Links for Keyword: Obesity

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A Heart-Healthy Diet May Be Good for the Brain

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

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: 26018 - Posted: 03.09.2019

Drug Companies and Doctors Battle Over the Future of Fecal Transplants

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

The Best Type of Exercise to Burn Fat

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.

Think You’ve Gained Weight This Winter? Check Out These Squirrels

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

Germs in Your Gut Are Talking to Your Brain. Scientists Want to Know What They’re Saying

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

Outrunning Hunger

By Gretchen Reynolds Exercise and eating have a fraught, unsettled relationship with each other. Workouts can blunt or boost appetites. People who start an exercise program often overeat and gain weight — and yet studies and lived experience demonstrate that regular exercise is needed to avoid regaining the weight lost during a successful diet. Intrigued by these contradictory outcomes, researchers at the University of Texas Southwestern Medical Center, along with colleagues from other institutions, ran an experiment on the melanocortin circuit, a brain network in the hypothalamus known to be involved in metabolism. The resulting study, published in December in Molecular Metabolism, suggests that intense exercise might change the workings of certain neurons in ways that could have beneficial effects on appetite and metabolism. The melanocortin circuit consists mainly of two types of neurons. The neuropeptide Y (NPY) cells relay signals encouraging the body to seek food, while the pro-opiomelanocortin (POMC) neurons countermand those orders, reducing interest in food. Animals, including humans, that lack healthy POMC neurons usually become morbidly obese. The researchers focused on what exercise would do to these cells in mice, whose melanocortin circuits resemble ours. Healthy adult male mice either ran on small treadmills or, in a control group, were placed on unmoving treadmills. The exercise routine consisted of 60 minutes of fast, intense running, broken into three 20-minute blocks. Afterward, the mice were free to eat or not, as they chose. The researchers then checked neuronal activity in some of their brains by microscopically probing individual cells in living tissue to measure their electrical and biochemical signals. The tests were repeated throughout the study, which ran for as many as 10 days for some mice. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 5: The Sensorimotor System
Link ID: 25911 - Posted: 01.29.2019

For Real Weight Control, Try Portion Control

By Jane E. Brody I had hoped to avoid ushering in the new year with yet another weight/diet column, but three circumstances prompted me to reconsider: 1) The latest data released by the Centers for Disease Control and Prevention showed that the weight of American men and women has continued its upward climb, with the average B.M.I. now almost at the cutoff for obesity; 2) The Food and Drug Administration is rolling out changes in serving sizes on packaged foods that could very well make matters worse, especially for consumers of ice cream and soda, and 3) Some good news for a change: the publication of an eminently sensible approach to weight loss, “Finally Full, Finally Slim,” written by a leading expert on portion control, Lisa R. Young, a registered dietitian and adjunct professor of nutrition at New York University. Unlike the myriad diet fads that have yet to stem the ever-increasing girth of American men and women, what Dr. Young describes is not a diet but a practical approach to food and eating that can be adapted to almost any way of life, even if most meals are eaten out or taken out. It is not prescriptive or even proscriptive. It does not cut out any category of food, like carbohydrates or fats, nor does it deprive people of their favorite foods, including sweet treats. And it works. I know, because more than half a century ago I lost 40 pounds in two years following Dr. Young’s approach, and I’ve kept the weight off ever since without dieting or deprivation. It fills me up with delicious, nutritious foods and allows me to enjoy a frequent nightcap of ice cream — half a cup (measured) at 150 calories or less. © 2019 The New York Times Company

Skinny genes the 'secret to staying slim'

By Smitha Mundasad Global Health Correspondent, BBC News Scientists say they have discovered the secret behind why some people are skinny while others pile on the pounds easily. Their work reveals newly discovered genetic regions linked to being very slim. The international team say this supports the idea that, for some people, being thin has more to do with inheriting a "lucky" set of genes than having a perfect diet or lifestyle. The study appears in PLOS Genetics. In the past few decades, researchers have found hundreds of genetic changes that increase the chance of a person being overweight - but there has been much less focus on the genes of people who are thin. In this investigation, scientists compared DNA samples from 1,600 healthy thin people in the UK - with a body mass index (BMI) of less than 18 - with those of 2,000 severely obese people and 10,400 people of normal weight. They also looked closely at lifestyle questionnaires - to rule out eating disorders, for example. Researchers found people who were obese were more likely to have a set of genes linked to being overweight. Meanwhile, people who were skinny not only had fewer genes linked to obesity but also had changes in gene regions newly associated with healthy thinness. Lead researcher Prof Sadaf Farooqi, from the University of Cambridge, called on people to be less judgemental about others' weight. "This research shows for the first time that healthy thin people are generally thin because they have a lower burden of genes that increase a person's chances of being overweight and not because they are morally superior, as some people like to suggest," she said. © 2019 BBC.

