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Researchers pinpoint neurons that prevent eating too much, too fast

By Catherine Offord As millions in the United States settle down to Thanksgiving dinner this week, few will be pondering a major question in neuroscience: Why, when so much of life across the animal kingdom revolves around finding and consuming food, do we ever stop eating? Scientists have identified brain regions and even specific cells involved in terminating meals. But exactly how this process is coordinated remains murky. Now, using brain recordings from mice tucking into food, researchers have for the first time identified how specific neurons in a region called the caudal nucleus of the solitary tract (cNTS) switch on during a meal to slow down and eventually end eating. “Nobody has really been able to [do this] in awake, behaving animals” before, says Nicholas Betley, a neuroscientist at the University of Pennsylvania who was not involved in the work. The findings, published today in Nature, suggest the brain manages a coordinated sequence of behavioral responses to food as it travels from the mouth through the gastrointestinal tract, and could provide new insight into humans’ eating behaviors and disorders, he adds. Previous research on what causes animals to stop eating has largely focused on two types of cells located in the cNTS. One is prolactin-releasing hormone (PRLH) neurons, which have been linked to many functions, including the inhibition of feeding behavior. The other is GCG neurons, which produce glucagon-like peptide-1—the appetite-suppressing hormone mimicked by newly popular weight loss drugs such as Wegovy. Studies of anesthetized animals have found that both neuron types become active in response to the stomach filling, which researchers mimic by inflating a balloon in the stomach or by directly infusing food. But such techniques are a poor proxy for what happens in real life, says Zachary Knight, a neurobiologist and Howard Hughes Medical Institute investigator at the University of California, San Francisco (UCSF). “You don’t really have any sense of what’s happening dynamically.”

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: 29023 - Posted: 11.26.2023

In the Gut’s ‘Second Brain,’ Key Agents of Health Emerge

By Yasemin Saplakoglu From the moment you swallow a bite of food to the moment it exits your body, the gut is toiling to process this strange outside material. It has to break chunks down into small bits. It must distinguish healthy nutrients from toxins or pathogens and absorb only what is beneficial. And it does all this while moving the partially processed food one way through different factories of digestion — mouth, esophagus, stomach, through the intestines and out. “Digestion is required for survival,” said Marissa Scavuzzo, a postdoctoral researcher at Case Western Reserve University in Ohio. “We do it every day, but also, if you really think about it, it sounds very foreign and alien.” Breaking down food requires coordination across dozens of cell types and many tissues — from muscle cells and immune cells to blood and lymphatic vessels. Heading this effort is the gut’s very own network of nerve cells, known as the enteric nervous system, which weaves through the intestinal walls from the esophagus down to the rectum. This network can function nearly independently from the brain; indeed, its complexity has earned it the nickname “the second brain.” And just like the brain, it’s made up of two kinds of nervous system cells: neurons and glia. Glia, once thought to be mere glue that fills the space between neurons, were largely ignored in the brain for much of the 20th century. Clearly, neurons were the cells that made things happen: Through electrical and chemical signaling, they materialize our thoughts, feelings and actions. But in the last few decades, glia have shed their identity as passive servants. Neuroscientists have increasingly discovered that glia play physiological roles in the brain and nervous system that once seemed reserved for neurons. A similar glial reckoning is now happening in the gut. A number of studies have pointed to the varied active roles that enteric glia play in digestion, nutrient absorption, blood flow and immune responses. Others reveal the diversity of glial cells that exist in the gut, and how each type may fine-tune the system in previously unknown ways. One recent study, not yet peer-reviewed, has identified a new subset of glial cells that senses food as it moves through the digestive tract, signaling to the gut tissue to contract and move it along its way. All Rights Reserved © 2023

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 11: Emotions, Aggression, and Stress
Link ID: 29018 - Posted: 11.22.2023

