Links for Keyword: Obesity

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By PAGAN KENNEDY Abby Solomon suffers from a one-in-a-billion genetic syndrome: After just about an hour without food, she begins to starve. She sleeps in snatches. In her dreams she gorges on French fries. But as soon as she wakes up and nibbles a few bites, she feels full, so she ends up consuming very few calories. At 5 feet 10 inches tall, she weighs 99 pounds. Now 21 years old, she is one of the few people in the world to survive into adulthood with neonatal progeroid syndrome, a condition that results from damage to the FBN1 gene. This mutation mangles noses and eyes and destroys the layer of fat under the skin so that even teenagers look middle-aged. It also interferes with the body’s ability to make a hormone called asprosin, which regulates blood sugar. Atul Chopra, a medical geneticist at Baylor College of Medicine, told me that people with the disorder don’t experience ordinary hunger — instead they waver on the edge of hypoglycemia and must constantly snack to keep from passing out. And yet when I asked Ms. Solomon if she wished she could magically repair her damaged gene, she answered without hesitation: “I wouldn’t change it for anything.” This is because her painful body may hold the clues to a lifesaving treatment for millions of people with obesity and diabetes. Dr. Chopra told me that, as far as medical science is concerned, Abby Solomon is worth thousands of the rest of us. By observing her, scientists can see how a hormone deficiency affects a living person, from her thoughts to her liver function. Several years ago, she spent a day inside a metabolic chamber in a lab so that Dr. Chopra could measure everything she breathed and ate. The results showed that Ms. Solomon takes in about half the calories of a typical woman her age, and also expends half as much energy. “Nothing comes close to starting with people who are naturally different,” he said. This is why he searches out patients at the extreme ends of the spectrum — those who are wired to weigh 80 pounds or 380 pounds. He said, “We have the opportunity to help a bigger swath of humanity when we learn from these outliers.” © 2016 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22919 - Posted: 11.28.2016

By Tracy Vence Lose weight, gain it back. That’s the frustrating routine for many individuals who have experienced only short-term success with diets. To examine the microbial and metabolic factors underlying this weight loss-regain cycle, researchers at the Weizmann Institute of Science in Rehovot, Israel, ran a series of experiments using a mouse model of recurrent obesity. The composition of a mouse’s microbiome is predictive of post-diet weight regain, which is in part modulated by metabolites released by the bugs, the researchers found. Their results were published today (November 24) in Nature. “This work adds some insight on how the microbiome acts as a buffer to changes in our diet,” study coauthor Eran Segal of the Weizmann Institute said during a press briefing this week (November 22). In particular, the researchers found evidence to suggest that mice that were once obese tend to experience alterations in microbiome composition that persist during and after weight loss. They also linked the metabolic health of mice to levels of the dietary flavonoids apigenin and naringenin, among other metabolites exchanged between the host and microbiome. See “How Diet Influences Host-Microbiome Communication in Mice” There is hope, however. Segal and colleagues also reported that microbiome- and metabolite-mediating therapies—such as antibiotic treatment, fecal transplant, or postbiotic supplementation—can ameliorate the rate of weight regain in mice predisposed to recurrent obesity. © 1986-2016 The Scientist

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22916 - Posted: 11.26.2016

By Julie Hecht If you assume dogs are always ready for more food, try again. Like you, dogs make decisions about which types of food to eat. For example, if someone shows you two plates, one with a glorious piece of your favorite pie and another plate with a piece of your favorite pie with a side of carrots, many of you are going to go for the pie alone. You'd adopt a less-is-more strategy because pie plus carrots is kinda gross. Monkeys do this too. In 2012, Kralik and colleagues found that while monkeys will eat grapes on their own and cucumbers on their own, when given the choice between a grape alone and a grape accompanied by a slice of cucumber, monkeys preferred the grape alone. It’s not that monkeys won't eat cucumbers, they’d just prefer grapes by themselves. Monkeys based their choice not on the overall quantity of the food, but instead on a qualitative decision. How about dogs? A recent study by Kristina Pattison and Thomas Zentall of the University of Kentucky examined whether companion dogs also adopt a less-is-more strategy. The researchers first determined whether dogs had a preference between two foods, in this case carrots and cheese. Ten companion dogs—all of whom would voluntarily eat both string cheese and baby carrots—were found to prefer the cheese over the carrots (all the dogs occasionally chose carrots, suggesting that carrots are not valueless). But when given the choice to eat a piece of cheese on its own or a piece of cheese together with carrot, dogs chose a single piece of cheese over a piece of cheese "tainted" by the presence of carrot. © 2016 Scientific American,