Memories of eating influence your next meal – new research pinpoints brain cells involved

Marise Parent Of course you know that eating is vital to your survival, but have you ever thought about how your brain controls how much you eat, when you eat and what you eat? This is not a trivial question, because two-thirds of Americans are either overweight or obese and overeating is a major cause of this epidemic. To date, the scientific effort to understand how the brain controls eating has focused primarily on brain areas involved in hunger, fullness and pleasure. To be better armed in the fight against obesity, neuroscientists, including me, are starting to expand our investigation to other parts of the brain associated with different functions. My lab’s recent research focuses on one that’s been relatively overlooked: memory. For many people, decisions about whether to eat now, what to eat and how much to eat are often influenced by memories of what they ate recently. For instance, in addition to my scale and tight clothes, my memory of overeating pizza yesterday played a pivotal role in my decision to eat salad for lunch today. Memories of recently eaten foods can serve as a powerful mechanism for controlling eating behavior because they provide you with a record of your recent intake that likely outlasts most of the hormonal and brain signals generated by your meal. But surprisingly, the brain regions that allow memory to control future eating behavior are largely unknown. Studies done in people support the idea that meal-related memory can control future eating behavior. © 2010–2019, The Conversation US, Inc.

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 25866 - Posted: 01.15.2019

Doubts Raised About Brain Stimulation to Reduce Food Cravings

Abby Olena In the never-ending search for ways to help people eat healthy, scientists have been looking into brain stimulation, specifically, sending a weak electrical current to the brain through two scalp electrodes—a technique called transcranial direct current stimulation. It has previously shown promise in limiting both food cravings and consumption in people, but in a study published yesterday (January 9) in Royal Society Open Science, researchers didn’t find any effects of tDCS on food-related behavior, indicating that the technique’s use needs another look. “The good things about the study are the large sample size and the fact that it’s fairly rigorous,” says Mark George, a psychiatrist and neurologist at the Medical University of South Carolina who did not participate in the study. “The problem [is] interpreting studies where there’s a failure to find. All you can say is that it didn’t work . . . with this group.” During tDCS, one to two milliamps of electricity—enough to feel tingles or pins and needles, but far less than the 800 or so milliamps used for electroconvulsive therapy—are delivered to the brain. Over the last two decades, scientists have reported targeting the technique to the dorsolateral prefrontal cortex, a brain area that’s been shown to be involved in food-related behavior. They’ve found it has helped people crave less and, to a lesser extent, eat fewer sweets and other tempting foods. Yet these experiments have generally included groups of 20 or fewer people, and other studies have failed to replicate their effects. © 1986 - 2019 The Scientist.

Tiny implantable wireless devices could help people repair nerves and lose weight

By Robert F. Service BOSTON—Implanted electronics can steady hearts, calm tremors, and heal wounds—but at a cost. These machines are often large, obtrusive contraptions with batteries and wires, which require surgery to implant and sometimes need replacement. That's changing. At a meeting of the Materials Research Society here last month, biomedical engineers unveiled bioelectronics that can do more in less space, require no batteries, and can even dissolve when no longer needed. "Huge leaps in technology [are] being made in this field," says Shervanthi Homer-Vanniasinkam, a biomedical engineer at University College London. By making bioelectronics easier to live with, these advances could expand their use. "If you can tap into this, you can bring a new approach to medicine beyond pharmaceuticals," says Bernhard Wolfrum, a neuroelectronics expert at the Technical University of Munich in Germany. "There are a lot of people moving in this direction." One is John Rogers, a materials scientist at Northwestern University in Evanston, Illinois, who is trying to improve on an existing device that surgeons use to stimulate healing of damaged peripheral nerves in trauma patients. During surgery, doctors suture severed nerves back together and then provide gentle electrical stimulation by placing electrodes on either side of the repair. But because surgeons close wounds as soon as possible to prevent infection, they typically provide this stimulation for an hour or less. © 2018 American Association for the Advancement of Science

