Links for Keyword: Obesity

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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

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

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: 26368 - Posted: 06.28.2019

By Anahad O’Connor Many nutrition experts blame processed foods for the obesity epidemic, suggesting that a return to home cooking would turn it around. But now some researchers are pushing back against that idea, arguing that it oversimplifies the obstacles that poor and middle-class families face. The case against processed foods has been growing. A flurry of studies last month provided new evidence that these foods, which are typically loaded with salt, sugar, fat and chemical additives, heighten the risk of obesity and chronic disease. Scientists at the National Institutes of Health found that people ate more calories and quickly gained weight on a diet of mostly ultra-processed foods like frozen entrees, diet beverages, fruit juices, pastries, baked potato chips, canned foods and processed meats. Then a pair of large studies in the journal BMJ showed that people who ate significant amounts of these foods had increased mortality rates and cardiovascular disease compared to people who avoided them. These findings and others prompted health experts — including Dr. Francis Collins, the director of the N.I.H. — to urge Americans to limit their intake of ultra-processed foods. But that might be easier said than done. Highly processed foods have become the dominant food source for many Americans, accounting for almost 60 percent of the calories we eat. Americans across the socioeconomic spectrum consume them in increasing amounts. But studies show that their intake is highest among low-income families. Many households depend on them because they are cheap, convenient and, in some cases, their only option. © 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: 26325 - Posted: 06.12.2019

By Malia Wollan “Fasting is mental over physical, just like basketball and most other stuff in life,” says Enes Kanter, the 6-foot-11 center for the Portland Trail Blazers. Raised in Turkey, Kanter, 27, is a Muslim who has fasted from sunrise to sunset during the month of Ramadan since he was 8. This season, Ramadan aligned with the N.B.A. playoffs, so Kanter fasted through seven playoff games. During the year he forgoes food and water a day or two a week. “Don’t be scared to try it,” he says. Intermittent fasting has become a trendy tool for losing weight and boosting mental acuity and productivity. Adherents typically restrict eating to a window of eight or fewer hours during the day, or they limit caloric intake a few days per week. Studies suggest that following such diets can lead to weight loss and reduced risk of cardiovascular disease and may even protect against age-related neurological disorders like Alzheimer’s. For his part, though, Kanter is trying desperately not to lose any weight. His team’s trainers worried about him going 16 hours without food or water on game days, and so before dawn and twice after dark he partook of carbohydrate feasts: pasta, quesadillas, burritos, sandwiches, sports drinks and nutrition bars. “As many calories as I can put in my body,” he says. Don’t fast if you are at all prone to eating disorders or have a medical condition that might make it dangerous. (While Ramadan fasting is compulsory for Muslims, exceptions are made for children, pregnant women and the ill, among others.) Break your fast carefully by resisting the hurried, gobbler mind-set. “Don’t lose control of yourself,” Kanter says. “Go slow.” Start with lighter fare like soup or salad. Wait 10 minutes before beginning heavier courses. © 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: 26320 - Posted: 06.11.2019

Mara Gordon Kids with obesity face a host of health problems related to their weight, like high blood pressure, diabetes, and joint problems. Research points to another way heavier children and teens are at risk: their own doctors' bias. This prejudice has real health consequences for kids, making families less likely to show up for appointments or get recommended vaccines. I am a family physician at a community health center in Washington, D.C., and many of my young patients have obesity. It's no surprise. Obesity is the most common chronic disease that affects children and teens in the U.S. One third of American kids are overweight or obese. But I often feel totally unprepared to talk about it in a way that puts kids at ease. We have to cram in a physical exam, shots, and parent questions into a 15-minute appointment, and a discussion about a healthy lifestyle sometimes feels like an afterthought. I remember one recent visit with a teenage girl and her mom, tripping over the words I chose. "Let's talk about your weight," I said, offering a reassuring smile. It didn't seem to work. I still think about the look of shame on my patient's mom's face, as if her daughter's obesity were a personal failing. © 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: 26302 - Posted: 06.05.2019

