Why chromosome ends shorten with each division
Telomeres are repetitive DNA caps (the sequence TTAGGG in humans) at the ends of chromosomes, bound by protective proteins. They shield the coding genome from being mistaken for broken DNA. Because of the end-replication problem, the cell's DNA-copying machinery cannot fully duplicate the very tips, so a small stretch of telomere is lost at each division.
The enzyme telomerase can rebuild telomeres, but most adult somatic cells express little of it, so telomeres gradually erode over a lifetime. Oxidative stress and inflammation can speed the loss.
The critical-length threshold and its consequences
When telomeres in a cell shorten below a critical length, they can no longer cap the chromosome effectively. This triggers a DNA-damage response that pushes the cell into senescence or apoptosis, a limit known historically as the Hayflick limit on division.
Average telomere length varies widely between people of the same age, so it is a noisy individual marker rather than a precise clock, and reactivating telomerase carries cancer-related concerns. This is general educational information about cell biology, not medical advice; consult a qualified professional.