Smoking: Genetics May Play A Role In Survival Of Some Long-Lived Smokers

Smoking is linked to an increased risk of numerous health issues, including cardiovascular problems, high blood pressure, stroke and more. Yet new findings published in the Journals of Gerontology: Medical Sciences examine how not all smokers experience early death. In fact, some will even manage to survive to older ages. Certain genetic factors may ultimately play a role in whether or not some smokers live longer than others, researchers say.

"We identified a set of genetic markers that together seem to promote longevity. What's more, many of these markers are in pathways that were discovered to be important for aging and lifespan in animal models," Morgan Levine, corresponding author of the study, said in a statement. "There is evidence that these genes may facilitate lifespan extension by increasing cellular maintenance and repair. Therefore, even though some individuals are exposed to high levels of biological stressors, like those found in cigarette smoke, their bodies may be better set up to cope with and repair the damage."

In this recent study, researchers analyzed data from long-lived smokers. They identified a network of SNPs (a DNA sequence variation that commonly occurs within a population) that allows certain individuals to better withstand certain environmental damages, including smoking and mitigate damage. Collectively, these SNPs were strongly associated with high survival rates.

The study findings suggest that longevity, rather than being entirely based on certain environmental factors, may ultimately be determined by the regulation of certain complex genetic networks that can influence stress resistance and genomic stability. In fact, researchers found that some long-lived smokers carrying certain genes had an 11 percent lower cancer prevalence than the smokers who did not carry them.

Thus, the study results suggest that some long-lived smokers may represent a biologically distinct group endowed with genetic variants that allow them to respond differentially to environmental stressors. Furthermore, genomic instability also appears to be one of the hallmarks of cancer pathogenesis. 

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