Links for Keyword: Obesity

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Marise Parent Of course you know that eating is vital to your survival, but have you ever thought about how your brain controls how much you eat, when you eat and what you eat? This is not a trivial question, because two-thirds of Americans are either overweight or obese and overeating is a major cause of this epidemic. To date, the scientific effort to understand how the brain controls eating has focused primarily on brain areas involved in hunger, fullness and pleasure. To be better armed in the fight against obesity, neuroscientists, including me, are starting to expand our investigation to other parts of the brain associated with different functions. My lab’s recent research focuses on one that’s been relatively overlooked: memory. For many people, decisions about whether to eat now, what to eat and how much to eat are often influenced by memories of what they ate recently. For instance, in addition to my scale and tight clothes, my memory of overeating pizza yesterday played a pivotal role in my decision to eat salad for lunch today. Memories of recently eaten foods can serve as a powerful mechanism for controlling eating behavior because they provide you with a record of your recent intake that likely outlasts most of the hormonal and brain signals generated by your meal. But surprisingly, the brain regions that allow memory to control future eating behavior are largely unknown. Studies done in people support the idea that meal-related memory can control future eating behavior. © 2010–2019, The Conversation US, Inc.

Related chapters from BN8e: 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: 25866 - Posted: 01.15.2019

Abby Olena In the never-ending search for ways to help people eat healthy, scientists have been looking into brain stimulation, specifically, sending a weak electrical current to the brain through two scalp electrodes—a technique called transcranial direct current stimulation. It has previously shown promise in limiting both food cravings and consumption in people, but in a study published yesterday (January 9) in Royal Society Open Science, researchers didn’t find any effects of tDCS on food-related behavior, indicating that the technique’s use needs another look. “The good things about the study are the large sample size and the fact that it’s fairly rigorous,” says Mark George, a psychiatrist and neurologist at the Medical University of South Carolina who did not participate in the study. “The problem [is] interpreting studies where there’s a failure to find. All you can say is that it didn’t work . . . with this group.” During tDCS, one to two milliamps of electricity—enough to feel tingles or pins and needles, but far less than the 800 or so milliamps used for electroconvulsive therapy—are delivered to the brain. Over the last two decades, scientists have reported targeting the technique to the dorsolateral prefrontal cortex, a brain area that’s been shown to be involved in food-related behavior. They’ve found it has helped people crave less and, to a lesser extent, eat fewer sweets and other tempting foods. Yet these experiments have generally included groups of 20 or fewer people, and other studies have failed to replicate their effects. © 1986 - 2019 The Scientist.

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 25861 - Posted: 01.14.2019

By Robert F. Service BOSTON—Implanted electronics can steady hearts, calm tremors, and heal wounds—but at a cost. These machines are often large, obtrusive contraptions with batteries and wires, which require surgery to implant and sometimes need replacement. That's changing. At a meeting of the Materials Research Society here last month, biomedical engineers unveiled bioelectronics that can do more in less space, require no batteries, and can even dissolve when no longer needed. "Huge leaps in technology [are] being made in this field," says Shervanthi Homer-Vanniasinkam, a biomedical engineer at University College London. By making bioelectronics easier to live with, these advances could expand their use. "If you can tap into this, you can bring a new approach to medicine beyond pharmaceuticals," says Bernhard Wolfrum, a neuroelectronics expert at the Technical University of Munich in Germany. "There are a lot of people moving in this direction." One is John Rogers, a materials scientist at Northwestern University in Evanston, Illinois, who is trying to improve on an existing device that surgeons use to stimulate healing of damaged peripheral nerves in trauma patients. During surgery, doctors suture severed nerves back together and then provide gentle electrical stimulation by placing electrodes on either side of the repair. But because surgeons close wounds as soon as possible to prevent infection, they typically provide this stimulation for an hour or less. © 2018 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 25786 - Posted: 12.13.2018

