Is Post-Traumatic Stress Disorder Associated with Premature Senescence? A Review of the Literature

Objective: Post-traumatic stress disorder (PTSD) has major public health significance.
Evidence that PTSD may be associated with premature senescence (early or accelerated
aging) would have major implications for quality of life and healthcare policy.
We conducted a comprehensive review of published empirical studies relevant to
early aging in PTSD. Method: Our search included the PubMed, PsycINFO, and PILOTS
databases for empirical reports published since the year 2000 relevant to early
senescence and PTSD, including: 1) biomarkers of senescence (leukocyte telomere
length [LTL] and pro-inflammatory markers), 2) prevalence of senescence-associated
medical conditions, and 3) mortality rates. Results: All six studies examining LTL
indicated reduced LTL in PTSD (pooled Cohen’s d ¼ 0.76). We also found consistent
evidence of increased pro-inflammatory markers in PTSD (mean Cohen’s ds),
including C-reactive protein ¼ 0.18, Interleukin-1 beta ¼ 0.44, Interleukin-6 ¼ 0.78,
and tumor necrosis factor alpha ¼ 0.81. The majority of reviewed studies also indicated
increased medical comorbidity among several targeted conditions known to be
associated with normal aging, including cardiovascular disease, type 2 diabetes
mellitus, gastrointestinal ulcer disease, and dementia. We also found seven of 10
studies indicated PTSD to be associated with earlier mortality (average hazard ratio:
1.29). Conclusion: In short, evidence from multiple lines of investigation suggests
that PTSD may be associated with a phenotype of accelerated senescence. Further
research is critical to understand the nature of this association. There may be a need
to re-conceptualize PTSD beyond the boundaries of mental illness, and instead as a
full systemic disorder. (Am J Geriatr Psychiatry 2015; 23:709e725)