Chapter 13. Homeostasis: Active Regulation of the Internal Environment

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By Kim Tingley It’s simple, we are often told: All you have to do to maintain a healthy weight is ensure that the number of calories you ingest stays the same as the number of calories you expend. If you take in more calories, or energy, than you use, you gain weight; if the output is greater than the input, you lose it. But while we’re often conscious of burning calories when we’re working out, 55 to 70 percent of what we eat and drink actually goes toward fueling all the invisible chemical reactions that take place in our body to keep us alive. “We think about metabolism as just being about exercise, but it’s so much more than that,” says Herman Pontzer, an associate professor of evolutionary anthropology at Duke University. “It’s literally the running total of how busy your cells are throughout the day.” Figuring out your total energy expenditure tells you how many calories you need to stay alive. But it also tells you “how the body is functioning,” Pontzer says. “There is no more direct measure of that than energy expenditure.” Though scientists have been studying metabolism for at least a century, they have not been able to measure it precisely enough — in real-world conditions, in enough people, across a broad-enough age range — to see how it changes throughout the human life span. It is clear that the bigger someone is, the more cells they have, and thus the more total calories they burn per day. But it has been much harder to assess whether variables like age, sex, lifestyle and illness influence our rate of energy expenditure. This lack of data led to assumptions rooted in personal experience: for instance, that significant hormonal changes like those that take place during puberty and menopause cause our metabolism to speed up or slow down, prompting us to burn more or fewer calories per day; or that men have inherently faster metabolisms than women, because they seem able to shed pounds more easily; or that our energy expenditure slows in midlife, initiating gradual and inevitable weight gain. “I’m in my 40s; I feel different than I did in my 20s — I buy it, too,” Pontzer says. “All that intuition was never backed up by data. It just seemed so sure.” © 2021 The New York Times Company

Keyword: Obesity
Link ID: 27994 - Posted: 09.15.2021

Natalie Grover Losing weight through exercise appears to be more difficult for obese people, research suggests. Initially, researchers thought that the total energy we spend in a day is the sum of energy expended due to activity (ranging from light gardening to running a marathon) and energy used for basic functioning (what keeps us ticking even when we are doing nothing, such as immune function and wound healing). But preliminary lab research indicates that that simple addition could be misleading – estimates of total daily expenditure tend to be less than the sum of baseline and activity expenditure in individuals. To explore this further, a group of international scientists analysed measurements of energy expenditure from 1,754 adults from a dataset collected over decades and supplied by the International Atomic Energy Agency. They found that increasing levels of activity by exercising more, for instance, led to each person’s body compensating by limiting the energy expended on basic metabolic functions over a longer period, according to the study published in the journal Current Biology. For instance, if you go for a run and your activity tracker says you burned 300 calories (and you didn’t eat any differently) – you may assume that your total daily energy expenditure went up by 300 calories. That may be the case in the short term, but over the long term the body starts to compensate for this extra energy exertion by reducing the energy spent on other processes, said lead author Prof Lewis Halsey from the University of Roehampton. “It’s like the government trying to balance the budget – if it’s spending more on education for instance, then it might need to spend less on roads,” he said. © 2021 Guardian News & Media Limited

