Chapter 13. Homeostasis: Active Regulation of the Internal Environment

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Obesity is not a choice and making people feel ashamed results only in them feeling worse about themselves, a report by top psychologists says. It calls for changes in language to reduce stigma, such as saying "a person with obesity" rather than an "obese person". And it says health professionals should be trained to talk about weight loss in a more supportive way. A cancer charity's recent ad campaign was criticised for "fat shaming". Obesity levels rose by 18% in England between 2005 and 2017 and by similar amounts in Scotland, Wales and Northern Ireland. This means just over one in four UK adults is obese while nearly two-thirds are overweight or obese. But these increases cannot be explained by a sudden loss of motivation across the UK - it is a lot more complicated than that, according to the British Psychological Society report, which concludes it "is not simply down to an individual's lack of willpower". "The people who are most likely to be an unhealthy weight are those who have a high genetic risk of developing obesity and whose lives are also shaped by work, school and social environments that promote overeating and inactivity," it says. "People who live in deprived areas often experience high levels of stress, including major life challenges and trauma, often their neighbourhoods offer few opportunities and incentives for physical activity and options for accessing affordable healthy food are limited." Psychological experiences also play a big role, the report says, with up to half of adults attending specialist obesity services having experienced difficulties in childhood. And stress caused by fat shaming - being made to feel bad about one's weight - by public health campaigns, GPs, nurses and policymakers, often leads to increased eating and more weight gain. © 2019 BBC

Keyword: Obesity
Link ID: 26640 - Posted: 09.24.2019

A landmark French trial is due to begin to decide whether a diabetes pill prescribed for weight loss was behind the deaths of up to 2,000 people. Servier, the drug's manufacturer, is accused of deceiving users over the killer side effects of a drug later used to treat overweight diabetics. Believed to be one of France's biggest healthcare scandals, the firm is on trial for manslaughter and deceit. Servier has denied the charges, saying it did not lie about the side effects. French health experts believe the drug known as Mediator could have killed anywhere between 500 and 2,000 people before it was finally taken off the market in 2009. The country's state drug regulator, accused of not acting to prevent deaths and injuries, is also on trial. The trial will involve more than 2,600 plaintiffs and 21 defendants, and is expected to run over the course of six months. It will also look into why the drug, which was introduced in 1976, was allowed to sell for so long despite various warnings. Lawyers representing the plaintiffs argue that the drug manufacturer purposely misled patients for decades, and that this was bolstered by lenient authorities. Servier has been accused of profiting at least €1bn ($1.1bn, £880m) from the drug's sales. "The trial comes as huge relief. Finally, we are to see the end of an intolerable scandal," Dr Irene Frachon, a pulmonologist credited with lifting the lid on the side effects, told Reuters news agency. Dr Frachon's research drew on medical records across France and concluded that there was a clear pattern of heart valve problems among Mediator users. This prompted many more studies which ultimately led to the drug's ban. One study concluded that 500 deaths could be linked to Mediator between 1976 and 2009. A second one put the figure at 2,000. Those numbers have been disputed by Servier, which has said that there are only three documented cases where death can be clearly attributed to the use of Mediator. In other cases, it says, aggravating factors were at work. © 2019 BBC

Keyword: Obesity
Link ID: 26639 - Posted: 09.24.2019

By Perri Klass, M.D. Cesarean delivery can save a baby — or a mother — at a moment of medical danger. However, cesarean births have been linked to an increased risk of various long-term health issues for both women and children, and a recent study shows an association between cesarean birth and the risk of developing autism or attention deficit disorder. The study, published in August in JAMA Network Open, was a meta-analysis. It looked at data from 61 previously published studies, which together included more than 20 million deliveries, and found that birth by cesarean section was associated with a 33 percent higher risk of autism and a 17 percent higher risk of attention deficit disorder. The increased risk was present for both planned and unplanned cesarean deliveries. The first and most important thing to say is that these were observational studies, and that association is not the same as causation. The children born by cesarean section may be different in important ways from the children born vaginally, and those differences may include factors that could affect their later neurodevelopment, from maternal health issues to developmental problems already present during pregnancy to prematurity to difficult deliveries. If your child was born by cesarean section, there’s nothing you can do to change that, and knowing about this association may make you worry, while if you’re pregnant it may make you even more anxious about how the delivery will go. But the information about long-term associations and mode of birth should help to drive further research and understanding of how and why these associations play out. Tianyang Zhang, a Ph.D. student in clinical neuroscience at the Karolinska Institute in Stockholm who was the first author on the article, said that earlier research had shown various associations between cesarean delivery and long-term health problems, including higher rates of obesity and asthma in children. This study looked at a range of developmental and mental health issues. Though it did find an association between cesarean delivery and autism spectrum and attention deficit disorders, it did not find significant associations with others, such as tic disorders, obsessive-compulsive disorders or eating disorders. © 2019 The New York Times Company

