While the popular GLP-1 medications continue to help people control diabetes and weight, the versatile drugs are also starting to address other health conditions as well.

On Aug. 28, the U.S. Food and Drug Administration (FDA) approved Mounjaro to lower the risk of heart events, including heart attack, in people with diabetes. Made by Eli Lilly and Company, Mounjaro is already approved to help manage blood sugar.

Mounjaro affects two of the hormones in the incretin class—GLP-1 and GIP—that have become powerful targets for controlling blood sugar and weight. In the study Lilly submitted to the FDA, researchers compared heart events among people with Type 2 diabetes who either took Mounjaro or another Lilly drug for diabetes, called Trulicity, which targets only GLP-1. People taking Mounjaro had an 8% lower rate of heart attack, stroke, or heart-related death compared to those taking Trulicity. In previous studies, Trulicity helped people with and without a history of heart conditions to lower their risk of having a heart event by 12% compared to those receiving placebo.

“This study was in patients with Type 2 diabetes, in whom the No. 1 cause of death is cardiovascular disease,” says Dr. Rachel Batterham, senior vice president of medical innovation and external engagement for cardiometabolic health at Lilly. “So reducing that risk is critically important.”

Batterham says Lilly decided to compare Mounjaro’s potential in reducing heart risk to an existing drug, Trulicity, that already reduced heart risk to see if Mounjaro would have any additional benefit. “We set ourselves a very high bar,” she says.

But the study design means that the heart benefit results cannot be directly compared to Mounjaro’s competitor drug, Ozempic, from Novo Nordisk. Ozempic, which is approved to treat diabetes, and Novo Nordisk’s Wegovy, approved to treat overweight and obesity, are both approved to lower the risk of heart disease risk by 20%. Lilly is, however, currently conducting a study tracking people who don’t have Type 2 diabetes who take the weight-loss version of their drug, Zepbound, for heart events. In that study, says Batterham, the researchers will be looking at whether Zepbound can prevent second heart events from occurring in people who have already had one, as well as whether the drug can prevent first heart events from occurring.

For now, she says, the new indication means that for people with Type 2 diabetes already taking Mounjaro, doctors can discuss the fact that in addition to controlling their blood sugar, the drug may also help them to lower their risk of having heart events. And for those who don’t have diabetes and are taking Zepbound for weight loss only, “what we could say is that we know people with Type 2 diabetes see this [heart] benefit, but as yet we don’t have the data to say that this same benefit applies in people without diabetes—but we will have those data next year.”

Heart disease remains the leading killer of people worldwide, and one of the key risk factors driving deaths is elevated levels of cholesterol.

In a new article published in the New England Journal of Medicine, researchers report that a gene-editing therapy helped people with increased levels of cholesterol and triglycerides maintain lower levels of these lipids for at least a year. The findings build on earlier results of the therapy, reported last November.

The gene-editing treatment, developed by the biotech company CRISPR Therapeutics, uses CRISPR technology to precisely edit a gene involved in cholesterol regulation. The gene, called ANGPTL3, makes an enzyme that blocks the breakdown of bad cholesterol (LDL) and triglycerides. But scientists discovered a long-lived population in Italy in which people born with a mutation in ANGPTL3—rendering it defective—had low levels of LDL and triglycerides and very little heart disease. The CRISPR therapy mimics this naturally occurring mutation; people who have received it now have this mutation in their ANGPTL3, which means they can now break down cholesterol and triglycerides properly.

In the small study, 15 people with severe forms of high cholesterol and triglycerides showed drops in the two lipids of up to 50%, which the latest results show lasted for at least a year.

“From an efficacy standpoint, it’s a pretty big win,” says Samarth Kulkarni, CEO of CRISPR Therapeutics.

