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By Jeneen Interlandi In the mid-2010s, when they were still postdoctoral fellows at the Massachusetts Institute of Technology, Mathilde Poyet and Mathieu Groussin kept bumping into different sides of the same obstacle. Poyet, an ecologist and a microbiologist, was trying to study rare bacterial species, the kind that had never been grown in a lab before. Groussin, a computational biologist in the same lab, wanted to understand how humans and microbes evolved together over millenniums. Each was focused on microbes that make their homes in and on the human body, what scientists collectively refer to as the human microbiome. But the only samples they could find to work with came from the same small sliver of humanity, namely populations that were wealthy, Western and white. “About 90 percent of all human diversity has been completely left out of the picture,” Groussin told me recently. It was as if someone had shone a bright flashlight on one small segment of a giant canvas and left the rest shrouded in darkness. The bright spot was well defined (imagine the face of a man). But they couldn’t really tell what they were looking at (whether that man was a monk, for example, or a matador) without seeing the rest of the canvas. Scientists refer to this vast, unexplored terrain as biology’s dark matter. Our bodies are home to more bacteria — on our skin, up our noses, in our guts and mouths and around our genitals — than there are stars in the Milky Way. These microbes have evolved not only with us but inside us, and scientists who study them closely say that hardly a biological process or system exists in which they do not play a role. They helped create our digestive systems and our immune systems. They influence the size and shape of our bodies. At least some research suggests that they also affect our brains, moods, personalities and behaviors. And yet, most of them have still not been identified, let alone studied. It was tantalizing to think about what a fuller picture might reveal. In recent years, scientists had linked the gut microbiome to a long list of conditions, including Crohn’s and irritable bowel syndrome, Parkinson’s, dementia and autism, and they were hopeful that a better understanding of those links would lead to treatments, if not cures. They were also sifting through the nearly unfathomable array of molecules that microbes produce, in search of biological treasures: not only potential medications but also compounds capable of breaking down pollutants or repairing damaged ecosystems. © 2026 The New York Times Company

Fructose silences hunger-driving neurons less than glucose does

By Sarah Thau Hunger pangs build with activity in Agouti-related protein (AgRP) neurons, and when we eat, these cells fall silent, signaling to the body that it’s full. Until recently, researchers thought these neurons responded to calorie intake alone, but a new study shows fructose quiets them less effectively than glucose does, even though both simple monomeric sugars carry the same number of calories. “We were really surprised when we tested these different sugars and found that fructose looks much different than glucose,” says study investigator Amber Alhadeff, a member of the Monell Chemical Senses Center and adjunct assistant professor of neuroscience at the University of Pennsylvania. Fiber photometry recordings of individual AgRP neurons in mice consuming fructose or glucose solutions first tipped the lab off to the fact that fructose is the weaker inhibitor. The same difference surfaced when the team infused the solutions directly into the animals’ guts, controlling for the fact that the mice tended to take more licks of the glucose than fructose. Glucose does not require the vagus nerve to inhibit AgRP neurons, according to previous work from Alhadeff’s group, but fructose does, the new study demonstrates. This study is the first to show “that the brain is responding to these things in different ways, and with a real mechanistic underpinning,” says Martin Myers, professor of diabetes research at the University of Michigan Medical School, who was not involved in the research. “This is an absolutely fabulous lab that is doing things that few, if any, other people in the world can do.” Once the team discovered that fructose acts through the vagus nerve, Alhadeff’s graduate student Aaron McKnight hit the mechanistic ground running. He worked for five years, according to Alhadeff, to show that fructose activates the vagus nerve, releasing a hormone called PYY that signals Y2 receptor-expressing vagal afferent neurons and then inhibits AgRP neurons. Glucose does not lead to increased PYY levels, acting through gut-spinal afferent signaling—a separate peripheral pathway. © 2026 Simons Foundation

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 30306 - Posted: 07.01.2026

New powerful GLP-1 drugs drop a lot of weight fast. How does that affect health?

