Chapter 13. Homeostasis: Active Regulation of the Internal Environment

Follow us on Facebook or subscribe to our mailing list, to receive news updates. Learn more.

Links 1 - 20 of 1957

By Erin Garcia de Jesús DENVER — A weight-loss drug used to treat obesity and diabetes has shown promise to treat another disorder: opioid addiction. Early results from a small clinical trial, presented February 17 at the annual meeting of the American Association for the Advancement of Science, suggest that a close relative of the weight-loss drugs Wegovy and Ozempic significantly lessened cravings for opioids in people with opioid use disorder. “For them to have any time when they might be free of that craving seems to be very hopeful,” Patricia “Sue” Grigson, a behavioral neuroscientist at Penn State College of Medicine in Hershey said at the conference. The vast majority of drug overdose deaths in the United States are due to opioids (SN: 2/14/24). The drug, called liraglutide, mimics a hormone called GLP-1 that the body releases after people eat. Wegovy and Ozempic — brand names for semaglutide, a molecule that induces weight loss more effectively than liraglutide — also imitate the hormone. It’s unclear exactly how the drugs work when it comes to weight loss, but researchers think such GLP-1 dupes prompt the body and brain to make people feel full (SN: 12/13/23). There are hints that such drugs could work for addiction, too. People taking Wegovy or Ozempic have reported lessened desire for not just food but also alcohol and nicotine. What’s more, Grigson and colleagues showed in a previous study in rats that liraglutide can cut down on heroin-seeking behavior, perhaps by changing the animals’ brain activity (SN: 8/30/23). © Society for Science & the Public 2000–2024.

Keyword: Drug Abuse; Obesity
Link ID: 29150 - Posted: 02.20.2024

By Kristin Kiesel and Richard J. Sexton Many public health advocates and scholars see sugar-sweetened-beverage taxes (often simply called soda taxes) as key to reducing obesity and its adverse health effects. But a careful look at the data challenges this view. We reviewed close to 100 studies that have analyzed current taxes in more than 50 countries and conducted our own research on the effectiveness of soda taxes in the US. There is no conclusive evidence that soda taxes have reduced how much sugar or calories people consume in any meaningful way. Soda taxes alone simply cannot nudge consumers toward healthier food choices. The World Health Organization estimates that more than 17 million people die prematurely each year from chronic noncommunicable diseases. Being overweight or obese is a major risk factor for many of these conditions, including type 2 diabetes, cardiovascular diseases, asthma and several types of cancer. A widely publicized 2019 Lancet Commission report pegged annual obesity-related health-care costs and economic productivity losses at $2 trillion, about 3 percent of the global gross domestic product. Consuming large amounts of added sugars is a key part of this problem. A single 12-ounce can of soda can have more than 10 teaspoons of sugar; drinking just one exceeds the American Heart Association’s recommended daily limits on added sugars. It is easy to see why reducing soda consumption has been a popular target in the war against obesity. One would think that taxing sodas would raise their prices and discourage consumers from purchasing them. With this idea in mind, a wave of taxes has been slapped on sugar-sweetened beverages across the world. For example, cities in California’s Bay Area have imposed a tax of 1 cent per ounce on sugary beverages (a seemingly large price increase given soda’s cost of about 5 cents per ounce in the western US).

