccine into the ovaries stimulates an immune response and it’s where you need it the most,” says Annette Kleiser, the CEO of biotech company Dalan Animal Health that created the vaccine. “A lot of these diseases are when the larvae get infected in the first few days when they hatch.”

[Related: Do we still need to save the bees?]

In the current study, two queen honeybees were vaccinated with either the vaccine or the placebo before entering their hive and laying eggs. After the eggs hatched, the two hives were brought to the lab (to avoid infecting other colonies in the wild) and exposed to AFB spores for several days. The team found that vaccinating the queen decreased the risk of AFB by 30 to 50 percent. What’s more, the vaccine did not impact the health of bee colonies. The study authors saw no difference in hive losses between the placebo and vaccinated groups before spore exposure.

“They have shown a proof-of-concept,” says Ramesh Sagili, a professor of apiculture at Oregon State University who was not affiliated with the study. He notes, however, the study took place in an isolated, lab-controlled setting and the challenge with this type of technology is the lack of success when tested in the field. One suggestion is to conduct large-scale field studies, expanding from two honeybee hives to thousands split between vaccine and placebo groups. Other questions Sagili would like answered in future research is how the vaccine fares against different AFB strains and how long immunity lasts in the long-run.

“I’m convinced they have something promising here, but only if they do some large-scale field studies with the beekeeping industry,” adds Sagili. If successful, he says this could open doors to the production of vaccines for other viral diseases plaguing honeybees.

Still, finding solutions to assist honeybees with illness is important: “A declining honeybee population has made it difficult to pollinate enough food for everyone to eat,” explains Kleiser.

Honeybees pollinate one-third of food in the US. Beyond honey, they are essential for the production of apples, broccolis, melons, and even your favorite cup of java. But as much service honeybees provide, humanity has provided them a disservice in keeping them safe and alive. Beekeepers estimated a 45.5 percent loss in honeybee colonies from April 2020 to April 2021, which is largely associated with human activity. According to the United Nations, if bees continue to disappear, we may see permanent disruptions in our food supply chain and the disappearance of fruits, vegetables, and other crops heavily dependent on pollination.

[Related: Temperature tells honey bees what time it is]

There are other options currently on the table to mitigate the spread of AFB. Once beekeepers notice the first signs of disease, they can burn the honey, tools, and other equipment in contact with the hive. Additionally, they could quarantine the hive to prevent infected bees from swarming nearby colonies. However, both options aren’t ideal because they slow down honey production and affect the food supply chain. “You have a withdrawal period where you have to wait and that costs money to beekeepers,” says Kleiser. “The flowers won’t wait so if you miss the season you miss your entire yield.” 

Another option is antibiotics. Sagili explains that antibiotics are effective against AFB, and beekeepers have been using antibiotics to manage the spread of spores. Because of its availability, he says it doesn’t rise to the level of other challenges that honeybees presently face. That said, there is always a risk of antibiotic resistance that could lower honeybees’ protection against the bacterium. “Beekeepers have options, but it would be nice to have a vaccine for [AFB] so they have one less problem to deal with,” Sagili says.

Right now, the vaccine is pending conditional license by the US Department of Agriculture Center of Veterinary Biologics. Kleiser emphasizes the vaccine would not only benefit bees, but the larger ecosystem as well. “It’s a survival issue,” she says. “We have to understand the critical importance of these animals.”

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The Cordyceps mushroom, an exotic fungus, grows by infecting insects with its spores. The spores use the animals’ bodies as all-you-can-eat buffets, feasting on their flesh. This parasitic relationship ends only when the spores fully grow and mature, sprouting out and mercilessly killing their hosts. Despite its unorthodox but popular survival method—Cordyceps are the inspiration behind some apocalyptic films and video games—the mushroom has some sought-after medicinal properties. For years, scientists have attempted to replicate this process in the lab, because the mushroom is hard to find in the wild. Using brown rice, a common experimental substitute for bugs, often fell short.

It turns out the best way to grow the ever-elusive Cordyceps mushroom is on the backs of fatty insects, finds a new study published Wednesday in Frontiers in Microbiology. Cultivating this rare species of fungus could increase the availability of a bioactive compound called cordycepin, which boasts potential antiviral and antitumor properties.

“Cordycepin has diverse biological effects such as anticancer and anti-inflammation, several aspects that must be considered for the treatment of diseases,” explains Mi Kyeong Lee, a professor of pharmacy at Chungbuk National University in South Korea and senior study author. “In addition, Cordyceps mushrooms may be widely used for prevention of diseases through immune enhancement.” 

Lee’s interest in the fungi came after searching for bioactive ingredients from natural products. However, Cordyceps mushrooms are rare in nature, and when grown on brown rice the fungus produces little cordycepin, perhaps because the grain has low protein content. In the outside world, Cordyceps mushrooms prefer snacking on insects and the study authors hypothesized they may prefer insects with a high protein content. “In particular, insects have recently been approved as a protein substitute in Korea,” Lee says. 

In the new study, Lee and his team sought to replicate how Cordyceps mushrooms grow in the wild with the goal of maximizing cordycepin levels. But first they would need to know whether the type of insect it ate mattered.

[Related: This deadly mushroom can literally shrink your brain—and it’s probably more widespread than we thought]

The team collected an assortment of insects—crickets, silkworm pupae, grasshoppers, Japanese rhinoceros beetles, mealworms, and white-spotted flower chafer larvae—exposed to the spores of the Cordyceps mushroom. The fungi grew for two months with the largest ones coming out of the bodies of silkworm pupae and mealworms. Mushrooms that bloomed out of chafer larvae and grasshoppers grew the smallest mushrooms. 

The size of the fungus, though, doesn’t matter for cordycepin levels. Cordyceps mushrooms that sprouted out of Japanese rhinoceros beetles were the most rich in the cordycepin compound, which had nearly 100 times more cordycepin than those grown out of brown rice. And compared to the giant mushrooms from silkworm pupae, Cordyceps cultivated from Japanese rhinoceros beetles had 34 times more cordycepin.

It was not the amount of protein that made a difference, the scientists determined, but the fat content in the invertebrates. Insects with high amounts of a fatty acid called oleic acid seemed to make more cordycepin. (For example, the Japanese rhinoceros beetle held 10.8 percent of oleic acid while silkworms only had 0.4 percent of oleic acid.)

What’s more, genes involved in the production of cordycepin, cns1 and cns2, were found at higher levels in the beetle than the other insects. Adding oleic acid to a low-performing insect raised cordycepin levels by 50 percent.

[Related: A South Pacific island could help us understand how fungi evolve]

“Raising medicinal fungi on farmed insects is a more sustainable practice than collecting these species in the wild,” notes Nicholas P. Money, a mycologist at Miami University in Ohio who was not affiliated with the study. However, he warns that “the clinical benefits of the metabolite examined in this study”–referring to cordycepin–“remain a matter of faith rather than science.” Ongoing research suggests cordycepin may have the potential to ward off viruses such as influenza and SARS-CoV-2 by acting as an inhibitor for viral replication as well as mitigating any severe symptoms by lowering inflammation levels. However, there is a lack of evidence from preclinical and clinical studies to support these claims.

Yet with an improved supply of Cordyceps, which the new work aims to provide, researchers will have an easier time studying its therapeutic potential. Lee says his goal is to find the optimal living environment for producing the highest quality of Cordyceps mushrooms. His next work will test different plant species as another possible breeding ground for the fungi to grow.

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Whether you’re channeling your inner Morbius or Dracula, chugging a goblet of blood is not a gory practice you’d want to reenact in real life. Blood, a necessity for human life, is ironically poisonous to drink. Medical experts warn you can get very sick from drinking it every day and invite a number of infections into your own supply.

One reason blood is dangerous to human health is it carries risky viruses. “Human blood is a biohazard,” says Laura Purdy, a family medicine physician and chief medical officer of telehealth company OpenLoop. “By exposing ourselves to someone else’s blood, you are potentially exposing yourself to infections that live in the bloodstream.” Just a few drops from the impure liquid is enough to transmit infectious blood-borne diseases such as HIV, hepatitis B, or hepatitis C. You can get syphilis too by exposing yourself to another person’s blood, though it is more commonly spread through sexual contact, Purdy says.

Now. having a quick lick of uncontaminated human blood wouldn’t exactly harm your health, says Rosmy Barrios, a regenerative medicine specialist and medical advisor for Health Reporter. Celebrities like Machine Gun Kelly and Megan Fox have admitted to drinking a few drops of each other’s blood for “ritualistic purposes,” and seem to survive just fine. But drinking it daily could build up toxins in your body. 

[Related: What is a toxin?]

If you’ve ever had a cut in your mouth or tasted a sprinkle of plasma and hemoglobin, you might have realized the sanguine fluid carries a bitter metallic flavor. The metal you taste comes from the high iron levels in blood—a normal range in adults is 60 to 170 micrograms per deciliter. Unlike vampire bats, which have evolved to stomach large doses of iron, humans carry a gene that prevents absorption of the mineral. Barrios says humans cannot properly digest blood and its rich iron content, along with all the nutrients we get from our usual diet. “An excess [of iron] is toxic to humans, and in some cases, even fatal,” she warns. “An overdose of iron can cause severe vomiting, diarrhea, abdominal pain, dehydration, and even death in children.” 

Iron overload, or hemochromatosis, can produce symptoms of fatigue, joint pain in the hands and knees, low sex drive, and darkening skin color—a stark contrast to the glittery white skin Edward Cullen pulls off. What’s more, complications of hemochromatosis can lead to the development of cirrhosis, diabetes, or heart failure. 

Both Purdy and Barrios say there is insufficient research to support any benefit of drinking human blood. (It won’t make you younger or give you a better high.) And while blood is a cocktail of different vitamins and minerals, we can find these same nutrients in food. “There is no exclusive benefit drinking human blood would give you that you couldn’t get from another dietary source,” explains Purdy. “If you’re looking for iron, you can eat red meat or spinach.” Besides, blood doesn’t have enough of every nutrient a person needs to survive: The human body cannot produce vitamin C, which is usually obtained from citrus, cruciferous vegetables, and supplements. 

[Related on PopSci+: Has the fountain of youth been in our blood all along?]

Another complication to living out any vampire fantasies: mismatching blood types. In normal circumstances, the consumed blood would be processed and eliminated through your GI tract. However, if someone has an ulcer or another open wound in their digestive system, Purdy says there is a chance of the blood getting mixed into your own. If the other person has a blood type that does not match up, you risk an intense immune reaction. “On the off chance incompatible blood types did mix, red blood cells would break down and form antibodies that attack each other,” she explains.

If you still have a morbid curiosity to see what human blood tastes like, both experts suggest trying only a few drops. But before you experiment, consider testing the sample to make sure the blood type is compatible with yours and there are no transmittable diseases. Purdy says that “as with all exchanges of bodily fluids, do so wisely with a well-informed understanding of the other person’s medical condition.” Hopefully, Megan and Machine Gun checked with their doctors first.

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You have little say in how tall you’ll grow. Height is based on variation in genes–lots of them. Research in 2020 found that 10,000 genes could possibly explain differences in human height. Now, the same statistical geneticists have teamed up with the international GIANT consortium to investigate additional genetic links to height. 

In the largest genome-wide association study for height to date, they’ve updated their calculations, adding 2,111 more genetic variants that influence a person’s stature, according to the report published Wednesday in the journal Nature. About 40 percent of the differences in height from people of European ancestry were explained by the identified genes. 

It’s a common misconception that certain traits such as height, intelligence, or eye color have one or two “master genes” that determine the final outcome, says Rebecca Darrah, an associate professor of genetics and genome sciences at the Case Western Reserve University School of Medicine who was not affiliated with the study. But in reality, thousands of genetic variables interact with the environment to determine these features. “This fascinating study shows that there are actually over 12,000 distinct genetic variants that contribute to height in European populations,” Darrah says, “and likely many, many more than that for even more complex traits like weight.”

Height makes for a good model trait to study, the paper’s authors point out. Eirini Marouli, a senior lecturer in computational Biology at Queen Mary University of London and joint co-first author of the study says height is easy to measure–adult tallness does not vary over time like weight or a person’s IQ–and it has high heritability, meaning your parents more likely pass down the genes that influence height. Genes, though, are not the only predictors of height. Environmental factors, such as a lack of dietary protein, exposure to certain infectious diseases, and exercise, also interact with genes and influence a person’s overall growth. 

[Related: The genes behind your fingerprints just got weirder]

With the GIANT consortium, the team expanded their sample size from an initial 700,000 to 4.1 million to now 5.4 million people from 281 contributing studies. Unlike the prior genetic research, which only sampled the genomes of individuals of European ancestry, this study included more than one million participants of East Asian, Hispanic, African, and South Asian ancestries (though most of the results came from people of European ancestry).

Based on the 5 million DNA samples, the study found 12,111 single-nucleotide polymorphisms (SNP)—single base substitutions in a DNA sequence—that could explain differences in height, making up about 21 percent of the genome’s length. 

Human genetic material consists of more than the actual genes themselves. Most of the identified genetic variants that influence height exist in 7,209 non-overlapping segments outside the genes. These include proteins that regulate how genes are expressed. Because these are “likely related to more subtle changes,” Darrah says, it could explain why most people, and everyone in the study, have heights within a typical range. However, dramatic changes such as a genetic mutation in these regions, she says, likely contribute to genetic conditions such as overgrowth or dwarfism.

[Related: We’re just beginning to understand how our genes and COVID-19 mix]

Prior to the 2020 study, research in twins indicated that genes explained about 60 to 80 percent of height differences. The study authors predicted genetic variants could influence 50 percent of variations in height. Indeed, the 12,111 genes explained differences in height for 40 percent of people of European ancestry. However, the identified genes explained only 10 to 20 percent of height variations in those with non-European ancestry. 

While this study had an enormous sample size, a lack of geographical diversity among non-European populations remains, pointed out Karoline Kuchenbaecker, a professor of genetic epidemiology at the University College London, in an editorial accompanying the Nature study. For example, while the research had data on people of African descent, only 0.4 percent of participants actually came from the African continent. Kuchenbaecker argues that because a person’s environment influences genes, it’s likely that the study did not capture Africa’s diversity.

Marouli agrees future work needs to better capture the ancestral diversity of non-European populations. “Increasing the number of individuals of non-European ancestry is essential to improve prediction accuracy and may help find genetic variants unique to particular groups,” she says. Understanding height at a genomic level could then give clinicians the ability to diagnose and treat genetic disorders that cause sizable changes in a person’s height.

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Flu season is making a comeback. In the past two years, influenza and other respiratory viruses took a backseat to the more contagious COVID-19 variants. Pandemic precautions caused flu cases to drop to so low that at least one strain of the pathogen may have gone extinct. However, as restrictions loosen and kids return to school in-person, infectious disease experts are predicting high infection rates this year. Currently, there have been two confirmed reports of influenza in Delaware.

There are a few clear-cut indicators that this season will spell trouble for the US, infectious disease scientists say. In most years, flu seasons are a guessing game for those experts. Because the virus is constantly mutating, it’s hard to say for certain whether or not it’ll be a severe one. “We’ve been saying for the last few years to expect bad flu seasons, and that didn’t pan out,” explains Andrew Handel, a pediatric infectious disease specialist at Stony Brook University. “I think the public gets very frustrated with our predictions about flu seasons, but it’s all a prediction based on the best information we have available.” 

This time, however, a bad flu season abroad and low US vaccination rates for the flu are ominous forecasts for a rough winter ahead.  

Australia’s tough flu season

Jennifer Lighter, a pediatric infectious disease doctor at NYU Langone Health explains that flu seasons typically start in the southern hemisphere and move north. For this reason, the US turns to places like Australia to glimpse what we should expect to see in the fall and winter. Australia’s 2022 flu season was one of the worst in five years, according to a report from Australia’s Department of Health and Aged Care. Children between 5 to 9 had the highest flu case rates followed by children younger than 5 and people between 10 to 19 years old.

[Related: The back-to-school guide for fighting common viruses]

Fortunately, there’s some good news. Another reason virologists closely follow Australia’s flu season is to identify which strains are circulating in the region. These strains are then considered in the final design of the annual flu vaccine, increasing the chances it will be highly effective. Lighter says that scientists don’t really have the estimates of how effective this year’s vaccine is until after cases emerge, but “we know that the current vaccine is matching well with what’s circulating in communities in the southern hemisphere.”

Low vaccination rates

Few people get their flu vaccines, and the COVID-19 pandemic made a flu shot less of a priority. The Centers for Disease Control and Prevention reports only 57 percent of children were immunized against influenza during the 2021-2022 season—a 5.6 percent drop from the pre-pandemic 2019-2020 season. The vaccine rates for adults were even lower; coverage for 2021-2022 ranged from 35.9 percent to 60 percent. 

“It’s always been a struggle to get a large portion of the population vaccinated against the flu,” explains Handel. “And over the last couple of years, fewer and fewer people have gotten flu vaccines, and that’s one more hole in the layer of protection against infections.”

There are many factors that go into a person’s decision not to get a vaccine. More recently, Handel says the discussions over COVID vaccine safety may have made Americans more hesitant about getting another shot in their arm. What’s more, people are experiencing vaccine fatigue—feeling burned out after constant immunizations and vaccine news.“People don’t want to spend time getting all of these vaccines, when they feel it’s not really all that beneficial or necessary,” Handel adds, even when the best evidence shows a flu shot helps.

Waning immunity

At the start of the pandemic, the flu and other respiratory viruses hit an all-time low. Public health practices including masking in public, online school, and social distancing prevented the influenza virus from spreading from person to person. 

While experts incorrectly predicted an enormous surge for 2021-2022 flu season as places opened back up, there is cause for concern for this upcoming season. To start, this will mark the third year in which most of the population’s immune systems have not been exposed to the flu virus. Both experts say it’s likely everyone’s immunity against influenza has waned. Waning immunity could lead to a greater chance of getting infected and having more severe illness.

[Related: A viral descendent of the deadly 1918 flu is probably still going around]

Winter respiratory viruses that normally circulate in the cold season, such as RSV, have also been running rampant in the last few months and overwhelming children’s hospitals. Young children are at especially high risk for severe flu because of their developing immune systems. “It might be their first time getting infected or because they’re getting exposed to multiple respiratory viruses all at once,” Handel explains. Even if your child has had a past flu case, he says it’s been a long time so there’s a chance their immunities are not as strong as it once was.” 

Other people at high risk for severe flu are people with asthma, COPD, older adults, and immunocompromised individuals. “The problem with kids not having a lot of immunity, and we’ve seen this with a lot of infections, is that these viruses are the ones that tend to pass on to grandparents and other adults who then spread it within the community,” says Handel.

