1. Study suggests anorexia nervosa has a genetic basis

    June 24, 2017 by Ashley

    From the Medical University of Vienna press release:

    A large-scale, international whole-genome analysis has now revealed for the first time that anorexia nervosa is associated with genetic anomalies on chromosome 12. This finding might lead to new, interdisciplinary approaches to its treatment. The study was led by the University of North Carolina and has been published in the American Journal of Psychiatry. Child and adolescent psychiatrist Andreas Karwautz from MedUni Vienna’s Department of Child and Adolescent Psychiatry was responsible for the Austrian contribution.

    There are currently around 7,500 adolescents in Austria suffering from anorexia nervosa. Girls make up around 95% of those suffering from this serious and protracted disease, which leads to serious health problems due to excessive weight loss. The disease is currently curable in 80% of cases but is still associated with an annual mortality rate of 0.5%. At the present time, the Department of Child and Adolescent Psychiatry at MedUni Vienna is treating around 70 seriously ill adolescents, both as in-patients and out-patients.

    Although we already knew from genetic tests on monozygotic twins that genes are approximately 60% responsible for the development of anorexia nervosa, we did not know with any certainty which gene loci were involved. A study initiated by the US University of North Carolina has now been conducted worldwide, involving 220 researchers in international medical centres analysing the genetic material of 3,500 anorexics. It was found that, compared with the control group of 11,000 people, anorexics had a significant locus on chromosome 12 that contributes towards an elevated risk of developing anorexia nervosa.

    The researchers also explored whether there was any correlation with other disorders. This revealed that the significant locus lies on chromosome 12, in a region associated with Type I diabetes and autoimmune disorders, as well as insulin metabolism. Moreover, genetic correlations were found between anorexia nervosa, neuroticism and schizophrenia, supporting the idea that anorexia is a psychiatric illness.

    Child and adolescent psychiatrist Karwautz regards the findings of this study as significant proof that, in addition to the psychosocial component, biological factors also play an extremely important role in the onset of anorexia nervosa. This has huge implications in terms of improving treatment. Says Karwautz: “Such studies form a basis for providing patients and their relatives with a logical and realistic explanation for this persistent disorder, which is the third commonest disorder in this adolescent age group. Prevention programmes will also benefit from these new findings.”


  2. A flip switch for binge-eating?

    June 8, 2017 by Ashley

    From the American Association for the Advancement of Science press release:

    Researchers have identified a subgroup of neurons in the mouse brain that, upon activation, immediately prompt binge-like eating. Furthermore, repeated stimulation of these neurons over time caused the mice to gain weight. The zona incerta (ZI) is a relatively understudied part of the brain.

    Intriguingly, patients receiving deep brain stimulation of the subthalamus, which includes the ZI, for the treatment of movement disorders can exhibit characteristics of binge eating. To explore this phenomenon in greater detail, Xiaobing Zhang and Anthony N. van den Pol optogenetically labelled GABA neurons in the ZIs of mice.

    They found that stimulating ZI GABA neurons with axons extending into the paraventricular thalamus (PVT) prompted immediate binge-like eating, just two to three seconds after stimulation. Within ten minutes of continuous ZI GABA stimulation, mice rapidly consumed 35% of their daily high-fat food store, meant to be eaten over a 24-hour period.

    The researchers also found that ghrelin, a hormone that signals a reduced energy state in the gut, excited ZI GABA neurons. Upon stimulating the subgroup of ZI neurons for five minutes every three hours over a period of two weeks, the mice significantly increased their food intake, and gained weight.

    Yet, once photostimulation was over, the mice showed a significantly reduced food intake compared with that of controls.

    Lastly, the authors found that stimulation of excitatory axons from the parasubthalamic nucleus to PVT or direct stimulation of glutamate neurons in the PVT reduced food intake.


  3. Prenatal stress predisposes female mice to binge eating

    June 1, 2017 by Ashley

    From the Cell Press press release:

    Stress changes our eating habits, but the mechanism may not be purely psychological, research in mice suggests. A study published May 30 in Cell Metabolism found that stressed mouse mothers were more likely to give birth to pups that would go on to exhibit binge-eating-like behavior later in life. The female mouse pups from stressed mothers shared epigenetic tags on their DNA, but these epigenetic markers only made a difference when the researchers put the young offspring into a stressful situation. Furthermore, the researchers were able to prevent their binge eating by putting the young mice on a diet with “balanced” levels of nutrients such as Vitamin B12 and folate.