By Bethany Brookshire Once people understood glucagonlike peptide 1 (GLP-1) drugs’ potential for weight loss, the race among pharmaceutical companies was on. Among the current options, Wegovy can help people lose an average of 10 percent of their body weight in a year, while people taking Zepbound have had about a 15 percent loss, on average, in the same period. Soon the most powerful GLP-1 treatment to date could hit the market: retatrutide. Already popular on the online peptide gray market, the new drug, originally developed by Eli Lilly, caused participants in a recent clinical study to lose more than a quarter of their body weight over 80 weeks at the highest dose—results comparable to bariatric surgery. U.S. Food and Drug Administration approval could soon follow. But bodies don’t just drop weight with no potential adverse effects. Weight loss on its own can change muscle, bone and more. As new-generation GLP-1 drugs promote higher rates of loss, clinicians want to ensure that the desire to shed pounds and see improvements such as better cardiovascular health are balanced with the very real risks that may come with the treatment. Fat, Muscle or Bone? People typically lose weight when they eat fewer calories than their body expends. A common way to cut calories is to diet, while bariatric surgery removes or changes part of the gastrointestinal tract to reduce food—and therefore calorie—absorption. GLP-1 is a gut hormone released in response to a meal that helps people feel full. It also increases insulin release and reduces glucose in the blood. Semaglutide (sold as Ozempic and Wegovy by Novo Nordisk) binds to the hormone’s receptor for longer periods of time, making people feel fuller for longer and eat less. Newer versions of GLP-1 drugs, such as tirzepatide (sold as Zepbound and Mounjaro by Eli Lilly) and Novo Nordisk’s upcoming drug CagriSema target more than one type of gut hormone receptor, while retatrutide hits three. © 2026 SCIENTIFIC AMERICAN

The Day the Food Noise Died

By Gina Kolata Before the new obesity drugs came on the market, almost no one used the term food noise. Researchers studying and developing drugs like Ozempic, Wegovy, Mounjaro and Zepbound analyzed doses, side effects, weight loss and improvements in conditions such as diabetes, heart disease and sleep apnea. Incessant thoughts about food and internal dialogues about what to eat, what not to eat, when to eat, how to resist eating — these were not on the research agenda. But if the obesity-drug researchers weren’t talking about food noise, people taking GLP-1s had a lot to say about it. For as long as they could remember, users of the drugs said, they had been plagued by food noise. But they thought it was just a normal part of life. They thought everyone had it. Until they took one of the new drugs. Suddenly, food noise was silenced. And that effect is leading to new questions about the drugs. If researchers can clarify the source of this inner buzz and what makes it go away, that could lead to a clearer understanding of what causes obesity in the first place. ‘You Don’t Want the Salad’ People who struggle with their weight describe relentless thoughts of food. Lena Smith Parker, 53, of Hamden, Conn., spent decades dieting and regaining weight. All the while, she said, she was plagued by internal voices urging her to eat and shaming her for eating. © 2026 The New York Times Company

GLP-1 microdosers are chasing longevity

By Jamie Ducharme More than 10 percent of U.S. adults take GLP-1 drugs. But not all of them are taking full doses. Around one in seven users has “microdosed” injections, a recent survey by the health tracking app Evidation found. Some take tiny portions for practical reasons, such as cutting costs. Others have loftier ambitions: They hope to harness the drugs’ powerful effects to achieve better health and longer lives without losing a lot of weight or experiencing side effects such as GI issues and muscle loss. Medications such as Ozempic and Wegovy mimic the body’s GLP-1 hormone, which helps regulate appetite, metabolism and blood sugar. That has made the drugs blockbuster treatments for type 2 diabetes and obesity. But to date, “there is no rigorous scientific data to support microdosing,” says bariatric medicine specialist Katy Williams of the University of Missouri Health Care in Jefferson City. That hasn’t stopped some intrepid biohackers from trying it, though. Companies like AgelessRx, a longevity-focused telehealth clinic, explicitly sell GLP-1 microdoses for this purpose, advertising them as “a powerful new path to promoting long-term wellness.” There is some research to suggest GLP-1s can promote healthy aging by improving overall health. The drugs have been found to reduce inflammation and oxidative stress, lower risks of major cardiovascular problems, lower cancer risk and more. Such findings have prompted scientists to study the drugs as potential treatments for illnesses as diverse as Alzheimer’s disease and arthritis. Some experts have even wondered whether the drugs’ systemic effects might slow cellular aging and prevent age-related chronic conditions, potentially making them the first true longevity drugs to hit the market. © Society for Science & the Public 2000–2026.