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: 25786 - Posted: 12.13.2018

What We Know About Diet and Weight Loss

By Gina Kolata You’d think that scientists at an international conference on obesity would know by now which diet is best, and why. As it turns out, even the experts still have widely divergent opinions. At a recent meeting of the Obesity Society, organizers held a symposium during which two leading scientists presented the somewhat contradictory findings of two high-profile diet studies. A moderator tried to sort things out. In one study, by Christopher Gardner, a professor of medicine at Stanford, patients were given low-fat or low-carb diets with the same amount of calories. After a year, weight loss was the same in each group, Dr. Gardner reported. Another study, by Dr. David Ludwig of Boston Children’s Hospital, reported that a low-carbohydrate diet was better than a high-carbohydrate diet in helping subjects keep weight off after they had dieted and lost. The low-carbohydrate diet, he found, enabled participants to burn about 200 extra calories a day. So does a low-carbohydrate diet help people burn more calories? Or is the composition of the diet irrelevant if the calories are the same? Does it matter if the question is how to lose weight or how to keep it off? There was no consensus at the end of the session. But here are a few certainties about dieting amid the sea of unknowns. What we know People vary — a lot — in how they respond to dieting. Some people thrive on low-fat diets, others do best on low-carb diets. Still others succeed with gluten-free diets or Paleo diets or periodic fasts or ketogenic diets or other options on the seemingly endless menu of weight-loss plans. Most studies comparing diets have produced results like Dr. Gardner’s: no difference © 2018 The New York Times Company

A New Connection between the Gut and the Brain

By Jonathan D. Grinstein It is well known that a high salt diet leads to high blood pressure, a risk factor for an array of health problems, including heart disease and stroke. But over the last decade, studies across human populations have reported the association between salt intake and stroke irrespective of high blood pressure and risk of heart disease, suggesting a missing link between salt intake and brain health. Interestingly, there is a growing body of work showing that there is communication between the gut and brain, now commonly dubbed the gut–brain axis. The disruption of the gut–brain axis contributes to a diverse range of diseases, including Parkinson’s disease and irritable bowel syndrome. Consequently, the developing field of gut–brain axis research is rapidly growing and evolving. Five years ago, a couple of studies showed that high salt intake leads to profound immune changes in the gut, resulting in increased vulnerability of the brain to autoimmunity—when the immune system attacks its own healthy cells and tissues by mistake, suggesting that perhaps the gut can communicate with the brain via immune signaling. Now, new research shows another connection: immune signals sent from the gut can compromise the brain’s blood vessels, leading to deteriorated brain heath and cognitive impairment. Surprisingly, the research unveils a previously undescribed gut–brain connection mediated by the immune system and indicates that excessive salt might negatively impact brain health in humans through impairing the brain’s blood vessels regardless of its effect on blood pressure. © 2018 Scientific American

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: 25754 - Posted: 12.06.2018

Limited Meal Times Prevent Obesity in Mice Prone to Gaining Weight

Abby Olena Mice with faulty circadian clocks are prone to obesity and diabetes. So are mice fed a diet high in fat. Remarkably, animals that have both of these obesity-driving conditions can stay lean and metabolically healthy by simply limiting the time of day when they eat. In a study published today (August 30) in Cell Metabolism, researchers report that restricting feeding times to mice’s active hours can overcome both defective clock genes and an unhealthy diet, a finding that may have an impact in the clinic. The work corroborates previous research showing how powerful restricted feeding can be to improve clock function, says Kristin Eckel-Mahan, a circadian biologist at the University of Texas Health Science Center at Houston who did not participate in the study. Over the last 20 years, biologists have found circadian clocks keeping physiologic time in almost every organ. They have also shown that mice with disrupted clocks often develop metabolic diseases, such as obesity, and that circadian clock proteins physically bind to the promoters of many metabolic regulators and instruct them when to turn on and off. For Satchidananda Panda of the Salk Institute, these lines of evidence came together in 2009, when his group published a study showing that in mice without the clock component Cryptochrome, feeding and fasting could drive the expression of some, but not all, of the metabolic regulators throughout the body. Other groups have also confirmed that even in the absence of the clock it is still possible to drive some genetic rhythms. In this latest study, he and colleagues wanted to look more closely at how the cycling of clock and metabolic transcripts induced by time-restricted feeding, rather than normal genetic rhythms, influences the health of mice. © 1986 - 2018 The Scientist