The fact that the people in the study were able to maintain lower levels of LDL and triglycerides for up to a year means that CRISPR was able to edit enough cells in the liver, where much of the body’s cholesterol and triglycerides are produced, to give patients the benefit of having lower levels of the lipids. It also shows that these edited cells continue to produce new generations of cells that carry the CRISPR edit in AGNPTL3. People who received the highest dose of the CRISPR therapy saw levels of the ANGPTL3 enzyme drop by nearly 80%, which contributed to a drop in LDL and triglycerides of about 50%. “This is a really big step for CRISPR to show the durability of the result,” says Dr. Luke Laffin, co-director of the Center for Blood Pressure Disorders at the Cleveland Clinic and lead author of the study.

The CRISPR therapy did not cause significant side effects—and researchers did not expect it to, since people born with the defective ANGPTL3 gene don’t seem to have serious diseases either. That means the one-time therapy could potentially replace the current treatment for high LDL and triglycerides: daily statin pills. While effective, many people don’t take the pills on a daily basis for years, which lowers their effectiveness. “We could look at a situation further down the line where we are able to give people a choice,” says Laffin. In the future, if someone has a serious family history of heart disease or high cholesterol, for example, “this therapy may be an option for them where we could treat them now, edit their [liver cells], and they can continue to have a genetic defect that we know is safe and will control their cholesterol.”

Kulkarni says the company has already begun the next phase of studies and anticipates additional results by the end of this year. That study will continue to focus on people with severe cases of high cholesterol and triglycerides, which affects about two to three million people in the U.S. If that study and further late-stage studies of the CRISPR therapy continue to show positive results, the company might consider conducting studies in people with more average elevations in their lipids.

“The biggest promise of gene-editing in cardiovascular medicine is the notion of a one-time treatment that would be all you need,” he says. “Once you reduce levels of ANGPTL3, it remains durably reduced—presumably for life, but at least for one year. It’s very exciting.”

Applying serums or creams with retinol—a vitamin A-derivative known for its anti-aging and acne-fighting properties—may be a mainstay in your skin-care routine. Some social-media influencers claim you can benefit by “eating your retinol” in the form of carrot-dense salads. Is that true? 

“The answer is yes and no,” says Dr. Lawrence Green, a clinical professor of dermatology at the George Washington University School of Medicine and Health Sciences and vice president of the American Academy of Dermatology.

The “eating your retinol” trend centers on the “retinol salad,” which typically includes ribboned carrots, garlic, vinegar, peppers, sesame oil, and lime juice, though recipes vary. The idea is that carrots are packed with beta-carotene (a precursor to vitamin A), which some influencers claim your body converts to retinol, similar to what’s found in skin-care products. 

“This is a great skin-saving salad, but I think the name is misleading,” says Dr. Rajani Katta, a dermatologist and author of Glow: The Dermatologist’s Guide to a Whole Foods, Younger Skin Diet. The retinol salad provides vitamin A, which is good for the skin, but it’s not the same as applying an over-the-counter retinol or prescription retinoid topically, she explains. 

Here’s what to know about the role of vitamin A and skin health, and whether the “retinol salad” offers any skin benefits. 

What’s the difference between the vitamin A in carrots vs. retinol? 

Vitamin A helps maintain the health of several vital organs, including the heart, reproductive system, eyes, and skin, says Amy Bragagnini, a spokesperson for the Academy of Nutrition and Dietetics.  

Beta-carotene, a natural pigment that gives red and orange fruits and vegetables their color, is a precursor to vitamin A, meaning your body needs to convert it to the vitamin, Bragagnini says. 

It’s true that the body converts beta-carotene into retinol (which is preformed vitamin A, or its active form). But it’s “not an efficient conversion,” Green says. “It happens, but it takes a lot of beta-carotene to get a lesser amount of retinol.” 

You can actually get retinol directly from foods, including eggs, milk, and beef liver, Katta adds. 

Is eating vitamin A the same as applying retinoids or retinol? 

A 2025 systematic review found that topical and dietary carotenoids (a group of plant compounds that include beta-carotene) offer anti-aging skin benefits, including lowered inflammation and improved hydration and elasticity. 

However, eating a retinol salad or other forms of beta-carotene “nowhere compares to putting retinol directly on your skin as a cream,” Green says. 

