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Binge Eating Disorder and genes

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
Brian C Harrington, Michelle Jimerson, Christina Haxton, David C Jimerson
Eating disorders are life-threatening conditions that are challenging to address; however, the primary care setting provides an important opportunity for critical medical and psychosocial intervention. The recently published Diagnostic and Statistical Manual of Mental Disorders, 5th ed., includes updated diagnostic criteria for anorexia nervosa (e.g., elimination of amenorrhea as a diagnostic criterion) and for bulimia nervosa (e.g., criterion for frequency of binge episodes decreased to an average of once per week)...
January 1, 2015: American Family Physician
Carmen Gamero-Villarroel, Raquel Rodriguez-Lopez, Mercedes Jimenez, Juan A Carrillo, Angustias Garcia-Herraiz, David Albuquerque, Isalud Flores, Guillermo Gervasini
We aimed to determine whether variability in the melanocortin-4 receptor (MC4R) gene, predisposing to hyperphagia and obesity, may also be present in nonobese patients with binge-eating behavior or be related to anthropometric or psychopathological parameters in these patients. The coding region of the MC4R gene was sequenced in nonobese patients with binge-eating behavior diagnosed with bulimia nervosa or binge-eating disorder (n=77); individuals with severe early-onset obesity (n=170); and lean women with anorexia nervosa (n=20)...
February 2015: Psychiatric Genetics
Tetsuya Ando, Naho Tamura, Takashi Mera, Chihiro Morita, Michiko Takei, Chiemi Nakamoto, Masanori Koide, Mari Hotta, Tetsuro Naruo, Keisuke Kawai, Toshihiro Nakahara, Chikara Yamaguchi, Toshihiko Nagata, Kazuyoshi Ookuma, Yuri Okamoto, Takao Yamanaka, Nobuo Kiriike, Yuhei Ichimaru, Toshio Ishikawa, Gen Komaki
The functional c.385C>A single-nucleotide polymorphism (SNP) in the fatty acid amide hydrolase (FAAH) gene, one of the major degrading enzymes of endocannabinoids, is reportedly associated with anorexia nervosa (AN). We genotyped the c.385C>A SNP (rs324420) in 762 lifetime AN and 605 control participants in Japan. There were significant differences in the genotype and allele frequencies of c.385C>A between the AN and control groups. The minor 385A allele was less frequent in the AN participants than in the controls (allele-wise, odds ratio = 0...
July 2014: Molecular Genetics & Genomic Medicine
Stacey J Winham, Alfredo B Cuellar-Barboza, Susan L McElroy, Alfredo Oliveros, Scott Crow, Colin L Colby, Doo-Sup Choi, Mohit Chauhan, Mark A Frye, Joanna M Biernacka
BACKGROUND: Bipolar disorder (BD) is a highly heritable disease. While genome-wide association (GWA) studies have identified several genetic risk factors for BD, few of these studies have investigated the genetic etiology of specific disease subtypes. In particular, BD is positively associated with eating dysregulation traits such as binge eating behavior (BE), yet the genetic risk factors underlying BD with comorbid BE have not been investigated. METHODS: Utilizing data from the Genetic Association Information Network study of BD, which included 729,454 single nucleotide polymorphisms (SNPs) genotyped in 1001 European American bipolar cases and 1034 controls, we performed GWA analyses of bipolar subtypes defined by the presence or absence of BE history, and performed a case-only analysis comparing BD subjects with and without BE history...
August 2014: Journal of Affective Disorders
V Boraska, C S Franklin, J A B Floyd, L M Thornton, L M Huckins, L Southam, N W Rayner, I Tachmazidou, K L Klump, J Treasure, C M Lewis, U Schmidt, F Tozzi, K Kiezebrink, J Hebebrand, P Gorwood, R A H Adan, M J H Kas, A Favaro, P Santonastaso, F Fernández-Aranda, M Gratacos, F Rybakowski, M Dmitrzak-Weglarz, J Kaprio, A Keski-Rahkonen, A Raevuori, E F Van Furth, M C T Slof-Op 't Landt, J I Hudson, T Reichborn-Kjennerud, G P S Knudsen, P Monteleone, A S Kaplan, A Karwautz, H Hakonarson, W H Berrettini, Y Guo, D Li, N J Schork, G Komaki, T Ando, H Inoko, T Esko, K Fischer, K Männik, A Metspalu, J H Baker, R D Cone, J Dackor, J E DeSocio, C E Hilliard, J K O'Toole, J Pantel, J P Szatkiewicz, C Taico, S Zerwas, S E Trace, O S P Davis, S Helder, K Bühren, R Burghardt, M de Zwaan, K Egberts, S Ehrlich, B Herpertz-Dahlmann, W Herzog, H Imgart, A Scherag, S Scherag, S Zipfel, C Boni, N Ramoz, A Versini, M K Brandys, U N Danner, C de Kovel, J Hendriks, B P C Koeleman, R A Ophoff, E Strengman, A A van Elburg, A Bruson, M Clementi, D Degortes, M Forzan, E Tenconi, E Docampo, G Escaramís, S Jiménez-Murcia, J Lissowska, A Rajewski, N