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.

Keyword: Obesity
Link ID: 29933 - Posted: 09.20.2025

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

Keyword: Obesity
Link ID: 29930 - Posted: 09.17.2025

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

Keyword: Obesity
Link ID: 29929 - Posted: 09.17.2025

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

Keyword: Obesity
Link ID: 29916 - Posted: 09.06.2025

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.

Keyword: Obesity
Link ID: 29910 - Posted: 09.03.2025

By R. Douglas Fields It is late at night. You are alone and wandering empty streets in search of your parked car when you hear footsteps creeping up from behind. Your heart pounds, your blood pressure skyrockets. Goose bumps appear on your arms, sweat on your palms. Your stomach knots and your muscles coil, ready to sprint or fight. Now imagine the same scene, but without any of the body’s innate responses to an external threat. Would you still feel afraid? Experiences like this reveal the tight integration between brain and body in the creation of mind — the collage of thoughts, perceptions, feelings and personality unique to each of us. The capabilities of the brain alone are astonishing. The supreme organ gives most people a vivid sensory perception of the world. It can preserve memories, enable us to learn and speak, generate emotions and consciousness. But those who might attempt to preserve their mind by uploading its data into a computer miss a critical point: The body is essential to the mind. How is this crucial brain-body connection orchestrated? The answer involves the very unusual vagus nerve. The longest nerve in the body, it wends its way from the brain throughout the head and trunk, issuing commands to our organs and receiving sensations from them. Much of the bewildering range of functions it regulates, such as mood, learning, sexual arousal and fear, are automatic and operate without conscious control. These complex responses engage a constellation of cerebral circuits that link brain and body. The vagus nerve is, in one way of thinking, the conduit of the mind. How could stimulating a single nerve potentially have such wide-ranging psychological and cognitive benefits? Nerves are typically named for the specific functions they perform. Optic nerves carry signals from the eyes to the brain for vision. Auditory nerves conduct acoustic information for hearing. The best that early anatomists could do with this nerve, however, was to call it the “vagus,” from the Latin for “wandering.” The wandering nerve was apparent to the first anatomists, notably Galen, the Greek polymath who lived until around the year 216. But centuries of study were required to grasp its complex anatomy and function. This effort is ongoing: Research on the vagus nerve is at the forefront of neuroscience today. © 2025Simons Foundation

Keyword: Emotions
Link ID: 29909 - Posted: 08.30.2025

Simon Makin Andrew Moseson experienced severe depression for many years. “Some days I wasn’t able to get out bed. I had long periods of unemployment and was living in my car for a time.” He struggled to find relief, nothing worked. “I tried medications, exercise, volunteering, psychedelics. I read books about happiness, about depression,” he says. “Everything helped a little, but it was still there.” Then, in the spring of 2023, he found a clinical trial that would change his life. The trial was for people with clinical depression who, like Moseson, had not found success with existing medication. It involved faecal microbiota transplantation (FMT), in which stool from a healthy donor is transferred into a recipient’s gastrointestinal tract to restore a healthy balance of gut bacteria. The procedure did not work as well for everyone who took part in the trial, but for Moseson the results were transformative — and they came fast. “Within about a week, I started feeling better,” he says. “I felt like my brain was refreshed.” Two years later, Moseson is still taking his previously prescribed medication. “My doctor doesn’t want me to quit my antidepressants,” he says. “There’s a thought that this transplant could make antidepressants work better.” Whatever the mechanism, the change seems stark. “I feel like I’ve been cured,” Moseson says. Numerous psychiatric and neurological conditions have been linked to disturbances in people’s gut microbiota — the community of trillions of microorganisms that live symbiotically in the gastrointestinal tract. These are just correlations, but studies in rodents show compelling evidence of causality, and other animal research points to multiple pathways through which the microbiota communicates with the brain. © 2025 Springer Nature Limited

