Editors' ChoicePsychiatry

A grim scorekeeper of biological aging

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Science Translational Medicine  27 May 2020:
Vol. 12, Issue 545, eabb7103
DOI: 10.1126/scitranslmed.abb7103

Abstract

An epigenetic clock set to predict lifespan shows accelerated biological aging processes in male veterans with posttraumatic stress disorder.

Accelerated biological aging has been linked with psychiatric disorders including depression, schizophrenia, and posttraumatic stress disorder (PTSD). PTSD has the largest effects on biological aging markers among adult psychiatric disorders; it also has persistent epigenetic effects that can span multiple generations.

Yang et al. recently tested whether an epigenetic clock designed to predict time-to-death, called GrimAge, would be accelerated relative to chronological age in male combat veterans with PTSD and healthy combat-exposed veterans without PTSD. GrimAge is an epigenetic marker of biological aging processes that is calculated using methylation-based markers of eight plasma proteins and a marker of smoking exposure, which were selected for their prediction of time-to-death. The authors found accelerated GrimAge in the PTSD group. The findings were replicated in an independent cohort, in which the authors reported an average difference of approximately 2 years of GrimAge acceleration in PTSD versus controls. Moreover, the effect size appeared even larger in a subset with longitudinal assessment 1 to 5 years after the initial evaluation. Individuals whose PTSD symptoms worsened showed a corresponding GrimAge acceleration, and PTSD symptom increases explained 15% of the variance in GrimAge acceleration. Epigenetic clocks like GrimAge represent a particularly interesting way to study biological aging. Epigenetic changes are a causal element in biological aging, and efforts are under way to develop methods to “reset” the epigenetic clock. It is plausible that efforts to treat the stress-related psychiatric symptoms of PTSD could one day be supplemented with corresponding treatments to reverse corresponding effects on physical health and aging.

Several outstanding questions remain. Given the male military sample, further research is needed in women and with other trauma types. It is also not yet clear whether PTSD-related stress contributes to early biological aging or whether early aging contributes to stress vulnerability in some way. The longitudinal approach taken in this study represents a first step in teasing this apart. It would also be interesting to test whether gold-standard PTSD treatments, such as cognitive behavioral therapy, allow GrimAge acceleration to recover toward a normative aging trajectory.

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