Chapter 13. Homeostasis: Active Regulation of the Internal Environment

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Katherine Hobson The theory behind artificial sweeteners is simple: If you use them instead of sugar, you get the joy of sweet-tasting beverages and foods without the downer of extra calories, potential weight gain and related health issues. In practice, it's not so simple, as a review of the scientific evidence on non-nutritive sweeteners published Monday shows. After looking at two types of scientific research, the authors conclude that there is no solid evidence that sweeteners like aspartame and sucralose help people manage their weight. And observational data suggest that the people who regularly consume these sweeteners are also more likely to develop future health problems, though those studies can't say those problems are caused by the sweeteners. The health effects of artificial sweeteners are important to study, because so many people use them. Another study published earlier this year found that a quarter of U.S. children and 41 percent of adults reported consuming them, most of them once per day. Even more people may be consuming them unwittingly in products such as granola bars or yogurt. "We were really interested in the everyday person who is consuming these products not to lose weight, but because they think it's the healthier choice, for many years on end," says Meghan Azad, lead author of the review and a research scientist at the University of Manitoba. While more research needs to be done, from what we know now, "there is no clear benefit for weight loss, and there's a potential association with increased weight gain, diabetes and other negative cardiovascular outcomes," says Azad. © 2017 npr

Keyword: Obesity
Link ID: 23845 - Posted: 07.18.2017

By TALYA MINSBERG When Marti Noxon set out to make “To the Bone,” a film about a 20-year-old battling an eating disorder, she initially faced the question: Was the topic too niche? The answer came in the form of a rousing premiere in January at the Sundance Film Festival, Netflix’s reported $8 million purchase of the film, a trailer that went viral with 54 million views in the first week and arguments over whether it glamorized excessive thinness. The film debuted on Netflix on Friday. The film is loosely based on Ms. Noxon’s experience with an eating disorder. She and its star, Lily Collins, are among the 30 million Americans — a third of them men — who have struggled with one. Ms. Collins plays Ellen, an anorexia patient who enters her fifth eating disorder treatment center, an unorthodox group home run by a doctor played by Keanu Reeves. Many of those reacting to the film’s trailer worried that watching it could trigger unhealthy thoughts in viewers who may be prone to eating disorders or already struggling with them. Indeed, some experts said that people who have had eating disorders should consider the state of their health before watching the film. “If you don’t feel solid in your recovery, don’t watch it right now. It could be triggering at any part of your life if you aren’t feeling strong and solid in your recovery,” Dr. Dena Cabera, executive clinical director at Rosewood Centers for Eating Disorders said. “It will always be there; you can look it up later.” Others say the film may help spur action. Eating disorders have the highest mortality rate of any psychiatric disorder, and can affect individuals across every demographic. “If the film helps raise awareness and more people seek treatment, that would be a success that we can be pleased with,” Dr. S. Bryn Austin, a professor at Boston Children’s Hospital and Harvard T.H. Chan School of Public Health, said. “Eating disorders can be successfully treated, they just need to take the first step in reaching out for care.” © 2017 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 23843 - Posted: 07.17.2017

Carina Storrs In the late 1960s, a team of researchers began doling out a nutritional supplement to families with young children in rural Guatemala. They were testing the assumption that providing enough protein in the first few years of life would reduce the incidence of stunted growth. It did. Children who got supplements grew 1 to 2 centimetres taller than those in a control group. But the benefits didn't stop there. The children who received added nutrition went on to score higher on reading and knowledge tests as adolescents, and when researchers returned in the early 2000s, women who had received the supplements in the first three years of life completed more years of schooling and men had higher incomes1. “Had there not been these follow-ups, this study probably would have been largely forgotten,” says Reynaldo Martorell, a specialist in maternal and child nutrition at Emory University in Atlanta, Georgia, who led the follow-up studies. Instead, he says, the findings made financial institutions such as the World Bank think of early nutritional interventions as long-term investments in human health. Since the Guatemalan research, studies around the world — in Brazil, Peru, Jamaica, the Philippines, Kenya and Zimbabwe — have all associated poor or stunted growth in young children with lower cognitive test scores and worse school achievement2. A picture slowly emerged that being too short early in life is a sign of adverse conditions — such as poor diet and regular bouts of diarrhoeal disease — and a predictor for intellectual deficits and mortality. But not all stunted growth, which affects an estimated 160 million children worldwide, is connected with these bad outcomes. Now, researchers are trying to untangle the links between growth and neurological development. Is bad nutrition alone the culprit? What about emotional neglect, infectious disease or other challenges? © 2017 Macmillan Publishers Limited

