The present results are consistent with previous findings identifying a subgroup of individuals with bulimia characterized by high psychiatric comorbidity and suggest that the 5-HTTLPR polymorphism and childhood trauma may both be pertinent to explaining the presence of greater psychiatric comorbidity in bulimia-spectrum disorders.
We evaluated the distribution of the functional 5-HTTLPR polymorphism in a series of 201 Italian, Caucasian, eating disorder patients (113 with AN and 88 with BN binge/purging (BP subtype) and in 150 Caucasian unrelated controls.
Reduced brain serotonin (5-hydroxytryptamine: 5-HT) transporter activity has been associated with susceptibility to various forms of psychopathology, including bulimia nervosa (BN) and related syndromes characterized by appetitive or behavioural dysregulation.
These findings support the view that polymorphic variants of the 5HTT promoter region do not play a part in predisposing to BN, whereas they seem to predispose bulimic individuals to nutritional impairment and increased harm avoidance.
These results suggest that the 196G/A SNP of the human BDNF gene does not contribute to the genetic susceptibility to BN and BED, but may predispose those patients to a more severe binge eating behavior.
This study: (1) assessed the role of leptin, melanocortin, and neurotrophin genetic variants in conferring risk for AN and BN; and (2) explored the involvement of these genes in body mass index (BMI) variations within AN and BN.
We have found that the Met66 variant is strongly associated to all ED subtypes (AN, ANR, binge-eating/purging AN and BN), and that the -270C BDNF variant has an effect on BN and late age at onset of weight loss.
Up to now, polymorphisms and variations in various genes (e.g. genes for 5-HT receptors, leptin gene, melanocortin MC(4) receptor gene) have been assessed for association and transmission disequilibrium pertaining to anorexia nervosa and/or bulimia nervosa.
This study: (1) assessed the role of leptin, melanocortin, and neurotrophin genetic variants in conferring risk for AN and BN; and (2) explored the involvement of these genes in body mass index (BMI) variations within AN and BN.
Sixty-six men and women with DSM-5 binge-eating disorder (BED) or bulimia nervosa (BN) were randomized to receive eight sessions of CBT-GSH + Noom (n = 33) or CBT-GSH (n = 33) over 12 weeks.
There were no significant group differences in COMTVal158Met alleles and genotype frequencies between patients and controls, for all EDs pooled together [range of odds ratios (ORs): 0.96-1.04, p-values: 0.46-0.97, I<sup>2</sup> = 0%] and when analysing separately patients with AN (ORs: 0.94-1.04, p-values: 0.31-0.61, I<sup>2</sup> = 0%) or BN (ORs: 0.80-1.09, p-values: 0.28-0.64, I<sup>2</sup> = 0-44%).
Eighty women receiving treatment for serious ED (52 for anorexia nervosa, 28 for bulimia nervosa) and 116 age-matched females in the control group underwent COMT genotyping for polymorphism in exon 4 (codon 158).
We explored the influence of interactions between polymorphisms acting upon postsynaptic receptors (DRD2 TaqA1 rs1800497 and DRD4 7R) and dopamine regulators (COMTrs4680 and DAT1) on the expression of eating symptoms and personality traits in women with bulimia-spectrum eating disorders.
We explored the influence of interactions between polymorphisms acting upon postsynaptic receptors (DRD2 TaqA1 rs1800497 and DRD4 7R) and dopamine regulators (COMT rs4680 and DAT1) on the expression of eating symptoms and personality traits in women with bulimia-spectrum eating disorders.