Genetic evidence shows that smoking causes us to age faster

A study of nearly 500,000 people has shown that smoking shortens the end fragments of chromosomes in the white blood cells of our immune systems. The length of these end fragments, called telomeres, is an indicator of how quickly we age and our cells’ ability to repair and regenerate. The work has been presented at the European Respiratory Society International Congress in Milan.

Telomeres are like the plastic or metal sheathes at the end of shoelaces, which prevent the shoelaces from fraying. They are lengths of repetitive DNA sequences that protect the ends of chromosomes. Each time a cell divides, the telomeres become slightly shorter, eventually becoming so short that the cell can no longer divide successfully, and it dies. This is part of the aging process. Telomere length in white blood cells (called leucocytes) has been linked previously to smoking, but, until now, there has been little research into whether smoking status and the quantity of cigarettes smoked actually caused the shortening in telomere length.

Researchers from Hangzhou Normal University and The Chinese University of Hong Kong analysed data from the UK Biobank, which contains genetic and health information from half a million UK participants. They used a method called Mendelian randomisation, which uses the variations in genes (known as single nucleotide polymorphisms or SNPs) that are inherited from our parents, to infer how exposure to a modifiable environmental factor (such as smoking) is causally related to a disease or health condition (such as shorter leucocyte telomeres). Mendelian randomisation avoids the problem of other, often unknown factors affecting the results, thereby enabling researchers to investigate whether a particular factor is the cause of a condition, rather than just being associated with it.

“We found that current smoking status was statistically significantly associated with shorter leucocyte telomere length, whereas previous smokers and people who had never smoked didn’t show significantly shorter leucocyte telomere length,” said Dr Siyu Dai, an assistant professor at Hangzhou Normal University. “Among people who used to smoke, there was a trend towards shorter telomere length, but this was not statistically significant. People who smoked the greater number of cigarettes had significantly shorter leucocyte telomere length. In summary, smoking may cause the shortening of leucocyte telomere length, and the more cigarettes smoked, the stronger the shortening effect.”

“In recent years, observational studies have linked shortened leucocyte telomere length with many diseases, such as cardiovascular disease, diabetes and muscle loss. This means that the effect of smoking on telomere length probably plays a critical role in these diseases, although more research is needed to understand the underlying mechanisms.

“Our study adds to the evidence that smoking causes ageing. As there are clear health benefits of smoking cessation, it is time to include cessation support as well as treatment into daily clinical management to help us to create a smoke-free environment for the next generation.”

Dai and her colleague Dr Feng Chen will carry out further research to validate the current findings. They are also interested in exploring further the effect of passive smoke exposure on tissue self-repair, regeneration and ageing, particularly in the way that it could affect children.

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