Links for Keyword: Obesity

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|By Charles Schmidt The notion that the state of our gut governs our state of mind dates back more than 100 years. Many 19th- and early 20th-century scientists believed that accumulating wastes in the colon triggered a state of “auto-intoxication,” whereby poisons emanating from the gut produced infections that were in turn linked with depression, anxiety and psychosis. Patients were treated with colonic purges and even bowel surgeries until these practices were dismissed as quackery. The ongoing exploration of the human microbiome promises to bring the link between the gut and the brain into clearer focus. Scientists are increasingly convinced that the vast assemblage of microfauna in our intestines may have a major impact on our state of mind. The gut-brain axis seems to be bidirectional—the brain acts on gastrointestinal and immune functions that help to shape the gut's microbial makeup, and gut microbes make neuroactive compounds, including neurotransmitters and metabolites that also act on the brain. These interactions could occur in various ways: microbial compounds communicate via the vagus nerve, which connects the brain and the digestive tract, and microbially derived metabolites interact with the immune system, which maintains its own communication with the brain. Sven Pettersson, a microbiologist at the Karolinska Institute in Stockholm, has recently shown that gut microbes help to control leakage through both the intestinal lining and the blood-brain barrier, which ordinarily protects the brain from potentially harmful agents. Microbes may have their own evolutionary reasons for communicating with the brain. They need us to be social, says John Cryan, a neuroscientist at University College Cork in Ireland, so that they can spread through the human population. © 2015 Scientific American

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: 20644 - Posted: 03.03.2015

by Penny Sarchet An injection and a dash of exercise could be the secret to keeping trim. These rainbow mice, imaged in infrared to reveal how much energy they are burning while on a treadmill, are revealing how a shot can boost a muscle's ability to burn calories. Red body parts show where lots of energy is being used. The mouse on the right has a red patch on its left hind leg, which corresponds to the spot where it received an injection of a substance developed by Denice Hodgson-Zingman from the University of Iowa and colleagues. The substance is a type of morpholino, a compound that can be designed to target specific genes, in this case to alter proteins responsible for storing energy. The disruption causes muscles to burn more energy even during mild exercise, such as a gentle trot on a treadmill. In contrast, the untreated mouse on the left, which is doing the same amount of exercise, is using less energy in the same spot, as illustrated by the colder green colour. The researchers hope the injection will help people who want to burn more calories do so through routine everyday activities, eliminating the need for intense exercise. Journal reference: Molecular Therapy, DOI: 10.1038/mt.2015.2141 © Copyright Reed Business Information Ltd.

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: 20610 - Posted: 02.24.2015

Scientists have uncovered more than 90 new gene regions that could help explain why some people are more likely to put on weight than others. The team scoured DNA libraries of more than 300,000 people, constructing the largest-ever genetic map of obesity. Looking for consistent patterns they found a link with genes involved in brain processes, suggesting obesity could partly have a neurological basis. The results are published in the journal Nature. Researchers from the international Giant consortium (Genetic Investigation of Anthropometric Trait), analysed the genetics behind body mass index (a ratio of weight and height ). And in a separate Nature paper they looked specifically at how genetics influence where fat is distributed around the body. Fat around the abdomen for example can cause more health problems than fat carried around the thighs. Some 33 newly pinpointed gene regions were linked to body fat distribution - giving further clues about why some people are pear-shaped while others put on weight more around the tummy. They also identified more than 60 genetic locations that influence body mass index - tripling the number previously known. And some of these regions have links with the nervous system. © 2015 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: 20572 - Posted: 02.13.2015

|By Erika Beras We know junk food can change the way bodies are shaped. Now, a study finds that those irresistible sweet and salty concoctions may also change the way brains are wired—at least in rats. Researchers divided rats into two groups—one labeled Cafeteria, the other called Chow. Both groups got a typical rat food diet, but the Cafeteria rats also got a bonus: meat pies, cakes and cookies. Both rat groups gained weight. But the Cafeteria rats gained significantly more than the Chows did—nearly half a pound more, which is a big body burden for a rat. But more important, over two weeks time the Cafeteria rats seemed to care less and less about even seeking out a balanced diet. This new behavior endured even after the rats were returned to their more healthy fare. The study is in the journal Frontiers in Psychology. [Amy C. Reichelt, Margaret J. Morris and R.F. Westbrook, Cafeteria diet impairs expression of sensory-specific satiety and stimulus-outcome learning] The researchers think junk-food diets cause lasting changes in the rewards circuits part of the brain—which plays a big role in decision-making. So if you’re a regular cookie eater and the next time you mindlessly reach for a cookie you wonder why you can’t help yourself—well, it could be because you’re not in charge, your rewired brain is. © 2015 Scientific American

