A family-based association study of the HTR1B gene in eating disorders

Abstract

Objective: To explore the association of three polymorphisms of the serotonin receptor 1Db gene (HTR1B) in the etiology of eating disorders and their relationship with clinical characteristics. Methods: We analyzed the G861C, A-161T, and A1180G polymorphisms of the HTR1B gene through a family-based association test (FBAT) in 245 nuclear families. The sample was stratified into anorexia nervosa (AN) spectrum and bulimia nervosa (BN) spectrum. In addition, we performed a quantitative FBAT analysis of anxiety severity, depression severity, and Yale-Brown-Cornell Eating Disorders Scale (YBC-EDS) in the AN and BN-spectrum groups.Results: FBAT analysis of the A-161T polymorphism found preferential transmission of allele A-161 in the overall sample. This association was stronger when the sample was stratified by spectrums, showing transmission disequilibrium between the A-161 allele and BN spectrum (z = 2.871, p = 0.004). Quantitative trait analysis showed an association between severity of anxiety symptoms and the C861 allele in AN-spectrum participants (z = 2.871, p = 0.004). We found no associations on analysis of depression severity or preoccupation and ritual scores in AN or BN-spectrum participants. Conclusions: Our preliminary findings suggest a role of the HTR1B gene in susceptibility to development of BN subtypes. Furthermore, this gene might have an impact on the severity of anxiety in AN-spectrum patients.

Serotonin deficiency induced after brain maturation rescues consequences of early life adversity

“…The observed increase in food, water and percentage sucrose consumption by Tph2 Δfl /− and Tph2 Δ fl / fl mice has also been reported in Tph2 − l − mice 20 , 71 , which reflects an increased energy need, rather than altered anhedonia as a symptom of depressive-like behavior. This supports the assertion that strong reductions in 5-HT metabolism in adulthood are implicated in the pathophysiology of eating disorders through various hormonal and receptor systems 72 , 73 , independent of 5-HT functions during development.…”

Risk factors for eating disorders: findings from a rapid review

“…Genes associated with other metabolic functions, including appetite and weight control endocrines (leptin, melanocortin, neurotrophin) have also been implicated in ED development and severity, however fewer differences between ED diagnoses are apparent. Polymorphisms in the genetic loci responsible for neurotransmitters associated with reward processing and appetite regulation hormones, including dopamine, serotonin, and cannabinoid have been identified as a risk factor across several ED diagnoses including AN, BN, and EDNOS [45,[50][51][52][53][54][55][56][57][58][59][60][61][62]. Additionally, genetic polymorphisms in the glucocorticoid receptor pathway responsible for the stress response have been linked to individuals who have experienced trauma and are associated with increased risk for BN [51,65,66].…”

“…A polymorphism of the oxytocin receptor gene (OXT-R) was also found to distinguish between risk of onset for restricting type EDs or binge/purge type EDs, indicating the potential role of oxytocin in the development and maintenance of EDs [ 58 ]. Additional research has identified an association between a polymorphism in a neurotransmitter inhibition gene (HTR1B) and an increased risk of developing BN as well as greater severity of AN symptoms, including low BMI [ 59 ].…”

Implementing High Energy Liquid Nutrition, Omega-3 Fatty Acids and Nutritional Supplements for the Treatment of Anorexia Nervosa

“…Genetics and environmental factors appear to play an important role in the pathogenesis and etiology of AN. The HTR1B gene (5-hydroxytryptamine receptor 1B) possibly has an effect on the 'severity of anxiety in AN-spectrum patients' 12 . Additionally, recent prospective studies in humans show a link between maternal stress and the development of eating disorders 13,14 .…”