By Gina Kolata You’d think that scientists at an international conference on obesity would know by now which diet is best, and why. As it turns out, even the experts still have widely divergent opinions. At a recent meeting of the Obesity Society, organizers held a symposium during which two leading scientists presented the somewhat contradictory findings of two high-profile diet studies. A moderator tried to sort things out. In one study, by Christopher Gardner, a professor of medicine at Stanford, patients were given low-fat or low-carb diets with the same amount of calories. After a year, weight loss was the same in each group, Dr. Gardner reported. Another study, by Dr. David Ludwig of Boston Children’s Hospital, reported that a low-carbohydrate diet was better than a high-carbohydrate diet in helping subjects keep weight off after they had dieted and lost. The low-carbohydrate diet, he found, enabled participants to burn about 200 extra calories a day. So does a low-carbohydrate diet help people burn more calories? Or is the composition of the diet irrelevant if the calories are the same? Does it matter if the question is how to lose weight or how to keep it off? There was no consensus at the end of the session. But here are a few certainties about dieting amid the sea of unknowns. What we know People vary — a lot — in how they respond to dieting. Some people thrive on low-fat diets, others do best on low-carb diets. Still others succeed with gluten-free diets or Paleo diets or periodic fasts or ketogenic diets or other options on the seemingly endless menu of weight-loss plans. Most studies comparing diets have produced results like Dr. Gardner’s: no difference © 2018 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 25775 - Posted: 12.11.2018

By Jonathan D. Grinstein It is well known that a high salt diet leads to high blood pressure, a risk factor for an array of health problems, including heart disease and stroke. But over the last decade, studies across human populations have reported the association between salt intake and stroke irrespective of high blood pressure and risk of heart disease, suggesting a missing link between salt intake and brain health. Interestingly, there is a growing body of work showing that there is communication between the gut and brain, now commonly dubbed the gut–brain axis. The disruption of the gut–brain axis contributes to a diverse range of diseases, including Parkinson’s disease and irritable bowel syndrome. Consequently, the developing field of gut–brain axis research is rapidly growing and evolving. Five years ago, a couple of studies showed that high salt intake leads to profound immune changes in the gut, resulting in increased vulnerability of the brain to autoimmunity—when the immune system attacks its own healthy cells and tissues by mistake, suggesting that perhaps the gut can communicate with the brain via immune signaling. Now, new research shows another connection: immune signals sent from the gut can compromise the brain’s blood vessels, leading to deteriorated brain heath and cognitive impairment. Surprisingly, the research unveils a previously undescribed gut–brain connection mediated by the immune system and indicates that excessive salt might negatively impact brain health in humans through impairing the brain’s blood vessels regardless of its effect on blood pressure. © 2018 Scientific American

Related chapters from BN8e: 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: 25754 - Posted: 12.06.2018

Abby Olena Mice with faulty circadian clocks are prone to obesity and diabetes. So are mice fed a diet high in fat. Remarkably, animals that have both of these obesity-driving conditions can stay lean and metabolically healthy by simply limiting the time of day when they eat. In a study published today (August 30) in Cell Metabolism, researchers report that restricting feeding times to mice’s active hours can overcome both defective clock genes and an unhealthy diet, a finding that may have an impact in the clinic. The work corroborates previous research showing how powerful restricted feeding can be to improve clock function, says Kristin Eckel-Mahan, a circadian biologist at the University of Texas Health Science Center at Houston who did not participate in the study. Over the last 20 years, biologists have found circadian clocks keeping physiologic time in almost every organ. They have also shown that mice with disrupted clocks often develop metabolic diseases, such as obesity, and that circadian clock proteins physically bind to the promoters of many metabolic regulators and instruct them when to turn on and off. For Satchidananda Panda of the Salk Institute, these lines of evidence came together in 2009, when his group published a study showing that in mice without the clock component Cryptochrome, feeding and fasting could drive the expression of some, but not all, of the metabolic regulators throughout the body. Other groups have also confirmed that even in the absence of the clock it is still possible to drive some genetic rhythms. In this latest study, he and colleagues wanted to look more closely at how the cycling of clock and metabolic transcripts induced by time-restricted feeding, rather than normal genetic rhythms, influences the health of mice. © 1986 - 2018 The Scientist