Keyword: Obesity
Link ID: 27971 - Posted: 09.01.2021

By Gina Kolata Everyone knows conventional wisdom about metabolism: People put pounds on year after year from their 20s onward because their metabolisms slow down, especially around middle age. Women have slower metabolisms than men. That’s why they have a harder time controlling their weight. Menopause only makes things worse, slowing women’s metabolisms even more. All wrong, according to a paper published Thursday in Science. Using data from nearly 6,500 people, ranging in age from 8 days to 95 years, researchers discovered that there are four distinct periods of life, as far as metabolism goes. They also found that there are no real differences between the metabolic rates of men and women after controlling for other factors. The findings from the research are likely to reshape the science of human physiology and could also have implications for some medical practices, like determining appropriate drug doses for children and older people. “It will be in textbooks,” predicted Leanne Redman, an energy balance physiologist at Pennington Biomedical Research Institute in Baton Rouge, La., who also called it “a pivotal paper.” Rozalyn Anderson, a professor of medicine at the University of Wisconsin-Madison, who studies aging, wrote a perspective accompanying the paper. In an interview, she said she was “blown away” by its findings. “We will have to revise some of our ideas,” she added. But the findings’ implications for public health, diet and nutrition are limited for the moment because the study gives “a 30,000-foot view of energy metabolism,” said Dr. Samuel Klein, who was not involved in the study and is director of the Center for Human Nutrition at the Washington University School of Medicine in St. Louis. He added, “I don’t think you can make any new clinical statements” for an individual. When it comes to weight gain, he says, the issue is the same as it has always been: People are eating more calories than they are burning. Metabolic research is expensive, and so most published studies have had very few participants. But the new study’s principal investigator, Herman Pontzer, an evolutionary anthropologist at Duke University, said that the project’s participating researchers agreed to share their data. There are more than 80 co-authors on the study. By combining efforts from a half dozen labs collected over 40 years, they had sufficient information to ask general questions about changes in metabolism over a lifetime. © 2021 The New York Times Company

Keyword: Obesity
Link ID: 27949 - Posted: 08.14.2021

By Rachel Fritts As you age, your brain slows down. You may forget where you left your glasses or have trouble picking up a new skill. Now there’s hope from rodent experiments that some of these declines could be reversed—but it takes guts. New research shows a transplant of gut microbes, in the form of feces, from young mice to old ones can turn back the clock on the aging brain. The study is “a tour de force” for the scope of data it collected, says Sean Gibbons, a gut microbe researcher at the Institute for Systems Biology. Still, he says, more work must be done before anyone considers doing anything similar with humans. The bacteria in our intestines influence everything from our daily moods to our overall health. This “gut microbiome” also changes over the course of our lives. But whereas some studies have shown young blood can have rejuvenating effects on old mice, the microbiome’s impact on age-related declines hasn’t been clear. To test whether a young microbiome could reverse signs of aging, researchers took fecal samples from 3- to 4-month-old mice, the equivalent of young adults, and transplanted them into 20-month-old animals—ancient by mouse standards. The scientists fed a slurry of feces to the old mice using a feeding tube twice a week for 8 weeks. As controls, old mice received transplants from fellow old mice, and young from young. The first thing the team noticed was that the gut microbiomes of the old mice given young mouse microbes began to resemble those of the younger ones. The common gut microbe Enterococcus became much more abundant in old mice, just as it is in young mice, for example. © 2021 American Association for the Advancement of Science

Keyword: Obesity; Development of the Brain
Link ID: 27939 - Posted: 08.11.2021

By Jane E. Brody No one with debilitating symptoms likes to be told “it’s all in your head.” Yet, this is often what distressed patients with irritable bowel syndrome hear, implicitly or explicitly, when a medical work-up reveals no apparent explanation for their repeated bouts of abdominal pain, bloating, diarrhea or constipation. In fact, irritable bowel syndrome, or I.B.S., is a real problem causing real symptoms, no matter how hard its sufferers may wish it gone. But unlike an infection or tumor, I.B.S. is what medicine calls a functional disorder: a condition with no identifiable cause. Patients have no visible signs of damage or disease in their digestive tracts. Rather, the prevailing theory holds that overly sensitive nerves in the patient’s gastrointestinal tract send distress signals to the brain that result in pain and malfunction. However, as medical science progresses, experts are beginning to find physical explanations for disorders that previously had no known biological cause. For example, conditions like epilepsy, Alzheimer’s disease and migraine were once considered functional disorders, but are now known to have measurable physical or biochemical underpinnings. And recent research has revealed at least one likely explanation for the symptoms of I.B.S.: an infection in the digestive tract that triggers a localized allergic reaction in the gut. As Dr. Marc E. Rothenberg wrote in The New England Journal of Medicine in June, “Patients with I.B.S. often report that their symptoms started at the time of a gastrointestinal infection.” Dr. Rothenberg, who is the director of the division of allergy and immunology at Cincinnati Children’s Hospital Medical Center, explained in an interview that the infection can temporarily disrupt the layer of cells that normally lines the bowel. These cells form a barrier that prevents allergy-inducing proteins in foods from being absorbed. When that barrier is penetrated, people can become intolerant to foods that previously caused them no issue. Sign up for the Well Newsletter Get the best of Well, with the latest on health, fitness and nutrition. Get it sent to your inbox. © 2021 The New York Times Company

