New research has found a link between post-traumatic stress disorder (PTSD) and accelerated aging.
“This is the first study of its type to link PTSD, a psychological disorder with no established genetic basis, which is caused by external, traumatic stress, with long-term, systemic effects on a basic biological process such as aging,” said Dilip V. Jeste, M.D., of the University of California, San Diego, senior author of the study.
That led Jeste, distinguished professor of Psychiatry and Neurosciences and director of the Center on Healthy Aging and Senior Care at UC San Diego, and his colleagues to conduct a comprehensive review of published empirical studies relevant to early aging in PTSD. The review covered multiple databases going back to 2000, investigating if PTSD might show a similar association to aging.
The researchers noted that there is no standardized definition of what constitutes premature or accelerated aging, also known as senescence. For guidance, they looked at early aging phenomena associated with non-psychiatric conditions, such as Hutchinson-Gilford progeria syndrome, HIV infection, and Down’s syndrome.
According to the researchers, the majority of evidence fell into three categories: Biological indicators or biomarkers, such as leukocyte telomere length (LTL); earlier occurrence or higher prevalence of medical conditions associated with advanced age; and premature mortality.
In their literature review, the researchers identified 64 relevant studies. They note that 22 were suitable for calculating overall effect sizes for biomarkers, and 10 for mortality.
All six studies looking specifically at LTL found reduced telomere length in people with PTSD, the researchers discovered. Leukocytes are white blood cells. Telomeres are stretches of protective, repetitive nucleotide sequences at the ends of chromosomes.
These sequences shorten with every cell replication and are considered a strong measure of the aging process in cells, the scientists explain.
The researchers also found evidence of increased pro-inflammatory markers, such as C-reactive protein and tumor necrosis factor alpha, associated with PTSD.
A majority of reviewed studies found increased medical comorbidity of PTSD with several conditions associated with normal aging, including cardiovascular disease, type II diabetes, gastrointestinal ulcer disease, and dementia.
Seven of 10 studies indicated a mild-to-moderate association of PTSD with earlier mortality, consistent with an early onset or acceleration of aging in PTSD, according to the analysis.
“These findings do not speak to whether accelerated aging is specific to PTSD, but they do argue the need to re-conceptualize PTSD as something more than a mental illness,” said first author James B. Lohr, M.D., professor of psychiatry.
“Early senescence, increased medical morbidity and premature mortality in PTSD have implications in health care beyond simply treating PTSD symptoms. Our findings warrant a deeper look at this phenomenon and a more integrated medical-psychiatric approach to their care.”
The study was published in the American Journal of Geriatric Psychiatry.