Ian Sample Science editor Losing weight can be a frustrating game: after months of successful slimming, the kilos may soon pile on again, leaving people back where they started. No one factor drives the yo-yo effect, but new research points to fatty tissue as a leading culprit. Fat “remembers” past obesity and resists attempts to lose weight, scientists found. Researchers identified the biological memory after examining fat tissue from people with obesity before and after they lost weight after bariatric surgery. The tissues were further compared with fat from healthy individuals who had never been obese. The analysis showed that fat cells were affected by obesity in a way that altered how they responded to food, potentially for years. In tests, the cells grew faster than others by absorbing nutrients more swiftly. Prof Ferdinand von Meyenn, a senior author on the study at the Federal Institute of Technology in Zurich, said: “Our study indicates that one reason maintaining body weight after initial weight loss is difficult is that the fat cells remember their prior obese state and likely aim to return to this state. “The memory seems to prepare cells to respond quicker, and maybe also in unhealthy ways, to sugars or fatty acids.” Further work on mouse cells traced the biological memory to chemical modifications on DNA or the proteins DNA is wrapped around. These epigenetic changes alter gene activity and metabolism. Writing in Nature, the scientists describe how formerly obese mice gained weight faster than others when put on a high-fat diet, suggesting a shift in metabolism that made it easier for them to gain weight. The memory of obesity in fat cells was not solely to blame, however. The scientists suspect a similar memory exists in brain cells that affects how much food animals consume and how much energy they expend. © 2024 Guardian News & Media Limited

Keyword: Obesity
Link ID: 29568 - Posted: 11.20.2024

By Kim Tingley There are two opposite paths to achievement in science. The first is straightforward: Identify a problem and set about solving it. The second is rather unscientific-sounding and perhaps more faith-based: Study in obscurity and hope serendipity strikes. In 1980, a young gastroenterologist named Jean-Pierre Raufman wound up taking the latter road through the digestive-diseases branch of the National Institutes of Health. His goal there was to gain research experience. While doing so, he chanced to meet the lead chemist of another laboratory, John Pisano, who had a passion for seeking out new and interesting examples of a specific kind of hormone, called a peptide, in animal venoms. Pisano regularly appealed to local insect and reptile enthusiasts in the classified pages of The Washington Post; in response, they would show up at his office door carrying plastic bags wriggling with possibility. Pisano offered some venom samples to Raufman for his meandering analyses. Over the following month, Raufman experimented with them to see if they stimulated pancreatic cells harvested from guinea pigs. The venom with the biggest effect by far came from a desert reptile that Raufman had never heard of: the Gila monster. Gila monsters — sluggish, thick-tailed ground dwellers — are native to southern Arizona and northern Mexico. They have blunt noses and bumpy black skin with tan, pink or orange squiggles. They spend 95 percent of their lives underground. Like their cousins to the south, Mexican beaded lizards, they are one of the very few lizard species that produces venom, which they excrete from mouth glands into grooves in their serrated teeth. The strength of their jaws is typically enough to subdue their prey (chicks, frogs, worms and the like). But if threatened and unable to escape or hide, they may bite a predator. Whenever they clamp down, piercing the skin, venom enters the victim’s bloodstream. This causes intense pain and can initiate a cascade of other symptoms that, in people, includes vomiting, dizziness, rapid heart rate, low blood pressure and, in rare circumstances, death. © 2024 The New York Times Company