Keyword: Development of the Brain
Link ID: 23831 - Posted: 07.13.2017

Aimee Cunningham An expectant mom might want to think twice about quenching her thirst with soda. The more sugary beverages a mom drank during mid-pregnancy, the heavier her kids were in elementary school compared with kids whose mothers consumed less of the drinks, a new study finds. At age 8, boys and girls weighed approximately 0.25 kilograms more — about half a pound — with each serving mom added per day while pregnant, researchers report online July 10 in Pediatrics. “What happens in early development really has a long-term impact,” says Meghan Azad, an epidemiologist at the University of Manitoba in Canada, who was not involved in the study. A fetus’s metabolism develops in response to the surrounding environment, including the maternal diet, she says. The new findings come out of a larger project that studies the impact of pregnant moms’ diets on their kids’ health. “We know that what mothers eat during pregnancy may affect their children’s health and later obesity,” says biostatistician Sheryl Rifas-Shiman of Harvard Medical School and Harvard Pilgrim Health Care Institute in Boston. “We decided to look at sugar-sweetened beverages as one of these factors.” Sugary drinks are associated with excessive weight gain and obesity in studies of adults and children. Rifas-Shiman and colleagues included 1,078 mother-child pairs in the study. Moms filled out a questionnaire in the first and second trimesters of their pregnancy about what they were drinking — soda, fruit drinks, 100 percent fruit juice, diet soda or water — and how often. Soda and fruit drinks were considered sugar-sweetened beverages. A serving was defined as a can, glass or bottle of a beverage. |© Society for Science & the Public 2000 - 2017

Keyword: Obesity; Development of the Brain
Link ID: 23820 - Posted: 07.11.2017

By Aggie Mika Microglia—the brain’s own macrophages—can prompt excess eating and subsequent weight gain in mice fed high-fat diets, according to a study published today (July 5) in Cell Metabolism. The researchers demonstrate that an appetite-promoting inflammatory cascade driven by these immune cells occurs within the mediobasal region of the hypothalamus, a structure that, according to a news release, “contains key groups of neurons that regulate food intake and energy expenditure.” Prior studies have demonstrated that when mice are fed a diet high in saturated fat, they consume more while expending fewer calories, leading them to gain weight, the news release states. Additionally, previous work in both obese mice and humans has also shown that microglia within the hypothalamus increase following high-fat feeding, prompting inflammation, the authors write in their report. In the current study, the researchers examined whether microglial activity in the mediobasal hypothalamus had anything to do with the increased food consumption and weight gain observed in mice consuming diets high in fat. First, they used a drug to wipe out microglia in this region brain and found that microglia-lacking, high-fat consuming mice gained less weight than their non-drugged, high-fat counterparts. They then genetically manipulated mice so that their microglia weren’t capable of mounting an inflammatory response, and these mice also ate less and gained less weight than normal mice on the high-fat diets. © 1986-2017 The Scientist

