Chapter 9. Homeostasis: Active Regulation of the Internal Environment
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Laura Sanders Faced with a shortage of the essential nutrient selenium, the brain and the testes duke it out. In selenium-depleted male mice, testes hog the trace element, leaving the brain in the lurch, scientists report in the Nov. 18 Journal of Neuroscience. The results are some of the first to show competition between two organs for trace nutrients, says analytical neurochemist Dominic Hare of the University of Technology Sydney and the Florey Institute of Neuroscience and Mental Health in Melbourne. In addition to uncovering this brain-testes scuffle, the study “highlights that selenium in the brain is something we can’t continue to ignore,” he says. About two dozen proteins in the body contain selenium, a nonmetallic chemical element. Some of these proteins are antioxidants that keep harmful molecules called free radicals from causing trouble. Male mice without enough selenium have brain abnormalities that lead to movement problems and seizures, neuroscientist Matthew Pitts of the University of Hawaii at Manoa and colleagues found. In some experiments, Pitts and his colleagues depleted selenium by interfering with genes. Male mice engineered to lack two genes that produce proteins required for the body to properly use selenium had trouble balancing on a rotating rod and moving in an open field. In their brains, a particular group of nerve cells called parvalbumin interneurons didn’t mature normally. © Society for Science & the Public 2000 - 2015.
Link ID: 21640 - Posted: 11.18.2015
Sarah Schwartz With outposts in nearly every organ and a direct line into the brain stem, the vagus nerve is the nervous system’s superhighway. About 80 percent of its nerve fibers — or four of its five “lanes” — drive information from the body to the brain. Its fifth lane runs in the opposite direction, shuttling signals from the brain throughout the body. Doctors have long exploited the nerve’s influence on the brain to combat epilepsy and depression. Electrical stimulation of the vagus through a surgically implanted device has already been approved by the U.S. Food and Drug Administration as a therapy for patients who don’t get relief from existing treatments. Now, researchers are taking a closer look at the nerve to see if stimulating its fibers can improve treatments for rheumatoid arthritis,heart failure, diabetes and even intractable hiccups. In one recent study, vagus stimulation made damaged hearts beat more regularly and pump blood more efficiently. Researchers are now testing new tools to replace implants with external zappers that stimulate the nerve through the skin. But there’s a lot left to learn. While studies continue to explore its broad potential, much about the vagus remains a mystery. In some cases, it’s not yet clear exactly how the nerve exerts its influence. And researchers are still figuring out where and how to best apply electricity. © Society for Science & the Public 2000 - 2015.
Link ID: 21633 - Posted: 11.14.2015
A single variation in the gene for brain-derived neurotropic factor (BDNF) may influence obesity in children and adults, according to a new study funded by the National Institutes of Health. The study suggests that a less common version of the BDNF gene may predispose people to obesity by producing lower levels of BDNF protein, a regulator of appetite, in the brain. The authors propose that boosting BDNF protein levels may offer a therapeutic strategy for people with the genetic variation, which tends to occur more frequently in African Americans and Hispanics, than in non-Hispanic Caucasians. The study is published in the journal Cell Reports. Obesity in children and adults is a serious issue in the United States, contributing to health conditions such as heart disease, stroke and type 2 diabetes. Importantly, genetic factors can predispose a person to obesity, as well as influence the effectiveness of weight-loss strategies. The body relies on cells to process and store energy, and changes in genes that regulate these functions can cause an imbalance that leads to excessive energy storage and weight gain. “The BDNF gene has previously been linked to obesity, and scientists have been working for several years to understand how changes in this particular gene may predispose people to obesity,” said Jack A. Yanovski, M.D., Ph.D., one of the study authors and an investigator at NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD). “This study explains how a single genetic change in BDNF influences obesity and may affect BDNF protein levels. Finding people with specific causes of obesity may allow us to evaluate effective, more-personalized treatments.”