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 25711 - Posted: 11.24.2018

Selene Meza-Perez, Troy D. Randall Fat is a loaded tissue. Not only is it considered unsightly, the excess flab that plagues more than two-thirds of adults in America is associated with many well-documented health problems. In fact, obesity (defined as having a body mass index of 30 or more) is a comorbidity for almost every other type of disease. But, demonized as all body fat is, deep belly fat known as visceral adipose tissue (VAT) also has a good side: it’s a critical component of the body’s immune system. VAT is home to many cells of both the innate and adaptive immune systems. These cells influence adipocyte biology and metabolism, and in turn, adipocytes regulate the functions of the immune cells and provide energy for their activities. Moreover, the adipocytes themselves produce antimicrobial peptides, proinflammatory cytokines, and adipokines that together act to combat infection, modify the function of immune cells, and maintain metabolic homeostasis. Unfortunately, obesity disrupts both the endocrine and immune functions of VAT, thereby promoting inflammation and tissue damage that can lead to diabetes or inflammatory bowel disease. As researchers continue to piece together the complex connections between immunity, gut microbes, and adipose tissues, including the large deposit of fat in the abdomen known as the omentum, they hope not only to gain an understanding of how fat and immunity are linked, but to also develop fat-targeted therapeutics that can moderate the consequences of infectious and inflammatory diseases. © 1986 - 2018 The Scientist.

Related chapters from BN8e: 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: 25710 - Posted: 11.24.2018

Abby Olena Anticipating something tasty can lead to a watering mouth and grumbling stomach, but these familiar responses aren’t the only ways the body prepares for nourishment. According to a study published today (November 15) in Cell, sensing food primes mice to process incoming nutrients by directions from the central nervous system to the liver. “It’s a great tour de force combining [several strategies] in one paper to then identify pathways by which food anticipation could alter hepatic metabolism,” says Christoph Buettner, a physician and researcher at Icahn School of Medicine at Mount Sinai in New York who was not involved in the study. “It’s interesting that even before your food hits your tongue or ends up in your stomach, there are changes that prepare an organism for nutrient storage.” Two types of cells in the brain’s hypothalamus have been shown in previous studies to play opposing roles in regulating how much an organism eats. AgRP neurons are turned on when energy stores are low, making an animal seek out food, while POMC neurons, activated when an animal is sated, inhibit eating. Up until a few years ago, the prevailing wisdom was that ingested food resulted in hormonal changes and subsequent neuronal activation after some lag time, says Jens Brüning, an endocrinologist and geneticist at the Max Planck Institute for Metabolism Research in Germany. But in 2015, researchers from the University of California, San Francisco, showed in mice that these neurons change their state of activation nearly instantaneously in response to the sight or smell of food. © 1986 - 2018 The Scientist

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 25709 - Posted: 11.24.2018

By Gina Kolata Whenever I see a photo from the 1960s or 1970s, I am startled. It’s not the clothes. It’s not the hair. It’s the bodies. So many people were skinny. In 1976, 15 percent of American adults were obese. Now the it’s nearly 40 percent. No one really knows why bodies have changed so much. Scientists do a lot of hand-waving about our “obesogenic environment” and point to favorite culprits: the abundance of cheap fast foods and snacks; food companies making products so tasty they are addictive; larger serving sizes; the tendency to graze all day. Whatever the combination of factors at work, something about the environment is making many people as fat as their genetic makeup permits. Obesity has always been with us, but never has it been so common. Everyone — from doctors to drug companies, from public health officials to overweight people themselves — would love to see a cure, a treatment that brings weight to normal and keeps it there. Why hasn’t anyone discovered one? It’s not for lack of trying. Yes, some individuals have managed to go from fat to thin with diets and exercise, and have kept off the weight. But they are the rare exceptions. Most spend years dieting and regaining, dieting and regaining, in a fruitless, frustrating cycle. There is just one almost uniformly effective treatment, and it is woefully underused: only about 1 percent of the 24 million American adults who are eligible get the procedure. That treatment is bariatric surgery, a drastic operation that turns the stomach into a tiny pouch and, in one version, also reroutes the intestines. Most who have it lose significant amounts of weight — but many of them remain overweight, or even obese. Their health usually improves anyway. Many with diabetes no longer need insulin. Cholesterol and blood pressure levels tend to fall. Sleep apnea disappears. Backs, hips and knees stop aching. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 25707 - Posted: 11.21.2018