Keyword: Obesity; Glia
Link ID: 23811 - Posted: 07.07.2017

By Mitch Leslie When you have a stuffy nose, a slice of freshly baked apple pie tastes like mush. But not being able to smell your food could have a surprising effect on your metabolism, potentially helping you remain thin even when you eat fatty foods, a new study in mice suggests. “This is a very exciting study, and the outcome is quite compelling,” says neuroendocrinologist Tamas Horvath of Yale School of Medicine, who wasn’t connected to the research. To conduct the study, molecular biologist Andrew Dillin of the University of California, Berkeley, and colleagues turned to a variety of genetically altered mice. The scientists gave them regular doses of the diphtheria toxin—which causes a temporary loss of odor-sensing neurons—to suppress their sense of smell. They then fed the rodents either a normal diet or fatty foods—the mouse equivalent of cheesecake and pizza—that usually induce obesity. After more than 3 months of noshing on regular chow, the odor-deprived rodents weighed slightly less than mice whose sense of smell was intact. In the group on the high-fat diet, however, the mice that couldn’t smell weighed 16% less than animals that could, which became obese. Losing the ability to smell also caused a different group of already-obese mice to lose weight, the researchers reveal today in Cell Metabolism. © 2017 American Association for the Advancement of Science.

Keyword: Obesity; Chemical Senses (Smell & Taste)
Link ID: 23810 - Posted: 07.06.2017

By Meredith Wadman The hallmark brain damage in Parkinson’s disease is thought to be the work of a misfolded, rogue protein that spreads from brain cell to brain cell like an infection. Now, researchers have found that the normal form of the protein—α-synuclein (αS)—may actually defend the intestines against invaders by marshaling key immune cells. But chronic intestinal infections could ultimately cause Parkinson’s, the scientists suggest, if αS migrates from overloaded nerves in the gut wall to the brain. “The gut-brain immune axis seems to be on a cusp of an explosion of new insights, and this work offers an exceptionally exciting new hypothesis,” says Charles Bevins, an expert in intestinal immunity at the University of California, Davis, who was not involved with the study. The normal function of αS has long been a mystery. Though the protein is known to accumulate in toxic clumps in the brain and the nerves of the gut wall in patients with Parkinson’s disease, no one was sure what it did in healthy people. Noting that a region of the αS molecule behaves similarly to small, microbe-targeting proteins that are part of the body’s immune defenses, Michael Zasloff, an immunologist at Georgetown University Medical Center in Washington, D.C., set out to find whether αS, too, might help fend off microbial invaders. © 2017 American Association for the Advancement of Science

Keyword: Parkinsons
Link ID: 23784 - Posted: 06.28.2017

Cassie Martin Long typecast as the strong silent type, bones are speaking up. In addition to providing structural support, the skeleton is a versatile conversationalist. Bones make hormones that chat with other organs and tissues, including the brain, kidneys and pancreas, experiments in mice have shown. “The bone, which was considered a dead organ, has really become a gland almost,” says Beate Lanske, a bone and mineral researcher at Harvard School of Dental Medicine. “There’s so much going on between bone and brain and all the other organs, it has become one of the most prominent tissues being studied at the moment.” At least four bone hormones moonlight as couriers, recent studies show, and there could be more. Scientists have only just begun to decipher what this messaging means for health. But cataloging and investigating the hormones should offer a more nuanced understanding of how the body regulates sugar, energy and fat, among other things. Of the hormones on the list of bones’ messengers — osteocalcin, sclerostin, fibroblast growth factor 23 and lipocalin 2 — the last is the latest to attract attention. Lipocalin 2, which bones unleash to stem bacterial infections, also works in the brain to control appetite, physiologist Stavroula Kousteni of Columbia University Medical Center and colleagues reported in the March 16 Nature. After mice eat, their bone-forming cells absorb nutrients and release a hormone called lipocalin 2 (LCN2) into the blood. LCN2 travels to the brain, where it gloms on to appetite-regulating nerve cells, which tell the brain to stop eating, a recent study suggests. © Society for Science & the Public 2000 - 2017.