Heidi Ledford An analysis of 53 weight-loss studies that included more than 68,000 people has concluded that, despite their popularity, low-fat diets are no more effective than higher-fat diets for long-term weight loss. And overall, neither type of diet works particularly well. A year after their diets started, participants in the 53 studies were, on average, only about 5 kilograms (11 pounds) lighter. “That’s not that impressive,” says Kevin Hall, a physiologist at the US National Institute of Diabetes and Digestive and Kidney Diseases in Bethesda, Maryland. “All of these prescriptions for dieting seem to be relatively ineffective in the long term.” The study, published in The Lancet Diabetes and Endocrinology, runs counter to decades' worth of medical advice and adds to a growing consensus that the widespread push for low-fat diets was misguided. Nature looks at why low-fat diets were so popular and what diet doctors might prescribe next. Are the new findings a surprise? The advantages of low-fat diets have long been in question. “For decades we’ve been touting low-fat diets as the way to lose weight, but obesity has gone up,” says Deirdre Tobias, lead author of the study and an epidemiologist at Brigham and Women’s Hospital in Boston, Massachusetts. “It seemed evident that low-fat diets may not be the way to go.” © 2015 Nature Publishing Group,
Link ID: 21584 - Posted: 10.31.2015
By Jan Hoffman As the first semester of the school year reaches the halfway mark, countless college freshmen are becoming aware that their clothes are feeling rather snug. While the so-called freshman 15 may be hyperbole, studies confirm that many students do put on five to 10 pounds during that first year away from home. Now new research suggests that an underlying cause for the weight gain may be the students’ widely vacillating patterns of sleep. A study in the journal Behavioral Sleep Medicine looked at the sleep habits of first-semester freshmen. Researchers followed 132 first-year students at Brown University who kept daily sleep diaries. After nine weeks, more than half of them had gained nearly six pounds. There are many poor sleep habits that might have exacerbated their weight gains, a growing body of research indicates. Was it abbreviated sleep? Optimally, experts say, teenagers need about nine hours and 15 minutes a night. These freshmen averaged about seven hours and 15 minutes. In a study earlier this year, in the journal PLOS One, researchers found that when teenagers are sleep-deprived, they more readily reach for candy and desserts. Or were the Brown students’ late bedtimes the scale-tipping factor? On average, they went to bed around 1:30 a.m. A study this month in the journal Sleep that followed teenagers into adulthood found that each hour later bedtime was pushed during the school or workweek was associated with about a two-point increase in body mass index. While both the amount of sleep and the lateness of bedtime may have played a role, the researchers in the Brown study identified a new sleep factor for predicting weight gain: variability, or the extent to which a student’s bedtime and waking time changed daily. © 2015 The New York Times Company
By ALEX HUTCHINSON WHEN marketing researchers at the University of Pennsylvania’s Wharton School rigged shopping carts at a major East Coast supermarket with motion-tracking radio-frequency tags, they unwittingly stumbled on a metaphor for our path through the aisles of life. Route data from more than 1,000 shoppers, matched to their purchases at checkout, revealed a clear pattern: Drop a bunch of kale into your cart and you’re more likely to head next to the ice cream or beer section. The more “virtuous” products you have in your basket, the stronger your temptation to succumb to vice. Such hedonic balancing acts are neither unpredictable — who, after all, hasn’t rewarded themselves with a piece of cake or an extra beer after a killer workout? — nor inherently bad. But an emerging body of research into what psychologists call the “licensing effect” suggests that this tit-for-tat tendency is deeply wired in us, operating even when we’re not aware of it. And in a world where we’re bombarded by pitches for an endless array of health-boosting products of dubious efficacy, that can be a problem. The key insight underlying the licensing effect, which was first described in 2006 by Uzma Khan, then a professor of marketing at Carnegie Mellon University, and Ravi Dhar of the Yale School of Management, is that our choices are contingent: Since we each have a fairly stable self-concept of how good/bad, healthy/unhealthy or selfish/altruistic we are, when one decision swings too far from this self-concept, we automatically take action to balance it out. © 2015 The New York Times Company
By Carrie Arnold Most of the anorexia patients Dr. Joanna Steinglass sees in the inpatient eating-disorders unit at the New York State Psychiatric Institute have been to treatment before. While in the hospital or a residential treatment center, they generally gained weight and began to eat a wider variety of foods. But after they left, their old anorexic habits returned. They began skipping meals again or returning to their extreme exercise routines. All too soon, it seemed, the gains made in treatment and the hope for recovery that went along with it began to evaporate. According to the conventional wisdom around eating disorders, these relapses were really a misguided search for control. Or maybe the patients just weren’t ready for recovery yet. Or perhaps these were signs of self-control gone awry, spurred on by friends who marvel at their seemingly endless willpower. Interesting theories, and yet Steinglass disagreed. “Even when people show up at our hospital and want to make changes, they find it tough,” she said. Now a new study in Nature Neuroscience — which Steinglass co-authored — reveals why people with anorexia often struggle so much to integrate new ways of eating into their lives. In the brain, the behaviors associated with anorexia act a lot like habits, those daily decisions we make without thinking. And habits, according to both the scientific evidence and the colloquial wisdom, are phenomenally difficult to break. This new finding helps explain why anorexia has historically been so hard to treat: Anorexic patients are essentially fighting their own brains in an uphill battle for wellness. But more important, the new research may also point toward new and better ways to help those with the eating disorder overcome it. © 2015, New York Media LLC.