Can weight-loss pills replace injectables? What the science says

Mariana Lenharo The weight-loss drugs that took the world by storm a few years ago have a drawback for anyone afraid of needles: they must be injected weekly. But scientists have been racing to perfect anti-obesity pills — which are now coming to market. An oral anti-obesity drug called orforglipron is likely to be approved by US regulators by the end of April, pharmaceutical analysts say. In December, a pill version of the obesity drug semaglutide won US regulatory approval. Both drugs belong to the class of therapies called glucagon-like peptide-1 (GLP-1) receptor agonists. Semaglutide, sold as Wegovy, is made by Novo Nordisk in Bagsværd, Denmark; orforglipron is made by Eli Lilly and Company in Indianapolis, Indiana. Clinical-trial results have been positive. After around one year of treatment at the highest dosage, people taking orforglipron lost, on average, about 11% of their body weight1, and those taking semaglutide pills lost almost 14%2. But it’s uncertain whether pills could one day replace the GLP-1 pens that have become a weight-loss staple. Oral drugs face formidable developmental challenges, and several injected drugs cause greater weight loss than does either orforglipron or oral semaglutide: the approved injectable drug Zepbound, for example, leads to weight loss of up to 21% of body weight3. “It’s encouraging, and it’s fantastic to have double-digit weight loss with a pill,” says Daniel Drucker, an endocrinologist at the University of Toronto in Canada. “But so far, rather than replace, I would say they’re going to complement the options that we have.” There’s a good reason why the original GLP-1 receptor agonists, which mimic the natural hormone glucagon-like peptide-1, were sold in injectable form. The drugs are composed of peptides, which are relatively large molecules. Because of their size, digestive enzymes quickly break them down, and the intestinal lining limits their entry into the bloodstream. © 2026 Springer Nature Limited

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: Development of the Brain
Link ID: 30163 - Posted: 03.19.2026

Exercise rewires the brain — boosting the body’s endurance

Mariana Lenharo Exercise pumps up your muscles — but it might also be pumping up your neurons. According to a study published today in Neuron1, repeated exercise sessions on a treadmill strengthen the wiring in a mouse’s brain, making certain neurons quicker to activate. This ‘rewiring’ was essential for mice in the study to gradually improve their running endurance. The work reveals that the brain — in mice and, presumably, in humans — is actively involved in the development of endurance, the ability to get better at a physical activity with repeated practice, says Nicholas Betley, a neuroscientist at the University of Pennsylvania in Philadelphia, and a co-author of the paper. “You go for a run, and your lungs expand, your heart gets pumping better, your muscles break down and rebuild. All this great stuff happens, and the next time, it gets easier,” Betley says. “I didn’t expect that the brain was coordinating all of that.” Betley and his colleagues were curious about what happens in the brain as people get stronger through exercise. They decided to focus on the ventromedial hypothalamus, a brain region that regulates appetite and blood sugar. The team then zeroed in on a group of neurons in that region that produce a protein called steroidogenic factor 1 (SF1), which is known to play a part in regulating metabolism2. A previous study3 found that the deletion of the gene that codes for SF1 impairs endurance in mice. © 2026 Springer Nature Limited