2 different brain circuits influence our taste for salt

Jon Hamilton MICHEL MARTIN, HOST: If you are thinking about brining that turkey for Thanksgiving - and full disclosure here, I will be doing that - here is something to consider. Food and drinks that are really salty can be appealing one day and off-putting the next. And scientists think they've figured out why. NPR's Jon Hamilton reports on a study that found two separate brain circuits that affect the taste for salt. JON HAMILTON, BYLINE: Our relationship with salt is complicated. Yuki Oka, a scientist at Caltech, says sodas, sports drinks and even tap water all contain a little salt, also known as sodium chloride. YUKI OKA: You enjoy low-sodium water, but if you imagine very high concentration of sodium, like ocean water, you really hate it. HAMILTON: Unless your body is really low on salt. That's pretty rare in people these days, but Oka says experiments with animals show that when salt levels plummet, the tolerance for salty water goes up. OKA: If your body needs sodium, then animals immediately start liking ocean water. HAMILTON: They crave sodium, and they can tolerate it in high concentrations they would normally avoid. Oka wanted to know how this system works in the brain, so he and a team of scientists studied mice. They showed that one set of neurons toward the back of the brain regulates the craving for salt. OKA: If you stimulate these neurons, then animals run to sodium source and then start eating. HAMILTON: Another group of neurons toward the front of the brain normally sets an upper limit on salt tolerance, but when salt levels get low enough, Oka says, these neurons get switched off. OKA: This means that the sodium craving and the sodium tolerance are controlled by completely different types of neurons. HAMILTON: The finding, which appears in the journal Cell, is part of a growing field of study called interoception. It deals with internal sensations like hunger and pain. Stephen Liberles, a cell biologist at Harvard Medical School, says scientists already know a lot about how the brain deals with sensory information coming from the eyes, ears, nose and skin. © 2023 npr

Fructose may be the ultimate driver of obesity

Ross Pomeroy Numerous hypotheses attempt to explain obesity‘s meteoric rise over the past few decades. There’s the energy balance hypothesis, which states that weight gain is due to consuming more calories than the amount expended. There’s the carbohydrate-insulin hypothesis, which argues that excess consumption of carbohydrates stimulates an insulin response that drives cells to accumulate fat. Then there’s the protein-leverage hypothesis, which suggests that we don’t eat enough protein, driving incessant hunger. Now, researchers have put forth a new hypothesis that places the blame on a sugar ubiquitous in modern food: fructose. Commonly known as “fruit sugar,” fructose is a simple, monosaccharide sugar found in many plants. But the compound that sweetens your watermelon, apples, and oranges can mess with your cells’ energy metabolism, Richard Johnson, a professor of medicine at the University of Colorado, and his co-authors Laura G. Sánchez-Lozada and Miguel A. Lanaspa explain in a paper published October 17 in the journal Obesity. “We suggest that obesity is not a disease of energy excess but rather a disease of energy crisis,” they wrote. The fructose hypothesis As studies in rodents have elucidated, fructose uniquely suppresses the function of mitochondria compared to other nutrients. When these cellular powerhouses are slowed, the cells get stuck in a low-energy state, triggering hunger and thirst. Eating nutrients including fats and protein eventually restores cellular energy levels, but not before we’ve eaten more calories than we need. This excess gets stored as fat. In the long term, frequent fructose exposure can damage mitochondria and reduce the amount of mitochondria in cells, the researchers say, locking people in a low-energy state which drives chronic overeating.

Less snacking, more satisfaction: Some foods boost levels of an Ozempic-like hormone

Michaeleen Doucleff For several months now, I've been studying how the new medications, Ozempic and Wegovy, cause dramatic weight loss. Both medications contain a compound, semaglutide, that squelches hunger like a fly swatter smashes a mosquito. People who take the medication say they no longer have constant cravings for food, so they eat less frequently. The drug seems to quiet what some people call "food noise," the constant internal chatter telling them to eat. While reading study after study about Wevgovy and Ozempic, I learned that the drug mimics a hormone that our bodies naturally make when we're eating food. It's called GLP-1. This made me wonder: Could we increase levels of this hormone by changing our diet? Turns out, the answer is yes – you can increase your body's production of GLP-1 with your diet, says Frank Duca, who studies metabolic diseases at the University of Arizona. One of the key foods that triggers its release is a food most Americans struggle to eat enough of, even though it comes with a cornucopia of health benefits. Yup, I'm talking about fiber. "Whenever my family finds out that I'm studying obesity or diabetes, they say, 'Oh, what's the wonder drug? What do I need to take? What do I need to do?'" Duca explains. "And I say, 'Eat more fiber.' " But here's the hitch. Not all fiber works the same way. Duca and other researchers are beginning to show that particular types of fibers are more potent at triggering GLP-1 release and at regulating hunger than others. "We're seeing now that companies are adding fiber to foods, but a lot of the time, they don't add the kind of fiber that's super beneficial for you," Duca says. To understand why fiber is so important for producing GLP-1, let's look at what happens when you don't eat much fiber. Let's say you wake up in the morning feeling hungry and you eat two slices of white bread and a fried egg. As the digested food moves into the small intestine, many of the nutrients, such as the carbohydrates, fats and amino acids, trigger an avalanche of activity in your blood and brain. "The food activates cells in your intestine, which then release a ton of hormones," says Sinju Sundaresan, who's a gut physiologist at Midwestern University. About 20 of these hormones, including GLP-1, are known as satiation hormones. © 2023 npr

