A new paper in the online version of The Lancet has shown in a direct fashion that both smoking and obesity decrease lifespan.
Researchers evaluated a group of female identical twins to determine the effects of smoking, obesity and serum leptin levels on telomere length. Telomeres are little bits of genetic material that act almost as coupons allowing the cells to divide. As each cell divides, it has to turn in a coupon to do so. When the coupons run out, the cell can no longer divide and dies. When all our cells run out of coupons and die, we die along with them. So telomere length—the longer the telomere, the more coupons available—basically determines the amount of life left in a cell. The more rapidly ones’ telomeres are consumed, the more quickly one ages.
The data from this study shows that women who smoke have shorter telomeres than those who are genetically identical but don’t smoke. Women who never smoked have longer telomeres than those who quit who have longer telomeres than those who still smoke. A strong relationship exists between number of packs smoked and telomere shortening.
A strong relationship also exists between serum leptin levels and telomere shortening. Leptin is a hormone made by fat cells; a high levels of circulating leptin usually equates to a larger fat mass. Interestingly, when the researchers initially compared BMI to telomere length there appeared to be a fairly strong negative correlation between the two, i.e., as BMI goes up, telomere length goes down. After applying a linear regression (a form of statistical analysis) to this data, however, the BMI/telomere length relationship faded to statistical insignificance, a finding I was happy to see because I hate using BMI to estimate the state of obesity. Serum leptin levels, in my opinion, along with body fat percentage evaluation are a much better way to determine the state of one’s excess fat, which is, after all, what were interested in.
The researchers conclude:

Our findings suggest that obesity and cigarette smoking accelerate human ageing. Our cross-sectional data underscore the considerable variation in telomere length between individuals. Thus large cohorts are needed to capture the effects of inflammation and oxidative stress.1 However, in view of the hypothesis that telomere length in vivo represents cellular turnover and exposure to oxidative and inflammatory damage, the difference in telomere length between being lean and being obese corresponds to 8·8 years of ageing; smoking (previous or current) corresponds on average to 4·6 years of ageing; and smoking a pack per day for 40 years corresponds to 7·4 years of ageing. Our results emphasise the potential wide-ranging effects of the two most important preventable exposures in developed countries—cigarettes and obesity.

So there you have it. If you are both overweight AND smoke, you can almost hear the telomeres tearing away.

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