Links for Keyword: Obesity

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By Laura Sanders Bulging stomachs often take the blame for ending holiday indulging. But bulging guts might be the real appetite killer, a study in mice suggests. The results, published November 14 in Cell, could point out new ways to treat obesity, or even help explain how gastric bypass surgeries limit eating. Those procedures result in food moving faster through the stomach into the intestines, stretching the gut in a way that might signal fullness, the authors speculate. Zachary Knight, a neuroscientist at the University of California, San Francisco, and colleagues identified and studied nerve cells in mice’s intestines that sense mechanical stretching. To simulate full intestines, the team activated these nerve cells with light and chemicals. As a result, the mice ate less food. Physically stretching the mice’s intestines with a salty liquid or a diuretic also caused the mice to eat less. Different stretch-sensing cells in the stomach also curbed mice’s appetites, but to a lesser extent, the researchers found. These nerve cell endings relay messages up the vagus nerve (SN: 11/13/15), which then zips signals to the brain. These messages about intestinal stretching help influence the eat-or-not decision, researchers suspect. L. Bai et al. Genetic identification of vagal sensory neurons that control feeding. Cell. Vol. 179, November 14, 2019, p. 1129. doi: 10.1016/j.cell.2019.10.031 © Society for Science & the Public 2000–2019.

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 26834 - Posted: 11.20.2019

By David S. Ludwig and Steven B. Heymsfield Most diet trials in the best journals fail even the most basic of quality control measures. That’s the finding of a study by us to be published today in JAMA Network Open. Investigators receiving funding for any clinical trial from the National Institutes of Health must register in advance what they plan to test, among other design features, to ensure that the data are fairly analyzed. Comparing the original registries with the final published studies, we found that diet trials in the past decade were about four times as likely as drug trials to have a discrepancy in the main outcome or measurement — raising concern for bias. This quality-control problem of diet trials in comparison to ones on pharmaceuticals leads to a bigger issue: underinvestment in nutrition research and in how we tackle the mysteries of a healthy diet. Although the problems with observational studies have received much attention (“Association doesn’t prove causation,” as scientists say), clinical trials can suffer from equally important limitations. In a clinical trial, investigators assign volunteers to receive different treatments — such as a a low-carbohydrate versus low-fat diet — ideally in random order. Beyond registry issues, trials may provide misleading results for many reasons, including small size, short duration and weak interventions (they lack power to actually make the intended change in behavior). These failures are disturbing because epidemics of diet-related disease will shorten life expectancy and impose huge economic costs on the United States in coming years. We continue to lack effective dietary prevention, in part because clinical trials have been too poorly designed and conducted to reach definitive conclusions. We’re still debating questions that have raged for decades: Should we focus on reducing carbs or fat? Is red meat harmful? Is sugar toxic? What about artificially sweetened beverages or moderate amounts of alcohol? © 2019 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 26820 - Posted: 11.14.2019

By Anahad O’Connor In recent years, hospitals and medical centers across the country have stopped selling sugar-sweetened beverages in an effort to reduce obesity and diabetes. Now a new study carried out at the University of California, San Francisco, has documented the health impact of a soda sales ban on its employees. Ten months after a sales ban went into effect, U.C.S.F. workers who tended to drink a lot of sugary beverages had cut their daily intake by about half. By the end of the study period, the group had, on average, reduced their waist sizes and belly fat, though they did not see any changes in their body mass index. Those who cut back on sugary beverages also tended to see improvements in insulin resistance, a risk factor for Type 2 diabetes. The new research, published on Monday in JAMA Internal Medicine, is the first peer-reviewed study to examine whether a workplace sales ban on sugary drinks could lead to reduced consumption of the beverages and improve employee health. At least nine other University of California campuses have said they are going to adopt similar initiatives to reduce sugary beverage sales and promote water consumption. “This was an intervention that was easy to implement,” said Elissa Epel, an author of the study and director of the Aging, Metabolism, and Emotions Center at U.C.S.F. “It’s promising because it shows that an environmental change can help people over the long run, particularly those who are consuming large-amounts of sugary beverages, and possibly even lead to a reduction in their risk of cardiometabolic disease.” In recent years, the link between sugar and obesity has drawn increasing scientific attention. Health authorities say that Americans have gotten fatter because they are consuming too many calories of all kinds. But some experts have singled out the role of added sugar consumption, which increased more than 30 percent between 1977 and 2010. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 26763 - Posted: 10.29.2019