Keyword: Obesity
Link ID: 29143 - Posted: 02.10.2024

By Matt Richtel For decades, eating disorders were thought to afflict mostly, if not exclusively, women and girls. In fact, until 2013, the loss of menstruation had long been considered an official symptom of anorexia nervosa. Over the last decade, however, health experts have increasingly recognized that boys and men also suffer from eating disorders, and they have gained a better understanding of how differently the illness presents in that group. A small but growing body of scientists and physicians have dedicated themselves to identifying the problem, assessing its scope and developing treatments. Recently, two of these experts spoke to The New York Times about how the disease is affecting adolescent boys, what symptoms and behaviors parents should look for, and which treatments to consider. Dr. Jason Nagata is a pediatrician at the University of California, San Francisco, who specializes in eating disorders; he is senior editor of the Journal of Eating Disorders and editor of the book “Eating Disorders in Boys and Men.” Dr. Sarah Smith is a child and adolescent psychiatrist at the University of Toronto who specializes in eating disorders; she was the lead author on a study published in JAMA Open Network in December that showed sharp increases in the rates of hospitalizations for boys with eating disorders. The medical and scientific understanding of eating disorders is changing and expanding. What happened? Dr. Smith: Historically, eating disorders have been conceptualized mostly as anorexia, which has been portrayed as an illness of adolescent females who want to lose weight for aesthetic reasons. Dr. Nagata: There’s increasing recognition, particularly in the last decade or so, that some people with body image dissatisfaction are not trying to lose weight at all. Some men and boys are trying to become large and muscular. In fact, one-third of teenage boys across the United States report that they’re trying to bulk up and get more muscular. And a subset of those may develop eating disorders or muscle dysmorphia that can lead to significant psychological distress and physical health complications. © 2024 The New York Times Company

Keyword: Anorexia & Bulimia; Sexual Behavior
Link ID: 29140 - Posted: 02.08.2024

By Harriet Brown The minute I saw the headline — “Should Patients Be Allowed to Die From Anorexia?” — in The New York Times Magazine last month, my heart sank. Over the last two years, more and more psychiatrists have floated the idea that it’s OK to stop trying to cure some people with anorexia nervosa. People with anorexia develop a deep fear of food and eating, often losing so much weight that they die of starvation or complications. About 20 percent die by suicide. Anorexia is a terrible disease, one that inflicts maximum pain on the person diagnosed and their families and friends. The suffering is continuous and intense, and it gets even worse during recovery. Our family experienced this for eight years. Having to watch my daughter suffer made me realize that anorexia is not a choice or a question of vanity but a tsunami of fear and anxiety that makes one of the most basic human acts, the act of eating, as terrifying as jumping out of a plane without a parachute. It usually takes years of steady, consistent, calorie-dense eating to fully heal the body and brain of a person with anorexia. Without the right kind of support and treatment, it’s nearly impossible. So when psychiatrists suggest that maybe some people can’t recover and should be allowed to stop trying, they’re sidestepping their own responsibility. What they should be saying instead is that current views on and treatments of anorexia are abysmal, and medicine needs to do better. If you’ve never experienced anorexia firsthand, consider yourself blessed. Anorexia has one of the highest mortality rates of any psychiatric illness. People with anorexia are 18 times as likely to die from suicide as their peers. Fewer than half of those with anorexia make a full recovery.

Keyword: Anorexia & Bulimia
Link ID: 29139 - Posted: 02.08.2024

April Smith Did you know that anorexia is the most lethal mental health condition? One person dies from an eating disorder every hour in the U.S. Many of these deaths are not from health consequences related to starvation, but from suicide. Up to 1 in 5 women and 1 in 7 men in the U.S. will develop an eating disorder by age 40, and 1 in 2 people with an eating disorder will think about ending their life. About 1 in 4 people with anorexia nervosa or bulimia nervosa will attempt to kill themselves, and those with anorexia have a risk of death by suicide 31 times higher than peers without the disorder. In fact, nonsuicidal self-injury, suicidal ideation, suicide attempts and suicide deaths are all more prevalent among those with any type of eating disorder compared to those without an eating disorder. Why might that be? I am a clinical psychologist who studies eating disorders and self-harm, and I have spent the past 15 years researching this question. We still don’t have the answer. But new work on perception of the internal state of the body points to some promising possibilities for treatment. And what we’re learning could help anyone improve their relationship with their body. To understand why people with eating disorders are at risk of dying by suicide, I first want to ask you to do a little thought exercise. I’d like you to really think about your body: Think about your hair, face, arms, stomach, chest and legs. What words and feelings come to mind? Are there any things you wish you could change? Feel free to close your eyes and try this out. © 2010–2024, The Conversation US, Inc.

