Chapter 13. Homeostasis: Active Regulation of the Internal Environment

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By Kate Murphy Maybe it was because when the waiter asked, “Still or sparkling?” you chose sparkling. It could have also been that you were ravenous and ate a little too much. Or, possibly, it was your ex, who happened to be dining at the same restaurant and stood a little too long over your table making awkward small talk. All of these things, hic, might cause spasms, hic, in your diaphragm, hic. Referred to in the medical literature as singultus (from the Latin singult, which means gasp or sob), hiccups are familiar to anyone who has ever taken a breath. In fact, you begin to hiccup while still in the womb. Most people hiccup the most during childhood, with the bouts becoming less frequent over time, but even in adulthood, hiccups are still a common, and annoying, occurrence. Just as we all have our own particular way of sneezing, we all have a unique way of hiccuping that can range from four to 60 hiccups per minute. Most hiccups are benign and last only a few minutes or hours. But sometimes hiccups are indicative of a more serious health issue, particularly when they recur or don’t go away for days, weeks or years. Beyond being embarrassing, the muscle contractions can be physically exhausting. They can interrupt sleep and make it hard to eat. Approximately 4,000 people in the United States are admitted to the hospital every year for hiccups. The patient with the longest recorded case, according to Guinness World Records, was Charles Osborne of Anthon, Iowa, who hiccuped for 68 years straight. He claimed it started while attempting to weigh a hog before slaughtering it. Doctors say there are as many causes for hiccups as there are crazy remedies, including tugging on your tongue, standing on your head and swallowing granulated sugar. Some actually work. Others are more likely just entertainment for friends and family who watch while you try to cure yourself. © 2019 The New York Times Company

Keyword: Miscellaneous
Link ID: 26503 - Posted: 08.15.2019

Tina Hesman Saey Subtle defects in the immune system may lead to obesity and type 2 diabetes, a study of mice suggests. Mice gained weight and developed health problems when they carried a genetic defect that dampens some immune functions, researchers report in the July 26 Science. The immune problems were linked to shifts in the gut microbiome — the collection of friendly bacteria and other microbes living in the intestines. Altering the gut microbe mix, particularly in the small intestine, may lead to increased absorption of fat from the diet, the researchers found. These findings, if they hold up in human studies, could lead to strategies for boosting immune system function in order to help prevent obesity and associated health problems. People with obesity and those with type 2 diabetes also have gut microbe compositions and subtle immune system deficiencies similar to those seen in the mice, says June Round, a microbiome researcher at the University of Utah School of Medicine in Salt Lake City. “It’s possible that things that are happening in our mice are also happening in individual [humans],” she says. Round and colleagues noticed that mice with a defect in the Myd88 gene started gaining weight at about 5 months old. By about a year old, those mice, which lack Myd88 protein in immune cells called T cells, weighed up to 60 grams — about twice as much as a normal mouse. The mutant mice also had developed metabolic problems associated with obesity, such as insulin resistance, a hallmark of type 2 diabetes in people. |© Society for Science & the Public 2000 - 2019

Keyword: Obesity; Neuroimmunology
Link ID: 26453 - Posted: 07.26.2019

Tina Hesman Saey A friendly gut bacterium can help lessen ALS symptoms, a study of mice suggests. Mice that develop a degenerative nerve disease similar to amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease, fared better when bacteria making vitamin B3 were living in their intestines, researchers report July 22 in Nature. Those results suggest that gut microbes may make molecules that can slow progression of the deadly disease. The researchers uncovered clues that the mouse results may also be important for people with ALS. But the results are too preliminary to inform any changes in treating the disease, which at any given time affects about two out of every 100,000 people, or about 16,000 people in the United States, says Eran Elinav, a microbiome researcher at the Weizmann Institute of Science in Rehovot, Israel. “With respect to ALS, the jury is still out,” says Elinav, also of the German Cancer Research Center in Heidelberg. “We have to prove that what we found in mice is reproducibly found in humans.” Elinav and his colleagues examined the gut microbiomes — bacteria, archaea and other microbes that live in the colon, or large intestine — of mice that produce large amounts of a mutated form of the SOD1 protein. In the mice, as in human ALS patients, faulty SOD1 proteins clump together and lead to the death of nerve cells. |© Society for Science & the Public 2000 - 2019