    Previous studies have found an epidemiological link between binge eating and traumatic or stressful events during early life, but untangling the biology behind that correlation has proved difficult. “Here we established a model where we can actually show that early life stress increases the likelihood of binge eating in females,” says senior co-author Alon Chen, a neurobiologist at the Weizmann Institute in Israel and the Max Planck Institute of Psychiatry in Munich, Germany. “The second thing that is really interesting is that prenatal stress is causing an epigenetic signature in the embryo’s brain,” says Mariana Schroeder, the postdoctoral fellow that led this study.

    To test the impact of prenatal stress, the researchers genetically engineered a line of mice, where the brain circuit responsible for releasing cortisol and other stress hormones could be manipulated. Many different systems within the brain contribute to “stress,” but the researchers wanted to be able to zero in on one specific neuroendocrine circuit — called the corticotropin-releasing factor (CRF) system — to see if it had an effect. In humans, high levels of CRF activity have been linked to increased anxiety, suppressed appetite, and inflammation, all of which can take a long-term toll.

    When these mice became pregnant, the researchers activated the CRF system during their “third trimester” in order to kick the stress circuit into high gear. Their goal was to simulate chronic CRF stress in isolation, but because being handled by humans usually causes all of a mouse’s stress circuits to kick in, they developed a CRF-triggering technique with minimal intervention. “We didn’t actually handle the mice at all; we just changed the water that included the genetic trigger in the third trimester,” Chen says. Handling the mice is usually a source of stress.

    They found that female pups from these stressed mice exhibited epigenetic markers in tissue from their hypothalami. However, the presence of epigenetic methyl tags alone was not enough to cause binge eating. The mouse pups’ tendency to binge only surfaced when they were placed in a stressful situation where the researchers restricted their access to food. The mice on the “limited access” diet could eat as much this very rewarding food as they wanted, but they only had access to food for 2-hour windows three times per week, prompting some mice to eat excessively large amounts of food very quickly during the meal windows.

    Interestingly, all 10 of the female mice that were subjected to the restricted feeding scenario exhibited a binge-eating phenotype. The researchers used an equal number of female offspring from the stressed out mothers that were not subjected to the restricted feeding schedule as a control. If the same pathways are involved in human eating disorders, it could partly explain why women diagnosed with eating disorders outnumber their male counterparts.

    The chemicals that cells use to epigenetically annotate their genes come from food sources. In this case, the epigenetic marker was a methyl tag, and the cell grabs methyl groups from vitamins such as B12 and folate for epigenetic tagging, so the researchers decided to test what would happen if they adjusted the levels of methyl-donating vitamins in the mice’s diet. The genetically predisposed mice on the methyl-balanced diet did not exhibit the binge-eating-like behavior, suggesting that non-invasive dietary interventions may be able to prevent binge eating.

    However, the researchers emphasize that this is a pre-clinical study in mice. We don’t know yet what a methyl-balanced diet for humans would look like or whether it would even have an effect on human eating disorders. “We found a balance, but it might not be the relevant balance for humans. This is something that needs to be tested,” says Chen.

    Chen hopes that this work will help researchers understand the neurobiology behind eating disorders. “The general public is less aware of the fact that we are dealing with a very biological mechanism that changes a person. People say, ‘Oh, it’s only in the brain.’ And yes, it’s in the brain. It involves changes in your genes, in your epigenome, and your brain circuits.”

    All of this underscores the importance of avoiding stressful situations as much as possible during pregnancy. “We all know this, but people ignore it for various social or economic reasons,” says Chen. “But the price we pay later in life — whether it’s psychiatric disorders, metabolic syndromes, or heart-related illnesses — is heavily impacted by the way your brain was programmed early in life.”