Szeszenia-Dabrowska, A Slopien, J Hauser, L Karhunen, I Meulenbelt, P E Slagboom, A Tortorella, M Maj, G Dedoussis, D Dikeos, F Gonidakis, K Tziouvas, A Tsitsika, H Papezova, L Slachtova, D Martaskova, J L Kennedy, R D Levitan, Z Yilmaz, J Huemer, D Koubek, E Merl, G Wagner, P Lichtenstein, G Breen, S Cohen-Woods, A Farmer, P McGuffin, S Cichon, I Giegling, S Herms, D Rujescu, S Schreiber, H-E Wichmann, C Dina, R Sladek, G Gambaro, N Soranzo, A Julia, S Marsal, R Rabionet, V Gaborieau, D M Dick, A Palotie, S Ripatti, E Widén, O A Andreassen, T Espeseth, A Lundervold, I Reinvang, V M Steen, S Le Hellard, M Mattingsdal, I Ntalla, V Bencko, L Foretova, V Janout, M Navratilova, S Gallinger, D Pinto, S W Scherer, H Aschauer, L Carlberg, A Schosser, L Alfredsson, B Ding, L Klareskog, L Padyukov, P Courtet, S Guillaume, I Jaussent, C Finan, G Kalsi, M Roberts, D W Logan, L Peltonen, G R S Ritchie, J C Barrett, X Estivill, A Hinney, P F Sullivan, D A Collier, E Zeggini, C M Bulik
Anorexia nervosa (AN) is a complex and heritable eating disorder characterized by dangerously low body weight. Neither candidate gene studies nor an initial genome-wide association study (GWAS) have yielded significant and replicated results. We performed a GWAS in 2907 cases with AN from 14 countries (15 sites) and 14 860 ancestrally matched controls as part of the Genetic Consortium for AN (GCAN) and the Wellcome Trust Case Control Consortium 3 (WTCCC3). Individual association analyses were conducted in each stratum and meta-analyzed across all 15 discovery data sets...
October 2014: Molecular Psychiatry
Emily M Pisetsky, Laura M Thornton, Paul Lichtenstein, Nancy L Pedersen, Cynthia M Bulik
We evaluated whether the prevalence of lifetime suicide attempts/completions was higher in women with a lifetime history of an eating disorder than in women with no eating disorder and assessed whether eating disorder features, comorbid psychopathology, and personality characteristics were associated with suicide attempts in women with anorexia nervosa, restricting subtype (ANR), anorexia nervosa, binge-purge subtype (ANBP), lifetime history of both anorexia nervosa and bulimia nervosa (ANBN), bulimia nervosa (BN), binge eating disorder (BED), and purging disorder (PD)...
November 2013: Journal of Abnormal Psychology
Monica Algars, Lu Huang, Ann F Von Holle, Christine M Peat, Laura M Thornton, Paul Lichtenstein, Cynthia M Bulik
OBJECTIVE: The relation between eating disorders and menstrual function has been widely studied, but it is unknown whether the behavior of binge eating itself is related to menstrual dysfunction. METHODS: The 11,503 women included in this study were from the Swedish Twin study of Adults: Genes and Environment. The associations between menstrual dysfunction and binge eating were analyzed using logistic regression or multiple linear regression models with generalized estimation equations...
January 2014: Journal of Psychosomatic Research
Christine M Peat, Lu Huang, Laura M Thornton, Ann F Von Holle, Sara E Trace, Paul Lichtenstein, Nancy L Pedersen, D Wayne Overby, Cynthia M Bulik
OBJECTIVE: Symptoms of both gastroesophageal reflux disease (GERD) and irritable bowel syndrome (IBS) are frequently reported by individuals who binge eat. Higher body mass index (BMI) has also been associated with these disorders and with binge eating (BE). However, it is unknown whether BE influences GERD/IBS and how BMI might affect these associations. Thus, we examined the potential associations among BE, GERD, IBS, and BMI. METHODS: Participants were from the Swedish Twin study of Adults: Genes and Environment (STAGE) and provided information on disordered eating behavior, BMI, gastrointestinal (GI) disorders, and commonly comorbid psychiatric and somatic illnesses...
November 2013: Journal of Psychosomatic Research
M Valette, C Poitou, E Kesse-Guyot, F Bellisle, C Carette, J Le Beyec, S Hercberg, K Clément, S Czernichow
Melanocortin-4 receptor (MC4R) gene mutations are involved in the leptin-melanocortin pathways that control food intake. The effect of these mutations on eating behavior phenotypes is still debated. To determine the association between functional MC4R mutations and eating behaviors, dietary intake and physical activity, we sequenced the MC4R gene in 4653 obese adults. Among them, 19 adults carriers of functional MC4R mutation were matched on age, sex and body mass index with two randomly-paired controls without MC4R mutation (n=57)...
June 2014: International Journal of Obesity: Journal of the International Association for the Study of Obesity
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