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Binge Eating Disorder and genes

G Gervasini, L M Gonzalez, S Mota-Zamorano, C Gamero-Villarroel, J A Carrillo, I Flores, A Garcia-Herraiz
BACKGROUND: Dopamine physiological functions make dopaminergic genes suitable candidates for association studies in eating disorders (ED). A Val158Met polymorphism in the catechol-O-methyltransferase (COMT) gene, which is involved in dopamine degradation, has been studied in relation to ED. OBJECTIVE: We aimed to analyze the association between this polymorphism and general psychopathological symptoms that are often coupled to these disorders. METHOD: A total of 303 ED patients, diagnosed according to DSM-5 criteria, completed the SCL-90R questionnaire and were genotyped for the Val158Met polymorphism...
June 7, 2018: Current Molecular Medicine
Yang Zhang, Yan Sun, Jie Liang, Lin Lu, Jie Shi
Similar symptomatology manifestations and high co-morbidity in substance and non-substance addictions suggest that there may be a common pathogenesis between them. Associated with impulse control and emotional processing, the monoamine neurotransmitter system genes are suggested to be related to both substance and non-substance addictions, such as dopamine (DA) system, 5-hydroxytryptamine/serotonin (5-HT) system, the endogenous opioid system and so on. Here we reviewed the similarities and differences in genetics between classic substance addiction and common types of non-substance addiction, e...
2017: Advances in Experimental Medicine and Biology
Alexandra J Mayhew, Marie Pigeyre, Jennifer Couturier, David Meyre
Eating disorders (ED) including anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED) affect up to 5% of the population in Western countries. Risk factors for developing an ED include personality traits, family environment, gender, age, ethnicity, and culture. Despite being moderately to highly heritable with estimates ranging from 28 to 83%, no genetic risk factors have been conclusively identified. Our objective was to explore evolutionary theories of EDs to provide a new perspective on research into novel biological mechanisms and genetic causes of EDs...
2018: Neuroendocrinology
Michael Lutter, Ethan Bahl, Claire Hannah, Dabney Hofammann, Summer Acevedo, Huxing Cui, Carrie J McAdams, Jacob J Michaelson
OBJECTIVE: Eating disorders develop through a combination of genetic vulnerability and environmental stress, however the genetic basis of this risk is unknown. METHODS: To understand the genetic basis of this risk, we performed whole exome sequencing on 93 unrelated individuals with eating disorders (38 restricted-eating and 55 binge-eating) to identify novel damaging variants. Candidate genes with an excessive burden of predicted damaging variants were then prioritized based upon an unbiased, data-driven bioinformatic analysis...
2017: PloS One
Anjali Chawla, Zachary A Cordner, Gretha Boersma, Timothy H Moran
Binge eating disorder (BED) is defined as recurrent, distressing over-consumption of palatable food (PF) in a short time period. Clinical studies suggest that individuals with BED may have impairments in cognitive processes, executive functioning, impulse control, and decision-making, which may play a role in sustaining binge eating behavior. These clinical reports, however, are limited and often conflicting. In this study, we used a limited access rat model of binge-like behavior in order to further explore the effects of binge eating on cognition...
October 15, 2017: Physiology & Behavior
Nicolas Ramoz, Julia Clarke, Philip Gorwood
Eating disorders (EDs) are complex and multifactorial psychiatric illnesses that induce significant and sustained pathological disruption of food intake. The Diagnostic and Statistical Manual of Mental Illnesses (DSM-5) describes the clinical criteria of major disorders including anorexia nervosa (AN), bulimia nervosa (BN) and binge eating disorder (BED). The neurobiological basis of food intake is well characterized. Epidemiological studies reported a heritability about 70% in AN and 60% in BN, suggesting that genetic factors are involved in the vulnerability to EDs...
2017: Biologie Aujourd'hui
Giovanni Castellini, Marica Franzago, Silvia Bagnoli, Lorenzo Lelli, Michela Balsamo, Milena Mancini, Benedetta Nacmias, Valdo Ricca, Sandro Sorbi, Ivana Antonucci, Liborio Stuppia, Giovanni Stanghellini
Eating Disorders (EDs) show a multifactorial etiopathogenesis including environmental, psychological and biological factors. In the present study, we propose a model of interactions between genetic vulnerability-represented by Fat Mass and Obesity-Associated (FTO) gene-and stable psychopathological traits, such as bodily disorders and emotion dysregulation for EDs patients. The distribution of a polymorphism of the FTO (rs9939609 T>A) was evaluated in a series of 250 EDs patients and in a group of 119 healthy control subjects...
