Telomeres, the specific DNA–protein structures found at both ends of each chromosome, protect genome from nucleolytic degradation, unnecessary recombination, repair, and interchromosomal fusion. Telomeres therefore play a vital role in preserving the information in our genome. As a normal cellular process, a small portion of telomeric DNA is lost with each cell division. When telomere length reaches a critical limit, the cell undergoes senescence and/or apoptosis. Telomere length may therefore serve as a biological clock to determine the lifespan of a cell and an organism. Certain agents associated with specific lifestyles may expedite telomere shortening by inducing damage to DNA in general or more specifically at telomeres and may therefore affect health and lifespan of an individual. In this review we highlight the lifestyle factors that may adversely affect health and lifespan of an individual by accelerating telomere shortening and also those that can potentially protect telomeres and health of an individual.
Telomere length can be prevented from shortening by an enzyme Telomerase. Telomerase has a protein subunit (hTERT) and an RNA subunit (hTR). This enzyme is active in germline and stem cells and maintains their telomere length by adding ‘TTAGGG’ repeats to the ends of chromosomes. Therefore, telomeres do not shorten in these types of cells. Telomerase is inactive in normal somatic cells. These cells, therefore, lose telomeres over time and when telomere length reaches below a critical limit, cells either senesce or die. In the absence of appropriate signals for senescence or apoptotic death, continued cell division leads to severe telomere shortening and genomic instability.