Chapter 9. Homeostasis: Active Regulation of the Internal Environment

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By Emily Underwood When a 53-year-old man asked Dutch doctors to treat his obsessive-compulsive disorder (OCD) several years back, they suggested a new but promising surgical treatment: implanted electrodes that would stimulate deep brain tissue involved in decision-making, reward-seeking, and motivation. The treatment apparently helped him go off one of his psychiatric medications, but it came with a surprising side effect—it also seemed to improve his type 2 diabetes. Now, researchers think they know why. A new study suggests that a boost in the activity of dopamine, a neurotransmitter involved in motivation and pleasure, improves the body’s ability to process sugar. This is the first time such a pathway, previously seen in mice, has been found in humans, says Mike Michaelides, a neuroscientist at the National Institute on Drug Abuse in Baltimore, Maryland, who was not involved in the new research. That doesn’t make deep brain stimulation (DBS) realistic for most people with diabetes, but other, less invasive brain therapies that target dopamine might one day be feasible. Diabetes occurs when glucose, or sugar, in a person’s bloodstream remains in chronically high concentrations. Type 1, which typically begins in childhood, results when the immune system destroys the pancreatic cells that make insulin, the hormone that lets our cells use sugar as food. Type 2 diabetes, typically triggered by a combination of bad genes, poor eating habits, and a lack of exercise, also damages the body’s ability to produce its own insulin. As time goes on, cells are hard-pressed to remove sugar from the blood, and people require larger and larger amounts of insulin to keep their blood sugar stable. There is no cure for either disease. © 2018 American Association for the Advancement of Science

Keyword: Obesity
Link ID: 25018 - Posted: 05.24.2018

Hartmut Wekerle Some immunologists regard the central nervous system (CNS) as a no-man’s-land, avoided by immune cells and therefore uninteresting. But, in fact, the CNS has a vigorous immune potential that remains dormant in normal conditions but is awakened after injury. The switch that controls the brain’s immune microenvironment involves non-neuronal cells called glia — not only microglia, which are sometimes called the immune cells of the CNS, but also multifunctional cells called astrocytes1. In a paper in Nature, Rothhammer et al.2 describe how these two glial cell types communicate on a molecular level to influence inflammation in the CNS, and show that this interaction is controlled remotely by microbes that inhabit the gut. A decade ago, the group that performed the current study, along with another research group, discovered3,4 an unexpected immunoregulatory role for a ligand-activated transcription factor called the aryl hydrocarbon receptor (AHR), which at the time was best known as a receptor for environmental toxins5. The two groups showed that AHR modulates the progression of experimental autoimmune encephalomyelitis (EAE) — an autoimmune disease in mice in which the immune system becomes overactive and attacks the CNS. EAE is often used a model of multiple sclerosis (MS). Initially, the groups focused on how AHR might affect EAE by regulating pathogenic and protective subsets of immune cells outside the CNS. But it later emerged that AHR is also strongly expressed in the CNS, particularly in microglia and astrocytes6, raising the question of whether AHR in the CNS has a role in autoimmune diseases. © 2018 Macmillan Publishers Limited,

Keyword: Neuroimmunology; Obesity
Link ID: 25010 - Posted: 05.23.2018

Nicola Davis With 26% of adults classified as obese in the UK in 2016, the hunt for causes and solutions to expanding waistlines is on. While public health messages have focused largely on the food we eat, some scientists suspect there is another factor at play: substances being dubbed as “obesogens” – found in our packaging, household goods and furnishings that might affect our hormones and the buildup of fat in the body. However, experts are sceptical, particularly in the light of one report this week. It has made the bold claim that “removing shoes when entering the house and swapping carpet for wooden floors could help people stay slim”, citing a talk by researchers at the universities of Aveiro and Beira Interior in Portugal, who have suggested that preventing obesogens accumulating in the house by frequently sweeping and dusting could stop us gaining weight. As Prof Russell Viner, president of the Royal College of Paediatrics and Child Health, says: “For some medical reasons, such as protection against allergies, yes, it’s advised to keep a dust-free home and so, too, is removing shoes to avoid bringing in dirt from outside, but these things will not make you a healthy weight. Only a balanced diet and regular exercise will do that.” It is not the first study to moot the idea of the existence of obesogens. Earlier this year, researchers at Harvard University suggested compounds called perfluoroalkyl substances (PFAS) – widely used in products such as stain repellents and known to have a number of negative effects on human health – might lead to weight gain. © 2018 Guardian News and Media Limited