Milkshake neuroscience: how the brain nudges us toward fatty foods

Max Kozlov Rich, high-fat foods such as ice cream are loved not only for their taste, but also for the physical sensations they produce in the mouth — their ‘mouthfeel’. Now scientists have identified a brain area that both responds to the smooth texture of fatty foods and uses that information to rate the morsel’s allure, guiding eating behaviour1. These findings, published on 16 October in The Journal of Neuroscience, “add a new dimension” of the eating experience to scientists’ understanding of what motivates people to choose certain foods, says Ivan de Araujo, a neuroscientist at the Max Planck Institute for Biological Cybernetics in Tübingen, Germany, who was not involved in the study. To explore how food textures influence eating habits, Fabian Grabenhorst, a neuroscientist at the University of Oxford, UK, and his colleagues set out to quantify the mouthfeel of fatty foods. The authors prepared several milkshakes with varying fat and sugar contents and placed a sample of each between two pig tongues procured from a local butcher. The researchers then slid the tongues across each other and measured the amount of friction between the two surfaces, providing a numerical index of each shake’s smoothness. The researchers then gave 22 participants milkshakes with the same compositions as those tested on the pig tongues. After tasting each milkshake, participants placed bids on how much they would spend to drink a full glass of it after the experiment. Accompanying brain scans showed that activity patterns in an area called the orbitofrontal cortex (OFC), which is involved in reward processing, reflected the shakes’ texture. The scans also identified OFC activity patterns that reflected participants’ bids, suggesting that this brain region links mouthfeel to the value placed on that food. © 2023 Springer Nature Limited

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: 28966 - Posted: 10.17.2023

Anti-obesity drugs’ side effects: what we know so far

Mariana Lenharo The treatment of obesity has been revolutionized by new drugs such as semaglutide and tirzepatide. In clinical trials, these medications led to substantial weight loss — as much as an average of 21% of participants’ body weight1 — and semaglutide has also been shown to cut the risk of severe cardiovascular problems, which specialists celebrated as a groundbreaking result. But as demand for the drugs increases, there’s a growing interest in investigating their potential side effects. Researchers have been looking into the gastrointestinal problems and loss of muscle mass connected with the medications and shared some findings earlier this month. Gastrointestinal problems The latest generation of anti-obesity drugs mimic a hormone called glucagon-like peptide 1 (GLP-1), which is associated with appetite regulation. Semaglutide was approved by the US Food and Drug Administration in 2017, under the name Ozempic, to treat type 2 diabetes, and later, in 2021, as Wegovy, for the treatment of obesity. Tirzepatide, marketed as Mounjaro, was approved in 2022 to treat diabetes, but is also prescribed off-label for weight loss. A research letter published last week in JAMA2 looked at a sample of people with obesity in a large health-insurance database. The authors found that the incidence of pancreatitis — inflammation of the pancreas — was 4.6 times higher in people taking semaglutide than in people taking a weight-loss medication that does not mimic GLP-1. The study also found that semaglutide and liraglutide, another GLP-1 medication, were associated with an increased incidence of gastroparesis, a disorder that slows or stops the movement of food from the stomach to the intestine. Clinical trials had already shown an association between GLP-1 drugs and gastrointestinal side effects, including nausea, constipation and rare cases of pancreatitis3. “What’s new is that, for all of them, we actually gave an incidence number,” says Mahyar Etminan, an epidemiologist at the University of British Columbia in Vancouver, Canada, and an author of the JAMA research. © 2023 Springer Nature Limited