Keyword: ALS-Lou Gehrig's Disease
Link ID: 26439 - Posted: 07.23.2019

Kelly Crowe · CBC News Scientists are slowly chipping away at one of the most mysterious aspects of weight loss: why does the lost weight often seem to come back? It's now clear that it's not simply a matter of willpower. "We know people are good at losing weight with diet and exercise," said Gregory Steinberg, Canada Research Chair in Metabolism and Obesity at McMaster University. "It's not that people just give up." The problem is rooted in the body's physiology. After people lose weight, their bodies' energy use also changes by burning fewer calories. "Quickly you hit a plateau at five to 10 per cent weight loss and you can't lose more weight than that because your metabolism slows down too much," said Steinberg. "This explains why relapse weight gain is so high." But why the body's calorie-burning capacity drops has so far not been explained. "No one knows why," said Steinberg. There are theories that something is putting the brakes on the body's ability to turn up its fat-burning machinery. And last week, a new paper published in Cell Reports, describes one possible system. At New York University, Ann Marie Schmidt is studying a receptor on fat cells that appears to interfere with weight loss. When she created a mouse model without any of those receptors the mice didn't get fat even though they ate more food. "When you delete [the receptor] it completely resets their metabolic program so that they are resistant to the diet-induced obesity," said Schmidt. "It's totally unexpected and it has so many implications for human health." Although scientists have identified the receptor — called RAGE — in humans, so far most of the research has been done in mice. ©2019 CBC/Radio-Canada.

Keyword: Obesity
Link ID: 26437 - Posted: 07.23.2019

By Jessica Hamzelou Anorexia nervosa isn’t just a psychiatric condition – it is a metabolic one, too, according to a genetic study of around 72,500 people. The findings help to explain some of the symptoms of anorexia, and could help to shape future treatments. Anorexia affects between 0.9 and 4 per cent of women and 0.3 per cent of men, but is still poorly understood. “Anorexia has the highest mortality rate of any psychiatric disorder,” says Cynthia Bulik at the University of North Carolina at Chapel Hill. “We’re not very good at treating anorexia. There’s no medication, and that’s probably because we don’t understand the underlying causes.” Previous research has found that genetic factors, as well as environmental ones, can increase a person’s risk of anorexia. To investigate, Bulik and her colleagues compared the genomes of just under 17,000 people with anorexia with those of 55,500 people who didn’t have the condition. The team used a technique that applies thousands of markers to the genome, and compares these markers across all the volunteers. “It points you to where in the genome the differences lie,” says Bulik. The search pinpointed eight locations across the genome that seem to play a role in anorexia. But this is likely to represent only a tiny fraction of all the genetic factors involved in the condition, says Bulik. “It’s a complex trait, so we expect lots of genes to each have a small to moderate effect,” she says. © Copyright New Scientist Ltd.

