0116 GMT October 22, 2019
"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.
There is no standardized definition of what constitutes premature or accelerated senescence. For guidance, the researchers looked at early aging phenomena associated with non-psychiatric conditions, such as Hutchinson-Gilford progeria syndrome, HIV infection and Down's syndrome. The majority of evidence fell into three categories of 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, EurekAlert reported.
In their literature review, the UC San Diego team identified 64 relevant studies; 22 were suitable for calculating overall effect sizes for biomarkers, 10 for mortality.
All six studies looking specifically at LTL found reduced telomere length in persons with PTSD. 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 also found consistent 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 targeted conditions associated with normal aging, including cardiovascular disease, type 2 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.