Keyword: Hormones & Behavior
Link ID: 23762 - Posted: 06.22.2017

By GRETCHEN REYNOLDS Better grades might be found on the playground. A new study of elementary-age children shows that those who were not part of an after-school exercise program tended to pack on a particular type of body fat that can have deleterious impacts on brain health and thinking. But prevention and treatment could be as simple as playing more games of tag. Most children do not meet the federal health guidelines for exercise, which call for at least an hour of it a day for anyone under the age of 18. Physical inactivity can result in weight gain, especially around the midsection — including visceral fat, a type of tissue deep inside the abdomen that is known to increase inflammation throughout the body. It is also linked to heightened risks for diabetes and cardiovascular complications, even in children, and may contribute to declining brain function: Obese adults often perform worse than people of normal weight on tests of thinking skills. But little has been known about visceral fat and brain health in children. For a soon-to-be-published study, researchers from Northeastern University in Boston and the University of Illinois at Urbana-Champaign tracked hundreds of 8-to-10-year-old children in a nine-month after-school exercise program in Urbana. Every day, one group of children played tag and other active games for about 70 minutes. The subjects in a control group continued with their normal lives, with the promise that they could join the program the following year. All the children completed tests of fitness, body composition and cognitive skills at the start and end of the program. The researchers did not ask the children to change their diets. © 2017 The New York Times Company

Keyword: Obesity
Link ID: 23747 - Posted: 06.17.2017

By MATT RICHTEL More than 10 percent of the world’s population is now obese, a marked rise over the last 30 years that is leading to widespread health problems and millions of premature deaths, according to a new study, the most comprehensive research done on the subject. Published Monday in The New England Journal of Medicine, the study showed that the problem had swept the globe, including regions that have historically had food shortages, like Africa. The study, compiled by the Institute for Health Metrics and Evaluation at the University of Washington and funded by the Gates Foundation, looked at 195 countries, essentially the world’s population, finding that rates of obesity at least doubled in 73 countries — including Turkey, Venezuela and Bhutan — from 1980 to 2015, and “continuously increased in most other countries.” Analyzing some 1,800 data sets from around the world, researchers found that excess weight played a role in four million deaths in 2015, from heart disease, diabetes, kidney disease and other factors. The per capita death rate was up 28 percent since 1990 and, notably, 40 percent of the deaths were among people who were overweight but not heavy enough to be classified as obese. The study defined obese as a body mass index of 30 or higher and overweight as a B.M.I. from 25 to 29. By those measures, nearly 604 million adults worldwide are obese and 108 million children, the authors reported. Obesity rates among children are rising faster in many countries than among adults. In the United States, 12.5 percent of children were obese, up from 5 percent in 1980. Combining children and adults, the United States had the dubious distinction of having the largest increase in percentile points of any country, a jump of 16 percentage points to 26.5 percent of the overall population. © 2017 The New York Times Company

Keyword: Obesity
Link ID: 23734 - Posted: 06.13.2017

Children born to women with gestational diabetes whose diet included high proportions of refined grains may have a higher risk of obesity by age 7, compared to children born to women with gestational diabetes who ate low proportions of refined grains, according to results from a National Institutes of Health study. These findings, which appear online in the American Journal of Clinical Nutrition, were part of the Diabetes & Women’s Health Study, a research project led by NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD). Gestational diabetes, or high blood sugar during pregnancy, affects about 5 percent of all pregnancies in the United States and may lead to health problems for mothers and newborns. The authors noted that previous studies have linked diets high in refined grains — such as white rice — to obesity, type 2 diabetes and heart disease. The researchers compared records from 918 mother-child pairs who took part in the Danish National Birth Cohort, a study that followed the pregnancies of more than 91,000 women in Denmark. They found that children born to women with gestational diabetes who consumed the most refined grain (more than 156 grams per day) were twice as likely to be obese at age 7, compared to children born to women with gestational diabetes who ate the least amount of refined grain (less than 37 grams per day). The link between maternal grain consumption during pregnancy and obesity by age 7 still persisted when the researchers controlled for factors that could potentially influence the children’s weight — such as physical activity level and consumption of vegetables, fruit and sweets. The authors called for additional studies to confirm their results and to follow children through later childhood, adolescence and adulthood to see if the obesity risk persists later in life.

