What does chronic stress do to your DNA?
Chronic stress accelerates the wear of your DNA protectors (telomeres) in a way that corresponds to years of extra cellular ageing. You cannot prevent this entirely, but limiting prolonged stress is probably one of the most direct ways to slow biological ageing.
Telomeres are the protective 'caps' at the ends of your chromosomes. They shorten slightly with every cell division, and when they become too short, the cell enters a kind of dormant state or dies. Women with the highest stress levels had telomeres corresponding to roughly ten years of extra cellular ageing compared with low-stress women. At the same time, their production of the enzyme telomerase, which can maintain telomeres, was lower, and their level of oxidative damage was higher.
The biological explanation runs through three mutually reinforcing pathways. Stress hormones (such as cortisol), inflammatory substances, and so-called free radicals damage telomere DNA and inhibit repair. Telomere DNA is especially vulnerable to such oxidative damage: its repair capacity is poorer there than elsewhere in the genetic material. This makes telomeres a kind of weakest link: chronic stress wears them down faster than normal cell division already does.
Notably, this damage can begin before birth. In a small study of 24 mother-child pairs, newborns of mothers with high psychosocial stress during pregnancy were born with measurably shorter telomeres. The starting position of biological ageing can therefore already be determined during foetal development. This is still a preliminary finding from a small study, but the direction is clear.
There are also indications that short telomeres are partly passed on to the next generation, both through the germ cells of parents and through prenatal stress exposure. How strong that effect is, and through exactly which pathway, requires further research.
Relaxation techniques such as meditation are sometimes mentioned as a counterweight, but direct evidence that they actually slow telomere shortening in humans is absent from the available studies. That is a hypothesis, not yet an established effect. What is clear is that long-term excess weight operates through similar inflammatory and ageing pathways as psychological stress, even at a young adult age.
Findings are based on observational and associative human studies, one longitudinal and one small prospective cohort study (n=24). A causal relationship is plausible on the basis of mechanistic research, but has not been proven through large randomised trials. The prenatal and intergenerational findings are limited in certainty.