Keyword: Autism; ADHD
Link ID: 26638 - Posted: 09.23.2019

By James Gallagher Health and science correspondent, BBC News Babies born by Caesarean section have dramatically different gut bacteria to those born vaginally, according to the largest study in the field. The UK scientists say these early encounters with microbes may act as a "thermostat" for the immune system. And they may help explain why Caesarean babies are more likely to have some health problems later in life. The researchers stress women should not swab babies with their vaginal fluids - known as "vaginal seeding". How important are gut bacteria? Our bodies are not entirely human - instead we are an ecosystem with around half our body's cells made up of microbes such as bacteria, viruses and fungi. Most of them live in our gut and are collectively known as our microbiome. The microbiome is linked to diseases including allergy, obesity, inflammatory bowel disease, Parkinson's, whether cancer drugs work and even depression and autism. This study - by Wellcome Sanger Institute, UCL, and the University of Birmingham - assessed how the microbiome forms when we leave our mother's sterile womb and enter a world full of bugs. Regular samples were taken from the nappies of nearly 600 babies for the first month of life, and some provided faecal samples for up to a year. © 2019 BBC

Keyword: Development of the Brain
Link ID: 26637 - Posted: 09.23.2019

Teen girls — but not boys — who prefer to go to bed later are more likely to gain weight, compared to same-age girls who go to bed earlier, suggests a study funded by the National Institutes of Health. The findings by researchers at Kaiser Permanente in Oakland, California, and other institutions appear in JAMA Pediatrics. A total of 804 adolescents (418 girls and 386 boys) ages 11 to 16 took part in the study. The children responded to questionnaires on their sleep habits and wore an actigraph — a wrist device that tracks movement. Researchers measured their waist size and calculated their proportion of body fat using a technique called dual-energy x-ray absorptiometry. They also estimated the children’s social jet lag — the difference between their weeknight and weekend bedtimes. Those who stayed up far later on weekends than weeknights were considered to have high social jet lag. The authors noted that previous studies had found that adults who preferred to stay up late and had high social jet lag were more likely to gain weight than those who went to be earlier and did not have social jet lag. The researchers undertook the current study to determine if the same associations would be seen in young people. For girls, staying up later was associated with an average .58 cm increase in waist size and a .16 kg/m2 increase in body fat. Each hour of social jet lag was associated with a 1.19 cm larger waste size and a 0.45 kg/m2 increase in body fat. These associations were reduced—but still remained—after the researchers statistically adjusted for other factors known to influence weight, such as sleep duration, diet, physical activity and television viewing. Although the researchers found slight associations between these measures and waist size and body fat in boys, they were not statistically significant. The researchers concluded that improving sleep schedules may be helpful in preventing obesity in childhood and adolescence, especially in girls.

Keyword: Obesity; Biological Rhythms
Link ID: 26618 - Posted: 09.17.2019

By Maanvi Singh The world’s most widely used insecticides may delay the migrations of songbirds and hurt their chances of mating. In the first experiment to track the effects of a neonicotinoid on birds in the wild, scientists captured 24 white-crowned sparrows as they migrated north from Mexico and the southern United States to Canada and Alaska. The team fed half of those birds with a low dose of the commonly used agricultural insecticide imidacloprid and the other half with a slightly higher dose. An additional 12 birds were captured and dosed with sunflower oil, but no pesticide. Within hours, the dosed birds began to lose weight and ate less food, researchers report in the Sept. 13 Science. Birds given the higher amount of imidacloprid (3.9 milligrams per kilogram of body mass) lost 6 percent of their body mass within six hours. That’s about 1.6 grams for an average bird weighing 27 grams. Tracking the birds (Zonotrichia leucophrys) revealed that the pesticide-treated sparrows also lagged behind the others when continuing their migration to their summer mating grounds. The findings suggest that neonicotinoid insecticides, already implicated in dropping bee populations, could also have a hand in the decline of songbird populations across North America. From 1966 to 2013, the populations of nearly three-quarters of farmland bird species across the continent have precipitously dropped. The researchers dosed the birds in the lab with carefully measured amounts of pesticide mixed with sunflower oil. In the wild, birds might feed on seeds coated with imidacloprid. The highest dose that “we gave each bird is the equivalent of if they ate one-tenth of [a single] pesticide-coated corn seed,” says Christy Morrissey, a biologist at the University of Saskatchewan in Saskatoon, Canada. “Frankly, these were minuscule doses we gave the birds.” © Society for Science & the Public 2000–2019.