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 30120 - Posted: 02.14.2026

Using GLP-1s to maintain a normal weight? There are benefits and risks

Yuki Noguchi At just over 5 foot, 5 inches, Christie Woodard weighs a lean 125 pounds. She's also open about relying on a low-dose GLP-1 to keep her weight there. She says sometimes people question why she's on the drug, "because they look at me and think I'm at healthy weight, or maybe they even think I'm thin." What people don't see is Woodard's previous struggles with obesity, which began in her 30s, and landed her at 260 pounds. She took up running half-marathons, but at that weight, it was painful. "I was not fast," she says. "I had massive issues; I was in physical therapy constantly. I tore my meniscus." Woodard, now 53 and living in Easton, Md., got gastric bypass surgery four years ago and cut her weight in half. Elated, she set a goal of completing half-marathons in all 50 states. Her weight remained stable until last year, when pounds began creeping back, despite adhering to a strict diet and lots of exercise. "I feel it in my knees, and mainly I feel it in my soul," she says. "I feel it in my confidence. It's messing with my head in a big way. I was terrified that I was going to go back to what I was." So her bariatric surgeon, Dr. Betsy Dovec, prescribed a low dose of the drug Zepbound, even though Woodard's body mass index didn't technically classify her as overweight. Dovec says Woodard isn't her only normal-weight patient on GLP-1s. "I prescribe medications for all types of people," she says. Though, she clarifies, she does not give the drugs to people for purely aesthetic reasons, like someone trying to shed a few pounds before an event, for example. © 2026 npr

Loss of ‘hunger hormone’ has made snakes masters of fasting

By Jake Buehler Though fearsome predators, snakes can go weeks or even months without eating. Now, scientists think they may know how they do it. Snakes have lost the genes to produce ghrelin, a key hormone that regulates appetite, digestion, and fat storage, researchers report today in Royal Society Open Biology. Chameleons and a group of desert lizards called toadhead agamas that also have huge spaces between meals have also lost the same genes, hinting that cutting off ghrelin is a key way to excel at fasting, possibly by suppressing appetite and holding onto fat stores. “I give [the researchers] a lot of credit for looking more deeply into the data that was staring us all in the face—myself included,” says Todd Castoe, a genomicist at the University of Texas at Arlington not involved with the study. The hormone is ubiquitous across vertebrates, from fish to mammals. So finding that reptiles have repeatedly ditched it is “pretty remarkable,” he says. When scientists first discovered ghrelin nearly 30 years ago, they thought this “hunger hormone” could be key to fighting obesity in humans. But it hasn’t been that simple. Since then, researchers have found that ghrelin has a complicated role within a network of hormones constantly tweaking hunger and energy stores. And even though ghrelin is commonly found in vertebrates, it’s been unclear how it has evolved across various groups of vertebrates. So in the new study, Rui Resende Pinto, an evolutionary biologist at the University of Porto, and his colleagues focused on reptiles, many of which can go long periods without food. The researchers scanned the genomes of 112 species. In snakes, chameleons, and toadhead agamas, ghrelin genes were either missing or so warped by mutations they could no longer encode the hormone, the team found. The degree of the genes’ erosion also varied considerably between snake families: Some snakes such as boas and pythons had malformed ghrelin genes, but others, such as vipers, cobras, and their relatives, barely had anything left.

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 30104 - Posted: 02.04.2026

Could Weight Loss Drugs Turn Fat Cats Into Svelte Ozempets?

By Emily Anthes In just a few short years, new diabetes and weight loss drugs like Ozempic, Wegovy and Mounjaro have taken the world by storm. In the United States, one in eight adults say they’ve tried one of these medications, which are known as GLP-1 drugs, and that number seems sure to rise as prices fall and new oral formulations hit the market. Fluffy and Fido could be next. On Tuesday, Okava Pharmaceuticals, a biopharmaceutical company based in San Francisco, is set to announce that it has officially begun a pilot study of a GLP-1 drug for cats with obesity. The company is testing a novel approach: Instead of receiving weekly injections of the drugs, as has been common in human patients, the cats will get small, injectable implants, slightly larger than a microchip, that will slowly release the drug for as long as six months. “You insert that capsule under the skin, and then you come back six months later, and the cat has lost the weight,” said Dr. Chen Gilor, a veterinarian at the University of Florida, who is leading the study. “It’s like magic.” Results are expected next summer. If they are promising, they could represent the next frontier for a class of drugs that has upended human medicine, and a potentially transformative treatment option for millions of pets. Some veterinarians have already begun administering human GLP-1 drugs, off label, to diabetic cats, and Okava is not the only company developing a product specifically for companion animals. “I think this is going to be the next big thing,” said Dr. Ernie Ward, a veterinarian and the founder of the Association for Pet Obesity Prevention. Veterinarians, he added, are “on the precipice of a complete new era in obesity medicine.” © 2025 The New York Times Company