  4. Parents’ use of emotional feeding increases emotional eating in school-age children

    May 6, 2017 by Ashley

    From the Society for Research in Child Development press release:

    Emotional eating — eating when you feel sad or upset or in response to another negative mood — is not uncommon in children and adolescents, but why youth eat emotionally has been unclear. Now a new longitudinal study from Norway has found that school-age children whose parents fed them more to soothe their negative feelings were more likely to eat emotionally later on. The reverse was also found to be the case, with parents of children who were more easily soothed by food being more likely to feed them for emotional reasons.

    The findings come from researchers at the Norwegian University of Science and Technology, King’s College London, University College London, and the University of Leeds. They appear in the journal Child Development.

    Understanding where emotional eating comes from is important because such behavior can increase the risk for being overweight and developing eating disorders,” according to the study’s lead author, Silje Steinsbekk, associate professor of psychology at the Norwegian University of Science and Technology. “If we can find out what influences the development of emotional eating in young children, parents can be given helpful advice about how to prevent it.”

    When children eat to soothe their negative feelings, their food tends to be high in calories (e.g., sweets) so they consume more calories. If they emotionally overeat often, they are also more likely to be overweight. Emotional eating is also tied to the development of later eating disorders (e.g., bulimia and binge eating). This study sought to determine why children eat emotionally and is the first research to consider the issue in school-age children.

    Researchers examined emotional feeding and eating in a representative group of 801 Norwegian 4-year-olds, looking at these issues again at ages 6, 8, and 10. They sought to determine whether parents involved in the study (mostly mothers) shaped their children’s later behavior by offering food to make them feel better when they were upset (emotional feeding), and whether parents whose children were easily soothed by food (those who calmed when given food) were more likely to offer them more food for comfort at a subsequent time. Parents were asked to complete questionnaires describing their children’s emotional eating and temperament (how easily they became upset, how well they could control their emotions), as well as their own emotional feeding. Approximately 65% of the children displayed some emotional eating.

    The study found that young children whose parents offered them food for comfort at ages 4 and 6 had more emotional eating at ages 8 and 10. But the reverse was also true: Parents whose children were more easily comforted with food were more likely to offer them food to soothe them (i.e., to engage in emotional feeding). Thus, emotional feeding increased emotional eating, and emotional eating increased emotional feeding. The findings held even after accounting for children’s body-mass index and initial levels of feeding and eating.

    Moreover, higher levels of negative affectivity (i.e., becoming angry or upset more easily) at age 4 increased children’s risk for emotional eating and feeding at age 6. And this contributed to the bidirectional relation between emotional feeding and emotional eating.

    “We know that children who are more easily upset and have more difficulty controlling their emotions are more likely to eat emotionally than calmer children, perhaps because they experience more negative emotions and eating helps them calm down,” notes Lars Wichstrøm, professor of psychology at the Norwegian University of Science and Technology, who coauthored the study. “Our research adds to this knowledge by showing that children who are more easily upset are at highest risk for becoming emotional eaters.”

    The authors suggest that instead of offering children food to soothe them when they are sad or upset, parents and other caregivers try to calm youngsters by talking, offering a hug, or soothing in ways that don’t involve food. “Food may work to calm a child, but the downside is teaching children to rely on food to deal with negative emotions, which can have negative consequences in the long run,” adds Steinsbekk.

    The authors caution that because the study was conducted in Norway, which has a relatively homogenous and well-educated population, the findings should not be generalized to more diverse populations or to cultures with other feeding and eating practices without further study.


  5. Identifying children at risk of eating disorders is key to saving lives

    January 6, 2017 by Ashley

    From the Newcastle University media release:

    Spotting eating disorder symptoms in children as young as nine years old will allow medics to intervene early and save lives, experts say.

    A team from Newcastle University has identified that girls and boys with more eating disorder symptoms at age nine also had a higher number of symptoms at age 12.

    A new study published in the academic journal, Appetite, reveals the need to treat eating disorder problems as early as possible to help prevent children developing the life-threatening illness.

    The six-year study identified three areas that parents, teachers and doctors should be alert to when looking to detect and help youngsters at risk of the mental health problem.

    These factors are: boys and girls with body dissatisfaction, girls with depressive symptoms, and boys and girls who have had symptoms at an earlier stage.

    It is believed that this research will help pave the way for early interventions to help young patients deal with their eating disorder.

    Dr Elizabeth Evans, Research Associate at Newcastle University’s Institute of Health and Society, led the study.