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22915 - Posted: 11.26.2016

Mo Costandi Lucy Cheke and her colleagues at the University of Cambridge recently invited a few participants into her lab for a kind of ‘treasure hunt’. The participants navigated a virtual environment on a computer screen, dropping off various objects along their way. They then answered a series of questions to test their memory of the task, such as where they had hidden a particular object. When examining what might have influenced their performance, you might expect that Cheke would have been more concerned with the participant’s IQ – not their waistline. Yet she found a clear relationship between their Body Mass Index – a measure of your weight relative to your height – and apparent memory deficits: the higher a participant’s BMI, the worse they performed on the Treasure Hunt task. In doing so, Cheke has contributed to a small but growing body of evidence showing that obesity is linked to brain shrinkage and memory deficits. This research suggests that obesity may contribute to the development of neurodegenerative conditions such as Alzheimer’s Disease. Surprisingly, it also seems to show that the relationship between obesity and memory is a two-way street: being overweight or obese not only impacts on memory function, but may also affect future eating behaviour by altering our recollections of previous eating experiences. Cheke’s interest in the subject began unexpectedly. “At the time I was looking at the ability to imagine a future state, particularly in terms of making decisions about food,” says Cheke. “If you’re hungry, you’ll imagine your future self as being hungry, too, but obese people seem to make such decisions on fact-based judgements rather than imagining.” © 2016 Guardian News and Media Limited

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22910 - Posted: 11.25.2016

Hannah Devlin Science correspondent People who struggle to maintain a healthy weight after dieting may do so because their gut bacteria retains a “memory” of their past weight, according to scientists. The study, in mice, suggests that yo-yo dieting is not simply a reflection of people returning to unhealthy eating habits, but could be driven by long-term changes in gut bacteria brought about by obesity. The scientists observed that the changes to the gut microbiome brought about by obesity persisted for five times as long as the actual period spent dieting and predisposed the mice to rapidly regain weight. Eran Elinav, an immunologist at the Weizmann Institute in Israel and lead author, said that the findings, if replicated in people, could help develop more evidence-based methods for weight loss. “It may explain some – more than some – of our failure to control weight by dieting,” he said. Simon Cork, a medical researcher at Imperial College London, said the study was one of the first to show that gut bacteria could actively drive weight gain, rather than simply being associated with it. However, he cautioned that it was unclear whether the findings could be extrapolated to people. “We do know that this yo-yo effect is caused by quite a few different mechanisms and it’s likely that gut bacteria is only going to play a small role,” he said. “Ultimately, the main reason why people yo-yo is because they don’t stick to the diet.” In the study, published in Nature, obese mice were switched from a high fat diet to balanced nutrition until they were indistinguishable from a control group of mice in terms of weight and a range of metabolic factors, such as blood sugar levels. © 2016 Guardian News and Media Limited