How to protect yourself

Both experts agree the best way to stay protected this season is to get vaccinated. They recommend getting the flu vaccine now and scheduling it at the same time as your COVID boosters, which are already available in pharmacies. Besides achiness and fatigue, Lighter says you should not feel concerned about getting a shot in each arm on the same day. The flu shot will protect you as well as your family and community from the worst cases, she emphasizes. 

“The flu shot is analogous to the COVID shot. There may be breakthroughs but they’re both preventing severe disease and keeping you out of the hospital,” Lighter says. “And that’s really the main purpose of a vaccine—to keep you from getting significantly sick.”

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If people over 80 with exceptional memory—a group who Northwestern researchers call “super-agers”—had a symbol in the style of Superman’s “S”, it might be the “super neurons” in their brains. The brains of super-agers age more slowly than normal, though until now no one understood what cellular trait qualified someone to be in this unique group. A new study published September 30 in The Journal of Neuroscience found that super-agers have significantly larger neurons in a specific brain region compared to the neurons of people of the same age and of individuals 20 to 30 years younger. 

The brain area in question, the entorhinal cortex, acts as a hub for consolidating new memories into long-term ones. It’s also one of the first targets of Alzheimer’s disease. Senior author Tamar Gefen, an assistant professor of psychiatry and behavioral sciences at the Northwestern University Feinberg School of Medicine, says her team was interested in looking at the entorhinal cortex in super-agers because their exceptional brain may hold a clue on what makes a person resistant to Alzheimer’s disease. 

The study examined six brains of recently deceased super-agers, seven cognitively average older adults of similar age, six young individuals, and five individuals with early Alzheimer’s. The researchers’ focused on the six layers of the entorhinal cortex, each with its own role in memory. In layer II of the entorhinal cortex, the researchers observed larger and healthier neurons than you would normally see in this brain area. 

[Related: Your brain uses different neurons to add and subtract]

“What surprised me most was that neurons in the entorhinal cortex of super-agers were significantly larger than neurons found in individuals much younger—as young as age 27,” Gefen explains. While not directly tested in the study, the research authors suggest these super neurons may be a unique biological signature that’s imprinted on a super-ager since birth.

Unlike other cells, these large layer II neurons remained healthy and large throughout life and were significantly more resistant to the formation of tau tangles, large clumps of protein that accumulate inside neurons. Super-agers showed fewer tau tangles in layer II of the entorhinal cortex compared to people of similar ages. According to the researchers, the difference in tau tangle density could explain why some cells shrink and others stay large and healthy.

In healthy cells, tau proteins bind and stabilize microtubules, cylindrical structures that give cells their shape and help transport nutrients. But in early-stage Alzheimer’s, tau proteins detach from microtubules and stick to other tau molecules, eventually forming tangles that block the transport system and cause the cell to die. These deaths can weaken communication between neurons.

[Related: What the recording of a dying human brain could tell us]

“The presence of these structurally distinct nerve cells in ‘super-agers’ that do not show age-related cognitive decline, and very often evidence superior cognitive (memory) capability, may be significant,” notes James Giordano, a professor of neurology and biochemistry at Georgetown University Medical Center who was not affiliated with the study.

The next question to answer will be why some people grow these super-sized cells while others do not. This will involve probing the cellular environment and finding out the mechanism behind these neurons’ resiliency.

Understanding how super-agers stay sharp may help scientists one day create treatments to ensure a person’s brain stays cognitively resilient. Future research will also have to expand to other brain areas involved in memory to paint a more complete picture of how super-agers ward off neurodegenerative diseases. By doing so, Giordano says, this could open up a new realm of interventions that could potentially preserve cognitive function across the lifespan while identifying individuals at most risk of age-related cognitive decline.

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Its lights outs for Puerto Rico, again. After dealing with devastation to the electric grid from Hurricane Maria five years ago, the US territory has struggled to create a hurricane-proof way to protect themselves from future blackouts. Now, two weeks after Hurricane Fiona swept over the island, a quarter of Puerto Rico’s residents are still without electricity. While efforts are underway to restore power locally, there’s been a revival of interest in transitioning to renewable energy—from leaders igniting conversations to locals rallying protests. Experts say diversifying the grid will help to “climatize” the energy system, reducing the chances of another island-wide blackout while simultaneously cutting residents’ carbon footprint and energy costs.

“We had a very fragile grid before the hurricane, and we hadn’t made the long-term repairs that needed to be made,” explains Sergio Marxuach, the policy director and general counsel at the Center for a New Economy in Puerto Rico. “But it’s old technology, and eventually the entire world needs to move to renewables due to climate change.”

In 2019, Puerto Rico passed a climate law mandating 100 percent of the island’s electricity come from renewable sources like solar and wind-powered facilities by 2050. While that’s still decades away, the territory has struggled to ramp up renewable energy use and phase out fossil fuel. Fossil fuels currently make up 97 percent of Puerto Rico’s electricity. In 2021, natural gas made up 44 percent of the total energy followed by petroleum at 37 percent. Benchmarks towards the 2050 plan include becoming 50 percent renewable by the end of the current decade, but the number is currently only at two to three percent, according to Max Lainfiesta, a manager at the Rocky Mountain Institute’s (RMI) Islands Energy Program.

[Related: Hurricane Fiona leaves most of Puerto Rico without power]

There are several short- and long-term routes Puerto Rico can take to reach its renewable energy goal. Marxuach says that right now Puerto Rico has an island-wide interconnected grid, but that current structure has a significant weak point. “If one part of the grid goes down, everything else shuts down because of the way [they] built the system to protect itself,” he explains. Creating seven to eight regional grids stationed across the island would not only prevent future disruptions to infrastructure, but would also slowly introduce renewable energy to areas and create locally sourced power. This segmented system can boost larger infrastructure, but also function independently when there is a hurricane or other disastrous event.

However, Marxuach acknowledges there are some challenges to creating an interconnected energy grid. For one, there’s been debate on how much renewable energy can be incorporated to the island right now, and whether Puerto Rico has the energy storage technology to overturn the entire system. Another issue is the geography of the island. He says that even though Puerto Rico is only 3,515 square miles—three times the size of Rhode Island but smaller than Connecticut—there are mountains and isolated communities that could make it difficult to establish new transmission lines for regional grids. 

What’s more, Marxuach says the US government has already approved $12 billion dollars to get the renewables transition underway in the territory, but bureaucracy from federal agencies such as FEMA and the Department of Energy had slowed down efforts to start using the funds before the hurricane. “Ironically, the new hurricane gave us a window to start a new reconstruction process to deal with the damage caused by Fiona and get moving on the grid,” he notes. “There are things we can do by next year to be better prepared, but the real modernization and phasing out natural gas will take more than five to eight years.”

[Related: You’ll need to solve Puerto Rico’s debt crisis to win this new board game]

Lainfiesta points out that because of the unreliability in the grid, residents have taken matters into their own hands and have invested in solar-plus battery systems for their homes. But from his perspective, these can get very expensive and further deepen the gap between higher- and lower-income neighborhoods on the island. People in middle- and lower-class neighborhoods cannot afford to pay for expensive installations and are usually the last to be reconnected after a power outage. The RMI team’s approach to “climatizing” Puerto Rico is to prioritize critical facilities—areas whose services are necessary for the community—first. Called the Community Energy Resilience Initiative, Lainfiesta and his collaborators help finance solar and storage microgrids for places such as pharmacies, grocery stores, and gas stations, so that in an event of another blackout, people have a way to buy food and water, charge their phone, and get their medicine.

“In Puerto Rico, everyone is talking about electricity, because people have been suffering from poor [utility] service all the time,” Lainfiesta explains. Costs are topping 30 cents per kilowatt hour (the average in the US is about 12 cents per kilowatt hour) for an unreliable grid, “and the most vulnerable population are mostly the ones paying for it,” he adds. The silver lining is that the recent hurricanes have motivated people in Puerto Rico, and possibly others worldwide, to talk and make real efforts to adopt renewable energy.

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Polyethylene is one of the world’s most commonly used plastics, found in bottles and packaging film, but it’s also one of the hardest to break down. By itself, it would take polyethylene hundreds of years to completely decompose. Scientists have been working to tackle this problem as polyethylene trash is clogging up landfills and littering beaches and oceans. 

A major obstacle to breaking down polyethylene is a feature of its molecular structure. It contains unreactive carbon chains, which are covalent bonds that hold atoms together so tightly it takes a high amount of force and energy to pull them apart. But scientists have been making efforts to find a solution for breaking down polyethylene. A new study published Thursday in the journal Science proposes a method to effectively transform polyethylene into propylene, a chemical that’s easier to use for future chemical reactions.

Turning polyethylene into usable polymers can increase the plastic’s value and provides an alternative to throwing it away, explains Susannah Scott, a professor of chemistry at the University of California, Santa Barbara, and an author of a seperate new study that used a similar technique to achieve the same goal. In that preprint study, published on Tuesday, Scott and her co-authors also described an approach in which they removed hydrogen from the polyethylene chains, creating reactive bonds that are easier to cut apart. 

Polyethylene has been around since the 1930s, but it took 20 years for scientists to refine the plastic to make it stiffer, harder, and more heat-resistant. Fast forward to the present, and polyethylene’s carbon-carbon and carbon-hydrogen bonds are nearly unbreakable, which has helped in creating a variety of materials from plastic water bottles to cable insulation. However, those same chemical bonds have made it difficult to break down without incurring a high energy cost. 

[Related: Will we ever be able to recycle all our plastic?]

To destroy the carbon-carbon single bonds in polyethylene, you would normally need to heat them up at a high temperature under special conditions: without oxygen, or using a catalyst and adding hydrogen. However, neither approach can completely eliminate the unreactive bonds. John Hartwig, a professor of chemistry at University of California, Berkeley, and senior author of the study in Science, sought a way to split up these carbon chains by installing a more reactive bond between each atom pair. 

The bond, known as a double bond, results when two pairs of electrons are shared between atoms. While a double bond is stronger than a single bond, it is less stable, making it easier to cleave. They, like Scott’s team, sequentially removed hydrogen from smaller and smaller carbon chains, making very tiny pieces of reactive material. When the double bond was cleaved, the scientists were left with products that also had reactive bonds, enabling the pieces to be used again. They then linked the small pieces together in a different arrangement to make propylene, another polymer.

About 80 percent of the end products made by this reaction was propylene. “Other methods have formed mixtures of products” that may only have niche applications, explains Hartwig. Creating mostly propylene is important, he says, because it’s in very high demand. Propylene is a key building block for a number of other chemicals, used in processes to make rubbing alcohol and polyesters.

That propylene yield is “quite exciting” says Mahdi Abu-Omar, a professor of green chemistry at the University of California, Santa Barbara, who was not affiliated with the study, because in the end product, every two of the three carbon atoms comes from waste material. 

[Related: A close look at the Great Pacific Garbage Patch reveals a common culprit]

In the new preprint study, Scott and her colleagues’ method produced 94 percent propylene. While similar to the procedure published in Science, she says, the method in the preprint study had a more continuous flow and used less of an organic chemical called ethylene. This is because they simultaneously added ethylene while removing the propylene as it formed. “We call this circularity where you take the polymer apart, get the pieces back, and put them back together in a new way to make a polymer from them,” Scott says. 

These studies fall in line with past efforts to degrade polyethylene. A 2020 paper suggested a model for an organic reaction where carbon-carbon double bonds could be redistributed using a metal catalyst to accelerate the process. 

While polyethylene by itself is nontoxic, it can interact with other molecules that may be toxic and able to contaminate the plastic’s surface. What’s more, when polyethylene degrades in the environment, there is a chance that animals will ingest tiny bits of polymer, known as microplastic, which may also be absorbed in the soil. While we still don’t know the true ecological impact of microplastics, research suggests human ingestion of microplastics can lead to cell damage, developmental toxicity, and an increased risk of cancer.

“It’s an interesting scientific and societal challenge,” says Scott. “We all realize [plastic degradation] is a problem we urgently need to solve, and that’s exciting as people are moving this whole field forward at a pace you don’t generally see in research.” 

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The baby formula shortage is far from over, but to prevent future scarcity, the United States is taking a critical look at what went wrong earlier this year. On September 20, the Food and Drug Administration (FDA) released an internal report on the fumbles and mishaps that led to a delay in response to the formula crisis. A number of reasons were listed, including outdated data systems, insufficient emergency response systems capable of managing multiple public health emergencies, and lack of consumer education on how to handle and prepare infant formula. The agency also acknowledged that there are many unknowns about the bacterial contaminant Cronobacter, which was reportedly found in baby formula products from Abbott Nutrition. 

“The baby formula shortage was a perfect storm,” explains Jenelle Ferry, neonatologist and director of feeding, nutrition, and infant development at Pediatrix Neonatology of Florida. “You had a combination of COVID pandemic restrictions, supply chain issues, and now you’re involving a situation with a company [Abbott Nutrition] that is a major manufacturer of formula products.” 

On February 17, 2022, the FDA sent out a warning to consumers to stop using powdered infant formula from Abbott Nutrition after concerns of bacterial contamination in its products. Shortly after, Abbott voluntarily recalled infant formula products and shut down the facility during the ongoing FDA investigation. Before the recall, the company was responsible for 40 percent of infant formula production. The uncertainty of when products would be back on shelves led to panic buying, making them hard to find. “The situation created unrest and distrust of the whole process, and I think families did not know what to believe or what was safe for their babies,” says Ferry.

[Related: What the FDA is doing about the US baby formula shortage]

Ferry explains part of the reason for the mistrust is the lack of understanding behind what actually happened to the babies who allegedly drank formula contaminated with Cronobacter. An initial report indicated that babies got sick with Cronobacter after drinking similar—but not the same—formula from Abbott, she says. “It’s very misleading to say the formulas was contaminated because it’s not clear [if] the two infants that died did because of Cronobacter.” Testing later revealed that Cronobacter was on some surfaces of the manufacturing plant, but tests to identify the bacterial strains in the infants found they did not match those found in the factory. Ferry says the results get “muddier” because the strains found in the baby formulas were different from each other, which suggests that it’s unclear where the bacteria originally came from.

This isn’t the first time Cronobacter has been a problem in such products—the bacteria is a known contaminant of infant formula. Richard Martinello, an infectious disease expert at Yale School of Medicine, says that the bacteria is naturally present in the environment and has a preference for very dry environments, such as dry powdered baby formula. It is an opportunistic bacteria that causes severe infections in vulnerable populations such as infants with less developed immune systems. While Cronobacter infections rarely happen—two to four cases are reported each year in the US—an infected infant (less than one year old) may experience symptoms ranging from fever, seizures, to meningitis. If untreated, there is a high chance of death or for the meningitis to lead to long-term neurological issues.

Ferry stresses that when you look at the contamination, you have to ask what was first exposed and where. She says the Cronobacter was not directly found in any of the recalled items—making it possible that the product was exposed to bacteria from other environmental conditions or handling rather than a contaminated ingredient. There are also a lot more opportunities for the formula to have picked up the bacteria, such as on countertops, storage, and even at home when the infant formula is not safely handled or prepared. 

Among the FDA’s suggested areas of improvement, Martinello says it is important to create a system to make Cronobacter cases a reportable disease where states can identify infections. Doing so will help better understand the frequency of cases and allow more opportunities for scientists to study the bacteria.

[Related: 3 solutions for when you can’t find your baby’s formula]

Infant formula is regulated as a food product, but experts agree it’s a life-saving item for babies under six months, when milk is the primary source of nutrition. Arik Alper, a pediatric gastroenterologist and assistant professor of pediatrics at Yale School of Medicine, explains that infants and toddlers with special needs were hit hardest by the low stock of infant formulas. Abbott is a major producer of special formulas for babies that have food allergies, an inability to digest certain proteins in the diet, or have a disease where they need non-dairy formulas, says Alper. “If you need a standard formula there are other options, but we have a problem when special formulas are not available,” he says. “It’s not easy [for babies] to adjust to a new formula and the transition may be associated with gastrointestinal problems such as vomiting or irregular bowel movement.”

Ferry says the only alternative to safely and adequately feed a baby under six months when infant formulas aren’t available is breast milk. However, she points out that often people choose infant formula because breastfeeding is not an option for all caregivers. Another possibility is to find other brands of infant formulas, although that is less of an option for infants with special needs. Though he does not recommend it, Alper has seen some parents create their own formula recipes in a blender at home. He says this would be better suited for older children and if a parent insisted on making their own stock, the process should be supervised by a nutritionist to ensure a nutritious and balanced diet. One thing he advises against is parents diluting their existing stock of formula to make it last. To provide a growing child 100 percent nutrition, “you need to make sure they get enough calories—they need enough nutrients, vitamins, and fiber,” Alper says.

Production at Abbott’s Michigan plant resumed in early July. Currently, the FDA is forming groups that will work on improving the gaps uncovered in the baby shortage investigation and will reevaluate their progress in a year.

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Your urine, or lack of it, could be a sign of diabetes, and scientists have finally pinned down a possible explanation. A Nature Communications study published on September 20 found that diabetes lowers a peptide called psoriasin that doubles as an internal antibiotic. When psoriasin levels decrease, it impairs the function of the urinary bladder’s cell barrier, making it easier for bacteria to travel up the urethra and into the organ, causing recurring urinary tract infections (UTIs).

About 11.3 percent of people living in the United States have diabetes. Of the 37.3 million, 8.5 million are undiagnosed. The high blood sugar levels triggered in diabetes weaken the innate immune system, raising a person’s chances of having regular infections, including UTIs. S. Adam Ramin, a urologist and medical director of Urology Cancer Specialists who was not involved in the new study, says people with diabetes also tend to have problems with urinary incontinence, or problems with incomplete bladder emptying, which can also lead to UTIs.

“Diabetes is a very common disease affecting, and in many respects changing, the lives of many people,” notes Annelie Brauner, a microbiology researcher at the Karolinska Institutet in Sweden and senior study author. What’s more, UTIs are commonly treated with antibiotics, which ups the risk of creating antibiotic-resistant bacterial strains and creates a need for alternative options for treating or preventing the infections.

[Related: Why your UTI keeps coming back]

The team collected urinary bladder cells and blood samples from people with type 1, type 2, or prediabetes to investigate a potential relationship between their glucose levels and the levels of an antimicrobial peptide known as psoriasin. Antimicrobial peptides such as psoriasin act as natural antibiotics to the body, also known as endogenous antibiotics. Their job is to destroy foreign bacteria. So if psoriasin levels are low, Brauner explains that it would be easier for bacteria to cause an infection. “It was a surprise that the difference was so clear between patients with and without diabetes,” she says.

