Background: The serotonin transporter gene promoter polymorphism (5HTTLPR) and child abuse have been associated with an increased risk for depression. We previously reported the long/long (l/l) genotype of 5HTTLPR being associated with higher heart rate among patients with a history of child abuse compared with those without a history of child abuse, whereas the short allele carriers did not have heart rate differences dependent on child abuse history. This time, we extended our investigation to other outcomes with body mass index (BMI), and diabetes mellitus (DM) diagnosis.
Methods: A retrospective chart review identified 185 White female depressed inpatients who were genotyped for 5HTTLPR. Child abuse history, BMI, and DM diagnosis were recorded. The relationship between 5HTTLPR, child abuse, and BMI, as well as a prevalence of DM were analyzed.
Results: Among the l/l genotype group, patients with a history of child abuse had a higher prevalence of DM (14.3 vs. 0%, P=0.06), and higher BMI (32.3 vs. 27.3 kg/m2, P=0.03) compared with those without. Patients with the short allele (s/s or s/l) had fewer differences on the basis of abuse history.
Conclusion: A potential interaction between 5HTTLPR and child abuse influenced metabolic profiles of White female depressed inpatients. In contrast with the widely recognized ‘reactivity’ associated with the short allele of 5HTTLPR, our White female depressed psychiatric inpatients with the l/l genotype showed relatively greater clinical pathology in metabolic profiles if they have a history of child abuse than inpatients with at least one short allele who had a history of child abuse.
aDepartments of Psychiatry and Psychology, Mayo Clinic, Rochester, Minnesota
bMental Health Service Line, Sioux Falls VA Medical Center, Sioux Falls
cDepartment of Psychiatry, University of South Dakota, South Dakota, USA
Correspondence to Dr Gen Shinozaki, MD, Departments of Psychiatry and Psychology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA Tel: +1 507 255 9187; fax: +1 507 255 9416; e-mail: email@example.com
Received May 4, 2011
Accepted September 25, 2011