    She said: “This research was not about investigating eating disorders themselves, rather we investigated risk factors for developing early eating disorder symptoms.

    “Most previous work on children and young adolescents has only looked at the symptoms at one point in time so cannot tell which factors precede others.

    “Our research has been different in that we have specifically focused on the factors linked with the development of eating disorder symptoms to identify children at the greatest risk.

    Results suggest the need to detect eating disorder symptoms early, since a higher level of symptoms at nine years old was the strongest risk factor for a higher level of symptoms at 12 years old.”

    Eating disorders are rare at age nine (1.64 per 100,000) but more prevalent at age 12 (9.51 per 100,000). The most common age for hospitalisation is 15 years old for both boys and girls.

    Many more children have symptoms but do not develop a full eating disorder. Symptoms can include rigid dieting, binge-eating, making oneself sick after eating, and high levels of anxiety about being fat or gaining weight. Eating disorders are serious and can be fatal.

    For the research, children from a birth cohort, the Gateshead Millennium Study, completed questionnaires about eating disorder symptoms, depressive feelings and body dissatisfaction when they were seven, nine and 12.

    The North East has the highest rate of eating disorder hospital admissions in the UK, at approximately six per 100,000. Many more sufferers are treated as outpatients.

    The research highlights that some risk factors precede the symptoms of the condition and others occur at the same time.

    At age 12, boys and girls who are more dissatisfied with their bodies have greater numbers of eating disorder symptoms. Body dissatisfaction is an important indicator of increased risk of the condition.

    Girls with depressive symptoms at 12 years old also have greater numbers of eating disorder symptoms. This relationship was not seen in boys.

    The study is being followed up by repeating the questionnaires with the same cohort of children at 15 years old. This will allow researchers to assess what happened next for the youngsters with greater numbers of eating disorders at age 12.

    Dr Evans said: “Future studies we do will investigate if our findings with young adolescents hold true for older adolescents, or whether we detect new risk factors.

    “Both possibilities will further inform our efforts to promote and target early prevention for eating disorders.”

     


  6. No sweet surrender: Glucose actually enhances self-control, study shows

    June 7, 2016 by Ashley

    From the Taylor & Francis media release:

    blueberries blackberriesIn the age of the ‘sugar tax’, good news about glucose is hard to come by. But an Australian scientist has just proposed a new understanding of the established link between the sweet stuff and improved .

    As Neil Levy, from Macquarie University, explains in the journal Philosophical Psychology, the current ‘ego depletion’ model of the link between glucose and self-control holds that self-control is a depletable resource. Or put another way, glucose is the fuel for the engine of self-control.

    But Dr Levy isn’t convinced. After examining all the available evidence, he proposes a rival ‘opportunity costs’ model. Glucose isn’t a ‘fuel’ to support self-control, he suggests, but a signal of environmental quality. He explains that, “a resource-poor environment is one in which it is relatively urgent to pursue shorter-sooner rewards; a resource-rich environment is one in which there is little urgency.”

    [Glucose] is a signal that the environment is such that there is relatively less urgency to pursue [smaller sooner] rewards, and that strategies aimed at securing [larger later] rewards are likely to be relatively more successful.” As Levy explains, when people in a resource-rich environment are less sensitive to ‘competing rewards’, they tend to work longer at tasks for which the payoff or reward is delayed: the very definition of self-control.

    “The opportunity costs of allocating attentional and cognitive resources … to a particular task are relatively low; therefore, the subject persists longer or performs better at the task,” he writes. “The subject persists longer because the subject continues to deploy resources without shifting them; the subject performs better because the subject allocates proportionally more resources to the task, as a consequence of not needing to devote resources to scouring for competing opportunities.” Despite his commitment to his theory, Levy acknowledges that glucose might only be one signal of environmental richness. “Any cue that signals a lack of urgency to pursue immediate reward should be expected to have the same effect,” he observes.

    It’s also unlikely that sensing glucose alone would be enough for the body to change its strategy; it may be the case that the body picks up on glucose only when other signals of poverty, conflict or instability are absent. “It is not glucose per se that constitutes the signal: it is glucose correlated with the absence of cues indicating the need to pursue it immediately,” he concludes.

