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

Keyword: Obesity
Link ID: 29629 - Posted: 01.15.2025

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.

Keyword: Obesity
Link ID: 29607 - Posted: 12.21.2024

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

Keyword: Obesity
Link ID: 29602 - Posted: 12.14.2024

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

Keyword: Obesity
Link ID: 29601 - Posted: 12.14.2024

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

Keyword: Obesity
Link ID: 29600 - Posted: 12.14.2024

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.

Keyword: Obesity
Link ID: 29594 - Posted: 12.11.2024

By Shane O’Neill In 2018, Matt Christensen kicked heroin by replacing drugs with drinking. When he stopped drinking in 2022, he turned to food. He put on 95 pounds. His doctor recommended he try Wegovy, part of a class of drugs known as GLP-1 receptor agonists, to help him lose weight. Eventually he switched to a different drug called Zepbound, which targets both GLP-1 and GIP agonists. The drugs worked. Get concise answers to your questions. Try Ask The Post AI. But a funny thing happened on his weight-loss journey: His cravings for food had diminished but so had his cravings for drugs and alcohol. Christensen, 42, started drinking at age 9 and using heroin at 17. For decades, catching a cold meant reaching for a hot toddy. Work stress meant numbing out with Xanax. Even passing through certain neighborhoods in Chicago where he used to buy drugs would lead to cravings. But after he started taking GLP-1 agonists, those triggers became, well, less triggering. “It was the weirdest thing,” he said. “It was just quiet. I just found it really easy all of a sudden.” More than that, Christensen noticed that an unease he had always felt in his body — a discomfort he perpetually tried to quell with fidgeting, food or drugs — was diminishing. “That’s a feeling that I’ve had my entire life,” he said. “Taking these drugs has toned that down. “There’s no silver bullet for addiction or mental illness, but for me, in concert with the other treatments, it has been an absolute game changer,” he said. Matt Christensen says weight-loss drugs like Ozempic and Zepbound have been “an absolute game changer” when it comes to his addiction struggles.

Keyword: Drug Abuse; Obesity
Link ID: 29589 - Posted: 12.07.2024

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

Keyword: Obesity; Brain imaging
Link ID: 29588 - Posted: 12.04.2024

Amy Fleming Nine years ago, Nikki Schultek, an active and healthy woman in her early 30s, experienced a sudden cascade of debilitating and agonising symptoms – including cognitive and breathing problems and heart arrhythmia – and was investigated for multiple sclerosis. But three brain scans and numerous X-rays later, there was still no diagnosis or treatment plan. “It was like living in a nightmare, imagining not watching my children – three and five years old – grow up,” says Schultek. Now, speaking on a video call from North Carolina, she is as bright as a button and shows no signs of degenerative brain disease. It turned out she had multiple chronic infections, including Borrelia burgdorferi bacteria, which causes Lyme disease and which had stealthily reached her brain. Antibiotics restored her health, but B burgdorferi is hard to eradicate once in the brain. She may need maintenance treatment to keep the disease at bay. Schultek is not the only person whose neurological disorder turned out to be caused by microbes in the brain. A recent paper she jointly lead-authored, published in Alzheimer’s and Dementia, compiled a long list of case reports where infectious disease was discovered to be the primary cause of dementia, meaning that, in many cases, the dementia was reversible. A few of the patients died, but most survived and saw significant improvements in cognitive function, including a man in his 70s who had been diagnosed with Alzheimer’s disease after his swift cognitive decline saw him unable to drive or, eventually, leave the house alone. A sample of his cerebrospinal fluid was taken and revealed a fungal infection caused by Cryptococcus neoformans. Within two years of taking antifungal medication, he was driving again and back at work as a gardener. Richard Lathe, a professor of infectious medicine at the University of Edinburgh and another lead author of the paper, says these patients “were by accident found to be suffering from various fungal, bacterial or viral infections, and when they treated the patient with antifungals, antivirals or antibiotics, the dementia went away”. He, among others, has been investigating the possibility that, like the gut, the brain hosts a community of microbes – an area of largely scientifically uncharted waters, but with huge life-saving potential. © 2024 Guardian News & Media Limited

Keyword: Alzheimers; Obesity
Link ID: 29587 - Posted: 12.04.2024

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

Keyword: Obesity
Link ID: 29584 - Posted: 12.04.2024

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

Keyword: Obesity
Link ID: 29580 - Posted: 11.30.2024

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

Keyword: Obesity
Link ID: 29569 - Posted: 11.20.2024

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