Keyword: Neurotoxins; Obesity
Link ID: 29555 - Posted: 11.13.2024

By Shaena Montanari In the Sterling Hall of Medicine at Yale University, a sign on a walk-in refrigerator door tells people to keep their voices down. Inside, about 250 ground squirrels are hibernating, each surrounded by shredded paper fluff and curled up in a clear plastic box. Shelves lined with these makeshift nests are bathed in red light that only the researchers can see, leaving the motionless animals in complete darkness. From about September to April—roughly the hibernation season for these thirteen-lined ground squirrels, which have stripes reminiscent of a chipmunk—the temperature inside the homemade hibernaculum is set at 4 degrees Celsius. The tiny rodents’ body temperature is the same as the chilly air, and their breathing and heart rates slow to just a handful of breaths and beats per minute—an energy-conserving response known as torpor. Scientists have studied this extreme physiological state for more than a century, says Elena Gracheva, whose bustling lab sits just outside the silent hibernaculum. But to date, they have focused mainly on physiological changes in individual peripheral organs that help an animal survive in cold temperatures. It is still unknown how the central nervous system regulates the process, she says. “We know a lot about physiology, but we don’t know the molecular basis.” Gracheva, professor of physiology and neuroscience at Yale University, is part of a small cadre of scientists who have set their sights on revealing those neural hibernation controls, using advanced tools to explore how the brain and other organ systems work together to maintain homeostasis. Their efforts are opening a “new era” in hibernation research, says Shona Wood, associate professor of Arctic chronobiology and physiology at the Arctic University of Norway. © 2024 Simons Foundation

Keyword: Sleep
Link ID: 29550 - Posted: 11.09.2024

By Skyler Ware The occasional sweet treat likely won’t ruin your health. But too much added sugar at a young age could increase the risk of health complications later in life. Limiting added sugars during the first 1,000 days after conception — so during pregnancy and a baby’s first two years — reduces the risk of a child developing diabetes and hypertension in adulthood, researchers report October 31 in Science. “In the first 1,000 days of life, the brain and body are gearing up to finish developing,” says Sue-Ellen Anderson-Haynes, a registered dietician in Boston and a spokesperson for the Academy of Nutrition and Dietetics. Nutrition during that timeframe is particularly important, she says, because “everything the mother eats gets transformed into nutrients for the fetus.” Current nutritional guidelines recommend that adults consume less than 40 grams of added sugars per day and that children under age 2 consume no added sugars. But by age 2, the average American child consumes about 29 grams of added sugars a day; the average adult consumes nearly 80 grams per day. To study the effects of excess added sugars early in life, economist Tadeja Gracner of the University of Southern California in Los Angeles and colleagues took advantage of a natural experiment: the end of sugar rationing in the United Kingdom after World War II. While rationing was in effect, each person was allotted about 8 ounces (about 227 grams) of sugar per week. Once sugar rationing ended in September 1953, daily sugar consumption for adults jumped to around 80 grams per day. Even though other foods were rationed during and after WWII, sugar intake increased the most after rationing was lifted. Consumption of other rationed foods, such as cheese, milk and fresh fruits remained relatively constant once rationing ended. Similarly, the end of butter rationing caused many families to switch from margarine, with its unsaturated fats, back to butter, so overall fat consumption did not increase significantly. © Society for Science & the Public 2000–2024

Keyword: Obesity
Link ID: 29538 - Posted: 11.02.2024

By Mariana Lenharo Feeding a baby born by caesarean section milk containing a tiny bit of their mother’s poo introduces beneficial microbes to their gut, according to a clinical trial. The approach might one day help to prevent diseases during childhood and later in life. The study — which reported early results last week during IDWeek, a meeting of infectious-disease specialists and epidemiologists in Los Angeles, California — is the first randomized controlled trial to test the ‘poo milkshake’ concept. The preliminary findings confirm researchers’ hypothesis that a small faecal-matter transplant is enough to have a positive effect on the infant’s microbiome, says Otto Helve, director of the public-health department at the Finnish Institute for Health and Welfare in Helsinki, Finland, and the study’s primary investigator. Inherited microbes Some studies show that babies born by c-section, rather than vaginal birth, have a higher risk of asthma, inflammation of the digestive system and other diseases associated with a dysfunctional immune system1. Scientists think that these differences arise because babies born by c-section aren’t exposed to and rapidly colonized by the microbes in their mothers’ vaginas and guts. Studies have even shown that c-section babies are more vulnerable to pathogens in hospitals than are babies born by vaginal birth2. Experiments have attempted to compensate for that by swabbing babies born by c-section with microbes from their mother’s vagina or giving them these microbes orally, a practice known as ‘vaginal seeding’. But this technique has had limited success, because vaginal microbes, scientists have learnt, cannot effectively colonize infants’ guts, says Yan Shao, a microbiome scientist at the Wellcome Sanger Institute in Hinxton, UK. © 2024 Springer Nature Limited