Keyword: Obesity
Link ID: 25005 - Posted: 05.22.2018

by Juli Fraga Individuals with anorexia, binge eating disorder and bulimia often feel anxious and overwhelmed when surrounded by food. This anxiety can make grocery shopping and cooking a challenge. A new form of telemedicine in which people can video-chat with a nutritional counselor while at the supermarket aims to help. According to the National Institute of Mental Health, approximately 1 percent of Americans suffer from anorexia, a sometimes deadly psychiatric illness. Along with anorexia, millions of Americans also struggle with binge eating disorder. Jamie Lynn Pelletier, 28, of Greensboro, N.C., was just 13 when she began counting calories and skipping meals, behavior that eventually led to anorexia, which is characterized by food restriction, extreme weight loss and distorted body image. “In junior high, I began to feel unattractive and self-conscious about my body. To lose weight, I started dieting and overexercising,” Pelletier said. Since 2015, Pelletier has completed several residential and outpatient treatment programs in the battle to stop starving herself. Her struggle shows how tough it can be for anorexics to stop seeing food as the enemy. Recently, Pelletier’s dietitian recommended grocery store therapy, which allows her to connect with a dietitian via video chat. “Going to the grocery store is stressful because seeing foods labeled as low-carb and low-fat can make me feel like buying the real thing is not okay. With virtual therapy, I FaceTime with my dietitian at the store,” said Pelletier, referring to Apple’s video-chat application. “For privacy, I put in my headphones so I can talk to her discreetly while I’m shopping.” © 1996-2018 The Washington Post

Keyword: Anorexia & Bulimia
Link ID: 25004 - Posted: 05.22.2018

Robin McKie, science editor Fasting every other day to lose weight could have damaging side effects. That is the conclusion of a group of scientists speaking this weekend at the European Society of Endocrinology’s annual meeting. Their findings suggest that fasting-based diets may impair the action of sugar-regulating hormone insulin, and lead to increased risk of diabetes. Care should be taken before starting such programmes, say researchers. Ana Bonassa, whose team from the University of São Paulo in Brazil carried out the study, said: “This is the first study to show that, despite weight loss, intermittent fasting diets may actually damage the pancreas and affect insulin function in normal healthy individuals, which could lead to diabetes and serious health issues.” Advertisement In recent years intermittent fasting diets have gained popularity. Participants fast for two days out of seven, or on alternate days. However, evidence of their success has been contradictory and there is debate among doctors about their potential to trigger harmful long-term effects. Previous research has also shown that short-term fasting can produce molecules called free radicals, highly reactive chemicals that can cause damage to cells in the body and which may be associated with impaired organ function, cancer risk and accelerated ageing. © 2018 Guardian News and Media Limited

Keyword: Obesity
Link ID: 25001 - Posted: 05.21.2018

By Abby Olena The gut-brain axis is line of communication between the two organs, involved in everything from brain development to the progression of neurological diseases, with gut microbiota often pitching in to the conversation. In a study published today (May 16) in Nature, researchers present evidence that multiple sclerosis (MS) may also be influenced by commensal microbes in the gut acting upon cells in the brain. They show in a mouse model of the disease that metabolites from gut bacteria alter the behavior of microglia—immune cells that reside in the brain—which in turn regulate the activity of astrocytes to promote or prevent inflammation. The authors also found evidence in vitro and in patient samples that a similar gut-brain connection exists in people with MS, suggesting that microbes and the cells that receive their signals could be targets for disease treatment. “The beauty of this paper is that it provides a very detailed mechanistic understanding of how things work,” Jonathan Kipnis, a neuroscientist at the University of Virginia who did not participate in the study, tells The Scientist. Previous research linked the microbiome and the development of MS in mice, he says, but “we never understood how the gut communicates with the brain.” In work published in Nature Medicine in 2016, Francisco Quintana of Brigham and Women’s Hospital in Boston and colleagues found part of the answer to the question of gut-brain communication. In that study, they showed that mouse and human astrocytes—star-shape glial cells—respond to molecules generated by microbes from the intestine. And because prior work from other groups had demonstrated that microglia can regulate astrocyte behavior, Quintana says, “one of the biggest unanswered questions we had is: what mediates the crosstalk between microglia and astrocytes?” © 1986-2018 The Scientist

