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Weight loss jabs in obese children can help avoid mealtime rows

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

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: 29786 - Posted: 05.14.2025

What Nearly Brainless Rodents Know About Weight Loss and Hunger

By Gina Kolata Do we really have free will when it comes to eating? It’s a vexing question that is at the heart of why so many people find it so difficult to stick to a diet. To get answers, one neuroscientist, Harvey J. Grill of the University of Pennsylvania, turned to rats and asked what would happen if he removed all of their brains except their brainstems. The brainstem controls basic functions like heart rate and breathing. But the animals could not smell, could not see, could not remember. Would they know when they had consumed enough calories? To find out, Dr. Grill dripped liquid food into their mouths. “When they reached a stopping point, they allowed the food to drain out of their mouths,” he said. Those studies, initiated decades ago, were a starting point for a body of research that has continually surprised scientists and driven home that how full animals feel has nothing to do with consciousness. The work has gained more relevance as scientists puzzle out how exactly the new drugs that cause weight loss, commonly called GLP-1s and including Ozempic, affect the brain’s eating-control systems. The story that is emerging does not explain why some people get obese and others do not. Instead, it offers clues about what makes us start eating, and when we stop. While most of the studies were in rodents, it defies belief to think that humans are somehow different, said Dr. Jeffrey Friedman, an obesity researcher at Rockefeller University in New York. Humans, he said, are subject to billions of years of evolution leading to elaborate neural pathways that control when to eat and when to stop eating. © 2025 The New York Times Company

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 9: Hearing, Balance, Taste, and Smell
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 29762 - Posted: 04.26.2025

Companies seek a second obesity treatment revolution—in pill form

By Rachel Brazil Drugs that mimic glucagonlike peptide-1 (GLP-1), such as semaglutide—marketed as Ozempic or Wegovy—have revolutionized the treatment of obesity and type 2 diabetes, but they have major drawbacks. “[They] are expensive to manufacture, they have to be refrigerated, and they often have to be injected because they cannot go through the gastrointestinal tract without being degraded,” explains Alejandra Tomas, a cell biologist at Imperial College London who studies the cellular receptor GLP-1 drugs target. That’s all because they consist of peptides, or long chains of amino acids. A small-molecule version of the therapy, on the other hand, could be given as a daily pill and would be much cheaper to produce. Companies including Eli Lilly, Pfizer, and Roche have launched clinical trials of such compounds. Results from Lilly’s first phase 3 trial of its oral drug are expected later this year. But Pfizer announced this week it was halting development of its candidate after signs of liver injury in a trial participant. The candidates furthest along in development activate the same receptors as peptide drugs do, in much the same way. But several firms are exploring more innovative small molecules that target different sites on those receptors—and could lead to even more effective treatments with fewer side effects. “In the next 4 or 5 years, this field will mature and more patients ultimately should be able to get these medicines,” says Kyle Sloop, a molecular biologist at Lilly Research Laboratories. By mimicking a natural hormone, semaglutide and other drugs in its class help regulate blood sugar by increasing insulin secretion from the pancreas in response to glucose, and suppress appetite by slowing down digestion. The first generation of peptide drugs were essentially copies of GLP-1, with modifications to prevent the peptide from quickly degrading once in the body. Novo Nordisk first won U.S. approval for semaglutide to treat type 2 diabetes in 2017. It needed to be injected, but in 2019 the company added a pill form, which includes an absorption-enhancing ingredient that allows the peptide to penetrate the stomach wall. However, it requires a high dose and has to be taken while fasting, with minimal liquid.

