Chapter 9. Homeostasis: Active Regulation of the Internal Environment
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by Rachel Ehrenberg Eating artificial sweeteners may spur the very health problems that dieters try to avoid. A new multipronged study of mice and a small number of people finds that saccharin meddles with the gut’s microbial community, setting in motion metabolic changes that are associated with obesity and diabetes. Other zero-calorie sweeteners may cause the same problems, researchers say September 17 in Nature. Though the finding is preliminary, four of seven human volunteers eating a diet high in saccharin developed impaired glucose metabolism, a warning sign for type 2 diabetes. “This is very interesting and scary if it really does hold for humans,” says Robert Margolskee of the Monell Chemical Senses Center in Philadelphia, who was not involved with the work. “There could be unintended consequences of these artificial sweeteners.” Until recently, most sugar substitutes were thought to pass through the gut undigested, exerting little to no effect on intestinal cells. As ingredients in diet soda, sugar-free desserts and a panoply of other foods, the sweeteners are touted as a way for people with diabetes and weight problems to enjoy a varied diet. But the new study, led by computational biologist Eran Segal and immunologist Eran Elinav of the Weizmann Institute of Science in Rehovot, Israel, suggests that rather than helping people, the sweeteners may promote problems. © Society for Science & the Public 2000 - 2014.
by Bethany Brookshire Most of us wish we ate better. I know I certainly do. But when hunger strikes, and you’re standing in line at the grab-and-go food joint, that salad seems really lackluster sitting next to that tasty-looking cookie. I can’t help but think that my diet — and my waistline — would look a lot better if I just craved lettuce a little more. Now a new study shows that although we may never cease to love cookies, we might be able to make that carrot a little more appealing. In overweight people, a behavioral intervention was associated with changes in how their brains responded to high- and low-calorie foods. The small pilot study is intriguing, but with just 13 participants, a larger study is needed before scientists will know if training the brain can make us abstain. “Everyone responds more strongly to high-calorie foods than low-calorie foods. It’s just normal,” says study coauthor Susan Roberts, a behavioral nutrition scientist from Tufts University in Medford, Mass. While most people prefer brownies over beets, people who are overweight or obese have a harder time avoiding high-calorie foods, she says. “When someone becomes overweight, there’s a dampening effect on a number of brain structures, including the reward system,” she says. “It’s harder to enjoy food generally, and so when someone becomes overweight, they really want to eat those high-calorie foods, because those are the foods that activate reward systems to the biggest extent.” Craving is a particular issue. Craving is distinct from hunger and focuses on a particular food, often foods that are high calorie. Other studies show that people who are obese have more cravings than those who are not. © Society for Science & the Public 2000 - 2014
People who are obese may be more susceptible to environmental food cues than their lean counterparts due to differences in brain chemistry that make eating more habitual and less rewarding, according to a National Institutes of Health study published in Molecular Psychiatry External Web Site Policy. Researchers at the NIH Clinical Center found that, when examining 43 men and women with varying amounts of body fat, obese participants tended to have greater dopamine activity in the habit-forming region of the brain than lean counterparts, and less activity in the region controlling reward. Those differences could potentially make the obese people more drawn to overeat in response to food triggers and simultaneously making food less rewarding to them. A chemical messenger in the brain, dopamine influences reward, motivation and habit formation. “While we cannot say whether obesity is a cause or an effect of these patterns of dopamine activity, eating based on unconscious habits rather than conscious choices could make it harder to achieve and maintain a healthy weight, especially when appetizing food cues are practically everywhere,” said Kevin D. Hall, Ph.D., lead author and a senior investigator at National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of NIH. “This means that triggers such as the smell of popcorn at a movie theater or a commercial for a favorite food may have a stronger pull for an obese person — and a stronger reaction from their brain chemistry — than for a lean person exposed to the same trigger.” Study participants followed the same eating, sleeping and activity schedule. Tendency to overeat in response to triggers in the environment was determined from a detailed questionnaire. Positron emission tomography (PET) scans evaluated the sites in the brain where dopamine was able to act.