By Kim Tingley In the United States and other Western countries, diet and nutrition researchers face an urgent imperative: Figure out how to solve the crisis of obesity. About 40 percent of the adults and 19 percent of the children and adolescents in the United States have obesity, according to the Centers for Disease Control and Prevention. More and more of them face the increased risks of suffering from diabetes, cardiovascular disease and countless other negative health effects. This situation looks like a single problem from a population standpoint — one that simple guidelines for balancing calorie consumption and expenditure should be able to solve. Instead, a seeming infinitude of variables influence what each of us eats and how the body responds. That is: Obesity, like cancer, “is not one disease,” says Elizabeth Mayer-Davis, a professor of nutrition and medicine at the University of North Carolina at Chapel Hill. In order to treat it, “you really have to be thinking about biology and behavior and society and culture and policy all at the same time. Because if you miss any one of those pieces, your intervention or your diet — it’s less likely to actually work.” The same diet can affect even identical twins differently. “It’s also why there have been so many conflicting studies in nutrition,” Mayer-Davis says. “The public is very frustrated.” Indeed, just last month a paper in Annals of Internal Medicine created controversy when it argued that there’s not enough evidence to say whether red and processed meats are bad for us, despite years of guidance claiming just that. It also reignited a growing debate: How valuable can universal diet guidelines be for individuals? In recent decades, popular weight-loss plans have largely seesawed between low-fat strategies, which U.S. health agencies have also promoted, and low-carbohydrate ones. Many of them appear to work especially well for some people and not well for others; on average, however, in studies comparing the two kinds of regimens, participants lose the same moderate amount of weight. In those cases when opposing diets produce equivalent results, Kevin Hall, a researcher at the National Institutes of Health, wondered if there was, in fact, an explanation other than the nutrients. He noticed that many of those diets tended to have at least one rule in common: Avoid ultraprocessed food, the sort of packaged fare containing artificial flavorings and ingredients you wouldn’t find in your kitchen that make processed food cheap, convenient, tasty and shelf-stable — and popular. It currently accounts for 57 percent of the American diet (a proportion that is rising). Previous studies have found correlations between ultraprocessed-food consumption and obesity but no proof that it’s a cause. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 26749 - Posted: 10.25.2019

By Elizabeth Pennisi The more researchers look, the more connections they find between the microbes in our intestines and those in our brain. Gut bacteria appear to influence everything from depression to autism. Now, a study on how mice overcome fear is starting to reveal more about the mysterious link between gut and mind. “This work is amazing,” says Peng Zheng, a neuroscientist at Chongqing Medical University in China who was not involved with the research. The study, he says, could provide new insight into several mental disorders. The research used a classic Pavlovian test: Shock a mouse on the foot while playing a tone and the rodent will quickly learn to associate the noise with pain, flinching whenever it hears the sound. But the association doesn’t last forever. After several sessions of hearing the tone but not getting the shock, the mouse will forget the association, and the sound will have no effect. This “forgetting” is important for people as well; it’s impaired, for example, in those with chronic anxiety and post-traumatic stress disorder. David Artis, an immunologist and microbiologist at Weill Cornell Medicine in New York City, wondered whether gut bacteria played any role in the learning and forgetting responses. He and colleagues treated mice with antibiotics to totally rid them of the bacteria in their gut, collectively known as the microbiome. They then played a tone and right after gave the mouse a mild shock, doing this multiple times. © 2019 American Association for the Advancement of Science.

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 26747 - Posted: 10.24.2019

By Nicholas Bakalar Trans fatty acids, known to increase the risk for heart disease, stroke and diabetes, have now been linked to an increased risk for dementia. Researchers measured blood levels of elaidic acid, the most common trans fats, in 1,628 men and women 60 and older and free of dementia. Over the following 10 years, 377 developed some type of dementia. Trans fats, which are added to processed food in the form of partially hydrogenated vegetable oils, increase levels of LDL, or “bad” cholesterol. Meat and dairy products naturally contain small amounts of trans fats, but whether these fats raise bad cholesterol is unknown. After controlling for other factors, the scientists found that compared with those in the lowest one-quarter in blood levels of elaidic acid, those in the highest were 50 percent more likely to develop any form of dementia and 39 percent more likely to develop Alzheimer’s disease in particular. Elaidic acid levels were not associated with vascular dementia considered alone. The study is in Neurology. The senior author, Dr. Toshiharu Ninomiya, a professor of public health at Kyushu University in Japan, said the study is observational so cannot prove cause and effect. “It is difficult to avoid trans fats completely, and the risk of a small amount of trans fats is unclear,” he said. “But it would be better to try to avoid them as much as possible.” © 2019 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 26744 - Posted: 10.24.2019

/ By Elizabeth Preston On the first page of Heinz Koop’s fecal analysis test results, a bar showed where he fell on a gradient from green to red. A label above said, in German: “Overall dysbiosis.” Koop was not in the green or even the yellow regions, but a worrisome orange. It was a bad result — but, he says, “I was kind of happy.” Doctors hadn’t given him a satisfying answer about his recurring bloody diarrhea and other gut troubles. But Koop had learned on Facebook that he could test his gut microbiome — the community of bacteria and other organisms living in his gastrointestinal tract — to look for problems. Koop ordered a test from a German laboratory called Medivere. The results said his gut microbes were imbalanced, which was something he thought he could treat. Soon he would be attempting to correct this imbalance by chauffering a friend’s fresh stool samples home to implant up his own colon. Trillions of microbes living on and in our bodies, especially our guts, make up our microbiome. The bugs in our bowel are not just there to slow down our poop, as one researcher speculated in 1970, but are intricately connected to our health. Gut microbes help us digest our food, make critical vitamins, and keep pathogens out. Over the past decade or so, research into the microbiome has exploded as researchers have tried to tease apart the complex connections between our diseases and our resident microbes. Today, at least 10 percent of published microbiome papers use the term dysbiosis to describe changes in the microbiome, estimates Katarzyna Hooks, a computational biologist now at Evotec, a global biotechnology company headquartered in Germany. Some scientists say the term is useful for communicating a specific finding, though they acknowledge its limitations. Other scientists hate it. Copyright 2019 Undark