Why there's always room for dessert, according to brain science

By Emily Kwong You probably know the feeling of having a hearty meal at a restaurant, and feeling full and satisfied … only to take a peek at the dessert menu and decide the cheesecake looks just irresistible. So why is it that you just absolutely couldn't have another bite, but you somehow make an exception for a sweet treat? Or as Jerry Sienfeld might put it back in the day "Whhaaaat's the deal with dessert?!" Scientists now have a better understanding of the neural origins of this urge thanks to a recent study published in the journal Science. Sponsor Message Working with mice, researchers tried to set up a scenario similar to the human experience described above. They started by offering a standard chow diet to mice who hadn't eaten since the previous day. That "meal" period lasted for 90 minutes, and the mice ate until they couldn't eat any more. Then it was time for a 30-minute "dessert" period. The first round of the experiment, researchers offered mice more chow for dessert, and the mice ate just a little bit more. The second time around, during the "dessert" period, they offered a high sugar feed to the mice for 30 minutes. The mice really went for the sugary feed, consuming six times more calories than when they had regular chow for dessert. In the mice, researchers monitored the activity of neurons that are associated with feelings of fullness, called POMC neurons. They're located in a part of the brain called the hypothalamus, which is "very important for promoting satiety," says Henning Fenselau, one of the study authors and a researcher at the Max Planck Institute for Metabolism Research in Cologne, Germany. © 2025 npr

Dozens of new obesity drugs are coming: these are the ones to watch

By Elie Dolgin For Kristian Cook, every pizza box he opened was another door closed on the path to overcoming obesity. “I had massive cravings for pizza,” he says. “That was my biggest downfall.” At 114 kilograms and juggling a daily regimen of medications for high cholesterol, hypertension and gout, the New Zealander resolved to take action. In late 2022, at the age of 46, Cook joined a clinical trial that set out to test a combination of the weight-loss drug semaglutide — better known by its brand names, Ozempic or Wegovy — and an experimental drug designed to preserve muscle while shedding fat. Muscle loss is a big concern for people on anti-obesity medications such as semaglutide. These ‘GLP-1 agonists’ mimic a natural gut hormone — glucagon-like peptide 1 — to suppress appetite and regulate metabolism. But reducing calories leads to an energy deficit, which the body often makes up for by burning muscle. The experimental drug that Cook received, called bimagrumab, seems to counteract this muscle loss. It’s one of more than 100 anti-obesity drug candidates that are in various stages of development. The next wave of medications, which are likely to hit pharmacy shelves in the next few years, resemble drugs that are already on the market. But close behind are numerous therapies being developed specifically for their muscle-sparing weight-loss potential. Dozens more are aimed at different biological pathways and could redefine obesity treatment in decades to come. “We’re working to create the next generation of healthy weight-loss solutions,” says Philip Larsen, who played a key part in the early development of GLP-1 drugs and is now chief executive of SixPeaks Bio, an obesity-focused start-up company in Basel, Switzerland. The surge in anti-obesity drug development has been made possible by the blockbuster success of semaglutide and its rival drug tirzepatide — sold as Zepbound or Mounjaro. These drugs have unlocked the potential for a global market that is projected to surpass US$100 billion by the end of the decade. © 2025 Springer Nature Limited

New obesity definition sidelines BMI to focus on health

By Giorgia Guglielmi Amid the rising buzz around Ozempic and similar weight-loss drugs, a group of 58 researchers is challenging the way obesity is defined and diagnosed, arguing that current methods fail to capture the complexity of the condition. They offer a more nuanced approach. The group’s revised definition, published in The Lancet Diabetes & Endocrinology1 on 14 January, focuses on how excess body fat, a measure called adiposity, affects the body, rather than relying only on body mass index (BMI), which links a person’s weight to their height. They propose two categories: preclinical obesity, when a person has extra body fat but their organs work normally, and clinical obesity, when excess fat harms the body’s organs and tissues. This shift could improve clinical care, public-health policies and societal attitudes toward obesity, says Elisabeth van Rossum, an endocrinologist at the Erasmus University Medical Center Rotterdam in the Netherlands. “Now the idea is, eat less, move more, and you’ll lose weight,” says van Rossum, who wasn’t involved in the work. Although a healthy lifestyle is important, she adds, “if it would be so simple, we wouldn’t have an epidemic, and this paper is an excellent contribution to the discussion about the complexity of obesity”. Global problem More than 1 billion people worldwide live with obesity, and the condition is linked to about 5 million deaths every year2 from disorders such as diabetes and cardiovascular disease. Because it is easy to measure and compare, BMI has long been used as a tool to diagnose obesity. But it doesn’t offer a full picture of a person’s health, because it doesn’t account for differences in body composition, such as muscle versus fat. © 2025 Springer Nature Limited

Restricting calories may extend life. Can this molecule do it without the hunger pangs?

