Wednesday, June 17, 2026

Hiding who you are can have real effects on your mental health

A person has a hood tied tight, covering their face except for one eye peeking out.

The decision to reveal or conceal a core part of one’s identity may seem like a small, everyday choice, but new research suggests those moments can have meaningful consequences for emotional well-being.

The study found that sexual and gender minority (SGM) young adults who felt compelled to hide their identities were more likely to experience emotional distress and uncertainty about themselves. In contrast, participants who felt able to be open about who they are reported greater confidence, self-understanding, and positivity.

The findings offer a rare glimpse into the day-to-day experiences that shape mental health among sexual and gender minority individuals—a population that experiences higher rates of depression than their non-SGM peers.

The research adds to growing empirical evidence for something many of us intuitively understand: Social norms and institutional policies that limit identity expression have a very real negative mental health impact, not just in the long term but in each moment that someone feels pressure to hide an important piece of themselves, says Sienna Nielsen, a University of Michigan psychology graduate student and study lead author.

According to Nielsen and colleagues, building a strong queer community to resist this effect is crucial in a period of intense anti-LGBTQ+ attitudes and legislation. Many studies have documented mental health disparities among sexual and gender minority populations, but we know much less about how those challenges unfold in everyday life.

“Our findings suggest that daily experiences related to identity visibility may play an important role in emotional well-being,” Nielsen says.

The researchers followed 252 SGM young adults over eight days, collecting more than 4,300 real-time reports about participants’ emotions, identity experiences and social interactions. The study primarily included bi+ cisgender women and nonbinary individuals assigned female at birth.

The researchers examined how participants felt when they concealed or openly expressed their sexual or gender identities. They found that moments of concealment were associated with greater emotional strain and lower confidence in one’s sense of self. Conversely, being open about one’s identity was linked to stronger feelings of self-clarity and identity positivity.

While the researchers did not find a direct link between these day-to-day experiences and depression symptoms during the study period, negative emotions appeared to play an important indirect role, particularly when participants felt pressure to hide aspects of who they were.

The findings highlight how seemingly ordinary interactions can accumulate over time and influence emotional health.

“Being able to live authentically may help reinforce a stronger sense of self, while concealing important aspects of identity can create emotional challenges that affect daily well-being,” Nielsen says.

The researchers say the study provides an important foundation for future work aimed at understanding and reducing mental health disparities among sexual and gender minority populations.

The study appears in Clinical Psychological Science.

Additional coauthors are from UM and the University of Pittsburgh.

The research was supported by the University of Pittsburgh Clinical and Translational Science Institute.

Source: University of Michigan

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Monday, June 15, 2026

‘Peach fuzz’ could hold clues to new chronic itch treatments

A close up shot of one peach among a bunch.

Working with mouse models, research has revealed previously hidden biology of how touch-sensitive hairs create itching sensations.

This fundamental discovery opens new avenues to better understand and potentially address human health conditions characterized by persistent itchiness.

“Itch is one of the major symptoms in most chronic skin inflammation patients,” says Bo Duan, associate professor in the molecular, cellular, and developmental biology department at the University of Michigan.

“What we’ve discovered is a pathway that we believe plays a very important role for both acute and chronic itch sensation.”

The team discovered a previously unrecognized class of hairs in mice, known as vellus-like hairs, and a specialized population of touch-sensitive neurons that connect to them. As their name suggests, these hairs are similar to the fine, short, light-colored vellus hairs found on humans, though we more commonly refer to them as peach fuzz.

The work, supported in part by funding from the National Institutes of Health, appears in the journal Neuron.

For one set of experiments, the team worked with mice that had chronic skin inflammation, which is known as eczema in humans. Mice that expressed these neurons scratched normally, as one would expect. But, for mice that lacked those neurons or in which the neurons were inactive, the itching response was greatly reduced.

While there are a number of ways to help soothe chemical itch caused by things like mosquito bites and poison ivy, those treatments are ineffective against itch caused by skin inflammation, Duan says. This study suggests treatments that target the “mechanical itch” pathway could be more successful.

“We need a new pathway to target if we want to treat chronic itch,” Duan says. “And our research suggests that this population of neurons could be a target in the future. We have ongoing projects looking at this.”

Although the team can’t run experiments to directly identify the same or related pathways in humans, the researchers are already building the case with other forms of evidence. For starters, humans do possess genes required to make these touch-sensitive neurons.

The team also discovered proteins in mice that help transmit the itch signal from hairs to the spinal cord via the specialized neurons. Human neurons grown in cultures respond to the same proteins, the team found.