By Larissa Zimberoff At the urging of doctor friends and a few popular books, I embarked on a diet plan earlier this year called intermittent fasting. The basics are that I could eat the foods I enjoyed and most of my regular meals, but it had to be within a short time frame of eight to 10 hours. Outside of that, I would stick to water, tea and black coffee. Proponents of the plan, also known as time-restricted eating, say that intermittent fasting could help me lose weight, always a worthwhile goal. It would also give my gut a much-needed break from processing food, improve focus and lessen daily inflammation. In the long-term, it might even help me live longer. I’ll admit, the words “intermittent fasting” sounded a little daunting. But Dr. Jason Fung, author of “The Obesity Code,” assured me that it could easily be incorporated into my daily routine. “Anytime you’re not eating is a fast — anything above four hours is fasting,” he said. “A lot of times people eat because they have to, versus really enjoying what they are eating. If you don’t want the sandwich, skip it. Your body knows what to do, it will take your body fat. That’s why you carry it around with you.” In other words, by voluntarily submitting to an absence of food for long periods during the day, my body would transition from burning sugar for fuel to burning fat. Two things made me think I might be able to stick with an intermittent fasting plan. First, I have Type 1 diabetes, which means eating requires thinking. For most of my life, I have spent my days making in-air computations about what I might or might not consume: weighing pros and cons about specific foods while factoring in things like carbs, fat and fiber. Protein too, if I’m super diligent. The more I eat, the more I have to think. © 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: 26296 - Posted: 06.04.2019

By Jane E. Brody When a child is born with a rare disorder that few doctors recognize or know how to manage, it can pay big dividends for parents to be proactive, learn everything they can about the condition, and with expert medical guidance, come up with the best way to treat it. That is the approach Lara C. Pullen of Chicago adopted when her son, Kian Tan, was born 15 years ago last month at 7½ pounds, seemingly well-formed and healthy. But within 24 hours, Dr. Pullen, who already had two daughters, said Kian had stopped moving, wouldn’t nurse and felt as floppy as a rag doll. Two and a half weeks later, a genetic test showed that Kian had Prader-Willi syndrome, a genetic disorder that occurs once in every 15,000 to 25,000 live births. While at first it is a struggle to get enough food into these babies because they’re too weak to suck, within two or three years their main symptom is an insatiable appetite that results in extreme obesity unless the child, who is driven by constant hunger, is kept from sneaking and stealing food. Prader-Willi syndrome is caused by the failed expression of several genes on chromosome 15 derived from the child’s father. The genes are either missing or inactivated by a mistake that occurs during sperm development or, in some cases, the father’s entire chromosome 15 is not inherited by the fetus. The disorder is only rarely inherited, but when a father has Prader-Willi syndrome caused by a deletion in chromosome 15, there’s a 50 percent chance each child he fathers will inherit the defective chromosome. In addition to an excessive appetite, its range of symptoms includes short stature, sleep apnea, extreme daytime sleepiness, visual defects, underdeveloped genital organs, poor coordination, mild to moderate intellectual disability, speech problems, a high tolerance for pain, temper tantrums, obsessive behaviors and blood sugar irregularities. © 2019 The New York Times Company

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: 26292 - Posted: 06.03.2019

By James Gallagher Health and science correspondent, BBC News Ultra-processed foods - such as chicken nuggets, ice cream and breakfast cereals - have been linked to early death and poor health, scientists say. Researchers in France and Spain say the amount of such food being eaten has soared. Their studies are not definite proof of harm but do come hot on the heels of trials suggesting ultra-processed foods lead to overeating. Experts expressed caution but called for further investigation. What are ultra-processed foods? The term comes from a way of classifying food by how much industrial processing it has been through. The lowest category is "unprocessed or minimally processed foods", which include: • fruit • vegetables • milk • meat • legumes such as lentils • seeds • grains such as rice • eggs "Processed foods" have been altered to make them last longer or taste better - generally using salt, oil, sugar or fermentation. This category includes: • cheese • bacon • home-made bread • tinned fruit and vegetables • smoked fish • beer Then come "ultra-processed foods", which have been through more substantial industrial processing and often have long ingredient lists on the packet, including added preservatives, sweeteners or colour enhancers. Prof Maira Bes-Rastrollo, from the University of Navarra, told BBC News: "It is said that if a product contains more than five ingredients, it is probably ultra-processed." Examples include: • processed meat such as sausages and hamburgers • breakfast cereals or cereal bars • instant soups • sugary fizzy drinks • chicken nuggets • cake • chocolate • ice cream • mass-produced bread • many "ready to heat" meals such as pies and pizza | meal-replacement shakes How bad were the findings? The first study, by the University of Navarra, in Spain, followed 19,899 people for a decade and assessed their diet every other year. There were 335 deaths during the study. But for every 10 deaths among those eating the least ultra-processed food, there were 16 deaths among those eating the most (more than four portions a day). © 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: 26278 - Posted: 05.30.2019