Why do your telomeres get shorter as you age?

Every cell division costs a piece of telomere. When a cell copies its DNA in order to divide, the copying enzyme cannot capture the very last bits at the ends. As a result, a small amount of telomere length is lost with each division. This mechanism is called replication attrition and is the fundamental underlying process behind telomere shortening during ageing. The more often a cell has divided, the shorter its telomeres tend to be.

Free radicals accelerate this process. Free radicals, also known as reactive oxygen species (ROS), are aggressive molecules that our bodies produce during metabolism and that also enter from the outside. They damage DNA, and telomeres are particularly vulnerable to this. They thus act as a link in the chain: lifestyle factors such as smoking, an unhealthy diet, sleep deprivation and UV radiation increase the production of free radicals, which in turn accelerates telomere shortening.

Chronic stress and low-grade inflammation amplify the damage further. Prolonged psychological stress increases the production of stress hormones (glucocorticoids), which in turn stimulate free radicals and inflammatory substances. Those inflammatory substances also damage telomeres. In this way, stress, free radicals and inflammation reinforce one another in a vicious cycle. Longitudinal studies in humans show that people with chronically high stress levels have, on average, shorter telomeres than people with low stress.

Your starting point at birth counts at least as much. Telomere length at birth appears to be the most important predictor of telomere length throughout life. New research using advanced DNA sequencing shows that the pattern of which chromosome ends are relatively long or short is already established in umbilical cord blood and remains remarkably stable as a person ages. In addition, parents can pass short telomeres directly to their children through their genes, although the evidence for this is still limited.

When telomeres become too short, the cell enters an alarm state. Telomeres are normally wrapped in a protective protein complex that prevents the cell from recognising the end as damaged DNA. Once telomeres reach a critical minimum or lose that protective wrapping, the cell raises the alarm: it permanently stops dividing (senescence) or dies off (apoptosis). An accumulation of such arrested cells in tissues contributes to the decline of organs that we experience as ageing.