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Author (up) Alcock, J.; Maley, C.C.; Aktipis, C.A. file  url
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  Title Is eating behavior manipulated by the gastrointestinal microbiota? Evolutionary pressures and potential mechanisms Type Journal Article
  Year 2014 Publication BioEssays : News and Reviews in Molecular, Cellular and Developmental Biology Abbreviated Journal Bioessays  
  Volume 36 Issue 10 Pages 940-949  
  Keywords Animals; *Biological Evolution; *Feeding Behavior; Gastrointestinal Tract/*microbiology; Humans; *Microbiota; Models, Biological; Obesity/etiology; Cravings; Evolutionary conflict; Host manipulation; Microbiome; Obesity  
  Abstract Microbes in the gastrointestinal tract are under selective pressure to manipulate host eating behavior to increase their fitness, sometimes at the expense of host fitness. Microbes may do this through two potential strategies: (i) generating cravings for foods that they specialize on or foods that suppress their competitors, or (ii) inducing dysphoria until we eat foods that enhance their fitness. We review several potential mechanisms for microbial control over eating behavior including microbial influence on reward and satiety pathways, production of toxins that alter mood, changes to receptors including taste receptors, and hijacking of the vagus nerve, the neural axis between the gut and the brain. We also review the evidence for alternative explanations for cravings and unhealthy eating behavior. Because microbiota are easily manipulatable by prebiotics, probiotics, antibiotics, fecal transplants, and dietary changes, altering our microbiota offers a tractable approach to otherwise intractable problems of obesity and unhealthy eating.  
  Call Number Serial 2002  
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Author (up) Backberg, M.; Meister, B. file  url
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  Title Abnormal cholinergic and GABAergic vascular innervation in the hypothalamic arcuate nucleus of obese tub/tub mice Type Journal Article
  Year 2004 Publication Synapse (New York, N.Y.) Abbreviated Journal Synapse  
  Volume 52 Issue 4 Pages 245-257  
  Keywords Acetylcholine/*metabolism; Adaptor Proteins, Signal Transducing; Animals; Arcuate Nucleus of Hypothalamus/blood supply/*metabolism; Blood Vessels/innervation; Carrier Proteins/metabolism; Glutamate Decarboxylase/metabolism; Immunohistochemistry; *Membrane Transport Proteins; Mice; Mutation; Obesity/*physiopathology; Polymerase Chain Reaction; Presynaptic Terminals/metabolism; Proteins/*genetics; Synaptophysin/metabolism; Vesicular Acetylcholine Transport Proteins; *Vesicular Transport Proteins; gamma-Aminobutyric Acid/*metabolism  
  Abstract Tubby and tubby-like proteins (TULPs) are encoded by members of a small gene family. An autosomal recessive mutation in the mouse tub gene leads to blindness, deafness, and maturity-onset obesity. The mechanisms by which the mutation causes the obesity syndrome has not been established. We compared obese tub/tub mice and their lean littermates in order to find abnormalities within the mediobasal hypothalamus, a region intimately associated with the regulation of body weight. Using an antiserum to the vesicular acetylcholine transporter (VAChT), a marker for cholinergic neurons, many unusually large VAChT-immunoreactive (-ir) nerve terminals, identified by colocalization with the synaptic vesicle protein synaptophysin, were demonstrated in the hypothalamic arcuate nucleus of obese tub/tub mice. Double-labeling showed that VAChT-ir nerve endings also contained glutamic acid decarboxylase (GAD), a marker for gamma-aminobutyric acid (GABA) neurons. The VAChT- and GAD-ir nerve terminals were in close contact with blood vessels, identified with antisera to platelet endothelial cell adhesion molecule-1 (PECAM; also called CD31), laminin, smooth muscle actin (SMA), and glucose transporter-1 (GLUT1). Such large cholinergic and GABAergic nerve terminals surrounding blood vessels were not seen in the arcuate nucleus of lean tub/+ mice. The presence of abnormal cholinergic/GABAergic vascular innervation in the arcuate nucleus suggests that alterations in this region, which contains neurons that receive information from the periphery and which relays information about the energy status to other parts of the brain, may be central in the development of the obese phenotype in animals with an autosomal recessive mutation in the tub gene.  
