Why do your telomeres get shorter as you age?

Every time a cell divides, a small piece of telomere is lost. The copying enzyme simply cannot replicate the very last bits at the ends of your DNA. The more often a cell has divided, the shorter its telomeres tend to be. This is the basic mechanism behind telomere shortening and has been robustly demonstrated.

Free radicals accelerate this process. These are aggressive molecules that your body produces during metabolism, but that also enter through smoking, unhealthy eating, sleep deprivation, and UV radiation. Telomeres are particularly vulnerable to this kind of damage. Free radicals therefore form a direct link between your lifestyle and faster telomere shortening.

Chronic stress and low-grade inflammation make things worse. Prolonged stress raises stress hormones, which in turn fuel free radicals and inflammatory substances. Those inflammatory substances also damage telomeres. Studies in humans show that people with chronically high stress levels have, on average, shorter telomeres than people with low stress.

Your starting position at birth counts at least as heavily. The telomere length you have at birth appears to be the strongest predictor of your telomere length throughout your entire life. Research shows that the pattern of long and short telomeres is already established in umbilical cord blood and remains remarkably stable. Parents can also pass shorter telomeres on to their children through their genes, although the evidence for this is still limited.

When telomeres become too short, the cell shuts itself down. Normally, telomeres are wrapped in a protective protein shell that prevents the cell from recognising the end as damaged. Once that no longer works, the cell permanently stops dividing or dies. An accumulation of such shut-down cells in tissues is one of the driving forces behind the aging of organs.