Nicola Davis Being overweight can cause depression, researchers say, with the effects thought to be largely psychological. While previous studies have found that people who are obese are more likely to have depression, it has been unclear whether that is down to depression driving weight changes or the reverse. Now, in the largest study of its kind, experts say having genetic variants linked to a high body mass index (BMI) can lead to depression, with a stronger effect in women than men. What’s more, they say the research suggests the effect could be down to factors such as body image. “People who are more overweight in a population are more depressed, and that is likely to be at least partly [a] causal effect of BMI [on] depression,” said Prof Tim Frayling, a co-author of the study, from the University of Exeter medical school. Get Society Weekly: our newsletter for public service professionals Read more Writing in the International Journal of Epidemiology, the researchers from the UK and Australia describe how they used data from the UK Biobank, a research endeavour involving 500,000 participants aged between 37 and 73 who were recruited in 2006-10. The researchers looked at 73 genetic variants linked to a high BMI that are also associated with a higher risk of diseases such diabetes and heart disease. They also looked at 14 genetic variants linked to a high percentage of body fat but which were associated with a lower risk of such health problems. While the former group could be linked to depression through biological or psychological mechanisms, the latter would only be expected to have a psychological effect. © 2018 Guardian News and Media Limited

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 25677 - Posted: 11.13.2018

By Kelly Servick SAN DIEGO, CALIFORNIA—We know the menagerie of microbes in the gut has powerful effects on our health. Could some of these same bacteria be making a home in our brains? A poster presented here this week at the annual meeting of the Society for Neuroscience drew attention with high-resolution microscope images of bacteria apparently penetrating and inhabiting the cells of healthy human brains. The work is preliminary, and its authors are careful to note that their tissue samples, collected from cadavers, could have been contaminated. But to many passersby in the exhibit hall, the possibility that bacteria could directly influence processes in the brain—including, perhaps, the course of neurological disease—was exhilarating. “This is the hit of the week,” said neuroscientist Ronald McGregor of the University of California, Los Angeles, who was not involved in the work. “It’s like a whole new molecular factory [in the brain] with its own needs. … This is mind-blowing.” The brain is a protected environment, partially walled off from the contents of the bloodstream by a network of cells that surround its blood vessels. Bacteria and viruses that manage to penetrate this blood-brain barrier can cause life-threatening inflammation. Some research has suggested distant microbes—those living in our gut—might affect mood and behavior and even the risk of neurological disease, but by indirect means. For example, a disruption in the balance of gut microbiomes could increase the production of a rogue protein that may cause Parkinson’s disease if it travels up the nerve connecting the gut to the brain. © 2018 American Association for the Advancement of Science

Related chapters from BN8e: 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: 25664 - Posted: 11.10.2018