by Laura Beil The obesity crisis has given prehistoric dining a stardom not known since Fred Flintstone introduced the Bronto Burger. Last year, “Paleo diet” topped the list of most-Googled weight loss searches, as modern Stone Age dieters sought the advice of bestsellers like The Paleo Solution or The Primal Blueprint, which encourages followers to “honor your primal genes.” The assumption is that America has a weight problem because human metabolism runs on ancient genes that are ill equipped for contemporary eating habits. In this line of thinking, a diet true to the hunter-gatherers we once were — heavy on protein, light on carbs — will make us skinny again. While the fad has attracted skepticism from those who don’t buy the idea whole hog, there’s still plenty of acceptance for one common premise about the evolution of obesity: Our bodies want to stockpile fat. For most of human history, the theory goes, hunter-gatherers ate heartily when they managed to slay a fleeing mastodon. Otherwise, prehistoric life meant prolonged stretches of near starvation, surviving only on inner reserves of adipose. Today, modern humans mostly hunt and gather at the drive-thru, but our Pleistocene genes haven’t stopped fretting over the coming famine. The idea that evolution favored calorie-hoarding genes has long shaped popular and scientific thinking. Called the “thrifty gene” hypothesis, it has arguably been the dominant theory for evolutionary origins of obesity, and by extension diabetes. (Insulin resistance and diabetes so commonly accompany obesity that doctors have coined the term “diabesity.”) However, it’s not that difficult to find scientists who call the rise of the thrifty gene theory a feat of enthusiasm over evidence. Greg Gibson, director of the Center for Integrative Genomics at Georgia Tech in Atlanta, calls the data “somewhere between scant and nonexistent — a great example of crowd mentality in science.” © Society for Science & the Public 2000 - 2014
Link ID: 20042 - Posted: 09.06.2014
By ANAHAD O’CONNOR People who avoid carbohydrates and eat more fat, even saturated fat, lose more body fat and have fewer cardiovascular risks than people who follow the low-fat diet that health authorities have favored for decades, a major new study shows. The findings are unlikely to be the final salvo in what has been a long and often contentious debate about what foods are best to eat for weight loss and overall health. The notion that dietary fat is harmful, particularly saturated fat, arose decades ago from comparisons of disease rates among large national populations. But more recent clinical studies in which individuals and their diets were assessed over time have produced a more complex picture. Some have provided strong evidence that people can sharply reduce their heart disease risk by eating fewer carbohydrates and more dietary fat, with the exception of trans fats. The new findings suggest that this strategy more effectively reduces body fat and also lowers overall weight. The new study was financed by the National Institutes of Health and published in the Annals of Internal Medicine. It included a racially diverse group of 150 men and women — a rarity in clinical nutrition studies — who were assigned to follow diets for one year that limited either the amount of carbs or fat that they could eat, but not overall calories. “To my knowledge, this is one of the first long-term trials that’s given these diets without calorie restrictions,” said Dariush Mozaffarian, the dean of the Friedman School of Nutrition Science and Policy at Tufts University, who was not involved in the new study. “It shows that in a free-living setting, cutting your carbs helps you lose weight without focusing on calories. And that’s really important because someone can change what they eat more easily than trying to cut down on their calories.” © 2014 The New York Times Company
Link ID: 20018 - Posted: 09.02.2014
By CARL ZIMMER Your body is home to about 100 trillion bacteria and other microbes, collectively known as your microbiome. Naturalists first became aware of our invisible lodgers in the 1600s, but it wasn’t until the past few years that we’ve become really familiar with them. This recent research has given the microbiome a cuddly kind of fame. We’ve come to appreciate how beneficial our microbes are — breaking down our food, fighting off infections and nurturing our immune system. It’s a lovely, invisible garden we should be tending for our own well-being. But in the journal Bioessays, a team of scientists has raised a creepier possibility. Perhaps our menagerie of germs is also influencing our behavior in order to advance its own evolutionary success — giving us cravings for certain foods, for example. “One of the ways we started thinking about this was in a crime-novel perspective,” said Carlo C. Maley, an evolutionary biologist at the University of California, San Francisco, and a co-author of the new paper. “What are the means, motives and opportunity for the microbes to manipulate us? They have all three.” The idea that a simple organism could control a complex animal may sound like science fiction. In fact, there are many well-documented examples of parasites controlling their hosts. Some species of fungi, for example, infiltrate the brains of ants and coax them to climb plants and clamp onto the underside of leaves. The fungi then sprout out of the ants and send spores showering onto uninfected ants below. How parasites control their hosts remains mysterious. But it looks as if they release molecules that directly or indirectly can influence their brains. © 2014 The New York Times Company