Keyword: Multiple Sclerosis; Glia
Link ID: 24992 - Posted: 05.18.2018

By Roni Dengler Just looking at a picture of a skinny model on the cover of Glamour or Elle makes many women feel bad about their own weight. Now, science is backing them up. The largest study of its kind finds images of thinner women make even healthy weight women less satisfied with their own bodies—but looking at heavier women makes them feel better. Researchers showed nearly 200 18- to 25-year-old female study participants with a “healthy” body mass index score between 19 and 25 images of normal-, underweight-, or overweight-looking women of the same age and ethnicity. All the images were originally of healthy weight women, but researchers altered some of the pictures to make the models appear larger or smaller by increasing or decreasing the width of the images by 150 pixels. Women who viewed images of the resulting healthy and “overweight” models reported feeling more satisfied with their own body size than women who viewed images of “underweight” models did. After looking at pictures of “underweight” models, women’s satisfaction with their own bodies hardly changed, whereas after seeing healthy weight models, women reported feeling nearly 9% more satisfied with their own body size, for example. Plus, women who viewed images of normal and overweight models perceived their own bodies as smaller, including women who came into the study already feeling highly dissatisfied with their bodies—similar to how eating disorder patients feel. Participants rated whether they thought they were too thin or too fat on a 0-to-10 scale when looking at themselves in a mirror. How they scored themselves dropped by almost 6% after looking at pictures of healthy and overweight models, researchers report today in Royal Society Open Science. In addition, these women felt better about themselves after seeing images of overweight women. And those differences in body satisfaction stuck around for 24 hours. © 2018 American Association for the Advancement of Science.

Keyword: Anorexia & Bulimia
Link ID: 24950 - Posted: 05.09.2018

By Kirstie Brewer BBC News People might think battling obesity is down to sheer willpower, but medical research says otherwise. Here are five potentially surprising factors that can affect your weight, as unearthed by The Truth About Obesity . 1. Gut microbes Gillian and Jackie are twins - but one weighs over six stone (41kg) more than the other. Prof Tim Spector has been tracking their progress over 25 years, as part of the Twins Research UK study. He believes a lot of their weight differences are down to the tiny organisms - microbes - that live deep in the gut. "Every time you eat anything, you're feeding a hundred trillion microbes. You're never dining alone," he says. A stool sample from each twin revealed Gillian, the thinner of the two, had a very diverse range of microbes, whereas Jackie had very few species living in her gut. "The greater the diversity, the skinnier the person. If you're carrying too much weight, your microbes aren't as diverse as they should be," says Prof Spector, who found the same pattern in a study of 5,000 people. Image copyright Science Photo Library Having a healthy and varied diet, rich in different sources of fibre, has been shown to create a more diverse range of gut microbes. Prof Spector warns most Britons eat only half the fibre they should. 2. The gene lottery Why do some people diligently follow diets and exercise regularly but still struggle to see results, while others do very little and don't pile on the pounds? Scientists at Cambridge University believe 40-70% of the effect on our weight is down to variation in the genes we inherit. © 2018 BBC

Keyword: Obesity
Link ID: 24922 - Posted: 04.30.2018

By Kerry Grens Thermometers in the mouse brain are responsible for a lack of appetite the animals feel after a vigorous workout. Simply firing up heat-sensing receptors on cells in the mouse hypothalamus can reproduce the same appetite-suppressing effects of exercise, researchers report today (April 24) in PLOS Biology. “Our study provides evidence that body temperature can act as a biological signal that regulates feeding behavior, just like hormones and nutrients do,” says coauthor Young-Hwan Jo, a neuroscientist at Albert Einstein College of Medicine, in a press release. It’s a fairly common observation among people that working out staves off hunger for a short while afterward. And it turns out the same is true in mice. Jo’s group had mice run a treadmill for 40 minutes, and observed that their brains were warmer and they ate less for the next hour. To see what might be responsible for this effect, Jo and his colleagues centered in on the hypothalamus, given its role in regulating eating. They found that in mice, neurons in the hypothalamus—specifically, in the arcuate nucleus (ARC) of the hypothalamus—produce heat-sensitive receptors called TRPV1. Through a variety of methods, including the application of capsaicin, a compound found in hot chili peppers, the investigators revealed that flipping on TRPV1 could tamp down mice’s appetites. On the flip side, disrupting the receptor wiped out the appetite-suppressing effects of exercise. © 1986-2018 The Scientist