“Our study indicates that humans may have this same kind of mechanism to transmit mechanical itch,” Duan says. “It also reveals that the body has a dedicated system for this type of sensation.”

It’s one of Duan’s favorite science demonstrations, one that he gave while interviewing for his job and one that he still shows to students joining his lab.

First, you take a tissue and roll one of its corners into a long, fine point. Then take that point and, ever so gently, stroke at the hairs around your lips. Not the thicker, darker hairs, which are called terminal hairs, but the thin, light vellus hairs. If you graze one just right, that peach fuzz will make you itch.

“Humans and animals experience this kind of itch, but no one knew the molecular and cellular mechanisms behind it,” Duan says. The new study identifies the sensory pathway that links specialized hairs to itch and, together with earlier research from Duan and his teammates, helps explain how these signals are transmitted through the nervous system.

It was more than a century ago that scientists first noted that the vellus-like hairs of mice, which are especially concentrated behind their ears, beneath their lips and at the base of their paws, were “special.” Yet these hairs have remained largely understudied in sensory science, Duan says.

Because of that, there really weren’t any standard procedures to test whether and how mice responded to mechanical itch. That meant Duan and his colleagues had to develop their own methods.

“A mouse can’t say that it’s itchy,” Duan says. “But it will scratch.”

For the new study, the team mechanically stimulated itch in mice using a small loop of thread and stroking the animal’s vellus-like hairs. Once they identified the neurons that gave rise to the itching response, the researchers could then make those neurons sensitive to blue light. Shining light on a mouse’s skin and observing it scratch in the same way it did with mechanical stimulation helped confirm the specific neurons’ role in itch.

Peach fuzz and peach fuzz-like hairs grow in higher numbers near human and mice mouths and ears, Duan says. This suggests they may have evolved as a warning system for mammals to alert them when pests or parasites are trying to get in.

But human bodies are covered in vellus hair (with some notable exceptions like the palms of our hands) and you may wonder why we’re not constantly scratching if we’re coated with such sensitive touch receptors. Another one of Duan’s earlier projects studying itch in mice could also explain that: Within the spinal cord, there are “gating” circuits at work that essentially block the mechanical itch signal unless it’s activated in a particular way.

Source: University of Michigan

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This GLP-1 drug may be best for weight loss

A person opens a GLP-1 medication injector.

GLP-1 medications are marketed to help you lose weight, but one may be better at it than the rest, according to a new meta-analysis.

Tirzepatide, better known as Zepbound for weight loss and Mounjaro for treatment of type 2 diabetes, helped patients lose more than 20% of their starting body weight across the reviewed studies.

Semaglutide (marketed under the brand name Wegovy) and liraglutide (Saxenda) did lead to weight loss, but it was significantly less at 15% and 8%, respectively.

The review is the first to compare efficacy of the three FDA-approved GLP-1 medications in nondiabetic patients using the drugs for weight loss.

“We were interested in finding which drug gives the most weight loss and doesn’t have higher rates of side effects like nausea and gastrointestinal problems. Tirzepatide seems to be the better option,” says Pooja Gokhale, corresponding author of the review and a doctoral student in the Unversity of Georgia College of Pharmacy.

Chances are someone you know is taking a GLP-1 medication.

Short for glucagon-like peptide-1, GLP-1s are highly effective FDA-approved medications that treat type 2 diabetes. Increasingly, they’re being used by more people to lose weight.

About one in every eight Americans is currently taking a GLP-1, according to a recent poll from KFF, formerly known as the Kaiser Family Foundation. And one in five have taken the medication in the past.

“Some people call these ‘miracle drugs’ because the weight loss effect is real,” says Lorenzo Villa-Zapata, coauthor of the paper and an assistant professor in the UGA College of Pharmacy.

“But what some people don’t understand is that when they stop taking the medication, they may gain all that weight back.” (The current study did not evaluate weight gain after the discontinuation of GLP-1 medications.)

GLP-1 medications act as a pharmaceutical version of a natural hormone in the gut, lowering blood sugar, keeping you feeling fuller longer, and slowing down digestion.

But where brand names like Wegovy and Saxenda are solely focused on mimicking GLP-1 receptors, tirzepatide targets both GLP-1 receptors and another gut hormone known as GIP.

That may make all the difference for people looking to maximize weight loss, the researchers say.

The researchers analyzed the results of 15 randomized controlled Phase 3 clinical trials, comprising more than 14,000 patients.