Mapping the Sense of What’s Going On Inside

By Carl Zimmer Last year, Ardem Patapoutian got a tattoo. An artist drew a tangled ribbon on his right arm, the diagram of a protein called Piezo. Dr. Patapoutian, a neuroscientist at Scripps Research in San Diego discovered Piezo in 2010, and in 2021 he won a Nobel Prize for the work. Three years later, he decided to memorialize the protein in ink. Piezo, Dr. Patapoutian had found, allows nerve endings in the skin to sense pressure, helping to create the sense of touch. “It was surreal to feel the needle as it was etching the Piezo protein that I was using to feel it,” he recalled. Dr. Patapoutian is no longer studying how Piezo informs us about the outside world. Instead, he has turned inward, to examine the flow of signals that travel from within the body to the brain. His research is part of a major new effort to map this sixth, internal sense, which is known as interoception. Scientists are discovering that interoception supplies the brain with a remarkably rich picture of what is happening throughout the body — a picture that is mostly hidden from our consciousness. This inner sense shapes our emotions, our behavior, our decisions, and even the way we feel sick with a cold. And a growing amount of research suggests that many psychiatric conditions, ranging from anxiety disorders to depression, might be caused in part by errors in our perception of our internal environment. Someday it may become possible to treat those conditions by retuning a person’s internal sense. But first, Dr. Patapoutian said, scientists need a firm understanding of how interoception works. “We’ve taken our body for granted,” he said. Everyone has a basic awareness of interoception, whether it’s a feeling of your heart racing, your bladder filling or a flock of butterflies fluttering in your stomach. And neuroscientists have long recognized interoception as one function of the nervous system. Dr. Charles Sherrington, a Nobel Prize-winning neuroscientist, first proposed the existence of “intero-ceptors,” in 1906. © 2025 The New York Times Company

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 30030 - Posted: 11.26.2025

How obesity drugs quiet ‘food noise’ in the brain

Mariana Lenharo The obesity drug tirzepatide, sold as Mounjaro or Zepbound, can suppress patterns of brain activity associated with food cravings, a study suggests. Researchers measured the changing electrical signals in the brain of a person with severe obesity who had experienced persistent ‘food noise’ — intrusive, compulsive thoughts about eating — shortly after the individual began taking the medication. The study is the first to use electrodes to directly measure how blockbuster obesity drugs that mimic the hormone GLP-1 affect brain activity in people, and to hint at how they curb extreme food cravings. “It’s a great strategy to try and find a neural signature of food noise, and then try to understand how drugs can manipulate it,” says Amber Alhadeff, a neuroscientist at the Monell Chemical Senses Center in Philadelphia, Pennsylvania. The findings were published today in Nature Medicine1. Casey Halpern, a neurosurgeon-scientist at the University of Pennsylvania in Philadelphia, and his colleagues did not set out to investigate the effects of obesity drugs on the brain. The team’s goal was to test whether a type of deep brain stimulation — a therapy that involves delivering a weak electrical current directly into the brain — can help to reduce compulsive eating in people with obesity for whom treatments such as bariatric surgery haven’t worked. The scientists set up a study in which participants had an electrode implanted into their nucleus accumbens, a region of the brain that is involved in feelings of reward. It also expresses the GLP-1 receptor, notes Christian Hölscher, a neuroscientist at the Henan Academy of Innovations in Medical Science in Zhengzhou, China, “so we know that GLP-1 plays a role in modulating reward here”. This type of electrode, which can both record electrical activity and deliver an electrical current when needed, is already used in people to treat some forms of epilepsy. © 2025 Springer Nature Limited

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 14: Attention and Higher Cognition
Link ID: 30016 - Posted: 11.19.2025