  Call Number Serial 1460  
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Author (up) Bjork, J.; Albin, M.; Grahn, P.; Jacobsson, H.; Ardo, J.; Wadbro, J.; Ostergren, P.-O.; Skarback, E. file  url
openurl 
  Title Recreational values of the natural environment in relation to neighbourhood satisfaction, physical activity, obesity and wellbeing Type Journal Article
  Year 2008 Publication Journal of Epidemiology & Community Health Abbreviated Journal Journal of Epidemiology & Community Health  
  Volume 62 Issue 4 Pages e2-e2  
  Keywords Recreational values; Physical activity; Obesity; Environment  
  Abstract Objectives: The aim of this population-based study was to investigate associations between recreational values of the close natural environment and neighbourhood satisfaction, physical activity, obesity and wellbeing.

Methods: Data from a large public health survey distributed as a mailed questionnaire in suburban and rural areas of southern Sweden were used (N  =  24 819; 59% participation rate). Geocoded residential addresses and the geographical information system technique were used to assess objectively five recreational values of the close natural environment: serene, wild, lush, spacious and culture.

Results: On average, a citizen of the Scania region, inner city areas excluded, only had access to 0.67 recreational values within 300 metres distance from their residence. The number of recreational values near the residence was strongly associated with neighbourhood satisfaction and physical activity. The effect on satisfaction was especially marked among tenants and the presence of recreational values was associated with low or normal body mass index in this group. A less marked positive association with vitality among women was observed. No evident effect on self-rated health was detectable.

Conclusions: Immediate access to natural environments with high recreational values was rare in the study population and was distributed in an inequitable manner. Moreover, such access was associated with a positive assessment of neighbourhood satisfaction and time spent on physical activity, which can be expected to reduce obesity and increase vitality by having a buffering effect on stress.
 
  Call Number Serial 2130  
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Author (up) Boggiano, M.M.; Wenger, L.E.; Turan, B.; Tatum, M.M.; Morgan, P.R.; Sylvester, M.D. file  url
openurl 
  Title Eating tasty food to cope. Longitudinal association with BMI Type Journal Article
  Year 2015 Publication Appetite Abbreviated Journal Appetite  
  Volume 87 Issue Pages 365-370  
  Keywords *Adaptation, Psychological; Adolescent; Adult; *Body Mass Index; Body Weight; Bulimia/psychology; Cross-Sectional Studies; Eating/*psychology; Emotions; Feeding Behavior/psychology; Female; Humans; Linear Models; Longitudinal Studies; Male; Motivation; Obesity/psychology; Overweight/psychology; Reproducibility of Results; Risk Factors; Self Report; Students; Young Adult; Assessment; Binge-eating; Emotions; Motivation; Obesity; Reward  
  Abstract The goals of this study were to determine if a change in certain motives to eat highly palatable food, as measured by the Palatable Eating Motives Scale (PEMS), could predict a change in body mass index (BMI) over time, to assess the temporal stability of these motive scores, and to test the reliability of previously reported associations between eating tasty foods to cope and BMI. BMI, demographics, and scores on the PEMS and the Binge Eating Scale were obtained from 192 college students. Test-retest analysis was performed on the PEMS motives in groups varying in three gap times between tests. Regression analyses determined what PEMS motives predicted a change in BMI over two years. The results replicated previous findings that eating palatable food for Coping motives (e.g., to forget about problems, reduce negative feelings) is associated with BMI. Test-retest correlations revealed that motive scores, while somewhat stable, can change over time. Importantly, among overweight participants, a change in Coping scores predicted a change in BMI over 2 years, such that a 1-point change in Coping predicted a 1.76 change in BMI (equivalent to a 10.5 lb. change in body weight) independent of age, sex, ethnicity, and initial binge-eating status (Cohen's f(2) effect size = 1.44). The large range in change of Coping scores suggests it is possible to decrease frequency of eating to cope by more than 1 scale point to achieve weight losses greater than 10 lbs. in young overweight adults, a group already at risk for rapid weight gain. Hence, treatments aimed specifically at reducing palatable food intake for coping reasons vs. for social, reward, or conformity reasons, should help achieve a healthier body weight and prevent obesity if this motive-type is identified prior to significant weight gain.  