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: 20564 - Posted: 02.09.2015

By Brady Dennis The Food and Drug Administration on Wednesday approved a device aimed at helping obese people shed weight in a novel way – by targeting the nerve pathway between the brain and the stomach that controls feelings of hunger and fullness. The Maestro Rechargeable System, as it is known, consists of an electrical charge generator, wire leads and electrodes that are implanted surgically into a patient’s abdomen. It sends electrical pulses designed to interfere with the vagus nerve, which signals to the brain when the stomach is full or empty. Though researchers don't know exactly how such electrical stimulation leads to weight loss, the approach seems promising. In a year-long clinical trial involving 233 patients with a body-mass index, or BMI, of 35 or greater, those who received a working Maestro device lost 8.5 percent more weight than those without it. About half those in the experimental group lost at least 20 percent of their excess weight, and more than a third lost more than 25 percent of their excess weight. The overall figure was below the original goal of the trial, which was to show weight loss of 10 percent more excess weight in the control group than in those using the new device. Nevertheless, an FDA advisory group said the data showed sustained weight loss among participants and argued that the benefits of the device outweigh its risks for certain patients. In the clinical trial, some patients experienced nausea, vomiting, surgical complications and other side effects. The FDA is requiring the device's manufacturer, EnteroMedics, to conduct a five-year, post-approval study to gather additional data about its safety and effectiveness.

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: 20488 - Posted: 01.15.2015

Carl Zimmer Among scientists who study how our DNA affects our weight, a gene called FTO stands out. “It’s the poster child for the genetics of obesity,” said Struan F. Grant, an associate professor of pediatrics at the University of Pennsylvania School of Medicine. In 2007, researchers discovered that people with a common variant of FTO tend to be heavier than those without it. Since then, studies have repeatedly confirmed the link. On average, one copy of the risky variant adds up to 3.5 extra pounds of weight. Two copies of the gene bring 7 extra pounds — and increase a person’s risk of becoming obese by 50 percent. But the gene doesn’t seem to have always been a problem. If scientists had studied FTO just a few decades ago, they would have found no link to weight whatsoever. A new study shows that FTO became a risk only in people born after World War II. The research, published this week in the Proceedings of the National Academy of Sciences, raises questions that extend far beyond obesity. Genes clearly influence our health in many ways, but so does our environment; often, it is the interplay between them that makes the difference in whether we develop obesity or cancer or another ailment. But the relative importance of certain genes may shift over the years, the new study suggests, as our environment changes. James Niels Rosenquist of Massachusetts General Hospital and his colleagues were inspired to conduct the study by recent research documenting how people’s experiences alter the effects of their genes. A variant of a gene called AKT1, for example, can raise the risk of psychosis — but only if the carrier smokes a lot of marijuana. If he avoids smoking, the AKT1 variant doesn’t cause a problem. © 2015 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: 20451 - Posted: 01.01.2015

by Andy Coghlan It may not sound very appetising, but an edible powder made from waste excreted by bacteria in our guts may help people to avoid gaining weight. Stabilising a person's weight could have a major health impact, says Gary Frost of Imperial College London, because as people on Western diets grow older, they tend to put on between 0.3 and 0.8 kilograms per year on average. A fatty acid called propionate is released when the bacteria in our gut digest fibre. Propionate makes people feel full by activating cells in the large intestine that produce the satiety hormones GLP-1 and PYY: these tell the brain that it's time to stop eating. But to trigger a big enough dose of this appetite-suppressing signal from gut bacteria alone, people would have to eat extremely large amounts of fibre. To get around that, Frost and his team made the molecule in a concentrated form called inulin-propionate ester (IPE). "That gives you eight times the amount of someone following a typical Western diet," he says. To test its appetite-stemming properties, the team gave powdered IPE, mixed in with fruit juice or a milkshake, to a group of overweight volunteers every day for six months. A type of ordinary fibre was given to another set of people, who acted as controls. Only one of the 25 volunteers taking IPE put on more than 3 per cent of their body weight over that time, compared with six of the 24 controls. One reason for this might be that the IPE recipients ate around 9 per cent less over the six months. © Copyright Reed Business Information Ltd.