Keyword: Obesity; Development of the Brain
Link ID: 29525 - Posted: 10.26.2024

By Elie Dolgin Cutting calorie intake can lead to a leaner body — and a longer life, an effect often chalked up to the weight loss and metabolic changes caused by consuming less food. Now, one of the biggest studies1 of dietary restrictions ever conducted in laboratory animals challenges the conventional wisdom about how dietary restriction boosts longevity. The study, involving nearly 1,000 mice fed low-calorie diets or subjected to regular bouts of fasting, found that such regimens do indeed cause weight loss and related metabolic changes. But other factors — including immune health, genetics and physiological indicators of resiliency — seem to better explain the link between cutting calories and increased lifespan. “The metabolic changes are important,” says Gary Churchill, a mouse geneticist at the Jackson Laboratory in Bar Harbor, Maine, who co-led the study. “But they don’t lead to lifespan extension.” To outside investigators, the results drive home the intricate and individualized nature of the body’s reaction to caloric restriction. “It’s revelatory about the complexity of this intervention,” says James Nelson, a biogerontologist at the University of Texas Health Science Center in San Antonio. The study was published today in Nature by Churchill and his co-authors, including scientists at Calico Life Sciences in South San Francisco, California, the anti-ageing focused biotech company that funded the study. Counting calories Scientists have long known that caloric restriction, a regimen of long-term limits on food intake, lengthens lifespan in laboratory animals2. Some studies3,4 have shown that intermittent fasting, which involves short bouts of food deprivation, can also increase longevity. © 2024 Springer Nature Limited

Keyword: Obesity
Link ID: 29516 - Posted: 10.12.2024

By Giorgia Guglielmi As the famed tale “Hansel and Gretel” makes clear, hunger can change behavior. The two lost and starving siblings give in to the temptation of a gingerbread cottage and ignore the danger lurking within—a wicked witch who has created the delicious house as a trap. Hunger is such a powerful driver that animals often pursue food at the expense of other survival needs, such as avoiding predators or recovering from injury. Hungry vicuñas, for example, will sometimes increase their risk of predation by pumas to get something to eat, behavioral ecologists have shown. Scientists know many of the key cells and circuits behind these competing drives—such as the hypothalamic “hunger neurons” that regulate food intake. But how the brain juggles the need to eat amidst other urges has remained mysterious, says Henning Fenselau, who leads the Synaptic Transmission in Energy Homeostasis group at the Max Planck Institute for Metabolism Research in Köln, Germany. “This is still a huge question [in neuroscience],” he says. In recent years, however, new clues about where and how hunger collides with rival motivations have come from technology to manipulate and monitor individual neurons across multiple brain regions at once. Those findings suggest that hunger neuron activity can override some brain signals, such as fear and pain. Exploring the brain’s ability to handle multiple needs simultaneously may offer insights into decision-making, anxiety and other neuropsychiatric conditions—helping to explain why people sometimes make maladaptive choices, says Nicholas Betley, associate professor of biology at the University of Pennsylvania. © 2024 Simons Foundation

Keyword: Obesity; Attention
Link ID: 29515 - Posted: 10.12.2024

By Mariana Lenharo There’s a bar in Baltimore, Maryland, that very few people get to enter. It has a cocktail station, beer taps and shelves stacked with spirits. But only scientists or drug-trial volunteers ever visit, because this bar is actually a research laboratory. Here, in a small room at the US National Institutes of Health (NIH), scientists are harnessing the taproom ambience to study whether blockbuster anti-obesity drugs might also curb alcohol cravings. Evidence is mounting that they could. Animal studies and analyses of electronic health records suggest that the latest wave of weight-loss drugs — known as glucagon-like peptide 1 (GLP-1) receptor agonists — cut many kinds of craving or addiction, from alcohol to tobacco use. “We need randomized clinical trials as the next step,” says Lorenzo Leggio, an addiction researcher at the NIH in Baltimore. In the trial he is leading, volunteers sit at the bar and get to see, smell and hold their favourite drinks, while going through tests such as questions about their cravings; separately, participants will have their brains scanned while looking at pictures of alcohol. Some will be given the weight-loss drug semaglutide (marketed as Wegovy) and others will get a placebo. George Koob and Lorenzo Leggio pose for a photograph in a research laboratory designed as a bar inside the National Institutes of Health’s hospital. Curbing addiction isn’t the only potential extra benefit of GLP-1 drugs. Other studies have suggested they can reduce the risk of death, strokes and heart attacks for people with cardiovascular disease1 or chronic kidney ailments2, ease sleep apnoea symptoms3 and even slow the development of Parkinson’s disease4. There are now hundreds of clinical trials testing the drugs for these conditions and others as varied as fatty liver disease, Alzheimer’s disease, cognitive dysfunction and HIV complications (see ‘Diseases that obesity drugs might treat’ at the end of this article). © 2024 Springer Nature Limited