Why BMI is flawed — and how to redefine obesity

McKenzie Prillaman Players in an ‘overweight football league’ warm up before a match in Germany. To join, members must have a BMI of at least 31. Credit: Ina Fassbender/AFP via Getty As an obesity physician, Fatima Cody Stanford has treated many people whose weight was causing them health problems. She has plenty of success stories: one woman, for instance, returned “stunning” cholesterol, blood-pressure and blood-sugar readings after working with Stanford for about ten years. But the woman still wanted more treatment. She was fixated on her body mass index, or BMI, which classified her as having obesity. “She wants to lose more weight”, says Stanford, who is at Massachusetts General Hospital and Harvard Medical School in Boston. BMI, which is calculated by dividing weight by height squared, has been used for several decades as an international standard to determine healthy weights. It serves as a proxy for body fat, and higher numbers can indicate increased risk for metabolic disease and death. But BMI does not measure body fat, and it also ignores factors that affect how healthy someone is at a given weight, including age, sex and race. Not everyone with a high BMI has poor health or a raised risk of death1–3. That’s why there is a small but growing movement to go beyond BMI when diagnosing and treating obesity, which the World Health Organization (WHO) recognizes as a chronic disease. In June, the American Medical Association (AMA) called for more weight-related metrics to be used in conjunction with BMI owing to its imperfections and questionable history. But, with global rates of obesity having tripled over the past 50 years, and a wave of cutting-edge weight-loss drugs now hitting the market, a high BMI still reigns as the main criterion for obesity treatment. Specialists worry that the surging demand for the drugs will exacerbate reliance on BMI as a solo diagnostic tool.

I try to be a body-positive doctor. It's getting harder in the age of Ozempic

Mara Gordon Right around the time Ozempic came out, I started to change the way I practice medicine. As the new class of weight-loss drug ushered in a highly medicalized era of Americans' obsession with being thin, I decided I was done with trying to get my patients to lose weight. Sometimes I call myself a "body-positive doctor," but that isn't it, exactly, because I don't expect all of my patients to love their bodies at all times. With my students, I call it practicing "weight-neutral medicine." I've found a great community of like-minded health care providers with the Health at Every Size movement, which promotes the idea that people can be healthy without focusing on weight loss. This change started for me, as many of my major realizations do, from reading. I read memoirs by fat authors like Roxane Gay, Lindy West, and Kiese Laymon, who wrote about the many ways they were made to feel terrible about their bodies, often at the doctor's office. It was unsettling to recognize myself in some of the encounters they described. I had told my own patients, dozens of times: "Your knee pain might get better if you just lost a few pounds." As if my patients hadn't thought of that already. As if they hadn't already tried. Reading these books also forced me to reckon with my own relationship to my weight and my experiences in health care. As a chubby teen, I remember a visceral unease before each appointment at the pediatrician's office, the fear I felt stepping on the scale. I remember the doctor who chided my mom for buying 2% milk, not skim. Then, when I lost weight in my 20s, appointments with the doctor were transformed. I could focus on the issues I wanted to discuss, rather than visits being dominated by talk of cutting calories. © 2023 npr

The origins of the obesity epidemic may be further back than we thought

By Molly Rains Over the past 50 years, worldwide obesity rates have tripled, creating a public health crisis so widespread and damaging that it is sometimes referred to as an epidemic. Most accounts put the roots of the problem firmly in the modern age. But could it have been brewing since before World War II? That’s one provocative conclusion of a study published today in Science Advances that purports to push the obesity epidemic’s origin back to as early as the 1930s. Historical measurements from hundreds of thousands of Danish youth show that in the decades before the problem was officially recognized, the heaviest members of society were already getting steadily bigger. The findings raise questions about the accepted narrative of the obesity epidemic, says Lindsey Haynes-Maslow, an obesity expert at the University of North Carolina at Chapel Hill who was not involved in the study. “This paper is an opportunity … to say maybe we’ve been looking at this wrong, maybe we should go back to the beginning—or, when was the beginning?” she says. Most epidemiologists trace that beginning to the 1970s, when health officials first observed an uptick in the prevalence of obesity—defined as a body mass index (BMI) above 30—in many Western nations. The crisis is usually blamed on the increased postwar availability of cheap, highly processed, and calorie-rich foods, as well as increasingly sedentary lifestyles and growing portion sizes. But University of Copenhagen epidemiologist Thorkild Sørensen was skeptical of that story. Years of slowly increasing body size typically precede obesity, and might show up in historical data, he suspected. And Sørensen wasn’t convinced that the so-called obesogenic diet and lifestyle were the only factors at play. Historical data, he hoped, could reveal whether other, yet-unknown factors had contributed to the crisis.