Keyword: Anorexia & Bulimia
Link ID: 29127 - Posted: 02.03.2024

By David Levin It can start small: a peculiar numbness; a subtle facial tic; an inexplicably stiff muscle. But then time goes by — and eventually, the tremors set in. Roughly a million people in the United States (and roughly 10 million people worldwide) live with Parkinson’s disease, a potent neurological disorder that progressively kills neurons in the brain. As it does so, it can trigger a host of crippling symptoms, from violent tremors to excruciating muscle cramps, terrifying nightmares and constant brain fog. While medical treatments can alleviate some of these effects, researchers still don’t know exactly what causes the disease to occur in the first place. A growing number of studies, however, are suggesting that it may be tied to an unlikely culprit: bacteria living inside our guts. Every one of us has hundreds or thousands of microbial species in our stomach, small intestine and colon. These bacteria, collectively called our gut microbiome, are usually considerate guests: Although they survive largely on food that passes through our insides, they also give back, cranking out essential nutrients like niacin (which helps our body convert food into energy) and breaking down otherwise indigestible plant fiber into substances our bodies can use. As Parkinson’s advances in the brain, researchers have reported that the species of bacteria present in the gut also shift dramatically, hinting at a possible cause for the disease. A 2022 paper published in the journal Nature Communications recorded those differences in detail. After sequencing the mixed-together genomes of fecal bacteria from 724 people — a group with Parkinson’s and another without — the authors saw a number of distinct changes in the guts of people who suffered from the disease. The Parkinson’s group had dramatically lower amounts of certain species of Prevotella, a type of bacterium that helps the body break down plant-based fiber (changes like this in gut flora could explain why people with Parkinson’s disease often experience constipation). At the same time, the study found, two harmful species of Enterobacteriaceae, a family of microbes that includes Salmonella, E. coli and other bugs, proliferated. Those bacteria may be involved in a chain of biochemical events that eventually kill brain cells in Parkinson’s patients, says Tim Sampson, a biologist at Emory University School of Medicine and coauthor of the study.

Keyword: Parkinsons
Link ID: 29098 - Posted: 01.13.2024

By Tim Vernimmen It is increasingly well understood that the countless microbes in our guts help us to digest our food, to absorb and produce essential nutrients, and to prevent harmful organisms from settling in. Less intuitive — perhaps even outlandish — is the idea that those microbes may also affect our mood, our mental health and how we perform on cognitive tests. But there is mounting evidence that they do. For nearly two decades, neuroscientist John Cryan of University College Cork in Ireland has been uncovering ways in which intestinal microbes affect the brain and behavior of humans and other animals. To his surprise, many of the effects he’s seen in rodents appear to be mirrored in our own species. Most remarkably, research by Cryan and others has shown that transplanting microbes from the guts of people with psychiatric disorders like depression to the guts of rodents can cause comparable symptoms in the animals. These effects may occur in several ways — through the vagus nerve connecting the gut to the brain, through the influence of gut bacteria on our immune systems, or by microbes synthesizing molecules that our nerve cells use to communicate. Cryan and coauthors summarize the science in a set of articles including “Man and the Microbiome: A New Theory of Everything?,” published in the Annual Review of Clinical Psychology. Cryan told Knowable Magazine that even though it will take much more research to pin down the mechanisms and figure out how to apply the insights, there are some things we can do already. This conversation has been edited for length and clarity.