When applied topically, retinol penetrates your skin, where it can speed up cell turnover and boost collagen production, Katta says. Research shows that topical retinol can improve fine lines, hyperpigmentation, roughness, and signs of sun damage. Retinol can also exfoliate and plump the skin and help treat and manage acne.

Consuming carrots or other foods rich in beta-carotene is an inefficient way to get these benefits, since your body has to go through the process to convert it into vitamin A, Katta explains. 

The retinol salad is still good for your skin. But its benefits mainly come from the antioxidants in the ingredients, rather than the potential to add retinol to your diet, Green says. 

Antioxidants help maintain skin health by reducing the effects of oxidative stress from the environment, such as ultraviolet light radiation and pollution, research shows. Antioxidants also protect against free radicals, or unstable molecules that lead to premature aging and collagen breakdown, Katta says. 

Are there any downsides to the ‘retinol salad’? 

Beta-carotene from dietary sources is typically safe for most people, even in high levels, according to the Harvard School of Public Health. However, too much preformed vitamin A, which you could get from overusing vitamin A supplements—or, less commonly, by eating too many vitamin A-rich foods—could be toxic, potentially causing blurry vision, dry skin, nausea, or vomiting. 

One potential downside to the salad, Bragagnini says, is that eating too many carrots could cause beta-carotene to build up in your blood and possibly turn your skin a “yellow-orange color.” 

If you don’t normally consume vegetables, which are fiber-rich, eating too many at once could upset your digestive system, she says. 

What’s the best diet for healthy skin? 

“I encourage my patients to make sure they are eating a variety of colorful fruits and vegetables,” at least five servings a day, Bragagnini says. 

Fruits and vegetables contain different antioxidants that protect your skin from damage from UV rays and pollution, she says. Omega-3 fatty acids, found in oily fish, walnuts, and flaxseeds, reduce inflammation in the body, which may guard against skin conditions. 

Also, limit sugar, alcohol, and ultra-processed foods, like cookies, bacon, and sugar-sweetened beverages, Bragagnini adds. These foods may increase oil production in the skin and affect collagen production.  

Overall, Green recommends the Mediterranean diet, which incorporates many of these principles and has been shown to benefit overall health. Research shows that the diet can also help manage inflammatory skin conditions, like acne or psoriasis. 

Yet diet alone is “not going to necessarily change your skin in a month,” Katta says. It’s a long-term approach.  

When to see a dermatologist about your skin 

If you’re struggling with acne or are bothered by age-related changes like wrinkles, sagginess, or sun spots, see a dermatologist.  

For acne, doctors can prescribe topical retinoids like tazarotene or tretinoin, oral retinoids such as isotretinoin, or other types of medications, Green says. The goal is to clear breakouts, prevent new ones, and minimize scarring, Katta adds. Dermatologists may also recommend dietary or other lifestyle changes. 

Addressing wrinkles, pigmentation changes, and other age-related changes depends on the individual person and their skin issue, Green says. For example, dermatologists may prescribe retinoids or recommend Botox, fillers, laser treatments, or microneedling. 

“We can look at your skin and help direct you,” Green says, and that includes helping you develop a tailored skin-care routine. 

Over-the-counter retinol serums, creams, and other products are available, too. Katta says they’re beneficial but not as potent as prescription retinoids. Retinol also hasn't been studied as extensively as retinoids, so there’s not as much evidence on its effectiveness, Green says. 

Taking care of your skin should be a holistic approach that includes diet, and the retinol salad can be a part of that. Green says the dish is a “nice idea for the antioxidant benefits,” but won’t treat acne or address any unwanted signs of aging. 

The first heat wave of summer hits like a wall. One day the air is crisp and cool, and the next it’s impossible to go out without sweating through a shirt. The store feels like it’s on the far side of the Amazon, or maybe the Gobi. And yet, the thermometer reveals a number that is not all that high, compared to later in the season. So why is the heat so unbearable? 

Scientists who study temperature regulation have found that the body takes time to adjust to seasonal changes and other thermal changes: a process called heat acclimatization. Research suggests that in people who regularly spend time outside, the body adjusts how it sheds heat to make the environment less stressful. “We can adapt to the heat we're in, and it's obviously progressive,” says Julien Périard, a professor at University of Canberra in Australia who studies the phenomenon. Your body in the summer, it turns out, might be fundamentally different from your body in the winter.

