Objective: There is less information about the biological basis of Antisocial Personality Disorder (ASPD), although some of its initial symptoms appear in childhood or adolescence and it is a psychological disorder that causes problems in the individual’s academic, economic, and social life. The aim of this study is to explore the presence of methylene tetrahydrofolate reductase (MTHFR) mutation and its correlation with psychometric tests among subjects with antisocial personality disorder.
Methods: One hundred and eight male subjects meeting DSM-IV-TR diagnostic criteria for ASPD who had been admitted to the outpatient unit of the Department of Psychiatry at GATA Haydarpasa Training Hospital were included in the study. The patients and control subjects were assessed by a semi-structured socio-demographic form, Structured Clinical Interview Diagnosis for DSM-IV (SCID-I), Structured Clinical Interview Diagnosis for DSM-III-R Personality Disorders (SCID-II), Hare Psychopathy Checklist-Revised, Barratt Impulsiveness Scale (BIS-11), Resilience Scale for adults and Temperament and Character Inventory. Real time PCR method is used in order to identify MTHFR mutation among subjects.
Results: In this study; all of the groups showed more “non-planning, lack of control impulsiveness” than other kinds. Also groups were not resilient in “perception of future”, “structured style” and “social competence” subgroups, groups with heterozygous and homozygous mutations were and group without mutation wasn’t resilient in “perception of self” subgroup, group with heterozygous mutation+ without mutation were and group with homozygous mutation wasn’t resilient in “family cohesion” and “social resources” subgroups. For all TCI temperament trait subgroups, there was no significant correlation with the results. But we found high novelty seeking, harm avoidance, cooperativeness, self-directedness points and low reward dependence, self-transcendence points. As a result of psychometric tests, there was no significant correlation identified between the MTHFR enzyme mutation and test results. On the other hand, it has been found that the impulsiveness among subjects with ASPD was of non-planning type.
Conclusion: In our study, no significant correlation was identified between the MTHFR enzyme mutation and ASPD. We thought that limitation of our study sample and not measuring MTHFR enzyme activity may play a role in producing these results. Additional work is needed to examine in large groups and with MTHFR enzyme activity measure.