Abstract
Background: Rape is a common traumatic event which may result in the development of posttraumatic stress disorder (PTSD), yet few studies have investigated risk biomarkers in sexually traumatised individuals. Adiponectin is a novel cytokine within inflammatory and cardiometabolic pathways with evidence of involvement in PTSD. Objective: This prospective exploratory study in a sample of female rape survivors investigated the association of single nucleotide polymorphisms (SNPs) in the adiponectin gene (ADIPOQ) and posttraumatic stress symptom (PTSS) severity, and the interaction of these SNPs of interest with childhood trauma in modifying the association with PTSS severity. Method: The study involved 455 rape-exposed black South African women (mean age (SD), 25.3 years (±5.5)) recruited within 20 days of being raped. PTSS was assessed using the Davidson Trauma Scale (DTS) and childhood trauma was assessed using a modified version of the Childhood Trauma Scale-Short Form Questionnaire. Eight ADIPOQ SNPs (rs17300539, rs16861194, rs16861205, rs2241766, rs6444174, rs822395, rs1501299, rs1403697) were genotyped using KASP. Mixed linear regression models were used to test additive associations of ADIPOQ SNPs and PTSS severity at baseline, 3 and 6 months following rape. Results: The mean DTS score post-sexual assault was high (71.3 ± 31.5), with a decrease in PTSS severity shown over time for all genotypes. rs6444174TT genotype was inversely associated with baseline PTSS in the unadjusted model (β = -13.6, 95% CI [-25.1; -2.1], p = .021). However, no genotype was shown to be significantly associated with change in PTSS severity over time and therefore ADIPOQ SNP x childhood trauma interaction was not further investigated. Conclusion: None of the ADIPOQ SNPs selected for investigation in this population were shown to be associated with change in PTSS severity over a 6-month period and therefore their clinical utility as risk biomarkers for rape-related PTSD appears limited. These SNPs should be further investigated in possible gene-gene and gene-environment interactions.