Keyword: Anorexia & Bulimia
Link ID: 21560 - Posted: 10.24.2015
By Tara Parker-Pope Children who regularly use antibiotics gain weight faster than those who have never taken the drugs, according to new research that suggests childhood antibiotics may have a lasting effect on body weight well into adulthood. The study, published in the International Journal of Obesity, examined the electronic medical records of 163,820 children ages 3 to 18, counting antibiotic prescriptions, body weight and height. The records, which covered pediatric exams from 2001 through 2012, showed that one in five — over 30,000 children — had been prescribed antibiotics seven or more times. By the time those children reached age 15, they weighed, on average, about 3 pounds more than children who had received no antibiotics. While earlier studies have suggested a link between antibiotics and childhood weight gain, they typically have relied on a mother’s memories of her child’s antibiotic use. The new research is significant because it’s based on documented use of antibiotics in a child’s medical record. “Not only did antibiotics contribute to weight gain at all ages, but the contribution of antibiotics to weight gain gets stronger as you get older,” said Dr. Brian S. Schwartz, the first author and a professor in the department of environmental health sciences at the Johns Hopkins Bloomberg School of Public Health. Scientists have known for years that antibiotic use promotes weight gain in livestock, which is why large food producers include low doses of antibiotics in the diets of their animals. © 2015 The New York Times Company
By LISA SANDERS, M.D. The middle-aged couple knocked at the door of the townhouse. When no one answered, the woman took her key and let them in. She called her daughter’s name as she hurried through the rooms. They had been trying to reach their 27-year-old daughter by phone all day, and she hadn’t answered. They found her upstairs, lying in bed and mumbling incoherently. The mother rushed over, but her daughter showed no signs of recognition. She and her husband quickly carried her to the car. Four months before, the mother told the emergency-room doctor at SSM Health St. Mary’s Hospital in St. Louis, her daughter had a procedure called gastric-sleeve surgery to help her lose weight. She came home after just a couple of days and felt great. She looked bright and eager. Once she started to eat, though, nausea and vomiting set in. After almost every meal, she would throw up. It’s an unusual but well-known complication of this kind of surgery. The cause is not clearly understood, but the phenomenon is sometimes linked to reflux. The surgeon tried different medications to stop the nausea and vomiting and to reduce the acid in her stomach, but they didn’t help. She had the surgery in order to lose weight, but now she was losing weight too quickly. After a month of vomiting, her doctors thought maybe she had developed gallstones — a common problem after rapid weight loss. But even after her gallbladder was removed, the young woman continued to vomit after eating. © 2015 The New York Times Company
Susan Gaidos CHICAGO — Eating a high-fat diet as a youngster can affect learning and memory during adulthood, studies have shown. But new findings suggest such diets may not have long-lasting effects. Rats fed a high-fat diet for nearly a year recovered their ability to navigate their surroundings. University of Texas at Dallas neuroscientist Erica Underwood tested spatial memory for rats fed a high-fat diet for either 12 weeks or 52 weeks, immediately after weaning. After rats placed in a chamber-filled box containing Lego-like toys became familiar with the box, the researchers moved the toys to new chambers. Later, when placed in the box, rats who ate high-fat foods for 12 weeks appeared confused and had difficulty finding the toys. But rats that ate high-fat foods for nearly a year performed as well as those fed a normal diet. Underwood repeated the experiment, posing additional spatial memory tests to new groups of rats. The findings were the same: Over the long-term, rats on high-fat diets recovered their ability to learn and remember. Studies of brain cells revealed that rats on the long-term high-fat diet showed reduced excitability in nerve cells from the hippocampus, the same detrimental effects seen in rats on the short-term high-fat diet. “The physiology that should create a dumber animal is there, but not the behavior,” said Lucien Thompson of UT Dallas, who oversaw the study. Underwood and Thompson speculate that some other part of the brain may be compensating for this reduction in neural response. © Society for Science & the Public 2000 - 2015.