Neuropeptide Y May Have Made Humans Smart and Overindulgent

By Joanna Thompson= Like many people, Mary Ann Raghanti enjoys potatoes loaded with butter. Unlike most people, however, she actually asked the question of why we love stuffing ourselves with fatty carbohydrates. Raghanti, a biological anthropologist at Kent State University, has researched the neurochemical mechanism behind that savory craving. As it turns out, a specific brain chemical may be one of the things that not only developed our tendency to overindulge in food, alcohol and drugs but also helped the human brain evolve to be unique from the brains of closely related species. A new study, led by Raghanti and published on September 11 in the Proceedings of the National Academy of Sciences USA, examined the activity of a particular neurotransmitter in a region of the brain that is associated with reward and motivation across several species of primates. The researchers found higher levels of that brain chemical—neuropeptide Y (NPY)—in humans, compared with our closest living relatives. That boost in the reward peptide could explain our love of high-fat foods, from pizza to poutine. The impulse to stuff ourselves with fats and sugars may have given our ancestors an evolutionary edge, allowing them to develop a larger and more complex brain. “I think this is a first bit of neurobiological insight into one of the most interesting things about us as a species,” says Robert Sapolsky, a neuroendocrinology researcher at Stanford University, who was not directly involved in the research but helped review the new paper. Advertisement Neuropeptide Y is associated with “hedonic eating”—consuming food strictly to experience pleasure rather than to satisfy hunger. It drives individuals to seek out high-calorie foods, especially those rich in fat. Historically, though, NPY has been overlooked in favor of flashier “feel good” chemicals such as dopamine and serotonin. © 2023 Scientific American,

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory and Learning
Link ID: 28905 - Posted: 09.13.2023

Humans aren’t the only fat primate

By Ann Gibbons Go to the Democratic Republic of the Congo, and you’re unlikely to encounter chimps so plump they have trouble climbing trees or vervet monkeys so chubby they huff and puff as they swing from branch to branch. Humans are a different story. Walk down a typical U.S. street and almost half of the people you encounter are likely to have obesity. Scientists have long blamed our status as the “fattest primate” on genes that help us store fat more efficiently or diets overloaded with sugars or fat. But a new study of 40 species of nonhuman primates, ranging from tiny mouse lemurs to hulking gorillas, finds many pack on the pounds just as easily as we do, regardless of diet, habitat, or genetic differences. All they need is extra food. “Lots of primates put on too much weight, the same as humans,” says Herman Pontzer, a biological anthropologist at Duke University and author of the new study, published this week in the Philosophical Transactions of the Royal Society B. “Humans are not special.” Some researchers have suggested our species is prone to obesity because our ancestors evolved to be incredibly efficient at storing calories. The adaptation would have helped our ancient relatives, who often faced famine after the transition to agriculture, get through lean times. This selection pressure for so-called thrifty genes set us apart from other primates, the thinking goes. But other primates can get fat. Kanzi, the first ape to show he understands spoken English, was triple the average weight of his bonobo species after years of being rewarded with bananas, peanuts, and other treats during research; scientists eventually put him on a diet. And then there was Uncle Fatty, an obese macaque who lived on the streets of Bangkok where tourists fed him milkshakes, noodles, and other junk food. He weighed an astonishing 15 kilograms—three times more than the average macaque—before he went to the monkey equivalent of a fat farm. © 2023 American Association for the Advancement of Science.