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: 20416 - Posted: 12.13.2014

By Nsikan Akpan Gut surgery is often the only option for life-threatening obesity and diabetes, but what if doctors could cut the pounds without using a knife? Scientists have engineered an antiobesity drug that rivals the dramatic benefits seen with surgery, dropping excess body weight by a third. Though the work was done only in rodents, the drug is the first to influence three obesity-related hormones in the gut at once. Bariatric surgery, including gastric bypass, typically involves limiting food intake by removing part of the stomach or intestines. Yet it does more than shrink the size of patient’s stomach or intestines. It also changes the release of multiple gut-related hormones, explains clinical endocrinologist Stephen O'Rahilly of the University of Cambridge in the United Kingdom, who wasn’t involved with the study. That’s important, because years of eating a diet high in fat and sugar can throw a person’s metabolism into disarray. Cells undergo genetic reprogramming that negatively impacts how they process sugar and store fat, locking in obesity. This pattern makes it harder and harder to lose weight, even if a person changes their diet and begins exercising. Bariatric surgery interrupts that cycle by stimulating the production of several hormones that reduce blood sugar, burn fat, and curb appetite. (It may also change the composition of the gut’s microbes.) Three of these hormones are called glucagon-like peptide-1 (GLP-1), gastric inhibitory peptide (GIP), and glucagon. Cells in your gut release GLP-1 and GIP after a meal to keep your body’s blood sugar levels in a normal range. GLP-1 also curbs appetite, signaling to your brain that you are full. In type 2 diabetes, the body stops responding to GLP-1 and GIP, which contributes to hyperglycemia, or too much blood sugar. Hyperglycemia causes the devastating hallmarks of diabetes, such as kidney injury, cardiovascular disease, and nerve damage. © 2014 American Association for the Advancement of Science.

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: 20408 - Posted: 12.10.2014

by Michael Slezak The elusive link between obesity and high blood pressure has been pinned down to the action of leptin in the brain, and we might be able to block it with drugs. We've known for more than 30 years that fat and high blood pressure are linked, but finding what ties them together has been difficult. One of the favourite candidates has been leptin – a hormone produced by fat cells. Under normal circumstances, when fat cells produce leptin, the hormone sends the message that you've had enough food. But in people with obesity, the body stops responding to this message, and large levels of leptin build up. Leptin is known to activate the regulatory network called the sympathetic nervous system, and it's the activation of sympathetic nerves on the kidneys that seem to be responsible for raising blood pressure. Leptin has thus been linked to blood pressure. However, conclusive evidence has been hard to come by. Michael Cowley of Monash University in Melbourne, Australia, and his colleagues have now conducted a string of experiments that provide some evidence. Through genetic and drug experiments in mice, they have pinpointed an area in the mouse brain that increases blood pressure when it is exposed to high leptin levels. This region is called the dorsomedial hypothalamus, and is thought to be involved in controlling energy consumption. Their findings show that high levels in leptin do indeed boost blood pressure, via this brain region. © Copyright Reed Business Information Ltd.

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: 20398 - Posted: 12.06.2014

By Nicholas Bakalar Researchers have found that people diagnosed with diabetes in their 50’s are significantly more likely than others to suffer mental decline by their 70’s. The study, published Monday in the Annals of Internal Medicine, started in 1990. Scientists examined 13,351 black and white adults, aged 48 to 67, for diabetes and prediabetes using self-reported physician diagnoses and glucose control tests. They also administered widely used tests of memory, reasoning, problem solving and planning. About 13 percent had diabetes at the start. The researchers followed them with five periodic examinations over the following 20 years. By that time, 5,987 participants were still enrolled. After adjusting for numerous health and behavioral factors, and for the large attrition in the study, the researchers found people with diabetes suffered a 30 percent larger decline in mental acuity than those without the disease. Diabetes can impair blood circulation, and the authors suggest that the association of diabetes with thinking and memory problems may be the result of damage to small blood vessels in the brain. “People may think cognitive decline with age is inevitable, but it’s not,” said the senior author, Elizabeth Selvin, an associate professor of epidemiology at the Johns Hopkins Bloomberg School of Public Health. “Factors like diabetes are potentially modifiable. If we can better control diabetes we can stave off cognitive decline and future dementia.” © 2014 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 20377 - Posted: 12.02.2014