  Call Number Serial 1202  
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Author (up) Cummings, D.E. file  url
openurl 
  Title Ghrelin and the short- and long-term regulation of appetite and body weight Type Journal Article
  Year 2006 Publication Physiology & Behavior Abbreviated Journal Physiol Behav  
  Volume 89 Issue 1 Pages 71-84  
  Keywords Animals; Appetite/*physiology; Body Weight/*physiology; Energy Metabolism; Ghrelin; Humans; Obesity; Peptide Hormones/*metabolism; Receptors, G-Protein-Coupled/physiology; Receptors, Ghrelin; Time Factors  
  Abstract Ghrelin, an acylated upper gastrointestinal peptide, is the only known orexigenic hormone. Considerable evidence implicates ghrelin in mealtime hunger and meal initiation. Circulating levels decrease with feeding and increase before meals, achieving concentrations sufficient to stimulate hunger and food intake. Preprandial ghrelin surges occur before every meal on various fixed feeding schedules and also among individuals initiating meals voluntarily without time- or food-related cues. Ghrelin injections stimulate food intake rapidly and transiently, primarily by increasing appetitive feeding behaviors and the number of meals. Preprandial ghrelin surges are probably triggered by sympathetic nervous output. Postprandial suppression is not mediated by nutrients in the stomach or duodenum, where most ghrelin is produced. Rather, it results from post-ingestive increases in lower intestinal osmolarity (information probably relayed to the foregut via enteric nervous signaling), as well as from insulin surges. Consequently, ingested lipids suppress ghrelin poorly compared with other macronutrients. Beyond a probable role in meal initiation, ghrelin also fulfills established criteria for an adiposity-related hormone involved in long-term body-weight regulation. Ghrelin levels circulate in relation to energy stores and manifest compensatory changes in response to body-weight alterations. Ghrelin crosses the blood-brain barrier and stimulates food intake by acting on several classical body-weight regulatory centers, including the hypothalamus, hindbrain, and mesolimbic reward system. Chronic ghrelin administration increases body weight via diverse, concerted actions on food intake, energy expenditure, and fuel utilization. Congenital ablation of the ghrelin or ghrelin-receptor gene causes resistance to diet-induced obesity, and pharmacologic ghrelin blockade reduces food intake and body weight. Ghrelin levels are high in Prader-Willi syndrome and low after gastric bypass surgery, possibly contributing to body-weight alterations in these settings. Extant evidence favors roles for ghrelin in both short-term meal initiation and long-term energy homeostasis, making it an attractive target for drugs to treat obesity and/or wasting disorders.  
  Call Number Serial 1442  
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Author (up) Durant, N.H.; Bartman, B.; Person, S.D.; Collins, F.; Austin, S.B. file  url
doi  openurl
  Title Patient provider communication about the health effects of obesity Type Journal Article
  Year 2009 Publication Patient Education and Counseling Abbreviated Journal Patient Educ Couns  
  Volume 75 Issue 1 Pages 53-57  
  Keywords Adolescent; Adult; African Americans; European Continental Ancestry Group; Female; *Health Knowledge, Attitudes, Practice; Hispanic Americans; Humans; Logistic Models; Male; Multivariate Analysis; Obesity/*ethnology/*prevention & control; *Patient Education as Topic; *Professional-Patient Relations; United States  
  Abstract OBJECTIVE: We assessed the influence of race/ethnicity and provider communication on overweight and obese patients' perceptions of the damage weight causes to their health. METHODS: The study included 1071 overweight and obese patients who completed the 2002 Community Health Center (CHC) User survey. We used logistic regression analyses to examine determinants of patients' perceptions of the impact of their weight on their health. Models were adjusted for covariates and weighting was used to account for the sampling design. RESULTS: Forty-one percent of respondents were overweight and 59% were obese. Non-Hispanic Blacks and Hispanics were half as likely as non-Hispanic Whites to believe weight was damaging to their health while controlling for covariates. Overweight/obese CHC patients who were told they were overweight by healthcare providers were almost nine times more likely to perceive that weight was damaging to their health compared to those not told. CONCLUSIONS: We observed large racial/ethnic disparities in the perception that overweight is unhealthy but provider communication may be a powerful tool for helping patients understand that overweight is damaging to health. PRACTICE IMPLICATIONS: Given obesity is a national epidemic, further attention to the role of patient provider communication in illness is essential with important implications for both health professional training and health care provision.  