Belly Fat Has a Role to Play in Fighting Infections

Selene Meza-Perez, Troy D. Randall Fat is a loaded tissue. Not only is it considered unsightly, the excess flab that plagues more than two-thirds of adults in America is associated with many well-documented health problems. In fact, obesity (defined as having a body mass index of 30 or more) is a comorbidity for almost every other type of disease. But, demonized as all body fat is, deep belly fat known as visceral adipose tissue (VAT) also has a good side: it’s a critical component of the body’s immune system. VAT is home to many cells of both the innate and adaptive immune systems. These cells influence adipocyte biology and metabolism, and in turn, adipocytes regulate the functions of the immune cells and provide energy for their activities. Moreover, the adipocytes themselves produce antimicrobial peptides, proinflammatory cytokines, and adipokines that together act to combat infection, modify the function of immune cells, and maintain metabolic homeostasis. Unfortunately, obesity disrupts both the endocrine and immune functions of VAT, thereby promoting inflammation and tissue damage that can lead to diabetes or inflammatory bowel disease. As researchers continue to piece together the complex connections between immunity, gut microbes, and adipose tissues, including the large deposit of fat in the abdomen known as the omentum, they hope not only to gain an understanding of how fat and immunity are linked, but to also develop fat-targeted therapeutics that can moderate the consequences of infectious and inflammatory diseases. © 1986 - 2018 The Scientist.

Just the Sight of Food Gets the Liver Ready for Action

Abby Olena Anticipating something tasty can lead to a watering mouth and grumbling stomach, but these familiar responses aren’t the only ways the body prepares for nourishment. According to a study published today (November 15) in Cell, sensing food primes mice to process incoming nutrients by directions from the central nervous system to the liver. “It’s a great tour de force combining [several strategies] in one paper to then identify pathways by which food anticipation could alter hepatic metabolism,” says Christoph Buettner, a physician and researcher at Icahn School of Medicine at Mount Sinai in New York who was not involved in the study. “It’s interesting that even before your food hits your tongue or ends up in your stomach, there are changes that prepare an organism for nutrient storage.” Two types of cells in the brain’s hypothalamus have been shown in previous studies to play opposing roles in regulating how much an organism eats. AgRP neurons are turned on when energy stores are low, making an animal seek out food, while POMC neurons, activated when an animal is sated, inhibit eating. Up until a few years ago, the prevailing wisdom was that ingested food resulted in hormonal changes and subsequent neuronal activation after some lag time, says Jens Brüning, an endocrinologist and geneticist at the Max Planck Institute for Metabolism Research in Germany. But in 2015, researchers from the University of California, San Francisco, showed in mice that these neurons change their state of activation nearly instantaneously in response to the sight or smell of food. © 1986 - 2018 The Scientist

Why Are We Still So Fat?

By Gina Kolata Whenever I see a photo from the 1960s or 1970s, I am startled. It’s not the clothes. It’s not the hair. It’s the bodies. So many people were skinny. In 1976, 15 percent of American adults were obese. Now the it’s nearly 40 percent. No one really knows why bodies have changed so much. Scientists do a lot of hand-waving about our “obesogenic environment” and point to favorite culprits: the abundance of cheap fast foods and snacks; food companies making products so tasty they are addictive; larger serving sizes; the tendency to graze all day. Whatever the combination of factors at work, something about the environment is making many people as fat as their genetic makeup permits. Obesity has always been with us, but never has it been so common. Everyone — from doctors to drug companies, from public health officials to overweight people themselves — would love to see a cure, a treatment that brings weight to normal and keeps it there. Why hasn’t anyone discovered one? It’s not for lack of trying. Yes, some individuals have managed to go from fat to thin with diets and exercise, and have kept off the weight. But they are the rare exceptions. Most spend years dieting and regaining, dieting and regaining, in a fruitless, frustrating cycle. There is just one almost uniformly effective treatment, and it is woefully underused: only about 1 percent of the 24 million American adults who are eligible get the procedure. That treatment is bariatric surgery, a drastic operation that turns the stomach into a tiny pouch and, in one version, also reroutes the intestines. Most who have it lose significant amounts of weight — but many of them remain overweight, or even obese. Their health usually improves anyway. Many with diabetes no longer need insulin. Cholesterol and blood pressure levels tend to fall. Sleep apnea disappears. Backs, hips and knees stop aching. © 2018 The New York Times Company