Keyword: Anorexia & Bulimia
Link ID: 26424 - Posted: 07.16.2019

By Thomas Stackpole The run happened — or didn’t — maybe five days into the raw-diet experiment. I had formed a sort of fitness pact with a friend to forgo cooked food, and after days of nothing but salads, almonds, sashimi and black coffee, my body felt taut and ready for action. And for about half a mile, it was, my strides floating above the pavement as a few fistfuls of raw kale percolated in my belly. Then suddenly I sputtered, feeling an unambiguous alarm go off: Tank is empty, sorry, this is the end of the line. After a pause, I tried running again but made it maybe a block before my legs revolted again and I slowed to a walk. My new healthy diet, it seemed, didn’t accommodate any actual exercise. When I told all this to my co-workers the next morning, it was fodder for a good laugh. My obsessions were — and often still are — a kind of running joke. I’ve been conducting a series of shifting and poorly planned “wellness” experiments on myself for about a decade. I’ve eaten keto, low-carb and sometimes not at all. One time, I ate almost nothing but lean ground turkey and broccoli over greens for maybe two months as part of a YouTube bodybuilder’s plan. More than once, I’ve lost 10 pounds in a week. I’ve also obsessed over bulking up, gaining 25 pounds over about six months of lifting, before pivoting and deciding to train for a marathon to run it off. Then there were the gut biome vitamins, the metabolism-boosting mushrooms, the experiments with LSD microdosing and calorie trackers. Despite years of cycling through boutique insanities, it didn’t occur to me that I might have a problem until earlier this year, when the Twitter founder turned Silicon Valley wellness influencer Jack Dorsey detailed his fasting regimen. The news that he eats one meal a day during the week and nothing on the weekend provoked scornful cries that he was advocating little more than anorexia with a bro-y tech-world veneer. I, on the other hand, saw a kindred spirit. © 2019 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 26418 - Posted: 07.15.2019

By Madeleine Connors At the age of 16, my mother spent hours waiting in bread lines in communist Poland, biting at her nails. The year was 1972. The line was mostly women. Their bellies rattled with hunger, anticipation of food burning in their throats. My mother has said that waiting in a bread line was not much different from a time later in her life when she had moved to America and stood in line for hours for an Eric Clapton concert. “It’s all about wanting something. You want something, you wait for it,” she recited with a tone so deadpan that it reminded me that my mom was once a teenage girl. My experience of teenage girlhood was vastly different, growing up in Sonoma, Calif. I was many things; hungry was not one of them. I picked mushrooms out of tacos with reckless abandon. I would surrender pieces of toast under the breakfast table to my dachshund. But in 1972, food rationing in Poland had become widespread. My mother would wake up at the crack of dawn with ambitions of bringing back flour to her family. She would clench and study her bread coupon, only to look up and see an outbound train full of canned goods and hams hurtling toward Russia. Even then she knew: food was for other people. People who were better, more deserving; worth nourishing. When I was young, I ate to overcompensate for her hunger. Costco became the patron saint of my mother’s immigrant anxieties and bulk was her prayer. She bought American dream-size buckets full of almonds. She bought offensive amounts of pastas. She bought enough snacks to feed a bus full of kids on a travel soccer team. Shopping with my mother became an arms race. Shuffling through aisles along with other newly American mothers, my mom lived to give me a different life than the one she experienced. © 2019 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 26392 - Posted: 07.05.2019

By Gretchen Reynolds People hoping to lose weight with exercise often wind up being their own worst enemies, according to the latest, large-scale study of workouts, weight loss and their frustrating interaction. The study, which carefully tracked how much people ate and moved after starting to exercise, found that many of them failed to lose or even gained weight while exercising, because they also reflexively changed their lives in other, subtle ways. But a few people in the study did drop pounds, and their success could have lessons for the rest of us. In a just and cogent universe, of course, exercise would make us thin. Physical activity consumes calories, and if we burn calories without replacing them or reducing our overall energy expenditure, we enter negative energy balance. In that condition, we utilize our internal energy stores, which most of us would call our flab, and shed weight. But human metabolisms are not always just and cogent, and multiple past studies have shown that most men and women who begin new exercise routines drop only about 30 percent or 40 percent as much weight as would be expected, given how many additional calories they are expending with exercise. Why exercise underwhelms for weight reduction remains an open question, though. Scientists studying the issue agree that most of us compensate for the calories lost to exercise by eating more, moving less, or both. Our resting metabolic rates may also decline if we start to lose pounds. All of this shifts us back toward positive energy balance, otherwise known as weight gain. © 2019 The New York Times Company