Keyword: Depression; Obesity
Link ID: 29894 - Posted: 08.20.2025

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

Keyword: Obesity
Link ID: 29887 - Posted: 08.13.2025

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

Keyword: Obesity
Link ID: 29867 - Posted: 07.26.2025

By Sofia Caetano Avritzer The original paleo diet might have included fewer succulent steaks and more juicy maggots. Neandertals are often depicted at the top of the food chain for their time, consuming as much meat as lions or hyenas. But maggots growing on rotting meat might have been the real signature dish of the Neandertal diet, researchers report July 25 in Science Advances. The idea that Neandertals were extreme carnivores comes partly from the high levels of a specific type of nitrogen called N-15 in their bones. Nitrogen has two stable forms. N-14 is lighter and a lot more common in nature, while N-15 is heavier and much rarer. When an animal eats a plant with both types of nitrogen, it will keep more N-15 than N-14 in its body after digestion. If that animal gets eaten, its predator will have an even higher proportion of N-15. That makes this molecule more prominent in animals that eat a lot of meat, says Melanie Beasley, a biological anthropologist at Purdue University in West Lafayette, Ind. The proportion of N-15 to N-14 found in Neandertal bones is similar to that found in animals like hyenas, which eat almost exclusively meat, Beasley says. But humans can’t consume as much meat as specialized carnivores, says Karen Hardy, a prehistoric archeologist at the University of Glasgow in Scotland. Without a balanced diet, the human body transforms protein into energy instead of using it to develop muscle, hormones and more. This creates toxic waste products that can cause nausea, diarrhea and even death. So, if Neandertals probably couldn’t eat as much meat as lions or hyenas, where does all the N-15 come from? Rotting meat. © Society for Science & the Public 2000–2025.

Keyword: Evolution; Obesity
Link ID: 29866 - Posted: 07.26.2025

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.

Keyword: Obesity; Pain & Touch
Link ID: 29846 - Posted: 07.02.2025

By Gordy Slack, MindSite News Lauren Kennedy West was still a teenager when she began to smell and hear things that weren’t there. Then to see things, too, that were invisible to others. Meanwhile, her moods began to intensify, sometimes turning very, very dark. “It was confusing, disturbing, and depressing,” she recalls. She had periods of elation, too. But when she came down from these, she’d keep descending until she hit emotional bottom. It got so bad that in her early 20s, at college, Kennedy West tried to end her life twice. Finally, when she was 25, she was diagnosed with schizoaffective disorder, a form of schizophrenia with powerful mood swings. The medications she was prescribed eased her worst symptoms, she said, but they also had troubling side effects that ranged from extreme weight gain and “dry mouth” to feeling lethargic and an episodic condition called oculogyric crisis which causes people to continually, involuntarily, gaze upward. Worst of all, she said, was the feeling of being “emotionally blunted.” Learning that she’d likely be taking those medications for the rest of her life was a blow, but the diagnosis gave Kennedy West a meaningful framework for her struggle. To be as stable, happy, and engaged as possible she would have to cultivate acceptance of her condition and the limitations it imposed, she was told. Driven by a hope that others might be spared the disabling confusion and depression she suffered before her diagnosis, Kennedy West and her partner started a YouTube Channel, which they called “Living Well with Mental Illness” (now “Living Well with Schizophrenia“) In frequent posts, Kennedy West recounted her own struggles and triumphs and interviewed experts on mental illness and related subjects. In early 2023, Christopher Palmer was a guest on the channel.