Peter Andrey Smith Nearly a year has passed since Rebecca Knickmeyer first met the participants in her latest study on brain development. Knickmeyer, a neuroscientist at the University of North Carolina School of Medicine in Chapel Hill, expects to see how 30 newborns have grown into crawling, inquisitive one-year-olds, using a battery of behavioural and temperament tests. In one test, a child's mother might disappear from the testing suite and then reappear with a stranger. Another ratchets up the weirdness with some Halloween masks. Then, if all goes well, the kids should nap peacefully as a noisy magnetic resonance imaging machine scans their brains. “We try to be prepared for everything,” Knickmeyer says. “We know exactly what to do if kids make a break for the door.” Knickmeyer is excited to see something else from the children — their faecal microbiota, the array of bacteria, viruses and other microbes that inhabit their guts. Her project (affectionately known as 'the poop study') is part of a small but growing effort by neuroscientists to see whether the microbes that colonize the gut in infancy can alter brain development. The project comes at a crucial juncture. A growing body of data, mostly from animals raised in sterile, germ-free conditions, shows that microbes in the gut influence behaviour and can alter brain physiology and neurochemistry. © 2015 Nature Publishing Group
By ERICA GOODE Women who suffer from anorexia are often thought of as having an extraordinary degree of self-control, even if that discipline is used self-destructively. But a new study suggests that the extreme dieting characteristic of anorexia may instead be well-entrenched habit — behavior governed by brain processes that, once set in motion, are inflexible and slow to change. The study’s findings may help explain why the eating disorder, which has the highest mortality rate of any mental illness, is so stubbornly difficult to treat. But they also add to increasing evidence that the brain circuits involved in habitual behavior play a role in disorders where people persist in making self-destructive choices no matter the consequences, like cocaine addiction or compulsive gambling. In the case of anorexia, therapists often feel helpless to interrupt the relentless dieting that anorexic patients pursue. Even when patients say they want to recover, they often continue to eat only low-fat, low-calorie foods. Neither psychiatric medications nor talk therapies that are used successfully for other eating disorders are much help in most cases. And research suggests that 50 percent or more of hospitalized anorexic patients who are discharged at a normal weight will relapse within a year. “The thing about people with anorexia nervosa is that they can’t stop,” said Dr. Joanna E. Steinglass, an associate professor in clinical psychiatry at the New York State Psychiatric Institute at Columbia University Medical Center and a co-author of the new study, which appears in the journal Nature Neuroscience. “They come into treatment saying they want to get better, and they can’t do it,” Dr. Steinglass added. Karin Foerde, a research scientist at the psychiatric institute and Columbia, was the lead author on the study. © 2015 The New York Times Company
By Nicholas Bakalar There may be a link between later bedtimes and weight gain, new research suggests. Researchers studied 3,342 adolescents starting in 1996, following them through 2009. At three points over the years, all reported their normal bedtimes, as well as information on fast food consumption, exercise and television time. The scientists calculated body mass index at each interview. After controlling for age, sex, race, ethnicity and socioeconomic status, the researchers found that each hour later bedtime during the school or workweek was associated with about a two-point increase in B.M.I. The effect was apparent even among people who got a full eight hours of sleep, and neither TV time nor exercise contributed to the effect. But fast food consumption did. The study, in the October issue of Sleep, raises questions, said the lead author, Lauren D. Asarnow, a graduate student at the University of California, Berkeley. “First, what is driving this relationship?” she said. “Is it metabolic changes that happen when you stay up late? And second, if we change sleep patterns, can we change eating behavior and the course of weight change?” The scientists acknowledge that their study had limitations. Their sleep data depended on self-reports, and they did not have complete diet information. Also, they had no data on waist circumference, which, unlike B.M.I., can help distinguish between lean muscle and abdominal fat. © 2015 The New York Times Company
By Kelly Servick Children born to obese mothers arrive already predisposed to obesity and other health problems themselves. Exactly what happens in the uterus to transmit this risk still isn’t clear, but a new study on mice points to the placenta as a key actor. The study shows that a hormone acting on the placenta can protect the offspring of obese mice from being born overweight. It suggests ways to break the cycle of obesity in humans—although other researchers caution there's a long way to go. Researchers discovered decades ago that conditions in the uterus can “program” a fetus to be more susceptible to certain health problems. People conceived during the 1944 famine in the Netherlands, for example, suffered higher rates of cardiovascular disease, diabetes, cancer, and other problems later in life. Recent animal studies suggest that malnourishment in the womb changes the expression of DNA in ways that can be passed down for generations. But researchers are now increasingly concerned with the opposite problem. Obese women tend to give birth to larger babies with more body fat, and these children are more likely to develop metabolic syndrome—the cluster of conditions including obesity and high blood sugar that can lead to diabetes and heart disease. To probe the roots of fetal “overgrowth,” developmental biologists at the University of Colorado, Denver, looked to the placenta—the whoopee cushion–shaped organ wedged between the fetus and the wall of the uterus, where branching arteries from the umbilical cord take up oxygen and nutrients from the mother’s blood vessels. The placenta “has always been viewed as a passive organ—whatever happens to the mother is translated toward the fetus,” says lead author Irving Aye, now at the University of Cambridge in the United Kingdom. However, recent research has shown that the placenta is less an indiscriminate drainpipe than a subtle gatekeeper. © 2015 American Association for the Advancement of Science.