Staying on the keto diet long term could carry health risks

By Meghan Rosen Maybe you’ve seen an influencer make French fries out of almond flour. Or a sandwich recipe that swaps bread for fried cheese. They’re called keto meals, and they’re largely shared for one reason: to help people lose weight. In the ketogenic diet, fat is king, and carbs are public enemy number one. Going keto means restricting carbs to the bare minimum and replacing those lost calories with fat. It’s the antithesis of the low-fat diet craze of the 1990s. Losing fat on keto diets typically means eating fat — and lots of it. The idea may sound paradoxical. But without our typical go-to energy source (sugar), our bodies learn to rely on a different type of fuel. In keto dieters, the liver converts fat into molecules called ketone bodies, which the body can burn instead of sugar. That can lead to weight loss, despite an unusually high intake of fat. Such results may explain why so many Americans have tried the keto diet on for size. “I think a lot of people look at a ketogenic diet and think, ‘I’ll lose weight, I’ll be healthier,’” says Molly Gallop, a physiologist at Earlham College in Richmond, Ind. On the surface, they may be right. But staying on the diet long-term could carry some risks, a new study in mice suggests. Mice fed a ketogenic diet for up to about a year — decades in human time — experienced health problems including glucose intolerance and signs of liver and cardiovascular disease, Gallop and her colleagues report September 19 in Science Advances. The work uncovers some potential hidden costs to going keto, says physiologist Amandine Chaix, at the University of Utah in Salt Lake City. “It’s a cautionary tale,” she says. People sticking to this high-fat plan need to be careful, she says, “because this is not a magical dietary approach.” © Society for Science & the Public 2000–2025.

Daily weight loss pill can help cut body weight by a fifth

Andrew Gregory Health editor A daily pill for weight loss can help people reduce their body weight by as much as a fifth, according to a trial that could pave the way for millions more people to shed pounds. The drug, called orforglipron, is manufactured by Eli Lilly and targets the same GLP-1 receptors as weight loss injections such as Mounjaro and Wegovy. In a trial of 3,127 adults, one in five people who took the once-a-day tablet for 72 weeks lost 20% or more of their body weight. Weight loss jabs have been transformative but pill versions are seen as a holy grail because they are easier to store, distribute and administer and are also expected to be cheaper, offering fresh hope for the millions of people trying to lose weight. Orforglipron is a GLP-1 agonist, a type of medication that helps lower blood sugar levels, slows the digestion of food and can reduce appetite. The weight loss seen among people taking the tablet is not as stark as that among patients taking tirzepatide (Mounjaro), which is also made by Eli Lilly, but experts believe the tablet will be more accessible and convenient compared with injections. Orforglipron is not yet approved by the US Food and Drug Administration (FDA) or regulators in other countries. Eli Lilly has said it expects substantial demand when the new pill is launched. The company published a snapshot of the results in August and the full paper detailing the findings has now been published in the New England Journal of Medicine and presented to the annual meeting of the European Association for the Study of Diabetes in Vienna, Austria. © 2025 Guardian News & Media Limited

Are ultra-processed foods really so unhealthy?

Nic Fleming In the early 2000s, Brazilian nutrition researcher Carlos Monteiro made a puzzling discovery that led to an epiphany. While trawling survey data on household spending to try to understand why rates of obesity and type 2 diabetes were rising so rapidly in his home country, he was surprised to note that people were buying smaller quantities of sugar, salt and other ingredients generally associated with these conditions than they had in previous decades. Only when Monteiro and his colleagues dug deeper did they find the culprit. People were buying less sugar to prepare cakes and desserts, but eating more of it in pre-made pastries and breakfast cereal. They were buying less salt, but consuming more of it in frozen pizzas, chicken nuggets and dehydrated packet soups. “We realized the problem was our traditional dietary patterns were being replaced by foods that are processed so many times that they can no longer be recognized in the final products. We called them ultra-processed foods.” Monteiro, a nutrition and public-health researcher at the University of São Paulo, first used the term ultra-processed food (UPF) in a paper in 2009, arguing that people interested in promoting healthy diets should focus more on the degree, extent and purpose of processing than on nutrient profiles1. It was a radical idea that caught the attention of other researchers, who, over the next decade or so, published dozens of papers linking UPFs with obesity and a range of other health problems. Governments took notice, too. In 2014, Brazil began advising people to avoid UPFs. Other countries, including France, Belgium and Israel, followed suit. Robert F. Kennedy Jr, secretary of the US Department of Health and Human Services (HHS), has been a critic of UPFs, saying in January that they are “poisoning the American people”. In May, the US government announced plans for a research agenda to support nutrition policy and improve people’s diets, in part by improving understanding of the impacts of UPFs on health. © 2025 Springer Nature Limited

