Lifetime stress accelerates epigenetic aging
Cumulative exposure to stress hormones affects the regulation of genes associated with aging and age-related diseases
One plausible mechanism that may mediate the adverse effects of stress on the aging process is epigenetic regulation. Epigenetic actions do not change the actual genetic code but alter its accessibility by i.e. attaching chemical groups to or removing them from the DNA. A team supervised by Elisabeth Binder, director at the Max Planck Institute of Psychiatry, investigated the effect of lifetime stress on a DNA methylation-based age predictor in blood samples from a cohort of highly traumatized African American individuals.
Cumulative stress exposure throughout the lifetime alters the accessibility and activity of genes associated with aging and age-related diseases.
“Glucocorticoids are molecular effectors of our response to stress and can exert actions in essentially every body organ via activation of the stress-hormone receptor. The stress hormone receptor regulates gene expression by binding to specific response elements in the DNA. This can also lead to long lasting “epigenetic reprogramming,” explains Anthony Zannas, leading scientist in the current study. “ We found that such a stress-induced reprogramming happens in sites that are associated with aging.”
The study showed that individuals exposed to high levels of lifetime stress were epigenetically older than their true biological age. Such a premature “biological” aging has been shown to increase the risk for a number of age-related diseases. Exposure to stress may thus lead to more aging-related diseases by long-lasting epigenetic effects induced by the chronic activation of stress-hormone receptors.
Measuring the epigenetic age in peripheral blood cells may be a possibility to identify chronically stressed individuals at high risk for cardiovascular diseases or dementia and to initiate timely prevention programs.
EB, AN, JK