Keyword: Obesity; Development of the Brain
Link ID: 23720 - Posted: 06.08.2017

Children born to women who had gestational diabetes and drank at least one artificially sweetened beverage per day during pregnancy were more likely to be overweight or obese at age 7, compared to children born to women who had gestational diabetes and drank water instead of artificially sweetened beverages, according to a study led by researchers at the National Institutes of Health. Childhood obesity is known to increase the risk for certain health problems later in life, such as diabetes, heart disease, stroke and some cancers. The study appears online in the International Journal of Epidemiology. According to the study authors, as the volume of amniotic fluid increases, pregnant women tend to increase their consumption of fluids. To avoid extra calories, many pregnant women replace sugar-sweetened soft drinks and juices with beverages containing artificial sweeteners. Citing prior research implicating artificially sweetened beverages in weight gain, the study authors sought to determine if diet beverage consumption during pregnancy could influence the weight of children. “Our findings suggest that artificially sweetened beverages during pregnancy are not likely to be any better at reducing the risk for later childhood obesity than sugar-sweetened beverages,” said the study’s senior author, Cuilin Zhang, Ph.D., in the Epidemiology Branch at NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD). “Not surprisingly, we also observed that children born to women who drank water instead of sweetened beverages were less likely to be obese by age 7.”

Keyword: Obesity; Development of the Brain
Link ID: 23717 - Posted: 06.07.2017

By JANE E. BRODY Harding Senior High, a public school in St. Paul, Minn., has long been known as a 90-90-90 school: 90 percent of students are minorities, nearly 90 percent come from poor or struggling families and, until recently, 90 percent graduate (now about 80 percent) to go on to college or a career. Impressive statistics, to be sure. But perhaps most amazing about this school is that it recognizes and acts on the critical contribution that adequate food and good nutrition make to academic success. Accordingly, it provides three balanced meals a day to all its students, some of whom might otherwise have little else to eat on school days. For those who can’t get to school in time for early breakfast, a substitute meal is offered after first period, to be eaten during the second period. Every student can pick up dinner at the end of the school day, and those who play sports after school can take the dinner with them to practices and games. To Jennifer Funkhauser, a French teacher at Harding and hands-on participant in the meal program, making sure the students are well fed is paramount to their ability to succeed academically. Ms. Funkhauser and the staff at Harding are well aware of the many studies showing that children who are hungry or malnourished have a hard time learning. After she noticed that some youngsters were uncomfortable eating with hundreds of others in a large, noisy lunchroom, Ms. Funkhauser created a more private, quieter “lunch bunch” option for them. The attitude and atmosphere at Harding are in stark contrast to the humiliating lunchroom experiences suffered by students at some schools, where youngsters are sometimes shamed in front of their classmates and their meals confiscated and dumped in the garbage when parents have an unpaid lunch bill. © 2017 The New York Times Company

Keyword: Development of the Brain
Link ID: 23706 - Posted: 06.05.2017

By Amina Zafar, CBC News When men postpone meal times, it delays one of the body's clocks, British researchers say, a finding that sheds light on a potential way to overcome jet lag and health harms for shift workers. Our bodies run a roughly 24-hour cycle called the circadian or sleep/wake rhythm. It is controlled by a master "clock" in the brain that responds to light signals from the retina, synchronizing other clocks throughout the body. Now investigators have discovered that a five-hour delay in meal time causes a five-hour delay in blood glucose rhythms. "We think this is due to changes in clocks in our metabolic tissues but not the 'master' clock in the brain," said Jonathan Johnston of the University of Surrey, one of the authors of the study published in Thursday's issue of the journal Current Biology. "This work is important because it demonstrates for the first time that a relatively subtle change of standard human feeding pattern re-synchronizes key metabolic rhythms in the body." Currently, people disoriented by the sluggish time warp of jet lag may take melatonin supplements and time their light exposure to help synchronize their clocks. While the study introduces the idea of adding meal timing to the clock reset toolkit, the practical details of how to do so still need to be worked out. In the experiment, 10 healthy young men came to a specialized sleep lab for 13 days. At first, breakfast was set for 30 minutes after waking. Then, after the men got used ©2017 CBC/Radio-Canada.