Keyword: Stress
Link ID: 27935 - Posted: 08.07.2021

By Jennifer Couzin-Frankel They rose to fame as the world’s fattest mice. At about 130 grams, the rodents were “the equivalent of 600 pounds in humans,” says diabetes researcher Philipp Scherer. They were born to genetically engineered mouse parents in his lab at the University of Texas Southwestern Medical Center. One set of parents lacked the hormone leptin, an appetite suppressant that signals when it’s time to stop eating. The other parents overproduced the hormone adiponectin, churned out by fat cells, which is thought to support metabolic health, protecting against obesity-linked diseases such as type 2 diabetes. Scherer’s mouse pups melded their parents’ traits. They ate constantly and became obese. But unlike other leptin-deficient mice (and people), the animals had healthy cholesterol and blood glucose levels and didn’t develop metabolic illnesses such as type 2 diabetes. “ They were exceptionally quote-unquote healthy,” Scherer says, though he wonders whether it’s possible to be truly well while carrying such a considerable fat burden. Despite their metabolic health, the mice didn’t live a normal life span: Their weight left them so off balance that they often flipped over and got stuck, causing dehydration and death. Still, to Scherer, who described the animals in 2007 and continues to study them, the rodents sharpened an emerging message for people as well as mice: Weight and health can be uncoupled. Many researchers and doctors—and broader societies—take it as a given that obesity means ill health. In fact, says Ruth Loos, who studies the genetics of obesity at the University of Copenhagen, “We can be obese but remain healthy.” Scherer, Loos, and other researchers worldwide are examining genes, animal models, and humans to understand how factors such as the distribution of fat in the body and the nature of fat itself can blunt or compound any health impacts of extra weight. The researchers are also working to define metabolically healthy obesity (MHO) and examine how common it is and how long it persists. © 2021 American Association for the Advancement of Science

Keyword: Obesity
Link ID: 27930 - Posted: 08.04.2021

By Jonathan Lambert Winter on the Qinghai-Tibetan Plateau is unfriendly to pikas. Temperatures across the barren, windy highlands routinely dip below –30° Celsius, and the grass that typically sustains the rabbitlike mammals becomes dry and brittle. It would seem the perfect time for these critters to hibernate, or subsist on stores of grass in burrows to stay warm, like the North American pika. Instead, plateau pika (Ochotona curzoniae) continue foraging in winter, but reduce their metabolism by about 30 percent to conserve energy, researchers report July 19 in the Proceedings of the National Academy of Sciences. Some pikas also resort to unusual rations: yak poop. Camera data from four sites confirmed that pikas regularly brave the cold to forage. “Clearly they’re doing something fancy with their metabolism that’s not hibernation,” says John Speakman, an ecophysiologist at the University of Aberdeen in Scotland. Speakman and colleagues measured daily energy expenditure of 156 plateau pikas in summer and winter, and implanted 27 animals with temperature sensors. While many nonhibernating animals keep warm in winter by using more energy, these pikas did the opposite (SN: 1/22/14). On average, pikas reduced their metabolism by 29.7 percent, in part by cooling their bodies a couple degrees overnight. The animals were also less active, relative to summertime levels. © Society for Science & the Public 2000–2021.