The other end of the weight spectrum: Very thin people

By Ute Eberle Before weight coach Bella Barnes consults with new clients, she already knows what they’ll say. The women struggle with their weight, naturally. But they don’t want to lose pounds. They want to gain them. Her clients find themselves too thin, and they’re suffering. “Last week, I signed up a client who wears leggings that have bum pads in them,” says Barnes, who lives in Great Britain. “I’ve had another client recently that, in summer, wears three pairs of leggings just to try and make herself look a bit bigger.” These women belong to a demographic group that has been widely overlooked. As the world focuses on its billion-plus obese citizens, there remain people at the other end of the spectrum who are skinny, often painfully so, but don’t want to be. Researchers estimate that around 1.9 percent of the population are “constitutionally thin,” with 6.5 million of these people in the United States alone. YOU MAY ALSO LIKE Conceptual illustration shows three dinner plates, two at night with crescent moons are empty, representing a nightly fast, and a third with a sun theme, full of food and representing the benefits of eating during a limited time during the day. Constitutionally thin individuals often eat as much as their peers and don’t exercise hard. Yet their body mass index is below 18.5 — and sometimes as low as 14, which translates to 72 pounds on a five-foot frame — and they don’t easily gain weight. The condition is “a real enigma,” write the authors of a recent paper in the Annual Review of Nutrition. Constitutional thinness, they say, challenges “basic dogmatic knowledge about energy balance and metabolism.” It is also understudied: Fewer than 50 clinical studies have looked at constitutionally thin people, compared with thousands on unwanted weight gain. © 2025 Annual Reviews

How to Help People Stay on Their Weight-Loss Drugs

By Joshua Cohen Roughly 40 percent of adult Americans are considered obese, and weight-loss drugs have come to play a central role in medical treatment over the past few years. As of the spring of 2024, one in eight U.S. adults had taken drugs including Wegovy, Zepbound, or Ozempic, among others, for weight loss. These products belong to a class of drugs known as glucagon-like peptide-1 agonists, or GLP-1s, which can be remarkably effective, but when patients go off GLP-1s, weight rebound occurs. And as it turns out, a relatively large portion of patients discontinue these medications within one year. Prime Therapeutics, a company that manages prescription drug coverage benefits for insurers, employers, and government programs, has been documenting this phenomenon. In 2023, the company published research indicating that merely 32 percent of patients remained on their GLP-1 at the end of one year. A follow-up analysis found that by year two, only 15 percent remained on the drug. And in a new review, the company found that only 8 percent of patients remained on the drugs after three years. The main reason for discontinuation — cited by almost half of patients in a large-scale survey — is concern about the medications’ side effects. People may quit their medication after experiencing common side effects, such as uncomfortable gastrointestinal issues. They may also quit out of fear of more serious ones, like certain cancers — although research suggests GLP-1s are associated with a lower risk for many types of cancer. Additionally, some GLP-1 users may also be at risk of nutrient deficiency and muscle or bone loss without a proper diet and exercise regimen. Health and nutrition experts suggest that optimizing the benefits conferred by GLP-1s requires lifestyle interventions aimed at modifying patient behavior. GLP-1 medicines work for weight loss by curbing hunger and slowing digestion, but they don’t replace the need for improved diet and increased physical activity. Rather, these prescription pharmaceuticals and other non-GLP-1 obesity drugs work together with nutrition and exercise to promote optimal health. In an email to Undark, Jody Dushay, an assistant professor at Harvard Medical School, wrote that “nutrition and exercise hugely benefit overall health” and increase the positive effects of the medications.

What Does It Mean To Be Thirsty?

