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Accelerated DNA Methylation Age: Associations with PTSD and Mortality.
Psychosomatic Medicine 2017 July 21
OBJECTIVE: Recently-developed indices of cellular age based on DNA methylation (DNAm) data, referred to as DNAm age, are being used to study factors that influence the rate of aging and the health correlates of these metrics of the epigenetic clock. This study evaluated associations between trauma exposure, posttraumatic stress disorder (PTSD) symptoms, and accelerated versus decelerated DNAm age among military veterans. We also examined if accelerated DNAm age predicted mortality over the course of a 6.5-year medical record review period.
METHODS: 339 genotype-confirmed white, non-Hispanic, middle-aged, trauma-exposed veterans underwent psychiatric assessment and genome-wide DNAm analysis. DNAm age was calculated using a previously validated algorithm. Medical records were available for a subset of 241 veterans and were reviewed approximately 6.5 years after DNA collection and PTSD assessment.
RESULTS: PTSD hyperarousal symptoms were associated with accelerated DNAm age (β = .20, p = .009) but trauma exposure and total PTSD severity were not. Accelerated DNAm age was also associated with 13% increased risk for all-cause mortality (HR: 1.13, 95% CI: 1.01 - 1.26) during the medical record review period.
CONCLUSIONS: Findings of this study replicate the association between PTSD and accelerated DNAm age and suggest this effect may be specific to the hyperarousal symptom cluster. Results point to the potential utility of DNAm age algorithms for identifying individuals who are aging at an accelerated rate and for determining the factors that influence this process.
METHODS: 339 genotype-confirmed white, non-Hispanic, middle-aged, trauma-exposed veterans underwent psychiatric assessment and genome-wide DNAm analysis. DNAm age was calculated using a previously validated algorithm. Medical records were available for a subset of 241 veterans and were reviewed approximately 6.5 years after DNA collection and PTSD assessment.
RESULTS: PTSD hyperarousal symptoms were associated with accelerated DNAm age (β = .20, p = .009) but trauma exposure and total PTSD severity were not. Accelerated DNAm age was also associated with 13% increased risk for all-cause mortality (HR: 1.13, 95% CI: 1.01 - 1.26) during the medical record review period.
CONCLUSIONS: Findings of this study replicate the association between PTSD and accelerated DNAm age and suggest this effect may be specific to the hyperarousal symptom cluster. Results point to the potential utility of DNAm age algorithms for identifying individuals who are aging at an accelerated rate and for determining the factors that influence this process.
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