Keyword: Obesity; Drug Abuse
Link ID: 29494 - Posted: 09.25.2024

By Max Kozlov A build-up of sticky goo that traps neurons in an appetite-control centre in the brain has been implicated in worsening diabetes and obesity, according to research on mice1. The goo also prevents insulin from reaching brain neurons that control hunger. Inhibiting production of the goo led mice to lose weight, experiments found. These findings points to a new driver of metabolic disorders and could help scientists to identify targets for drugs to treat these conditions. These results were published today in Nature. Metabolic diseases such as type 2 diabetes and obesity can develop when the body’s cells become insensitive to insulin, a hormone that regulates blood-sugar levels. Scientists searching for the mechanism that causes this insulin resistance have homed in on a part of the brain called the arcuate nucleus of the hypothalamus, which senses insulin levels and, in response, adjusts energy expenditure and sensations of hunger. As the animals develop insulin resistance, a type of cellular scaffolding, called the extracellular matrix, that holds the hunger neurons in place becomes a disorganized goo. Previously, researchers had noticed that this scaffolding changes when mice are fed a high-fat diet2. The researchers wanted to see whether these brain changes might drive insulin resistance rather than merely developing alongside it. The authors fed mice a high-fat, high-sugar diet for 12 weeks and monitored the scaffolding around the hunger neurons by taking tissue samples and monitoring gene activity. © 2024 Springer Nature Limited

Keyword: Obesity
Link ID: 29489 - Posted: 09.21.2024

By Gina Kolata and Stephanie Nolen The Lasker Awards, a prestigious set of prizes given for advances in medicine and public health research, were given on Thursday to scientists whose research helped lead to the discovery of a new class of obesity drugs, infectious disease specialists who worked on the drivers of H.I.V. infection and how to stop it, and a scientist who discovered a way the body protects itself from infectious diseases and cancer. The Laskers are highly regarded in the fields of biomedicine and are sometimes seen as foretelling recipients of the Nobel Prizes in the sciences. This year’s Lasker-DeBakey Clinical Medical Research Award went to three scientists for their work on GLP-1, the hormone that led to drugs like Wegovy (the same compound is the basis for Ozempic), which have transformed the treatment of obesity. They are Dr. Joel Habener, Svetlana Mojsov and Lotte Bjerre Knudsen. Each of the three honorees played a role at a key moment: finding the new hormone; finding the biologically active shorter form of GLP-1; and, finally, showing that the shorter form elicits weight loss. Of course, as almost always happens in science, many others also played key roles, and the Lasker Foundation mentioned some as part of its citation. And one of the honorees, Dr. Mojsov, is receiving what many deem a long overdue recognition. The story of GLP-1 begins with Dr. Habener, an endocrinologist who arrived in the mid-1970s at Massachusetts General Hospital, where he decided to work on diabetes. Most of the focus had been on insulin, which lowers blood sugar levels. But there is another hormone, glucagon, that raises it. Dr. Habener decided to try to find the gene for glucagon, hoping it would lead to a way to squelch the hormone and so lower blood sugar. Working with anglerfish, he discovered a gene for another mysterious protein that resembles glucagon. © 2024 The New York Times Company