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22909 - Posted: 11.25.2016

By Andy Coghlan It may sound like a healthy switch, but sometimes people who drink diet soft drinks put on more weight and develop chronic disorders like diabetes. This has puzzled nutritionists, but experiments in mice now suggest that in some cases, this could partly be down to the artificial sweetener aspartame. Artificial sweeteners that contain no calories are synthetic alternatives to sugar that can taste up to 20,000 times sweeter. They are often used in products like low or zero-calorie drinks and sugar-free desserts, and are sometimes recommended for people who have type 2 diabetes. But mouse experiments now suggest that when aspartame breaks down in the gut, it may disrupt processes that are vital for neutralising harmful toxins from the bacteria that live there. By interfering with a crucial enzyme, these toxins seem to build up, irritating the gut lining and causing the kinds of low-level inflammation that can ultimately cause chronic diseases. “Our results are providing a mechanism for why aspartame may not always work to keep people thin, or even cause problems like obesity, heart disease, diabetes and metabolic syndrome,” says Richard Hodin at Massachusetts General Hospital in Boston. Irritating bacteria © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 22908 - Posted: 11.25.2016

By Joshua A. Krisch “In Drosophila, there is a well-documented interaction between sleep and metabolism, whereby flies suppress sleep or increase their activity when starved,” said coauthor William Ja of the Scripps Research Institute in Florida, in a press release. “However, the acute effects of food consumption on sleep have not yet been tested, largely because there was no system available to do so.” Ja and colleagues placed fruit flies in a small plastic chamber, which allowed the researchers to record fly activity before and after feeding. The recordings revealed that the fruit flies became lethargic or fell asleep for about 30 minutes following a large meal and that, the more the flies ate, the longer they remained asleep. Then, the researchers focused on a subset of leucokinin receptors previously implicated as potential drivers of post-meal sleep. Indeed, the researchers found that flies in which leucokinin receptor neurons were silenced remained alert even after a large meal. “Using an animal model, we’ve learned there is something to the food coma effect, and we can now start to study the direct relationship between food and sleep in earnest,” Ja said in the press release. “This behavior seems conserved across species, so it must be valuable to animals for some reason.” © 1986-2016 The Scientist

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22905 - Posted: 11.25.2016

Sara Reardon Lasers shone into the brains of mice can now activate individual neurons — and change the animals behaviour. Scientists have used the technique to increase how fast mice drink a milkshake, but it could also help researchers to map brain functions at a much finer scale than is currently possible. Neuroscientists at Stanford University in California conducted their experiments on mice that were genetically engineered to have light-sensitive neurons in a brain region called the orbitofrontal cortex. That area is involved in perceiving, and reacting to, rewards. By shining a laser at specific neurons, the researchers increased the pace at which the mice consumed a high-calorie milkshake. The results, reported on 12 November at the annual meeting of the Society for Neuroscience in San Diego, California, illustrate for the first time that the technique, known as optogenetics, can control behaviour by activating a sequence of individual cells. One goal of optogenetics is to create automated systems that manipulate the brain on the fly using only light, says Michael Häusser, a neuroscientist at University College London, UK. This might be done by engineering neurons to contain one protein that makes the cell fire when activated by a flash of coloured light, and another that causes the cell to flash in a different colour when it fires. A device that detected this second colour could quickly determine sites of activity associated with certain behaviours and customize which cells the first light would stimulate in response. Such a system might be able to alter the neural processes that link alcohol with reward in addiction, or a visual trigger with flashbacks in post-traumatic stress disorder. © 2016 Macmillan Publishers Limited,

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 22884 - Posted: 11.18.2016

Laura Sanders SAN DIEGO — A nerve-zapping headset caused people to shed fat in a small preliminary study. Six people who had received the stimulation lost on average about 8 percent of the fat on their trunks in four months, scientists reported November 12 at the annual meeting of the Society for Neuroscience. The headset stimulated the vestibular nerve, which runs just behind the ears. That nerve sends signals to the hypothalamus, a brain structure thought to control the body’s fat storage. By stimulating the nerve with an electrical current, the technique shifts the body away from storing fat toward burning it, scientists propose. Six overweight and obese people received the treatment, consisting of up to four one-hour-long sessions of stimulation a week. Because it activates the vestibular system, the stimulation evoked the sensation of gently rocking on a boat or floating in a pool, said study coauthor Jason McKeown of the University of California, San Diego. After four months, body scans measured the trunk body fat for the six people receiving the treatment and three people who received sham stimulation. All six in the treatment group lost some trunk fat, despite not having changed their activity or diet. In contrast, those in the sham group gained some fat. Researchers suspect that metabolic changes are behind the difference. “The results were a lot better than we thought they’d be,” McKeown said. |© Society for Science & the Public 2000 - 2016.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 22869 - Posted: 11.15.2016

