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

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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

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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

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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

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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

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Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 26278 - Posted: 05.30.2019

By Gretchen Reynolds Skipping breakfast before exercise might reduce how much we eat during the remainder of the day, according to a small but intriguing new study of fit young men. The study finds that the choice to eat or omit a meal before an early workout could affect our relationship to food for the rest of the day, in complicated and sometimes unexpected ways. Weight management is, of course, one of the great public — and private — health concerns of our time. But the role of exercise in helping people to maintain, lose or, in some instances, add pounds is problematic. Exercise burns calories, but in many past studies, people who begin a new exercise program do not lose as much weight as would be expected, because they often compensate for the energy used during exercise by eating more later or moving less. These compensations, usually subtle and unintended, indicate that our brains are receiving internal communiqués detailing how much energy we used during that last workout and, in response, sending biological signals that increase hunger or reduce our urge to move. Our helpful brains do not wish us to sustain an energy deficit and starve. Previous studies show that many aspects of eating and exercise can affect how much people compensate for the calories burned during exercise, including the type and length of the exercise and the fitness and weight of the exercisers. Skipping or consuming breakfast also can matter. When we eat a meal, our bodies rely on the carbohydrates in those foods as a primary source of energy. Some of those carbohydrates are stored in our bodies, but those internal stores of carbohydrates are small compared to the stores of fat. Some researchers believe that our brains may pay particular attention to any reductions in our carbohydrate levels and rush to replace them. © 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: 26257 - Posted: 05.22.2019

By Gina Kolata At least six million obese teenagers in the United States are candidates for weight-loss surgery, experts estimate. Fewer than 1,000 of them get it each year. Many of these adolescents already have complications of obesity, like diabetes or high blood pressure. But doctors have been uncertain just how well surgery works for young patients, and whether they can handle the consequences, including a severely restricted diet. A new study provides some hopeful answers. Researchers followed 161 teenagers aged 13 to 19, and 396 adults aged 25 to 50, for five years after weight-loss surgery. The teenagers actually fared better than the adults. The adolescents lost at least as much weight, and were more likely to see high blood pressure and diabetes ease or go away, the investigators reported on Wednesday in the New England Journal of Medicine. “This really changes the game,” said Dr. Amir Ghaferi, a bariatric surgeon at the University of Michigan, who was not involved in the research. The paper, he said, added to evidence that obesity, like cancer, is best treated early, before long-term damage from related conditions, such as high blood pressure and diabetes, sets in. To have the surgery, teenagers in the study had to meet the same criteria as adults: a body mass index of at least 35 — for instance, a person who is 5 feet 2 inches tall and weighs 192 pounds or more — and obesity-related health problems. Alternately, the adolescents could have a B.M.I. of at least 40 — such as a person who is 5 feet 2 inches tall and weighs at least 220 pounds — without other conditions linked to obesity. There is no exact data on the number of teenagers who meet those criteria in the United States, said Dr. Thomas Inge, chief of pediatric surgery at Children’s Hospital Colorado and lead author of the new study. © 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: 26242 - Posted: 05.17.2019

Aimee Cunningham Nutrition advice can be confusing. Studies that bolster the health benefits of a food or nutrient seem inevitably to be followed by other work undercutting the good news. One reason for the muddle is that nutrition studies sometimes depend on people’s self-reporting of past meals. And because people may forget or even lie about what they’ve been consuming, that data can be flawed, creating conflicting reports about what’s healthy and what’s not, research has shown. But even if people had a photographic memory of all of their meals, that alone wouldn’t provide enough information. How bodies react to and process food can vary widely from person to person and be dependent on genes, the microbes that live inside the gut, a person’s current health, what the food contains or even how it was made (SN: 1/9/16, p. 8). “The problem is that nutrition research is rocket science,” says David Ludwig, a pediatric endocrinologist at Boston Children’s Hospital. “There are potentially thousands of different nutrients and factors in food that could influence our biology or our senses as we eat. Those can interact in unpredictable and complicated ways.” Given the complexity that comes with researching diet, one approach is to study people in a controlled environment, so that researchers know exactly what the participants are eating. A study that tied eating highly processed foods to weight gain, published online May 16 in Cell Metabolism, did just that. Here’s what the researchers learned — and what they still can’t answer. © 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: 26241 - Posted: 05.17.2019