Keyword: Neurotoxins; Obesity
Link ID: 26608 - Posted: 09.13.2019

By Anahad O’Connor Dr. Elaine Yu, an endocrinologist at Massachusetts General Hospital in Boston, was inundated with volunteers when she put out a call a few years ago for overweight people who were willing to take part in a study of obesity and the microbiome. People as far away as Alaska and Hawaii were eager to enroll. But the most surprising part was what they were willing to do. The study required them to swallow capsules containing stool to test whether gut bacteria from lean donors could improve their metabolic health. “We had this concern that it would be difficult to recruit people because there’s a certain yuck factor with having to take a poop pill,” Dr. Yu said. “But we had an overwhelming number of volunteers wanting to participate.” The link between the gut and metabolic disease is a growing area of obesity research. In recent years, scientists have uncovered clues that the microbiota, the community of trillions of microbes that live in the gut, plays a role in weight gain and metabolic disease. Now, in small studies, they are exploring whether they can spur changes in metabolism and potentially in body weight through a therapy known as fecal microbiota transplants, or F.M.T., which transfers gut bacteria from lean donors to the guts of obese patients. The research, which is still in its infancy, has yielded mixed results and plenty of skepticism. Experts say fecal transplants will never replace diet, exercise, behavioral therapies and other standard interventions for obesity and Type 2 diabetes. But some believe they could lead to the discovery of bacteria that protect against metabolic disease, and perhaps become one of many tools that help obese patients who are struggling to shed pounds. “Obesity is a very complex disorder,” said Dr. Jessica Allegretti, the director of the Fecal Microbiota Transplant Program at Brigham and Women’s Hospital. “Perhaps the microbiome is a contributing part of it, and maybe for everyone it’s slightly different. But even for patients where the microbiome is playing a big part, I think this would be something that is part of a larger weight loss program.” © 2019 The New York Times Company

Keyword: Obesity
Link ID: 26597 - Posted: 09.10.2019

By Roni Caryn Rabin Every year, hundreds of thousands of obese Americans undergo weight-loss surgery in a last-ditch effort to shed pounds and control their Type 2 diabetes. Now a new study suggests that bariatric surgery may also have other significant health benefits, cutting the overall risk of serious cardiovascular events and premature death by almost half. The study, published in the medical journal JAMA on Monday, is not definitive. Though it compared the long-term outcomes of about 2,300 bariatric surgery patients with some 11,500 closely matched patients who had not undergone surgery, it was an observational study, not a randomized controlled trial of the kind considered the gold standard in medicine. But the findings were so striking that an editorial accompanying the paper suggested that weight-loss surgery, rather than medications, should be the preferred treatment for Type 2 diabetes in certain patients with obesity. “The new information here is the ability of bariatric surgery to control macrovascular events like strokes, heart attacks, heart failure and kidney disease,” not just improve weight and diabetes control, said Dr. Edward H. Livingston, the editorial’s author. “That’s a big deal.” A bariatric surgeon himself, Dr. Livingston said he had long been known as a “curmudgeon” who was reluctant to make claims about the long-term health benefits of weight-loss surgery. “This is the first time I’ve come out publicly saying, ‘You know what, this may be a better way to go,’” he said, adding that insurers should cover the procedure more liberally. © 2019 The New York Times Company