Keyword: Obesity; Neuroimmunology
Link ID: 29488 - Posted: 09.21.2024

By Daniela J. Lamas In the near future, the story of drugs like Ozempic may no longer be primarily about weight loss and diabetes. We now know that these drugs can reduce heart and kidney disease. They could very well slow the progression of dementia. They might help women struggling with infertility to get pregnant. They are even tied to lower mortality from Covid. It’s easy to attribute this to the dramatic weight loss provided by Ozempic and other drugs in its class, known as GLP-1 receptor agonists. But that isn’t the whole story. Rather, the drugs’ numerous benefits are pointing to an emerging cause of so much human disease: inflammation. As a critical care doctor, I have long considered inflammation a necessary evil, the mechanism through which our bodies sound an alarm and protect us from threat. But a growing body of research complicates that understanding. Inflammation is not just a marker of underlying disease but also a driver of it. The more medicine learns about inflammation, the more we are learning about heart disease and memory loss. This should serve as a reminder of the delicate balance that exists in our bodies, of the fact that the same system that protects us can also cause harm. Inflammation is the body’s response to infection or injury. Our innate immune system — the body’s first line of defense against bacterial or viral intruders — protects us by triggering an inflammatory response, a surge of proteins and hormones that fight infection and promote healing. Without that response, we would die of infectious disease in childhood. But by the time we make it to our 50s and beyond, our innate immune system can become more of a hindrance as inflammation begins to take a toll on the body. Acute inflammation, which happens in response to an illness, for instance, is often something we can see — an infected joint is swollen and red. But chronic inflammation is usually silent. Like high blood pressure, it’s an invisible foe. Sign up for the Opinion Today newsletter Get expert analysis of the news and a guide to the big ideas shaping the world every weekday morning. Get it sent to your inbox. © 2024 The New York Times Company

Keyword: Obesity
Link ID: 29487 - Posted: 09.21.2024

By Julian Nowogrodzki Millions of adults around the world take potent drugs such as Wegovy to shed pounds. Should kids do the same? That question is growing more urgent in the face of mounting evidence that children and adolescents, as well as adults, slim down if they take the latest generation of obesity drugs. Clinical trials1,2 have shown that many adolescents with obesity lose substantial amounts of weight on these drugs, which work by mimicking a natural hormone called glucagon-like peptide 1 (GLP-1). The GLP-1 mimics semaglutide, commonly sold as Ozempic and Wegovy, and liraglutide, marketed as Saxenda and Victoza, are approved in the United States and Europe to treat obesity in children as young as 12. Now a trial has produced some of the first data on anti-obesity drugs in even younger children: those aged 6 to 11. The study3 reports that children who were treated with liraglutide showed a decrease in their body mass index (BMI), a measure of obesity. The results were published on 10 September in The New England Journal of Medicine. Nature asked specialists in obesity about the costs and benefits of giving the GLP-1 mimics to youngsters who are still growing and developing. Why test powerful weight-loss drugs on kids? Most kids with obesity become teens with obesity and then adults with obesity. Many young children with severe obesity have “already developed significant health issues”, says physician Sarah Ro, who directs the University of North Carolina Physicians Network Weight Management Program and has served as a consultant to Novo Nordisk, the manufacturer of semaglutide. Her clinic in Hillsborough treats children with severe obesity who have health issues such as high blood pressure, type 2 diabetes or an advanced form of liver disease linked to excess weight. © 2024 Springer Nature Limited

Keyword: Obesity; Development of the Brain
Link ID: 29482 - Posted: 09.18.2024

By Max Kozlov A low-cost diabetes drug slows ageing in male monkeys and is particularly effective at delaying the effects of ageing on the brain, finds a small study that tracked the animals for more than three years1. The results raise the possibility that the widely used medication, metformin, could one day be used to postpone ageing in humans. Monkeys that received metformin daily showed slower age-associated brain decline than did those not given the drug. Furthermore, their neuronal activity resembled that of monkeys about six years younger (equivalent to around 18 human years) and the animals had enhanced cognition and preserved liver function. This study, published in Cell on 12 September, helps to suggest that, although dying is inevitable, “ageing, the way we know it, is not”, says Nir Barzilai, a geroscientist at the Albert Einstein College of Medicine in New York City, who was not involved in the study. Metformin has been used for more than 60 years to lower blood-sugar levels in people with type 2 diabetes — and is the second most-prescribed medication in the United States. The drug has long been known to have effects beyond treating diabetes, leading researchers to study it against conditions such as cancer, cardiovascular disease and ageing. Data from worms, rodents, flies and people who have taken the drug for diabetes suggest the drug might have anti-ageing effects. But its effectiveness against ageing had not been tested directly in primates, and it is unclear whether its potential anti-ageing effects are achieved by lowering blood sugar or through a separate mechanism. This led Guanghui Liu, a biologist who studies ageing at the Chinese Academy of Sciences in Beijing, and his colleagues to test the drug on 12 elderly male cynomolgus macaques (Macaca fasciucularis); another 16 elderly monkeys and 18 young or middle-aged animals served as a control group. Every day, treated monkeys received the standard dose of metformin that is used to control diabetes in humans. The animals took the drug for 40 months, which is equivalent to about 13 years for humans. © 2024 Springer Nature Limited