Keyword: Depression; Stress
Link ID: 29091 - Posted: 01.11.2024

By Gina Kolata People taking the wildly popular drugs Ozempic, to treat diabetes, and Wegovy, to combat obesity, are slightly less likely to have suicidal thoughts than people who are not taking them, researchers reported on Friday. Millions of people take Ozempic and Wegovy, which are considered to be among the biggest blockbusters in medical history. But last year a European drug safety agency said it was investigating whether the drugs cause suicidal thoughts. The new study, published in the journal Nature Medicine, was funded by the National Institutes of Health and used a huge population. The findings provide data that may potentially reassure people who take the drugs. Novo Nordisk, maker of the drugs, had no role in the study, and the study’s investigators had no conflicts of interest. The investigators used anonymized electronic health records from a database of 100.8 million people. That allowed them to look at two groups: 240,618 who were prescribed Wegovy or other weight loss drugs, and 1,589,855 who were prescribed Ozempic or other medicines to lower their blood sugar. Suicidal thoughts were included in patients’ records as part of routine monitoring of their health. The investigators compared the incidence of suicidal thoughts in people who were taking the drugs with the incidence among similar people who were not taking them but were taking other weight loss and anti-diabetes medications. They also asked if there was an increase in the recurrence of suicidal thoughts among those taking the drugs who had previously reported thoughts of suicide. The database’s size allowed the researchers to look at subgroups such as sex, race and age groups. “No matter how hard we tried we did not see any increased risk,” said Rong Xu, director of the Center for Artificial Intelligence in Drug Discovery at Case Western Reserve University in Cleveland. Dr. Xu conceived the study and interpreted the data with Dr. Nora D. Volkow, director of the National Institute on Drug Abuse. But it was an observational study, so it is impossible to draw conclusions about cause and effect. Such studies can only show associations. “More studies are absolutely needed,” Dr. Volkow said. © 2024 The New York Times Company

Keyword: Obesity; Depression
Link ID: 29078 - Posted: 01.06.2024

By Katie Engelhart The doctors told Naomi that she could not leave the hospital. She was lying in a narrow bed at Denver Health Medical Center. Someone said something about a judge and a court order. Someone used the phrase “gravely disabled.” Naomi did not think she was gravely disabled. Still, she decided not to fight it. She could deny that she was mentally incompetent — but this would probably just be taken as proof of her mental incompetence. Of her lack of insight. She would, instead, “succumb to it.” It was early 2018. She had come to the hospital voluntarily, because she was getting so thin. In the days before, she had felt her electrolyte levels dip toward the danger zone — and she had decided that, even after everything, she did not want to be dead. By then, Naomi was 37 and had been starving herself for 26 years, and she was exquisitely attuned to her body’s corrupted chemistry. At the hospital, she was admitted to the ACUTE Center for Eating Disorders & Severe Malnutrition for medical stabilization. There, doctors began what was once called refeeding but is now more commonly called nutritional rehabilitation, using an intravenous line that fed into her neck. Reintroducing food to an emaciated body can be dangerous and even lethal if done too quickly. Physicians identified this phenomenon in the aftermath of World War II, when they observed skeletal concentration-camp survivors and longtime prisoners of war eat high-caloric foods and then drop dead of cardiac failure. “Well, here I am,” Naomi said in a video message that she recorded for her parents. “I am alive, but am I happy? I don’t know. … It’s pretty pathetic. I don’t know how I feel about the fact that I would have died had I not come.” In the video, she was wearing a hot pink tank top, even though it was cool in the hospital room, because she wanted to shiver, because shivering burned calories. A few days later, when she was not imminently dying anymore, Naomi announced that she was going home — and the hospital responded by placing her on a 72-hour mental-health hold. Clinicians then obtained what Colorado calls a short-term certification, which required, by judicial order, that Naomi be detained and treated, in her case until she reached what physicians determined to be 80 percent of her “ideal body weight.” In Colorado, as in most states, a patient can be treated against her will if she is mentally ill and found incapable of making informed decisions. That day, Naomi was transferred to a residential program at Denver’s Eating Recovery Center (E.R.C.) © 2024 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 29075 - Posted: 01.03.2024