By NICHOLAS BAKALAR Is use of antibiotics in infancy tied to childhood obesity? Some studies suggest so, but a new analysis suggests the link may be with infections, rather than antibiotics. Using records of a large health maintenance organization, researchers tracked 260,556 infants born from January 1997 through the end of March 2013. The database included details on antibiotic use, diagnosis and height and weight measurements from birth through age 18. The study is in Lancet Diabetes and Endocrinology. The scientists compared children who had no infections and no antibiotic use in the first year of life with those who had untreated infections. They found that an infant with one untreated infection had a 15 percent increased risk for childhood obesity, and the risk increased to 40 percent in those with three untreated infections. But there was no difference in obesity risk between infants treated with antibiotics and those with a similar infection left untreated. In other words, infections, but not the use of antibiotics, were associated with childhood obesity. “If there is an infection during infancy, particularly a respiratory or ear infection, it should be treated,” said the lead author, Dr. De-Kun Li of the Kaiser Permanente Division of Research. “You shouldn’t avoid antibiotics because you are concerned about childhood obesity.” © 2016 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22823 - Posted: 11.03.2016

By GINA KOLATA Americans believe that obesity is the biggest health threat in the nation today — bigger even than cancer. But though scientific research shows that diet and exercise are insufficient solutions, a large majority say fat people should be able to summon the willpower to lose weight on their own. The findings are from a nationally representative survey of 1,509 adults released on Tuesday by the National Opinion Research Center at the University of Chicago, an independent research institution. The study, funded by the American Society for Metabolic and Bariatric Surgery, found that concerns about obesity have risen. Just a few years ago, in a more limited survey, cancer was seen as the most serious health threat. The lead researcher, Jennifer Benz of the survey group at the University of Chicago, said that to her knowledge no other survey has provided so comprehensive a view of Americans’ beliefs about obesity, including how to treat it, whether people are personally responsible for it and whether it is a disease. Researchers say obesity, which affects one-third of Americans, is caused by interactions between the environment and genetics and has little to do with sloth or gluttony. There are hundreds of genes that can predispose to obesity in an environment where food is cheap and portions are abundant. Yet three-quarters of survey participants said obesity resulted from a lack of willpower. The best treatment, they said, is to take responsibility for yourself, go on a diet and exercise. Obesity specialists said the survey painted an alarming picture. They said the findings went against evidence about the science behind the disease, and showed that outdated notions about obesity persisted, to the detriment of those affected. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22815 - Posted: 11.01.2016

By Meredith Knight In June, international diabetes organizations endorsed provocative new guidelines suggesting physicians should consider gastric bypass surgery for a greatly expanded number of diabetics—those with a body mass index of 30 and above as opposed to just those with a BMI of 40 or more. Research has shown that the surgery helps people lose more weight, maintain the loss longer and achieve better blood glucose levels than those who slim down by changing diet and exercise habits. Now a study in mice suggests the effectiveness of bariatric surgery may stem in part from changes it causes in the brain. According to the study, published in the International Journal of Obesity, gastric bypass surgery causes the hyperactivation of a neural pathway that leads from stomach-sensing neurons in the brain stem to the lateral parabrachial nucleus, an area in the midbrain that receives sensory information from the body, and then to the amygdala, the brain's emotion- and fear-processing center. The obese mice underwent so-called Roux-en-Y bypass surgery, in which surgeons detach most of the stomach, leaving only a tiny pouch connected to the small intestine. Shortly after the surgery, the mice begin to show increased activation in this neural pathway, along with reduced meal size and a preference for less fatty food. They also begin to secrete higher levels of satiety hormones. Similar behavioral and hormonal patterns are found in humans after bypass surgery, suggesting that the brain changes may also be similar—but the authors say looking at this particular circuit in humans with brain imaging is difficult because the resolution is not up to the task. © 2016 Scientific American,