2017: PloS One
Stacey L Kirkpatrick, Lisa R Goldberg, Neema Yazdani, R Keith Babbs, Jiayi Wu, Eric R Reed, David F Jenkins, Amanda F Bolgioni, Kelsey I Landaverde, Kimberly P Luttik, Karen S Mitchell, Vivek Kumar, W Evan Johnson, Megan K Mulligan, Pietro Cottone, Camron D Bryant
BACKGROUND: Eating disorders are lethal and heritable; however, the underlying genetic factors are unknown. Binge eating is a highly heritable trait associated with eating disorders that is comorbid with mood and substance use disorders. Therefore, understanding its genetic basis will inform therapeutic development that could improve several comorbid neuropsychiatric conditions. METHODS: We assessed binge eating in closely related C57BL/6 mouse substrains and in an F2 cross to identify quantitative trait loci associated with binge eating...
May 1, 2017: Biological Psychiatry
Nadia Micali, Marta Crous-Bou, Janet Treasure, Elizabeth A Lawson
This study aimed to investigate associations between oxytocin receptor gene (OXT-R) polymorphisms (rs53576 and rs2254298), their interaction with maternal care (GxE), and ED behaviours in a community sample. We studied 3698 women from the Avon Longitudinal Study of Parents and Children (ALSPAC) who participated in a two-phase prevalence study of lifetime ED and had genotype data. The GG rs53576 genotype was associated with binge eating and purging, and the rs2254298 AG/AA genotype with restrictive eating lifetime...
January 2017: European Eating Disorders Review: the Journal of the Eating Disorders Association
Rebecca L W Corwin, Francis H E Wojnicki, Derek J Zimmer, R Keith Babbs, Lauren E McGrath, Diana R Olivos, Elizabeth G Mietlicki-Baase, Matthew R Hayes
OBJECTIVE: Binge eating is characterized by repeated intermittent bouts of compulsive overconsumption of food. Treatment is challenging given limited understanding of the mechanisms underlying this type of disordered eating. The hypothesis that dysregulation of mesocortical dopaminergic and GABAergic systems underlie binge eating was tested. METHODS: Analysis of gene expression within the ventral tegmental area and its terminal mesocortical regions was examined in bingeing rats before and after bingeing occurred...
October 2016: Obesity
Giovanni Castellini, Lorenzo Lelli, Andrea Tedde, Irene Piaceri, Silvia Bagnoli, Ersilia Lucenteforte, Sandro Sorbi, Alessio Maria Monteleone, James J Hudziak, Benedetta Nacmias, Valdo Ricca
Childhood overweight and the SNP rs41423247 of the glucocorticoid receptor gene (GR) were reported to represent predisposing factors for Eating Disorders (EDs). The distribution of the polymorphism was evaluated in 202 EDs patients, and in 116 healthy subjects. The Structured Clinical Interview for the DSM-IV and self-reported questionnaires were administered at the admission to the clinic and at 3 time points (end of a cognitive behavioral therapy, 3 and 6 years follow up). G-allele was associated with childhood overweight, depressive disorder comorbidity, and diagnostic instability...
September 30, 2016: Psychiatry Research
Chloe Luck, Martha H Vitaterna, Rachel Wevrick
The etiology of abnormal eating behaviors, including binge-eating disorder, is poorly understood. The neural circuits modulating the activities of the neurotransmitters dopamine and serotonin are proposed to be dysfunctional in individuals suffering from eating disorders. Prader-Willi syndrome is a neurodevelopmental disorder that causes extreme food seeking and binge-eating behaviors together with reduced satiety. One of the genes implicated in Prader-Willi syndrome, Magel2, is highly expressed in the regions of the brain that control appetite...
August 2016: Behavioral Neuroscience
Amélie Bonnefond, Ramsi Keller, David Meyre, Fanny Stutzmann, Dorothée Thuillier, Dimitre G Stefanov, Philippe Froguel, Fritz F Horber, John G Kral
OBJECTIVE: Data on the effects of eating behavior and genetics on outcomes of gastrointestinal surgery for diabesity have been sparse, often flawed, and controversial. We aimed to assess long-term outcomes of bariatric operations in patients characterized for eating behavior and rare mutations in the melanocortin-4 receptor (MC4R) gene, which is strongly implicated in energy balance. RESEARCH DESIGN AND METHODS: Between 1996 and 2005, 1,264 severely obese Swiss patients underwent current laparoscopic adjustable gastric banding, gastroduodenal bypass, or a hybrid operation...
