Lack of association of genetic variants in genes of the endocannabinoid system with anorexia nervosa

Müller, Timo; Reichwald, Kathrin; Brönner, Günter; Kirschner, Jeanette; Nguyen, Thuy Trang; Scherag, André; Herzog, Wolfgang; Herpertz‐Dahlmann, Beate; Lichtner, Peter; Meitinger, Thomas; Platzer, Matthias; Schäfer, Helmut; Hebebrand, Johannes; Hinney, Anke

doi:10.1186/1753-2000-2-33

Cited by 41 publications

(31 citation statements)

References 55 publications

(68 reference statements)

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“…The authors found a significant increase in the frequency of both polymorphisms in AN and BN patients, a result in sharp contrast with the previous findings by Muller et al [89] that showed a lack of association of these polymorphisms with AN. Additionally, Monteleone et al [91] found a synergistic effect of the two polymorphisms in AN but not in BN.…”

Section: Cannabinoids and Eating Disorderscontrasting

confidence: 56%

“…However, upon dividing the samples to restricting and binging/purging subtypes of AN, the data analysis revealed a preferential transmission of different alleles in each of the subtypes, suggesting restricting AN and binging/purging AN may be associated with different alleles of the CNR1 gene [88]. However, a subsequent study involving up to 91 German AN trios (patient Dis Disord, 2017 doi: 10.15761/JDD.1000103 with AN and both biological parents) was unable to confirm these results, nor did it show an association for any of 15 single nucleotide polymorphisms representative of regions with restricted haplotype diversity in FAAH, NAAA, and MAGL genes [89].…”

Section: Cannabinoids and Eating Disordersmentioning

confidence: 65%

“…In this respect, have been studied CNR1 and CNR2 (the genes encoding cannabinoid CB1Rs and CB2Rs, respectively), as well as the genes encoding the main enzyme responsible in the degradation of AEA (FAAH), NAAA (N-Acylethanolamine-hydrolyzing acid amidase [88][89][90][91][92][93].…”

Section: Cannabinoids and Eating Disordersmentioning

confidence: 99%

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The role of endocannabinoids in the control of eating disorders

Milano¹,

Tecce²,

Capasso³

2017

Dis Disord

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Eating Disorder (ED) is a syndrome characterized by persistent alteration of eating behavior and the conditions that cause an insufficient ingestion and/or adsorption of foods. There are three different ED diseases: Anorexia Nervosa (AN), Bulimia Nervosa (BN) and Binge Eating Disorders (BED). ED are complex conditions that arise from a combination of long-standing behavioral, emotional, psychological, interpersonal, and social factors. The neuronal circuits that control the ingestion of food are mainly related to catecholaminergic, serotoninergic and peptidergic systems. In this respect, while serotonin, dopamine and prostaglandin promote the ingestion of food, by contrast, neuropeptide Y, norepinephrine, GABA and opioid peptides inhibit food ingestion thus causing the occurrence of ED. The drugs mainly used in the treatment of ED are antidepressants such as selective serotonin reuptake inhibitors and tricyclic antidepressant. Additionally, mood stabilizers (lithium), anxiolytics, serotonin and noradrenalin reuptake inhibitors and antipsychotic drugs are often used in the treatment of ED.Several studies indicate that the endocannabinoid system is involved in ED supporting the idea that the cannabinoid signaling system is a key modulatory element in the activity in the brain area associated with ED.

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Section: Cannabinoids and Eating Disorderscontrasting

confidence: 56%

Section: Cannabinoids and Eating Disordersmentioning

confidence: 65%

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The role of endocannabinoids in the control of eating disorders

Milano¹,

Tecce²,

Capasso³

2017

Dis Disord

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“…Genetic polymorphisms in the CNR1 gene have been associated with basal metabolic index, obesity and various metabolic parameters (Aberle et al, 2007;Baye et al, 2008;Benzinou et al, 2008;Gazzerro et al, 2007;Jaeger et al, 2008;Peeters et al, 2007;Russo et al, 2007), however some negative studies have also been reported (Aberle et al, 2007;Lieb et al, 2009;Muller et al, 2007). Significant association of polymorphisms in CNR1 with anorexia nervosa and bulimia nervosa have also been reported (Monteleone et al, 2009;Siegfried et al, 2004), despite one negative report (Muller et al, 2008). Based on these many significant findings, we hypothesized that CNR1 might be associated with antipsychotic-induced weight gain.…”