/ By Susan D’Agostino I’d had intestinal distress before, but never like this. I was excreting not just waste, but blood and bits of my colon’s lining — up to 30 times per day. My abdominal pain hit deeper and felt less productive than the pain of giving birth, epidural-free, to my second child. Even shingles, which stung like a dental drill against my face, paled in comparison. Such was the agony of Clostridium difficile. Commonly known as C. diff., Clostridium difficile is an antibiotic-resistant superbug carried by approximately 5 percent of the adult population. The harmful gut bacterium is normally kept in check by other, good bacteria in the gut’s microbiome. But when the microbial balance is upset — for example, by a dose of antibiotics — C. diff. can gain a foothold. Left to multiply unchecked, it may kill its human host. In 2013, the Centers for Disease Control and Prevention estimated that 14,000 Americans die each year from C. diff. Thanks to an ill-considered decision by the U.S. Food and Drug Administration, and the willful ignorance of a string of doctors charged with my care, I was nearly one of them. Things started innocently enough. In early 2013, my doctor diagnosed me with a bacterial infection and prescribed an antibiotic. I had lived antibiotic-free for nearly four decades — a streak I was not inclined to break. But my doctor insisted on antibiotics, and I reluctantly complied. Soon after, my stomach turned against me. I went to an emergency room and was sent home with a prescription for vancomycin, an antibiotic reserved for serious bacterial infections. But the drug proved little match for the microbes that had bum-rushed my colon. My weight and fluid loss accelerated. My colon risked perforation. Copyright 2018 Undark

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 25663 - Posted: 11.10.2018

By David Prologo “Exercise isn’t really important for weight loss” has become a popular sentiment in the weight-loss community. “It’s all about diet,” many say. “Don’t worry about exercise so much.” This idea crept out amid infinite theories about dieting and weight loss, and it quickly gained popularity, with one article alone citing 60 studies to support and spread this notion like wildfire. The truth is that you absolutely can — and should — exercise your way to weight loss. So why is anyone saying otherwise? For 10 years, I have been studying the epidemic of failed weight-loss attempts and researching the phenomenon of hundreds of millions of people embarking on weight-loss attempts — then quitting. Meanwhile, exercise remains the most common practice among nationally tracked persons who are able to maintain weight loss over time. Ninety percent of people who lose significant weight and keep it off exercise at least one hour a day, on average. There are a few reasons that exercise for weight loss gets a bad rap. First, the public is looking, in large part, for a quick fix — and the diet and weight-loss industry exploits this consumer desire for an immediate solution. Many studies have shown that exercise changes your body’s composition, improves your resting metabolism and alters your food preferences. These plain and simple facts have stood the test of time, but go largely unnoticed compared to most sensationalized diet products (change through exercise over time is a much tougher sell than a five-day “cleanse”). Moreover, many people consider one hour a day for exercise to be unreasonable or undoable, and find themselves looking elsewhere for an easier fix. © 1996-2018 The Washington Post

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 25645 - Posted: 11.05.2018

Sukanya Charuchandra L. Wu et al., “Human ApoE isoforms differentially modulate brain glucose and ketone body metabolism: Implications for Alzheimer’s disease risk reduction and early intervention,” J Neurosci, 38:6665­–81, 2018. Humans carry three different isoforms of the ApoE gene, which affects Alzheimer’s risk. Liqin Zhao of the University of Kansas and her colleagues previously found that the gene plays a role in brain metabolism when expressed in mice; in a new study, they looked for the pathways involved. LEAVING AN IMPRESSION Zhao’s team engineered female mice to express the human versions of either ApoE2, ApoE3, or ApoE4, and analyzed expression of 43 genes involved in energy metabolism in their cortical tissue. BLOCKADE Mice with ApoE2 showed higher levels of proteins needed for glucose uptake and metabolism in their brains relative to animals harboring the most common isoform in humans, ApoE3. Mice with ApoE4 had lower levels of such proteins. The brain tissue’s glucose transport efficiency also varied across the genotypes, and levels of a key glucose-metabolizing enzyme, hexokinase, were reduced in ApoE4 brains. However, ApoE2 and ApoE4 brains contained similar levels of proteins involved in using ketone bodies, a secondary source of energy, while ApoE3 brains had lower levels of those proteins. “Brain glycolytic function may serve as a significant mechanism underlying the differential impact of ApoE genotypes,” Zhao says. © 1986 - 2018 The Scientist.