Keyword: Obesity
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

Keyword: Obesity
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

Keyword: Obesity
Link ID: 26368 - Posted: 06.28.2019

Nicola Davis Evidence that Parkinson’s disease may start off in the gut is mounting, according to new research showing proteins thought to play a key role in the disease can spread from the gastrointestinal tract to the brain. The human body naturally forms a protein called alpha-synuclein which is found, among other places, in the brain in the endings of nerve cells. However, misfolded forms of this protein that clump together are linked to damage to nerve cells, a deterioration of the dopamine system and the development of problems with movement and speech – hallmarks of Parkinson’s disease. The latest findings, which are based on studies in mice, back up a long-held theory that abnormally folded alpha-synuclein may start off in the gut and then spread to the brain via the vagus nerve – a bundle of fibres that starts in the brainstem and transports signals to and from many of the body’s organs, including the gut. “It supports and really provides the first experimental evidence that Parkinson’s disease can start in the gut and go up the vagus nerve,” said Ted Dawson, professor of neurology at the Johns Hopkins University school of medicine and co-author of the research. The researchers say the way the misfolded alpha-synuclein spreads in the brains of the mice, and the animals’ symptoms, closely mirrors the disease in humans. Parkinson's disease 'could be detected early on by brain changes' © 2019 Guardian News & Media Limited

Keyword: Parkinsons; Obesity
Link ID: 26360 - Posted: 06.26.2019

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

Keyword: Obesity
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

Keyword: Obesity
Link ID: 26320 - Posted: 06.11.2019

By Joshua Sokol For half the year, a little brown bird on the northernmost islands of the Galápagos uses its wickedly sharp beak to pick at seeds, nectar and insects. But when the climate dries out, it drinks blood. Yes, there is such a thing as a vampire finch. Yes, it is what it sounds like. Galápagos finches have been used since Darwin’s time to illustrate evolution in action. Even among them, Geospiza septentrionalis is an outlier, one of the few birds in the world to intentionally draw and drink blood. And the species is only found on Wolf and Darwin islands, two of the most remote and off-limits places in the entire archipelago. The vampire finch has a method. First, one bird hops on the back of a resting Nazca booby, pecks at the base of the seabird’s wing, and drinks. Blood stains the booby’s white feathers. Other finches crowd around to wait their turn, or to watch and learn. Because adult boobies can fly away, the attacks are almost never fatal. The only casualties are chicks that flee from the finches on foot and, unable to find their way back, starve. Drinking blood is an unusual diet, and research published last year showed that vampire finches have evolved specialized bacteria in their guts to aid digestion. Even more surprising, according to a paper this week in the journal Philosophical Transactions of the Royal Society B, is that some of these bacteria are similar to ones found in the vampire bats of Central and South America. Se Jin Song, a biologist at the University of California San Diego and the study’s lead author, had previously studied the convergent evolution of gut bacteria. Do disparate animals with the equivalent of fad diets — eating only ants and termites, for instance — develop similar gut microbiota over evolutionary time? © 2019 The New York Times Company