by Bethany Brookshire Last weekend, I ran the Navy-Air Force half-marathon. After pounding pavement for an hour or so, my legs began to feel light. Slightly numb. I felt fantastic. I had to remind myself to run, not to stop and dance, and that singing along to my candy-pop workout music — even at mile 10 — is not socially acceptable. It’s the hope of this euphoria — this runner’s high — that keeps me running. We’re not totally sure what’s responsible for this incredible high. Some studies call out our body’s endorphins. Others point to cannabinoids — chemicals related to the active compound in marijuana. A new study suggests that the appetite hormone leptin may play a role in getting us going. And from an evolutionary perspective, it makes good sense. When our dinner might make a quick getaway, it’s important to link our drive to run with our need to feed. But it’s probably not the whole story. Like many other neurobiological events, the exact recipe for runner’s high is complex and hazy. It takes a whole suite of chemicals to help us get started and to make sure we want to go the distance. Those who get runner’s high know it when they feel it. But a clinical definition is a little more slippery. “I remember someone saying the runner’s high was the moment when the body was disconnected from the brain,” says Francis Chaouloff, who studies running and motivation in mice at the French Institute of Health and Medical Research in Bordeaux. This sense of extreme euphoria, he says, is generally limited to people running or exercising for long periods of time, over many miles or hours. © Society for Science & the Public 2000 - 2015.
By Sarah C. P. Williams When the human body needs extra energy, the brain tells fat cells to release their stores. Now, for the first time, researchers have visualized the nerves that carry those messages from brain to fat tissue. The activation of these nerves in mice, they found, helps the rodents lose weight—an observation that could lead to new slimming treatments for obese people. “The methods used here are really novel and exciting,” says neuroendocrinologist Heike Muenzberg-Gruening of Louisiana State University’s Pennington Biomedical Research Center in Baton Rouge, who was not involved in the new study. “Their work has implications for obesity research and also for studying these nerves in other tissues.” Diagrams of the chatter between the brain and fat tissues have long included two-way arrows: Fat cells produce the hormone leptin, which travels to the brain to lower appetite and boost metabolism. In turn, the brain sends signals to the fat cells when it’s time to break down their deposits of fatty molecules, such as lipids, into energy. Researchers hypothesized that there must be a set of nerve cells that hook up to traditional fat tissue to carry these messages, but they’d never been able to indisputably see or characterize them. Now they have. Thanks to two forms of microscopy, neurobiologist Ana Domingos, of the Instituto Gulbenkian de Ciência in Oeiras, Portugal, produced images showing bundles of nerves clearly enveloping fat cells in mice. She and her colleagues went on to show, using various stains, that the nerves were a type belonging to the sympathetic nervous system that stretches outward from the spinal cord and keeps the body’s systems in balance. © 2015 American Association for the Advancement of Science
Link ID: 21448 - Posted: 09.26.2015
By Sarah C. P. Williams Immune cells are usually described as soldiers fighting invading viruses and bacteria. But they may also be waging another battle: the war against fat. When mice lack a specific type of immune cell, researchers have discovered, they become obese and show signs of high blood pressure, high cholesterol, and diabetes. The findings have yet to be replicated in humans, but they are already helping scientists understand the triggers of metabolic syndrome, a cluster of conditions associated with obesity. The new study “definitely moves the field forward,” says immunologist Vishwa Deep Dixit of the Yale School of Medicine, who was not involved in the work. “The data seem really solid.” Scientists already know that there is a correlation between inflammation—a heightened immune response—and obesity. But because fat cells themselves can produce inflammatory molecules, distinguishing whether the inflammation causes weight gain or is just a side effect has been tricky. When he stumbled on this new cellular link between obesity and the immune system, immunologist Yair Reisner of the Weizmann Institute of Science in Rehovot, Israel, was studying something completely different: autoimmune diseases. An immune molecule called perforin had already been shown to kill diseased cells by boring a hole in their outer membrane. Reisner’s group suspected that dendritic cells containing perforin might also be destroying the body’s own cells in some autoimmune diseases. To test the idea, Reisner and his colleagues engineered mice to lack perforin-wielding dendritic cells, and then waited to see whether they developed any autoimmune conditions. © 2015 American Association for the Advancement of Science