Richard Harris Scientists who recently announced an experimental genetic test that can help predict obesity got immediate pushback from other researchers, who wonder whether it is really useful. The story behind this back-and-forth is, at its core, a question of when it's worth diving deep into DNA databanks when there's no obvious way to put that information into use. The basic facts are not in dispute. Human behavior and our obesity-promoting environment have led to a surge in this condition over the past few decades. Today about 40% of American adults are obese and even more are overweight. But genetics also plays an important role. People inherit genes that make them more or less likely to become seriously overweight. While some diseases (like Huntington's and Tay-Sachs) are caused by a single gene gone awry, that's certainly not the case for common conditions, including obesity. Instead, untold thousands of genes apparently play a role in increasing obesity risk. Many of those gene variants contribute a miniscule risk. Sekar Kathiresan, a cardiologist at Harvard and a geneticist at the Broad Institute, set out to see whether he and his team could find a bunch of these genetic variants and add up their effects. The goal was to identify genetic patterns that put people at the highest risk. This genetic information "could explain why somebody's so big, why they have so much trouble keeping their weight down," Kathiresan says. His team identified more than 2 million DNA variants of potential interest. He figures most of those variants are irrelevant, but his hunch is, hidden somewhere in there are a few thousand changes that each contribute at least a tiny bit to a person's risk of developing obesity. © 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: 26214 - Posted: 05.07.2019

By Gina Kolata The study subjects had been thin all their lives, and not because they had unusual metabolisms. They just did not care much about food. They never ate enormous amounts, never obsessed on the next meal. Now, a group of researchers in Britain may have found the reason. The people carry a genetic alteration that mutes appetite. It also greatly reduces their chances of getting diabetes or heart disease. The scientists’ study, published on Thursday in the journal Cell, relied on data from the U.K. Biobank, which includes a half million people aged 40 to 69. Participants have provided DNA samples and medical records, and have allowed researchers to track their health over years. A second study in the same journal also used data from this population to develop a genetic risk score for obesity. It can help predict, as early as childhood, who is at high risk for a lifetime of obesity and who is not. Together, the studies confirm a truth that researchers wish more people understood. There are biological reasons that some struggle mightily with their weight and others do not, and the biological impacts often are seen on appetite, not metabolism. People who gain too much weight or fight to stay thin feel hungrier than naturally thin people. The study of the appetite-dulling mutation was led by Dr. Sadaf Farooqi, professor of metabolism and medicine at the University of Cambridge, and Nick Wareham, an epidemiologist at the university. The study drew on Dr. Farooqi’s research into a gene, MC4R. She has probed it for 20 years, but for the opposite reason: to understand why some people are overweight, not why some are thin. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 26156 - Posted: 04.19.2019

Tina Hesman Saey There’s a new way to predict whether a baby will grow into an obese adult. Combining the effect of more than 2.1 million genetic variants, researchers have created a genetic predisposition score that they say predicts severe obesity. People with scores in the highest 10 percent weighed, on average, 13 kilograms (about 29 pounds) more than those with the lowest 10 percent of scores, the team reports April 18 in Cell. The finding may better quantify genes’ roles in obesity than previous prediction scores, but still fails to account for lifestyle, which may be more important in determining body weight, other researchers say. Still, the study shows that “your genetics really start to take hold very early in life,” says coauthor Amit Khera, a cardiologist at Massachusetts General Hospital and the Broad Institute of MIT and Harvard. Weight differences showed up as early as age 3, and by age 18, those with the highest scores weighed 12.3 kilograms more on average than those with the lowest scores, Khera and his colleagues found. Some people with high genetic scores had normal body weights, but those people may have to work harder to maintain a healthy weight than others, he says. People with the highest scores were 25 times more likely to have severe obesity — a body mass index (BMI) greater than 40 — than those with the lowest scores. BMI is a measurement of body fat based on height and weight. A BMI of 18.5 (calculated as kilograms per meters squared of height) to 24.9 is considered healthy. BMIs 30 and above are considered obese. |© Society for Science & the Public 2000 - 2019

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 26155 - Posted: 04.19.2019

By Nicholas Bakalar Eating a heart-healthy diet beginning in your 20s may provide brain benefits in middle age, new research suggests. The study, in Neurology, ranked 2,621 people on their degree of adherence to three different diets considered to be good for the heart. All emphasize vegetables, fruits and whole grains and minimize saturated fat consumption: the Mediterranean diet, which involves mainly plant-based foods and moderate alcohol intake; a research-based diet plan that rates food groups as favorable or not; and the DASH diet, which stresses low-sodium foods. Researchers tracked their diet compliance at ages 25, 32 and 45, and tested mental acuity at 50 and then again at 55. Those who adhered most strictly to the Mediterranean or the food group diet scored higher than those who did not, especially on tests of executive function, which involves organizing and planning. After adjusting for many health and behavioral factors, people with the strictest adherence to these diets had a 46 to 52 percent lower risk of poor cognitive function. But adherence to the DASH diet, which does not consider alcohol consumption, was not associated with cognitive test scores. Which diet is best? “We can say at this point that a heart-healthy diet like the Mediterranean diet is a good option,” said the lead author, Claire T. McEvoy, a dietitian and epidemiologist at Queen’s University Belfast. “It’s palatable and adaptable, and in that respect it’s a pretty good dietary pattern.” © 2019 The New York Times Company

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Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 26018 - Posted: 03.09.2019