By Mitch Leslie It’s a dismaying thought during a holiday season full of cookies and big meals, but severely restricting calories consumed is one of the best supported strategies for a healthier, longer life. Slicing food consumption stretches the lives of animals in lab experiments, and similar deprivation seems to improve health in people, although almost no one can sustain such a calorie-depleted diet for long. Now, researchers in China studying animals on lean rations have identified a molecule made by gut bacteria that delivers some of the same benefits. When given on its own, the molecule makes flies and worms live longer and refurbishes age-weakened muscles in mice, all without leaving the animals hungry. Although the molecule’s effects in people remain unclear, the discovery is “a really important step forward,” says gerontologist Richard Miller of the University of Michigan, who wasn’t connected to the research. The work, reported in two studies today in Nature, “is very thorough.” Research over the past 90 years has shown that calorie restriction—which to scientists typically means a diet with between 10% and 50% fewer calories than normal—can extend longevity in organisms as diverse as yeast, nematodes, and mice. One experiment also found an effect in monkeys. Trials to test whether calorie restriction increases human life span would take too long, but participants in the 2-year CALERIE trial, which ran from 2007 to 2010 and aimed to cut calorie intake by 25%, enjoyed a slew of improvements, including lower levels of low-density lipoprotein cholesterol, increased sensitivity to insulin, and a 10% reduction in weight. However, the trial also illustrates what makes calorie restriction so challenging: Participants on average cut their caloric intake by only half the experiment’s goal. So, scientists have been hunting for molecules that trigger health-promoting, longevity-stretching effects without privation. To identify new candidates, molecular biologist and biochemist Sheng-Cai Lin of Xiamen University and colleagues took a systematic approach, analyzing the levels of more than 1200 metabolic molecules in blood samples from calorically restricted mice and from counterparts with no dietary limits. They discovered that just over 200 molecules became more abundant when food was in short supply.

To beat the heat, hypothalamus neurons in mice ramp up their firing

By Calli McMurray A strong, long-lasting sensory stimulus—be it visual, auditory, olfactory or tactile—triggers plasticity in the neurons that respond to it. But as a scientist long interested in temperature, Jan Siemens wondered: Does the same principle apply to prolonged heat? In mammals, the body changes when temperatures soar—blood vessels dilate, heat-generating brown adipose tissue shuts off, the heart rate lowers, locomotion slows—but it wasn’t clear if the brain played a role in these changes, or even changed itself, says Siemens, professor of pharmacology at the University of Heidelberg. Siemens and his team started a search for heat-induced neuronal plasticity in the ventromedial preoptic area of the hypothalamus (VMPO) in mice. They chose the region because of its involvement in regulating body temperature and generating fever; neurons there receive temperature information downstream from cells innervating the skin, whereas others are themselves warm-sensitive. They identified cells to target by measuring the expression of c-FOS, a gene that is activated by neuronal activity, after housing the mice at 36 degrees Celsius for up to eight hours. At first, however, their investigative trail went cold. In brain slices, those warm-responding cells showed only slight and inconsistent changes in synaptic plasticity. “That was actually quite humbling and disappointing,” Siemens says. But then they made a “serendipitous observation,” he says: A subgroup of neurons expressing the leptin receptor became almost constantly active after four weeks of heat acclimation. The firing was so synchronized and regular that Wojciech Ambroziak, a postdoctoral scholar in the lab at the time, described it as “soldiers marching in a line,” Siemens recalls. © 2024 Simons Foundation