Keyword: Biological Rhythms; Obesity
Link ID: 23695 - Posted: 06.02.2017

Alexandra Sifferlin Like most people, Kevin Hall used to think the reason people get fat is simple. "Why don't they just eat less and exercise more?" he remembers thinking. Trained as a physicist, the calories-in-vs.-calories-burned equation for weight loss always made sense to him. But then his own research--and the contestants on a smash reality-TV show--proved him wrong. Hall, a scientist at the National Institutes of Health (NIH), started watching The Biggest Loser a few years ago on the recommendation of a friend. "I saw these folks stepping on scales, and they lost 20 lb. in a week," he says. On the one hand, it tracked with widespread beliefs about weight loss: the workouts were punishing and the diets restrictive, so it stood to reason the men and women on the show would slim down. Still, 20 lb. in a week was a lot. To understand how they were doing it, he decided to study 14 of the contestants for a scientific paper. Hall quickly learned that in reality-TV-land, a week doesn't always translate into a precise seven days, but no matter: the weight being lost was real, speedy and huge. Over the course of the season, the contestants lost an average of 127 lb. each and about 64% of their body fat. If his study could uncover what was happening in their bodies on a physiological level, he thought, maybe he'd be able to help the staggering 71% of American adults who are overweight. © 2017 Time Inc.

Keyword: Obesity
Link ID: 23670 - Posted: 05.29.2017

Laura Sanders Nerve cells in a poorly understood part of the brain have the power to prompt voracious eating in already well-fed mice. Two to three seconds after blue light activated cells in the zona incerta, a patch of neurons just underneath the thalamus and above the hypothalamus, mice dropped everything and began shoveling food into their mouths. This dramatic response, described May 26 in Science, suggests a role in eating behavior for a part of the brain that hasn’t received much scrutiny. Scientists have previously proposed a range of jobs for the zona incerta, linking it to attention, movement and even posture. The new study suggests another job — controlling eating behavior, perhaps even in humans. “Being able to include the zona incerta in models of feeding is going to help us understand it better,” says study coauthor Anthony van den Pol, a neuroscientist at Yale University. The new results may also help explain why a small number of Parkinson’s disease patients develop binge-eating behavior when electrodes are implanted in their brains to ease their symptoms. Those electrodes may be stimulating zona incerta nerve cells, van den Pol suspects. He and his collaborator Xiaobing Zhang, also of Yale, studied the mice with a technique called optogenetics. Mice were engineered so that some nerve cells in the zona incerta fired off signals when hit with blue light. When the light activated these cells, the mice immediately found the food and began eating, the researchers reported. “It’s really quick,” van den Pol says. |© Society for Science & the Public 2000 - 2017.

Keyword: Obesity
Link ID: 23664 - Posted: 05.26.2017

Claude Messier, Alexandria Béland-Millar, The short answer is yes: certain brain regions do indeed consume more energy when engaged in particular tasks. Yet the specific regions involved and the amount of energy each consumes depend on the person’s experiences as well as each brain’s individual properties. Before we delve into the answer, it is important to understand how we measure a brain’s energy expenditure. Picture the colorful brain images researchers use to display neural activity. The colors typically represent the amount of oxygen or glucose various brain regions use during a task. Our brain is always active on some level—even when we are not engaged in a task—but it requires more energy to accomplish something that demands concentration such as moving, seeing or thinking. A simple example is that our primary visual cortex lights up more in brain scans—consuming more energy—when our eyes are open than when they are closed. Similarly, our primary motor cortex uses more energy if we move our hands than if we keep them still. Say you are learning a new skill—how to juggle or speak Spanish. Neuroscientists have made the fascinating observation that when we do something completely novel, a broad range of brain areas becomes active. As we become more skilled at the task, however, our brain becomes more focused: we require only the essential brain regions and need increasingly less energy to perform that task. Once we have mastered a skill—we become fluent in Spanish—only the brain areas directly involved remain active. Thus, learning a new skill requires more brainpower than a well-practiced activity. © 2017 Scientific American