Keyword: Obesity
Link ID: 27916 - Posted: 07.21.2021

By Gretchen Reynolds We all know that lifting weights can build up our muscles. But by changing the inner workings of cells, weight training may also shrink fat, according to an enlightening new study of the molecular underpinnings of resistance exercise. The study, which involved mice and people, found that after weight training, muscles create and release little bubbles of genetic material that can flow to fat cells, jump-starting processes there related to fat burning. The results add to mounting scientific evidence that resistance exercise has unique benefits for fat loss. They also underscore how extensive and interconnected the internal effects of exercise can be. Many of us pigeonhole resistance training as muscle building, and with good reason. Lifting weights — or working against our body weight as we bob through push-ups, squats or chair dips — will noticeably boost our muscles’ size and strength. But a growing number of studies suggest weight training also reshapes our metabolisms and waistlines. In recent experiments, weight workouts goosed energy expenditure and fat burning for at least 24 hours afterward in young women, overweight men and athletes. Likewise, in a study I covered earlier this month, people who occasionally lifted weights were far less likely to become obese than those who never lifted. But how weight training revamps body fat remains murky. Part of the effect occurs because muscle is metabolically active and burns calories, so adding muscle mass by lifting should increase energy expenditure and resting metabolic rates. After six months of heavy lifting, for example, muscles will burn more calories just because they are larger. But that doesn’t fully explain the effect, because adding muscle mass requires time and repetition, while some of the metabolic effects of weight training on fat stores seem to occur immediately after exercise. © 2021 The New York Times Company

Keyword: Obesity
Link ID: 27915 - Posted: 07.21.2021

Yuki Noguchi Health conditions exacerbated by obesity include heart disease, stroke, Type 2 diabetes and certain types of cancer, according to the CDC. Researchers say the newly approved drug Wegovy could help many who struggle with obesity lose weight. adamkaz/Getty Images When a promising new drug to treat obesity was approved by the Food and Drug Administration for sale in the U.S. last month, it was the first such treatment to gain approval since 2014. In clinical trials, weekly injections of semaglutide — or Wegovy, as it's been branded — helped people drop an average of 15% of their body weight. That's an average of about 34 pounds over 16 months, before their weight plateaued — roughly triple what's achieved with other drugs on the market. At least as important, Wegovy raised none of the alarm bells with the FDA or obesity doctors that it might trigger serious side effects of the sort some people experienced by taking fen-phen or other previous medical treatments for obesity. But with a price tag for Wegovy of $1,000 to $1,500 a month, a big question remains: Will insurers cover its significant cost for the millions such as Marleen Greenleaf who might benefit? Greenleaf grew up on the island of Trinidad, where her family paid little heed to what they ate and paid a high medical price, she says: "My husband has diabetes, my sister has diabetes, my brother has diabetes." Since then, she's tried — and failed — at numerous diets, says Greenleaf, now 58 and an administrator at a charter school in Washington, D.C. Then, in 2018, she signed up for the clinical trial of a new drug — a once-weekly shot that changes the way her brain signals hunger. © 2021 npr

Keyword: Obesity
Link ID: 27896 - Posted: 07.08.2021

By Rodrigo Pérez Ortega For some people, no amount of exercise and dieting keeps the kilograms off. For others, leanness comes naturally. Now, scientists might know one reason why. In one of the most comprehensive studies of the genetics of obesity to date, a research team has identified rare gene variants that protect lucky carriers from putting on weight. The work is “a tour de force of genetics,” says Sadaf Farooqi, an obesity researcher at the University of Cambridge who was not involved with the study. Geneticists generally look for mutations that cause disease, but people can also carry subtly different versions of a gene that promote good health. Finding rare variants that offer protection against a disease is very hard because sequencing studies are usually small, Farooqi notes. Yet such variants can lead to new drug targets, she adds. At least 2.8 million people die every year from being overweight or clinically obese. Obesity increases the risk of developing type 2 diabetes, heart disease, some cancers, and even severe COVID-19. Diet and exercise can help people with obesity lose weight, but genetics also strongly influence whether a person develops the disease. Studies that focused on people with extreme obesity have identified common gene variants—like a “broken” copy of the MC4R gene, linked to appetite regulation—that make people more likely to be overweight. Other work has found thousands of genetic variants, each of which has a tiny impact on body weight; together, they can significantly increase the likelihood of obesity. In the new study, researchers sequenced the genomes of more than 640,000 people from Mexico, the United States, and the United Kingdom, homing in on only the exome—the part of the genome that codes for proteins. © 2021 American Association for the Advancement of Science.