These neurons in the abdomen help form the gut-brain connection

Jon Hamilton Not all brain cells are found in the brain. For example, a team at Caltech has identified two distinct types of neurons in the abdomens of mice that appear to control different aspects of digestion. The finding, reported in the journal Nature, helps explain how clusters of neurons in the body play a key role in the gut-brain connection, a complex two-way communication system between the brain and digestive system. It also adds to the evidence that neurons in the body can take on specialized functions, "just like in the brain," says Yuki Oka, an author of the study. "The peripheral nervous system is smart," says Frank Duca of the University of Arizona, who was not involved in the study. "You have specific neurons within this system that are performing a wide variety of functions, either with the brain's help or sometimes even without the brain's input," he says. The study focused on a subset of the peripheral nervous system called the sympathetic nervous system, which becomes active when the brain detects danger. "Your adrenaline goes up and your glucose level in the blood is really high because you need to fight or flight," Oka says. At the same time, the sympathetic nervous system dials back functions that are less urgent, like digestion and moving food through the gut. © 2024 npr

Fasting can reduce weight — but also hair growth

By Max Kozlov A popular weight-loss regimen stunts hair growth, data collected from mice and humans suggest1. The study’s findings show that intermittent fasting, which involves short bouts of food deprivation, triggers a stress response that can inhibit or even kill hair-follicle stem cells, which give rise to hair. The results, published in today in Cell, suggest that although short-term fasting can provide health benefits, such as increased lifespan in mice, not all tissue and cell types benefit. “I was shocked to hear these results,” says Ömer Yilmaz, a stem-cell biologist at the Massachusetts Institute of Technology in Cambridge who was not involved in the study. “We’ve come to expect that fasting is going to be beneficial for most, if not all cell types and good for stem cells. This is the inverse of what we expected, and the finding seems to hold true in humans.” Deliberate deprivation During the past decade, intermittent fasting has become one of the most popular dieting regimens; by one count, about 12% of adults in the United States practised it in 2023. One of the most common forms is time-restricted eating, which involves eating only within a limited time frame each day. Stem cells seem to be particularly vulnerable to changes in diet. For example, Yilmaz and his colleagues reported2 in August that stem cells in the guts of mice showed a burst of activity during post-fast feasting. This activity helped to repair damage in the animals’ intestines. To learn whether dieting affects hair regrowth, which can be affected by stress, Bing Zhang, a regenerative biologist at Westlake University in Zhejiang, China, and his colleagues shaved mice and subjected them to one of two intermittent-fasting regimens: time-restricted eating and alternate-day fasting, in which animals fasted for 24 hours and then ate their normal diet for the following 24 hours. By the end of the three-month study, the dieting mice had not regrown as much hair as control animals that ate a similar number of calories, the authors found. © 2024 Springer Nature Limited

Are Weight-Loss Drugs Contributing to a Fall in the Obesity Rate?

By Joshua Cohen Earlier this fall, the Centers for Disease Control and Prevention reported data showing that adult obesity rates — long trending upwards — had fallen modestly over the past few years, from 41.9 to 40.3 percent. The decline sparked discussion on social media and in major news outlets about whether the U.S. has passed so-called “peak obesity” — and whether the growing use of certain weight-loss drugs might account for the shift. An opinion piece in the Financial Times suggested that the public health world might look back on the current moment in much the same way that it now reflects on 1963, when cigarette sales hit their high point and then dropped dramatically over the following decades. The article’s author, John Burn-Murdoch, speculated that the dip is “highly likely” to be caused by the use of glucagon-like peptide-1 receptor agonists, or GLP-1s, for weight loss. It’s easy to see why one might make that connection. Although GLP-1s have been used for nearly two decades in the treatment of type 2 diabetes, their use for obesity only took off more recently. In 2014, the Food and Drug Administration approved a GLP-1 agonist named Saxenda specifically for this purpose. Then in the late 2010s, a GLP-1 drug named Ozempic, made from the active ingredient semaglutide, began to be used off-label. The FDA also authorized Wegovy, another semaglutide-based GLP-1 medication, explicitly for weight loss in 2021. Still, it is premature to declare that GLP-1s have caused overall declining obesity rates in the U.S. There are a number of ways to interpret the CDC data, and not all of them suggest that obesity rates have actually fallen. Further, recent evidence indicates that GLP-1s might not be as effective for weight loss as initially thought. And there are reasons to question the comparison to cigarette sales. Taken together, all of this suggests that we may need to wait to understand how this new class of drugs affects weight loss at the population level.