Keyword: Brain imaging
Link ID: 23647 - Posted: 05.23.2017

By Catherine Caruso If you give a mouse a beer, he is going to want a cookie—and another, and another. If you give a person enough beer, she might find herself wolfing down a plate of greasy nachos or some other caloric snack. A study published in January in Nature Communications helps to explain why binge drinking, in both mice and humans, so often leads to binge eating even though alcohol is, itself, high in calories. In the first part of the study, neuroscientists Craig Blomeley and Sarah Cains, both at the Francis Crick Institute Mill Hill Laboratory in London, injected mice with the equivalent of roughly two bottles of wine once a day for three consecutive days, mimicking a weekend of heavy drinking. Sure enough, the inebriated mice ate far more than sober mice in a control group. To figure out why, the researchers then exposed thin-sliced postmortem mouse brains to alcohol and measured the resulting neural activity using fluorescent tags and electrodes. They found that ethanol exposure alters calcium exchange in the cells, causing specialized nerve cells called agouti-related protein (AgRP) neurons to fire more frequently and easily. These neurons normally fire when our body needs calories, and research has shown that activating them artificially will cause mice to chow down even when they are full. The study results suggest that alcohol activates AgRP neurons in the brain, giving drunk mice the munchies. The same is likely true for humans because this brain circuitry has been highly conserved across mammal species, Cains says: “I don't doubt that AgRP neurons are activated in humans, and that's why you see this effect.” © 2017 Scientific American

Keyword: Drug Abuse; Obesity
Link ID: 23645 - Posted: 05.22.2017

Sarah Boseley in Porto A crinkly plate, designed with ridges that cunningly reduce the amount of food it holds, may be heading for the market to help people concerned about their weight to eat less. The plate is the brainchild of a Latvian graphic designer, Nauris Cinovics, from the Art Academy of Latvia, who is working with a Latvian government agency to develop the idea and hopes to trial it soon. It may look like just another arty designer plate, but it is intended to play tricks with the mind. “My idea is to make food appear bigger than it is. If you make the plate three-dimensional [with the ridges and troughs] it actually looks like there is the same amount of food as on a normal plate – but there is less of it,” said Cinovics. “You are tricking the brain into thinking you are eating more.” The plate will be made of clear glass and could turn eating dinner into a more complex and longer process than it is usually for most of us. Negotiating the folds in the glass where pieces of fish or stray carrots may lurk will slow down the speed with which people get through their meal. Cinovics has also designed heavy cutlery, with the idea of making eating more of a labour – that therefore lasts longer. His knife, fork and spoon weigh 1.3kg each. “We tested this and it took 11 minutes to finish a meal with this cutlery rather than seven minutes,” he said.

Keyword: Obesity; Attention
Link ID: 23639 - Posted: 05.20.2017

By: Ted Dinan, M.D., Ph.D, and John F. Cryan, Ph.D. O ver the past few years, the gut microbiota has been implicated in developmental disorders such as schizophrenia and autism, neurodegenerative disorders such as Alzheimer’s disease and Parkinson’s disease, mood disorders such as depression, and even addiction disorders. It now seems strange that for so many decades we viewed the gut microbiota as bacteria that did us no harm but were of little benefit. This erroneous view has been radically transformed into the belief that the gut microbiota is, in effect, a virtual organ of immense importance. What we’ve learned is that what is commonly referred to as “the brain-gut-microbiota axis” is a bidirectional system that enables gut microbes to communicate with the brain and the brain to communicate back to the gut. It may be hard to believe that the microbes in the gut collectively weigh around three pounds—the approximate weight of the adult human brain—and contain ten times the number of cells in our bodies and over 100 times as many genes as our genome. 1 If the essential microbial genes were to be incorporated into our genomes, it is likely that our cells would not be large enough for the extra DNA. Many of those genes in our microbiota are important for brain development and function; they enable gut bacteria to synthesize numerous neurotransmitters and neuromodulators such as γ-aminobutyric acid (GABA), serotonin, dopamine, and short-chain fatty acids. While some of these compounds act locally in the gut, many products of the microbiota are transported widely and are necessary for the proper functioning of diverse organs. This is a two-way interaction: gut microbes are dependent on us for their nourishment. Any pathological process that reduces or increases food intake has implications for our microbes. © 2017 The Dana Foundation. All Rights Reserved.

Keyword: Parkinsons
Link ID: 23636 - Posted: 05.19.2017