Eating disorders (ED) are classic examples of complex psychiatric phenotypes having both genetic and environmental determinants. Many data, mainly obtained from animal studies, suggest that the endocannabinoid system is involved in food intake and energy-balance control through the modulation of several mechanisms (Cota et al., 2003). In a recent study, the homozygous FAAH A385A genotype was associated with obesity (Sipe et al., 2005). A family-based study suggests that anorexia nervosa (AN) may be associated with different alleles of the CNR1 gene (Siegfried et al., 2004). The aims of this preliminary study are to investigate whether an association exists between the (AAT)n triplet repeat in the 30 flanking region of the CNR1 gene and the FAAH cDNA 385 C-A polymorphism and ED. The participants were 47 patients (42 females) with ED (13 AN restricting type, 21 AN bingeing/purging type, and 13 bulimia nervosa purging type according to the Diagnostic and Statistical Manual of Mental Disorders, 4th edition) and 116 healthy controls. We studied the (AAT)n triplet repeat in the 30 flanking region of the CNR1 gene and the FAAH cDNA 385 C-A polymorphism. The analysis did not suggest any significant difference in the alleles and genotypes distribution between the whole sample of ED patients compared with controls. However, we found a lack of allele 8 of the AAT repeat in female ED patients compared with female controls, but did not reach significant statistical levels (Fisher’s exact test: P = 0.1), and an excess of allele 7, mainly in the AN group (32.8 vs. 18.0% in the female control group, Fisher’s exact test: P=0.03; odds ratio: 1.22, 95% confidence interval: 1.01–1.49). Bulimic symptoms assessed by Eating Disorders Inventory-Bulimia and Bulimic Investigatory Test Edinburgh-Symptoms subscales were less severe in those patients with a long AAT allele (P=0.05 and 0.02, respectively).
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