    Dr Levy acknowledges that his theory needs further exploration — but when the experiments involve glucose, he’s unlikely to have any shortage of volunteers.

     


  7. Overeating and depressed? There’s a connection, and maybe a solution

    January 8, 2016 by Ashley

    From the Yale University media release:

    midnight snackChronic overeating and stress are tied to an increased risk of depression and anxiety, and in a new study, Yale researchers explain why that happens and suggest a possible solution.

    The researchers report that the anesthetic ketamine reverses depression-like symptoms in rats fed a high-fat diet in a similar way it combats depression and synaptic damage of chronic stress in people.

    The effects of a high-fat diet overlap with those of chronic stress and could also be a contributing factor in depression as well as metabolic disorders such as Type 2 diabetes,” said Ronald Duman, the Elizabeth Mears and House Jameson Professor of Psychiatry, professor of neurobiology, and senior author of the paper published in the journal Neuropharmacology.

    Scientists at Yale have shown that ketamine, also known as “Special K” and abused as a recreational drug, can quickly and dramatically reduce symptoms of chronic depression in patients who are resistant to typical antidepressant agents. Subsequent research showed that ketamine activates the mTORC pathway, which regulates the synthesis of proteins involved in creation of synaptic connections in the brain that are damaged by stress and depression.

    The pathway is also involved in cellular responses to energy and metabolism, and people with metabolic disorders like Type 2 diabetes are also at higher risk of depression. A Yale team headed by lead author Sophie Dutheil in Duman’s lab decided to explore whether diet might influence behavior of rats fed six times the normal amount of fat. They found that after four months of the diet, pathways involved with both synaptic plasticity and metabolism were disrupted, and the rats exhibited signs of depression and anxiety.

    They also found that a single low dose of ketamine reversed those symptoms quickly, and reversed the disruption of mTORC signaling pathways.

    Duman cautioned that the effects of ketamine on metabolism need more research and its proper dosage and use for depression are still a subject of clinical trials.

     


  8. Have an apple-shaped body? You may be more susceptible to binge eating

    November 20, 2015 by Ashley

    From the Drexel University media release:

    healthy_decisionsWomen with apple-shaped bodies — those who store more of their fat in their trunk and abdominal regions — may be at particular risk for the development of eating episodes during which they experience a sense of “loss of control,” according to a new study from Drexel University.

    The study also found that women with greater fat stores in their midsections reported being less satisfied with their bodies, which may contribute to loss-of-control eating.

    This study marks the first investigation of the connections between fat distribution, body image disturbance and the development of disordered eating.

    Eating disorders that are detected early are much more likely to be successfully treated. Although existing eating disorder risk models comprehensively address psychological factors, we know of very few biologically-based factors that help us predict who may be more likely to develop eating disorder behaviors,” said lead author Laura Berner, PhD, who completed the research while pursuing a doctoral degree at Drexel.

    “Our preliminary findings reveal that centralized fat distribution may be an important risk factor for the development of eating disturbance, specifically for loss-of-control eating,” said Berner. “This suggests that targeting individuals who store more of their fat in the midsection and adapting psychological interventions to focus specifically on body fat distribution could be beneficial for preventing eating disorders.”

    The study, titled “Examination of Central Body Fat Deposition as a Risk Factor for Loss-of-Control Eating,” was published in the American Journal of Clinical Nutrition.

    Berner is now a postdoctoral research fellow at the Eating Disorders Center for Treatment and Research at UC San Diego Health. Michael R. Lowe, PhD, a professor in Drexel’s College of Arts and Sciences, was a co-author, along with Danielle Arigo, PhD, who was a postdoctoral research fellow at Drexel and is now an assistant professor of psychology at the University of Scranton; Laurel Mayer, MD, associate professor of clinical psychiatry at the Columbia University College of Physicians and Surgeons and the New York State Psychiatric Institute; and David B. Sarwer, PhD, professor of psychology in Psychiatry and Surgery at the Perelman School of Medicine at the University of Pennsylvania as well as director of clinical services at the Center for Weight and Eating Disorders.

    Mounting evidence suggests that experiencing a sense of loss-of-control during eating — feeling driven or compelled to keep eating or that stopping once one has started is difficult — is the most significant element of binge-eating episodes regardless of how much food is consumed, according to the researchers.