By Laura Sanders In this busy holiday season, many of us multitask. Arctic reindeer are no exception. Reindeer can eat and sleep at the same time, a new study suggests. This timesaving strategy, described December 22 in Current Biology, adds to the number of ingenious ways animals can catch some z’s under tough conditions (SN: 11/30/23). Arctic reindeer are quite busy in the summer — eating when the sun shines around the clock and the food is abundant. Like other ruminants, reindeer spend a considerable amount of time chewing on regurgitated food, making it smaller and easier to digest. Finding time to sleep amid all this cud chewing might be tough. But not if the reindeer could sleep while they chewed. To find out if the reindeer could actually sleep-eat, neuroscientist Melanie Furrer and chronobiologist Sara Meier, along with their colleagues, trained four female Eurasian tundra reindeer (Rangifer tarandus tarandus) to tolerate a pen and electrodes on shaved patches of skin. The process involved some kicks and lots of lichen treats, “which is like candy to them,” says Meier, of the University of Zurich. The researchers were looking for the brain waves that appear during non-REM sleep, a deep, restorative sleep phase. These waves appeared when the reindeer were chewing cud, though the chewing motion itself made it hard to say whether the signal was identical to that of a regular sleep session. “We couldn’t go into detail by looking only at the brain waves, because we have this chewing in there that disturbs it a bit,” says Furrer, also of the University of Zurich. Still, other signs also pointed to sleep while chewing. The reindeer were calm while chewing, often with their eyes closed. “They were in a very relaxed state that resembles the body position of non-REM sleep,” Furrer says. Ruminating reindeer were also harder to disturb; rustling from neighboring reindeer was less likely to get a look from a ruminating reindeer. When reindeer are kept awake, they need catch-up recovery sleep. But time spent chewing decreased this time spent in recovery sleep, the researchers found. © Society for Science & the Public 2000–2023.

Keyword: Sleep; Attention
Link ID: 29072 - Posted: 12.31.2023

Alex Johnson The holiday season is upon us, and with it, opportunities to indulge in festive treats. The proverbial saying “you eat with your eyes first” seems particularly relevant at this time of year. The science behind eating behavior, however, reveals that the process of deciding what, when and how much to eat is far more complex than just consuming calories when your body needs fuel. Hunger cues are only part of why people choose to eat. As a scientist interested in the psychology and biology that drives eating behavior, I’m fascinated with how the brain’s experiences with food shape eating decisions. Food-related visual cues can shape feeding behaviors in both people and animals. For example, wrapping food in McDonald’s packaging is sufficient to enhance taste preferences across a range of foods – from chicken nuggets to carrots – in young children. Visual food-related cues, such as presenting a light when food is delivered, can also promote overeating behaviors in animals by overriding energy needs. In fact, a whole host of sensory stimuli – noises, smells and textures – can be associated with the pleasurable consequences of eating and influence food-related decisions. This is why hearing a catchy radio jingle for a food brand, seeing a television ad for a restaurant or walking by your favorite eatery can shape your decision to consume and sometimes overindulge.

Keyword: Obesity; Chemical Senses (Smell & Taste)
Link ID: 29060 - Posted: 12.22.2023

By Gina Kolata Dr. Edward Lewis, a pediatrician in Rochester, N.Y., has seen hundreds of children with obesity over the years in his medical practice. He finally may have a treatment for their medical condition — the powerful weight loss drug Wegovy. But that does not mean Dr. Lewis is prescribing it. Nor are most other pediatricians. “I am reluctant to prescribe medications we don’t use on a day-to-day basis,” Dr. Lewis said. And, he added, he is disinclined to use “a medicine that is a relative newcomer to the scene in kids.” Regulators and medical groups have all said that these drugs are appropriate for children as young as 12. But like Dr. Lewis, many pediatricians hesitate to prescribe Wegovy to young people, fearful that too little is known about long term effects, and mindful of past cases when problems emerged years after a drug was approved. Twenty-two percent of adolescents age 12 to 19 have obesity. Research shows that most are unlikely to ever overcome the condition — advice to diet and exercise usually has not helped. The reason, obesity researchers say, is that obesity is not caused by a lack of will power. Instead, it is a chronic disease characterized by an overwhelming desire to eat. Of particular concern to doctors are the 6 percent of children and adolescents with severe obesity, which is defined as having a body mass index at or above 120 percent of the 95th percentile for height and weight. “We are not talking about kids who are mildly overweight,” said Susan Yanovski, co-director of the office of obesity research at the National Institute of Diabetes and Digestive and Kidney Diseases. Such extreme obesity in adolescents, she said, often has “a really severe course.” These teenagers develop diabetes, heart disease, high blood pressure, kidney failure and eye damage much earlier than adults with obesity. “It is terrifying,” Dr. Yanovski added. The seriousness of health outcomes for obese teenagers motivated the American Academy of Pediatrics to recommend weight loss drugs like Wegovy for adolescents in January, after the Food and Drug Administration approved it for people age 12 and older. When that happened, experts in obesity medicine were elated, knowing full well the scope of the problem. “We said, Wow, we finally have something we can offer,” Dr. Yanovski said. Still, drugs like Wegovy are new, and the impediments to using them are snowballing. Doctors also worry about the dearth of data on long-term safety. And those who want to prescribe Wegovy say that they are beset by roadblocks put up by health insurers along with severe and continuing drug shortages. © 2023 The New York Times Company