The study authors discovered that having high blood sugar levels was associated with lower levels of psoriasin. The lower psoriasin levels led to changes in bladder cell membranes and cytoskeletons, compromising the uterine barrier and allowing more bacteria to flood through the urethra and into the bladder. The findings/results reveal a specific pathway that explains why patients with diabetes may get UTIs, says Ramin. “This protein is effectively the first line of defense against bacteria in the bladder,” he says. “Because they have a decreased ability to make this protein, they’re more prone to getting infections.”

Both experts agree it’s important for people with diabetes to keep their blood sugar under control. Avoiding high glucose levels improves immune function and, according to the study, raises psoriasin levels to help fend off bacteria. Ramin also advises that keeping a healthy weight and drinking lots of fluids to stay hydrated and prevent constipation can lower the likelihood of getting UTIs.

[Related: Doctors add diabetes to the list of COVID-triggered conditions]

Another potential way to increase psoriasin levels is by administering estrogen. Previous work from Brauner’s team observed that estrogen helped ‘glue’ together the gaps between the cells lining the damaged urinary wall. In the current study, the team tested estrogen treatment on cells exposed to high glucose levels. They found estrogen restored psoriasin levels and the function of uroepithelial cells in charge of killing invading bacteria. Clinically, this may support giving estrogen supplements to postmenopausal people with diabetes. “In some of the older female patients who are diabetic, we sometimes recommend they use estrogen vaginal cream or tablets, which can also help with this particular situation,” adds Ramin.

Brauner says deepening her understanding of why recurrent UTIs occur in people with diabetes will help create alternative ways of treating and preventing them, and potentially other infections associated with diabetes. Beyond this, she says her results may eventually help with explaining why certain people without diabetes have recurrent UTIs and how to help them.

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Children are swallowing more button batteries than ever before. A study recently published in Pediatrics reported an alarming increase in kids’ battery-related emergency room (ER) visits from 2010 to 2019. While ingested button batteries—ranging from 5 to 25 millimeters—are excreted through the stool, having them pass through the body can cause severe and potentially fatal harm to multiple tissues and organs.

Button batteries are in everyday household items that kids can quickly get their hands on, from watches and key fobs to toys and sing-along books. Mark Chandler, a research scientist at Safe Kids Worldwide and lead author of the study, says children are naturally curious to explore and understand their environment, often placing objects in their mouths, noses, and ears. “Parents often aren’t aware of the ingestion dangers posed by button batteries and how they can often be easily removed from devices,” Chandler explains.

These small coin-shaped batteries are popular because they have a lower chance of self-discharge through specific chemical reactions that gradually reduce the stored charge, resulting in a longer shelf life than regular batteries. Kelly Johnson-Arbor, a medical toxicologist and co-medical director of the National Capital Poison Center, says that with items such as mobile devices using more button batteries, we’ll likely see more exposure cases in children each year.

The research study used the National Electronic Injury Surveillance System to collect data on ER visits where children had either ingested a battery, placed it around or in their mouth, or inserted it into their ears or nose. In the past decade, there were 70,322 battery-related ER visits (9.5 per every 100,000 children yearly). Button batteries were the most common battery ingested, making up 84.7 percent of visits. 

[Related: Babies and pets might freak out during fireworks shows, but you can help them relax]

Children five years and younger had the highest rates of hospital visits. The average age was about three years old. What’s more, the number of battery-related ER visits increased from 2010 to 2017. “While we suspected an increase, we were surprised to find more children had visited the emergency room for battery-related injuries in the decade between 2010 and 2019 than in the previous two decades combined,” comments Chandler. “The proportion of patients hospitalized also increased, indicating that battery-related injuries may be becoming more severe.”

Each year, nearly 2,000 button battery ingestion cases are reported to US poison control centers in children under six years old, explains Johnson-Arbor. Around two percent of cases involve life-threatening symptoms that require medical intervention or even death. 

Johnson-Arbor explains it can take two hours to see serious injuries after a child swallows a button battery. In the esophagus, the chemicals in the button batteries can burn holes in the muscular tube. As batteries travel down the esophagus, it can become lodged in the throat and the pressure on the walls can cause tissue damage. 

While it’s still dangerous for the battery to be in the stomach and intestines, she explains there is more free-flowing movement than in the esophagus. “It’s unlikely that a battery will stay in one place long enough in the stomach and intestines to cause direct tissue damage.”

One of the more concerning battery-related damage is electrical injury. Johnson-Arbor explains that when a button battery is swallowed, the electrical current created between the two poles of the battery causes a hydrolysis reaction in the fluid in the esophagus. The hydrolysis reaction forms corrosive hydroxide ions that cause chemical burns to nearby tissues. Thisreaction continues until the battery runs out of energy. Still, Johnson-Arbor adds, “it’s important to remember that ‘dead’ batteries can still generate current and cause potentially dangerous injuries.”

[Related: What is botulism, anyway?]

Chandler hopes that the study’s findings will remind all parents and caregivers to be extra vigilant when children are using devices with button batteries. If the product is damaged or the button battery compartment cannot be secured, immediately discard the product. Both experts advise the following to prevent further battery-related incidents:

• Buy only the batteries that you need and buy only single units 
• Lock up or store unused batteries out of the reach of young children
• Don’t change button batteries in front of children
• Tape up or secure button batteries tightly within their devices

If  you suspect your one-year or older child has ingested a battery in the past 12 hours, there are some immediate actions you can take. Both experts advise giving two teaspoons of honey every ten minutes for up to six doses and then going straight to the ER. Johnson-Arbor warns that honey is never an acceptable alternative to seeking medical care for a swallowed battery, however, it can temporarily help as honey coats the battery and reduces the production of hydroxide ions. This would delay corrosive tissue injury to the esophagus as you head to the hospital. “Do not delay going to an ER by stopping at a grocery store or going to a neighbor’s house to get honey because button battery treatment is extremely time-sensitive,” Johnson-Arbor  says. 

Because of a potential botulism risk, honey should not be given to children younger than a year. Other precautions involve not inducing vomiting and stopping your child from eating or drinking until you see a doctor. For more information, visit the National Battery Ingestion Hotline at 1-800-498-8666.

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Leaving the lights on at night makes it hard to sleep, and it also may endanger our health and local ecosystems. A new study published today in Science Advances reconstructed nighttime light pollution in Europe and found an increase in artificial blue lights across the continent. While LED technology can help illuminate poorly visible streets and roads, the authors warn that high amounts of blue light emissions could alter natural nighttime cycles for humans and animals.

One of the greatest risks to artificial light is how it alters animal behavior, says lead study author Alejandro Sánchez de Miguel. “Many times the nighttime is the time to eat, pollinate, navigate, nest, or rest, and all those processes are disturbed by the artificial light,” says Sánchez de Miguel, an astrophysicist studying light pollution at the University of Exeter in the UK. These light sources can cause harm by “sometimes exposing the animals to predators, other times directly by messing up with their physiology,” he says.

Scientists have only tracked artificial light before in smaller areas since it’s hard to map on a wider scale. What’s more, other studies have used satellites to produce panchromatic images—gray-scale pictures that combine red, blue, and green bands for high-resolution—but they leave no information on specific wavelengths. The team bypassed this issue using pictures taken on digital cameras by astronauts on the International Space Station. “It is a complicated data source, but it is currently the only one that we have public and can be up to 150 times more resolution than the most popular satellite,” says Sánchez de Miguel. 

[Related: The world needs dark skies more than ever. Here’s why.]

Collating these images, the study authors were able to map the light spectrum in Europe between 2012 to 2013 and 2014 to 2020. Compared to the beginning of the decade, the study authors observed a shift from high-pressure sodium lighting—lights with a warm yellow glow that’s often used in roadways and parking lots—to broad white LEDs. The study’s spectral map showed the move toward white LEDs varied by country. Italy, Ireland, and the UK showed the greatest shift towards blue light emissions, while Belgium and Germany showed the least change. 

Cities are turning towards LEDs to provide more brightness to dark skies than the monochrome yellow tone from high-pressure sodium lighting. Another benefit the study authors suggest is that LED lights are marketed as an energy-efficient alternative. However, the findings show LED lights give off more blue light emissions. Blue light has shorter waves (ranging from 450 to 495 nanometers) that provide more energy and a cooler color than other longer wavelengths, such as red light waves. We’re often exposed to blue light on our electronic devices like smartphones and television. 

Thomas Kilkenny, the director of the Institute Sleep Medicine at Staten Island University Hospital who was not affiliated with the study, says that blue light exposure can disrupt sleep by inhibiting the production of melatonin. “This is the hormone that makes you feel sleepy. It is normally stimulated by darkness just before sleep.” With blue light, however, your brain is tricked into thinking it’s still daylight, keeping you awake and prolonging the time it takes to fall asleep.

[Related: Artificial light poses a growing threat to nocturnal wildlife]

On the bright side, “blue light added to the streetlights may make people feel more awake when they are driving and decrease accidents,” points out Kilkenny. On the downside, “it may also have the unintended consequence of increasing the amount of insomnia in the population,” he adds. “Sleep deprivation is already a major problem in society and in itself may lead to more traffic accidents, illnesses, depression, and lost time at work.”

The authors also revisited past research studies and found that artificial nighttime lights may explain changes in human melatonin levels, star visibility, as well as bat and insect behavior. “LEDs are not being used in a sustainable way, and they are not reducing light pollution,” warns Sánchez de Miguel. “In the context of an energy crisis like now, we should remember that light pollution is a plain air pollutant and a waste of energy.”

According to the research authors, this is one of the first studies that has mapped the full spectrum of LED lights across the European continent at night. Sánchez de Miguel explains that they are currently working on trying to automate some of the processes involved in mapping with the goal to create a world map showing the environmental risks associated with artificial lighting across the entire planet.

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One-third of Pakistan is now underwater. The country is currently dealing with one of the worst floods in a decade, with record-breaking rains leaving 1,325 people dead and more than 33 million without homes. Climate change experts say that these extreme weather conditions did not come out of the blue, suggesting that global warming is likely the cause behind the flooding and will likely instigate future flooding events.

While studies have yet to confirm the official cause behind the disastrous waters in Pakistan, the flood “has all the signs of a climate change-enhancing event,” says Benjamin Zaitchik, a climate change scientist at Johns Hopkins University. There are several leads that researchers, such as Zaitchik, are following to understand why the relentless monsoon occurred and what weather conditions should be monitored to prepare for events in the future. 

One of the most likely scenarios involves greenhouse gases. With greenhouse gases warming the air, Zaitchik explains that extreme precipitation rates are expected to increase in many regions. This is because warm air holds more water vapor than cold air. As you warm air, it transports more moisture, creating the right conditions for extreme rainfall. 

Another potential cause for the intense flooding in Pakistan could be related to meandering jet streams. Jet streams are fast flowing, strong winds five to seven miles above the atmosphere. The air currents travel across the globe but there are times when they “wiggle around” slightly, explains Zaitchik, causing cold air to come in from the north or warm air to come from the south.

[Related: A ‘monsoon on steroids’ has submerged a third of Pakistan]

Jet streams blow from west to east with the flow shifting from north and south. “It’s the difference between the really warm air at the equator and the cold air at the pole that keeps the jet streams in line as they whip around the planet,” he says. The bigger the temperature difference in the air, the better the balance at keeping the jet stream. During the winter when the temperature gap is at an all-time high, jet streams travel with strong and fast cold winds to the south. But in the summer, the warm air drives jet streams to travel slowly up north. 

However, under global warming, the jet streams are flowing more often in a meandering pattern: some currents are dipping and rising, even splitting away more often than they should. Zaitchik explains that when you warm the planet with greenhouse gases, the difference in cold air from the poles and warm air from the equator gets smaller. As jet streams wiggle around more often, Zaitchik says it can create situations called blocking patterns, where a jet stream blocks the air and creates a particular high or low pressure current that stays longer over an area. This can  cause prolonged weather patterns than usual, like a heatwave. 

Heat waves on land could also be a potential culprit. Zaitchik explains that as warm air rises, it creates a low-pressure system over regions like in Pakistan, which already experience hot and dry temperatures. The low pressure sucks the air coming in and removes moisture from the ocean. Martin Stute, a hydrologist and environmental science professor at Barnard College, says that the world is currently in a La Niña period that tends to make Pakistan and other Asian countries wetter in the summer. Warm moisture taken from the ocean feeds into storms, intensifying winds and rainfall. The “heat wave leads to dry and hot conditions that bring more wet fuel, to power the event,” explains Zaitchik.

[Related: What is a flash flood?]

Another type of wet fuel for extreme flooding is the melting of glaciers in Pakistan. The country has over 7,200 glaciers, one of the largest number of glaciers outside the North and South Poles. With glaciers rapidly melting from constant high temperatures, Stute says they are contributing to higher stream flow. The runoff could have then fed lakes and rivers that overflowed into nearby towns and villages.

Although Zaitchik blames particularly rich first-world countries, such as the US and China, with large carbon footprints for the greenhouse gas emissions charging these natural disasters, the rest of the world often has to face the consequences. ​​Pakistan’s carbon use has grown in the past few years but its footprint is much smaller than developed countries. For example, Pakistan has a 0.67 percent carbon emission rate while the US is nearly 14 percent. ”We’re seeing some of the poor countries with relatively low per capita carbon emissions, but also low infrastructure and climate resilience, bearing the brunt of the impacts,” says Zaitchik. 

Pakistan’s flooding is devastating, but expected. As a developing country, Pakistan has made strides in exporting textile and leather goods as well as energy production. However, its troubles with housing, health, and poverty may make it difficult to reconstruct millions of lost homes. 

Stute says cities and nations need to adapt for more floods, whether it’s through raising settlements or installing more deep wells for access to clean drinking water. “We expect this flooding to be more common in the future,” he says. “Even if we stopped emitting greenhouse gases tomorrow we will see further increases in global temperatures [because] the Earth’s climate system needs time to adjust.”

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The change in season is coming with a change in COVID-19 vaccines. Last week, the Food and Drug Administration (FDA) authorized the use of another round of boosters, with the Pfizer-BioNTech shot green lit for people 12 years and older and the Moderna shot for people 18 and older. The shots can only be received after at least two months following the primary vaccination series.

Unlike previous doses, the new booster is a bivalent vaccine which includes an updated formula containing the mRNA of the original SARS-CoV-2 strain to broadly protect against COVID-19 infection, as well as the mRNA of the more recent Omicron BA.4 and BA.5 variants. As of September, the BA.5 variant is currently the dominant variant circulating in the United States, making up 88.6 percent of cases.

Infectious disease experts are bracing for another surge of cases in the fall and winter, but they are cautiously optimistic that the new COVID-19 boosters will provide immunity against severe disease and illness. These vaccinations will be available soon—here’s what you need to know before you get one.

When can I get the new boosters?

By the end of the week. The White House COVID-19 Response Team said in a September 6 press briefing that they have already shipped millions of doses once they received the FDA’s authorization on August 31. They announced that by Friday, September 9, “over 90 percent of Americans will live within five miles of these new updated vaccines.”

You can visit Vaccines.gov to find sites carrying the new boosters. Appointments at pharmacies such as CVS and Walgreens will become available this weekend with a majority of slots opening up next week. You can also contact your primary care provider or local health clinic to see if they are taking vaccine appointments and which booster they are carrying.

Should I go with the Moderna or the Pfizer-BioNTech booster?

Michael Chang, a pediatric infectious disease specialist at UTHealth Houston and Memorial Hermann Hospital, says there’s not much evidence to suggest one is better than the other. However, he says pre-clinical data showed little difference between the two and both were effective in preventing illness and hospitalization. 

Sharon Nachman, chief of the division of pediatric infectious diseases at Stony Brook Children’s Hospital, recommends trying for a mix-and-match strategy this time around. “If you’ve gotten Pfizer as your primary series, it’s a great idea to swap out and go for the Moderna booster and vice versa.” She says because the vaccines are formulated a little differently and there’s more research to suggest that mixing and matching gives you an extra boost of immunity, you’re likely to have a higher degree of protection.

I already had a COVID booster. Do I need this one?

Yes. The Centers for Disease Control and Prevention (CDC) says you’re not up to date with your vaccines until you’ve finished your primary series and the most recently authorized booster. Even if you received a booster earlier this year, Chang says these new shots are better at targeting Omicron strains. “It will better cover the currently circulating variants and potentially provide broader immunity against future variants,” he explains. Since the newer boosters are more effective, they will replace the previous boosters, which will not be offered anymore to people over the age of 12, Chang adds. 

[Related: Omicron boosters are the future of COVID vaccines in the US]

Chang says if you received your booster even three to four months ago, your antibody levels are probably falling. Both he and Nachman agree that getting the bivalent vaccine will raise the country’s collective immunity and provide as much protection as possible going forward. As the US transitions from pandemic to endemic mode, the priorities have shifted towards learning how to live with? and manage the virus. 

“COVID is here to stay,” adds Nachman. “It’s going to be part of our lives and I suspect we’ll have annual dosing like the flu vaccine every year.”

I just recovered from COVID. How long can I hold off on getting a booster?

Yes, you can wait, but not for too long. Fighting off a recent battle with COVID temporarily gives you antibodies to avoid catching another infection. The CDC advises delaying your booster shot for no more than three months from when your symptoms first emerged or when you received a positive test result. 

Studies measuring antibody levels after each strain of infection shows a lot of variation with naturally acquired protection, Nachman explains. In some cases, she says antibodies lasted a couple of months while others saw levels dropping sooner than that. “Would I run and get the booster a day [after testing negative]? No,” she says. “Would I wait six months? Absolutely not.”

When is the best time to get the bivalent booster?

If you recently recovered from infection and delay the dose for three to four months, Chang says you’ll likely have your highest antibody levels during the winter, a time when infectious disease experts expect to see a surge in cases after the holidays. “You will probably have peak antibodies within two weeks or so [after immunization].” Chang also recommends waiting three to four months for people who received a booster in the summer or in the last two weeks.

Nachman says that in an ideal world, people would wait until October or November to get the booster to prepare for a bad winter. But if you have underlying immune issues or are living with someone with multiple medical problems, she recommends getting the vaccine immediately. If you’re planning on traveling outside of the country, she says it’d be ideal to get your vaccine a month before to protect yourself against a potential outbreak in another country. “There’s no one right answer,” she cautions. When in doubt, Nachman highly recommends speaking with your doctor about the right timing for you to get the booster shot.

[Related: China approves world’s first nasal COVID-19 vaccine booster]

Will the booster have any side effects?