Keyword: Obesity
Link ID: 26560 - Posted: 09.02.2019

By Anahad O’Connor Low-carbohydrate diets have fallen in and out of favor since before the days of Atkins. But now an even stricter version of low-carb eating called the ketogenic diet is gaining popular attention, igniting a fierce scientific debate about its potential risks and benefits. Both the Atkins and ketogenic diets encourage followers to cut carbs from their diets. But while the Atkins diet gradually increases carbs over time, keto places firm limits on carbs and protein. This way of eating depletes the body of glucose, forcing it to primarily burn fat and produce an alternate source of fuel called ketones. A typical ketogenic diet restricts carbs to less than 10 percent of calories and limits protein to 20 percent, while fat makes up the rest. The keto diet has been popularized in best-selling books, promoted by celebrities and touted on social media as an antidote to various ailments. Proponents say it causes substantial weight loss and can help those with Type 2 diabetes dramatically improve their blood sugar levels, which fall when people avoid carbs. There have been many studies of the ketogenic diet over the years, but most have been small and of fairly short duration. A federal registry of clinical research shows that more than 70 trials looking at the diet’s impact on brain, cardiovascular and metabolic health are either underway or in the beginning stages. Dr. Ethan Weiss, a researcher and preventive cardiologist at the University of California, San Francisco, had long been skeptical of low-carb diets but decided to experiment with the ketogenic diet a couple years ago. In a typical day he skips breakfast and eats mostly salads, nuts, cheese, roasted vegetables and grilled chicken, fish or tofu, as well as dark chocolate for dessert. The result, he says: He lost 20 pounds and had to buy a new wardrobe. © 2019 The New York Times Company

Keyword: Obesity
Link ID: 26520 - Posted: 08.20.2019

By Kate Murphy Maybe it was because when the waiter asked, “Still or sparkling?” you chose sparkling. It could have also been that you were ravenous and ate a little too much. Or, possibly, it was your ex, who happened to be dining at the same restaurant and stood a little too long over your table making awkward small talk. All of these things, hic, might cause spasms, hic, in your diaphragm, hic. Referred to in the medical literature as singultus (from the Latin singult, which means gasp or sob), hiccups are familiar to anyone who has ever taken a breath. In fact, you begin to hiccup while still in the womb. Most people hiccup the most during childhood, with the bouts becoming less frequent over time, but even in adulthood, hiccups are still a common, and annoying, occurrence. Just as we all have our own particular way of sneezing, we all have a unique way of hiccuping that can range from four to 60 hiccups per minute. Most hiccups are benign and last only a few minutes or hours. But sometimes hiccups are indicative of a more serious health issue, particularly when they recur or don’t go away for days, weeks or years. Beyond being embarrassing, the muscle contractions can be physically exhausting. They can interrupt sleep and make it hard to eat. Approximately 4,000 people in the United States are admitted to the hospital every year for hiccups. The patient with the longest recorded case, according to Guinness World Records, was Charles Osborne of Anthon, Iowa, who hiccuped for 68 years straight. He claimed it started while attempting to weigh a hog before slaughtering it. Doctors say there are as many causes for hiccups as there are crazy remedies, including tugging on your tongue, standing on your head and swallowing granulated sugar. Some actually work. Others are more likely just entertainment for friends and family who watch while you try to cure yourself. © 2019 The New York Times Company

Keyword: Miscellaneous
Link ID: 26503 - Posted: 08.15.2019

Tina Hesman Saey Subtle defects in the immune system may lead to obesity and type 2 diabetes, a study of mice suggests. Mice gained weight and developed health problems when they carried a genetic defect that dampens some immune functions, researchers report in the July 26 Science. The immune problems were linked to shifts in the gut microbiome — the collection of friendly bacteria and other microbes living in the intestines. Altering the gut microbe mix, particularly in the small intestine, may lead to increased absorption of fat from the diet, the researchers found. These findings, if they hold up in human studies, could lead to strategies for boosting immune system function in order to help prevent obesity and associated health problems. People with obesity and those with type 2 diabetes also have gut microbe compositions and subtle immune system deficiencies similar to those seen in the mice, says June Round, a microbiome researcher at the University of Utah School of Medicine in Salt Lake City. “It’s possible that things that are happening in our mice are also happening in individual [humans],” she says. Round and colleagues noticed that mice with a defect in the Myd88 gene started gaining weight at about 5 months old. By about a year old, those mice, which lack Myd88 protein in immune cells called T cells, weighed up to 60 grams — about twice as much as a normal mouse. The mutant mice also had developed metabolic problems associated with obesity, such as insulin resistance, a hallmark of type 2 diabetes in people. |© Society for Science & the Public 2000 - 2019