By Dan Samorodnitsky Water is the most fundamental need for all life on Earth. Not every organism needs oxygen, and many make their own food. But for all creatures, from deep-sea microbes and slime molds to trees and humans, water is nonnegotiable. “The first act of life was the capture of water within a cell membrane,” a pair of neurobiologists wrote in a recent review. Ever since, cells have had to stay wet enough to stay alive. Water is the medium in which all chemical reactions in an organism take place, and those reactions are finely tuned to a narrow range of ratios between water and salt, another essential ingredient in life’s chemistry. The cells in your body are permeable to water, so if the water-salt balance of the surrounding fluid — blood, lymph or cerebrospinal fluid, for example — is outside its healthy range, cells can swell or shrink, shrivel or potentially burst. An imbalance can cause brain cells to malfunction, losing their ability to manage ion concentrations across their membranes and propagate action potentials. Although these effects of insufficient water are felt by every cell in the body, cells themselves do not cry out in thirst. Instead, it’s the brain that monitors the body’s water levels and manifests the experience of thirst — a dry tongue, hot throat and rapid onset of malaise — which compels a behavior: acquire water. “These neural circuits that control hunger and thirst are located deep in primitive brain structures like the hypothalamus and brainstem,” said Zachary Knight (opens a new tab), a neuroscientist at the University of California, San Francisco, who recently co-authored a review paper in Neuron (opens a new tab) on the neurobiology of thirst. Because these brain areas are difficult to study — due not only to their location, but also to their composition, with many different cell types and crisscrossed circuitry — it’s only in the last decade or so that neuroscientists have begun to understand how thirst fundamentally works. The body, researchers have found, is filled with sensors that feed clues to the brain about how much water or salt an organism needs to consume. How those sensors work, or what they even are, continues to elude scientists. Their existence offers a tantalizing insight: Water may be fundamental to life, but thirst is an educated guess. © 2025 Simons Foundation

You can't outrun a bad diet. Food — not lack of exercise — fuels obesity, study finds

Maria Godoy Back in the 1800s, obesity was almost nonexistent in the United States. Over the last century, it's become common here and in other industrialized nations, though it remains rare among people who live more traditional lifestyles, such as the Hadza hunter-gatherers of Tanzania. So what's changed? One common explanation is that as societies have developed, they've also become more sedentary, and people have gotten less active. The assumption is that as a result, we burn fewer calories each day, contributing to an energy imbalance that leads to weight gain over time, says Herman Pontzer, a professor of evolutionary biology and global health at Duke University who studies how human metabolism has evolved. Sponsor Message But in a major new study published in the journal PNAS, Pontzer and an international team of collaborators found that's not the case. They compared the daily total calorie burn for people from 34 different countries and cultures around the world. The people involved ran the spectrum from hunter-gatherers and farming populations with low obesity rates, to people in more sedentary jobs in places like Europe and the U.S., where obesity is widespread. "Surprisingly, what we find is that actually, the total calories burned per day is really similar across these populations, even though the lifestyle and the activity levels are really different," says Pontzer. And that finding offers strong evidence that diet — not a lack of physical activity — is the major driver of weight gain and obesity in our modern world. © 2025 npr

By Laura Sanders GLP-1 drugs may possess a new power: Easing migraines. In a small, preliminary study, a GLP-1 drug nearly halved the number of days people spent with a migraine in a given month. The results, presented June 21 at the European Academy of Neurology Congress in Helsinki, Finland, expand the possible benefits of the powerful new class of obesity and diabetes drugs. These pernicious, debilitating headaches are estimated to affect one billion people worldwide. Earlier studies have shown that GLP-1 agonists can reduce the pressure inside the skull, a squeeze that’s been implicated in migraines. Neurologist Simone Braca of the University of Naples Federico II in Italy and his colleagues explored whether liraglutide, an older relative of Ozempic and Wegovy, might help migraine sufferers. Thirty-one adults, 26 of them women, got daily injections of liraglutide for 12 weeks. These adults all had obesity and continued to take their current migraine medicines too. At the start of the experiment, participants had headaches on about 20 days out of a month. After 12 weeks of liraglutide, the average number dropped to about 11 days. “Basically, we observed that patients saw their days with headache halved, which is huge,” Braca says. Participants’ weight stayed about the same during the trial, suggesting that headache reductions weren’t tied to weight loss. If the results hold up in larger studies, they may point to treatments for migraine sufferers who aren’t helped by existing drugs. The results may also lead to a deeper understanding of the role of pressure inside the head in migraines, Braca says. © Society for Science & the Public 2000–2025.

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