Eating Disorder Symptoms and CYP2D6 Variation in Cuban Healthy Females: A Report from the Ibero-American Network of Pharmacogenetics

CYP2D6 is involved in the metabolism of antidepressants drugs and of the endogenous neurotransmitter serotonin. We have previously shown an increased number of CYP2D6 active alleles, indicative of higher enzyme hydroxylation capacity, among patients with eating disorders. From a population genetic heterogeneity standpoint, there is a need to extend this line of inquiry to populations hitherto understudied. Moreover, because environmental factors do vary regionally, genetic/pharmacogenetic studies need to be broadened in different populations. In this study, we tested the role of CYP2D6 activity variation in a sample of women with regard to their risk of eating disorder symptoms from Havana, Cuba. Subjects, recruited from university students and staff with no prior history of psychopathology or psychotropic treatment, completed the Eating Disorder Inventory (EDI) (N=159). Subjects' CYP2D6 genotypes and phenotypic activity (debrisoquine metabolic ratio, MR) were determined. All subjects were at low-risk for “EDI-global”, “drive for thinness” or “body dissatisfaction” but 47.7% were at moderate-risk for “EDI-bulimia” in this sample. This moderate risk group for bulimia symptoms displayed a higher number of phenotypically ultrarapid (MR<0.1), and a lower number of poor metabolizers (MR>12.6), compared to the “EDI-Bulimia” low-risk group in the sample (p<0.01). To the best of our knowledge, this is the first study regarding this phenotype, which lends further support to prior observations on an association between CYP2D6 activity and risk of eating disorders.