By Elizabeth Pennisi The microbes that live in your body outnumber your cells 10 to one. Recent studies suggest these tiny organisms help us digest food and maintain our immune system. Now, researchers have discovered yet another way microbes keep us healthy: They are needed for closing the blood-brain barrier, a molecular fence that shuts out pathogens and molecules that could harm the brain. The findings suggest that a woman's diet or exposure to antibiotics during pregnancy may influence the development of this barrier. The work could also lead to a better understanding of multiple sclerosis, in which a leaky blood-brain barrier may set the stage for a decline in brain function. The first evidence that bacteria may help fortify the body’s biological barriers came in 2001. Researchers discovered that microbes in the gut activate genes that code for gap junction proteins, which are critical to building the gut wall. Without these proteins, gut pathogens can enter the bloodstream and cause disease. In the new study, intestinal biologist Sven Pettersson and his postdoc Viorica Braniste of the Karolinska Institute in Stockholm decided to look at the blood-brain barrier, which also has gap junction proteins. They tested how leaky the blood-brain barrier was in developing and adult mice. Some of the rodents were brought up in a sterile environment and thus were germ-free, with no detectable microbes in their bodies. Braniste then injected antibodies—which are too big to get through the blood-brain barrier—into embryos developing within either germ-free moms or moms with the typical microbes, or microbiota. © 2014 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 2: Cells and Structures: The Anatomy of the Nervous System; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 20338 - Posted: 11.20.2014

By Nicholas Bakalar Exposure to secondhand smoke and roadway traffic may be tied to increased body mass index in children and adolescents, a new study suggests. Researchers studied 3,318 children in 12 Southern California communities beginning at an average age of 10, and then followed them through age 18. They used parental questionnaires to establish exposure to smoking, and data on traffic volume and levels of nitrogen dioxide, ozone and particulates to track pollution. The study, in Environmental Health Perspectives, controlled for many other factors: sex, initial B.M.I., asthma, physical activity, insurance status, parental education and income, acres of parks and open space nearby, percentage of people living in poverty in each community. But even after accounting for these issues and more, they found that compared with children exposed to no secondhand smoke or near-roadway air pollution, B.M.I. was 0.80 higher in children exposed to pollution alone, 0.85 higher in those exposed to secondhand smoke alone, and 2.15 higher in those exposed to both. A normal B.M.I. for adults is 18.5 to 24.9. Higher than 25 is considered overweight, and above 30 obese. “It would be interesting to know more about the mechanism,” said the lead author, Dr. Rob McConnell, a professor of preventive medicine at the University of Southern California. “But the finding challenges the view that obesity is due solely to increased caloric intake and reduced physical activity. That’s not the whole story.” © 2014 The New York Times Company

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: 20322 - Posted: 11.18.2014

By Adam Brimelow Health Correspondent, BBC News A Mediterranean diet may be a better way of tackling obesity than calorie counting, leading doctors have said. Writing in the Postgraduate Medical Journal (PMJ), the doctors said a Mediterranean diet quickly reduced the risk of heart attacks and strokes. And they said it may be better than low-fat diets for sustained weight loss. Official NHS advice is to monitor calorie intake to maintain a healthy weight. Last month NHS leaders stressed the need for urgent action to tackle obesity and the health problems that often go with it. The PMJ editorial argues a focus on food intake is the best approach, but it warns crash dieting is harmful. Signatories of the piece included the chair of the Academy of Medical Royal Colleges, Prof Terence Stephenson, and Dr Mahiben Maruthappu, who has a senior role at NHS England. They criticise the weight-loss industry for focusing on calorie restriction rather than "good nutrition". And they make the case for a Mediterranean diet, including fruit and vegetables, nuts and olive oil, citing research suggesting it quickly reduces the risk of heart attacks and strokes, and may be better than low-fat diets for sustained weight loss. The lead author, cardiologist Dr Aseem Malhotra, says the scientific evidence is overwhelming. "What's more responsible is that we tell people to concentrate on eating nutritious foods. "It's going to have an impact on their health very quickly. We know the traditional Mediterranean diet, which is higher in fat, proven from randomised controlled trials, reduces the risk of heart attack and stroke even within months of implementation." The article also says adopting a Mediterranean diet after a heart attack is almost three times as effective at reducing deaths as taking cholesterol-lowering statin medication. BBC © 2014