Fish Have a Brain Microbiome. Could Humans Have One Too?

By Yasemin Saplakoglu Bacteria are in, around and all over us. They thrive in almost every corner of the planet, from deep-sea hydrothermal vents to high up in the clouds, to the crevices of your ears, mouth, nose and gut. But scientists have long assumed that bacteria can’t survive in the human brain. The powerful blood-brain barrier, the thinking goes, keeps the organ mostly free from outside invaders. But are we sure that a healthy human brain doesn’t have a microbiome of its own? Over the last decade, initial studies have presented conflicting evidence. The idea has remained controversial, given the difficulty of obtaining healthy, uncontaminated human brain tissue that could be used to study possible microbial inhabitants. Recently, a study published in Science Advances provided the strongest evidence yet (opens a new tab) that a brain microbiome can and does exist in healthy vertebrates — fish, specifically. Researchers at the University of New Mexico discovered communities of bacteria thriving in salmon and trout brains. Many of the microbial species have special adaptations that allow them to survive in brain tissue, as well as techniques to cross the protective blood-brain barrier. Matthew Olm (opens a new tab), a physiologist who studies the human microbiome at the University of Colorado, Boulder and was not involved with the study, is “inherently skeptical” of the idea that populations of microbes could live in the brain, he said. But he found the new research convincing. “This is concrete evidence that brain microbiomes do exist in vertebrates,” he said. “And so the idea that humans have a brain microbiome is not outlandish.” While fish physiology is, in many ways, similar to humans’, there are some key differences. Still, “it certainly puts another weight on the scale to think about whether this is relevant to mammals and us,” said Christopher Link (opens a new tab), who studies the molecular basis of neurodegenerative disease at the University of Colorado, Boulder and was also not involved in the work. © 2024 Simons Foundation

Novel neurons upend ‘yin-yang’ model of hunger, satiety in brain

By Giorgia Guglielmi For years, scientists have thought of hunger regulation as a tug-of-war between two types of neurons in the hypothalamus: those that express the AGRP gene and increase hunger, and those that express the POMC gene and act as a brake. Now a new study challenges this long-standing model, revealing a third player in the hunger-satiety network—a neuron type that expresses the BNC2 gene and suppresses hunger faster than those that express POMC. These BNC2 neurons are activated by leptin—a hormone that helps suppress appetite and boost metabolism. Their discovery “reshapes our understanding of feeding behavior,” says lead investigator Han Tan, “and how leptin regulates body weight.” Tan is a research associate in Jeffrey Friedman’s lab at Rockefeller University. “We’ve known for a long time there must be [other] neurons in the brain that are sensing leptin and decreasing appetite, but we didn’t know who they were until now,” says John Campbell, assistant professor of biology at the University of Virginia, who wasn’t involved in the study. The results jibe with two other recent reports of leptin-sensitive neurons in the arcuate nucleus—a region in the hypothalamus that processes signals related to hunger and satiety. The neurons generate feelings of fullness, an independent team reported in Science in June, and they dampen appetite by inhibiting AGRP-expressing “hunger neurons,” according to a preprint Campbell and his colleagues posted on bioRxiv in July. The studies all point to a unique group of neurons that inhibit hunger, says Martin Myers, professor of internal medicine and molecular and integrative physiology at the University of Michigan, who was not involved in the work. “The three groups essentially found [these neurons] simultaneously.” © 2024 Simons Foundation