How does the body adapt to seasonal temperature changes?

Spending most of your time indoors in the air conditioning might slow the body’s changes, come summer. “But if we spend time outside exercising, or even just being physically active outdoors, we'll adapt to those conditions,” Périard says.

When you go for a walk on a hot summer day, before you’ve adapted to the heat, both your skin temperature and your core temperature may go up. That sets off alarms in the body, announcing heat stress. “With that, we trigger lots of sweating, and we increase our skin blood flow,” says Périard. Sweat evaporates from the skin, cooling skin down, and blood sent to the surface of the body helps shed heat. 

The volume of blood pumping through the body also goes up. More blood volume allows more heat to be shed and supports greater sweating without dehydration. There are also changes at the level of the cell, with some proteins’ production going up to protect normal functioning in greater heat. The process of reaching a fully adapted state might take a few weeks, although the precise details will depend on the situation. 

These changes can be triggered in advance, with a little bit of exposure at a time. In fact, athletes and people working in warm conditions, like utility workers out in the Texas sun all day, may slowly ramp up their time in the heat to stay healthy under strain. 

Does adapting to heat reduce the risk of heat stroke?

Being adapted to the heat lowers the risks. But it isn’t carte blanche to go for a run at noon in Havana. People who’ve adapted are still vulnerable to heat-related illness, like heat stroke and heat exhaustion, says Glen Kenny, a professor of physiology at the University of Ottawa in Canada. 

What’s more, researchers who study heat adaptation are worried about the stresses that the future climate will bring, when warming may be so swift, and so extreme, that the body can’t react fast enough. In an experiment meant to mimic an extreme 3-day heat wave in 2021 that killed 619 people in British Columbia alone, Kenny spent three days at 104°F in a special chamber in his lab, which allowed him and his colleagues to monitor what happens to the body. “Over three days, you'll see that the body will show some progressive adaptation. But in this situation, you're seeing a decay in the physiological system supporting the maintenance of core temperature,” he says. He lost about 10 pounds in three days because he couldn’t hydrate fast enough. “You're losing so much sweat. You're seeing cell function deteriorate.” 

What happens if you lose your heat adaptation?

Spending a few weeks in a cooler climate can mean the body will roll back some of these changes. “But what's interesting is we have some sort of heat acclimation memory,” says Périard. “If within a month, for example, I've removed you from the heat, and then I've put you back in the heat, in three or four days you'll probably get adaptations that are similar” to what would have taken ten days to build up originally.

Does your body adapt to the cold, too? Yes, but there’s a lot less to work with, says Périard. “We've evolved to be tropical animals, so our heat-loss mechanisms are very potent. But if you think of conserving heat, the only two things we can do are physical constriction—to try and keep the warm blood in the central circulation, essentially—or shivering, which produces a bit of heat but not too much.” Exercising can warm you up, but an essential feature of human culture—clothing—has a far more important role to play here than biology. 

“You can exercise all you want. But if it's -40° outside, you're going to get cold pretty quickly if you don't have any clothes on,” he says.  

An alarming number of professional football players in the U.S. may someday have chronic traumatic encephalopathy (CTE), the neurodegenerative disease associated with repeated concussions and sub-concussive hits to the head, a new study suggests. 

The research, published in the BMJ, studied the brains of NFL players who died from 2016 to 2021 and found that one in four had CTE—a figure that is almost certainly an undercount, the researchers say. Depending on how they crunched the numbers, the CTE incidence rose as high as 91%. 

“The one in four figure is intentionally the most conservative estimate possible,” says lead author Dr. Daniel Daneshvar, chair of the department of physical medicine and rehabilitation at Mass General Brigham and associate professor at Harvard Medical School. “We know the true prevalence is higher than that.”