Keyword: Obesity; Genes & Behavior
Link ID: 27887 - Posted: 07.03.2021

By Kim Tingley Childhood obesity has increased significantly in the United States during the past four decades. In 1980, about 5 percent of the country’s children between 2 and 19 were experiencing obesity, according to the C.D.C.; as of 2018, more than 19 percent were — and an additional 16 percent were considered overweight. Because children are far more likely to gain an unhealthful amount of weight while out of school over the summer, experts were worried last spring when in-person schooling was suspended indefinitely because of the pandemic. They feared extended closures might “exacerbate the epidemic of childhood obesity and increase disparities in obesity risk,” as researchers from the Mailman School of Public Health at Columbia University and colleagues put it in a paper in the journal Obesity in June 2020. That, in turn, would mean more children living with related conditions such as Type 2 diabetes, hypertension and fatty-liver disease. Those concerns were warranted, according to a May study in Pediatrics. Based on measurements of body mass index taken for more than 500,000 children between the ages of 2 and 17 during visits to the Children’s Hospital of Philadelphia Care Network, researchers found that, on average, between January 2019 and December 2020 the prevalence of obesity increased by almost 2 percentage points overall, from 13.7 percent to 15.4 percent. (In the most recent years for which national data is available, the increase has been 1 percentage point or less.) Black and Latino children, as well as those from families with lower incomes, displayed sharper increases than children from other groups did. Such gains early in life make it more likely that children will have higher B.M.I.s when they grow up. (Obesity already affects more than 40 percent of American adults.) “This isn’t just baby fat that’s going to go away,” says Brian Jenssen, the study’s lead author and a pediatrician at Children’s. “That’s why I think this is so alarming.” © 2021 The New York Times Company

Keyword: Obesity
Link ID: 27875 - Posted: 06.26.2021

By Emily Underwood In the 1930s, neurosurgeon Wilder Penfield pioneered a daring new kind of cartography. As a stenographer took notes, he delicately touched an electrode to the exposed brains of his awake, consenting patients and asked what they felt as electrical current hit different areas. Penfield wanted to better predict which brain functions would be threatened when surgeons had to remove tumors or chunks of tissue that were triggering epileptic seizures. Stimulating adjacent brain regions, he found, produced sensations in corresponding body parts: hand, forearm, elbow. The result of his mapping was the iconic “homunculus”: a map on the brain’s wrinkled outer layer representing the surface of the body. Penfield then ventured into more mysterious territory. When he probed the insula, a deep fold of cortex, some patients felt nauseated or gassy; others belched or vomited. “My stomach is upset and I smell something like medicine,” one said. Penfield found those visceral signals harder to decipher than the brain’s map of the body’s surface. Brain regions responsible for different internal sensations seemed to overlap. Sensory regions were hard to distinguish from those that sent motor instructions such as telling the intestines to contract. Penfield once asked participants to swallow an electrode to detect changes in gut contractions while he stimulated their brains. But his map of the inner organs was blurry and ambiguous—and stayed that way for most of the next century. Decades later, scientists are starting to unravel how our wet, spongy, slippery organs talk to the brain and how the brain talks back. That two-way communication, known as interoception, encompasses a complex, bodywide system of nerves and hormones. Much recent exploration has focused on the vagus nerve: a massive, meandering network of more than 100,000 fibers that travel from nearly every internal organ to the base of the brain and back again. © 2021 American Association for the Advancement of Science.