|By Melinda Wenner Moyer For most people, “fat,” particularly the kind that bulges under the skin, is a four-letter word. It makes our thighs jiggle; it lingers despite our torturous attempts to eliminate it. Too much of it increases our risk for heart disease and type 2 diabetes (the most common form of the condition). For decades researchers have looked for ways to reduce our collective stores of fat because they seemed to do more harm than good. But biology is rarely that simple. In the late 2000s several research groups independently discovered something that shattered the consensus about the absolute dangers of body fat. Scientists had long known that humans produce at least two types of fat tissue—white and brown. Each white fat cell stores energy in the form of a single large, oily droplet but is otherwise relatively inert. In contrast, brown fat cells contain many smaller droplets, as well as chestnut-colored molecular machines known as mitochondria. These organelles in turn burn up the droplets to generate heat. Babies, who have not yet developed the ability to shiver to maintain their body temperature, rely on thermogenic deposits of brown fat in the neck and around the shoulders to stay warm. Yet investigators assumed that all brown fat disappears during childhood. The new findings revealed otherwise. Adults have brown fat, too. Suddenly, people started throwing around terms like holy grail to describe the promise of brown fat to combat obesity. The idea was appealingly simple: if researchers could figure out how to incite the body to produce extra brown fat or somehow rev up existing brown fat, a larger number of calories would be converted into heat, reducing deposits of white fat in the process. © 2014 Scientific American
Link ID: 19953 - Posted: 08.13.2014
James Gorman Deep in the mouse brain, scientists recently found that a very small network of cells, a few thousand at most, turns appetite on and off. They used the most sophisticated of modern techniques, but as has often happened in science — witness penicillin, Velcro and Viagra — the researchers discovered something they weren’t looking for. “This was an accidental discovery,” said David Anderson, of the California Institute of Technology, the senior scientist on the team that reported the finding, in Nature Neuroscience. The discovery may eventually lead to a better understanding and treatment of eating disorders. The surprise and drama of the finding are immediately clear, however, in lab videos. A mouse busily munches lab chow until a light signal is sent to its brain, and the mouse wanders off, no longer interested in food. His lab had previously studied this small group of neurons, in a part of the brain called the amygdala. That earlier research was on fear, an emotion strongly associated with the amygdala in both mice and humans. As a technique called optogenetics became more and more refined, he said, it seemed worth revisiting the neurons with this new tool. Optogenetics requires genetic manipulation of specific cells to make them sensitive to light in a certain wavelength, in this case blue light. Then fiber-optic cables are inserted into the brain, and when the light is turned on, neurons can be activated or turned off. Researchers in Dr. Anderson’s lab, including Haijiang Cai, a postdoctoral researcher and a co-author of the report, prepared the mice and conducted the experiment with the entirely unexpected result. © 2014 The New York Times Company
Link ID: 19945 - Posted: 08.12.2014
The gurgles made by a hungry belly are familiar to us all, but they are not just the side effect of an empty stomach. Brain cells not normally associated with communication send out a signal when they detect blood glucose levels are running low, and this triggers the stomach contractions. Richard Rogers of the Pennington Biomedical Research Center at Louisiana State University and colleagues used a drug called fluorocitrate to knock out the function of certain astrocytes and neurons in the brains of rats, blocking the sensation of hunger. Only when astrocyte function was restored did the gastric grumbles return, showing that it is these cells that respond to low glucose levels (Journal of Neuroscience, DOI: 10.1523/JNEUROSCI.1406-14.2014). The feeling of discomfort you get when hungry is called "hypoglycaemia awareness". "For most people this is only slightly unpleasant, but for diabetics whose glucose levels can drop significantly, [being hungry] can be dangerous," says Rogers. "It's important to understand how this mechanism works." © Copyright Reed Business Information Ltd.