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 26729 - Posted: 10.22.2019

Fatty tissue has been found in the lungs of overweight and obese people for the first time. Australian researchers analysed lung samples from 52 people and found the amount of fat increased in line with body mass index. They said their findings could explain why being overweight or obese increased asthma risk. Lung experts said it would be interesting to see if the effect could be reversed by weight loss. In the study, published in the European Respiratory Journal, scientists looked at post-mortem samples of lung donated for research. Fifteen had had no reported asthma, 21 had asthma but died of other causes and 16 died of the condition. The scientists used dyes to carry out detailed analyses of almost 1,400 airways from the lung samples under the microscope. The researchers found adipose (fatty) tissue in the walls of airways, with more present in people with a higher body mass index, And they say the increase in fat appears to alter the normal structure of the airways and cause inflammation in the lungs - which could explain the increased risk of asthma in overweight or obese people. Dr Peter Noble, an associate professor at the University of Western Australia, in Perth who worked on the study, said: "Being overweight or obese has already been linked to having asthma or having worse asthma symptoms. "Researchers have suggested that the link might be explained by the direct pressure of excess weight on the lungs or by a general increase in inflammation created by excess weight." But, he said, their study suggested "another mechanism is also at play". © 2019 BBC.

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 26722 - Posted: 10.19.2019

Tim McDonnell High rates of childhood obesity are a problem in a rising number of low- and middle-income countries, according to a new global assessment of child malnutrition by UNICEF. It's the agency's most comprehensive nutrition report in two decades. The report paints a complex, dire picture of the state of children's health. Overall, it found that around 200 million children under age 5, or 1 in 3 worldwide, are either undernourished or overweight. Wasting (below-average weight for height) and micronutrient deficiency remain persistent challenges in Africa and South Asia. Still, there's some good news: Stunting (below-average height for age) has dropped sharply in the last two decades on every continent except Africa. Meanwhile, at least 340 million adolescents worldwide between ages 5-19, and 40 million children under age 5, have been classified as overweight, the report found. The most profound increase has been in the 5-19 age group, where the global rate of overweight increased from 10.3% in 2000 to 18.4% in 2018. "It's a shockingly fast increase," says Laurence Chandy, director of UNICEF's Office of Global Insights and Policy and a lead author of the report. "It's hard to think of any development indicator where you see such a rapid deterioration." Most of those children live in high- and middle-income countries in North America, Eastern Europe, Pacific island nations and the Middle East. The U.S. is near the top of the list, with a rate of adolescent overweight around 42% (the highest rates, up to 65% are in Palau, Nauru and other in Pacific island nations, which have long struggled with obesity driven by a heavy reliance on imported food). © 2019 npr

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 26717 - Posted: 10.18.2019

By Aaron E. Carroll There’s a decent chance you’ll be reading about diet soda studies until the day you die. (The odds are exceedingly good it won’t be the soda that kills you.) The latest batch of news reports came last month, based on another study linking diet soda to an increased risk of death. As usual, the study (and some of the articles) lacked some important context and caused more worry than was warranted. There are specific reasons that this cycle is unlikely to end. 1. If it’s artificial, it must be bad. People suspect, and not always incorrectly, that putting things created in a lab into their bodies cannot be good. People worry about genetically modified organisms, and monosodium glutamate and, yes, artificial sweeteners because they sound scary. But everything is a chemical, including dihydrogen monoxide (that’s another way of saying water). These are just words we use to describe ingredients. Some ingredients occur naturally, and some are coaxed into existence. That doesn’t inherently make one better than another. In fact, I’ve argued that research supports consuming artificial sweeteners over added sugars. (The latest study concludes the opposite.) 2. Soda is an easy target In a health-conscious era, soda has become almost stigmatized in some circles (and sales have fallen as a result). It’s true that no one “needs” soda. There are a million varieties, and almost none taste like anything in nature. Some, like Dr Pepper, defy description. But there are many things we eat and drink that we don’t “need.” We don’t need ice cream or pie, but for a lot of people, life would be less enjoyable without those things. None of this should be taken as a license to drink cases of soda a week. A lack of evidence of danger at normal amounts doesn’t mean that consuming any one thing is huge amounts is a good idea. Moderation still matters. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 26696 - Posted: 10.14.2019

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

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
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

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 26639 - Posted: 09.24.2019

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.

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 10: Biological Rhythms and Sleep
Link ID: 26618 - Posted: 09.17.2019

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

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
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

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
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

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 26520 - Posted: 08.20.2019

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

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 11: Emotions, Aggression, and Stress
Link ID: 26453 - Posted: 07.26.2019

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.

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 26437 - Posted: 07.23.2019

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

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
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

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 26373 - Posted: 07.02.2019