Gene Evidence Indicates Smoking Accelerates Aging in the Human Body

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Gene Evidence Indicates Smoking Accelerates Aging in the Human Body

Gene Evidence Indicates Smoking Accelerates Aging in the Human Body.

A study involving nearly 500,000 individuals has revealed that smoking can shorten telomeres, which are the end segments of chromosomes in white blood cells closely associated with our immune system.

Measuring these telomeres can provide insights into our aging rate and the ability of cells to self-repair and rejuvenate.

Gene Evidence Indicates Smoking Accelerates Aging in the Human Body

Speaking at the International Congress of the European Respiratory Society held in Milan, Italy, Dr. Suyu Dai, an assistant professor at Hangzhou Normal University’s School of Clinical Medicine and an honorary postdoctoral fellow in the Department of Pediatrics at the Chinese University of Hong Kong, stated, “Our research suggests that smoking status and the quantity of smoking can lead to the shortening of white blood cell telomeres, which serve as indicators of tissue self-repair, regeneration, and aging. In other words, smoking accelerates the aging process, while quitting smoking may significantly reduce associated risks.”

Telomeres are akin to the plastic or metal aglets at the ends of shoelaces, protecting the ends of chromosomes. With each cell division, telomeres become slightly shorter, eventually shortening to a point where cells can no longer successfully divide and subsequently die.

This is a part of the aging process. While white blood cell telomere length has been previously associated with smoking, research on whether smoking status and quantity actually lead to telomere shortening has been limited until now.

Dr. Dai and her colleague Dr. Feng Chen from the Chinese University of Hong Kong analyzed data from the UK Biobank, which contains genetic and health information from 500,000 UK participants. They studied factors such as current smoking status, former smoking, never smoking, smoking addiction level, smoking quantity (pack-years), and white blood cell telomere length obtained from blood tests.

They utilized a method known as Mendelian randomization, which uses genetic variations inherited from parents (called single nucleotide polymorphisms or SNPs) to infer causal relationships between exposure to modifiable environmental factors (such as smoking) and disease or health conditions (like shortened white blood cell telomeres). Mendelian randomization avoids the issue of other factors (typically unknown ones) influencing outcomes, allowing researchers to study whether a specific factor is a cause of a particular disease rather than just associated with it.

The study included data from 472,174 UK Biobank participants and 113 SNPs related to smoking status (15 SNPs for current smokers, 78 SNPs for never smokers, 20 SNPs for former smokers).

“From a statistical perspective, we found a significant association between current smoking status and the shortening of white blood cell telomere length, while former smokers and never smokers did not exhibit significant telomere shortening. Among former smokers, there was a trend towards telomere length reduction, but it was not statistically significant. The more one smoked, the more pronounced the shortening of white blood cell telomeres. In summary, smoking is likely to lead to the shortening of white blood cell telomeres, and the effect is stronger with higher smoking frequency,” Dr. Dai remarked.

“In recent years, observational studies have linked shortened white blood cell telomere length to various diseases, such as cardiovascular diseases, diabetes, and muscle atrophy. This suggests that smoking’s impact on telomere length may play a crucial role in these diseases, although more research is needed to understand the underlying mechanisms. Our study adds to the evidence that smoking contributes to aging. Given the clear health benefits of quitting smoking, it’s time to integrate smoking cessation support and treatment into routine clinical management to create a smoke-free environment for the next generation.”

Dr. Dai and Dr. Chen will undertake further research to validate the current findings. They also express interest in further exploring the effects of passive smoking on tissue self-repair, regeneration, and aging, especially in children.

Professor Jonathan Gregg, Chair of the Tobacco Control Committee of the European Respiratory Society, was not involved in this study. He commented, “This study explores whether smoking affects telomere length. Telomeres protect the ends of chromosomes. If telomeres shorten, cells can no longer divide successfully and eventually die. Dr. Dai and her colleagues studied 500,000 adults and found a significant link between smoking and telomere shortening. This study employs Mendelian randomization, a well-established method providing strong evidence and demonstrating causality, which supports previous observational research indicating that smoking accelerates aging and quitting smoking may potentially reverse this effect. We eagerly await findings on the impact of passive smoking on telomere length.”