Examining the relation between the serotonin transporter 5-HTTPLR genotype x trauma exposure interaction on a contemporary phenotypic model of posttraumatic stress symptomatology: A pilot study

Background is known about the specificity of the interaction of serotonin transporter 5-HTTLPR genotype x trauma exposure in relation to contemporary structural models of PTSD symptomatology, which suggest that 4- or 5-factor models provide a better representation of the phenotypic expression of this disorder. s ndred forty-nine respondents of a representative sample of adults affected by Hurricane Ike were interviewed 2–5 months after this 2008 disaster. s adjustment for age, sex, and ancestral proportion scores, the interaction of 5-HTTPLR genotype x trauma exposure was significantly associated with both severity (β=.40, p<.001) and probable diagnosis (Wald=4.55, p=.033; odds ratio=3.81, 95% CI=1.11–13.03) of Ike-related PTSD. Respondents with the low-expression variant of the 5-HTTPLR polymorphism (S allele carriers) who were highly exposed to Hurricane Ike reported significantly greater severity of PTSD symptoms and were more likely to screen positive for PTSD than respondents homozygous for the L allele who were highly exposed to Hurricane Ike. Confirmatory factor analyses revealed that a 5-factor model of intercorrelated re-experiencing, avoidance, numbing, dysphoric arousal, and anxious arousal symptoms provided the best structural representation of PTSD symptomatology. The 5-HTTPLR genotype x exposure interaction was significant only for anxious arousal (β=.44, p<.001) and re-experiencing (β=.35, p<.001) symptoms, but not avoidance, numbing, or dysphoric arousal symptoms (all βs≤.20, all ps>.13). tions all sample size and employment of self-report measures may limit generalizability of these findings. sions s of this pilot study suggest that the low-expression variant of the 5-HTTLPR polymorphism modifies risk for PTSD, but that this effect may be specific to anxious arousal and re-experiencing symptoms.