Keyword: Development of the Brain; Obesity
Link ID: 29481 - Posted: 09.14.2024

By Roni Caryn Rabin Move over, body mass index. Make room for roundness — to be precise, the body roundness index. The body mass index, or B.M.I., is a ratio of height to weight that has long been used as a medical screening tool. It is one of the most widely used health metrics but also one of the most reviled, because it is used to label people overweight, obese or extremely obese. The classifications have been questioned by athletes like the American Olympic rugby player Ilona Maher, whose B.M.I. of 30 technically puts her on the cusp of obesity. “But alas,” she said on Instagram, addressing online trolls who tried to shame her about her weight, “I’m going to the Olympics and you’re not.” Advocates for overweight individuals and people of color note that the formula was developed nearly 200 years ago and based exclusively on data from men, most of them white, and that it was never intended for medical screening. Even physicians have weighed in on the shortcomings of B.M.I. The American Medical Association warned last year that B.M.I. is an imperfect metric that doesn’t account for racial, ethnic, age, sex and gender diversity. It can’t differentiate between individuals who carry a lot of muscle and those with fat in all the wrong places. “Based on B.M.I., Arnold Schwarzenegger when he was a bodybuilder would have been categorized as obese and needing to lose weight,” said Dr. Wajahat Mehal, director of the Metabolic Health and Weight Loss Program at Yale University. “But as soon as you measured his waist, you’d see, ‘Oh, it’s 32 inches.’” So welcome a new metric: the body roundness index. B.R.I. is just what it sounds like — a measure of how round or circlelike you are, using a formula that takes into account height and waist, but not weight. © 2024 The New York Times Company

Keyword: Obesity
Link ID: 29471 - Posted: 09.07.2024

By Max Kozlov A black and gold fork, knife and spoon lay on a pale blue plate over a white background in harsh sunlight Some of the health benefits of fasting kick in when food consumption resumes, animal experiments show.Credit: Getty Breaking a fast carries more health benefits than the fasting itself, a study in mice shows1. After mice had abstained from food, stem cells surged to repair damage in their intestines — but only when the mice were tucking into their chow again, the study found. But this activation of stem cells came at a price: mice were more likely to develop precancerous polyps in their intestines if they incurred a cancer-causing genetic change during the post-fasting period than if they hadn’t fasted at all. These results, published in Nature on 21 August, show that “regeneration isn’t cost-free”, says Emmanuelle Passegué, a stem-cell biologist at Columbia University Irving Medical Center in New York City, who wasn’t involved in the study. “There is a dark side that is important to consider.” Fast way to health Researchers have been investigating the potential health benefits of fasting for decades, and there is evidence that the practice can help to delay certain diseases and lengthen lifespan in rodents. But the underlying biological mechanisms behind these benefits have been a mystery. In 2018, Ömer Yilmaz, a stem-cell biologist at the Massachusetts Institute of Technology in Cambridge, and his colleagues found that stem cells are likely to be implicated. During fasting, these cells begin burning fats rather than carbohydrates as an energy source, leading to a boost in their ability to repair damage to the intestines in mice2. © 2024 Springer Nature Limited

