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. Author manuscript; available in PMC: 2008 Jun 29.
Published in final edited form as: JAMA. 2008 Mar 19;299(11):1291–1305. doi: 10.1001/jama.299.11.1291

Figure 2. Glucocorticoid Receptor Sensitivity, PTSD, and FKBP5 SNPs.

Figure 2

PTSD indicates posttraumatic stress disorder; SNPs, single-nucleotide polymorphisms. Mean serum cortisol concentration with 95% confidence interval (CI) is shown in participants who were tested at baseline and after 0.5 mg of dexamethasone (postdexamethasone suppression). The 4 panels represent the mean cortisol concentrations at baseline and postdexamethasone for individuals without probable PTSD (no PTSD) or with probable PTSD stratified by rs3800373, rs9296158, rs1360780, and rs9470080 genotypes. Individuals were categorized as risk allele carriers when they carried the C, A, T, or T alleles of these SNPs, respectively. Carriers of the AA, GG, CC, or CC homozygote genotypes of rs3800373, rs9296158, rs1360780, and rs9470080, respectively, were labeled as carrying the presumed protective genotypes. We found a significant interaction of genotype carrier- and PTSD-status on cortisol suppression (repeated measures analysis of variance: rs3800373, F1,76=6.03, P=.02; rs9296158, F1,78=8.76, P < .004; rs1360780, F1,79=3.95, P =.05; rs9470080, F1,77=5.32, P =.02; but also using permutation-based methods on percentage cortisol suppression). Although the risk alleles seem to be associated with less suppression (ie, glucocorticoid receptor resistance) in the no PTSD group, they are associated with greater suppression of cortisol from baseline to postdexamethasone in the group with PTSD. For rs9296158 GG carrier with no PTSD and rs9470080 CC carrier with no PTSD, the lower bound of the 95% CI had a negative value and was truncated at zero.