Participants saw the largest weight reduction when prescribed the maximum dose of tirzepatide (between 10 and 15 milligrams).

Liraglutide proved the least effective of the three drugs. It also requires daily injections compared to the weekly dosing schedule of tirzepatide and semaglutide medications.

At the time of the review, the FDA had not yet approved the Wegovy pill, an oral version of the GLP-1 medication that is now available in 25 mg pills.

However, the researchers did a sensitivity analysis of a 50 mg version and found that it was not as effective as tirzepatide in nondiabetic patients looking to lose weight. It was “almost as good as the injectable semaglutide,” though, Gokhale says.

The research appears in Obesity.

Source: University of Georgia

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Listen: How websites trick you with ‘dark patterns’

A person types on a laptop keyboard.

In a new podcast episode, a computer scientist explores tactics used in apps and online to deceive users—from subscription traps to collecting data.

Why does it seem so difficult to cancel a subscription, delete an account, or opt-out of data tracking?

You might think it’s just bad luck or a confusing user interface, but more often than not, it’s by design.

Marshini Chetty is a professor at the University of Chicago’s computer science department.

In this episode of Big Brains, Professor Chetty reveals the science behind “dark patterns”—the subtle, manipulative design choices woven into the apps and websites you use every day. Chetty digs into how these deceptive interfaces weaponize human psychology to keep us clicking, spending, and sharing our data:

Read the transcript of this episode.

Source: University of Chicago

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Tuesday, June 9, 2026

Dogs and humans are more alike than we thought

An older golden retriever gets pets from its owner.

The same biological signals that help predict lifespan in humans also appear in dogs, according to new research from the Dog Aging Project.

The finding could help scientists better understand aging in both species.

In a study in The Journals of Gerontology, researchers found that patterns of metabolites—small chemicals and molecules produced during normal bodily processes—were associated with earlier or later death in dogs in much the same way they have been shown in humans.

“The molecules that are risky for dogs or protective against a sooner death are very similar to those in people, showing that we share important features of aging biology, which is really interesting and rewarding,” says Kate Creevy, chief veterinary officer for the Dog Aging Project and a professor in the Texas A&M College of Veterinary Medicine and Biomedical Sciences, where the work of the Dog Aging Project is supported by the WoodNext Foundation.

“Our findings also highlight the value of pet dogs as a model for studying long-term health and lifespan.”

Because metabolites reflect what is happening at the cellular level, researchers can use them to study patterns associated with health outcomes.

In this project, the team analyzed blood samples from dogs enrolled in the Dog Aging Project, a community science study that asks owners to share detailed survey information and submit physical samples from their dogs over the course of the dog’s lifetime. These blood samples were examined for metabolic patterns associated with lifespan—specifically, whether dogs died sooner or later.

“Death is an easy outcome to understand,” Creevy says. “It is very easy to tell when a person or a dog has died, whereas other features of aging health are a bit more nuanced.”

By starting with that clear outcome, researchers can begin to work backward to identify the biological processes that influence aging, such as metabolism, inflammation or how cells respond to stress.

“If we understand why something happened, we have a greater chance of identifying ways to change it,” Creevy says.

To better understand those patterns, researchers examined thousands of metabolites at once to identify broader signals that could predict risk. Creevy says studying groups of metabolites provides a clearer picture of what may be happening inside cells.

“Some of my colleagues refer to it as a fingerprint,” Creevy says. “We often look at a pattern or grouping that has a relationship with better or worse outcomes rather than just looking at a single molecule.”

These measurable biological signals—known as biomarkers—help researchers anticipate health outcomes based on what’s happening inside the body.

“Importantly, those biomarkers do not necessarily cause an outcome; when we find a biomarker associated with sooner or later mortality, we don’t know that it’s causing it,” Creevy says. “But if we understand why that biomarker is present, we may be able to identify what the cause of the relationship is.”

By identifying these patterns, researchers can begin to better understand the biological processes linked to aging—and identify potential targets for improving health over time.

To determine whether the same kinds of metabolic signals appear in humans, researchers compared their findings in dogs with five large, published studies of human mortality that used similar metabolite-based approaches. In each case, the patterns linked to earlier or later death were similar.

The consistency across multiple human studies was one of the study’s most notable findings, reinforcing the idea that dogs and humans share fundamental aspects of aging biology.

“Frequently, we know a little more about this in people than we do in dogs,” Creevy says. “If we have the same targets, we’ll be able to leverage human research to benefit dogs.”

That overlap allows researchers to build on existing human research while using dogs to better understand how aging unfolds over time.

