A genetic study shows that alcohol accelerates biological aging

Results of a new analysis from Oxford Population Health show that alcohol damages DNA by shortening its protective telomeres.

Telomeres are repetitive DNA sequences that cap the ends of chromosomes, protecting them from damage. Telomere length is considered a potential biological marker of aging, since 50 to 100 base pairs are lost each time a cell replicates – extremely short telomeres prevent cell division and can even trigger cell death. Previous studies of leukocytes (cells of the immune system) have shown that shorter telomere lengths are associated with several age-related diseases, including Alzheimer’s disease, cancer, and coronary heart disease.

Longevity. Technology: Telomere length is a partly inherited trait, but other factors play a role, the usual suspects related to environment and lifestyle – especially exercise, diet and smoking – having a significant impact. Until now, studies on the impact of alcohol consumption on telomere length have been conflicting, in part due to the various methods used to measure telomeres and categorize alcohol consumption.

To provide more definitive research, Oxford Population Health researchers conducted the first genetic study of the association between alcohol consumption and telomere length. Their data comes from over 245,000 UK biobank participants and the results were published today in Molecular psychiatry.

The research team used a genetic approach called Mendelian Randomization (MR), using 93 genetic variants previously associated with weekly drinking and 24 variants previously associated with a diagnosis of alcohol use disorder. [1].

The MRI uses ‘genetic proxies’ to predict each participant’s level of exposure, and the team then looked at measurements of leukocyte telomere length (LTL), which were quantified using DNA samples collected when participants were recruited from the UK Biobank.

To complement the MR analysis, the researchers also performed an observational assessment based on study participants’ self-reported weekly alcohol consumption at the time of recruitment; most participants were current drinkers, with only 3% never drinking and 4% being past drinkers.

Discoveries at the bottom of the glass

The study found that there was a significant association between heavy alcohol consumption and shorter leukocyte telomere length. Compared to drinking less than 6 units of alcohol per week (approximately two large 250 ml glasses of wine), drinking more than 29 units per week (approximately ten drinks) was associated with a change in length telomeres between one and two years related to age.

As expected, therefore, people who were diagnosed with an alcohol use disorder had significantly shorter LTLs compared to controls – equivalent to between three and six years of alcohol-related change. ‘age.

Similarly, in the MR study, shorter telomere length was linked to genetically predicted higher alcohol consumption – an increase in weekly consumption of 10 to 32 units was associated with three years of aging.

The association between genetically predicted alcohol consumption and telomere length, however, was only significant for those who drank more than 17 units per week; this could mean that there is a minimum threshold of alcohol consumption that must be passed before telomere damage is sustained.

MR analysis also revealed a significant association between genetically predicted alcohol use disorder and telomere length, which is equivalent to approximately three years of aging.

Last orders

While these results don’t conclusively prove that alcohol directly affects telomere length, two study results confirm that this is the case. First, the effects were only found in current drinkers, not in previous or never-drinkers; and second, the most influential genetic variant in the MR analysis was AD1HB, an alcohol metabolism gene.

The study authors posit that a potential biological mechanism to explain the influence of alcohol on telomere length is increased oxidative stress and inflammation. The metabolism of ethanol metabolism can both produce reactive oxidant species that damage DNA and reduce levels of antioxidant compounds that protect against oxidative stress.

Dr Anya Topiwala, study leader, said: “These results support the suggestion that alcohol, especially at excessive levels, directly affects telomere length. Shortened telomeres have been proposed as risk factors for a number of serious age-related diseases, such as Alzheimer’s disease.

“Our results provide another piece of information for clinicians and patients looking to reduce the harmful effects of excess alcohol. Also, the dose of alcohol is important – even reducing consumption could have benefits [2].”

Dr Richard Piper, Managing Director of Alcohol Change UK, said: “We welcome all research into the effects of alcohol on the human body. This particular study shows clear links between alcohol consumption and aging, and points to a possible link between alcohol and Alzheimer’s disease.

“The researchers are transparent that this study does not prove causation, but they also present a well-argued case about the likely biological mechanism. In general, there is a growing body of science showing how, exactly, alcohol causes so many health problems and so many premature deaths. [3].”

[1] https://www.nature.com/articles/s41380-022-01690-9
[2] https://www.ndph.ox.ac.uk/news/genetic-study-provides-new-evidence-that-alcohol-accelerates-biological-aging
[3] https://www.techexplorist.com/study-offers-evidence-alcohol-accelerates-biological-aging/52727/

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