Section: Discussionmentioning

confidence: 94%

A Common Polymorphism in the Cannabinoid Receptor 1 (CNR1) Gene is Associated with Antipsychotic-Induced Weight Gain in Schizophrenia

Tiwari

Zai

Likhodi

et al. 2010

Neuropsychopharmacol

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Antipsychotic-induced weight gain has emerged as a serious complication in the treatment of patients with atypical antipsychotic drugs. The cannabinoid receptor 1 (CNR1) is expressed centrally in the hypothalamic region and associated with appetite and satiety, as well as peripherally. An antagonist of CNR1 (rimonabant) has been effective in causing weight loss in obese patients indicating that CNR1 might be important in antipsychotic-induced weight gain. Twenty tag SNPs were analyzed in 183 patients who underwent treatment (with either clozapine, olanzapine, haloperidol, or risperidone) for chronic schizophrenia were evaluated for antipsychotic-induced weight gain for up to 14 weeks. The polymorphism rs806378 was nominally associated with weight gain in patients of European ancestry treated with clozapine or olanzapine. 'T' allele carriers (CT + TT) gained more weight (5.96%), than the CC carriers (2.76%, p ¼ 0.008, FDR q-value ¼ 0.12). This translated into approximately 2.2 kg more weight gain in patients carrying the T allele than the patients homozygous for the CC genotype (CC vs CT + TT, 2.21±4.51 vs 4.33±3.89 kg; p ¼ 0.022). This was reflected in the allelic analysis (C vs T allele, 3.84 vs 5.83%, p ¼ 0.035). We conducted electrophoretic mobility shift assays which showed that the presence of the T allele created a binding site for arylhydrocarbon receptor translocator (ARNT), a member of the basic helix-loop-helix/Per-Arnt-Sim protein family. In this study, we provide evidence that the CNR1 gene may be associated with antipsychotic-induced weight gain in chronic schizophrenia patients. However, these observations were made in a relatively small patient population; therefore these results need to be replicated in larger sample sets.

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“…For instance, mixed findings involving the overtransmission of cannabinoid receptor 1 ( CNR1 ) variants in AN have been reported, 152,153 and preliminary case-control findings need replication. 154 As mentioned in the linkage section, preliminary results involving the OPRD1 gene have been reported in AN, 66,67 whereas opioid receptor mu 1 gene ( OPRM1 ) has been implicated in hedonic eating in one study with 300 participants.…”

Section: Molecular Genetic Studies Of Eating Disordersmentioning

confidence: 99%

Genetics and epigenetics of eating disorders

Yılmaz¹,

Hardaway²,

Bulik³

2015

AGG

131

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Eating disorders (EDs) are serious psychiatric conditions influenced by biological, psychological, and sociocultural factors. A better understanding of the genetics of these complex traits and the development of more sophisticated molecular biology tools have advanced our understanding of the etiology of EDs. The aim of this review is to critically evaluate the literature on the genetic research conducted on three major EDs: anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED). We will first review the diagnostic criteria, clinical features, prevalence, and prognosis of AN, BN, and BED, followed by a review of family, twin, and adoption studies. We then review the history of genetic studies of EDs covering linkage analysis, candidate gene association studies, genome-wide association studies, and the study of rare variants in EDs. Our review also incorporates a translational perspective by covering animal models of ED-related phenotypes. Finally, we review the nascent field of epigenetics of EDs and a look forward to future directions for ED genetic research.

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Lack of association of genetic variants in genes of the endocannabinoid system with anorexia nervosa

Cited by 41 publications

References 55 publications

The role of endocannabinoids in the control of eating disorders

The role of endocannabinoids in the control of eating disorders

A Common Polymorphism in the Cannabinoid Receptor 1 (CNR1) Gene is Associated with Antipsychotic-Induced Weight Gain in Schizophrenia

Genetics and epigenetics of eating disorders

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