Keyword: Obesity
Link ID: 29448 - Posted: 08.22.2024

By Ashley Andreou “I still don’t trust my parents’ ability to feed me,” confessed Sofia after I asked what she was most anxious about, nearing discharge after two months on an inpatient eating disorders unit where I worked as a psychiatry resident. The 14-year-old girl was brought to the pediatrician by her parents, worried about her eating. They learned that Sofia (whose name has been changed for her privacy) had lost 30 pounds over three months—she was eating only one piece of fruit a day in the weeks leading up to her admission. She could barely walk home from school, her menses ceased, her hair fell out in clumps, and her heart rate dangerously slowed. But Sofia was not the patient that people often envision with an eating disorder. Her family was Spanish-speaking and had emigrated from Peru. Her confession contained both her fears about losing control of her eating as well as real concern for her life after leaving the hospital. Her deeply caring family struggled with family sessions during her inpatient treatment, complicated by the need for interpreters, a prescribed inpatient diet that differed from the meals typically eaten at home, and a hesitancy to ask questions of the health care team. While Sofia was successfully restored to a healthy weight at discharge from the hospital, finding appropriate outpatient treatment presented yet another challenge. Family-based treatment is a standardized outpatient therapy, which aims to restore adolescent patients to a healthy weight with the support of their parents; the therapy consists of three phases where the parents begin with most of the feeding responsibility, and the patient gradually gains more autonomy as they become renourished. It is the gold standard for adolescent outpatient therapy. However, Medicaid did not fully cover most of these programs, and finding one with a Spanish-speaking therapist was even rarer. Despite a social worker’s efforts, Sofia was wait-listed for a family treatment program with a Spanish-speaking provider who offered sliding-scale payment. © 2024 SCIENTIFIC AMERICAN

Keyword: Anorexia & Bulimia
Link ID: 29437 - Posted: 08.19.2024

By Erin Garcia de Jesús An appetite-stimulating protein can reverse anorexia in mice. Mice with lack of appetite and weight loss — symptoms similar to people with anorexia — that were genetically tweaked to secrete a protein called ACBP ate more food and weighed more than anorexic animals with an ACBP deficit, researchers report August 14 in Science Translational Medicine. The finding points to a potential treatment target for people with the eating disorder. “Anorexia is a whole brain and body illness” that is difficult to treat, says psychiatrist and neuroscientist Rachel Ross, who wasn’t involved with the new work. “One of the major challenges is that the brain of a person with anorexia is directly fighting against their body.” While the body screams for food, the brain prioritizes the need to restrict weight (SN: 7/26/13). Globally, around 1 percent of women and 0.2 percent of men develop the disorder. Roughly just a third of those people fully recover. Yet, no drugs are available; treatment typically involves medical care to stabilize weight and therapy to mend patients’ relationships with food. Some cancer patients can also develop a similar disorder called cancer cachexia, which comes from an impaired metabolism, that is similarly tough to treat (SN: 7/30/24). “Anything that has the potential to provide some sort of mechanism that would be useful for creating a new therapeutic is huge,” says Ross, of Albert Einstein College of Medicine and Montefiore Health System in New York City. And although there’s no guarantee the results will apply to people, the new findings suggest that ACBP, a protein that helps turn on parts of the brain that arouse appetite, may have that potential. © Society for Science & the Public 2000–2024.

Keyword: Obesity; Hormones & Behavior
Link ID: 29435 - Posted: 08.15.2024

By Gina Kolata People with obesity now have a choice between two powerful drugs to help them lose weight. One is semaglutide, sold by Novo Nordisk as Wegovy for obesity treatment and as Ozempic for diabetes. The second, tirzepatide, is sold by Eli Lilly as Zepbound for obesity and as Mounjaro for diabetes. Many with neither obesity or diabetes take the drugs to get thinner. A recent study suggested that people lost more weight taking Mounjaro than they did taking Ozempic, and it may leave you wondering: Which should I take? And if I’m already taking one of them, should I switch? The answers, obesity medicine experts say, are not so simple. Here are some factors that can help sort out hype from realistic hope. Is one weight loss drug really better than the other? For now, it’s hard to say. All of the information available comes from “highly flawed studies,” said Dr. Diana Thiara, medical director of the weight loss clinic at the University of California, San Francisco. That includes the recent study comparing Mounjaro and Ozempic. Using electronic health records, the researchers reported that those taking Mounjaro lost an average of 15.3 percent of their weight after a year. Those taking Ozempic lost an average of 8.3 percent. While that sounds impressive, Dr. Susan Z. Yanovski, co-director of the Office of Obesity Research at the National Institute of Diabetes and Digestive and Kidney Diseases, said, “I wouldn’t make any decisions on my medical care based solely on a study like this.” There’s an inherent difficulty in using electronic health records, she noted, because it is not known why the patients were taking the drugs — the study was underway before Zepbound was approved for treating obesity. The investigators looked at prescriptions for Ozempic and Mounjaro, which were approved to treat diabetes. Yet many in the study did not have diabetes. © 2024 The New York Times Company