Yes. Both experts say you should expect to see similar side effects as your previous vaccines such as low-grade fever, muscle soreness around the injection site, and fatigue. Though Chang is hopeful that the side effects won’t be as severe as prior vaccinations. “In some cases with people who had vaccine side effects, we’re seeing a little less side effects with each booster.”

To prepare for the side effects, experts recommend getting a full night’s rest, gently moving your body to help with fatigue and muscle aches, and staying hydrated throughout the day. Nachman does not recommend taking pain relievers such as aspirin, Tylenol, or Motrin prior to vaccination. Instead, she says it’s better to take Tylenol a couple of hours after.

When will boosters be available for kids from 5 to 11?

There’s no clear timeline on when boosters will become available for kids between 5 to 11 years. Both experts say Moderna and Pfizer-BioNTech are already starting the groundwork to conduct studies on the appropriate dosage for this age group. 

Chang says the process toward authorizing boosters for kids should not take as long—he could even see more developments before the end of the year. Nachman’s prediction is a bit more grim. She says parents should not expect COVID booster eligibility for younger age groups until late winter 2023. The CDC recommends children 5 to 11 years old get a monovalent—containing only the original strain—booster dose in the meantime.

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For years, the beauty market has exploded with hundreds of different skincare products advertising themselves as a ‘must-have’ item for age-defying skin—Kim Kardashian’s recent skincare line is a nine-step process that retails for $630. And now a brand-new beauty routine is making the rounds on TikTok: skin cycling. Dermatologist Whitney Bowe, the creator of the new skin cycling trend, has used her platform to advocate for doing less work to get better-looking skin.

Skin cycling is a four-day regimen. On the first night, after you wash your face, you apply a physical or chemical exfoliant to peel off dead skin cells on the top layer of your skin. On the second night, you apply a retinol to unclog pores and increase skin cell production to give your face a more refreshed appearance. The drawback with constantly using an exfoliant and then retinol closely after is that it can irritate the skin. So Bowe advises her viewers to use days three and four for hydration and recovery, applying just a moisturizer after your regular face cleansing. 

TikTok users like _eaden are strong advocates for Bowe’s skin cycling regimen, calling it a game-changer. “When I started doing this a couple of months ago, someone literally came up to me in person the other day and said ‘Your skin looks like an Instagram filter,’” she recalls in one of her videos. 

But, like any fad you find on TikTok, does it actually work? 

“Other TikTok trends are from influencers that tried something and want to spread the word of a one-case scenario that worked on them,” says Melanie Kingsley, an associate professor of dermatology at Indiana University School of Medicine and dermatologist at Indiana University Health. “That’s when TikTok trends get a little dangerous because we don’t have the science behind them.”

[Related: The truth about activated charcoal in beauty products]

However, for some peace of mind, this routine is being recommended by a board-certified dermatologist who clinically treats people’s skin conditions. Bowe has “years of experience,” Kingsley reassures. “She’s formulated it in a way that has helped her patients and fine-tuned it over the years.”   

While there is no research studying skin cycling, Kingsley says there is some evidence that backs up the importance of getting rid of dead skin cells and using retinol to increase collagen production and remove skin damage. But instead of doing those two harsh steps over again and risking your skin drying out, she says that allowing the skin to heal gives you the benefit of exfoliation and retinol while not harming the barrier extensively, resulting in glowing and brighter skin.

Kingsley says she would recommend skin cycling for patients that want to restart their nighttime routine or do not currently have a skincare regimen but want something easy. “I think it’s a great option.”

Though not all skincare experts share the same enthusiasm over Bowe’s skin cycling methods. Amber Rose Johnson, a celebrity esthetician and founder of Facial Lounge, explains that skin cycling is helpful because it gives the skin time to receive treatment and recover. However, she points out that there is no one skin cycling protocol that is safe for all skin types. “There are a lot of different trends out there so I cannot recommend [Bowe’s] especially for sensitive skin.” Johnson also has her own preferred skin cycling method which revolves around deeper exfoliation during your menstrual cycle or every 28 days. “This is the natural exfoliation process of our body and it’s great to keep the process up.”

[Related: Does ‘vabbing’ work? The truth about vaginal pheromones.]

Pregnant people should be cautious of doing the skin cycling trend given that there is some evidence that retinols may cause birth defects. Having sensitivity to retinoids—such as people with rosacea, contact dermatitis, and eczema—could make the skin cycling routine intolerable. If you fall into one of these categories, Kingsley advises to forgo the retinol and instead focus on doing very gentle exfoliation and moisturizing. The key is to not overdo it and to take it slow.

“The skin loves to exfoliate but can be irritated and mad at you after the process,” adds Johnson. “You must give it some love with lots of hydration that is paraben and fragrance-free. Not only is this good for large pores, blackheads, fine lines, and scarring but definitely slows down the aging process.”

If you’re interested in skin cycling, but don’t know if it’s right for your skin, see a skincare expert first. They will help you identify your skin profile, sensitivities, and tailor treatments specific to your needs.

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To understand what environmental issues lie ahead for our warming planet, geographers often look back to the past for answers. A new study published on August 29 in Proceedings of the National Academy of Sciences details how the landscape of ancient Egypt allowed them to create the pyramids of Giza—one of the most iconic human-made phenomenons in the world. On a now-dried-up arm of the Nile River called the Khufu branch, the study authors found that people needed the waterway to transport tools and other materials such as stones and limestones to the Giza Plateau for pyramid construction. The Nile was a vital resource not only for transportation, but for food, land for farming, and water for ancient Egypt, explains Sheisha Hader, a physical geographer at the Aix-Marseille University in France and lead author of the study.

“Good [Nile] levels promised stability [to] the ancient Egyptian society,” Hader says. “By contrast, the drought as a result of low Nile levels would be catastrophic and a reason for social unrest and sometimes, civil wars.”

In May 2019, Hader and the team studied pollen grains taken after drilling the land next to where the Khufu branch of the Nile once stood. Two of the study sites were in the supposed Khufu basin. About 109 samples dating between the Predynastic and Early Dynastic-Old Kingdom periods were collected for analysis and divided into different groups based on seven vegetation patterns. The vegetation patterns combined with other data sets involving nearby volcanic activity that could drive weather changes, solar radiation, and African water levels at the time, helped the geographers trace back changing water levels and painted a picture of how the climate looked over the last 8,000 years in Egypt. This timeline encapsulated the dates when the three pyramids of Giza—Khufu, Khafre, and Menkaure—were estimated to be completed, between 2686 and 2160 BCE.

Hader says she wasn’t as much surprised but rather in awe of the “clever old kingdom’s engineers who could thoroughly harness their environment and the Nile dynamics for turning the impossible into reality.” With the river, she says the ancient Egyptians were capable of designing a harbor on the edge of the desert where the small Khufu channel would drive in water without the risk of flood. “They dredged the floodplain on the western part of the channel and let the water flow, and the ships navigate to provide the logistic supply for builders.”

Joseph Manning, a professor of classics and history at Yale University says that, before this study, how water got to the Giza pyramids was not well understood. “We’d known there was water that came pretty close to the Giza Plateau, which is how they’re getting stone from the Tura quarries [the Egyptians’ main source of limestone] across the river over to Giza,” he explains. “I thought they were building canals that connected, but it looks like it’s a natural river channel.“

Manning says that finding natural river features frames how humans interacted and took advantage of their environment, creating not-so-simple projects like the pyramids. However, one concern he points out in the study is how the researchers analyzed the data on volcanic eruptions during that time period. Their findings suggest volcanic eruptions played a major role in fluctuations in the Khufu branch, which in this case, led to a decrease in Nile summer flooding. “Just because you have a volcanic sequence doesn’t necessarily tell you anything about Nile conditions,” he explains. For instance, some large eruptions in high latitude regions, such as Iceland or Alaska, have been known to impact the East African monsoon—which can change the water levels on the Nile. But not every eruption has an effect, Manning says, explaining that that other factors such as the time of year, location, and the scale of the eruption will affect monsoon responses in the Middle East, instead. 

[Related: There’s apparently a giant void in the Great Pyramid. Here’s why we don’t know what’s in there.]

Christophe Morhange, an expert in geomorphology at Aix-Marseille University and senior study author, says the study goes beyond knowing the origin of these massive monuments. “It’s also the human imprints on the environment [and] the importance of landscape archaeology.”

The rise and fall of the ancient Egyptian empire was hinged to changes in the Nile, explains Hader. Looking back on a society that rose to power by tapping into the local ecosystem can teach/inform climate scientists today. 

It’s important to know how “the path of their history and how the environment could direct a flourishing empire like the old kingdom,” Hader says. “[But] the climate-environmental change being the same reason for which the empire collapsed is a crucial point to understand if we want to face our present and future environmental challenges.”

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Psilocybin, the psychedelic compound that causes the trippy effects of magic mushrooms, could help people with alcohol use disorder drink less and potentially quit altogether. A new clinical study published August 25 in JAMA Psychiatry found that two doses of psilocybin combined with psychotherapy reduced the amount people drank compared with people who only received psychotherapy. Psilocybin’s effects persisted for at least seven months after the second dose, suggesting it could be a potential long-term treatment for alcohol addiction. 

“The findings are promising and exciting,” says lead study author Michael Bogenschutz, director of the NYU Langone Center for Psychedelic Medicine. “We saw large and very persistent effects that could help us find out what place psilocybin will play in the treatment of alcohol use disorder and potentially co-occurring mood and anxiety disorders.”

Though it enrolled fewer than 100 people, the trial “represents the largest psilocybin study to date, and the relatively robust outcomes in both overall drinking, and drinking-related behaviors in a study of this size are therefore noteworthy,” says James Giordano, professor of neurology and biochemistry at Georgetown University Medical Center who was not a member of the research team.

The Food and Drug Administration does not approve psilocybin as a treatment for any disorder. But in the past decade, a growing scientific movement has explored possible mental health benefits of psychedelics. Psilocybin, most notably, has shown to provide immediate and long-term relief for people with depression. Research suggests psilocybin’s effectiveness increases when combined with therapy, especially for treatment-resistant depression. The current trial tested psilocybin’s health benefits towards another condition: alcoholism. 

About 14.5 million people in the US have alcohol use disorder; alcohol is the third-leading preventable cause of death among Americans. Heavy drinking rates have also soared during lockdown, with an increased 25 percent of alcohol-related deaths in the first year of the pandemic. While some medications and psychotherapy can effectively manage alcohol abuse, Bogenschutz says their effects are small. Only one person out of 60 with alcohol use disorder actually seek medical treatment.

The new randomized, double-blind clinical trial is based on the results of a 2015 pilot study led by Bogenschutz, in which his team tested the effects of two doses of psilocybin plus psychotherapy on 10 participants with alcohol dependence. While the previous study was not well-controlled, Bogenschutz observed that the treatment substantially decreased people’s drinking and there were no noticeable safety issues.

[Related: Is Dry January the best way to cut back on drinking?]

To build off those results, the researchers enrolled 93 men and women diagnosed with alcohol use disorder. Each person received 12 psychotherapy sessions for 12 weeks and was randomly assigned to receive either two doses of psilocybin (48 patients) or an antihistamine placebo (45 patients). The team tracked the participants’ health outcomes and their daily drinking patterns for eight months. After the eight months, every participant was offered a third session where they would knowingly receive psilocybin.

People in the psilocybin group drank significantly less than people in the placebo group during the first 32 weeks. The rate of heavy drinking–four or more drinks in men and three or more drinks in women in a single day–in people who took psilocybin was 9.7 percent. For people who had the antihistamine, it was 23.6 percent. The last follow-up showed psilocybin’s effects persisted for another seven months.

Twice as many people in the psilocybin group stopped drinking altogether compared with those who were abstinent in the placebo group (48 percent vs. 24 percent). “My greatest expectations for this were to be able to manage my cravings, and this surpassed that,” said John Costas, one of the first participants enrolled in the clinical trial, in a press conference about the study. “[Psilocybin] eliminated all my cravings to the point where it cured my alcoholism, and I don’t categorize myself as an alcoholic anymore.”

Paul Mavis, another study participant who received the placebo but then psilocybin in the optional third session, said he feels comfortable again going out to dinner with friends who are drinking in front of him. “No one would have thought that I would not be drinking, including myself… I haven’t had a drink or a craving, it was as if I never drank in my life.”

[Related: What is a hangover? And can you cure it?]

“This is a very encouraging preliminary study of psilocybin-assisted therapy for alcohol use disorder,” says Keith Heinzerling, an addiction medicine specialist and director of treatment and research in psychedelics at Providence Saint John’s Health Center who was not affiliated with the study. Not only were there improvements in heavy drinking, but Heinzerling noted taking psilocybin did not cause any serious side effects. He pointed out, though, that the study had trouble hiding who had the hallucinogen and who did not; participants quickly realized which group they were in. “This is a challenge in all psychedelic clinical trials and may have biased the results in favor of psilocybin.”

The study has the potential to expand psilocybin use to co-morbidities often associated with alcohol dependence, Giordano says. But it would have been helpful to observe how psilocybin affected people by gender, ethnicity, and age, he adds.

Bogenschutz and his team are planning to expand their findings into a three-year trial with more than 200 participants at 15 sites. If all goes well, the trial may be one step closer toward FDA approval of psilocybin, which Bogenschutz says would be “a real breakthrough in the treatment of alcohol use disorder.”

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A strong defense against online misinformation may be to administer a digital vaccine: Exposing yourself to common deception methods may help you recognize sensationalized headlines, misleading TikToks, or social media fabrications in the future. In collaboration with Google and its tech unit Jigsaw, a team of psychologists added short videos to YouTube’s ad lineup, educating people about how to spot common misinformation tactics. In an online campaign, they found these clips were an effective way to get people to identify what’s real and what’s fake news.

People who watched the videos were better able to identify misinformation techniques than those who didn’t see the clips, as the team reports in a study published in the journal Science Advances today. “It’s very possible on social media to reduce vulnerability and susceptibility to being manipulated,” says Jon Roozenbeek, a postdoctoral fellow at the University of Cambridge and the lead author of the study. “Maybe not all misinformation, but you can demonstrably improve people’s ability to detect when they’re being manipulated online.”

Misinformation happens when people spread false information, even if it wasn’t the person’s intention to mislead others. Misinformation happens regularly in our daily lives, says Sabrina Romanoff, a clinical psychologist who was not affiliated with the study, and it can be something as small as misremembering something you saw on television and telling someone else the wrong information. “You can think of it as analogous to the childhood game of ‘telephone,’” explains Romanoff, in which small errors become magnified through repetition. But through the megaphone of social media, wrong or misleading claims can become a harmful way to distort the truth.

[Related: The biggest consumers of fake news may benefit from this one tech intervention]

Anyone can fall prey to misinformation online, Romanoff says, though people who click on a story consistent with their pre-established beliefs are more susceptible. Being prone to impulsivity and feeling an overload of information could also make you more likely to spread fake news. 

The current study focuses on inoculation theory, where people learn about these types of misinformation techniques. Roozenbeek compares this theory to a vaccine: Introducing a weakened virus or virus-like material primes your immune system to recognize and destroy the pathogen in the future. Unlike fact-checking, which takes a more retroactive approach, inoculation theory stops people who are exposed to misinformation from spreading the content in the first place. “The idea was to inoculate people against these tropes, because if someone can successfully recognize a false dichotomy in content they’ve never seen before, they’re more resilient to any use of that particular manipulation technique on social media,” Roozenbeek says.

Roozenbeek and his team created five 1.5 minute videos covering common tactics used in online misinformation. To avoid any bias towards one group of people, the videos were designed to be nonpolitical, fictitious, and humorous. In the lab, the team invited over 6,000 participants to randomly watch either a video showing how to identify misinformation techniques or a neutral video that acted as a control. Afterward, the participants were shown 10 made-up social media posts that were manipulative or neutral. 

Roozenbeek then partnered with Google to expand the study. As part of a public ad campaign on YouTube, nearly 23,000 people watched one of two anti-misinformation videos. One video involved negative and exaggerated emotional language to encourage clicks and belief in fake news (Sample headline: “Baby formula linked to horrific outbreak of news, terrifying disease among helpless infants. Parents despair.”). The other one relied on presenting two points of views or facts as the only available options (The headline: “Improving salaries for workers means businesses will go bankrupt. The choice is between small businesses and workers. It’s simple mathematics.”). 

Within a day of seeing the video ads, one-third of people who watched the videos were randomly given a test question on YouTube where they were asked to identify the type of manipulation technique in a headline or sentence. People who watched the videos were better able to pick out misinformation techniques and misleading content.

“Finding a significant effect was actually quite surprising,” Roozenbeek says. This is because unlike a controlled laboratory setting, people on the internet can get easily distracted by other ads and videos. Additionally, there is no guarantee people actually watched the videos. While the videos were not allowed to be skipped, people could have turned off the sound or moved to another tab. “But despite all that, we still found a large and robust effect.”

[Related: Connecticut will pay a security analyst 150k to monitor election memes for misinformation]

Roozenbeek and other psychologists are wrapping up another study that looks into how long it takes for people to forget what they’ve learned from the videos. “It’s not reasonable to expect someone to watch a video once and remember the lesson for all eternity. Human memory doesn’t work that way,” he says. Ongoing results suggest ‌people might need a ‘booster shot,’ in the form of repeated video reminders. Another project in the works will use Twitter to see how watching these videos affects people’s behaviors, specifically how much they retweet misleading content.

To stay vigilant against misinformation as you scroll through the internet, Romanoff warns about these six common tactics:

• Fabricated content: Completely false or made-up stories
• Manipulated content: Information is intentionally distorted to fit a person’s agenda
• Misleading content: A person deceives others, such as presenting an opinion as a fact
• False context of connection: A person strings together facts to fit the narrative they are trying to convey, such as new stories using real images to create a false narrative of what happened
• Satire content: A person creates false but comical stories as if they were true
• Imposter content: A story is created through the branding and appearance of a legitimate news story, but is false such someone creating a video using someone else’s logo to seem legitimate

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With COVID, monkeypox, and West Nile virus, New York has had an onslaught of outbreaks this summer, and it doesn’t seem to be slowing down. Polio is spreading in the Empire State, with the first case in decades reported in Rockland County, followed by traces of the virus in New York City wastewater weeks later. Adding to concerns of a potential outbreak is an August 16 report by the Centers for Disease Control and Prevention (CDC) confirming the virus had actually been circulating in the area since April.

The past few years have been nothing short of public health emergencies, but given the new threat of a virus thought to be under control, you might be asking: Will the US see a new polio outbreak? 