Genetic link between obesity and depression uncovered, say scientists

Nicola Davis Being overweight can cause depression, researchers say, with the effects thought to be largely psychological. While previous studies have found that people who are obese are more likely to have depression, it has been unclear whether that is down to depression driving weight changes or the reverse. Now, in the largest study of its kind, experts say having genetic variants linked to a high body mass index (BMI) can lead to depression, with a stronger effect in women than men. What’s more, they say the research suggests the effect could be down to factors such as body image. “People who are more overweight in a population are more depressed, and that is likely to be at least partly [a] causal effect of BMI [on] depression,” said Prof Tim Frayling, a co-author of the study, from the University of Exeter medical school. Get Society Weekly: our newsletter for public service professionals Read more Writing in the International Journal of Epidemiology, the researchers from the UK and Australia describe how they used data from the UK Biobank, a research endeavour involving 500,000 participants aged between 37 and 73 who were recruited in 2006-10. The researchers looked at 73 genetic variants linked to a high BMI that are also associated with a higher risk of diseases such diabetes and heart disease. They also looked at 14 genetic variants linked to a high percentage of body fat but which were associated with a lower risk of such health problems. While the former group could be linked to depression through biological or psychological mechanisms, the latter would only be expected to have a psychological effect. © 2018 Guardian News and Media Limited

Do gut bacteria make a second home in our brains?

By Kelly Servick SAN DIEGO, CALIFORNIA—We know the menagerie of microbes in the gut has powerful effects on our health. Could some of these same bacteria be making a home in our brains? A poster presented here this week at the annual meeting of the Society for Neuroscience drew attention with high-resolution microscope images of bacteria apparently penetrating and inhabiting the cells of healthy human brains. The work is preliminary, and its authors are careful to note that their tissue samples, collected from cadavers, could have been contaminated. But to many passersby in the exhibit hall, the possibility that bacteria could directly influence processes in the brain—including, perhaps, the course of neurological disease—was exhilarating. “This is the hit of the week,” said neuroscientist Ronald McGregor of the University of California, Los Angeles, who was not involved in the work. “It’s like a whole new molecular factory [in the brain] with its own needs. … This is mind-blowing.” The brain is a protected environment, partially walled off from the contents of the bloodstream by a network of cells that surround its blood vessels. Bacteria and viruses that manage to penetrate this blood-brain barrier can cause life-threatening inflammation. Some research has suggested distant microbes—those living in our gut—might affect mood and behavior and even the risk of neurological disease, but by indirect means. For example, a disruption in the balance of gut microbiomes could increase the production of a rogue protein that may cause Parkinson’s disease if it travels up the nerve connecting the gut to the brain. © 2018 American Association for the Advancement of Science

When an FDA Ruling Curbed Fecal Transplants, I Performed My Own

/ By Susan D’Agostino I’d had intestinal distress before, but never like this. I was excreting not just waste, but blood and bits of my colon’s lining — up to 30 times per day. My abdominal pain hit deeper and felt less productive than the pain of giving birth, epidural-free, to my second child. Even shingles, which stung like a dental drill against my face, paled in comparison. Such was the agony of Clostridium difficile. Commonly known as C. diff., Clostridium difficile is an antibiotic-resistant superbug carried by approximately 5 percent of the adult population. The harmful gut bacterium is normally kept in check by other, good bacteria in the gut’s microbiome. But when the microbial balance is upset — for example, by a dose of antibiotics — C. diff. can gain a foothold. Left to multiply unchecked, it may kill its human host. In 2013, the Centers for Disease Control and Prevention estimated that 14,000 Americans die each year from C. diff. Thanks to an ill-considered decision by the U.S. Food and Drug Administration, and the willful ignorance of a string of doctors charged with my care, I was nearly one of them. Things started innocently enough. In early 2013, my doctor diagnosed me with a bacterial infection and prescribed an antibiotic. I had lived antibiotic-free for nearly four decades — a streak I was not inclined to break. But my doctor insisted on antibiotics, and I reluctantly complied. Soon after, my stomach turned against me. I went to an emergency room and was sent home with a prescription for vancomycin, an antibiotic reserved for serious bacterial infections. But the drug proved little match for the microbes that had bum-rushed my colon. My weight and fluid loss accelerated. My colon risked perforation. Copyright 2018 Undark

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