Keyword: Learning & Memory; Obesity
Link ID: 27850 - Posted: 06.11.2021

By Mitch Leslie For the past 3 years, about 6000 middle-aged and elderly Australians have pumped iron, loaded up on greens and whole grains, strived to quell stress, and challenged their wits with computer exercises, all in an effort to preserve their cognition. They’re part of a clinical trial called Maintain Your Brain, one of about 30 current or planned studies that eschew pharmaceutical interventions and test whether altering multiple aspects of participants’ lives improves brain health. Such multidomain studies may finally reveal whether modifying diet, exercise, and other factors can slow cognitive decline as people age—or even prevent dementia. “There’s a lot of hope for multidomain trials,” says psychologist Kaarin Anstey of the University of New South Wales, Sydney, one of the principal investigators of the Maintain Your Brain trial, which will finish by the end of this year. Although people can’t escape some mental decline as they get older, lifestyle exerts a powerful influence over the risk of developing dementia—the type of severe cognitive impairment seen in conditions such as Alzheimer’s disease. Last year, an international committee of scientists and psychiatrists known as the Lancet Commission on dementia prevention, intervention, and care estimated that so-called modifiable factors account for 40% of dementia risk. Their report highlighted a dozen factors, including many familiar villains—diabetes, high blood pressure, smoking, obesity, and lack of exercise. Researchers are still probing exactly how these risk factors steal people’s faculties, but they’ve identified some likely mechanisms. Lack of physical activity may impair cognition, for instance, because exercise stimulates formation of new neurons and soothes brain inflammation. © 2021 American Association for the Advancement of Science.

Keyword: Alzheimers; Obesity
Link ID: 27834 - Posted: 05.29.2021

By Gina Kolata Obesity has stalked Marleen Greenleaf, 58, all of her life. Like most people with obesity, she tried diet after diet. But the weight always came back. With that, she has suffered a lifetime of scorn and stigma. Jeering comments from strangers when she walked down the street. Family members who told her, when she trained for a half-marathon, “I don’t think it’s good for you.” Then, in 2018, Ms. Greenleaf, an administrator at a charter school in Washington, D.C., participated in a clinical trial for semaglutide, which is a new type of obesity drug, known as incretins. Over the course of the 68-week study, Ms. Greenleaf slowly lost 40 pounds. Until then, she had always believed that she could control her weight if she really tried. “I thought I just needed more motivation,” she said. But when she took semaglutide, she said that “immediately, the urge to eat just dissipated.” Incretins appear to elicit significant weight loss in most patients, enough to make a real medical and aesthetic difference. But experts hope that the drugs also do something else: change how society feels about people with obesity, and how people with obesity feel about themselves. If these new drugs allow obesity to be treated like a chronic disease — with medications that must be taken for a lifetime — the thought is that doctors, patients and the public might understand that obesity is truly a medical condition. © 2021 The New York Times Company

Keyword: Obesity; Hormones & Behavior
Link ID: 27821 - Posted: 05.15.2021

By Nicholas Bakalar Type 2 diabetes is a chronic, progressive illness that can have devastating complications, including hearing loss, blindness, heart disease, stroke, kidney failure and vascular damage so severe as to require limb amputation. Now a new study underscores the toll that diabetes may take on the brain. It found that Type 2 diabetes is linked to an increased risk for Alzheimer’s disease and other forms of dementia later in life, and the younger the age at which diabetes is diagnosed, the greater the risk. The findings are especially concerning given the prevalence of diabetes among American adults and rising rates of diabetes in younger people. Once referred to as “adult-onset diabetes” to distinguish it from the immune-related “juvenile-onset” Type 1 disease that begins in childhood, Type 2 diabetes is seen in younger and younger people, largely tied to rising rates of obesity. The Centers for Disease Control and Prevention estimates that more than 34 million American adults have Type 2 diabetes, including more than a quarter of those 65 and over. About 17.5 percent of those aged 45 to 64 have Type 2 disease, as do 4 percent of 18- to 44-year-olds. “This is an important study from a public health perspective,” said the director of the Yale Diabetes Center, Dr. Silvio Inzucchi, who was not involved in the research. “The complications of diabetes are numerous, but the brain effects are not well studied. Type 2 diabetes is now being diagnosed in children, and at the same time there’s an aging population.” © 2021 The New York Times Company

