Objective: To test the hypothesis that the interaction between the brain-derived neurotrophic factor (BDNF) and dopamine receptor D(2) (DRD2)/ANKK1 gene contributes to individual differences in alexithymia. The personality construct of alexithymia refers to difficulties in emotional self-regulation and contributes as a risk factor to several mental disorders. Alexithymic individuals show an impoverished conscious experience of emotions but an intact autonomic emotional response. Persons with high alexithymia scores reportedly show a reduced activation of the anterior cingulate cortex (ACC) during the processing of emotional stimuli. An interaction between two polymorphisms on the BDNF and DRD2/ANKK1 gene has been recently associated with reduced gray matter volume in the ACC and higher trait anxiety.
Methods: We conducted a genetic association study. A total of 664 healthy participants completed the Toronto Alexithymia Scale questionnaire and were genotyped for the BDNF Val66Met (rs6265) and the DRD2/ANKK1 Taq IA (rs1800497) polymorphisms.
Results: Carriers of at least one BDNF 66Met and one DRD2/ANKK1 A1 allele showed the highest scores in the total Toronto Alexithymia Scale and in the subscale "Difficulties Identifying Feelings."
Conclusion: In line with recent studies investigating the role of BDNF Val66Met and DRD2/ANKK1 Taq IA polymorphisms on anxiety and gray matter volume in the ACC, our findings provide the first evidence for a genetic contribution to alexithymia.