Eating two and a half times more than you should will leave you overweight and prone to type 2 diabetes, although no one is entirely sure why. Now a team that fed volunteers a whopping 6000 calories a day have found some clues. Obesity is only one problem caused by eating too much. An overly large food intake can also increase a person’s risk of diabetes, heart disease and some cancers, but no one is sure why this should be the case. Resistance to the hormone insulin seems to play a role. When a healthy person eats a meal, their blood glucose levels rise, and the body responds by making insulin. This hormone prompts the body to store un-needed glucose, but people who develop insulin resistance are not able to absorb excess glucose in the same way. This means that, after eating, their blood glucose levels remain high, and over time, this can damage the kidneys, nervous system and heart, for example. Guenther Boden and Salim Merali at Temple University, Philadelphia, and their team set out to investigate how overeating might lead to insulin resistance. They fed six healthy male volunteers 6000 calories’ worth of food every day for a week – around two and a half times what they should have been eating. “It was a regular, American diet, composed of pizzas, hamburgers and that sort of thing,” says Merali. Each volunteer stayed at a hospital for the duration of the experiment, where they were bed-bound, carefully monitored and prevented from doing any sort of exercise. © Copyright Reed Business Information Ltd.
Link ID: 21400 - Posted: 09.12.2015
By Nicholas Bakalar Being obese at age 50 may be tied to an increased risk of developing Alzheimer’s disease at a younger age. Previous studies have shown that being overweight at midlife is associated with an increased risk of developing Alzheimer’s. Now researchers have found that it also predicts occurrence at a younger age. Scientists studied 1,394 cognitively normal people, average age around 60, following them for an average of 14 years. During the study, 142 developed Alzheimer’s. After controlling for age, race, level of education and cardiovascular risk factors, they found that each unit increase in B.M.I., or body mass index, at age 50 was associated with a 6.7-month decrease in the age of onset of Alzheimer’s. The study, in Molecular Psychiatry, also found an association of higher B.M.I. with larger deposits of neurofibrillary tangles on autopsy, one of the characteristics of brain damage in Alzheimer’s disease. “Age of onset is not as well studied as risk,” said the senior author, Dr. Madhav Thambisetty, a neurologist at the National Institute on Aging. “As we try to cure Alzheimer’s disease, we also want to delay the onset of symptoms. Until we know what factors accelerate onset, we won’t be able to test any potential interventions. And that is perhaps as important as the search for treatment.” © 2015 The New York Times Company
by Bethany Brookshire You’ve already had a muffin. And a half. You know you’re full. But there they are, fluffy and delicious, waiting for the passersby in the office. Just thinking about them makes your mouth water. Maybe if you just slice one into quarters. I mean, that barely counts… And then we give in, our brains overriding our body’s better judgment. When I catch myself once again polishing off a whole plate of baked goods, I wish that there was something I could do, some little pill I could take that would make that last delicious bite look — and taste — a little less appealing. But the more scientists learn about the human body, the more they come to understand that there is no one set of hormones for hungry, with a separate set that kicks off your ice cream binge. Instead, our guts and their hormones are firmly entwined with our feelings of reward and motivation. That close relationship shows just how important it is to our bodies to keep us fed, and how hard it is to stop us from overeating. Researchers have long divided our feeding behavior into two distinct categories. One, the homeostatic portion, is primarily concerned with making sure we’ve got enough energy to keep going and is localized to the lateral hypothalamus in the brain. The reward-related, or “hedonic,” component is centralized in the mesolimbic dopamine system, areas of the brain usually referenced when we talk about the effects of sex, drugs and rock ’n’ roll. © Society for Science & the Public 2000 - 2015