Study Links PTSD With Accelerated Aging
Post-traumatic brain injury may be linked with a heightened risk for accelerated aging or premature senescence according to a new study published in the American Journal of Geriatric Psychiatry.
In the first study of its kind, researchers at University of California, San Diego School of Medicine and Veterans Affairs San Diego Healthcare System indicate that individuals with PTSD may also be at risk for 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, MD, Distinguished Professor of Psychiatry and Neurosciences and director of the Center on Healthy Aging and Senior Care at UC San Diego, who is the senior author of this study.
Past research has noted a possible link between psychiatric conditions, such as schizophrenia and bipolar disorder, and accelerated aging, and now Jeste and colleagues sought to see if a similar connection was present in PTSD. To explore this potential connection, the researchers reviewed published empirical studies related to early aging in PTSD from multiple databases dating back to 2000.
Complicating matters, there is no standard clinical definition for premature or accelerated senescence, so the researchers used early aging phenomena associated with non-psychiatric conditions as a guide.
The majority of evidence for a link between the PTSD and accelerated aging broke down 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.
Over the course of the review, the UC San Diego team identified 64 relevant studies, which contained 22 studies suitable for calculating overall effect sizes for biomarkers and 10 for mortality.
According to the report, all six studies which specifically focused on LTL found reduced telomere length in those with PTSD. Leukocytes are white blood cells, and telomeres are stretches of repetitive nucleotide sequences found at the ends of chromosomes. With each replication, these sequences shorten and are believed to be a reliable measure of the aging process in cells.
The report also found consistent evidence of increased pro-inflammatory markers, such as C-reactive protein and tumor necrosis factor alpha, which are linked with PTSD.
Out of all reviewed studies, the majority showed increased medical comorbidity of PTSD with several targeted conditions linked to normal aging, including cardiovascular disease, type 2 diabetes, gastrointestinal ulcer disease and dementia.
Seven of 10 studies found a mild-to-moderate association between PTSD and earlier mortality, which researchers say are consistent with accelerated aging in PTSD.
“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, MD, 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.”