Keyword: Schizophrenia
Link ID: 29842 - Posted: 06.28.2025

Diana Kwon There might be a paradox in the biology of ageing. As humans grow older, their metabolisms tend to slow, they lose muscle mass and they burn many fewer calories. But certain cells in older people appear to do the exact opposite — they consume more energy than when they were young. These potential energy hogs are senescent cells, older cells that have stopped dividing and no longer perform the essential functions that they used to. Because they seem idle, biologists had assumed that zombie-like senescent cells use less energy than their younger, actively replicating counterparts, says Martin Picard, a psychobiologist at Columbia University in New York City. But in 2022, Gabriel Sturm, a former graduate student of Picard’s, painstakingly observed the life course of human skin cells cultured in a dish1 and, in findings that have not yet been published in full, found that cells that had stopped dividing had a metabolic rate about double that of younger cells. For Picard and his colleagues, the energetic mismatch wasn’t a paradox at all: ageing cells accumulate energetically costly forms of damage, such as alterations in DNA, and they initiate pro-inflammatory signalling. How that corresponds with the relatively low energy expenditure for ageing organisms is still unclear, but the researchers hypothesize that this tension might be an important driver of many of the negative effects of growing old, and that the brain might be playing a key part as mediator2. As some cells get older and require more energy, the brain reacts by stripping resources from other biological processes, which ultimately results in outward signs of ageing, such as greying hair or a reduction in muscle mass (see ‘Energy management and ageing’). Picard and his colleagues call this concept the ‘brain–body energy-conservation model’. And although many parts of the hypothesis are still untested, scientists are working to decipher the precise mechanisms that connect the brain to processes associated with ageing, such as senescence, inflammation and the shortening of telomeres — the stretches of repetitive DNA that cap the ends of chromosomes and protect them. © 2025 Springer Nature Limited

Keyword: Obesity; Stress
Link ID: 29836 - Posted: 06.18.2025

By Tina Hesman Saey People trying to lose weight often count calories, carbs, steps and reps and watch the scales. Soon, they may have another number to consider: a genetic score indicating how many calories a person needs to feel full during a meal. This score may help predict whether someone will lose more weight on the drugs liraglutide or phentermine-topiramate, researchers report June 6 in Cell Metabolism. A separate study, posted to medRXiv.org in November, suggests that individuals with a higher genetic propensity for obesity benefit less from semaglutide compared to those with a lower genetic predisposition. Such genetic tests may one day help doctors and patients select personalized weight-loss treatments, some researchers say. But the genetic scores “are not perfect predictors of drug response,” says Paul Franks, a genetic epidemiologist at Queen Mary University of London who was not involved in either study. “They show a tendency.” For the Cell Metabolism study, Mayo Clinic researchers measured how many calories it took for about 700 adults with obesity to feel full when given an all-you-can-eat meal of lasagna, pudding and milk. The calorie intake varied widely, ranging from about 140 to 2,200 calories, with men generally needing more than women. The team used machine learning to compile a genetic score based on variants of 10 genes associated with obesity. That score is designed to reflect the calories people required to feel full. Then, the Mayo team and colleagues from Phenomix Sciences Inc, headquartered in Menlo Park, Calif., conducted two clinical trials. In one 16-week trial, people with obesity received either a placebo or liraglutide­ — a GLP-1 drug branded as Saxenda. GLP-1s are a class of diabetes drugs that have shown promise with weight loss. People with a lower genetic score lost more weight on liraglutide than those with higher genetic scores. © Society for Science & the Public 2000–2025.

Keyword: Obesity; Genes & Behavior
Link ID: 29830 - Posted: 06.14.2025

Elie Dolgin Sheree had maintained a healthy weight for 15 years, thanks to a surgery that wrapped a silicone ring around the top of her stomach. But when the gastric band repeatedly slipped and had to be removed, the weight came back — fast. She gained nearly 20 kilograms in just 2 months. Frustrated, she turned to the latest generation of anti-obesity medications, hoping to slow the rapid weight gain. She cycled through various formulations of the blockbuster therapies semaglutide (sold under the brand names Ozempic and Wegovy) and tirzepatide (sold as Zepbound for weight loss), finding some success with higher doses of these drugs, which mimic the effects of the appetite-suppressing hormone GLP-1. But each time, drug shortages disrupted her treatment, forcing her to start again with a new formulation or to go without the drugs for weeks. Tired of the uncertainty around the therapies, she decided to try something different. Sheree, who asked that her middle name be used to protect her privacy, underwent two minimally invasive procedures designed to reduce the size of her stomach and to blunt hunger cues. Developed over the past two decades, these ‘endoscopic’ procedures — performed using flexible tubes inserted through the mouth, and no scalpels — are just one part of a growing toolkit to help people who want to move away from GLP-1 therapy. More-conventional bariatric surgeries, used routinely since the 1980s to reroute the flow of food through the gut or to restrict the stomach’s size, might also gain wider appeal. And the search is picking up for other drugs that could offer lasting alternatives for a post-GLP-1 population. That momentum is driven by a convergence of factors: chronic shortages of GLP-1 therapies, high costs, insurance barriers and debilitating side effects. As a result, many people who start the drugs ultimately stop — with discontinuation rates in clinical trials ranging from 37% to 81% in the first year1. And once treatment ends, the weight lost often piles back on. © 2025 Springer Nature Limited