    “This sense of loss of control is experienced across a range of eating disorder diagnoses: bulimia nervosa, binge eating disorder and the binge-eating/purging subtype of anorexia nervosa,” said Berner. “We wanted to see if a measurable biological characteristic could help predict who goes on to develop this feeling, as research shows that individuals who feel this sense of loss of control over eating but don’t yet have an eating disorder are more likely to develop one.”

    Using a large dataset that followed female college freshman for two years, the researchers preliminarily investigated whether body fat distribution is linked to body dissatisfaction over time and increases risk for the development or worsening of loss-of-control eating.

    The nearly 300 young adult women completed assessments at baseline, six months and 24 months, that looked at height, weight and total body fat percentage and where it’s distributed. Participants, none of whom met the diagnostic criteria for eating disorders at the start of the study, were assessed for disordered eating behaviors through standardized clinical interviews in which experiences of sense of loss of control were self-reported.

    In this sample, the researchers found that women with greater central fat stores, independent of total body mass and depression levels, were more likely to develop loss-of-control eating and demonstrated steadier increases in loss-of-control eating episode frequency over time. Women with a larger percentage of their body fat stored in the trunk region were also less satisfied with their bodies, regardless of their total weight or depression level.

    The findings indicate that storage of body fat in trunk and abdominal regions, rather than elsewhere in the body, is more strongly predictive of loss-of-control eating development and worsening over time, and that larger percentages of fat stored in these central regions and body dissatisfaction may serve as maintenance or exacerbation for loss-of-control eating.

    “Our results suggest that centralized fat deposition increased disordered eating risk above and beyond other known risk factors,” said Berner. “The specificity of our findings to centralized fat deposition was also surprising. For example, a one-unit increase in the percentage of body fat stored in the abdominal region was associated with a 53 percent increase in the risk of developing loss-of-control eating over the next two years, whereas total percentage body fat did not predict loss-of-control eating development.”

    According to Berner, more research is needed to explain the mechanism behind these findings, though she speculates that there are a number of reasons why this might happen.

    “It’s possible that this kind of fat distribution is not only psychologically distressing, but biologically influential through, for example, alterations in hunger and satiety signaling,” she said. “Fat cells release signals to the brain that influence how hungry or satiated we feel. Our study didn’t include hormone assays, so we can’t know for sure, but in theory it’s possible that if a centralized distribution of fat alters the hunger and satiety messages it sends, it could make a person feel out of control while eating.”

    The findings may apply to other disordered eating behaviors beyond loss-of-control eating, but more research is needed. “Body fat distribution hasn’t been studied in disorders characterized by binge-eating behaviors as much as it has in anorexia nervosa,” said Berner. “The participants in our sample didn’t develop eating disorder diagnoses within the two year period that we studied them, but this study suggests that future research should investigate whether individuals with greater central fat stores are more likely to develop bulimia nervosa and binge eating disorder.”

     


  9. Scientists unravel brain circuits involved in cravings

    November 13, 2015 by Ashley

    From the Dartmouth College media release:

    mind mazeDartmouth researchers studying rats have discovered that activation of designer neural receptors can suppress cravings in a brain region involved in triggering those cravings.

    The study is the first to systematically show how designer brain receptors and designer drugs work together to change how cues for food stimulate motivation. The findings, which may help scientists to fight addiction, overeating and other habitual behavior in humans, appear in the European Journal of Neuroscience.

    In everyday life, we are bombarded with advertisements, or cues, that garner our attention and trigger us into purchasing products, or rewards. Consequently, these reward-paired cues can become attractive themselves. For example McDonald’s golden arches can produce cravings for fast food even though you haven’t seen the food or aren’t even hungry. Scientists study this phenomenon using sign-tracking, or autoshaping, an experimental conditioning in which the reward is given regardless of the subject’s behavior.

    “Although we have a sense of what brain circuits mediate reward, less is known about the neural circuitry underlying the transfer of value to cues associated with rewards,” says lead author Stephen Chang, a postdoctoral fellow. “We were primarily interested in whether the ventral pallidum, a brain region implicated in processing reward, is also involved in sign-tracking.”