Obesity Drugs Would Be Covered by Medicare and Medicaid Under Biden Proposal

By Margot Sanger-Katz The Biden administration, in one of its last major policy directives, proposed on Tuesday that Medicare and Medicaid cover obesity medications, a costly and probably popular move that the Trump administration would need to endorse to become official. The proposal would extend access of the drugs to millions of Americans who aren’t covered now. The new obesity drugs, including Wegovy from Novo Nordisk and Zepbound from Eli Lilly, have been shown to improve health in numerous ways, but legislation passed 20 years ago prevents Medicare from covering drugs for “weight loss.” The new proposal sidesteps that restriction, specifying that the drugs would be covered to treat the disease of obesity and prevent its related conditions. “We don’t want to see people having to wait until they have these additional diseases before they get treatment,” said Chiquita Brooks-LaSure, the administrator of the Centers for Medicare and Medicaid Services, or C.M.S., noting the growing medical consensus that obesity is a chronic health condition. The classification would also mean that every state Medicaid program would be required to cover the drugs. Currently, only a handful do. C.M.S. estimates that around 3.4 million more patients in Medicare would become eligible for obesity drugs, and around four million patients in Medicaid would gain coverage, costing the programs billions of dollars. Medicare mostly covers Americans 65 and older; Medicaid mostly covers poor and disabled Americans. The proposal is part of an annual policy update for all Medicare drug plans and private Medicare Advantage plans starting in 2026. In a conference call with reporters Tuesday, Daniel Tsai, the top Medicaid official, said Medicaid coverage could start sooner than 2026. © 2024 The New York Times Company

Ozempic Could Crush the Junk Food Industry. But It Is Fighting Back.

By Tomas Weber Trinian Taylor, a 52-year-old car dealer, pushed his cart through the aisles of a supermarket as I pretended not to follow him. It was a bright August day in Northern California, and I had come to the store to meet Emily Auerbach, a relationship manager at Mattson, a food-innovation firm that creates products for the country’s largest food and beverage companies: McDonald’s and White Castle, PepsiCo and Hostess. Auerbach was trying to understand the shopping behavior of Ozempic users, and Taylor was one of her case studies. She instructed me to stay as close as I could without influencing his route around the store. In her experience of shop-alongs, too much space, or taking photos, would be a red flag for the supermarket higher-ups, who might figure out we were not here to shop. “They’d be like, ‘You need to exit,’” she said. Auerbach watched in silence as Taylor, who was earning $150 in exchange for being tailed, propelled his cart through snack aisles scattered with products from Mattson’s clients. He took us straight past the Doritos and the Hostess HoHos, without a side glance at the Oreos or the Cheetos. We rushed past the Pop-Tarts and the Hershey’s Kisses, the Lucky Charms and the Lay’s — they all barely registered. Clumsily, close on his heels, Auerbach and I stumbled right into what has become, under the influence of the revolutionary new diet drug, Taylor’s happy place: the produce section. He inspected the goods. “I’m on all of these,” he told us. “I eat a lot of pineapple. A lot of pineapple, cucumber, ginger. Oh, a lot of ginger.” Taylor, who lives in Hayward, Calif., used to nurse a sugar addiction, he said, but he can no longer stomach Hostess treats. A few days earlier, his daughter fed him some candy. “I just couldn’t,” he said. “It was so sweet it choked me.” His midnight snack used to be cereal, but now he stirs at night with strange urges. Salads. Chicken. He has sworn off canned sodas and fruit juices and infuses his water with lemon and cucumber. He dropped a heavy bag of lemons into the cart and sauntered over to the leafy vegetables. “I love Swiss chard,” he said. “I eat a lot of kale.” For decades, Big Food has been marketing products to people who can’t stop eating, and now, suddenly, they can. The active ingredient in Ozempic, as in Wegovy, Zepbound and several other similar new drugs, mimics a natural hormone, called glucagon-like peptide-1 (GLP-1), that slows digestion and signals fullness to the brain. Around seven million Americans now take a GLP-1 drug, and Morgan Stanley estimates that by 2035 the number of U.S. users could expand to 24 million. © 2024 The New York Times Company

Fat ‘remembering’ past obesity drives yo-yo diet effect

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

Limiting sugar in infancy reduces the risk of diabetes and hypertension

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

‘Poo milkshake’ boosts the microbiome of c-section babies

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

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory and Learning
Link ID: 29525 - Posted: 10.26.2024

Eating less can lead to a longer life: massive study in mice shows why

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

Should I stay (and eat) or should I go? How the brain balances hunger with competing drives

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

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: 29515 - Posted: 10.12.2024

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