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 28902 - Posted: 09.10.2023

We Know Where New Weight Loss Drugs Came From, but Not Why They Work

By Gina Kolata Every so often a drug comes along that has the potential to change the world. Medical specialists say the latest to offer that possibility are the new drugs that treat obesity — Ozempic, Wegovy, Mounjaro and more that may soon be coming onto the market. It’s early, but nothing like these drugs has existed before. “Game changers,” said Jonathan Engel, a historian of medicine and health care policy at Baruch College in New York. Obesity affects nearly 42 percent of American adults, and yet, Dr. Engel said, “we have been powerless.” Research into potential medical treatments for the condition led to failures. Drug companies lost interest, with many executives thinking — like most doctors and members of the public — that obesity was a moral failing and not a chronic disease. While other drugs discovered in recent decades for diseases like cancer, heart disease and Alzheimer’s were found through a logical process that led to clear targets for drug designers, the path that led to the obesity drugs was not like that. In fact, much about the drugs remains shrouded in mystery. Researchers discovered by accident that exposing the brain to a natural hormone at levels never seen in nature elicited weight loss. They really don’t know why, or if the drugs may have any long-term side effects. “Everyone would like to say there must be some logical explanation or order in this that would allow predictions about what will work,” said Dr. David D’Alessio, chief of endocrinology at Duke, who consults for Eli Lilly among others. “So far there is not.” Although the drugs seem safe, obesity medicine specialists call for caution because — like drugs for high cholesterol levels or high blood pressure — the obesity drugs must be taken indefinitely or patients will regain the weight they lost. Dr. Susan Yanovski, a co-director of the office of obesity research at the National Institute of Diabetes and Digestive and Kidney Diseases, warned that patients would have to be monitored for rare but serious side effects, especially as scientists still don’t know why the drugs work. But, she added, obesity itself is associated with a long list of grave medical problems, including diabetes, liver disease, heart disease, cancers, sleep apnea and joint pain. “You have to keep in mind the serious diseases and increased mortality that people with obesity suffer from,” she said. © 2023 The New York Times Company

Weight-loss drug Wegovy cuts heart attack risk among obese, study says

By Laurie McGinley and David Ovalle The weight-loss drug Wegovy reduced the risk of strokes, heart attacks and other cardiovascular problems by 20 percent among overweight people with a history of heart disease, its manufacturer said Tuesday, results that could increase demand and bolster the case for insurance coverage for the medication. The better-than-expected result was announced by Danish pharmaceutical giant Novo Nordisk in a news release. Experts said the results of the trial, called Select, demonstrate that a new crop of drugs commonly used for weight loss, such as Wegovy, can provide important health benefits, not just cosmetic ones. Obesity should be treated as a serious illness given its connection to other problems such as heart disease, specialists said. Still, private insurers have been slow to cover Wegovy, and Medicare is barred from paying for weight-loss medications. With Wegovy costing more than $1,300 a month, the lack of insurance coverage has put the drug out of reach for many people. The study is important because it could shift perceptions of Wegovy and similar drugs, said Andres J. Acosta, an assistant professor of medicine and a consultant in gastroenterology and hepatology at the Mayo Clinic. Previously, the medications were highlighted for their cosmetic results. “It’s a new era,” Acosta said. “It matters because if you lose weight, your risk of dying is reduced.” The data from the highly anticipated trial have not been published. The results released Tuesday were top-line findings, and the company said it would release detailed results at a conference later this year. Steven Nissen, a Cleveland Clinic cardiologist, noted that while Tuesday’s announcement is promising, he wants to see the full results. “We have to be cautious until we actually see the peer-reviewed publication,” said Nissen, who is leading a similar trial involving Eli Lilly’s Mounjaro, a diabetes drug commonly used for weight loss.

3 Factors Keeping Americans From New Weight-Loss Drugs

By Gina Kolata A national survey released on Friday by KFF, a nonprofit organization focused on health policy, has found that Americans long for safe and effective drugs for weight loss. But the more they learn about new drugs like Wegovy that are transforming obesity treatment, the more their enthusiasm fades. The survey found that 59 percent of people who were trying to lose weight said they were interested in taking a safe and effective drug. But only 23 percent remained interested when asked if they would take such a drug if it had to be injected. And just 16 percent were still interested if their insurance would not pay for the drug. The list price of the drugs is about $1,300 a month. When they heard they would regain their lost weight it they stopped taking the drug, interest declined to 14 percent. “People always want that magic pill,” said Ashley Kirzinger, director of survey methodology at KFF. “There is no magic.” The survey was conducted in July online and by telephone with a representative sample of 1,327 U.S. adults. That’s the median weight loss experienced by people who take Wegovy, a drug from Novo Nordisk. The new drugs are the first truly effective obesity medicines. They act by stemming people’s appetites and cravings for food. Many patients started by taking Ozempic, a diabetes drug also by Novo Nordisk that led to weight loss as a side effect. But many more patients are asking for Wegovy, which is approved for obesity. Mounjaro, made by Eli Lilly and approved for treating diabetes, is expected to be approved soon for obesity. People taking it lose a median of 20 percent of their body weight. Obesity is a chronic disease that can result in diabetes and other conditions like high blood pressure, heart disease, sleep apnea and joint problems. But it was so difficult to treat obesity that many doctors and patients had all but given up. © 2023 The New York Times Company