Keyword: Obesity; Neuroimmunology
Link ID: 26453 - Posted: 07.26.2019

Tina Hesman Saey A friendly gut bacterium can help lessen ALS symptoms, a study of mice suggests. Mice that develop a degenerative nerve disease similar to amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease, fared better when bacteria making vitamin B3 were living in their intestines, researchers report July 22 in Nature. Those results suggest that gut microbes may make molecules that can slow progression of the deadly disease. The researchers uncovered clues that the mouse results may also be important for people with ALS. But the results are too preliminary to inform any changes in treating the disease, which at any given time affects about two out of every 100,000 people, or about 16,000 people in the United States, says Eran Elinav, a microbiome researcher at the Weizmann Institute of Science in Rehovot, Israel. “With respect to ALS, the jury is still out,” says Elinav, also of the German Cancer Research Center in Heidelberg. “We have to prove that what we found in mice is reproducibly found in humans.” Elinav and his colleagues examined the gut microbiomes — bacteria, archaea and other microbes that live in the colon, or large intestine — of mice that produce large amounts of a mutated form of the SOD1 protein. In the mice, as in human ALS patients, faulty SOD1 proteins clump together and lead to the death of nerve cells. |© Society for Science & the Public 2000 - 2019

Keyword: ALS-Lou Gehrig's Disease
Link ID: 26439 - Posted: 07.23.2019

Kelly Crowe · CBC News Scientists are slowly chipping away at one of the most mysterious aspects of weight loss: why does the lost weight often seem to come back? It's now clear that it's not simply a matter of willpower. "We know people are good at losing weight with diet and exercise," said Gregory Steinberg, Canada Research Chair in Metabolism and Obesity at McMaster University. "It's not that people just give up." The problem is rooted in the body's physiology. After people lose weight, their bodies' energy use also changes by burning fewer calories. "Quickly you hit a plateau at five to 10 per cent weight loss and you can't lose more weight than that because your metabolism slows down too much," said Steinberg. "This explains why relapse weight gain is so high." But why the body's calorie-burning capacity drops has so far not been explained. "No one knows why," said Steinberg. There are theories that something is putting the brakes on the body's ability to turn up its fat-burning machinery. And last week, a new paper published in Cell Reports, describes one possible system. At New York University, Ann Marie Schmidt is studying a receptor on fat cells that appears to interfere with weight loss. When she created a mouse model without any of those receptors the mice didn't get fat even though they ate more food. "When you delete [the receptor] it completely resets their metabolic program so that they are resistant to the diet-induced obesity," said Schmidt. "It's totally unexpected and it has so many implications for human health." Although scientists have identified the receptor — called RAGE — in humans, so far most of the research has been done in mice. ©2019 CBC/Radio-Canada.

Keyword: Obesity
Link ID: 26437 - Posted: 07.23.2019

By Jessica Hamzelou Anorexia nervosa isn’t just a psychiatric condition – it is a metabolic one, too, according to a genetic study of around 72,500 people. The findings help to explain some of the symptoms of anorexia, and could help to shape future treatments. Anorexia affects between 0.9 and 4 per cent of women and 0.3 per cent of men, but is still poorly understood. “Anorexia has the highest mortality rate of any psychiatric disorder,” says Cynthia Bulik at the University of North Carolina at Chapel Hill. “We’re not very good at treating anorexia. There’s no medication, and that’s probably because we don’t understand the underlying causes.” Previous research has found that genetic factors, as well as environmental ones, can increase a person’s risk of anorexia. To investigate, Bulik and her colleagues compared the genomes of just under 17,000 people with anorexia with those of 55,500 people who didn’t have the condition. The team used a technique that applies thousands of markers to the genome, and compares these markers across all the volunteers. “It points you to where in the genome the differences lie,” says Bulik. The search pinpointed eight locations across the genome that seem to play a role in anorexia. But this is likely to represent only a tiny fraction of all the genetic factors involved in the condition, says Bulik. “It’s a complex trait, so we expect lots of genes to each have a small to moderate effect,” she says. © Copyright New Scientist Ltd.