Keyword: Obesity
Link ID: 29044 - Posted: 12.13.2023

By Siddhant Pusdekar In the deepest stage of sleep, slow waves of electrical activity travel through your brain. They help consolidate memories and flush out the buildup of unwanted chemicals, getting you ready for the day. This midnight orchestra is responsible for many of the benefits of a good night’s sleep, such as improved attention, mood and energy levels. Scientists at the University of California, Berkeley, recently found that for some people, these waves could also serve as early warning signs of diabetes. The results, published in July in Cell Reports Medicine, suggest that getting a restful sleep may help control high blood sugar. People with type 2 diabetes are unable to metabolize sugar, leading to a damaging excess concentration in the blood. The approximately 515 million people globally with type 2 diabetes can manage blood sugar through diet, exercise and medications such as insulin. But researchers and clinicians have observed that quality of sleep seems to influence blood sugar, too. “We have known that something magic happens during sleep,” says New York University neuroscientist Gyorgy Buzsaki about the links between sleep and metabolism. Yet the mechanism behind that relationship has been a mystery, he says. To investigate, the July study’s co-lead author Raphael Vallat, then a postdoctoral researcher at U.C. Berkeley, analyzed blood glucose and sleep measurements from two large independent public datasets. In the first analysis, Vallat and his colleagues examined sleep patterns measured from polysomnography, a standard assessment that doctors recommend for people with sleep problems. The procedure, typically conducted at night, involves placing a bunch of wires on different parts of the head to record activity in specific brain regions. The ends of the wires act like “microphones” that “hear” brain waves, explains Vyoma Shah, a graduate student at U.C. Berkeley and co-lead author of the paper. Squiggles of different shapes and sizes on the polysomnography graphs represent the ebbs and flows of electrical activity in people’s head as they sleep throughout the night. It is only a surface-level view, however. © 2023 SCIENTIFIC AMERICAN,

Keyword: Sleep; Obesity
Link ID: 29035 - Posted: 12.09.2023

Jon Hamilton If this year's turkey seems over brined, blame your brain. The question of when salty becomes too salty is decided by a special set of neurons in the front of the brain, researchers report in the journal Cell. A separate set of neurons in the back of the brain adjusts your appetite for salt, the researchers showed in a series of experiments on mice. "Sodium craving and sodium tolerance are controlled by completely different types of neurons," says Yuki Oka, an author of the study and a professor of biology at Caltech. The finding could have health implications because salt ingestion is a "major issue" in many countries, including the United States, says Nirupa Chaudhari, a professor of physiology and biology at the University of Miami's Miller School of Medicine. Too much salt can cause high blood pressure and raise the risk for heart disease and stroke, says Chaudhari, who was not involved in the study. Craving, to a point The study sought to explain the complicated relationship that people and animals have with salt, also known as sodium chloride. We are happy to drink sodas, sports drinks, and even tap water that contain a little salt, Oka says. "But if you imagine a very high concentration of sodium like ocean water, you really hate it." This aversion to super salty foods and beverages holds unless your body is really low on salt, something that's pretty rare in people these days. But experiments with mice found that when salt levels plummet, the tolerance for salty water goes up. "Animals start liking ocean water," Oka says. The reason for this change involves at least two different interactions between the body and brain, Oka's team found. When the concentration of sodium in the bloodstream begins to fall below healthy levels, a set of neurons in the back of the brain respond by dialing up an animal's craving for salt. "If you stimulate these neurons, then animals run to a sodium source and start eating," Oka says. Meanwhile, a different set of neurons in the front of the brain monitors the saltiness of any food or water the mice are consuming. And usually, these neurons will set an upper limit on saltiness. © 2023 npr

Keyword: Chemical Senses (Smell & Taste); Obesity
Link ID: 29024 - Posted: 11.26.2023

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.”