Four key questions on the new wave of anti-obesity drugs

McKenzie Prillaman It’s rare to find a product so successful that its makers stop advertising it. But that’s what happened to the weight-loss drug Wegovy in May. In the United States, where prescription drugs can be advertised, developer Novo Nordisk pulled its television adverts because it couldn’t keep up with demand. The injectable medication, called semaglutide, works by imitating a hormone that curbs appetite and was approved as an obesity treatment by the US Food and Drug Administration (FDA) in 2021. In a study, participants who took semaglutide for over a year lost more than twice as much body weight on average — almost 16% — as did people taking an older weight-loss drug that mimics the same hormone1. Semaglutide’s approval for treatment of weight loss came four years after the drug was approved for type 2 diabetes under the trade name Ozempic, also made by Novo Nordisk, based in Bagsværd, Denmark. Demand for Ozempic has skyrocketed as physicians prescribe it for weight loss outside its approved use. Now, even more-potent medications for obesity are on the way. The drug tirzepatide, which is FDA-approved for type 2 diabetes under the name Mounjaro and made by Eli Lilly in Indianapolis, Indiana, imitates two hunger-related hormones. And the company’s drug retatrutide, which mimics three hormones, showed promising results for weight loss in its mid-stage clinical trial, announced at a conference in June. Neither of these newcomers has been approved for obesity. But treating the condition is more urgent than ever. Obesity rates have tripled in the past 50 years, and carrying significant extra weight often brings a heightened risk of other health complications, including type 2 diabetes, heart disease and some cancers. It can also impede quality of life in other ways, such as limiting a person’s range of movement or resulting in feelings of shame because of weight stigma. With this wave of drugs comes a fresh set of questions for researchers. “We are currently in such a dynamic phase of these transformative developments,” says physician-scientist Matthias Tschöp, chief executive of Helmholtz Munich, a research centre in Germany. “We’re still overwhelmed with curiosity.” © 2023 Springer Nature Limited

Intermittent fasting is as effective as counting calories

Will Stone Intermittent fasting has taken off in popularity in recent years as an alternative to more traditional weight loss advice, including counting calories, which can be cumbersome and hard to sustain for some people. Intermittent fasting can take different forms. One approach — called time-restricted eating — limits when people eat to a specific window of time, often around six to eight hours. Some research suggests this can be successful for weight loss in the short term because people end up eating less, but it has been less clear how well it works over a longer stretch of time. A study published Monday may have an answer. "We really wanted to see if people can lose weight with this over a year. Can they maintain the weight loss?" says Krista Varady, a professor of nutrition at the University of Illinois Chicago, who has studied intermittent fasting for the past two decades and led the new study. Varady's research finds that intermittent fasting can indeed help people lose weight and keep it off over the course of a year, with effects similar to tracking calories. The results of the clinical trial were published in the Annals of Internal Medicine. Sponsor Message The amount of weight loss wasn't dramatic — equivalent to about 5% of body weight — but the findings are encouraging to researchers in the field, in part because they underscore that people could keep this habit up over a long stretch of time. "That is pretty exciting," says Courtney Peterson, a professor of nutrition at the University of Alabama at Birmingham, who wasn't involved in the research. "This study has the most compelling results suggesting that people can stick with it, that it's not a fad diet in the sense that people can do it for three months and they fall off the wagon for a year." © 2023 npr