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22768 - Posted: 10.19.2016

Analysis of a trial that used the drug canagliflozin found that as people lost weight, their appetite increased proportionately, leading to consumption of more calories and weight loss plateau (leveling off). The findings provide the first measurement in people of how strongly appetite counters weight loss as part of the body’s feedback control system regulating weight. Results are currently available on BioRxiv (link is external) and will publish in Obesity during Obesity Week 2016. A team led by the NIH’s National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) analyzed data from a year-long, placebo-controlled, double-blind trial in people with type 2 diabetes who could eat and drink without restriction by the study. Of the 242 participants, 153 received canagliflozin, a drug that caused a substantial increase in the amount of glucose excreted in their urine. Those people were not directly aware of that calorie loss, which caused a gradual decrease in weight averaging about eight pounds. The team used a validated math model to calculate the changes in the amount of calories consumed during the study. They found no long-term calorie intake changes in the 89 people who got a placebo. However, for every pound of lost weight, the people treated with canagliflozin consumed about 50 calories per day more than they were eating before the study. This increase in appetite and calorie intake led to slowing of weight loss after about six months. The measurements are consistent with the researchers’ analysis of data from a separate trial on a commercial weight loss program not involving canagliflozin. In the weight loss program trial, despite the dieters’ consistent efforts to reduce calorie intake, their increased appetite resulted in a progressive increase in calorie intake — three times stronger than the changes in caloric expenditure that typically accompany weight loss — and weight loss plateau. Findings from the analyses suggest that persistent effort is required to avoid weight regain.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22756 - Posted: 10.15.2016

By GRETCHEN REYNOLDS Exercise may aid in weight control and help to fend off diabetes by improving the ability of fat cells to burn calories, a new study reports. It may do this in part by boosting levels of a hormone called irisin, which is produced during exercise and which may help to turn ordinary white fat into much more metabolically active brown fat, the findings suggest. Irisin (named for the Greek goddess Iris) entered the scientific literature in 2012 after researchers from Harvard and other universities published a study in Nature that showed the previously unknown hormone was created in working muscles in mice. From there, it would enter the bloodstream and migrate to other tissues, particularly to fat, where it would jump-start a series of biochemical processes that caused some of the fat cells, normally white, to turn brown. Brown fat, which is actually brown in color, burns calories. It also is known to contribute to improved insulin and blood sugar control, lessening the risk for Type 2 diabetes. Most babies, including human infants, are plump with brown fat, but we humans lose most of our brown fat as we grow up. By the time we are adults, we usually retain very little brown fat. In the 2012 study, the researchers reported that if they injected irisin into living mice, it not only turned some white fat into brown fat, it apparently also prevented the rodents from becoming obese, even on a high-fat, high-calorie diet. But in the years since, some scientists have questioned whether irisin affects fat cells in people to the same extent as it seems to in mice — and even whether the hormone exists in people at all. A study published last year in Cell Metabolism by the same group of researchers who had conducted the first irisin study, however, does seem to have established that irisin is produced in humans. They found some irisin in sedentary people, but the levels were much higher in those who exercise often. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22744 - Posted: 10.12.2016