Keyword: Obesity
Link ID: 29829 - Posted: 06.14.2025

By Amber Dance The experiment was a striking attempt to investigate weight control. For six weeks, a group of mice gorged on lard-enriched mouse chow, then scientists infected the mice with worms. The worms wriggled beneath the animals’ skin, migrated to blood vessels that surround the intestines, and started laying eggs. Bruno Guigas, a molecular biologist at the Leiden University Center for Infectious Diseases in the Netherlands, led this study some years back and the results, he says, were “quite spectacular.” The mice lost fat and gained less weight overall than mice not exposed to worms. Within a month or so, he recalls, the scientists barely needed their scale to see that the worm-infested mice were leaner than their worm-free counterparts. Infection with worms, it seems, reversed obesity, the researchers reported in 2015. While it’s true that worms gobble up food their hosts might otherwise digest, that doesn’t seem to be the only mechanism at work here. There’s also some intricate biology within the emerging scientific field of immunometabolism. Over the past couple of decades, researchers have recognized that the immune system doesn’t just fight infection. It’s also intertwined with organs like the liver, the pancreas and fat tissue, and implicated in the progression of obesity and type 2 diabetes. These and other metabolic disorders generate a troublesome immune response — inflammation — that worsens metabolism still further. Metabolic disease, in other words, is inflammatory disease. Scientists have also observed a metabolic influence of worms in people who became naturally infected with the parasites or were purposely seeded with worms in clinical trials. While the physiology isn’t fully understood, the worms seem to dampen inflammation, as discussed in the 2024 Annual Review of Nutrition.

Keyword: Obesity; Neuroimmunology
Link ID: 29828 - Posted: 06.14.2025

Myrian Wares for Quanta Magazine You’ve just gotten home from an exhausting day. All you want to do is put your feet up and zone out to whatever is on television. Though the inactivity may feel like a well-earned rest, your brain is not just chilling. In fact, it is using nearly as much energy as it did during your stressful activity, according to recent research. Sharna Jamadar (opens a new tab), a neuroscientist at Monash University in Australia, and her colleagues reviewed research from her lab and others around the world to estimate the metabolic cost of cognition (opens a new tab) — that is, how much energy it takes to power the human brain. Surprisingly, they concluded that effortful, goal-directed tasks use only 5% more energy than restful brain activity. In other words, we use our brain just a small fraction more when engaging in focused cognition than when the engine is idling. It often feels as though we allocate our mental energy through strenuous attention and focus. But the new research builds on a growing understanding that the majority of the brain’s function goes to maintenance. While many neuroscientists have historically focused on active, outward cognition, such as attention, problem-solving, working memory and decision-making, it’s becoming clear that beneath the surface, our background processing is a hidden hive of activity. Our brains regulate our bodies’ key physiological systems, allocating resources where they’re needed as we consciously and subconsciously react to the demands of our ever-changing environments. “There is this sentiment that the brain is for thinking,” said Jordan Theriault (opens a new tab), a neuroscientist at Northeastern University who was not involved in the new analysis. “Where, metabolically, [the brain’s function is] mostly spent on managing your body, regulating and coordinating between organs, managing this expensive system which it’s attached to, and navigating a complicated external environment.” © 2025 Simons Foundation.