  Call Number Serial 402  
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Author (up) Fisher, J.O.; Birch, L.L. file  url
openurl 
  Title Restricting access to foods and children's eating Type Journal Article
  Year 1999 Publication Appetite Abbreviated Journal Appetite  
  Volume 32 Issue 3 Pages 405-419  
  Keywords Child Behavior/*psychology; Child, Preschool; Feeding Behavior/*psychology; Female; Food Preferences; Humans; Male; *Mother-Child Relations; Nutritional Requirements; Obesity/psychology; Sex Factors  
  Abstract This study evaluated maternal restriction of children's access to snack foods as a predictor of children's intake of those foods when they were made freely available. In addition, child and parent eating-related “risk” factors were used to predict maternal reports of restricting access. Participants were 71, 3-to-5-year-old children (36 boys, 35 girls) and their parents. Children's snack food intake was measured immediately following a meal, in a setting offering free access to palatable snack foods. Child and maternal reports of restricting children's access to those snack foods were obtained. In addition, information on child and parent adiposity as well as parents' restrained and disinhibited eating was used to examine “risk” factors for restricting access. For girls only, child and maternal reports of restricting access predicted girls' snack food intake, with higher levels of restriction predicting higher levels of snack food intake. Maternal restriction, in turn, was predicted by children's adiposity. Additionally, parents' own restrained eating style predicted maternal restriction of girls' access to snack foods.  
  Call Number Serial 1690  
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Author (up) Gohir, W.; Ratcliffe, E.M.; Sloboda, D.M. file  url
openurl 
  Title Of the bugs that shape us: maternal obesity, the gut microbiome, and long-term disease risk Type Journal Article
  Year 2015 Publication Pediatric Research Abbreviated Journal Pediatr Res  
  Volume 77 Issue 1-2 Pages 196-204  
  Keywords Female; Gastrointestinal Tract/growth & development/*microbiology; Humans; *Maternal Nutritional Physiological Phenomena; *Maternal-Fetal Exchange; *Microbiota; Obesity/*complications/microbiology; Pregnancy; Prenatal Exposure Delayed Effects/immunology/*microbiology; Microbiome  
  Abstract Chronic disease risk is inextricably linked to our early-life environment, where maternal, fetal, and childhood factors predict disease risk later in life. Currently, maternal obesity is a key predictor of childhood obesity and metabolic complications in adulthood. Although the mechanisms are unclear, new and emerging evidence points to our microbiome, where the bacterial composition of the gut modulates the weight gain and altered metabolism that drives obesity. Over the course of pregnancy, maternal bacterial load increases, and gut bacterial diversity changes and is influenced by pre-pregnancy- and pregnancy-related obesity. Alterations in the bacterial composition of the mother have been shown to affect the development and function of the gastrointestinal tract of her offspring. How these microbial shifts influence the maternal-fetal-infant relationship is a topic of hot debate. This paper will review the evidence linking nutrition, maternal obesity, the maternal gut microbiome, and fetal gut development, bringing together clinical observations in humans and experimental data from targeted animal models.  