Allison Aubrey The World Health Organization has already urged us to cut back on sugar, limiting added sugars to no more than 10 percent of our daily calories. So, how might policymakers get people to follow this advice? In a new report, the WHO is urging governments around the world to tax soda and other sugary drinks. In its report, the World Health Organization points to systematic reviews of policies aimed at improving diet and preventing lifestyle diseases, such as obesity and diabetes. "The evidence was strongest and most consistent for the effectiveness of sugar-sweetened beverage taxes in the range of 20-50% in reducing consumption," the WHO's meta-review concludes. Dr. Douglas Bettcher, director of the WHO's Department for the Prevention of Noncommunicable Diseases, says that "consumption of free sugars, including products like sugary drinks, is a major factor in the global increase of people suffering from obesity and diabetes." "If governments tax products like sugary drinks, they can reduce suffering and save lives. They can also cut healthcare costs and increase revenues to invest in health services," Bettcher was quoted as saying in a WHO release on the report. The International Council of Beverages Associations, which represents soda companies and other beverage-makers around the globe, says it's disappointed with the new WHO report. "We strongly disagree with the committee's recommendation to tax beverages, as it is an unproven idea that has not been shown to improve public health based on global experiences to date," an ICBA release concludes. © 2016 npr

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22743 - Posted: 10.12.2016

By Michelle Roberts Some people are genetically wired to prefer the taste of fatty foods, putting them at increased risk of obesity, according to UK researchers. The University of Cambridge team offered 54 volunteers unlimited portions of chicken korma, followed by an Eton mess-style dessert. Some of the meals were packed with fat while others were low-fat versions. Those with a gene already linked to obesity showed a preference for the high-fat food and ate more of it. Fat genes The gene in question is called MC4R. It is thought about one in every 1,000 people carries a defective version of this gene which controls hunger and appetite as well as how well we burn off calories. Mutations in MC4R are the most common genetic cause of severe obesity within families that has so far been identified. Humans probably evolved hunger genes to cope in times of famine, say experts. When food is scarce it makes sense to eat and store more fat to fend off starvation. But having a defect in the MC4R gene means hunger can become insatiable. In the study, published in the journal Nature Communications, the researchers created a test menu that varied only in fat or sugar content. The three versions of the main meal on offer - chicken korma - were identical in appearance, and as far as possible, taste, but ranged in fat from low to medium and high. The volunteers were offered a small sample of each and then left to eat as much as they liked of the three dishes. The same was then done for a pudding of strawberries, meringue and cream, but this time varying the sugar content rather than the fat. © 2016 BBC.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 22726 - Posted: 10.05.2016

Joe Palca Most of us have been tempted at one time or another by the lure of sugar. Think of all the cakes and cookies you consume between Thanksgiving and Christmastime! But why are some people unable to resist that second cupcake or slice of pie? That's the question driving the research of Monica Dus, a molecular biologist at the University of Michigan. She wants to understand how excess sugar leads to obesity by understanding the effect of sugar on the brain. Dus's interest in how animals control the amount they eat started with a curious incident involving her two Bichon Frise dogs. One day, Cupcake and Sprinkles got into a bag of dog treats when Dus wasn't around. The dogs overdid it. "I couldn't believe that these two tiny, 15-pound animals had huge bellies for three days and they couldn't stop themselves from eating," she recalls. Dus was already an expert in fruit fly genetics, so she decided to study flies to see if she could unravel the puzzle of how the brain controls eating behavior. Her lab has a working hypothesis. Dus believes a diet high in sugar actually changes the brain, so it no longer does a good job of knowing how many calories the body is taking in. She thinks there are persistent molecular changes in the brain over time – changes that pave the way for excessive eating and eventually, obesity. Monica Dus is a researcher at the University of Michigan. She just won a $1.5 million Young Innovator grant from the National Institutes of Health to study how a high-sugar diet may lead to obesity by changing brain chemistry. © 2016 npr