Keyword: Attention; Brain imaging
Link ID: 29825 - Posted: 06.07.2025

Anna Bawden Health and social affairs correspondent Weight loss drugs could at least double the risk of diabetic patients developing age-related macular degeneration, a large-scale study has found. Originally developed for diabetes patients, glucagon-like peptide-1 receptor agonist (GLP-1 RA) medicines have transformed how obesity is treated and there is growing evidence of wider health benefits. They help reduce blood sugar levels, slow digestion and reduce appetite. But a study by Canadian scientists published in Jama Ophthalmology has found that after six months of use GLP-1 RAs are associated with double the risk of older people with diabetes developing neovascular age-related macular degeneration compared with similar patients not taking the drugs. Academics at the University of Toronto examined medical data for more than 1 million Ontario residents with a diagnosis of diabetes and identified 46,334 patients with an average age of 66 who were prescribed GLP-1 RAs. Nearly all (97.5%) were taking semaglutide, while 2.5% were on lixisenatide. The study did not exclude any specific brand of drugs, but since Wegovy was only approved in Canada in November 2021, primarily for weight loss, it is likely the bulk of semaglutide users in the study were taking Ozempic, which is prescribed for diabetes. Each patient on semaglutide or lixisenatide was matched with two patients who also had diabetes but were not taking the drugs, who shared similar characteristics such as age, gender and health conditions. The researchers then compared how many patients developed neovascular age-related macular degeneration over three years. © 2025 Guardian News & Media Limited

Keyword: Vision; Obesity
Link ID: 29822 - Posted: 06.07.2025

By Abby Ellin Sally Odenheimer starved herself because she was an athlete and thought she’d run faster on an empty stomach. Karla Wagner starved herself because she wanted to be in charge of at least one aspect of her life. Janice Bremis simply felt too fat. They all sought perfection and control. Not eating helped. They are women in their 60s and 70s who have struggled with anorexia nervosa since childhood or adolescence. Years later, their lives are still governed by calories consumed, miles run, laps swum, pounds lost. “It’s an addiction I can’t get rid of,” said Ms. Odenheimer, 73, a retired teacher who lives outside Denver. For decades, few people connected eating disorders with older people; they were seen as an affliction of teenage girls and young women. But research suggests that an increasing number of older women have been seeking treatment for eating disorders, including bulimia, binge eating disorder (known as BED) and anorexia, which has the highest mortality rate of any psychiatric disorder, and brings with it an elevated risk of suicide. In a 2017 paper in the journal BMC Medicine, researchers reported that more than 15 percent of 5,658 women surveyed met the criteria for a lifetime eating disorder while in their 30s and 40s. A 2023 review of recent research reported that the prevalence rates among women 40 and older with full diagnoses of eating disorders were between 2.1 and 7.7 percent. (For men, they were less than 1 percent.) © 2025 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 29816 - Posted: 06.04.2025

Anna Bawden in Málaga and agency Giving obese children weight loss jabs works and could help avoid arguments over mealtimes, according to research. Clinicians treating very obese children at a hospital in Sweden analysed whether liraglutide injections could be used as well as diet and lifestyle changes to increase weight loss. In real-life analysis of 1,000 children under 16 with severe obesity over a number of years, about a quarter of patients in 2023 were given the weight loss drug liraglutide in addition to receiving intensive health behaviour and lifestyle treatment at the National Childhood Obesity Centre in Stockholm. The clinicians found that nearly a third of these children dropped enough weight to improve their health, compared with about 27% in earlier treated groups with no access to the drugs. Patients starting the programme in 2024 have been given semaglutide but results from these children are not yet available. Semaglutide, better known as Wegovy, and liraglutide, sold as Saxenda, are both GLP-1 receptor agonists, which help curb appetite. In the UK they are available on the NHS only for adults with a BMI above 35 with a weight-related condition, although in certain circumstances specialist paediatric clinics can prescribe them. Dr Annika Janson, of Karolinska university hospital in Sweden, the lead author of the study, whose findings were presented at the European Congress on Obesity, said the beneficial impact of weight loss jabs on children’s weight could accelerate in future years. © 2025 Guardian News & Media Limited

Keyword: Obesity
Link ID: 29786 - Posted: 05.14.2025