Keyword: Anorexia & Bulimia
Link ID: 26424 - Posted: 07.16.2019

By Thomas Stackpole The run happened — or didn’t — maybe five days into the raw-diet experiment. I had formed a sort of fitness pact with a friend to forgo cooked food, and after days of nothing but salads, almonds, sashimi and black coffee, my body felt taut and ready for action. And for about half a mile, it was, my strides floating above the pavement as a few fistfuls of raw kale percolated in my belly. Then suddenly I sputtered, feeling an unambiguous alarm go off: Tank is empty, sorry, this is the end of the line. After a pause, I tried running again but made it maybe a block before my legs revolted again and I slowed to a walk. My new healthy diet, it seemed, didn’t accommodate any actual exercise. When I told all this to my co-workers the next morning, it was fodder for a good laugh. My obsessions were — and often still are — a kind of running joke. I’ve been conducting a series of shifting and poorly planned “wellness” experiments on myself for about a decade. I’ve eaten keto, low-carb and sometimes not at all. One time, I ate almost nothing but lean ground turkey and broccoli over greens for maybe two months as part of a YouTube bodybuilder’s plan. More than once, I’ve lost 10 pounds in a week. I’ve also obsessed over bulking up, gaining 25 pounds over about six months of lifting, before pivoting and deciding to train for a marathon to run it off. Then there were the gut biome vitamins, the metabolism-boosting mushrooms, the experiments with LSD microdosing and calorie trackers. Despite years of cycling through boutique insanities, it didn’t occur to me that I might have a problem until earlier this year, when the Twitter founder turned Silicon Valley wellness influencer Jack Dorsey detailed his fasting regimen. The news that he eats one meal a day during the week and nothing on the weekend provoked scornful cries that he was advocating little more than anorexia with a bro-y tech-world veneer. I, on the other hand, saw a kindred spirit. © 2019 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 26418 - Posted: 07.15.2019

By Madeleine Connors At the age of 16, my mother spent hours waiting in bread lines in communist Poland, biting at her nails. The year was 1972. The line was mostly women. Their bellies rattled with hunger, anticipation of food burning in their throats. My mother has said that waiting in a bread line was not much different from a time later in her life when she had moved to America and stood in line for hours for an Eric Clapton concert. “It’s all about wanting something. You want something, you wait for it,” she recited with a tone so deadpan that it reminded me that my mom was once a teenage girl. My experience of teenage girlhood was vastly different, growing up in Sonoma, Calif. I was many things; hungry was not one of them. I picked mushrooms out of tacos with reckless abandon. I would surrender pieces of toast under the breakfast table to my dachshund. But in 1972, food rationing in Poland had become widespread. My mother would wake up at the crack of dawn with ambitions of bringing back flour to her family. She would clench and study her bread coupon, only to look up and see an outbound train full of canned goods and hams hurtling toward Russia. Even then she knew: food was for other people. People who were better, more deserving; worth nourishing. When I was young, I ate to overcompensate for her hunger. Costco became the patron saint of my mother’s immigrant anxieties and bulk was her prayer. She bought American dream-size buckets full of almonds. She bought offensive amounts of pastas. She bought enough snacks to feed a bus full of kids on a travel soccer team. Shopping with my mother became an arms race. Shuffling through aisles along with other newly American mothers, my mom lived to give me a different life than the one she experienced. © 2019 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 26392 - Posted: 07.05.2019

By Gretchen Reynolds People hoping to lose weight with exercise often wind up being their own worst enemies, according to the latest, large-scale study of workouts, weight loss and their frustrating interaction. The study, which carefully tracked how much people ate and moved after starting to exercise, found that many of them failed to lose or even gained weight while exercising, because they also reflexively changed their lives in other, subtle ways. But a few people in the study did drop pounds, and their success could have lessons for the rest of us. In a just and cogent universe, of course, exercise would make us thin. Physical activity consumes calories, and if we burn calories without replacing them or reducing our overall energy expenditure, we enter negative energy balance. In that condition, we utilize our internal energy stores, which most of us would call our flab, and shed weight. But human metabolisms are not always just and cogent, and multiple past studies have shown that most men and women who begin new exercise routines drop only about 30 percent or 40 percent as much weight as would be expected, given how many additional calories they are expending with exercise. Why exercise underwhelms for weight reduction remains an open question, though. Scientists studying the issue agree that most of us compensate for the calories lost to exercise by eating more, moving less, or both. Our resting metabolic rates may also decline if we start to lose pounds. All of this shifts us back toward positive energy balance, otherwise known as weight gain. © 2019 The New York Times Company