Dogs are especially useful for aging research because they share many aspects of daily life with people, including environment, diet and activity levels. Those shared experiences make it easier to understand how lifestyle influences long-term health.

“One of the things we like most about learning from dogs as it pertains to aging is their widely varied lifestyles that mirror their owners’ lifestyles in a way that’s less true for other companion animals,” Creevy says.

For example, cats tend to have more consistent, independent lifestyles, while dogs tend to reflect their owners’ daily routines more closely.

Dogs’ shorter lifespans also allow researchers to study aging much quicker than would be possible in humans, because while humans, on average, live into their 70s, dogs, on average, live only 12-13 years, giving researchers an opportunity to observe comparable outcomes in dogs in a fraction of the time.

The study was made possible through the Dog Aging Project, a nationwide, long-term study of pet dogs living with owners across the United States. Participating owners share detailed information about their dogs’ lives, and a subset provide annual biological samples, giving researchers a unique opportunity to study aging over time.

“The owners who enroll their dogs make everything possible,” Creevy says. “The dedication and commitment of these owners to participate in research and discovery to better the health of dogs is remarkable.”

Creevy says the findings represent an important step in understanding the biology of aging, helping researchers move from identifying patterns to exploring what may be driving them.

“This is a starting point,” she says. “We’ve identified these metabolites, and now we know where to start looking.”

For dog owners, Creevy says the takeaway is simple: many of the habits that support healthy aging in people are likely just as important for dogs.

“Keeping them on a healthy diet, at a healthy body weight, and preserving mobility and cognitive health—just like we would do for ourselves,” Creevy says. “What’s good for us is probably good for them.”

Source: Texas A&M University

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Tuesday, June 2, 2026

Mosquitoes can learn to love DEET

A mosquito with a belly full of red blood stands on a white surface.

Mosquitoes can learn to like DEET, the world’s most powerful insect repellent, according to a new study.

Every summer, millions of people spray themselves with DEET to keep mosquitoes away. But the new research suggests mosquitoes may be able to learn to associate the repellent with food—and even become attracted to it.

The study in the Journal of Experimental Biology, was a collaboration between Clément Vinauger, associate professor at Virginia Tech, and Claudio Lazzari at the University of Tours in France.

“If someone applies DEET and the concentration fades over time, but a mosquito still manages to feed, the insect may begin associating that smell with a reward,” says Vinauger, part of the Department of Biochemistry in the College of Agriculture and Life Sciences.

“That’s a possibility we should take seriously when we think about how repellents are used in the real world.”

The study focused on the yellow fever mosquito, Aedes aegypti, a species that spreads dengue fever, Zika, yellow fever, and chikungunya, which infect tens of millions of people each year.

Researchers trained the mosquitoes using a form of Pavlovian conditioning—the same learning principle behind Ivan Pavlov’s famous experiments in which dogs learned to associate the sound of a bell with food.

Mosquitoes were restrained behind fabric mesh with a bag of warm blood positioned just out of reach. After the mosquitoes began to feed on the blood, researchers introduced the smell of DEET. After repeating the experiment four times, more than 60% of the insects tried to feed when presented with only the smell of DEET.

Next, mosquitoes were given a choice between two human hands—one untreated and one coated with DEET at normal concentrations. Untrained mosquitoes avoided the DEET-treated hand. Trained mosquitoes were drawn to it.

The researchers also found mosquitoes could form the same association when sugar, instead of blood, was used as the reward.

“The common assumption has always been that repellents work because of their chemistry—that DEET simply smells bad to mosquitoes and they flee or that its chemistry prevents mosquitoes from smelling us,” says Vinauger, who is also an affiliate of Fralin Life Sciences Institute’s Center for Emerging, Zoonotic, and Arthropod-borne Pathogens.

“But what we are showing is that the mosquito’s brain can rewrite that response based on experience. What the insect has learned matters just as much as what the chemical does. That, I think, is a paradigm shift.”

The findings do not mean people should stop using DEET, Vinauger says. It’s still one of the most effective repellents available, particularly in regions where mosquito-borne disease is common.

“If you’re in tropical regions where disease risk is real, you should use it,” he says.

But the study suggests timing and concentration may matter more than previously understood.

“Instead of applying a lot at once, you may want to reapply regularly so it’s always active and providing continuous protection,” Vinauger says.

He adds that treated clothing may also present challenges because DEET concentrations in fabric decline over time.