Related chapters from BN8e: 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: 25613 - Posted: 10.25.2018

Laura Sanders Researchers have found a new link between gut and brain. By signaling to nerve cells in the brain, certain microbes in the gut slow a fruit fly’s walking pace, scientists report. Fruit flies missing those microbes — and that signal — turn into hyperactive speed walkers. With the normal suite of gut microbes, Drosophila melanogaster fruit flies on foot cover an average of about 2.4 millimeters a second. But fruit flies without any gut microbes zip along at about 3.5 millimeters a second, Catherine Schretter, a biologist at Caltech, and her colleagues report October 24 in Nature. These flies with missing microbes also take shorter breaks and are more active during the day. “Our work suggests that microbes assist in maintaining a certain level of locomotion,” Schretter says. An enzyme made by Lactobacillus brevis bacteria normally serves as the brakes, the researchers found. When researchers supplied the enzyme, called xylose isomerase, to flies lacking bacteria, the flies began walking at a slower, more normal pace. Xylose isomerase acts on a sugar that’s thought to influence nerve cells in fruit flies’ brains that control walking. For still mysterious reasons, the bacterial influence on walking speed occurred only in female fruit flies, not males. Studying that difference will be “a very interesting potential direction for this work,” Schretter says. |© Society for Science & the Public 2000 - 2018

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 25612 - Posted: 10.25.2018

Ashley P. Taylor The activity in a cortical area involved in self-regulation was the best correlate of weight loss in a study published today (October 18) in Cell Metabolism. Previously, scientists thought that challenges to losing weight stemmed from imbalances between the hormones leptin, which produces a feeling of satiety, and ghrelin, which stimulates hunger. When people go on a diet, ghrelin levels go up and leptin levels go down. To see how brain activity fits into dieting physiology, Alain Dagher, a neurologist at McGill University, worked with 24 overweight and obese people who were starting a 1,200-calories-per-day diet at a weight-loss clinic. Before starting the regimen, participants had fMRIs—imaging scans that show brain activity—while looking at pictures of either appetizing, sometimes high-calorie food, or of scenery. The researchers repeated the scans one month and three months into the diet. Typically, food pictures activate the ventral medial prefrontal cortex, linked to desire, motivation, and value, Dagher says in a press release. Further, this region stimulates hunger when the body is burning more calories than it’s taking in, Dagher tells HealthDay. Over the course of the study, the ventral medial prefrontal cortex responded less and less to the pictures of food, but the decline in activity was greatest in people who lost the most weight, Dagher says in the release. On the other hand, activity in the lateral prefrontal cortex, involved in self-regulation, increased over the course of the diet, and the more it was active, the more weight people lost. © 1986 - 2018 The Scientist

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 25593 - Posted: 10.20.2018

Researchers say they have discovered a gene mutation that slows the metabolism of sugar in the gut, giving people who have the mutation a distinct advantage over those who do not. Those with the mutation have a lower risk of diabetes, obesity, heart failure, and even death. The researchers say their finding could provide the basis for drug therapies that could mimic the workings of this gene mutation, offering a potential benefit for the millions of people who suffer with diabetes, heart disease, and obesity. The study, which is largely supported by the National Heart, Lung, and Blood Institute (NHLBI), part of the National Institutes of Health, appears in the Journal of the American College of Cardiology (link is external). “We’re excited about this study because it helps clarify the link between what we eat, what we absorb, and our risk for disease. Knowing this opens the door to improved therapies for cardiometabolic disease,” said Scott D. Solomon, M.D., a professor of medicine at Harvard Medical School and a senior physician at Brigham and Women’s Hospital in Boston, who led the research. He explained that the study is the first to fully evaluate the link between mutations in the gene mainly responsible for absorbing glucose in the gut — SGLT-1, or sodium glucose co-transporter-1 — and cardiometabolic disease. People who have the natural gene mutation appear to have an advantage when it comes to diet, Solomon noted. Those who eat a high-carbohydrate diet and have this mutation will absorb less glucose than those without the mutation. A high-carbohydrate diet includes such foods as pasta, breads, cookies, and sugar-sweetened beverages.

