Yu Lee1, Pao-Yen Lin. 1. Department of Psychiatry, Chang Gung Memorial Hospital- Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Abstract
OBJECTIVE: Compelling evidence has suggested a role for serotonin system dysfunction in the pathogenesis of eating disorders (EDs), including anorexia nervosa (AN) and bulimia nervosa (BN). Studies have examined the association between EDs and a functional polymorphism of the serotonin transporter gene promoter (5-HTTLPR). These studies have yielded inconsistent results. The present study aimed to determine conclusively whether there is an association by using a meta-analytic method. METHOD: Data of over 2,000 participants from eight independent case-controlassociation studies were pooled by using a random effects model. RESULTS: AN was found to be significantly associated with the S allele (p < .001) and S carrier (SS + LS) genotype (p = .007). However, BN was associated neither with the S allele (p = .49) nor with the S carrier genotype (p = .33). DISCUSSION: These results suggested that the genetic variance of the serotonin transporter gene promoter contributed to the susceptibility of AN.
OBJECTIVE: Compelling evidence has suggested a role for serotonin system dysfunction in the pathogenesis of eating disorders (EDs), including anorexia nervosa (AN) and bulimia nervosa (BN). Studies have examined the association between EDs and a functional polymorphism of the serotonin transporter gene promoter (5-HTTLPR). These studies have yielded inconsistent results. The present study aimed to determine conclusively whether there is an association by using a meta-analytic method. METHOD: Data of over 2,000 participants from eight independent case-controlassociation studies were pooled by using a random effects model. RESULTS: AN was found to be significantly associated with the S allele (p < .001) and S carrier (SS + LS) genotype (p = .007). However, BN was associated neither with the S allele (p = .49) nor with the S carrier genotype (p = .33). DISCUSSION: These results suggested that the genetic variance of the serotonin transporter gene promoter contributed to the susceptibility of AN.
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