Keyword: Alzheimers; Obesity
Link ID: 27803 - Posted: 05.05.2021

by Peter Hess Deleting the autism-related gene CHD8 from the intestines induces significant gastrointestinal and behavioral changes in mice, according to a new unpublished study. The results suggest that changes to the gut are involved in some of the behavioral traits seen in people with CHD8 mutations, says lead researcher Evan Elliott, assistant professor of molecular and behavioral neuroscience at Bar-Ilan University in Ramat Gan, Israel. Elliott’s team presented the findings virtually this week at the 2021 International Society for Autism Research annual meeting. (Links to abstracts may work only for registered conference attendees.) Up to 90 percent of people with CHD8 mutations report gastrointestinal issues such as constipation, Elliott says. Most also have autism. Mice missing one copy of CHD8 have unusually thin and permeable small intestines, Elliott and his colleagues found. The reason seems to be that these mice have fewer mucus-producing goblet cells than controls, resulting in thinner organ walls and less mucus lining the digestive tract. CHD8 regulates the expression of other genes, so Elliott’s team looked at gene expression levels in the CHD8 mice’s intestinal epithelial cells via RNA sequencing. The mice expressed 920 genes differently than control mice did. These include an increase in the expression of genes involved in inflammatory responses and in antimicrobial activity. The latter set may be the body’s way of compensating for increased microbial populations, Elliott says. © 2021 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 27801 - Posted: 05.05.2021

by Angie Voyles Askham Mice that lack CNTNAP2, a gene linked to autism, have an atypical collection of microbes in their intestines, according to a new study. Treating the mice with a strain of gut bacteria commonly found in wildtype mice, people and other mammals improves their social behavior. The CNTNAP2 mice are hyperactive, and those raised in isolation prefer to spend time alone or with a familiar cagemate rather than with a stranger mouse. But when they grow up alongside wildtype littermates, their social deficits — but not their hyperactivity — disappear, the study shows. Because mice that live together eat one another’s feces, which can alter the microbial content of their guts, the researchers wondered if a change in the microbiome might be driving the change in the isolated animals’ social behaviors. “It was sort of a serendipitous discovery,” says lead investigator Mauro Costa-Mattioli, professor of neuroscience at Baylor College of Medicine in Houston, Texas. The findings highlight how some autism traits associated with genetic mutations may be shaped, and potentially eased, via changes to the gut microbiome. Figuring out which behaviors can be attributed to the environment is particularly helpful for thinking about treatments because the environment can be changed, whereas “genetics is still hard to correct,” says Sarkis Mazmanian, professor of microbiology at the California Institute of Technology in Pasadena, who was not involved in the work. © 2021 Simons Foundation

Keyword: Autism
Link ID: 27746 - Posted: 03.27.2021

Kayla Hounsell · CBC News · Sarah White has always been a 'picky eater' but says the pandemic exacerbated her difficult relationship with food. It ultimately led to a diagnosis of avoidant restrictive food intake disorder. (Eric Woolliscroft/CBC) Sarah White sets a timer to remind herself to eat. She sets it six times a day so that she eats three meals and three snacks. White says she's always been a "picky eater." But when she started working from home, her routine was interrupted and her already difficult relationship with food became dangerous. It ultimately led to an eating disorder diagnosis during the pandemic. "I had all of the time in the world to eat, but I was finding I wasn't eating nearly as much as I should have been," White, 33, said during a physically distanced interview at her Halifax apartment. "It started to feel a lot more serious than it had in the past." There's been an alarming spike in the number of people seeking help for eating disorders. The National Eating Disorder Information Centre says the volume of inquiries to its help line and online chat service has been up 100 per cent during the pandemic. "There's been literature coming out across the world really suggesting that the numbers are skyrocketing and we're trying to understand why that is," said Dr. Jennifer Couturier, principal investigator for the Canadian Consensus Panel for In May, the panel, which consists of clinicians, policymakers, parents and youth, received a $50,000 federal grant to determine how best to treat eating disorders during a pandemic, particularly in children and young adults under 25. Couturier says she feels this age group hasn't received a lot of attention when it comes to research generally. ©2021 CBC/Radio-Canada.

