title: 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.
abstract: BACKGROUND
  Little 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.
  
  
  METHODS
  One hundred forty-nine respondents of a representative sample of adults affected by Hurricane Ike were interviewed 2-5 months after this 2008 disaster.
  
  
  RESULTS
  After 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).
  
  
  CONCLUSIONS
  The small sample size and employment of self-report measures may limit generalizability of these findings.
  
  
  CONCLUSIONS
  Results 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.
authors.affiliation: Clinical Neurosciences Division, National Center for Posttraumatic Stress Disorder, Veterans Affairs Connecticut Healthcare System, West Haven, CT 06516, USA. robert.pietrzak@yale.edu
authors.forename: Robert H
authors.initials: RH
authors.lastname: Pietrzak
authors.forename: Sandro
authors.initials: S
authors.lastname: Galea
authors.forename: Steven M
authors.initials: SM
authors.lastname: Southwick
authors.forename: Joel
authors.initials: J
authors.lastname: Gelernter
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D055867:Cyclonic Storms; D004190:Disasters; D005260:Female; D059647:Gene-Environment Interaction; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D008957:Models, Genetic; D010641:Phenotype; D010865:Pilot Projects; D011110:Polymorphism, Genetic; D036301:Qualitative Research; D050486:Serotonin Plasma Membrane Transport Proteins / Q000235:genetics*; D013313:Stress Disorders, Post-Traumatic / Q000453:epidemiology* / Q000235:genetics*; D055815:Young Adult
chemical_list: D050486:Serotonin Plasma Membrane Transport Proteins