Studies on over half a million individuals have shown that tobacco smoking significantly shortens chromosome end fragments known as telomeres, and their length provides an indication of both our rate of aging and our cells’ capacity to regenerate and repair themselves.

This study shows that smoking status and number of cigarettes consumed can shorten leucocyte telomere length, an indicator of aging, tissue regeneration and self-repair. Therefore, smoking accelerates aging processes while quitting can significantly decrease risks associated with it.

Telomeres act like plastic sheaths on shoelaces to stop fraying. Telomeres are repetitive DNA sequence lengths protecting chromosome ends; each time cells divide they shorten gradually until their size limits their ability to divide further and eventually they die off completely.

Telomere shortening is part of aging. Smoking may shorten leucocyte telomere length; however, studies are limited as to whether smoking-related factors actually caused any reduction.

Data was obtained from the UK Biobank which contains health and genetic information on over half a million individuals, including information such as smoking status (current, former, never), nicotine addiction level, the total pack-years smoked as well as leucocyte telomere length information from blood tests.

Mendelian randomization, an approach utilizing gene variations called single nucleotide polymorphisms that we inherit and pass down through generations, was utilized to infer how exposure to environmental factors such as smoking was linked with conditions or health issues like shorter leucocyte telomeres.

Mendelian randomization allows researchers to circumvent the challenge posed by other, often unknown factors influencing results and examine if one factor causes rather than simply links with an illness or condition.