Keyword: Anorexia & Bulimia
Link ID: 27729 - Posted: 03.13.2021

By Andreas von Bubnoff The world is getting fatter. More than 40 percent of U.S. adults are obese — almost three times more than in 1980. One reason for this weight gain is Americans are consuming more: National figures suggest an increase of about 200 daily calories between the early 1970s and 2010. Another is more snacking. In 2010, U.S. adults ate about 20 percent more of their daily calories as snacks than they did 50 years ago. But there is more to rising obesity rates than endless grazing. What also matters is timing, some experts believe. We eat when we shouldn’t, and don’t give our bodies a long enough break in between. We didn’t evolve to eat day and night, says neuroscientist Dominic D’Agostino of the University of South Florida. Until the dawn of agriculture about 12,000 years ago, we subsisted on hunting and gathering and often had to perform those activities with empty bellies. “We are hard-wired,” D’Agostino says, “to undergo periodic intermittent fasting.” What’s more, people are now eating at times of the day when historically they would have been asleep, says Satchin Panda, a circadian biologist at the Salk Institute for Biological Studies in La Jolla, Calif., who co-wrote an overview on the timing of eating in the 2019 Annual Review of Nutrition. For thousands of years, he says, our nightly fast probably started much earlier than in these times of late-night television. Although the research is still mixed, the timing of eating seems to matter for body weight and health. Studies suggest significant potential benefits from fasting every other day or so — or, on a daily basis, eating only when we would normally be awake, within a window of 12 hours or fewer — a practice known as time-restricted eating. © 1996-2021 The Washington Post

Keyword: Obesity
Link ID: 27710 - Posted: 02.28.2021

By Anahad O’Connor Five years ago, a group of nutrition scientists studied what Americans eat and reached a striking conclusion: More than half of all the calories that the average American consumes comes from ultra-processed foods, which they defined as “industrial formulations” that combine large amounts of sugar, salt, oils, fats and other additives. Highly processed foods continue to dominate the American diet, despite being linked to obesity, heart disease, Type 2 diabetes and other health problems. They are cheap and convenient, and engineered to taste good. They are aggressively marketed by the food industry. But a growing number of scientists say another reason these foods are so heavily consumed is that for many people they are not just tempting but addictive, a notion that has sparked controversy among researchers. Recently, the American Journal of Clinical Nutrition explored the science behind food addiction and whether ultra-processed foods might be contributing to overeating and obesity. It featured a debate between two of the leading experts on the subject, Ashley Gearhardt, associate professor in the psychology department at the University of Michigan, and Dr. Johannes Hebebrand, head of the department of child and adolescent psychiatry, psychosomatics and psychotherapy at the University of Duisburg-Essen in Germany. Dr. Gearhardt, a clinical psychologist, helped develop the Yale Food Addiction Scale, a survey that is used to determine whether a person shows signs of addictive behavior toward food. In one study involving more than 500 people, she and her colleagues found that certain foods were especially likely to elicit “addictive-like” eating behaviors, such as intense cravings, a loss of control, and an inability to cut back despite experiencing harmful consequences and a strong desire to stop eating them. At the top of the list were pizza, chocolate, potato chips, cookies, ice cream, French fries and cheeseburgers. © 2021 The New York Times Company

Keyword: Obesity; Drug Abuse
Link ID: 27706 - Posted: 02.23.2021