Sarah C. P. Williams Every fall, grizzly bears pack on the pounds in preparation for their winter hibernation. In humans, such extreme weight gain would likely lead to diabetes or other metabolic diseases, but the bears manage to stay healthy year after year. Their ability to remain diabetes-free, researchers have now discovered, can be chalked up to the shutting down of a protein found in fat cells. The discovery could lead to new diabetes drugs that turn off the same pathway in humans. The findings are “provocative and interesting,” says biologist Sandy Martin of the University of Colorado, Denver, who was not involved in the new work. “They found a natural solution to a problem that we haven’t been able to solve.” As people gain weight, fat, liver, and muscle cells typically become less sensitive to the hormone insulin—which normally helps control blood sugar levels—and insulin levels rise. In turn, that increased insulin prevents the breakdown of fat cells, causing a vicious cycle that can lead to full-blown insulin resistance, or diabetes. Developing new diabetes drugs has been hampered by the fact that findings from many mouse models of diabetes have not translated to humans. So Kevin Corbit, a senior scientist at Thousand Oaks, California–based drug company Amgen, decided to start looking at obesity and metabolic disease in other animals. “When I was thinking about things that are quite fat, one of the first things I thought of was bears, and what they do to prepare to go into hibernation,” he says. “But of course you don’t see bears running around with diabetes and heart disease.” © 2014 American Association for the Advancement of Science
Link ID: 19919 - Posted: 08.06.2014
By Smitha Mundasad Health reporter, BBC News Scientists have discovered a central hub of brain cells that may put the brakes on a desire to eat, a study in mice shows. And switching on these neurons can stop feeding immediately, according to the Nature Neurosciences report. Researchers say the findings may one day contribute to therapies for obesity and anorexia. Experts say this sheds light on the many complex nerve circuits involved in appetite control. Scientists from the California Institute of Technology suggest the nerve cells act as a central switchboard, combining and relaying many different messages in the brain to help reduce food intake. Using laser beams they were able to stimulate the neurons - leading to a complete and immediate stop to food consumption. Prof David Anderson, lead author of the study told the BBC: "It was incredibly surprising. "It was like you could just flick a switch and prevent the animals from feeding." Researchers then used chemicals to mimic a variety of scenarios - including feelings of satiety, malaise, nausea and a bitter taste. They found the neurons were active in all situations, suggesting they may be integral in the response to many diverse stimuli. BBC © 2014
Link ID: 19887 - Posted: 07.28.2014
Obese women may have a "food learning impairment" that could explain their attitude to food, research from Yale School of Medicine suggests. Tests on groups of obese and healthy-weight people found that the obese women performed worst when asked to remember a sequence of food picture cards. Writing in Current Biology, Yale researchers tested 135 men and women. The findings could lead to new ways to tackle obesity, the study says. Study author Ifat Levy, assistant professor at Yale School of Medicine, said the difference in the performance of the obese women compared with the other groups was "really striking" and "significant". The tests looked at an individual's ability to learn and predict the appearance of pictures of food or money on coloured cards. The participants were told they would be given whatever appeared on these "reward" cards. In the first phase, the reward cards always followed a particular coloured card in a sequence. Later, the order was changed and the reward cards appeared following a different coloured card. During this time, participants were asked to predict the likelihood of a reward card appearing as the cards were shown one by one. The results showed that obese women performed worst because they overestimated how often the pictures of food, including pretzels or chocolate, appeared. Even after researchers had accounted for other factors, there was still a large difference in their learning performance. Prof Levy said: "This is not a general learning impairment, as obese women had no problem learning when the reward was money rather than food. BBC © 2014