Keyword: Obesity
Link ID: 26382 - Posted: 07.03.2019

By Nicholas Bakalar People with obesity-related disorders may benefit from supplements of a common gut bacterium, a small pilot study suggests. Researchers tested the bacterium, Akkermansia muciniphila, in 32 men and women who met the criteria for metabolic syndrome by having at least three of five conditions: high fasting blood sugar, high blood pressure, high triglycerides, low HDL (the “good” cholesterol) or excessive waist circumference. A. muciniphila is a normal inhabitant of the human gut that is less prevalent in people with metabolic syndrome. In a three-month trial, volunteers were randomized to one of three groups: daily tablets containing live bacteria, pasteurized bacteria or a placebo. Compared with the placebo group, those who took pasteurized A. muciniphila had significantly improved insulin sensitivity and total cholesterol, and decreases in several blood markers of inflammation and liver dysfunction. They also had decreased body weight, fat mass and waist circumference, though those differences were not statistically significant. From the team at NYT Parenting: Get the latest news and guidance for parents. We'll celebrate the little parenting moments that mean a lot — and share stories that matter to families. The live bacteria were largely ineffective. The study is in Nature Medicine. “I hope people will not see this as a miracle cure,” said the senior author, Patrice D. Cani, a professor at the Catholic University of Louvain in Brussels. “The finding is significant, but it has to be confirmed in a larger cohort. Keep in mind that the first treatment for cardiometabolic disorders is healthy diet and sufficient exercise.” © 2019 The New York Times Company

Keyword: Obesity
Link ID: 26373 - Posted: 07.02.2019

Laura Sanders A gut-busting diet may set the brain up for more of the same. After mice ate fatty food for just two weeks, cells in their brains that send a “stop eating” signal were quieter than those in mice that didn’t eat high-fat chow, researchers report in the June 28 Science. The result helps untangle the complex relationship between food and appetite, one that can become muddled when people overeat. Because food is crucial to survival, the brain has built-in redundancy — a multitude of overlapping pro-food systems to make sure animals eat enough. Neuroscientist Garret Stuber of the University of Washington in Seattle took aim at one brain area known to be involved in eating behavior. Called the lateral hypothalamus, this brain structure contains a large number of diverse cells. Stuber and his colleagues looked at gene behavior in single cells there, and found that one group, called glutamatergic nerve cells, showed particularly big changes in which genes were active when the team compared lean mice with obese mice. Earlier work suggested that these glutamatergic cells acted like a brake on feeding: When the cells were artificially blocked from firing signals, mice ate more food and gained more weight. But it wasn’t clear how these cells actually behaved over a more natural shift from leanness to obesity. |© Society for Science & the Public 2000 - 2019

Keyword: Obesity
Link ID: 26368 - Posted: 06.28.2019

Nicola Davis Evidence that Parkinson’s disease may start off in the gut is mounting, according to new research showing proteins thought to play a key role in the disease can spread from the gastrointestinal tract to the brain. The human body naturally forms a protein called alpha-synuclein which is found, among other places, in the brain in the endings of nerve cells. However, misfolded forms of this protein that clump together are linked to damage to nerve cells, a deterioration of the dopamine system and the development of problems with movement and speech – hallmarks of Parkinson’s disease. The latest findings, which are based on studies in mice, back up a long-held theory that abnormally folded alpha-synuclein may start off in the gut and then spread to the brain via the vagus nerve – a bundle of fibres that starts in the brainstem and transports signals to and from many of the body’s organs, including the gut. “It supports and really provides the first experimental evidence that Parkinson’s disease can start in the gut and go up the vagus nerve,” said Ted Dawson, professor of neurology at the Johns Hopkins University school of medicine and co-author of the research. The researchers say the way the misfolded alpha-synuclein spreads in the brains of the mice, and the animals’ symptoms, closely mirrors the disease in humans. Parkinson's disease 'could be detected early on by brain changes' © 2019 Guardian News & Media Limited

Keyword: Parkinsons; Obesity
Link ID: 26360 - Posted: 06.26.2019