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 25555 - Posted: 10.10.2018

Selene Meza-Perez, Troy D. Randall Fat is a loaded tissue. Not only is it considered unsightly, the excess flab that plagues more than two-thirds of adults in America is associated with many well-documented health problems. In fact, obesity (defined as having a body mass index of 30 or more) is a comorbidity for almost every other type of disease. But, demonized as all body fat is, deep belly fat known as visceral adipose tissue (VAT) also has a good side: it’s a critical component of the body’s immune system. VAT is home to many cells of both the innate and adaptive immune systems. These cells influence adipocyte biology and metabolism, and in turn, adipocytes regulate the functions of the immune cells and provide energy for their activities. Moreover, the adipocytes themselves produce antimicrobial peptides, proinflammatory cytokines, and adipokines that together act to combat infection, modify the function of immune cells, and maintain metabolic homeostasis. Unfortunately, obesity disrupts both the endocrine and immune functions of VAT, thereby promoting inflammation and tissue damage that can lead to diabetes or inflammatory bowel disease. As researchers continue to piece together the complex connections between immunity, gut microbes, and adipose tissues, including the large deposit of fat in the abdomen known as the omentum, they hope not only to gain an understanding of how fat and immunity are linked, but to also develop fat-targeted therapeutics that can moderate the consequences of infectious and inflammatory diseases. © 1986 - 2018 The Scientist

Related chapters from BN8e: 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: 25536 - Posted: 10.06.2018

By Gretchen Reynolds Are we born to be physically lazy? A sophisticated if disconcerting new neurological study suggests that we probably are. It finds that even when people know that exercise is desirable and plan to work out, certain electrical signals within their brains may be nudging them toward being sedentary. The study’s authors hope, though, that learning how our minds may undermine our exercise intentions could give us renewed motivation to move. Exercise physiologists, psychologists and practitioners have long been flummoxed by the difference between people’s plans and desires to be physically active and their actual behavior, which usually involves doing the opposite. Few of us exercise regularly, even though we know that it is important for health and well being. Typically, we blame lack of time, facilities or ability. But recently an international group of researchers began to wonder whether part of the cause might lie deeper, in how we think. For an earlier review, these scientists had examined past research about exercise attitudes and behavior and found that much of it showed that people sincerely wished to be active. In computer-based studies, for example, they would direct their attention to images of physical activity and away from images related to sitting and similar languor. But, as the scientists knew, few people followed through on their aims to be active. So maybe, the scientists thought, something was going on inside their skulls that dampened their enthusiasm for exercise. To find out, they recruited 29 healthy young men and women. All of the volunteers told the scientists that they wanted to be physically active, although only a few of them regularly were. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 5: The Sensorimotor System
Link ID: 25526 - Posted: 10.04.2018

By Diana Kwon How do we decide what we like to eat? Although tasty foods typically top the list, a number of studies suggest preferences about consumption go beyond palatability. Scientists have found both humans and animals can form choices about what to consume based on the caloric content of food, independent of taste. Research spanning many decades has shown nutrients in the gastrointestinal tract can shape animals’ flavor preferences. One of the earliest findings of this effect dates back to the 1960s, when Garvin Holman of the University of Washington reported hungry rats preferred consuming a liquid paired with food injected into the stomach rather than a solution coupled with a gastric infusion of water. More recently Ivan de Araujo, a neuroscientist at the Icahn School of Medicine at Mount Sinai, and his colleagues have shown calories can trump palatability: Their work has demonstrated mice prefer consuming bitter solutions paired with a sugar infusion injected in the gut rather than a calorie-free sweet solution. Advertisement For years De Araujo and his group have been working to tease apart how the contents of the gut produce pleasure in the brain. In mice they have found sugar in the digestive tract can activate the brain’s reward centers. In animals bred without the ability to taste sweetness, sugary snacks still triggered activity in the ventral striatum, a brain region involved in reward processing. But according to De Araujo, the specific pathway that relayed signals between the gut and the brain remained a mystery. © 2018 Scientific American

Related chapters from BN8e: 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: 25523 - Posted: 10.03.2018