By Andrew Jacobs CAMBRIDGE, Mass. — There’s a new war raging in health care, with hundreds of millions of dollars at stake and thousands of lives in the balance. The battle, pitting drug companies against doctors and patient advocates, is being fought over the unlikeliest of substances: human excrement. The clash is over the future of fecal microbiota transplants, or F.M.T., a revolutionary treatment that has proved remarkably effective in treating Clostridioides difficile, a debilitating bacterial infection that strikes 500,000 Americans a year and kills 30,000. The therapy transfers fecal matter from healthy donors into the bowels of ailing patients, restoring the beneficial works of the community of gut microbes that have been decimated by antibiotics. Scientists see potential for using these organisms to treat diseases from diabetes to cancer. At the heart of the controversy is a question of classification: Are the fecal microbiota that cure C. diff a drug, or are they more akin to organs, tissues and blood products that are transferred from the healthy to treat the sick? The answer will determine how the Food and Drug Administration regulates the procedure, how much it costs and who gets to profit. In 2013, the F.D.A. announced a draft decision to regulate the therapy as a new drug but said it would continue to study the matter before reaching a final decision — which is expected to happen soon. Critics say that approach is based on outdated science and could lead to increased costs for patients, most of whom currently rely on a nonprofit stool bank in Cambridge. At stake, some researchers say, is the future of pioneering therapies that harness the human microbiome — the trillions of organisms that colonize the body and are increasingly seen as critical for healthy brain development and immune function. © 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: 26006 - Posted: 03.05.2019

By Gretchen Reynolds A few minutes of brief, intense exercise may be as effective as much lengthier walks or other moderate workouts for incinerating body fat, according to a helpful new review of the effects of exercise on fat loss. The review finds that super-short intervals could even, in some cases, burn more fat than a long walk or jog, but the effort involved needs to be arduous. I have written many times about the health, fitness and brevity benefits of high-intensity interval training, which typically involves a few minutes — or even seconds — of strenuous exertion followed by a period of rest, with the sequence repeated multiple times. Most H.I.I.T. workouts require less than half an hour, from beginning to end (including a warm-up and cool-down), and the strenuous portions of the workout are even briefer. But despite this concision, studies show that interval workouts can improve aerobic fitness, blood sugar control, blood pressure and other measures of health and fitness to the same or a greater extent than standard endurance training, such as brisk walking or jogging, even if it lasts two or three times as long. People being people, though, the most common question I hear about quickie intervals and have asked, on my own behalf, is whether they also will aid in weight control and fat loss. Only a few past studies have directly compared the fat-burning effects of endurance training to those of short interval workouts, however, and their results have been inconsistent. Some indicate that intervals prompt significant fat loss and others that any losses are negligible when compared to the effects of endurance training.

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: 25994 - Posted: 02.28.2019

By C. Claiborne Ray Q. What keeps squirrels from gaining huge amounts of weight as they gorge on acorns and nuts each fall? A. In fact, many squirrels do achieve huge weight gain ahead of the privations of winter. Common gray squirrels may increase their weight by 25 percent in the harvest season. But not because they hibernate — they don’t. Winter foraging is hard, and gray squirrels tend to spend the winter months mostly in their nests. But they must make forays every few days to seek squirreled-away food and other nourishment. Among hibernating squirrels, much of the stored nourishment is needed to survive the cold season without foraging. A study of the Arctic ground squirrel found extreme weight gains during the active season: 42 percent among males and 63 percent among females. They slow their activity drastically before hibernating in order to maintain peak mass. While some do emerge from winter lighter, a significant share of their fat stores may remain. © 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: 25952 - Posted: 02.12.2019

By Carl Zimmer In 2014 John Cryan, a professor at University College Cork in Ireland, attended a meeting in California about Alzheimer’s disease. He wasn’t an expert on dementia. Instead, he studied the microbiome, the trillions of microbes inside the healthy human body. Dr. Cryan and other scientists were beginning to find hints that these microbes could influence the brain and behavior. Perhaps, he told the scientific gathering, the microbiome has a role in the development of Alzheimer’s disease. The idea was not well received. “I’ve never given a talk to so many people who didn’t believe what I was saying,” Dr. Cryan recalled. A lot has changed since then: Research continues to turn up remarkable links between the microbiome and the brain. Scientists are finding evidence that microbiome may play a role not just in Alzheimer’s disease, but Parkinson’s disease, depression, schizophrenia, autism and other conditions. For some neuroscientists, new studies have changed the way they think about the brain. One of the skeptics at that Alzheimer’s meeting was Sangram Sisodia, a neurobiologist at the University of Chicago. He wasn’t swayed by Dr. Cryan’s talk, but later he decided to put the idea to a simple test. “It was just on a lark,” said Dr. Sisodia. “We had no idea how it would turn out.” He and his colleagues gave antibiotics to mice prone to develop a version of Alzheimer’s disease, in order to kill off much of the gut bacteria in the mice. Later, when the scientists inspected the animals’ brains, they found far fewer of the protein clumps linked to dementia. Just a little disruption of the microbiome was enough to produce this effect. Young mice given antibiotics for a week had fewer clumps in their brains when they grew old, too. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 25915 - Posted: 01.29.2019