Keyword: Obesity; Pain & Touch
Link ID: 24901 - Posted: 04.26.2018

Alexey Ponomarenko & Tatiana Korotkova The body’s basic needs include a timely supply of nutrients and the avoidance of tissue damage, which are signalled in the brain by hunger and pain, respectively. But these needs cannot be fulfilled simultaneously, because their resolution involves mutually exclusive behaviours. How does the brain prioritize the more urgent need? Writing in Cell, Alhadeff et al.1 report that the brain’s priorities are set depending on the type of pain involved. Hunger-mediating neurons suppress long-term inflammatory pain, but acute pain, which signals an immediate threat, dampens the activity of these neurons and thus deprioritizes feeding. Alhadeff and colleagues deprived mice of food for 24 hours, and analysed how the hungry animals responded to pain. The researchers found that responses to long-term inflammatory pain — of the type associated with chronic disease and recovery from injury — were reduced in the food-deprived animals compared with controls. By contrast, short-term responses to acute pain that was induced by chemicals, heat or force remained intact in hungry mice. The brain’s hypothalamus contains several structures involved in regulating food intake. One of these, the arcuate nucleus, harbours a population of neurons that express agouti-related protein (AgRP), and help to signal nutritional needs — activation of these neurons evokes voracious feeding2, whereas their ablation leads to starvation3,4. Alhadeff et al. found that stimulation of the AgRP-expressing neurons mimicked the pain-inhibiting effect of hunger in mice. By contrast, silencing of these cells blocked the reduction of inflammatory pain. © 2018 Macmillan Publishers Limited,

Keyword: Obesity; Pain & Touch
Link ID: 24896 - Posted: 04.24.2018

By Kerry Grens A variant in the gene for a certain hormone is tied to people eating more carbs. Yet a new study of 451,000 people finds that the allele doesn’t universally mean poorer health. Researchers reported yesterday (April 10) in Cell Reports that those with the sweet-tooth variant actually have lower body fat than others, and no higher risk for type 2 diabetes. They did, however, find a link between the allele and high blood pressure and a thicker waistline. “This goes against the current perception that eating sugar is bad for health. It may reduce body fat because the same allele also results in a lower consumption of protein and fat in the diet,” study coauthor Timothy Frayling, a molecular geneticist at the University of Exeter Medical School in the U.K., says in a press release. “But whilst this version of the gene lowers body fat, it also redistributes fat to the upper body, where it’s more likely to cause harm, including higher blood pressure.” The gene of interest here is FGF21, which encodes fibroblast growth factor 21, a hormone involved in alcohol and sugar consumption and insulin sensitization. The authors note that it’s a target of weight loss interventions. People with a particular allele of FGF21—20 percent of Europeans are homozygous for the variant—tend to consume relatively more sugar and alcohol than those without the allele. To see what consequences this might have on people’s health, Frayling and his colleagues collected data on 451,000 people whose genetic and health information is part of the UK Biobank. © 1986-2018 The Scientist