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: 20316 - Posted: 11.17.2014

Sara Reardon Companies selling ‘probiotic’ foods have long claimed that cultivating the right gut bacteria can benefit mental well-being, but neuroscientists have generally been sceptical. Now there is hard evidence linking conditions such as autism and depression to the gut’s microbial residents, known as the microbiome. And neuroscientists are taking notice — not just of the clinical implications but also of what the link could mean for experimental design. “The field is going to another level of sophistication,” says Sarkis Mazmanian, a microbiologist at the California Institute of Technology in Pasadena. “Hopefully this will shift this image that there’s too much commercial interest and data from too few labs.” This year, the US National Institute of Mental Health spent more than US$1 million on a new research programme aimed at the microbiome–brain connection. And on 19 November, neuroscientists will present evidence for the link in a symposium at the annual Society for Neuroscience meeting in Washington DC called ‘Gut Microbes and the Brain: Paradigm Shift in Neuroscience’. Although correlations have been noted between the composition of the gut microbiome and behavioural conditions, especially autism1, neuroscientists are only now starting to understand how gut bacteria may influence the brain. The immune system almost certainly plays a part, Mazmanian says, as does the vagus nerve, which connects the brain to the digestive tract. Bacterial waste products can also influence the brain — for example, at least two types of intestinal bacterium produce the neurotransmitter γ-aminobutyric acid (GABA)2. © 2014 Nature Publishing Group

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 20310 - Posted: 11.13.2014

By James Gallagher Health editor, BBC News website Weight loss surgery can dramatically reduce the odds of developing type 2 diabetes, according to a major study. Doctors followed nearly 5,000 people as part of a trial to assess the health impact of the procedure. The results, published in the Lancet Diabetes and Endocrinology journal, showed an 80% reduction in type 2 diabetes in those having surgery. The UK NHS is considering offering the procedure to tens of thousands of people to prevent diabetes. Obesity and type 2 diabetes are closely tied - the bigger someone is, the greater the risk of the condition. The inability to control blood sugar levels can result in blindness, amputations and nerve damage. Around a tenth of NHS budgets are spent on managing the condition. Surgery The study followed 2,167 obese adults who had weight loss - known as bariatric - surgery. They were compared to 2,167 fellow obese people who continued as they were. There were 38 cases of diabetes after surgery compared with 177 in people left as they were - a reduction of nearly 80%. Around 3% of morbidly obese people develop type 2 each year, however, surgery reduced the figure to around 0.5%, which is the background figure for the whole population. Bariatric surgery, also known as weight loss surgery, is used as a last resort to treat people who are dangerously obese and carrying an excessive amount of body fat. This type of surgery is available on the NHS only to treat people with potentially life-threatening obesity when other treatments have not worked. Around 8,000 people a year currently receive the treatment. The two most common types of weight loss surgery are: Gastric band, where a band is used to reduce the size of the stomach so a smaller amount of food is required to make someone feel full Gastric bypass, where the digestive system is re-routed past most of the stomach so less food is digested to make someone feel full BBC © 2014

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: 20269 - Posted: 11.03.2014

Daniel Duane, Men's Journal For more than half a century, the conventional wisdom among nutritionists and public health officials was that fat is dietary enemy No. 1 — the leading cause of obesity and heart disease. It appears the wisdom was off. And not just off. Almost entirely backward. According to a new study from the National Institutes of Health, a diet that reduces carbohydrates in favor of fat — including the saturated fat in meat and butter — improves nearly every health measurement, from reducing our waistlines to keeping our arteries clear, more than the low-fat diets that have been recommended for generations. "The medical establishment got it wrong," says cardiologist Dennis Goodman, director of Integrative Medicine at New York Medical Associates. "The belief system didn't pan out." It's not the conclusion you would expect given the NIH study's parameters. Lead researcher Lydia Bazanno, of the Tulane University School of Public Health, pitted this high-fat, low-carb diet against a fat-restricted regimen prescribed by the National Cholesterol Education Program. "We told both groups to get carbs from green, leafy vegetables, because those are high in nutrients and fiber to keep you sated," Bazanno says. "We also told everyone to stay away from trans fats." The fat-restricted group continued to eat carbs, including bread and cereals, while keeping saturated fat — common in animal products — below 7 percent of total calories. By contrast, the high-fat group cut carbs in half and did not avoid butter, meat, and cheese. Most important, both groups ate as much as they wanted — no calorie counting, no going hungry.