According to medical experts, people should be vigilant enough to follow the news, but not concerned enough about it becoming another pandemic. “It’s a disease that’s been considered eradicated for the most part,” says Zachary Hoy, a doctor at Pediatrix Nashville Pediatric Infectious Disease. “With most people vaccinated and low circulating numbers, [you] should not be too worried.” 

While there’s only been one case of polio so far, viral traces in wastewater suggests there could be hundreds more unconfirmed cases. Your concerns about a potential polio outbreak are valid. Polio is dangerous. Fortunately, this isn’t the country’s first run-in with the virus, and infectious disease doctors have the answers you need to protect you and your loved ones. 

How good is the polio vaccine?

You might have heard that the paralytic polio case occurred in an unvaccinated individual exposed to a polio strain used in oral polio vaccines. The oral polio vaccine, which is still the go-to in some countries, uses three weakened strains of the virus to stimulate the immune system and build antibodies against it. Spearman says this type of vaccine is typically safe, but there is a very small risk—one in every two to three million doses—for the weakened virus to shed and develop mutations. If it gets a certain number of mutations, the immunized person or an unvaccinated person exposed to that mutated virus can end up with paralytic poliomyelitis. Of the ten billion doses of the oral drops, there have been less than 800 cases of vaccine-derived poliovirus in the past decade.

The inactivated polio vaccine is the only shot used in the US since 2000 and is considered extremely safe and effective. “It’s greater than 99 percent effective in protecting individuals against any disease from poliovirus,” says Paul Spearman, director of the division of infectious diseases at Cincinnati Children’s Hospital Medical Center. “Compared to the COVID vaccine, waning immunity is not much of an issue with the polio vaccines,” Hoy explains further.

[Related: During a devastating polio epidemic, a vaccine was finally on the horizon]

The vaccine is also very effective among children, especially those under 5, who are the most at risk for paralysis and death. Two doses of the inactivated polio vaccine are 90 percent effective or more against paralytic polio, while three doses increase protection to 99 to 100 percent. The World Health Organization warns it takes only one infected child to make other children at risk for polio, making it a mandatory vaccine in all 50 US states for students.

Spearman explains that the vaccines helped to nearly eradicate polio in the US in 1979. Since then, the rare cases that pop up are usually from someone who has traveled out of the country where the virus is still endemic. However, those instances are so well controlled with the current vaccines that they never have erupted into a large-scale outbreak. 

I got the oral polio vaccine as a kid. Will I need a booster?

Short answer: no. According to the CDC, the oral polio vaccine was discontinued because of the small risk of vaccine-derived poliovirus. But that does not mean it stops working. “The oral polio vaccines are effective and very immunogenic,” says Spearman.

Also known as the Sabin vaccine, the oral drops were one of the reasons why the polio epidemic ended in the US. “There were tens of thousands of polio cases yearly in the US in the 1940s and ‘50s,” explains Spearman. “Then the Salk vaccine and Sabin vaccine, which is the oral polio vaccine, came out and cases fell dramatically.” 

“People that have taken the oral polio vaccine versus the inactivated would still have appropriate immunity,” adds Hoy. “So it would not be recommended that they would have to get a polio booster.” At the time of publication, the CDC has not released any recommendation that individuals who received either vaccine series will need an extra dose of the inactivated vaccine.

Will I ever need a polio booster in the future?

Both infectious disease experts say it’s unlikely, given that the polio vaccines are highly effective in protecting against infection and curbing viral spread. But there are some exceptions.  

The CDC says people who are at increased risk of being exposed to the poliovirus, such as healthcare workers, and have already completed their shot series are eligible for a one lifetime booster of the inactivated polio vaccine.

[Related: Everything you should know about getting a second COVID booster]

Spearman mentions that doctors may also consider giving a booster on a case-by-case basis, with the highest priority going to people traveling to certain countries in Asia and Africa with known wild-type poliovirus circulating in the area. Another thing to consider is if an individual is immunocompromised and has a risk of contact with poliovirus. While the CDC is not offering additional boosters to this population, they may be more susceptible to infection by the virus and could also harbor it for longer periods of time, warns Spearman.

“The most important thing is if you have a good record of being fully vaccinated as a child, then you’re safe,” adds Spearman. “And you don’t have to worry at this point about getting any boosters.”

Can I get vaccinated for polio as an adult?

For people who know they are unvaccinated, it is possible to catch up as an adult. However, because the immunization is a three-shot series, you won’t be fully protected immediately. After the first dose, your second is scheduled one to two months later. Then your third dose is six to 12 months after the second dose. Given that “it’s not a routine adult vaccine,” Hoy advises calling ahead to ensure your family doctor carries the dose. If not, he recommends going to:

• Your county health department
• Travel clinics
• Urgent care
• Your family doctor

For those unsure about their vaccine status, there are a few ways to confirm old medical records:

• Your state’s electronic immunization registry
• Your old pediatrician
• Your parents

If you can’t find your records, Hoy says your doctor may be able to draw your blood and send it to a lab to check for polio titers. If the sample tests positive, you were probably vaccinated.

Are there other ways to protect myself from polio?

Both infectious disease experts agree vaccination is the best way to protect yourself from polio. But Hoy also says that it’s useful to know how the virus gets into people’s bodies. The poliovirus is spread through the fecal-oral route and lives in the host’s throat and intestines. Having a bit of stool on your hands from contaminated foods, water, or surfaces can make its way to the respiratory tract if you touch your mouth. Some recommendations include:

• Washing your hands with soap and water for at least 20 seconds
• Using hand sanitizer with at least 60-percent alcohol
• Rinsing raw foods before cooking
• Not sharing drinks with other people

“But if someone is unvaccinated, I wouldn’t just practice good hygiene,” Spearman says. “I would certainly get vaccinated.

The post What to know about polio boosters, oral vaccines, and your medical history records appeared first on Popular Science.

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Some of the most significant scientific inventions—penicillin, gunpowder, the microwave—were discovered by accident. Now a group of researchers investigating how some animals live in the freezing Arctic have another to tack on the list: natural antifreeze. A new study published today in the journal Evolutionary Bioinformatics found that a tiny snailfish species living in Greenland contained sky-high levels of antifreeze proteins that made it possible to survive subzero temperatures.

In 2019, study coauthor David Gruber, a research associate at the American Museum of Natural History in New York and a distinguished biology professor at CUNY’s Baruch College, was out with his team on an expedition to eastern Greenland to look for animals that glowed in the dark under the ice. Located in the Arctic Circle, this region of Greenland gets near-full days of summer sun, but is plunged in darkness during the winter months. The team’s goal was to understand the role light plays in marine species living in these environments with such drastic seasonal periods of never-ending and very limited sunlight. Their search led them to a juvenile biofluorescent snailfish, a small fish with a tadpole-like body typically found in frigid waters dipping well below freezing , at 28.4 degrees Fahrenheit. Biofluorescence is when an animal absorbs blue light and emits either green, red, or yellow light—a rarity among Arctic fishes that live in darkness for most of their lives.

To better understand how snailfish create light, the biology team examined its entire transcriptome—every gene it is making—where they were surprised to find that one of the most actively made proteins in the body was antifreeze proteins. “Similar to how antifreeze in your car keeps the water in your radiator from freezing in cold temperatures, some animals have evolved amazing machinery that prevent them from freezing, such as antifreeze proteins, which prevent ice crystals from forming,” Gruber said in a press release.

Marine biologists had already uncovered the existence of antifreeze proteins 50 years ago. Several species from fish, reptiles, insects, to bacteria are known to have evolved antifreeze proteins to survive in icy habitats. For snailfish, antifreeze protein is developed in the liver where it prevents large ice grains from forming inside cells and body fluids. Without antifreeze protein, the blood of snailfish would turn frozen solid. 

[Related: Fish blood could hold the answer to safer de-icing solutions during snowstorms]

Since the initial discovery, biologists have since found that antifreeze proteins are created through five different gene families. But marine biologists did not know how much energy snailfish spent in creating antifreeze proteins. “In retrospect it makes sense—of course a juvenile fish living on an iceberg is making lots of proteins that prevent it from freezing,” explained Gruber. In their genetic analysis, the team found two gene families in charge of encoding two types of antifreeze proteins, called Type I and LS-12-like proteins. These genes were highly expressed, making up the top 1 percent of expressed genes in snailfish.

The study authors suggest that the high expression levels for these antifreeze proteins are essential for living in extremely cold waters. Some marine biologists, however, have casted some doubts on how big of a conclusion to draw from these results. C.-H. Christina Cheng, an evolutionary biologist at the University of Illinois Urbana-Champaign who was not affiliated with the study, said that LS-12-like proteins also present in the Northwest Atlantic longhorn sculpin did not provide much help in preventing fish from freezing to death. Instead, she says it’s possible the snailfish could be expressing this protein for another developmental reason. What’s more, the expression Type I antifreeze protein found in the snailfish is different from other Type I proteins from the same species. 

Cheng said these discrepancies could be resolved by further looking at antifreeze protein activity directly in the blood plasma. “If all these detected transcripts are actually made into functional antifreeze proteins, the plasma antifreeze activity would be high,” she explains. “But if the plasma antifreeze activity is low, then it’s questionable that these transcripts are made into active antifreeze proteins.”

[Related: How polar animals cope with frigid darkness for months at a time]

Still, the new study does highlight the importance of antifreeze proteins in the survival of snailfish living in the Arctic—an environment that is particularly vulnerable to rising global temperatures. Since the past century, the Arctic has been warming four times as fast as the rest of the planet, with predictions projecting an ice-free Arctic ocean in 30 years.

As the region undergoes dramatic changes, ice-dwelling fish will be forced to adapt to warmer climates or face extinction. “For these juvenile snailfish, their superpower of making lots of antifreeze proteins will no longer be a superpower in an Arctic without icebergs,” Gruber said. To make matters worse, warmer waters may introduce more fish species that tend to reside in temperate climates, increasing competition for food and shelter.

In the future, Gruber and his team plan on further investigating the nuances of antifreeze in snailfish and other species living in these frozen environments. “Snailfishes are an interesting family as they have representatives that live at surface to beyond 8,000 meters deep [in the ocean],” he said. “We are curious to investigate if there are any connections between snailfishes ability to survive extreme cold and extreme pressure environments.”

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What do elephants, camels, and sauropod dinosaurs all have in common? Soft tissue pads beneath their heels support their enormous sizes and weights. A new study published in Science Advances found that sauropod dinosaurs were likely capable of evolving to heights up to 76 feet—almost as high as the White House—because their feet had cushions which helped their massive bodies move without crushing their foot bones.

The evolution of gigantic dinosaurs and how they carried their enormous stature has been a topic of debate among paleontologists for more than a century–that, until now, had no concrete answer. “What is exciting is that our research finally resolves this 120-year-old hypothesis by providing, for the first time, biomechanical evidence to show how gigantic sauropods could support their weight on land,” says Andréas Jannel, a research associate at The University of Queensland and lead author of the study. 

These gigantic plant-eating dinosaurs, iconic for their long necks and tails, roamed Earth in the Jurassic epoch as early as 201 million years ago. But it was not until 145 million years ago that they started evolving into bigger sizes—10 times the height of the modern-day African elephant. When paleontologists found the first sauropod tracks a century ago, Jannel says, the footprints seemed to show the animals were walking on heels. This led some paleontologists to speculate that giant dinosaurs had a kind of heel pad when walking—although there was no evidence to definitively support the theory. Hundred-year-old technology was unable to study soft tissue in fossils, which are rarely preserved in rock to begin with. 

[Related: Even dinosaurs couldn’t escape the sniffles]

Jannel and his co-authors created a new approach to study dinosaur foot anatomy that included the bones and soft tissue. Using fossil data from the Upper Triassic to the Upper Jurassic epoch, the researchers created 3D virtual models from five different sauropod species, which weighed between 1,984 to 74,957 pounds. They also created a model based on the foot of an existing African elephant. Virtually reconstructing the foot postures allowed them to track how the sauropods would walk on dry land with and without a soft tissue foot pad. 

Soft tissue pads underneath the heel were necessary for sauropod dinosaurs to walk without causing tissue damage or breaking any bones. Similar to elephants, the pad cushion directed the loads away from the bones.

Study author Olga Panagiotopoulou, a senior lecturer of anatomy and developmental biology at Monash University, says the idea of fleshy foot pads came from looking at the fat pads found in elephants, rhinoceroses, and other living giants. These animals evolved bottom cushions to serve as shock absorbers to redistribute the pressure on their feet. Panagiotopoulou says a 2011 study, which found that ancestral elephants evolved to have large foot fat pads as they grew in size, partly inspired their hypothesis that sauropods had similar structures to reduce the stress on their bones and avoid fractures.

[Related: Dinosaurs who stuck together, survived together]

Smaller members in the sauropod family, the scientists found, also shared their version of a cushy foot pad. Using the fossilized tracks of sauropod precursors known as Plateosaurus, the researchers created a reconstruction of their foot that had toes slightly raised off the ground with no heel pad. The results indicate there was no way the foot skeleton alone could support their weight without some form of additional padding. “Our work suggests that the presence of an incipient heel pad in sauropod precursors laid the foundations for the evolution of a more substantial structure,” says Jannel. 

Kimberley Chapelle, a Kalbfleisch postdoctoral fellow in the American Museum of Natural History’s Division of Paleontology who was not affiliated with the study, says before this paper, no other studies tested the theory of whether sauropods had fatty pads in their feet. “This provides yet another puzzle piece to how sauropod dinosaurs got so big.” Although Chapelle says her only reservation would be that, while the study methods were tested on a modern-day elephant, “it would have been useful to see what predictions the models made for other living animals that have fat pads such as camels and rhinos, as well as those who don’t.”

With evidence for fatty foot pads in sauropod dinosaurs, Panagiotopoulou says she is planning to investigate how exactly they distribute the stress of walking by studying the foot mechanics of elephants, rhinoceroses, and horses. 

Jannel, on the other hand, is working to expand the 3D computational models to an entire sauropod limb—complete with soft tissue such as muscles, which are also rarely preserved in fossils. “This research and methodology are relatively new in the field of paleontology,” he explains. “So stay tuned, because this has a lot of potential for more research in the future, not only in sauropods but also other dinosaurs and prehistoric animals!”

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Two years into the pandemic, and political leaders are finally taking strides towards understanding the complexities of long COVID. The Biden administration released two reports last week on August 3 that address the government’s plan to advance research towards the prevention, diagnosis, and treatment services of long COVID. But for the estimated 7.7 to 23 million people currently living with longer-term symptoms and health complications from COVID, the time it takes to recover fully is still unclear. 

“The short answer is it’s a bit up in the air,” says Scott Roberts, an infectious disease specialist at Yale Medicine. 

In 2020, the Centers for Disease Control and Prevention (CDC) initially reported that nearly 35 percent of people infected with COVID-19 take 2-3 weeks for symptoms to go away after testing positive. But new data now estimates that 13.3 percent—nearly one in ten people—who recuperate from illness will take a month to resolve their symptoms. For people with more severe infections, such as those needing hospitalization, the CDC says that 2.5 percent are predicted to have lingering side-effects, including but not limited to difficulty breathing, muscle pain, and trouble concentrating, for three months or more. 

Some scientists argue that certain individual cases will take longer to become healthy again. Over three-fourths of hospitalized COVID-19 patients in Wuhan, China showed prolonged symptoms of fatigue, muscle weakness, and sleep problems six months after discharge. A 2022 study found that one in four people took a year to fully recover from long COVID. A number of grim scenarios suggest that some people may live with long COVID for the rest of their lives. A July 2022 review of past studies of people with long COVID symptoms suggests nearly six percent of people will never recover their sense of smell and taste.

[Related: Long COVID can manifest in dozens of ways. Here’s what we know so far.]

One reason ‌why recovery times are so difficult to estimate is because COVID-19 infections affect multiple organs in the body. “When a virus damages the body in multiple ways, you’re going to have different timelines for recovery,” says Shruti Gohil, an assistant professor of infectious diseases and associate medical director at the University of California, Irvine. For example, she says an injured nerve is going to take more time to repair than an upper respiratory tract that’s causing congestion.

Another issue is that we still don’t know what’s causing long COVID in the first place. Infectious disease experts, however, have identified some possible leads: Gohil says long COVID symptoms may be the result of the body’s overactive immune response when fighting the virus. Widespread inflammation from such a response may cause collateral damage to nearby organs and tissues. 

Another prominent theory is that small, undetectable numbers of the virus are able to survive, says Sritha Rajupet, the primary care lead for the Post-COVID Clinic at Stony Brook Medicine. Rajupet explains that these persistently low viral particles might hide within nerves and tissues, causing the body to maintain a chronic inflammatory response. Another explanation is that the body could be exhibiting an abnormal immune response where it still thinks it’s fighting the initial infection. Roberts says one less popular but plausible cause is that an infection creates a hypercoagulable state, a condition that leads to increased micro blood clots from blood vessel damage, which could explain shortness of breath in people with long COVID.

[Related: The long road back to fitness after COVID]

The data is also unclear on who is more likely to endure long COVID for weeks versus months. Rajupet explains that recovery rates could depend on a person’s symptoms, age, and overall health. For instance, she says individuals with severe COVID-19 symptoms or multiorgan problems during infection are susceptible to developing other conditions involving the heart, brain, or even diabetes. People who are older or immunocompromised may also have a hard time recovering from any damage to the body, which could lead to persistent symptoms after infection. 

One thing all experts are sure about: vaccination helps. Research suggests vaccinated individuals with breakthrough infections were nearly half as likely than infected unvaccinated individuals to report long COVID symptoms at least four weeks after infection. However, the role of vaccines in long COVID is still up for debate. There’s other preliminary research to suggest that vaccines only help long COVID symptoms somewhat or not at all. A May 2022 study in Nature Medicine reported the vaccines only reduced the longer-term risk by 15 percent. 

Infectious disease experts are still trying to unpack if vaccination, even during long COVID, can help with symptoms, says Roberts. “There’s just a lot of unknowns,” he says. “It’s an ongoing science that I imagine over time, we’ll get more data about what is going on and hopefully how to prevent and treat it.”

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Raising the dead sounds like science fiction, but a team of medical scientists at Yale University have managed to achieve just that–at least on a cellular level. They successfully revived cells from pigs that were dead for an hour, as a Nature study published August 3 reports. While the study authors emphasize the technology is ages away from being used on people, the work could eventually help keep human tissues alive longer, increasing the supply of viable organs for transplants.

“These cells are functioning hours after they should not be,” said Nenad Sestan, a professor of neuroscience and comparative medicine at Yale and lead author of the study, in a news briefing per CNN. “And what this tells us is that the demise of cells can be halted. And their functionality restored in multiple vital organs. Even one hour after death.”