    Previously, it was impossible to inactivate brain areas like this repeatedly and temporarily to study how cues become valuable in themselves. But it is now possible with a new technology called DREADDs (designer receptors exclusively activated by designer drugs). Your brain cells are loaded with natural receptors, or molecules like jigsaw puzzles that are activated when another molecule arrives that fits like a missing piece. But DREADDs are engineered receptors introduced into neurons using viruses. Injection of a synthetic drug can activate these receptors, thus shutting down the neurons as a sort of remote control.

    This technology allowed the Dartmouth researchers to inactivate the ventral pallidum repeatedly and temporarily during tests in which a lever was inserted into the experimental chamber for 10 seconds, followed by a food pellet reward when the lever was withdrawn. Even though the food was delivered regardless of the rats’ behavior, the rats pressed and bit the lever as if it were the reward itself. The results showed that activating DREADDs in the ventral pallidum before each training session blocked that behavior. In addition, recordings of individual neurons in the ventral pallidum following DREADD activation showed that ventral pallidum activity can become suppressed or excited to varying speeds and amounts.

    “These results are the first to show that the ventral pallidum is necessary for the attribution of value to cues that are paired with rewards,” Chang says. “This is surprising because the ventral pallidum was historically considered to be just an area for expressing motivations in behavior. In terms of clinical applications, the results carry the potential for stripping away value from reward-paired cues in cases such as addiction. The ventral pallidum is a novel target for such work.”


  10. Teasing girls about weight is more than a playground joke, study finds

    by Ashley

    From the University of Houston media release:

    girls_bulliesCurrent research about childhood obesity has illustrated the complexity of the epidemic–how it intertwines with hunger, poverty, food deserts and socioeconomic status.

    A new University of Houston study examined a practice that may seem like a harmless playground antic, but could have long-lasting and harmful effects to a young girl’s perception of herself and of food.

    Professor Norma Olvera, health educator with the UH College of Education, examined the impact of teasing on minority, adolescent girls, specifically as predictors of disordered eating behaviors. Olvera said there are two reasons to pursue this kind of research.

    “First because Hispanic and African-American girls are at a higher risk of obesity, which may increase their desire to be thinner and lead them to engage in unhealthy eating behaviors,” she said. “Secondly, there is not a lot of research that explores these issues in minority girls.”

    Olvera’s study surveyed 135 girls who were all about 11-years-old. All the girls had high body fat; 81 percent were considered obese. Almost all the girls indicated they were unhappy with their body size, wishing they were thinner than their perceived size. When teasing was added to this climate about body size and weight, Olvera said, it sparked unhealthy, or what she called “disordered” eating behaviors.

    “Weight status may be a more sensitive issue for children who are overweight or obese, and being teased about it may elicit a stronger response from them as opposed to children who are not overweight or obese,” she said.

    Her findings are published in the Journal of Early Adolescence.

    The girls answered questions about peer-weight teasing at the hands of boys and girls. They also discussed their response to the teasing.

    Fifty-two percent of respondents indicated they had been teased about their weight by girls. Sixty percent had been teased by boys. Some of the teasing came from siblings.

    Olvera said the girls became at risk of developing disordered eating behaviors in order to control their weight and avoid the psychological disturbances and stigma of being overweight. Seventy percent of the girls reported implementing weight-control behaviors, such as cutting back or skipping meals, dieting or starving themselves in order to be thinner. Twelve percent said they engaged in binge and purge behaviors (feeling unable to stop eating followed by forcing themselves to throw up) in order to lose weight. Thirty-three percent said they engaged in emotional eating (eating more or less because they felt bored or upset) because of being teased about their weight.

    “Results from this study may guide health educators and practitioners to design interventions to teach coping strategies to these children to help them deal with peer-weight teasing,” Olvera said. “The findings also support social policies of no tolerance of weight-related teasing particularly in school settings.”

    Olvera is a fellow of The Obesity Society, which is dedicated to expanding research, preventions and treatment of obesity. She also is the founder and director of the BOUNCE program (Behavior Opportunities Uniting Nutrition Counseling and Education), a summer program for minority, adolescent girls to empower them and their families to adopt health lifestyles and positive self-esteem.