Keyword: Obesity
Link ID: 29023 - Posted: 11.26.2023

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

Keyword: Obesity; Glia
Link ID: 29018 - Posted: 11.22.2023

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

Keyword: Obesity
Link ID: 29013 - Posted: 11.22.2023

By Frieda Klotz Tess Olmsted stopped eating sugar when she was just 12 years old. She had previously been treated for obsessive compulsive disorder, or OCD, and soon found herself following rituals around eating. “For me it was never, ‘Oh I need to get skinnier,’” she recalls. Once she started to diet, she simply couldn’t stop. Two years later, on a summer day in 2019, her father saw her on the family’s patio wearing a loose-fitting swimsuit. He soon noticed how little Tess was eating and insisted she see the pediatrician. During a subsequent appointment with a specialist, he recalls, the family learned that Tess’s blood pressure and heart rate were dangerously low. She was admitted to a hospital in life-threatening condition. Across the United States, up to 2 million adults have had anorexia, a mental health condition in which a person severely restricts their food intake, often due to an intense fear of gaining weight. Almost 1 percent of all U.S. women will experience anorexia at some point in their lives. Patients are developing the condition increasingly early in life — sometimes as young as 8 years old — and new figures suggest that symptoms in children worsened during the Covid-19 pandemic, leading to increased numbers of hospitalizations. At one treatment center in Michigan, the admission rate of young people aged 10 to 23 more than doubled during the pandemic’s first year. These sobering developments are due, in part, to the fact that there are no drugs or devices approved by the U.S. Food and Drug Administration to treat the condition. For adults, there are three first-line treatments: an adapted form of cognitive behavioral therapy, known as CBT-E; a structured psychotherapy designed with patient input; and an approach that combines psychotherapy with nutritional support. Studies have shown that these approaches can help more than 50 percent of patients. But experts acknowledge that the studies are not high quality. Patients with anorexia are hard to engage in treatment, and as a result, studies are small and drop-out rates are high.

Keyword: Anorexia & Bulimia
Link ID: 29002 - Posted: 11.13.2023

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.

Keyword: Obesity
Link ID: 28993 - Posted: 11.08.2023

By Meghan Rosen In endurance athletes, some brain power may come from an unexpected source. Marathon runners appear to rely on myelin, the fatty tissue bundled around nerve fibers, for energy during a race, scientists report October 10 in a paper posted at In the day or two following a marathon, this tissue seems to dwindle drastically, brain scans of runners reveal. Two weeks after the race, the brain fat bounces back to nearly prerace levels. The find suggests that the athletes burn so much energy running that they need to tap into a new fuel supply to keep the brain operating smoothly. “This is definitely an intriguing observation,” says Mustapha Bouhrara, a neuroimaging scientist at the National Institute on Aging in Baltimore. “It is quite plausible that myelin lipids are used as fuel in extended exercise.” If what the study authors are seeing is real, he says, the work could have therapeutic implications. Understanding how runners’ myelin recovers so rapidly might offer clues for developing potential treatments — like for people who’ve lost myelin due to aging or neurodegenerative disease. Much of the human brain contains myelin, tissue that sheathes nerve fibers and acts as an insulator, like rubber coating an electrical wire. That insulation lets electrical messages zip from nerve cell to nerve cell, allowing high-speed communication that’s crucial for brain function. The fatty tissue seems to be a straightforward material with a straightforward job, but there’s likely more to it than that, says Klaus-Armin Nave, a neurobiologist at the Max Planck Institute for Multidisciplinary Sciences in Göttingen, Germany. “For the longest time, it was thought that myelin sheathes were assembled, inert structures of insulation that don’t change much after they’re made,” he says. Today, there’s evidence that myelin is a dynamic structure, growing and shrinking in size and abundance depending on cellular conditions. The idea is called myelin plasticity. “It’s hotly researched,” Nave says. © Society for Science & the Public 2000–2023.

Keyword: Glia; Multiple Sclerosis
Link ID: 28983 - Posted: 11.01.2023