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Comparative Study
. 2014 Dec 15;220(1-2):513-8.
doi: 10.1016/j.psychres.2014.08.037. Epub 2014 Aug 27.

COMT met allele differentially predicts risk versus severity of aberrant eating in a large community sample

Shannon D Donofry  1 , Kathryn A Roecklein  2 , Jennifer E Wildes  3 , Megan A Miller  4 , Janine D Flory  5 , Stephen B Manuck  4
Affiliations
Comparative Study

COMT met allele differentially predicts risk versus severity of aberrant eating in a large community sample

Shannon D Donofry et al. Psychiatry Res. .

Abstract

Prefrontal dopamine (DA) transmission participates in the reinforcement of reward-driven behaviors like eating. Because catechol-O-methyltransferase (COMT) degrades DA and is expressed in the prefrontal cortex, variation in the COMT gene may modulate eating behavior. Previous studies have shown that the met allele of the COMT val158met single nucleotide polymorphism (SNP) is associated with Bulimia Nervosa (BN). The specific aim of this study was to test whether the met allele increased risk for, and severity of, eating disorder symptomatology in community volunteers. Caucasian adults (N=1003; 51.2% female) from the University of Pittsburgh Adult Health and Behavior Project (AHAB) were genotyped and completed the Eating Disorders Inventory (EDI). Logistic and Poisson regression analyses assessed genotype-dependent presence and severity of eating disorder symptomatology. The met allele was significantly associated with the presence of symptoms on the Bulimia subscale and the severity of Body Dissatisfaction scores. All EDI subscales significantly predicted BMI. To our knowledge, these are the first data indicating that the COMT met allele increases risk for some symptoms of disordered eating, while increasing severity of others, in a community sample. These novel findings may have important implications for understanding the etiology of heterogeneous disordered eating phenotypes.

Keywords: Aberrant eating; Bulimia; Catechol-O-methyltransferase gene; Dopamine; Eating disorders; Prefrontal cortex.

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