It was in 1928 that pathologist Harrison Martland first described the condition now known as CTE in boxers experiencing what he called “punch drunk” syndrome. It was not until 2002 that the disease was first diagnosed in an NFL player, when neuropathologist Bennet I. Omalu examined the brain of Mike Webster, a former player for the Pittsburgh Steelers, and found the buildup of tau proteins around blood vessels, thinning of tissue, and overall brain atrophy that characterize the disease. CTE is only firmly diagnosable by autopsy, but the range of symptoms that point to the disease—including memory loss, confusion, aggression, depression, apathy, tremors, and slurred speech—can be pronounced during a person’s life.

“Many of these former players had dementia,” says Daneshvar, “meaning their cognitive symptoms were severe enough to interfere with their ability to function independently. These are not just microscopic changes that we happen to find when someone dies. We are talking about a disease that can profoundly affect people’s ability to think, work, maintain relationships, and live independently.”

What the research found

In the new study, Daneshvar and his colleagues examined the brains of 235 former NFL players who had donated their brains to science. (A total of 878 players died in that 2016-2021 window.) Of the brains studied,  215 were found to have CTE—or 91%. The researchers arrived at their much lower one-in-four figure by making the exceedingly cautious assumption that none of the remaining 643 brains would have shown signs of the disease—an assumption that Daneshvar believes would not stand up if the brains had been examined.

“Among the people who did not donate,” he says, “16% had dementia listed on their death certificate. That certainly does not mean they had CTE, but it illustrates how unrealistic it is to assume that every non-donor was disease-free.”

Another part of the study looked at a larger time window—from 2008 to 2021—during which 1,712 former NFL players died. Of those, 338, including the 235 already analyzed, donated their brains to research, and of that group, 315 had CTE. That makes for a possible CTE prevalence of as high as 93.2%, though if the researchers once again made the conservative—if unrealistic—estimate that all of the unexamined brains were disease-free, the figure would drop to 18.4%.

How to make football safer

What makes CTE particularly insidious is that it is a cumulative disease, one that builds up over a career’s-worth of hits that don’t begin when a player is tapped for the NFL, but can stretch back into college, high school, and even childhood play. In 2011, the NFL, mindful of the growing incidence of CTE, established its concussion protocol, sidelining players who take a hit and exhibit any signs of possible concussion, such as confusion, amnesia, ataxia—a lack of muscle control—or any loss of consciousness.  

That’s a big improvement over the days when concussed players were simply described as having had their “bell rung,” and then sent back out onto the field to continue the game. But concussions are only the most extreme symptoms of brain trauma; there’s a lot of damage that’s done invisibly, with no signs at all. According to one 2012 study in the Annals of Biomedical Engineering, a college football player may sustain up to 1,000 subconcussive hits to the head over the course of a single season of play.

“Concussion protocols are important,” says Daneshvar, “but concussion management and CTE prevention are not the same thing. The evidence increasingly suggests that CTE risk is related to cumulative exposure to repetitive head impacts, including the many impacts that never cause a diagnosed concussion. A player can follow every concussion protocol appropriately and still accumulate thousands of head impacts over a year.”

In addition to the concussion protocols, the NFL has made other rule changes to reduce the incidence of brain trauma, including outlawing both helmet-to-helmet hits and so-called blindside blocks, in which an unsuspecting player is struck from behind, often leading to head and neck injuries. Bigger changes could come during practice, when 70% of hits occur, Daneshvar says. These friendly collisions, he adds, do as much cerebral damage as actual blows sustained during a game.

“The NFL has already moved dramatically in this direction,” he says. “NFL players now have less than one full-contact practice per week.”

Another concern is that measures like this may be coming too late, since young players may be reaching the NFL having sustained brain damage already. Former New England Patriots player Aaron Hernandez, for example, was only 27 when he died by suicide while serving a life sentence for murder. He had spent just four years in the NFL and he was posthumously diagnosed with the worst case of CTE that Boston University researchers had ever seen in a person his age. 

“We don’t need to eliminate football to make it substantially safer,” says Daneshvar—but just like in the pros, high school and college football programs could be changed to minimize or eliminate collisions in practice, and to outlaw hits during games that could be exacerbating trauma to the brain.