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: 20251 - Posted: 10.28.2014

Clare Pain Eating a high fat and high carb diet resulted in inflammation in the brain - at least in male mice. We'll have to wait to see if the same process applies to male humans. The detrimental impact of junk food seems to be connected to inflammation in the brains of male mice, with the brains of females protected by oestrogen, according to research published today in Cell Reports. Dr Deborah Clegg, who led the study while at University of Texas Southwestern Medical Centre, Dallas, USA, was building on existing research that links brain inflammation with obesity and heart disease in male mice. "We embarked on this research because [the link with inflammation] had been shown in male mice, so we asked ourselves, do the same processes occur in females?" explains Clegg. Previous research has shown that one cause of inflammation in the hypothalamus - the part of the brain that controls energy balance - is palmitic acid, a saturated fatty acid found in palm oil, dairy products and meat, and common in high fat food. The team looked at male and female mice, fed either their normal diet or a 'high fat' diet. Besides containing 42 per cent fat, the high fat diet was also high in carbohydrates making it a good correlate of human junk food, says Clegg. © 2014 ABC

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 8: Hormones and Sex
Link ID: 20215 - Posted: 10.18.2014

BY Bethany Brookshire In this sweet, sweet world we live in, losing weight can be a dull and flavorless experience. Lovely stove-popped popcorn drenched in butter gives way to dry microwaved half-burnt kernels covered in dusty yellow powder. The cookies and candy that help us get through the long afternoons are replaced with virtuous but boring apples and nuts. Even the sugar that livens up our coffee gets a skeptical eye: That’s an extra 23 calories per packet you shouldn’t be eating. What makes life sweet for those of us who are counting calories is artificial sweeteners. Diet soda gives a sweet carbonated fix. A packet of artificial sweetener in your coffee or tea makes it a delicious morning dose. But a new study, published September 17 in Nature, found that the artificial sweetener saccharin has an unintended side effect: It alters the bacterial composition of the gut in mice and humans. The new bacterial neighborhood brings with it higher blood glucose levels, putting the humans and the murine counterparts at risk for diabetes. Many people wondered if the study’s effects were real. We all knew that sugar was bad, but now the scientists are coming for our Splenda! It seems more than a little unfair. But this study was a long time coming. The scientific community has been studying artificial sweeteners and their potential hazards for a long time. And while the new study adds to the literature, there are other studies, currently ongoing and planned for the future, that will determine the extent and necessity of our artificially sweetened future. © Society for Science & the Public 2000 - 2014.

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: 20153 - Posted: 10.02.2014

By Nicholas Bakalar Average waist circumference — but not body mass index— increased significantly in the United States between 1999 and 2012, a new study reports. Abdominal obesity — a “beer belly” or “beer gut” — is caused by fat around the internal organs. It is one of the indicators of metabolic syndrome, a group of five conditions that raises the risk for heart disease and diabetes. After adjusting for age, the overall mean waist circumference increased to 38.7 inches in 2012 from 37.5 in 1999. The increases were significant for men, women, non-Hispanic whites, non-Hispanic blacks and Mexican-Americans. They were greatest among non-Hispanic whites in their 40s, and non-Hispanic black men in their 30s. “I would encourage people to keep track of their waists,” said the lead author of the study, Dr. Earl S. Ford, a medical officer with the Centers for Disease Control and Prevention. “Standing on the scale every day is all good and well, but you can have a steady weight and still have an expanding waist. And that should be a signal for people to start looking at their diet and physical activity.” In 2012, 54.2 percent of Americans had abdominal obesity (defined as an age-adjusted waist circumference of more than 40 inches for men and more than 34.6 for women) compared with 46.4 percent in 1999. The study was published in JAMA. © 2014 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: 20103 - Posted: 09.23.2014

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.

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: 20093 - Posted: 09.18.2014