By GRETCHEN REYNOLDS Sleep is essential for good health, as we all know. But a new study hints that there may be an easy but unrealized way to augment its virtues: lower the thermostat. Cooler bedrooms could subtly transform a person’s stores of brown fat — what has lately come to be thought of as “good fat” — and consequently alter energy expenditure and metabolic health, even into daylight hours. Until recently, most scientists thought that adults had no brown fat. But in the past few years, scanty deposits — teaspoonfuls, really — of the tissue have been detected in the necks and upper backs in many adults. This is important because brown fat, unlike the more common white stuff, is metabolically active. Experiments with mice have shown that it takes sugar out of the bloodstream to burn calories and maintain core temperature. A similar process seems to take place in humans. For the new study, published in June in Diabetes, researchers affiliated with the National Institutes of Health persuaded five healthy young male volunteers to sleep in climate-controlled chambers at the N.I.H. for four months. The men went about their normal lives during the days, then returned at 8 every evening. All meals, including lunch, were provided, to keep their caloric intakes constant. They slept in hospital scrubs under light sheets. For the first month, the researchers kept the bedrooms at 75 degrees, considered a neutral temperature that would not prompt moderating responses from the body. The next month, the bedrooms were cooled to 66 degrees, a temperature that the researchers expected might stimulate brown-fat activity (but not shivering, which usually begins at more frigid temperatures). The following month, the bedrooms were reset to 75 degrees, to undo any effects from the chillier room, and for the last month, the sleeping temperature was a balmy 81 degrees. Throughout, the subjects’ blood-sugar and insulin levels and daily caloric expenditures were tracked; after each month, the amount of brown fat was measured. © 2014 The New York Times Company
Link ID: 19844 - Posted: 07.17.2014
by Azeen Ghorayshi Food could be a new weapon in shaking off the effects of jet lag after research in mice showed that the insulin released as a result of eating can be a key factor in restoring a disrupted body clock. Miho Sato and her colleagues at The Research Institute for Time Studies at Yamaguchi University in Japan did experiments in mice and tissue cultures to show, for the first time, that increases in insulin affect circadian rhythms. These daily rhythms affect alertness, sleep patterns, and mediate many other physiological processes. Your biological clock is regulated by two broad factors: first, the central rhythm is reset daily by light, as sensory input from the eyes is processed by a small part of the brain called the suprachiasmatic nucleus. The rise and fall of hormones linked to sleep, for example, match this rhythm. But circadian rhythms are also present in peripheral "clocks" in a wide range of cell types in the body. Some of these can be influenced by food. Sato demonstrated the role of insulin by shifting the peripheral body clock in the livers of mice by feeding them only at night. They then split the mice into two groups, supressed insulin levels in one group, and returned all the mice to daytime feeding. Four days later, the livers of the non-supressed mice had readjusted to a normal daily rhythm, as revealed by the daily rise and fall of liver-gene expression. The livers of the insulin-suppressed mice had still not returned to normal. © Copyright Reed Business Information Ltd.
