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

Abstract

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. 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. All six studies examining LTL indicated reduced LTL in PTSD (pooled Cohen’s d = 0.76). We also found consistent evidence of increased pro-inflammatory markers in PTSD (mean Cohen’s ds), including C-reactive protein = 0.18, Interleukin-1 beta = 0.44, Interleukin-6 = 0.78, and tumor necrosis factor alpha = 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 HR = 1.29). 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.

PTSD is associated with an increase in aged T cell phenotypes in adults living in Detroit

“…Overall, the present study adds to the mounting evidence from the literature that PTSD is associated with a phenotype of accelerated immune system aging (Lohr et al, 2015). The exact mechanisms underlying these associations remain unclear, but it is likely that the psychosocial stress associated with PTSD has strong influences on the neuroendocrine system, which may directly and indirectly contribute to immune aging, for example through the hypothalamic–pituitary–adrenal axis and the sympathetic–adrenal–medullary systems (Effros, 2011; Pace and Heim, 2011).…”

Longitudinal associations between post-traumatic stress disorder and metabolic syndrome severity

“…We suspect that PTSD-related MetS may reflect an underlying process wherein the stress and chronicity of PTSD symptoms contribute to accelerated cellular aging and premature disease onset (Miller et al, 2014; Lohr et al, 2015; Wolf et al, 2016). The prevalence of MetS is strongly associated with age in the US population (Ervin et al, 2009); however, we found that PTSD was associated with MetS independent of age, with a prevalence that was greater than expected by age.…”

Childhood and Adolescent Adversity and Cardiometabolic Outcomes: A Scientific Statement From the American Heart Association

“…Although investigators have examined posttraumatic stress disorder in relation to a range of health outcomes (including rheumatoid arthritis, stroke, heart disease, and cancer), some of the strongest empirical research, in terms of methodology and findings, has been with cardiometabolic diseases. 70,71 Numerous methodologically rigorous prospective population-based observational studies have found that posttraumatic stress disorder is associated with increased risk of incident CVD [72][73][74][75][76][77][78][79][80][81][82][83][84] and T2DM. [85][86][87] However, whether and how much of the relation between childhood adversity and cardiometabolic disease may be explained by posttraumatic stress disorder is unclear, especially because these studies have included traumatic events over the life course, with a substantial proportion of studies focused on veterans and military service-related trauma, not just adversity during childhood.…”