People on Drugs Like Ozempic Say Their ‘Food Noise’ Has Disappeared

By Dani Blum Until she started taking the weight loss drug Wegovy, Staci Klemmer’s days revolved around food. When she woke up, she plotted out what she would eat; as soon as she had lunch, she thought about dinner. After leaving work as a high school teacher in Bucks County, Pa., she would often drive to Taco Bell or McDonald’s to quell what she called a “24/7 chatter” in the back of her mind. Even when she was full, she wanted to eat. Almost immediately after Ms. Klemmer’s first dose of medication in February, she was hit with side effects: acid reflux, constipation, queasiness, fatigue. But, she said, it was like a switch flipped in her brain — the “food noise” went silent. “I don’t think about tacos all the time anymore,” Ms. Klemmer, 57, said. “I don’t have cravings anymore. At all. It’s the weirdest thing.” Dr. Andrew Kraftson, a clinical associate professor at Michigan Medicine, said that over his 13 years as an obesity medicine specialist, people he treated would often say they couldn’t stop thinking about food. So when he started prescribing Wegovy and Ozempic, a diabetes medication that contains the same compound, and patients began to use the term food noise, saying it had disappeared, he knew exactly what they meant. As interest has intensified around Ozempic and other injectable diabetes medications like Mounjaro, which works in similar ways, that term has gained traction. Videos related to the subject “food noise explained” have been viewed 1.8 billion times on TikTok. And some of the people who have managed to get their hands on these medications — despite persistent shortages and list prices that can near or surpass a thousand dollars — have shared stories on social media about their experiences. When food noise fades Wendy Gantt, 56, said she first heard the term food noise on TikTok, where she had also learned about Mounjaro. She found a telehealth platform and received a prescription within a few hours. She can remember the first day she started taking it last summer. “It was like a sense of freedom from that loop of, ‘What am I going to eat? I’m never full; there’s not enough. What can I snack on?’” she said. “It’s like someone took an eraser to it.” © 2023 The New York Times Company

New Obesity Drugs Come With a Side Effect of Shaming

By Gina Kolata Eileen Isotalo was always able to lose weight, but always gained it back. Now 66, her first diet was with Weight Watchers at age 14. She went on to try one diet after another and bought so many books on weight loss that she thinks she has more than the public library. In desperation, she finally went to a weight management clinic at the University of Michigan. She had sleep apnea and aching knees, but could not curb her appetite. “It’s just this drive to eat,” said Ms. Isoltalo, a retired interior design coordinator. “It’s almost like this panic feeling when you start craving food.” “My mental shame was profound,” she said. Now, though, since she started taking Wegovy, one of a new class of drugs for obesity that was prescribed by her doctor at the clinic, those cravings are gone. She has lost 50 pounds and jettisoned the dark clothes she wore to hide her body. Her obesity-related medical problems have vanished along with much of the stigma that caused her to retreat from family and friends. But like others at the clinic, she still struggles with the fear others will judge her for receiving injections to treat her obesity rather than finding the willpower to lose weight and keep it off. Yet the drug, she said, “changed my life.” Wegovy and drugs like it make this “a very exciting time in the field,” said Dr. Susan Yanovski, co-director of the office of obesity research at the National Institute of Diabetes and Digestive and Kidney Diseases. About 100 million Americans, or 42 percent of the adult population, have obesity, according to the Centers for Disease Control and Prevention. For the first time, people with obesity, who faced a lifetime of medical jeopardy, can escape the ruthless trap of fruitless dieting and see their obesity-related health problems mitigated, along with the weight loss. But there is still the taint. © 2023 The New York Times Company

The neurons that make us feel hangry

By Amber Dance Maybe it starts with a low-energy feeling, or maybe you’re getting a little cranky. You might have a headache or difficulty concentrating. Your brain is sending you a message: You’re hungry. Find food. Studies in mice have pinpointed a cluster of cells called AgRP neurons near the underside of the brain that may create this unpleasant hungry, even “hangry,” feeling. They sit near the brain’s blood supply, giving them access to hormones arriving from the stomach and fat tissue that indicate energy levels. When energy is low, they act on a variety of other brain areas to promote feeding. By eavesdropping on AgRP neurons in mice, scientists have begun to untangle how these cells switch on and encourage animals to seek food when they’re low on nutrients, and how they sense food landing in the gut to turn back off. Researchers have also found that the activity of AgRP neurons goes awry in mice with symptoms akin to those of anorexia, and that activating these neurons can help to restore normal eating patterns in those animals. Understanding and manipulating AgRP neurons might lead to new treatments for both anorexia and overeating. “If we could control this hangry feeling, we might be better able to control our diets,” says Amber Alhadeff, a neuroscientist at the Monell Chemical Senses Center in Philadelphia. AgRP neurons appear to be key players in appetite: Deactivating them in adult mice causes the animals to stop eating — they may even die of starvation. Conversely, if researchers activate the neurons, mice hop into their food dishes and gorge themselves. © 2023 Annual Reviews

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