Sestan and his colleagues received 100 pigs from a local breeder. They placed the pigs on ventilators and shocked the animals’ hearts to induce cardiac arrest. An hour after confirmed death, the Yale scientists used two systems to pump blood back into the bodies—an ECMO machine removed carbon dioxide and added oxygenated blood to one group, while another device, called OrganEx, pumped artificial blood back into the other. That fluid entered the blood vessels of the dead pigs, where synthetic forms of hemoglobin and other molecules protected cells from degradation and stopped blood clots. 

After six hours, the researchers recorded signs of oxygen recirculating into the pigs’ tissues. A heart scan confirmed signs of electrical activity in the heart of pigs on the OrganEx machine, though those organs did not fully restart. Elsewhere, there were signs of business as usual, too: The livers of the deceased pigs resumed production of a protein called albumin. Additionally, the cells of other vital organs were responsive to glucose, suggesting the pigs’ metabolic processes were working again.

The experiment is not the first time scientists have tried to redefine life and death. In the early 20th century, there were attempts to reboot the brains of deceased monkeys. And in 2019, neuroscientists reanimated the brains of decapitated pigs four hours after they died in a slaughterhouse.

Studies such as these raise questions about what it means to be dead. “We presume death is a thing, it is a state of being,” Nita Farahany, a Duke law professor who studies ethical, legal and social implications of emerging technologies, told The New York Times. “Are there forms of death that are reversible? Or not?”

The findings also call into question who is considered legally dead, especially as medicine adapts to make cardiac death one day reversible. “People tend to focus on brain death, but there’s not much consensus on when cardiac death occurs,” Arthur Caplan, a bioethicist at New York University told Nature News. “This paper brings that home in an important way.”

Ethical challenges abound if technology such as this were applied to people. In 2016 India’s medical research council, citing ethical concerns, blocked a planned clinical trial that aimed to revive brain-dead people to a minimally conscious state using a mix of stem cells and other techniques.

While the current study showed no signs of brain activity in the pigs, the researchers observed the heads, necks, and torsos moved. If brain activity was restored, there is no telling how functional or conscious the pigs would be, making it one of a slew of ethical questions scientists will need to answer as they breach this murky area of science.

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Earth itself can claim a new world record: Scientists studying our planet’s rotation confirmed that June 29 was the shortest day on record. As Earth completes one full rotation on its axis, the speed of the spin—nearly 24 hours, with tiny fluctuations—determines our length of day. But on June 29, Earth spun a bit faster than normal, shortening our day by 1.59 milliseconds.

The news is historic but unsurprising. Since the 1960s, astronomers have been using atomic clocks to record Earth’s rotation. In 1987, the International Astronomical Union and the International Union of Geodesy and Geophysics established the International Earth Rotation and Reference Systems Services to monitor Earth’s rotation and maintain global time. But in recent years, they have observed a peculiar pattern. Earth’s spin is getting faster. In 2020, our planet had the 28 shortest days on record—on July 19, 2020, midnight came 1.47 milliseconds sooner than expected. The speed of Earth’s spin did not slow down in 2021, though 2021 was fractionally longer than 2020.

2022 is shaping up to be speedy, too. June 29 wasn’t the only day to whirl by unusually fast. On July 26, the planet reached midnight 1.50 milliseconds ahead of schedule. And the planet may break that record again in the near future if it keeps spinning faster. 

[Related: What if the speed of Earth’s rotation suddenly got faster?]

Why is Earth in a hurry? Astronomers still don’t have an answer to this question, but they do have some theories. At the upcoming Asia Oceania Geosciences Society annual meeting, astronomers are expected to discuss the shortened length of day and how it’s related to a phenomenon called the “Chandler wobble.”

The Chandler wobble involves small and irregular movements that cause a slight change of spin in Earth’s rotation. It’s like the jiggling motion of a toy top when it starts to slow down. For Earth, pressure changes in the atmosphere and the ocean bottom are believed to cause wobbles that shift Earth’s axis of rotation. “The normal amplitude of the Chandler wobble is about three to four meters at Earth’s surface, but from 2017 to 2020 it disappeared,” Leonid Zotov, an astronomer from the International Astronomical Union, told Time and Date. Other theories behind Earth’s change in rotational speed involve less weight on poles from melting glaciers, seismic activity, and changes to the inner molten core. 

Chances are you didn’t realize midnight came early on June 29—we can’t count by the millisecond. But computers can, and astronomers are concerned that if Earth’s rotation continues to get faster, it could affect how those machines keep track of time. Since GPS satellites and smartphones, computers, and other communication devices use atomic clocks, a faster spinning speed will affect their function and render them unusable. 

International timekeepers have dabbled with the idea of a negative leap second at the end of December. The idea is to subtract a second from our clocks to keep our time in sync with Earth’s rotation. Not everyone is on board with this proposal, though: Facebook’s parent company Meta published a blog post on July 25 arguing a negative leap second is an outdated idea from the 1970s that would cause today’s data programs and technologies to crash.

No one knows whether Earth will eventually slow down or keep rushing–it’s just not clear, even to experts. “I think there’s a 70 percent chance we’re at the minimum [length of day],” Zotov told Time and Date, “and we won’t need a negative leap second.”

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Pandas love bamboo, but they might not have acquired a taste for this bitter, nutty-flavored plant until recently. Paleontologists discovered the fact while studying a newly described relative to giant pandas, named Agriarctos nikolovi, which hung out in Europe a few million years ago and sported a smaller set of teeth than their modern family. The findings, published on July 31 in the Journal of Vertebrate Paleontology, suggest the panda species was likely the last to live in Europe.

The fossil teeth were first unearthed in the late 1970s in northwestern Bulgaria in coal deposits that blackened the chompers. Because the Bulgarian National Museum of National History did not clearly list the specimens in their catalog of fossilized treasures, they remained untouched in storage until an accidental discovery by staff 40 years later.

“They had only one label written vaguely by hand,” Nikolai Spassov, a paleontologist and museum professor at Sofia University in California, explained in a press release. “It took me many years to figure out what the locality was and what its age was. Then it also took me a long time to realize that this was an unknown fossil giant panda.”

The upper canine and upper molar of the dental sample trace back to a species closely related to today’s giant pandas, which only live in southwest China. The ursids roamed the forested and swampy areas of Europe nearly 6 million years ago in the Miocene epoch. A. nikolovi had smaller teeth than present-day pandas, but bigger ones than other panda species of that time period. The study authors hypothesize that through evolution, the mammals’ canines and molars likely grew to protect them from predators. Bigger teeth also require a bigger mouth, suggesting these pandas were similar in size or just slightly smaller to present-day pandas.

[Related: Pandas have cute markings because their food supply sucks]

While this isn’t the first prehistoric panda found in Europe, the majority of the other specimens date back to around 10 million years ago. Given that the fossilized teeth at the Bulgarian National Museum of National History are more recent, it’s probable they belonged to the last panda species on the European continent. Though they are closely related, A. nikolovi is more of a cousin than a direct descendent of giant pandas. Previous research suggests the oldest direct descendent of the giant panda is a species found in Spain called the Kretzoiarctos beatrix. It existed at least 11.6 million years ago. 

Of further note, A. nikolovi was vegetarian, though bamboo was probably not part of its diet. Today’s giant pandas have strong jaws and large, flat teeth to help grind up the leaves, stem, and stalks of the sturdy plant. Bamboo makes up 99 percent of a giant panda’s diet: Adults can eat 26 to 83 pounds of it every day. But A. nikolovi’s smaller teeth indicate it probably did not have the strength to chew and mash up the plant’s tough and inedible stalks, and opted for softer greens for nourishment instead. 

“The likely competition with other species, especially carnivores and presumably other bears, explains the closer food specialization of [modern] giant pandas to vegetable food in humid forest conditions,” Spassov said in the press release.

So how did A. nikolovi go extinct? Climate change, and specifically the drying up of the Mediterranean basin, might have affected the entire ecosystem of plants the mammals thrived on. While this idea is still under investigation, paleontologists speculate that similar environmental conditions could have propelled other closely related panda species like Kretzoiarctos beatrix to move out of Europe and into Asia 8 million years ago. From there, ancient pandas would evolve into the Ailuropoda, making up the playful bamboo lovers we know today.

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The weekend forecast looks cloudy with a chance of raining space debris. On July 24, China launched its Long March 5B rocket to carry a laboratory module for the Tiangong space station it’s currently constructing. As it falls back to Earth, astronomers predict the 23-ton rocket body will break up into pieces big enough to survive the atmosphere. About 75 percent of those crash landings should be in water, desert, or jungle, making it unlikely to harm a person or damage any property. But the exact trajectories are not fully known.

Last week’s launch was the third time China used the Long March 5B rocket model since debuting it at the pad in 2020. In the first flight, the rocket’s entire main-core stage reached low orbit, allowing atmospheric friction to drag it back down to Earth and disintegrate most of the parts. 

This isn’t the first time China has been responsible for falling space junk. In May 2021, the second booster of the Long March 5B rocket launch landed in the Indian Ocean near the Maldives, but caused no injuries. In an incident the previous year, remnants of a separate Long March 5B hit the Ivory Coast, causing damage to several buildings in the African country. The reason both events were so disruptive is likely because the rocket model is not designed to dispose of itself and have a controlled reentry.

[Related on PopSci+: How harpoons, magnets, and ion blasts could help us clean up space junk]

NASA and other space agencies have gone through similar trials and tribulations, but have since taken extra steps with their rocket designs to minimize large space debris from plummeting back to the home planet. The US has criticized China’s negligence and its irresponsibility to maintain safe conditions in orbit and in the atmosphere. “Spacefaring nations must minimize the risks to people and property on Earth of re-entries of space objects and maximize transparency regarding those operations,” NASA administrator Bill Nelson said in a press statement after the Long March 5B firestorm in May 2021. “It is clear that China is failing to meet responsible standards regarding their space debris.”

Responding to criticism, China accused American officials of overexaggerating the chances of the current rocket core freefalling back to Earth. “The US and a few other countries have been hyping up the landing of the Chinese rocket debris over the past few days,” said Hua Chunying, a senior spokeswoman at China’s Ministry of Foreign Affairs, per the New York Times. “To date, no damage by the landing debris has been reported. US experts put the chances of that at less than one in a billion.”

[Related: What happens when a rocket hits the moon? It’s not always what astronomers predict.]

The latest Long March 5B is predicted to crash down as soon as July 30. Astronomers placed the risk as fairly low with a one-in-230 chance of someone getting hit or killed from the falling pieces. Still, the chances are higher than the usual one-in-10,000 risk of being crushed by space junk on the ground. “The worst case in this event is going to be less serious than a single cruise missile strike that we’ve been seeing every day in the Ukraine war, so let’s put it in some perspective here,” Jonathan McDowell, an astrophysicist and satellite tracker the Harvard-Smithsonian Center for Astrophysics, said during a July 28 social media livestream.

Right now, the rocket core is expected to make impact in a remote area that’s 1,240 miles long and 44 miles wide. Astronomers will have more answers on its landing site when it gets closer to re-entry.

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Two more patients have been successfully treated for HIV infections, according to results presented at the International AIDS Society meeting on Wednesday. In one case, a 66-year-old American was essentially cured of HIV, becoming the oldest and the fifth person to be rid of the virus. The other, a woman who received an immune-boosting therapy, is in long-term viral remission. 

In previous cases, patients cured of HIV had received bone marrow transplants from donors with a rare genetic mutation that makes immune cells naturally resistant to the virus. The American, anonymously identified as the City of Hope patient after the California hospital where he was treated, received a stem cell transplant in 2019 that also contained the same mutation. 

Although the results look promising, infectious disease scientists are hesitant to call stem cell or bone marrow transplants official cures for HIV. The therapies are meant to treat other illnesses, not HIV. The American received the blood stem cells because he has acute myeloid leukemia. 

[Related: The first people have received an experimental mRNA HIV vaccine]

Nor are these options widely available: Only 1 in 100 people of Northern European ancestry have the key mutation. The procedure also carries a strong risk of complications or death. The City of Hope patient is currently undergoing treatment for painful mouth ulcers because the donor stem cells are attacking his tissues. Marrow transplants do not always work, either, as two patients who were previously HIV-free saw the infection return years later.

Still, Steven Deeks, a professor of medicine at the University of California at San Francisco who previously took care of the first patient cured of HIV, told The Washington Post this is likely the fifth time “in which this type of transplant appeared to cure someone. This approach clearly works. It’s curative, and we know the mechanism.”

The City of Hope patient has been in remission for almost a year and a half. He had been on antiretroviral therapy for over 30 years to manage an HIV infection. “When I was diagnosed with HIV in 1988, like many others, I thought it was a death sentence,” the patient said in a statement from the hospital. “I never thought I would live to see the day that I no longer have HIV.”

The meeting included results of another case from Spain, where a woman is reported to be in long-term viral remission. She was originally enrolled in a clinical trial for antiretroviral medication, and was randomly selected to complete four immune-boosting treatments for 11 months. The woman has been taken off the medications, and her immune system has prevented the virus from spreading for 15 years. But, unlike the stem cell transplant recipient, she still has HIV in her body.

[Related: The first woman has been cured of HIV using donor stem cells]

“These cases are still interesting, still inspiring, and illuminate the search for a cure,” said Sharon Lewin, an infectious disease specialist at Australia’s University of Melbourne in a news conference, per NBC News, though she noted transplants are not viable for the majority of people with HIV.

About 1.2 million people in the United States are living with HIV. Since 2019, there have been 15,815 deaths in adults and adolescents with HIV. Thirteen percent of people do not know they are positive, and almost 40 percent of new cases come from people who are not aware they are infected. The Centers for Disease Control and Prevention recommends everyone between the ages of 13 and 64 get an HIV test at least once in their lives as part of their routine health care. 

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In the weeks since the Supreme Court’s decision to overturn Roe v. Wade, abolishing the nationwide right to an abortion, OB-GYNs and emergency room physicians are still figuring out how to provide the best care while working around vaguely worded and subjective bans. With little guidance, becoming eligible for emergency reproductive care is downright impossible in some states.

Amid mounting pressure, on July 8, President Joe Biden signed an executive order with steps to protect access to reproductive healthcare. Some involve access to reliable information for abortion and ensuring the right to emergency medical procedures for pregnant people. The executive order says the US Department of Health and Human Services will submit a report to him in 30 days outlining the plan.

While several reproductive rights organizations, such as Planned Parenthood and NARAL Pro-Choice America, have lauded Biden’s efforts to improving abortion rights, others are concerned that the executive order will not have much impact. “It’s nice that Biden has issued this statement, but I’m not sure that it has much enforcement to it for states that are really intent on criminalizing people in the abortion space,” says Jennifer Kerns, an associate professor of obstetrics, gynecology, and reproductive sciences at the University of California, San Francisco. She adds that the federal government can only do so much because most of the power is handed to the states. 

[Related: The dangers of digital health monitoring in a post-Roe world]

One reason is that there is no nationwide guideline on what warrants an emergency abortion, so any procedures fall into a gray area of legal medicine. “The executive order sounds great in practice. But my feeling is that a lot of physicians and clinicians are still hesitant to provide abortion care where it’s been made illegal,” says Jessica Lee, an assistant professor of obstetrics, gynecology, and reproductive sciences at the University of Maryland and a fellow at the Physicians for Reproductive Health. “These doctors are probably struggling to decide how sick they let the patient become before they can say their life is at risk and not deal with legal ramifications.”

States with abortion bans that list exceptions for emergency abortions have left the wording ambiguous. The reality is that one life-threatening pregnancy in one state may not be in the other. For example, a doctor in Indiana is currently embroiled in a state lawsuit for performing an emergency abortion on a 10-year-old rape victim from Ohio who was 6 weeks and 3 days pregnant. (Ohio has banned abortions after 6 weeks of pregnancy unless a person’s life is endangered or the pregnancy causes bodily harm; Indiana allows abortions up to 22 weeks of pregnancy). The OB-GYN is being sued for allegedly failing to report the abortion, and Indiana state attorneys are arguing she also did not have the license to perform the procedure. “[The doctor] is now in a position of having to defend herself with attorneys when she did something that was even within the law. So it’s really an unfair position to be putting healthcare providers,” says Kerns. 

Another issue the executive order does not address is how criminalizing all abortions, including emergency care, affects the future of medicine. Lee says the US should expect to see 26 out of 50 states with significant abortion restrictions in the coming months (eight states have already passed bans), which can affect the medical training for new OB-GYNs who may be taught abortion care in one school but not the other. If so, people who need to seek out a life-saving abortion, and may qualify, still could have trouble accessing one because no in-state doctors can perform the procedure. “We’re going to see patients suffer nationally because of that,” Lee explains.

[Related: What’s the difference between morning-after pills and abortion medications?]

One silver lining: It’s not 1972. Both experts say pregnant people have more options than before, like abortion pills. Biden’s executive order has made it a priority for people to have access to abortion medications that the US Foods and Drug Administration approved as safe and effective two decades ago. Non-governmental organizations are also connecting patients with out-of-state telemedicine appointments and prescriptions for the pills. That said, the medications might not be able to help in cases of life-threatening pregnancies. If a person needs an emergency abortion, they probably can’t afford to wait for the pills to get shipped to their door. Planned Parenthood, for instance, says prescriptions can be mailed overnight, but the process of completing a virtual doctor’s appointment, lab tests, and medical history review can take a full one to two weeks. 

“Our efforts really need to be focused on getting information to patients on how to access abortion safely, whether that’s across state lines, procedural abortion, or medications, either in their home state or across state lines,” says Kern. If you’re from a state where abortions are banned, she says, it’s not the best idea to talk to them about abortion options with your healthcare provider, unless you really trust them. Instead, ‌she advises people to turn to advocacy and community groups with reliable information on abortion, including National Abortion Federation, Plan C, AidAccess, Planned Parenthood, and I need an a.

Both experts expect access to all kinds of abortions to remain an uphill legal battle. For example, days after Biden’s executive order, the Texas attorney general sued the federal government for infringing on the state’s rights by mandating all hospitals provide emergency abortions. And while Kern says abortion access for pregnant people is the priority, she adds that healthcare workers need protection, too. Without it, she warns, “providers who want to do the right thing are scared to do it.”

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Saturn boasts the most iconic rings in our solar system, but it is not the only planet to have them. Images released earlier this month from the James Webb Space Telescope (JWST) gave the world a glimpse of Jupiter’s rings, though they are much darker and fainter than Saturn’s. Until now, astronomers were puzzled as to why Jupiter doesn’t have larger rings, but a new preprint study released on July 13 suggests it may have to do with the gas giant’s moons.