August 2016: Diabetes Care
Howard Steiger, Lea Thaler, Lise Gauvin, Ridha Joober, Aurelie Labbe, Mimi Israel, Audrey Kucer
Substance abuse is common in individuals with bulimia-spectrum (binge-purge) eating disturbances, a co-occurrence that has been attributed to shared neurobiological substrates--notably alterations in dopaminergic activity. We examined the implications of variations of selected, dopamine-relevant polymorphisms (DRD2 Taq1A, DRD4 7R, and COMT) for risk of substance abuse in women with binge-purge eating syndromes. We genotyped 183 women (66.1% showing full-threshold BN and 33.9% showing sub-syndromic variants), and assessed lifetime presence of alcohol, cannabis, cocaine, and stimulant abuse or dependence using structured interviews...
June 2016: Journal of Psychiatric Research
Melissa A Munn-Chernoff, Jessica H Baker
Eating disorders (EDs) and substance use disorders (SUDs) frequently co-occur; however, the reasons for this are unclear. We review the current literature on genetic risk for EDs and SUDs, as well as preliminary findings exploring whether these classes of disorders have overlapping genetic risk. Overall, genetic factors contribute to individual differences in liability to multiple EDs and SUDs. Although initial family studies concluded that no shared familial (which includes genetic) risk between EDs and SUDs exists, twin studies suggest a moderate proportion of shared variance is attributable to overlapping genetic factors, particularly for those EDs characterized by binge eating and/or inappropriate compensatory behaviours...
March 2016: European Eating Disorders Review: the Journal of the Eating Disorders Association
A M Maillard, L Hippolyte, B Rodriguez-Herreros, S J R A Chawner, D Dremmel, Z Agüera, A B Fagundo, A Pain, S Martin-Brevet, A Hilbert, S Kurz, R Etienne, B Draganski, S Jimenez-Murcia, K Männik, A Metspalu, A Reigo, B Isidor, C Le Caignec, A David, C Mignot, B Keren, M B M van den Bree, S Munsch, F Fernandez-Aranda, J S Beckmann, A Reymond, S Jacquemont
BACKGROUND: The 600 kb BP4-BP5 copy number variants (CNVs) at the 16p11.2 locus have been associated with a range of neurodevelopmental conditions including autism spectrum disorders and schizophrenia. The number of genomic copies in this region is inversely correlated with body mass index (BMI): the deletion is associated with a highly penetrant form of obesity (present in 50% of carriers by the age of 7 years and in 70% of adults), and the duplication with being underweight. Mechanisms underlying this energy imbalance remain unknown...
May 2016: International Journal of Obesity: Journal of the International Association for the Study of Obesity
Guillermo Gervasini, Carmen Gamero-Villarroel
In addition to the identification of mutations clearly related to Mendelian forms of obesity; genome-wide association studies and follow-up studies have in the last years pinpointed several loci associated with BMI. These genetic alterations are located in or near genes expressed in the hypothalamus that are involved in the regulation of eating behavior. Accordingly, it seems plausible that these SNPs, or others located in related genes, could also help develop aberrant conduct patterns that favor the establishment of eating disorders should other susceptibility factors or personality dimensions be present...
2015: Pharmacogenomics
Caroline Davis
This narrative review provides an overview of the epidemiology of binge eating disorder (BED), highlighting the medical history of this disorder and its entry as an independent condition in the Feeding and Eating Disorders section of the recently published Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. Estimates of prevalence are provided, as well as recognition that the female to male ratio is lower in BED than in other eating disorders. Evidence is also provided of the most common comorbidities of BED, including mood and anxiety disorders and a range of addiction disorders...
December 2015: CNS Spectrums
Jennifer L Bakalar, Lisa M Shank, Anna Vannucci, Rachel M Radin, Marian Tanofsky-Kraff
The Diagnostic and Statistical Manual of Mental Disorders (i.e., DSM-5) currently recognizes three primary eating disorders: anorexia nervosa, bulimia nervosa, and binge eating disorder. The origins of eating disorders are complex and remain poorly understood. However, emerging research highlights a dimensional approach to understanding the multifactorial etiology of eating disorders as a means to inform assessment, prevention, and treatment efforts. Guided by research published since 2011, this review summarizes recent findings elucidating risk factors for the development of eating disorders across the lifespan in three primary domains: (1) genetic/biological, (2) psychological, and (3) socio-environmental...
June 2015: Current Psychiatry Reports
Linda Booij, Kevin F Casey, Juliana M Antunes, Moshe Szyf, Ridha Joober, Mimi Israël, Howard Steiger
OBJECTIVE: Evidence associates anorexia nervosa (AN) with epigenetic alterations that could contribute to illness risk or entrenchment. We investigated the extent to which AN is associated with a distinct methylation profile compared to that seen in normal-eater women. METHOD: Genome-wide methylation profiles, obtained using DNA from whole blood, were determined in 29 women currently ill with AN (10 with AN-restrictive type, 19 with AN-binge/purge type) and 15 normal-weight, normal-eater control women, using 450 K Illumina bead arrays...
November 2015: International Journal of Eating Disorders
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