Keyword: Obesity; Genes & Behavior
Link ID: 24855 - Posted: 04.12.2018

By GRETCHEN REYNOLDS If you give a mouse a running wheel, it will run. But it may not burn many additional calories, because it will also start to move differently when it is not on the wheel, according to an interesting new study of the behaviors and metabolisms of exercising mice. The study, published in Diabetes, involved animals, but it could have cautionary implications for people who start exercising in the hopes of losing weight. In recent years, study after study examining exercise and weight loss among people and animals has concluded that, by itself, exercise is not an effective way to drop pounds. In most of these experiments, the participants lost far less weight than would have been expected, mathematically, given how many additional calories they were burning with their workouts. Scientists involved in this research have suspected and sometimes shown that exercisers, whatever their species, tend to become hungrier and consume more calories after physical activity. They also may grow more sedentary outside of exercise sessions. Together or separately, these changes could compensate for the extra energy used during exercise, meaning that, over all, energy expenditure doesn’t change and a person’s or rodent’s weight remains stubbornly the same. Proving that possibility has been daunting, though, in part because it is difficult to quantify every physical movement someone or something makes, and how their movements do or do not change after exercise. Mice, for instance, skitter, dart, freeze, groom, eat, roam, defecate and otherwise flit about in frequent fits and starts. But recently, animal researchers hit upon the idea of using infrared light beams to track how animals move at any given moment in their cages. Sophisticated software then can use that information to map daily patterns of physical activity, showing, second-by-second, when, where and for how long an animal roams, sits, runs or otherwise spends its time. © 2018 The New York Times Company

Keyword: Obesity
Link ID: 24848 - Posted: 04.11.2018

By Catherine Offord A tadpole has a lot of growing to do to get up to the size it needs to be to metamorphose into an adult frog or toad. Now, researchers at the University of Michigan suggest that this rapid growth is made possible by a lack of inhibitory feeding controls prior to metamorphosis. The team reports the absence of these controls, along with the hormonal regulation that accompanies it, today (March 28) in Proceedings of the Royal Society B. “Our findings are consistent with the hypothesis that the strong drive to eat prior to metamorphosis is due to the absence, or the relative immaturity of hypothalamic feeding control circuits,” the authors write in their paper. This lack of inhibition helps allow “the animal to maximize growth during this critical life-history stage.” Previous work by the researchers had implicated a role for leptin, a hormone that acts as a hunger inhibitor in vertebrates, in regulating the changing feeding habits of toads during early development. To investigate how this hormone might prepare juvenile amphibians for metamorphosis, the team analyzed levels of mRNA transcripts for leptin receptor proteins and for the hormone itself in tadpoles of the African clawed frog (Xenopus laevis). The researchers found that the tadpoles were essentially unresponsive to leptin, unlike their adult counterparts, and showed minimal expression of the leptin receptor in the hypothalamus—a key brain region in the regulation of feeding behavior. Instead, these responses develop as the relevant neural circuits mature during metamorphosis, the authors write. © 1986-2018 The Scientist

Keyword: Obesity
Link ID: 24796 - Posted: 03.29.2018

by David Kohn This is a story about the importance of good timing. Two-thirds of Americans are overweight or obese. This excess weight contributes to a variety of health problems. Despite enormous effort over decades, the problem has proved extremely difficult to solve. Biologist Satchin Panda thinks we’re missing a key variable: Instead of focusing so much on what we eat, he says, we should pay more attention to when we eat. A researcher at the Salk Institute in San Diego, Panda argues that eating within a certain time window each day can help people lose weight and may help prevent illnesses including diabetes, heart disease and cancer. In animal studies, he and others have shown that limiting food intake to a period of eight to 12 hours can boost cognitive and physical performance, and may even lengthen life span. Known as time-restricted feeding, or TRF, the approach is simple: Eat more or less what you want, but don’t consume anything before or after the allotted time. Panda argues that humans’ circadian rhythm is not designed for a world with 24-7 access to food. “If you’re eating all the time, it messes up that pattern,” he says. For many if not most Americans, that pattern is deeply out of whack, and many of us eat from early morning until late at night. © 1996-2018 The Washington Post