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22725 - Posted: 10.05.2016

By GINA KOLATA It is not easy to be fat in America, even though more than a third of adults are obese. Donald J. Trump brought the issue of fat shaming to the fore during and after last week’s debate, when he disparaged a former Miss Universe winner who gained weight and when he said the hacking of the Democratic National Committee’s emails might have been done by “somebody sitting on their bed that weighs 400 pounds.” But there also is a body of evidence showing that the effects of fat shaming and stigmatizing go far beyond such remarks, beyond the stares fat people get on the street, the cutting comments strangers make about their weight and the “funny” greeting cards featuring overweight people. It turns out that fat prejudice differs from other forms in ways that make it especially difficult to overcome. The problems with fat shaming start early. Rebecca Puhl, the deputy director of the University of Connecticut’s Rudd Center for Food Policy and Obesity, and her colleagues find that weight is the most common reason children are bullied in school. In one study, nearly 85 percent of adolescents reported seeing overweight classmates teased in gym class. Dr. Puhl and her colleagues asked fat kids who was doing the bullying. It turned out that it was not just friends and classmates but also teachers and — for more than a third of the bullied — parents. “If these kids are not safe at school or at home, where are they going to be supported?” Dr. Puhl asked. The bullying problem is not limited to the United States. Dr. Puhl and her colleagues found the same situation in Canada, Australia and Iceland. Women face harsher judgment than men, Dr. Puhl reports. The cutting remarks can begin when a woman’s body mass index is in the overweight range, while for men the shaming tends to start when they are obese. And women who are obese report more than three times as much shaming and discrimination as men of equal obesity. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 11: Emotions, Aggression, and Stress
Link ID: 22722 - Posted: 10.02.2016

The make-up of the bacteria found in human faeces may influence levels of dangerous fat in our bodies, say researchers from King's College London. Their analysis of stool samples in a study of more than 3,600 twins found evidence that some of this bacteria is inherited. What is contained in faeces bacteria could therefore partly explain why obesity passes down through families. The study is published in Genome Biology. The research team extracted information from study participants about the human faecal microbiome - the bacteria present in faeces samples - and compared these to six different measures of obesity, including body mass index (BMI) and different types of body fat. The researchers found the strongest links with visceral fat, where participants with a high diversity of bacteria in their faeces had lower levels of visceral fat. This type of body fat is bad news because it is stored in the stomach area around important organs such as the liver, pancreas and intestines and is linked with higher risks of cardiovascular disease and diabetes. Dr Michelle Beaumont, lead study author from the department of twin research and genetic epidemiology at King's College London, said although the study showed a clear link, it was not yet possible to explain why it existed. One theory is that a lack of variety in faecal bacteria could lead to the domination of high levels of gut microbes which are good at turning carbohydrates into fat. © 2016 BBC.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22694 - Posted: 09.26.2016

By GINA KOLATA You must lose weight, a doctor told Sarah Bramblette, advising a 1,200-calorie-a-day diet. But Ms. Bramblette had a basic question: How much do I weigh? The doctor’s scale went up to 350 pounds, and she was heavier than that. If she did not know the number, how would she know if the diet was working? The doctor had no answer. So Ms. Bramblette, 39, who lived in Ohio at the time, resorted to a solution that made her burn with shame. She drove to a nearby junkyard that had a scale that could weigh her. She was 502 pounds. One in three Americans is obese, a rate that has been steadily growing for more than two decades, but the health care system — in its attitudes, equipment and common practices — is ill prepared, and its practitioners are often unwilling, to treat the rising population of fat patients. The difficulties range from scales and scanners, like M.R.I. machines that are not built big enough for very heavy people, to surgeons who categorically refuse to give knee or hip replacements to the obese, to drug doses that have not been calibrated for obese patients. The situation is particularly thorny for the more than 15 million Americans who have extreme obesity — a body mass index of 40 or higher — and face a wide range of health concerns. Part of the problem, both patients and doctors say, is a reluctance to look beyond a fat person’s weight. Patty Nece, 58, of Alexandria, Va., went to an orthopedist because her hip was aching. She had lost nearly 70 pounds and, although she still had a way to go, was feeling good about herself. Until she saw the doctor. “He came to the door of the exam room, and I started to tell him my symptoms,” Ms. Nece said. “He said: ‘Let me cut to the chase. You need to lose weight.’” © 2016 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22693 - Posted: 09.26.2016