The study builds on years of mosquito learning and behavior research connected to Vinauger’s work. While pursuing his PhD in Lazzari’s lab in France, and later as a postdoctoral researcher at the University of Washington, Vinauger helped pioneer experiments showing mosquitoes can learn and remember odors associated with blood meals and defensive hosts.

At Virginia Tech, Vinauger’s lab studies how mosquitoes use sensory information to find hosts and adapt to changing environments. His team has shown that mosquitoes remember and avoid hosts who swat at them, combine smell and vision to track people with surprising precision, and gravitate toward and away from the smell of certain body soaps.

“Mosquitoes are remarkable at processing information about their environment,” Vinauger says. “What we are trying to understand is not only how they detect us, but how their brains interpret those cues and turn them into behavior.”

As Aedes aegypti expands into new regions and insecticide resistance grows worldwide, Vinauger says understanding mosquito behavior is becoming increasingly important for public health.

“We need to understand how mosquitoes keep outsmarting our control strategies,” Vinauger says. “And that takes understanding how they work—at the molecular level, the neural level, the behavioral level.”

Source: Virginia Tech

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Team finds protein that could help failing hearts recover

A heart spray painted in red on a white wall.

Researchers have identified a key protein that may help failing hearts regain function, offering new insight into why some hearts recover while others do not.

The discovery comes from studying patients treated with left ventricular assist devices, or LVADs, which are mechanical pumps that reduce strain on the heart and allow it to rest and recover.

While these devices can stabilize patients with advanced heart failure, only a subset experience meaningful recovery, and the biological reasons have remained unclear.

In a new study in the Journal of the American Heart Association, cardiovascular molecular researcher Junco Warren of Virginia Tech and cardiologist Stavros Drakos of the University of Utah found that a protein called PERM1 is fully restored in patients whose hearts recover after LVAD support. Patients who did not recover showed no such restoration.

The study brought together scientists at Virginia Tech’s Fralin Biomedical Research Institute at VTC and clinical collaborators at the University of Utah, combining molecular research with patient-based cardiac care.

Heart failure affects more than 6 million people in the United States, and predicting recovery remains a major challenge in care.

“This is the first muscle-specific molecular signal linked to recovery in human heart failure,” says Warren, assistant professor at the Fralin Biomedical Research Institute and co-corresponding author.

“We don’t yet know whether PERM1 drives recovery or reflects it, but it gives us a clear window into the biology of how recovery happens.”

The research team analyzed heart tissue from 19 patients, comparing samples collected before and after LVAD implantation. Patients were enrolled through the University of Utah cardiac transplant program, with tissue collected from the left ventricular apex during implantation and later during device removal or transplantation. Patients were categorized as responders or non-responders based on improvements in heart function.

Before treatment, PERM1 levels were reduced in all patients. After LVAD support, levels were restored to near-normal only in those whose hearts recovered, while remaining suppressed in non-responders.

“This study begins to explain why some patients recover heart function with LVAD support while others do not,” says Drakos, professor of cardiology at the University of Utah and co-corresponding author. “Identifying the biological signals behind recovery is essential to improving outcomes for patients with advanced heart failure.”

The findings showed a strong correlation between PERM1 levels and improved cardiac function. PERM1 regulates how heart cells produce and use energy, and recovery was associated with normalization of stress-related metabolic pathways.

Together, the results position PERM1 as both a potential biomarker and a target for future therapies.

“Current therapies help manage heart failure, but they do not repair the heart muscle itself,” says Warren, who is also an assistant professor in Virginia Tech’s human nutrition, foods, and exercise department in the College of Agriculture and Life Sciences.

“Our findings point to a pathway that directly targets cardiomyocytes—the heart muscle cells—and restores both energy production and contractile function, the two core deficits in heart failure.”

Previous work from Warren’s lab showed that increasing PERM1 improves heart function in experimental models. The approach has also been shown to prevent heart failure in preclinical studies and may support recovery in advanced disease, including in patients receiving mechanical heart support.

“Heart failure creates a vicious cycle where energy loss and reduced contraction reinforce each other,” Warren says. “PERM1 appears to act at the center of that cycle.”

While more research is needed to determine whether PERM1 directly causes recovery, the findings provide a step toward new treatment strategies.

To help advance these discoveries toward patient use, Warren and members of her research team have co-founded a company focused on developing PERM1-based gene therapies.

The study was supported by the National Institutes of Health, the American Heart Association, the US Department of Veterans Affairs, the Nora Eccles Treadwell Foundation, and internal funding from the Fralin Biomedical Research Institute.

Source: Virginia Tech

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