Jupiter, in theory, should have big rings. It’s the largest planet in our solar system—Saturn comes in at a close second—and it stands to reason the gas giant could pull even more space debris to create bigger and more vivid rings. 

“If Jupiter did have them, they’d appear even brighter to us, because the planet is so much closer than Saturn,” Stephen Kane, an astrophysicist at the University of California, Riverside and lead author of the study, said in a university press release. When Jupiter is closest to Earth, astronomers estimate it’s about 365 million miles away, whereas Saturn only gets about 746 million miles near Earth.

Uranus and Neptune have rings, too, along with Jupiter and Saturn. But only Saturn’s are visible without an advanced telescope. Unlike its predecessor telescopes such as Hubble, JWST can look at the universe in infrared light, which makes it easier to see the other planets’ less-majestic rings.

Studying rings can give astronomers insight into the planet’s history, revealing what type of collisions or events happened there. Saturn’s massive rings span the length of 27 Earths. They are made up of billions of pieces of comets, asteroids, and moons pulled in and torn apart by the planet’s gravity. 

If scientists can calculate the age of the materials that form the rings, they can deduce whether the chunks of space debris came from nearby moons or objects from the distant Kuiper belt. Knowing the origins behind planetary rings could answer some questions on how our solar system and the universe began.

In the current study, the authors used a computer model to simulate Jupiter’s orbit and the orbits of four of its moons—Ganymede, Callisto, Io, and Europa. The astrophysicists also included information on how long it takes for rings to take shape. “We found that the Galilean moons of Jupiter, one of which is the largest moon in our solar system, would very quickly destroy any large rings that might form,” Kane said, referring to the moons by their discoverer, Galileo Galilei. 

Since the moons are so big, their strong gravitational force ejects ice coming into Jupiter’s orbit instead of drawing it in. Based on the findings, the team suggests it’s unlikely that Jupiter had large rings in the past and later lost them, as they had originally theorized at the start of their study. 

The next step is to use the simulation to study Uranus’ rings. One question they’re hoping to answer is why Uranus orbits the sun tipped on its side. A possible explanation is that a massive collision shifted the planet’s position, and the rings may be leftover remnants from the impact. 

“For us astronomers, they are the blood spatter on the walls of a crime scene,” Kane said.  “When we look at the rings of giant planets, it’s evidence something catastrophic happened to put that material there.” 

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The US has detected its first case of polio in nearly a decade. On July 21, public health officials confirmed that an unvaccinated man in Rockland County, New York, had developed polio after using a banned version of the vaccine for the virus. Traces of a similar form of polio have recently been reported in other countries, such as the United Kingdom.

“We are monitoring the situation closely and working with the New York State Department of Health and the Centers for Disease Control and Prevention to respond to this emergent public health issue to protect the health and wellbeing of residents,” Patricia Schnabel Ruppert, the Rockland County Health Commissioner, said in a press release.

The poliovirus is a highly contagious and deadly disease that has devastated humanity for centuries. No one knows when the first cases began. However, historians have found early evidence of polio-like symptoms in ancient Egypt, where hieroglyphics depict a man with a weak leg who cannot walk without a walking stick. It wasn’t until the late 19th century when the US saw polio outbreaks. 

[Related: From the archives: A polio vaccine was finally on the horizon]

The virus can enter the body through the mouth from a number of sources, including contact with an infected person’s feces through contaminated food or water. While less common, droplets from the sneeze or cough of an infected person can also spread the virus. It mainly targets children below the age of five.

About 25 percent of people infected with polio will develop flu-like symptoms such as a sore throat, fever, stomach pain, and a headache for two to five days. Nearly 75 percent of people will have no visible symptoms. As it spreads through the body, the poliovirus can attack the brain and spinal cord, causing permanent damage. One in every 200 polio infections leads to paralysis, and about five to 10 percent of people paralyzed die because the muscles involved in breathing become immobilized as well.

By 1940, polio caused paralysis in nearly 20,000 people living in the US (including, famously, President Franklin D. Roosevelt). But in 1953, Jonas Salk discovered a polio vaccine that helped drop the US caseload to just 6,000 four years later. By 1979, the states were polio-free, although the disease can come back if someone is unvaccinated and exposed in a country with polio outbreaks or to a population that relies on the oral vaccine.

[Related: Researchers may finally know what’s causing the mysterious polio-like illness in kids]

The recent polio case in New York, occurred in an unvaccinated young adult. While the person is no longer contagious, they have become paralyzed. Health officials believe the patient contracted the disease after taking an oral version of the vaccine that uses the live virus. Since 2000, the US has been using an inactivated injectable vaccine with a dead virus that trains the immune system to recognize and destroy the pathogen. However, some countries still use the live attenuated vaccine, which delivers a weak but viable polio virus to create a lasting immune response. With this treatment, there is a small risk of the virus mutating and infecting  others. “It mimics natural infection, and people shed the virus, the vaccine virus, and that spreads to other people, and then they get immunized that way,” Amesh A. Adalja, senior scholar at Johns Hopkins Center for Health Security, explained to the New York Times.

“If there are unvaccinated communities, it can cause a polio outbreak,” Walter Orenstein, a polio expert at Emory University, told Stat News. “The inactivated polio vaccine we have is very effective and very safe and could have prevented this.”

The Centers for Disease Control and Prevention recommends all children get vaccinated with four doses of the inactivated polio vaccine starting at two months of age. Unvaccinated adults can get a routine series of the polio vaccine with their family doctor as well. Adults that were immunized during childhood but are at an increased risk of polio exposure are eligible for a booster dose.

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When a Falcon 9 rocket launches on Thursday, if all goes well, SpaceX will have sent 32 vehicles to space in 2022–breaking the previous yearly record of 31 launches it set in 2021. And SpaceX has many more blast-offs planned: The California-based commercial spaceflight company is on track to launch 50 rockets this year, almost one a week. 

On July 17, SpaceX completed a launch of 53 Starlink broadband satellites via one of its Falcon 9 rockets. This marked the 31st successful mission this year and the 13th launch using the same Falcon 9 rocket stage. SpaceX has also sent the most boosters to space this year. SpaceX’s US-based competitor United Launch Alliance has completed about one launch every 64 days. 

SpaceX is also launching more often than national space agencies. China planned to be the leader in rocket launches with an ambitious goal of 60 flights in 2020. It has since made efforts to reach that goal but, to date, has completed only 24; the country says it has more than 50 launches scheduled in 2022. NASA, meanwhile, has planned eight more missions, among other projects, through the end of the year. 

SpaceX is living up to its promise of recycling rockets. Reusing rocket parts has made it cost-efficient and faster for the company to prepare launches. The Falcon 9 rocket will use boosters that were refurbished for weeks and months before the next mission.

The road to 50 launches by the end of the year has been bumpy, though. On July 11, SpaceX’s Starship booster engines blew up in a fiery explosion during testing, which SpaceX CEO Elon Musk tweeted was “not good.” 

[Related: SpaceX Starships keep exploding, but it’s all part of Elon Musk’s plan]

Thursday’s mission, to deliver more Starlink broadband satellites to space, will take place at the Vandenberg Space Force Base in California. While sending the most rockets and boosters to space is a feat in itself, Musk has a larger vision in mind. His goal is for humans to reach the moon and Mars aboard a Starship rocket—making humans an interplanetary species. If everything goes to plan, according to SpaceX, a crewed mission to the Red Planet could happen as early as 2029. 

But on the way to our solar system neighbor, SpaceX may face some competition from two new companies, Relativity Space and Impulse Space. We may be at the start of a brand-new space race: The two upstarts claim they will reach Mars faster than SpaceX. 

For now, you can watch the record-breaking launch of Falcon 9 in a YouTube livestream Thursday starting at 1:13 p.m. Eastern, beginning 10 minutes before the launch.

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Talk about a major life hack. Scientists might have devised a way to help people live longer by carefully tweaking the genetic code in our cells. 

Researchers from Verve Therapeutics in Cambridge, Massachusetts, launched the first clinical trial last week of a new gene-editing technique that could help lower adult cholesterol levels. By making targeted changes to the DNA of a protein that regulates blood cholesterol levels, the experimental method  may permanently lower cholesterol and slash patients’ risk of heart attacks. The study, which involves 40 participants, will be followed by another clinical trial slated to begin later this year for sickle-cell disease.

The new gene-editing test uses a similar process to its gene-editing predecessor, CRISPR-Cas9, which was first put in use a decade ago. CRISPR-Cas9 uses a guide RNA to help the Cas9 enzyme locate the site of the mutation in the DNA that needs to be removed. The CASE9 enzyme then works like a pair of scissors to cut both strands of DNA. When the cell realizes there’s an issue with the genetic code, it sends over enzymes to patch up the hole and avoid any loss of genetic information or DNA structure.

[Related: CRISPR breaks ground as a one-shot treatment for a rare disease]

Deleting a large fragment of DNA and letting the DNA repair the strands back together can knock out or disable mutations, such as those that cause hereditary disorders. Another way researchers apply the technique is by taking advantage of the mistakes made in stitching up the strands to make new mutations. In this scenario, they send a DNA template alongside CRISPR/Cas9 that gets inserted into the genetic code during the repair process. The DNA template can make a brand new set of instructions for genes to put to action.

With CRISPR/Cas9 technology, scientists have genetically manipulated mosquitoes to reduce the spread of malaria, tinkered with the DNA of ticks to stop tick-borne diseases, and created mushrooms that do not brown as quickly. Some are even taking giant leaps to bring extinct animals back to life. But for all the good it’s done for the world, CRISPR/Cas9 is not perfect. While the technology allows experts to make detailed edits in a living organism, it has not been precise enough to make the exact edits needed to reverse or prevent genetic diseases. There’s also concern that multiple or incorrect edits could harm a person’s cells, introducing mutations in the selected DNA sequence that raise, say, the risk of cancer.

Cue in CRISPR’s cousin. As seen in the cholesterol trial, the new method cuts only one DNA strand instead of two, and uses another enzyme attached to Cas9 that works like a pencil to make a small edit to the genetic code. The base-editing enzyme chemically rewrites one letter of DNA to change it to another. “Of all the different genome editing ongoing on the clinic, this one could have the most profound impact because of the number of people who could benefit,” Eric Topol, a cardiologist and researcher at Scripps Research, told MIT Technology Review.

The upcoming heart disease trial will genetically alter the PCSK9 protein for people with heterozygous familial hypercholesterolemia (HeFH). HeFH is a genetic disorder that causes extremely elevated cholesterol levels because the liver cannot eliminate the cholesterol. PCSK9 is being targeted because it normally breaks down low-density lipoprotein receptors that remove excess cholesterol in the blood. The one-time gene therapy will create a one-letter misspelling to permanently turn the gene off, preventing the PCSK9 protein from destroying cholesterol-lowering receptors. In an experiment with monkeys, the gene editing treatment lowered the “bad” cholesterol by 60 percent—an effect that lasted for more than a year. 

“The number one cause of mortality in the world is heart attack,” said Sekar Kathiresan, CEO of Verve Therapeutics, the biotechnology company that created the base-editing technique, per MIT Technology Review. “If you are going to give a medicine that makes you avoid a heart attack, people are going to live longer.”

Cholesterol increases a person’s risk for heart disease, which kills almost 700,000 Americans a year. It also heightens an individual’s chances of having a heart attack. The Centers for Disease Control and Prevention estimates a heart attack happens every 40 seconds. 

[Related: 5 heart-healthy foods—and 2 to absolutely avoid]

It’s too early to know if this new adaptation of CRISPR-Cas9 is as effective or even better than the original. So far, only one New Zealander has participated in the cholesterol trial and seen positive results. There could be toxic side effects from the nanoparticles used to package the genetic instructions and carry them into the cell. For people already taking PCSK9 inhibitors to lower cholesterol, there is also a risk of muscle pain, among other side effects.

“It’s very exciting that the first clinical trials are starting, with CRISPR–Cas9 and now also with base editing,” Gerald Schwank, who studies the use of gene editing to treat diseases at the University of Zurich, Switzerland, said in an interview with Nature. “We’ve got a lot to learn.” Both clinical trials are expected to publicly report their results by 2023.

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The US is adding a new COVID vaccine to its pandemic toolbox. On July 13, the Food and Drug Administration gave emergency use authorization to Novavax’s COVID-19 shot, making it the fourth brand of vaccine cleared for use. The two-dose vaccine, which was already available in 170 countries, is only authorized for Americans 18 years and older who need their first immunization series.

Novavax’s COVID-19 vaccine is coming at a time when the US faces a lag in vaccination. As of July, 78.4 percent of the population has received at least one dose, and only 67 percent is fully vaccinated. What’s more, the rapid spread of multiple Omicron variants— BA.5 now makes up nearly 70 percent of coronavirus cases—has accelerated interest in variant-specific vaccines. On June 30, the FDA voted to change the formulation of the next set of COVID-19 boosters to include components of Omicron BA.4/5 for extra protection.

Novavax’s vaccine, though it arrives more than two years into the pandemic, is expected to boost vaccination rates among Americans wary of mRNA technology. In contrast with Pfizer-BioNTech and Moderna, Novavax uses a decades-old vaccine method, widely found in protections against other viruses such as influenza and hepatitis B.

The Novavax COVID-19 vaccine is a protein-based shot. It delivers copies of protein fragments of the virus for the immune system to recognize and destroy. Those protein copies are made in insect cells and packaged into nanoparticles that give off the appearance of a virus. Other ingredients, such as the bark of a South American tree, are included in the nanoparticles to serve as red flags—alerting the immune system to a suspicious character in the body. 

[Related: Omicron variants keep getting better at dodging our immune systems]

Each faux-virus particle is “basically a soap bubble. It’s made of stuff that you find in root beer,” Gregory Glenn, Novavax research chief told NBC Chicago.  “When an immune cell sees that, it becomes quite activated. … We supercharge the immune response.” 

In clinical trials, the Novavax vaccine was 90.4 percent effective in preventing mild, moderate, or severe COVID-19 infections. In people 65 years and older, the vaccine was 78.6 effective. It’s important to note, though, that the data was collected before Delta and Omicron appeared, and the vaccine is based on the genetic sequence from the first coronavirus strain.  

Still, US officials say this immunization will be helpful because it may be an appealing alternative to those who are holding off on getting vaccinated with mRNA vaccines. “Authorizing an additional COVID-19 vaccine expands the available vaccine options for the prevention of COVID-19, including the most severe outcomes that can occur such as hospitalization and death,” FDA commissioner Robert M. Califf said in a statement. 

The Biden-Harris Administration secured 3.2 million doses of Novavax’s COVID-19 vaccines, and like all other COVID-19 vaccines available in the US, the shots will be free of charge. You won’t see a Novavax vaccine offered at your local pharmacy just yet. The director of the Centers for Disease Control and Prevention will need to officially sign off on a recommendation for the two-dose shots, which is expected to happen after a CDC meeting on July 19. 

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A United Nations (UN) population report published on July 11 reported the world’s population will reach 8.5 billion by November 15, 2022. The latest projections indicate the slowest population growth in decades. Sixty-one countries are expected to see their population numbers drop by one percent between now and 2050. Despite the pace of growth slowing down, the world’s population is expected to increase to 10.4 billion people in the 2080s and remain there until 2100. Currently, the world population is at about 7.7 billion.

“The projected global population of 10.4 billion at the end of the century is more than a half a billion lower than what we projected three years ago,” John Wilmoth, the director of the Population Division at the Department of Economic and Social Affairs for the UN, commented in a press conference. The year 2020 marked the first time since 1950 that population growth slowed down by one percent.

More countries are experiencing slower increases because of low fertility rates. The average global fertility rate is 2.3 births per woman compared to 5 births per woman in 1950. Family planning programs, expanded contraception, and educating women are some ‌reasons for declining birth rates. 

[Related: Why birth rates are falling, and why it’s no big deal]

The countries with the two biggest populations, China and India, each now have 1.4 billion people. However, unlike India, China is facing an aging population problem, with 28 percent of its entire population being people over 60. India is expected to surpass China as the most populous country by 2023. Meanwhile, North America, along with countries in Europe and Latin America, are expecting to hit their peak populations and then see declines before 2100.

“Population growth is a tangible sign of our collective success in improving the living conditions of everyday people throughout the world,” Maria-Francesca Spatolisano, the Assistant Secretary-General for Policy Coordination and Inter-Agency Affairs for the United Nations, said in the July 11 press briefing. Additionally, the news “brings important responsibilities and highlights related challenges for social and economic development and environmental sustainability.”

[Related: Almost half of the world’s children live in dangerous climate conditions]

Despite a slower growth rate, population numbers are still rising globally because of decreased mortality rates and increased levels of life expectancy at birth in multiple countries. The report stated the world average age of death was 72.8 years in 2019—an increase of nine years since 1990. The COVID-19 pandemic did, however, lower global life expectancy from 72.8 to 71 years. The estimated death toll from COVID-19 is currently at 6.35 million. 

With increasing survival and declining fertility also comes an aging workforce. Based on the population trends, the UN advised countries in its report to prioritize access to healthcare and quality education for all ages to help people qualify for livable employment.

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Skygazers will have an eventful night this coming Wednesday. An enormous comet is cruising through our solar system, which coincides with a so-called supermoon—the biggest and brightest view of a full moon in 2022. The comet, named C/2017 K2 (PanSTARRS) and nicknamed K2, is estimated to be about 18 to 100 miles wide. Astronomers from NASA expect it to make its closest approach towards Earth on July 13 with the most visibility on July 14.

The K2 comet was first detected through the Hubble Space Telescope in May 2017 between the orbits of Saturn and Uranus—about 2.4 billion kilometers from the sun. NASA reported it was the farthest they have seen a comet enter the solar system’s planetary zone. The K2 comet is believed to have originated from the Oort Cloud, a spherical layer of icy objects where the temperature reaches -440 degrees Fahrenheit. The Oort Cloud is located in the outermost region of our solar system. 

NASA experts speculate most long-period comets—meteors that take more than 200 years to complete their orbit around the sun—come from the Oort Cloud. The city-sized comet of ice and dust may have been gravitationally expelled from the Oort Cloud, beginning a journey spanning millions of years that includes a passing visit to the Earth.

[Related: The biggest comet ever found is cruising through our solar system’s far reaches]

Despite the comet’s massive size, it might be hard to spot at first. While it makes its closest approach to Earth on July 13, it will still be about two Earth-sun distances away. ” It would easily have been a naked-eye comet had it arrived half a year earlier or later,” Quanzhi Ye, an astronomer at the University of Maryland who specializes in comets, told Space.com. 