  Call Number Serial 2080  
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Author (up) Gortmaker, S.L.; Swinburn, B.A.; Levy, D.; Carter, R.; Mabry, P.L.; Finegood, D.T.; Huang, T.; Marsh, T.; Moodie, M.L. file  url
openurl 
  Title Changing the future of obesity: science, policy, and action Type Journal Article
  Year 2011 Publication Lancet (London, England) Abbreviated Journal Lancet  
  Volume 378 Issue 9793 Pages 838-847  
  Keywords Cost-Benefit Analysis; Food Industry; *Government Programs; Health Care Costs; Health Personnel; *Health Policy; *Health Promotion; Humans; International Cooperation; Obesity/economics/*epidemiology/*prevention & control/therapy; United Nations  
  Abstract The global obesity epidemic has been escalating for four decades, yet sustained prevention efforts have barely begun. An emerging science that uses quantitative models has provided key insights into the dynamics of this epidemic, and enabled researchers to combine evidence and to calculate the effect of behaviours, interventions, and policies at several levels--from individual to population. Forecasts suggest that high rates of obesity will affect future population health and economics. Energy gap models have quantified the association of changes in energy intake and expenditure with weight change, and have documented the effect of higher intake on obesity prevalence. Empirical evidence that shows interventions are effective is limited but expanding. We identify several cost-effective policies that governments should prioritise for implementation. Systems science provides a framework for organising the complexity of forces driving the obesity epidemic and has important implications for policy makers. Many parties (such as governments, international organisations, the private sector, and civil society) need to contribute complementary actions in a coordinated approach. Priority actions include policies to improve the food and built environments, cross-cutting actions (such as leadership, healthy public policies, and monitoring), and much greater funding for prevention programmes. Increased investment in population obesity monitoring would improve the accuracy of forecasts and evaluations. The integration of actions within existing systems into both health and non-health sectors (trade, agriculture, transport, urban planning, and development) can greatly increase the influence and sustainability of policies. We call for a sustained worldwide effort to monitor, prevent, and control obesity.  
  Call Number Serial 1274  
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Author (up) Horstmann, A.; Dietrich, A.; Mathar, D.; Possel, M.; Villringer, A.; Neumann, J. file  url
openurl 
  Title Slave to habit? Obesity is associated with decreased behavioural sensitivity to reward devaluation Type Journal Article
  Year 2015 Publication Appetite Abbreviated Journal Appetite  
  Volume 87 Issue Pages 175-183  
  Keywords Adaptation, Physiological; Adult; Body Mass Index; Body Weight; Energy Intake; Feeding Behavior/*psychology; Health Behavior; Humans; Hunger; Hyperphagia/psychology; Linear Models; Male; Models, Biological; Motivation; Obesity/*psychology; *Reward; Satiation; Surveys and Questionnaires; Young Adult; Control of food intake; Devaluation; Goal-directed; Habitual; Obesity; Reward sensitivity  
  Abstract The motivational value of food is lower during satiety compared to fasting. Dynamic changes in motivational value promote food seeking or meal cessation. In obesity this mechanism might be compromised since obese subjects ingest energy beyond homeostatic needs. Thus, lower adaptation of eating behaviour with respect to changes in motivational value might cause food overconsumption in obesity. To test this hypothesis, we implemented a selective satiation procedure to investigate the relationship between obesity and the size of the behavioural devaluation effect in humans. Lean to obese men (mean age 25.9, range 19-30 years; mean BMI 29.1, range 19.2-45.1 kg/m(2)) were trained on a free operant paradigm and learned to associate cues with the possibility to win different food rewards by pressing a button. After the initial training phase, one of the rewards was devalued by consumption. Response rates for and wanting of the different rewards were measured pre and post devaluation. Behavioural sensitivity to reward devaluation, measured as the magnitude of difference between pre and post responses, was regressed against BMI. Results indicate that (1) higher BMI compared to lower BMI in men led to an attenuated behavioural adjustment to reward devaluation, and (2) the decrease in motivational value was associated with the decrease in response rate between pre and post. Change in explicitly reported motivational value, however, was not affected by BMI. Thus, we conclude that high BMI in men is associated with lower behavioural adaptation with respect to changes in motivational value of food, possibly resulting in automatic overeating patterns that are hard to control in daily life.  
  Call Number Serial 1264  
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