Keyword: Obesity
Link ID: 24785 - Posted: 03.27.2018

By Aaron E. Carroll The endless array of diets that claim to help you shed pounds tend to fall into two camps: low fat or low carbohydrate. Some companies even claim that genetics can tell us which diet is better for which people. A rigorous recent study sought to settle the debate, and it had results to disappoint both camps. On the hopeful side, as The New York Times noted, people managed to lose weight no matter which of the two diets they followed. The study is worth a closer look to see what it did and did not prove. Researchers at Stanford University took more than 600 people (which is huge for a nutrition study) aged 18 to 50 who had a body mass index of 28 to 40 (25-30 is overweight, and 30 and over is obese). The study subjects had to be otherwise healthy. They couldn’t even be on statins, or drugs for Type 2 diabetes or hypertension, which might affect weight or energy expenditure. They were all randomly assigned to a healthful low-fat or a healthful low-carbohydrate diet, and they were clearly not blinded to which group they were in. All participants attended 22 instructional sessions over one year in groups of about 17 people. The sessions were held weekly at first and were then spaced out so that they were monthly in the last six months. Everyone was encouraged to reduce intake of the avoided nutrient to 20 grams per day over the first eight weeks, then participants slowly added fats or carbohydrates back to their diets until they reached the lowest level of intake they believed could be sustained for the long haul. Everyone was followed for a year (which is an eternity for a nutrition study). Everyone was encouraged to maximize vegetable intake; to minimize added sugar, refined flour and trans fat intake; and to focus on whole foods that were minimally processed. The subjects were also encouraged to cook at home as much as possible. © 2018 The New York Times Company

Keyword: Obesity
Link ID: 24783 - Posted: 03.26.2018

Aimee Cunningham As mice plumped up on a high-fat diet, some of their taste buds vanished. This disappearing act could explain why some people with obesity seem to have a weakened sense of taste, which may compel them to eat more. Compared with siblings that were fed normal mouse chow, mice given high-fat meals lost about 25 percent of their taste buds over eight weeks. Buds went missing because mature taste bud cells died off more quickly, and fewer new cells developed to take their place. Chronic, low-level inflammation associated with obesity appears to be behind the loss, researchers report March 20 in PLOS Biology. Taste buds, each a collection of 50 to 100 cells, sense whether a food is sweet, sour, bitter, salty or umami (savory). These cells help identify safe and nourishing food, and stimulate reward centers in the brain. The tongue’s taste bud population is renewed regularly; each bud lasts about 10 days. Special cells called progenitor cells give rise to new taste bud cells that replace old ones. Some studies have suggested that taste becomes duller in people with obesity, although why that is has remained unclear. But if taste becomes less intense, “then maybe you don’t get the positive feeling that you should,” which could give way to more overeating, says study coauthor Robin Dando, who studies the biology of taste at Cornell University. Nearly 40 percent of U.S. adults have obesity, determined by a person’s body mass index, a ratio of weight to height. The condition is linked to a number of health problems, including heart disease, diabetes and cancer. |© Society for Science & the Public 2000 - 2018

Keyword: Obesity; Chemical Senses (Smell & Taste)
Link ID: 24777 - Posted: 03.21.2018

By JANE E. BRODY When The New York Times hired me to write about science and health 52 years ago, I was 40 pounds overweight. I’d spent the previous three years watching my weight rise as I hopped from one diet to the next in a futile attempt to shed the pounds most recently gained. No amount of exercise, and I did plenty of it, could compensate for how much I ate when I abandoned the latest weight loss scheme. I had become a living example of the adage: A diet is something one goes on to go off. Even daylong fasting failed me. When I finally ate supper, I couldn’t stop eating until I fell asleep, and sometimes awoke the next morning with partly chewed food in my mouth. I had dieted myself into a binge-eating disorder, and that really scared me. Clearly, something had to change. I finally regained control when I stopped dieting. I decided that if I was going to be fat, at least I could be healthy. I made a plan to eat three nutritious, satisfying meals every day with one small snack, which helped me overcome the temptation to binge in response to deprivation. Much to my surprise, a month later I had lost 10 pounds — eating! Eating good food, that is, and plenty of it. I continued the regimen without difficulty because it was not a diet. It was a way to live and a healthy one at that. And I continued to lose, about two pounds a month. Two years later, all the excess weight was gone. I never gained it back and never again went on a diet. (Even with a twin pregnancy, I gained only 36 pounds and lost them all when my sons were born at 6 pounds 13 ounces each.) The greatest challenge to lasting weight loss, especially for someone like me with a food addiction, is the fact that no one can give up eating. Rather, one has to learn a better — and permanent — way to handle food. © 2018 The New York Times Company