For a first-hand look at K2, your best bet is to use a small telescope or binoculars. You’ll want to scan for a dim patch of light, which is likely the tail of the comet, at around 11 p.m. EDT on July 14.

Depending on which night you hunt for it, the comet will appear in different places in the sky. On July 14, it will seem to be located near the star cluster called Messier 10; by mid-August, it will be positioned as though it’s at the tip of the constellation Scorpius. (A stargazing app such as Stellarium can be a big help to find celestial objects on the move.)

The comet will remain viewable for people living in the Northern Hemisphere with a telescope until September as it makes its way toward the sun near the end of the year. A live-stream for the K2 comet will be available Thursday at 6:15 p.m. EDT. 

The supermoon will also be visible the evening of July 13 through the morning of July 14. The Virtual Telescope Project is live-streaming the event starting at 3 p.m. EDT on Wednesday. Because the moon will appear at its brightest, without the right telescope, the dazzling light could make it hard to see fainter objects in the heavens like the K2 comet and summer stars.

Correction (July 12, 2022): On readers’ requests, this story has been updated to include additional information for locating K2. The times were also changed from EST to EDT.

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The hunt for dark matter is underway underground. In a first run with LUX-ZEPLIN (LZ) that lasted for more than three months and ended this April, the world’s most sensitive dark matter detector found no signs of hypothetical dark matter bits called Weakly Interacting Massive Particle (WIMPs) in space. Despite the lack of hard data, scientists confirmed the US Department of Energy-led experiment is working as planned, leaving the possibility of finding dark matter in future rounds.

“For now it’s kind of a weird thing, we’re saying that we’re the best in the world at finding nothing, but the prospect of finding new physics a few years from now is entirely feasible,” Chamkaur Ghag, an astroparticle physicist and professor at the University College London and team member of the LUX experiment, told New Scientist.

Dark matter is thought to make up 27 percent of the universe (the visible matter in stars and galaxies might only comprise 5 percent of it). That said, no one has ever detected it. That’s because dark matter contains particles that do not emit, absorb, or reflect light, making it difficult to even measure with electromagnetic radiation. But physicists and astronomers know dark matter exists because of the gravitational effects it has on visible objects, like keeping stars from slingshotting around space and preventing galaxies from collapsing. It is hypothesized to be the invisible glue holding the universe together.

[Related: Meet the mysterious particle that’s the dark horse in dark matter]

WIMPs have been scientists’ best bet at detecting dark matter. Other hypothesized dark matter such as photons or axions are very small and behave like waves. But WIMPs contain mass and rarely interact with other visible matter. Billions of WIMPs also pass through us every second. By studying dark matter, experts will have a better understanding of what the true base of the universe is—and what we can expect to happen to it in the future. 

The key to unlocking the secrets of the universe is buried a mile below the Black Hills of South Dakota. The LZ experiment is composed of two next titanium tanks filled with 10 tons of pure liquid xenon tanks. It also contains two arrays of photomultiplier tubes that can detect the faintest light. If dark matter in the form of WIMPs collide with a xenon atom, it will knock over loose electrons. The particle collision produces a brief shimmer of luminosity the LZ experiment picks up. 

The experiment is underground because cosmic radiation and the radiation from human bodies could muffle dark matter signals. So, submerging the detector helps increase its sensitivity and chances of finding a sign of dark matter. “You’re trying to hear a whisper. You do it in the middle of New York City, you’re not going to hear it, there’s just too much noise. You want to get away from our backgrounds—the cosmic rays and junk we’re bombarded by would hide the very rare signals we’re looking for,” Kevin Lesko, a senior physicist at the Lawrence Berkeley National Laboratory, who coordinates the LZ project, told Popular Science in 2020.

[Related: What we learned from the Large Hadron Collider on its first day back in business]

While, the first round of results did not find dark matter, it did show the machine is working well and functioning within expectation. “Considering we just turned it on a few months ago and during COVID restrictions, it is impressive we have such significant results already,” said Aaron Manalaysay, a physics coordinator from the Berkeley Lab that led the effort for the experiment’s initial run, in a Berkeley Lab press release.

“We are now out of the starting gate,” said Harry Nelson, a professor of physics at the University of California, Santa Barbara and former spokesperson of LZ in a second press release. “LZ is a far more powerful detector of dark matter than any ever built before, and is uniquely capable of making a discovery in the next few years.”

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Some animals wait their whole lives to breed, only to die right after. But for hundreds of ancient horny frogs, death came knocking during sex. On July 6, paleontologists unraveled the mystery behind the sudden disappearance of hundreds of mating frogs 45 million years ago. Their new study, published in the journal Papers in Palaeontology, suggests a swamp where frog mating took place 45 million years ago was actually a watery death trap.

The mucky graveyard lies in the Geiseltal area in central Germany—though it looks different from before. Nowadays, the swamp is home to thousands of fossils, and is a scientific jackpot for paleontologists who want a window into how life on Earth was like millions of years ago.

If you traveled back to the middle Eocene, you would find a much hotter Earth. The Geiseltal area itself was covered in a swampy subtropical forest; it was also a dangerous place to live as it was filled with ancient creatures such as large crocodiles, giant snakes, and different frogs and toads. Amphibians were not the only victims snared in the swamp’s trap: It also claimed the lives of more than 50,000 prehistoric birds, horses, bats, and fish.

[Related: Shifting ancient climates shaped human evolution]

Decades-old research on the frogs from the fossil deposit suggested they died because of a lack of dissolved oxygen in the swamp’s aquatic habitats. But the authors of the new study say this is unlikely because the frogs were capable of migrating to other bodies of water when conditions were harsh. So, the exact cause of death remained a mystery.

The paleontologists behind the new paper studied the skeletal remains of 168 frogs—most belonging to the Pelobatidae family—to find a clue to how they perished. Some of the common themes were the loss of abdominal bones and one or more limbs. “As far as we can tell, the fossil frogs were healthy when they died, and the bones don’t show any signs of predators or scavengers. There’s also no evidence that they were washed in during floods, or died because the swamp dried up,” said Daniel Falk, a PhD student at the University College Cork (UCC) in Ireland and lead author of the study, in a press release. As the team ruled out several causes of death, they were left with one plausible option: The frogs died during sex.

One piece of evidence to support this hypothesis is where the fossils were located. Geiseltal fossil frogs were primarily land-dwellers. They only returned to bodies of water, like the swamp, when they wanted to mate. The researchers suggest that exhaustion from constant breeding or drowning could have led to the frogs’ sudden demise.

[Related: 7 animal mating rituals that make horseshoe crab orgies look tame]

The likelihood of dying during sex is also common in modern-day amphibians like the South American Rhinella proboscidea. Males pile on the female in a fierce competition to mate, causing her to drown or suffocate. “Female frogs are at higher risk of drowning as they are often submerged by one or more males—this often happens in species that engage in mating congregations during the short explosive breeding season,” Maria McNamara, a professor of paleontology at UCC and senior study author, also said in the press release. “What’s really interesting is that fossil frogs from other sites also show these features, suggesting that the mating behaviors of modern frogs are really quite ancient and have been in place for at least 45 million years.”

While these ancient frogs paid a big price for a fling, it may be a great payoff for paleontologists looking into the Earth’s past. What’s more, the findings could help biologists understand how these ancient horndogs evolved to the slimy green amphibians we know today.

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After three years of upgrades and maintenance, the world’s largest and most powerful particle accelerator, the Large Hadron Collider (LHC) has fired up for a third run. On Tuesday at 10:47 a.m. EDT, the atom smasher shot beams of protons through a 16.7-mile ring of superconducting magnets in Switzerland. New upgrades will allow the LHC to achieve an increased collision energy of 13.6 trillion electron volts (previous runs were at 8 trillion and 13 trillion electron volts). Physicists project the machine will run for almost four years at this intensity—opening up new insights into the field of particle physics.

“This is a significant increase, paving the way for new discoveries,” said Mike Lamont, director for Accelerators and Technology at the European Organization for Nuclear Research (CERN), in a press release.

One goal of the new LHC era is to better understand the structure of the Higgs boson, a subatomic particle the collider uncovered a decade ago. The Higgs boson particle, which scientists theorize gives other particles such as electrons and quarks their mass, was created 10 to 12 seconds after the big bang that created the universe billions of years ago. 

[Related: The souped-up Large Hadron Collider is back to take on its weightiest questions yet]

Scientists at CERN, which runs the LHC, plan to measure how the Higgs boson decays into other matter, such as muons. “This would be an entirely new result in the Higgs boson saga, confirming for the first time that second-generation particles also get mass through the Higgs mechanism,” said CERN theorist Michelangelo Mangano, in a press release.

LHC’s upgrades will also more precisely measure other fundamental features in the universe, such as the origin of matter-antimatter asymmetry (the unsolved mystery of why more matter than antimatter exists). Other areas of interest include searching for dark matter and studying matter under extreme temperatures and density.

To hunt for these rare atomic bits, the LHC contains multiple accelerating structures to augment the energy of its particle beams. The machine uses thousands of magnets that help push the particles closer together, increasing the chance of a collision. Those beams travel almost at the speed of light before they smash together, allowing scientists to study the insides of atoms. 

Through particle collisions, physicists have learned a great deal about the smallest known building blocks of matter. Also on Tuesday, CERN presented evidence of three new exotic particles, a pentaquark and two tetraquarks. The discovery could help inform physicists how quarks—pairs of subatomic particles that carry a fractional electrical charge—form. When combined, quarks are believed to create the protons and neutrons, together known as hadrons, in an atomic nucleus. 

It may also help explain the creation of exotic hadrons, which are particles composed of more than three quarks. “Finding new kinds of tetraquarks and pentaquarks and measuring their properties will help theorists develop a unified model of exotic hadrons, the exact nature of which is largely unknown,” said Chris Parkes, a spokesperson for the experiment responsible for the discovery, in a separate CERN press release. With the LHC running, scientists may be one step closer to unraveling the secrets of the universe. 

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Four mathematicians won the prestigious Fields Medal on Monday for their significant contributions to mathematics. The 14-karat gold award, equivalent to an Olympic gold medal for math, is given out by the International Mathematical Union in Helsinki every four years to talented mathematicians under the age of 40. 

This year’s award recognizes groundbreaking research in subjects such as prime numbers and the packing, or efficiently arranging, of spheres in eight-dimensional space. The winning mathematicians–Hugo Duminil-Copin of France, June Huh of the US, Maryna Viazovska of Switzerland, and James Maynard of the UK–have answered questions that have stumped other experts for years. 

Duminil-Copin, of France’s Institut des Hautes Études Scientifiques, was awarded for his work on the probabilistic theory of phase transitions—how matter changes forms, such as water freezing to ice. Duminil-Copin’s work focuses on how ferromagnetic objects transition from a nonmagnetic to magnetic phase in what’s called the Ising model. Previous physicists have used it to create simplified one- and two-dimensional models of reality, but solving the Ising model in 3D is more difficult. “The ability to produce exact formulas just collapses completely,” Duminil-Copin told The New York Times. “Nobody has any idea how to compute things exactly.” While the 3D Ising model is not completely solved, Duminil-Copin’s work showed proof that phase transitions in a 3D Ising model resembled those in two dimensions. 

[Related: Your brain uses different neurons to add and subtract]

Princeton University’s Huh won for a range of work: He was the first to apply geometric concepts to combinatorics, the mathematics of counting. Working with his colleagues, he answered previously unsolved problems in combinatorics and provided a scheme to explain the mathematical properties of complex geometric objects. But despite these accomplishments, Huh tried to avoid math as much as he could growing up. “I was pretty good at most subjects except math,” Huh told The New York Times, adding he nearly failed his tests. Huh, who dropped out of school and wanted to become a poet, fell in love with math at 23 after studying under Heisuke Hironaka, a Japanese mathematician, who won the Fields Medal in 1970. 

For 13 years, Viazovska, a Ukrainian-born mathematician and professor at the Swiss Federal Institute of Technology in Lausanne, has worked on an arrangement called the E₈ lattice, which shows how to pack spheres in eight dimensions in the least amount of space possible. “Sphere packing is a very natural geometric problem. You have a big box, and you have infinite collection of equal balls, and you’re trying to put as many balls into the box as you can,” Viazovska, who is now trying to densely pack spheres in 24 dimensions, told New Scientist. Her win is the second time the committee has awarded the medal to a woman.

One mathematical theory is that there are an infinite number of prime numbers, but as numbers get larger the distance between two prime numbers gets farther apart. The University of Oxford’s James Maynard, in a prize-winning breakthrough, showed this is not always the case: There are instances where prime numbers can come close together. Yet, in other stretches, primes can be very distant.   

John Charles Fields, a Canadian mathematician, created the award in 1924, as a way to recognize early-career mathematicians for their accomplishments–and also to highlight researchers whose future work might dazzle, too. “Suddenly to be tossed up on this list,” Maynard told Quanta Magazine, “with these legends of mathematics who inspired me as [a child], is incredible but completely surreal.”

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Floating around in space sounds like fun, but doing so takes a massive toll on your body. A study published on June 30 in the journal Scientific Reports found that spending just a few months in space changes astronauts’ bones, causing a loss of density equivalent to what most humans would lose in a couple of decades on Earth. More concerning is that after a year, many astronauts do not fully recover their lost bone mass.

The connection between bone mass and spaceflight has been studied for quite some time. One prior NASA study from 2007 estimated a two to nine percent loss in bone mass within nine months of space travel. Another study published in 2020 simulated the impact of a three-year spaceflight to Mars, finding a 33 percent risk of osteoporosis for long-distance travelers. Decreases in bone density can weaken a person’s skeletal structure and increase the risk of back pain, bone fractures, and loss of height.

[Related: Astronauts are losing 3 million red blood cells every second in space]

The poor osteopathic health likely results from the lack of gravity in space. Despite moving around, weightlessness removes pressure from the legs when standing or walking, mimicking the effects of extreme physical inactivity. “Even with two hours of sport a day, it is like you are bedridden for the other 22 hours,” Guillemette Gauquelin-Koch, the head of medical research at France’s CNES space agency, who was not part of the study, told The Guardian. Unless scientists figure out if the lost bone mass is fully recoverable, the findings jeopardize the hope of sending humans to Mars in 2030. “It will not be easy for the crew to set foot on Martian soil when they arrive–it’s very disabling,” Gauquelin-Koch noted in the same interview.

One hypothesis that the new study tested is whether astronauts can recuperate their lost bone mass by spending enough time back on Earth. Medical experts with NASA and its collaborators scanned the wrists and ankles of 17 astronauts (majority male) before, during, and after they’d spent months on the International Space Station (ISS). After one year back at home, nine astronauts still hadn’t recovered the density of their shinbones. The total bone mass loss across the nine subjects was comparable to a decade’s worth of bone mass loss that aging people face on Earth.

[Related: Your bones do more than you give them credit for]

Astronauts who spent the longest time on the ISS—four to seven months—showed the slowest recovery of bone density. It’s still unclear whether there’s a maximum amount of bone loss a person could endure in space. “Will it continue to get worse over time or not? We don’t know,” Steven Boyd, director of the McCaig Institute for Bone and Joint Health at the University of Calgary and study coauthor also told The Guardian. “It’s possible we hit a steady state after a while, or it’s possible that we continue to lose bone. But I can’t imagine that we’d continue to lose it until there’s nothing left.”

One shred of good news is that some exercises worked better than others in helping astronauts recuperate the lost bone mass. Deadlifting rather than cycling or running seems to work better at strengthening the remaining bone mass, which suggests that heavy lower-body exercises would be beneficial in preparing for long space missions. 

Astronauts who were fit and in their 40s also did not seem impacted as much by the bone loss. “Fatigue, light-headedness, and imbalance were immediate challenges for me on my return. Bones and muscles take the longest to recover following spaceflight.” said Robert Thirsk, a former chancellor at The University of Calgary and a former Canadian Space Agency astronaut in a press release. “But within a day of landing, I felt comfortable again as an Earthling.”

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Along with exercising and eating a balanced meal, getting a good night’s sleep is vital for a strong and healthy heart. On Wednesday, the American Heart Association (AHA) updated its cardiovascular health checklist, adding sleep as one of eight key areas that measure a person’s heart health.

New data collected in the past decade has highlighted the importance of sleep to lower the risk for heart problems, prompting AHA to issue “Life’s Essential 8,” a new version of its heart guidelines. “Sleep is related to every single one of the other seven elements—it’s closely tied to weight, blood pressure, glucose metabolism, what we choose to eat,” Donald Lloyd-Jones, the AHA president, said in a Northwestern University press release. “There’s newer research that shows when we take the old seven and add sleep, we can predict cardiovascular disease and stroke even better.”

Heart disease is the leading cause of death in the United States, with a person estimated to die from the disease every 36 seconds. And a lack of sleep can contribute to worsening heart problems. According to the Centers for Disease Control and Prevention, sleeping lowers your blood pressure, controls blood sugar levels, and maintains your weight—all factors that can reduce the odds of heart attacks, heart disease, and stroke. 

[Related: We’re finally understanding why exercise is great for your heart]

The average adult needs between seven to nine hours of rest every night, but more than 1 in 3 Americans sleep less than seven hours a day. The quality of sleep matters, too. Sleep is divided into REM and non-REM sleep cycles, which refer to the rapid movements of your eyes. During  non-REM sleep, slumber is deeper, helping you physically heal. (There are mental benefits as well: Research also suggests non-REM sleep works in tandem with REM sleep to improve learning.)

Sleep brings AHA’s previous 2010 list from seven to eight factors, which also include maintaining a healthy diet, exercising regularly, avoiding nicotine, having a healthy weight and blood pressure, and having healthy levels of blood lipids and blood glucose. 

There are other fresh revisions to that checklist, too. One is changing how people track their diet. “We are recommending a 16-item questionnaire that can be used at regular intervals to assess healthy dietary habits that focuses on weekly amounts of food,” Eduardo Sanchez, the AHA’s chief medical officer for prevention, told CNN. Another change is expanding the category of avoiding nicotine to include vaping and secondhand smoke. 

One of the goals of the checklist is to measure heart health early in kids, and help them maintain their hearts as they age. “We’re losing a lot of cardiovascular health in the eating patterns as our kids age into later childhood and adolescence,” said Lloyd-Jones. “When we create healthier kids, they become healthier adults who then go on to have healthier pregnancies, and the benefits continue with their kids being healthier simply because their parents were healthier.”

The post Take heart: A good night’s sleep can boost cardiac health appeared first on Popular Science.

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