Keyword: Biological Rhythms
Link ID: 19830 - Posted: 07.15.2014
By Sharon Oosthoek, CBC News Mounting evidence that gut bacteria affect mood and behaviour has researchers investigating just how much power these tiny microbes wield over our mental health. "Many people with chronic intestinal conditions also have psychological disturbances and we never understood why," says McMaster University gastroenterologist Dr. Stephen Collins. Now, scientists such as Dr. Collins are starting to come up with answers. Our lower gastrointestinal tract is home to almost 100 trillion microorganisms, most of which are bacteria. They are, by and large, "good" bacteria that help us digest food and release the energy and nutrients we need. They also crowd out bacteria that can trigger disease. But when things go awry in our guts, they can also go awry in our brains. Up to 80 per cent of people with irritable bowel syndrome experience increased anxiety and depression. And those with autism — a syndrome associated with problems interacting with others — are more likely to have abnormal levels of gut bacteria. Dr. Collins and fellow McMaster gastroenterologist Premysl Bercik have done some of the seminal research into the bacteria-brain-behaviour connection. In a study published last year, they changed the behaviour of mice by giving them fecal transplants of intestinal bacteria. It involved giving adventurous mice bacteria from timid ones, thereby inducing timid behaviour. Before the transplant, adventurous mice placed in a dark, protected enclosure spent much of their time exploring an attached bright, wide-open area. After the transplant, they rarely ventured beyond their enclosure. © CBC 2014
by Helen Thomson You are what your grandmother ate, potentially, but maybe not what your great grandmother consumed. A study in mice shows that undernourishment during pregnancy increases the chances that the next two generations will develop obesity and diabetes. But by then the slate is wiped clean. If the same holds true for humans, it may mean that stressful events in our lives affect our grandchildren's health, but not great-grandchildren. Environmental stresses cause chemical changes to DNA that turn genes on and off. Many researchers believe that these changes can be passed down through sperm and eggs – a mechanism known as epigenetic inheritance. Low-calorie diet For example, studies have linked pregnant mothers that were undernourished during the second world war with gene changes in their children that put them at higher risk of becoming obese or getting cancer. But what happens to later generations is not clear. To model this effect, Anne Ferguson-Smith at the University of Cambridge and her colleagues fed pregnant mice a diet containing 50 per cent fewer calories than usual from the 12th day of gestation until the birth, which is normally after about 20 days. Offspring were smaller than average and developed diabetes when fed a healthy diet. When the male pups had offspring, they were also at higher risk of becoming diabetic. The team analysed the sperm of the offspring from the undernourished mothers to see how many genes had had their expression altered by the addition or removal of a methyl group – an epigenetic change. The team found a decrease in methylation in 111 regions of the DNA compared with sperm from mice born to mothers fed a healthy diet. © Copyright Reed Business Information Ltd
Erika Check Hayden Nearly 750,000 babies born each year in the United Kingdom are at risk of brain damage because of low oxygen during birth. Cooling babies who are at risk of brain damage provides long-lasting prevention of such injuries, researchers report today in the New England Journal of Medicine1. A team led by Denis Azzopardi, a neonatologist at King’s College London, lowered the body temperature of 145 full-term babies who were born after at least 36 weeks of gestation. All were at risk of brain damage because they had been deprived of oxygen during birth — a problem that is often caused by troubles with the placenta or umbilical cord, and affects nearly 750,000 babies a year in the United Kingdom. The researchers cooled the infants to between 33°C and 34°C for 72 hours, starting within 6 hours of birth. The technique is known to boost the chances that children avoid brain damage until they become toddlers2, but any longer-term benefits have remained unclear. The study finds treated babies had better mental and physical health than untreated infants through to ages 6 or 7: they were 60% more likely to have normal intelligence, hearing and vision. Those who survived to childhood also had fewer disabilities such as difficulty walking and seeing. "The bottom line is that this doubles a child’s chance of normal survival," says David Edwards, a neonatologist at King’s College London and an author of the study. Neonatologist David Rowitch from the University of California, San Francisco, who studies treatments for paediatric brain damage, says the new findings are important because they show sustained improvements. "This study is encouraging, adding to the weight of evidence showing both positive early indicators and also school-age benefits to hypothermia," Rowitch adds. © 2014 Nature Publishing Group,
Keyword: Development of the Brain
Link ID: 19814 - Posted: 07.10.2014
Adults with extreme obesity have increased risks of dying at a young age from cancer and many other causes including heart disease, stroke, diabetes, and kidney and liver diseases, according to results of an analysis of data pooled from 20 large studies of people from three countries. The study, led by researchers from the National Cancer Institute (NCI), part of the National Institutes of Health, found that people with class III (or extreme) obesity had a dramatic reduction in life expectancy compared with people of normal weight. The findings appeared July 8, 2014, in PLOS Medicine. “While once a relatively uncommon condition, the prevalence of class III, or extreme, obesity is on the rise. In the United States, for example, six percent of adults are now classified as extremely obese, which, for a person of average height, is more than 100 pounds over the recommended range for normal weight,” said Cari Kitahara, Ph.D., Division of Cancer Epidemiology and Genetics, NCI, and lead author of the study. “Prior to our study, little had been known about the risk of premature death associated with extreme obesity.” In the study, researchers classified participants according to their body mass index (BMI), which is a measure of total body fat and is calculated by dividing a person’s weight in kilograms by their height in meters squared. The 20 studies that were analyzed included adults from the United States, Sweden and Australia. These groups form a major part of the NCI Cohort Consortium, which is a large-scale partnership that identifies risk factors for cancer death. After excluding individuals who had ever smoked or had a history of certain diseases, the researchers evaluated the risk of premature death overall and the risk of premature death from specific causes in more than 9,500 individuals who were class III obese and 304,000 others who were classified as normal weight.