Keyword: Evolution; Obesity
Link ID: 26312 - Posted: 06.10.2019

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

Keyword: Obesity
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

Keyword: Obesity
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

Keyword: Obesity; Genes & Behavior
Link ID: 26292 - Posted: 06.03.2019

By Veronique Greenwood After a long hike on a hot day, few things are more rewarding than a tall, frosty glass of water. The rush of pleasure that comes with a drink might feel like a sign from your body that you’ve done the right thing, a reward for remedying your dehydration. But that pleasing sensation isn’t actually linked to your real need for a drink. In a study published Wednesday in the journal Neuron, a group of scientists who have studied how thirst works in the bodies of mammals report that the neural systems related to the feeling of reward work independently of those involved in monitoring water intake. Staying hydrated is high on most organisms’ list of priorities. Mammals have multiple ways of tracking the water they’ve consumed, a subject Yuki Oka, a neuroscientist at the California Institute of Technology, has long studied in mice. The mechanisms in other mammals, including humans, may be similar. One method he and colleagues explored in earlier research involves the gulping motion made by the throat as liquid is swallowed. That gulping sends a message to the brain that water has been consumed, quieting the neurons that generate the urge to drink. But that happens regardless of whether the substance gulped was water or oil, suggesting that the act of gulping only briefly convinces your brain that your thirst is quenched. The body also tracks the presence of water in the gut, and when it becomes clear that water is not arriving, thirst returns. Dr. Oka and colleagues report in their latest study that injecting water directly into the stomachs of mice did quench thirst, albeit after a longer lag. © 2019 The New York Times Company

Keyword: Drug Abuse
Link ID: 26287 - Posted: 06.01.2019

By Kelly Servick Genes are a powerful driver of risk for autism, but some researchers suspect another factor is also at play: the set of bacteria that inhabits the gut. That idea has been controversial, but a new study offers support for this gut-brain link. It reveals that mice develop autismlike behaviors when they are colonized by microbes from the feces of people with autism. The result doesn’t prove that gut bacteria can cause autism. But it suggests that, at least in mice, the makeup of the gut can contribute to some hallmark features of the disorder. “It’s quite an encouraging paper,” says John Cryan, a neuroscientist at University College Cork in Ireland who was not involved in the research. The idea that metabolites—the molecules produced by bacterial digestion—can influence brain activity “is plausible, it makes sense, and it will help push the field forward.” Many studies have found differences between the composition of the gut microbiomes in people with and without autism. But those studies can’t determine whether a microbial imbalance is responsible for autism symptoms or is a result of having the condition. To test the effect of the gut microbiome on behavior, Sarkis Mazmanian, a microbiologist at the California Institute of Technology (Caltech) in Pasadena, and collaborators put fecal samples from children with and without autism into the stomachs of germ-free mice, which had no microbiomes of their own. The researchers then mated pairs of mice colonized with the same microbiomes, so their offspring would be exposed to a set of human microbes early in development. © 2019 American Association for the Advancement of Science

Keyword: Autism
Link ID: 26283 - Posted: 05.31.2019

By Diana Kwon Few things are more refreshing than enjoying a cool beverage after spending a day under the hot summer sun. But gulping down a drink does not always quench thirst. Seawater, for example, may look appealing to someone stranded in the middle of the ocean, but taking a swig of it will only worsen dehydration. Scientists have now discovered that in rodents, signals from both the throat and gut control feelings of thirst. These distinct pathways may explain why consuming a beverage is typically refreshing but does not always sate one’s thirst, according to a study by Yuki Oka, a neuroscientist at the California Institute of Technology, and his colleagues at the California Institute of Technology, published May 29 in Neuron. Last year, Oka’s team reported that the simple act of gulping activated a circuit in the lamina terminalis, a region near the front of the brain, which ultimately led to the suppression of activity in neurons responsible for generating feelings of thirst. This throat-brain pathway, which the researchers identified in mice, switched on regardless of what an animal consumed—water, saline solution and oil produced similar effects. But the fact that all of these substances were able to inhibit the brain’s “thirst” neurons indicated that there was something missing. After all, if any liquid could satisfy an animal’s thirst, it might not consume enough water to remain hydrated. According to Oka, behavioral studies in animals dating back decades suggested that there was an additional mechanism in the gut that signaled the presence of water to the brain. So in their latest investigation, Oka’s team set out to map the brain circuits responsible for receiving these signals. By injecting fluids directly into the guts of mice, the researchers discovered that in order for the rodents to feel fully hydrated, this second gut-based circuit needed to be activated. Without these gastrointestinal signals—which, unlike ones from the throat, selectively responded to the presence of water—the brain’s “thirst” neurons quickly revved up again, driving the animals to drink more. © 2019 Scientific American

Keyword: Miscellaneous
Link ID: 26280 - Posted: 05.30.2019