Keyword: Obesity
Link ID: 24723 - Posted: 03.06.2018

By VERONIQUE GREENWOOD If you think about being thirsty at all, it seems like a fairly simple thought process: Find water. Drink it. Move on. But in fact there is something rather profound going on as you take that long, refreshing drink after a run or a hot day in the garden. As you become dehydrated, there is less water in your blood, and neurons in your brain send out the word that it’s time to look for water. Then, once you take a drink, you feel almost instantly satisfied. But if that is obvious, it is also mysterious. You aren’t pouring water directly into your bloodstream, after all. It will take at least 10 or 15 minutes, maybe longer, for the water in your stomach to make its way into the blood. And yet somehow, the brain knows. Sometimes that process isn’t as straightforward as it should be: People with a syndrome called polydipsia feel excessive thirst and drink enormous quantities of water. That can be dangerous, because if the blood is diluted too much, a person can die — a victim of water intoxication. As neuroscientists ponder how and why we thirst, a group of researchers at the California Institute of Technology has shed light on one small corner of the problem. Interested in how the brain keeps track of what the body is drinking, they have identified a set of neurons that receive messages as thirsty mice gulp down water. Passed around in the brain’s thirst centers, these messages seem to be behind the sensation of swift satisfaction that comes after a drink, and also suggest that it’s not just what is drunk, but how it is slurped down, that affects the brain. If the circuits work the same way in people, it may be key to understanding the neuroscience of what happens as we feel thirsty. In the last few years, biologists have been mapping the neurons within an area in the brain that regulates thirst, said Yuki Oka, a professor at Caltech and senior author of the new paper, which was published Wednesday in Nature. Cells in this region had been observed going quiet after an animal had water, but it was not clear exactly why. © 2018 The New York Times Company

Keyword: Miscellaneous
Link ID: 24715 - Posted: 03.01.2018

By NICHOLAS BAKALAR Some experts have suggested that there is an “obesity paradox,” the idea that obese people live longer than those of normal weight. But a new study found that obesity was associated with an increased risk for cardiovascular disease and a two- to three-year shorter life span. The study, in JAMA Cardiology, pooled data from 10 studies of 190,672 people followed from 1964 to 2015. Compared with those of normal weight, overweight men (body mass index of 25 to 29.9) had a 21 percent higher lifetime risk of cardiovascular disease and women a 32 percent higher risk. Among the obese (B.M.I. of 30 to 39.9), the risk was 67 percent higher for men and 85 percent higher for women, with even higher risk for those with a B.M.I. over 40. Longevity in men who were overweight but not obese was similar to that of men of normal weight. But they had an increased risk of cardiovascular disease at a younger age. “We were able to measure how much time is spent in healthy life years rather than just life span,” said the study’s senior author, Dr. Sadiya S. Khan, an assistant professor of medicine at Northwestern. “Maintaining a healthy B.M.I. is associated with a longer, healthier life, with less risk for cardiovascular disease.” © 2018 The New York Times Company

Keyword: Obesity
Link ID: 24712 - Posted: 03.01.2018

By NICHOLAS BAKALAR Overweight mothers are more likely to have overweight babies, and the gut bacteria the babies inherit may in part be to blame. Researchers report that overweight mothers are more likely to have a cesarean section, and that babies born by cesarean to those mothers have species of gut bacteria different from those in babies born to normal weight women. And that difference in the gut microbiome — specifically an abundance of bacteria of the family Lachnospiraceae in infants of overweight mothers — may contribute to an increased risk for obesity. The study included 935 mother-infant pairs. Compared to children born to normal weight mothers, those born vaginally to overweight women were more than three times as likely to be overweight by age 3. But C-section babies born to overweight mothers were more than five times as likely to be overweight. For normal weight mothers, vaginal or C-section delivery made no difference in the risk for overweight babies. The study, in JAMA Pediatrics, controlled for breast-feeding, antibiotic exposure and other factors. The senior author, Anita L. Kozyrskyj, a professor of pediatrics at the University of Alberta, said that there is no probiotic that would lead to a positive change in gut bacteria. “If a cesarean is unavoidable, there is no easy answer,” she added, “but breast-feeding is effective in helping to prevent infants from becoming overweight.” © 2018 The New York Times Company

Keyword: Obesity
Link ID: 24711 - Posted: 03.01.2018