Link ID: 19812 - Posted: 07.10.2014
|By Emilie Reas A poor diet can eat away at brain health. Now a study in Neurology helps elucidate why. It suggests that eating a lot of sugar or other carbohydrates can be hazardous to both brain structure and function. Diabetes, which is characterized by chronically high levels of blood glucose, has been linked to an elevated risk of dementia and a smaller hippocampus, a brain region critical for memory. The new study sought to identify whether glucose had an effect on memory even in people without the disease because having it could induce other brain changes that confound the data. In the experiment, researchers at the Charité University Medical Center in Berlin evaluated both short- and long-term glucose markers in 141 healthy, nondiabetic older adults. The participants performed a memory test and underwent imaging to assess the structure of their hippocampus. Higher levels on both glucose measures were associated with worse memory, as well as a smaller hippocampus and compromised hippocampal structure. The researchers also found that the structural changes partially accounted for the statistical link between glucose and memory. According to study co-author Agnes Flöel, a neurologist at Charité, the results “provide further evidence that glucose might directly contribute to hippocampal atrophy,” but she cautions that their data cannot establish a causal relation between sugar and brain health. These findings indicate that even in the absence of diabetes or glucose intolerance, higher blood sugar may harm the brain and disrupt memory function. Future research will need to characterize how glucose exerts these effects and whether dietary or lifestyle interventions might reverse such pathological changes. © 2014 Scientific American
Link ID: 19798 - Posted: 07.08.2014
Priyanka Pulla Not everyone who is obese is unhealthy. So say some researchers, who note that a small fraction of overweight people have normal blood sugar levels and blood pressure, and are thus “healthy obese.” Now, scientists have identified a single protein that seems to determine whether obesity is harmful or benign. The protein is a new player in our understanding of how obesity leads to disease, says Alan Saltiel, a cell biologist at the University of Michigan, Ann Arbor, who was not involved in the study. It is well known that obesity leads to a wide range of health problems, from diabetes to heart disease to cancer. So established is the link between extra pounds and illness that last year the American Medical Association voted to classify obesity itself as a disease. Although some researchers have suggested that a small number of obese people are healthy, that idea remains controversial. Instead, the emerging consensus is that healthy obesity is a transient phase, says Ravi Retnakaran, an endocrinologist at the Leadership Sinai Centre for Diabetes in Toronto, Canada. Sooner or later, he says, these outliers will develop metabolic syndrome, a condition in which glucose, cholesterol, and lipid levels soar, causing diabetes and heart disease. In fact, so-called healthy obese people may already have early signs of disease, which are too muted to show up on routine tests. In a study of more than 14,000 metabolically healthy Korean people last year, scientists found early plaque buildup in the arteries of obese subjects more often than they did in the lean ones. © 2014 American Association for the Advancement of Science
Link ID: 19797 - Posted: 07.04.2014