Keyword: Obesity
Link ID: 29402 - Posted: 07.23.2024

By Mitch Leslie Millions of people have taken glucagon-like peptide-1 (GLP-1) agonist drugs such as Ozempic to lose weight, despite the fact that the drugs can cause severe nausea and vomiting. But a new mouse study shows distinct groups of neurons in the brain diminish appetite and trigger nausea, a finding that could lead to less stomach-turning treatments that activate one set of cells and not the other. “It’s a very solid paper,” says neuroscientist Chuchu Zhang of the University of California, Los Angeles, who wasn’t connected to the study. “It shows us something new” about the activity of GLP-1 agonists. Scientists haven’t pinned down exactly how GLP-1 agonist drugs work, and previous studies have produced conflicting results on where they exert their effects. Some research suggests the drugs curb appetite by targeting the hypothalamus, a control center for physiological functions such as thirst and hunger that is located in the center of the brain. Other findings point to the rear portion of the brain, known as the hindbrain, and still others implicate the vagus nerve, which carries messages to and from organs such as the stomach and heart. All of these locations contain cells bearing GLP-1 receptors, to which the drugs bind. Another key question is whether the drugs cause weight loss primarily because people feel full or because they feel nauseated—a side effect suffered by more than half of individuals who take the drugs. “Do we need the nausea and aversion [to food] to see the appetite suppression and weight loss?” asks neuroscientist Amber Alhadeff of the Monell Chemical Senses Center. To answer that question, she and her colleagues first tried to pinpoint where GLP-1 agonists act. Using a genetically modified virus containing genes for either of two cell-killing molecules, they selectively eliminated cells bearing GLP-1 receptors in the hypothalamus, the hindbrain, or the vagus nerve. Only destroying the hindbrain cells prevented weight loss when mice received a GLP-1 agonist, suggesting this region curtails appetite. In a follow-up experiment, the researchers stimulated cells in the hindbrain and found that even slender mice lost weight. © 2024 American Association for the Advancement of Science.

Keyword: Obesity
Link ID: 29390 - Posted: 07.11.2024

By Teddy Rosenbluth The process for diagnosing a child with autism heavily relies on a parent's description of their child’s behavior and a professional’s observations. It leaves plenty of room for human error. Parents’ concerns may skew how they answer questionnaires. Providers may hold biases, leading them to underdiagnose certain groups. Children may show widely varying symptoms, depending on factors like culture and gender. A study published Monday in Nature Microbiology bolsters a growing body of research that suggests an unlikely path to more objective autism diagnoses: the gut microbiome. After analyzing more than 1,600 stool samples from children ages 1 to 13, researchers found several distinct biological “markers” in the samples of autistic children. Unique traces of gut bacteria, fungi, viruses and more could one day be the basis of a diagnostic tool, said Qi Su, a researcher at the Chinese University of Hong Kong and a lead author of the study. A tool based on biomarkers could help professionals diagnose autism sooner, giving children access to treatments that are more effective at a younger age, he said. “Too much is left to questionnaires,” said Sarkis Mazmanian, a microbiome researcher at the California Institute of Technology. “If we can get to something we can measure — whatever it is — that’s a huge improvement.” For decades, researchers have scoured the human genome, medical histories and brain scans for a reliable indicator of A.S.D., with limited success. The Food and Drug Administration has approved two diagnostic tests based on eye-tracking software, which Dr. Su said required significant involvement from a psychiatrist. © 2024 The New York Times Company

Keyword: Autism
Link ID: 29386 - Posted: 07.09.2024