Researchers reviewed data of over 245,000 UK individuals to assess how alcohol impacts aging. Shorter telomeres were found in those who drank heavily or had alcohol use disorder. No effect on telomeres was seen in light-to-moderate drinkers. Telomere length is linked to biological aging and disease onset. The pros and cons of drinking alcohol are frequently relayed, and there’s a new addition to the ever-growing list. Research conducted by Oxford Population Health, part of the University of Oxford, indicates excessive alcohol consumption can speed up the aging process at a biological level. The , published in Molecular Psychiatry, is the largest of its kind to date. It involved more than 245,000 individuals aged between 40 and 69 years old, with their data obtained from the UK Biobank. Three percent of participants were classed as ‘never drinkers’, four percent ‘previous drinkers’, and 93 percent ‘current drinkers’. Data on participants’ weekly alcohol consumption — self-reported when joining the Biobank — was used as the basis of an observational analysis. Researchers also used Mendelian randomization (MR) to investigate whether any genetic markers (that have been previously linked to AUD) might play a role in telomere length. The results? Observational analysis findings indicated that heavy alcohol drinkers and those with alcohol use disorder (AUD) were significantly more likely to have shorter telomeres — an essential part of our chromosomes linked to aging and the onset of various health concerns. Meanwhile, the MR analysis also found a strong link between telomere length and genetically-predicted AUD. The most influential gene was discovered to be AD1HB, which acts as an alcohol metabolizer in the body.
How much alcohol has an impact? The observational analysis found drinking more than 29 units each week was most detrimental. Compared to individuals enjoying six units weekly, this level of consumption was associated with telomere shortening equivalent to two years’-worth of aging. In layman’s terms, 29 units is equivalent to around 10 250ml-sized glasses of wine (with 12 percent alcohol by volume, ABV). If you’re a beer drinker, this equates to about 17 330ml-sized bottles (at five percent ABV). Meanwhile, in the MR analysis, drinking 32 units each week (as opposed to 10 units) was linked to telomere shortening akin to three years of aging. Those with a genetic disposition for AUD also showed a similar level of telomere damage. However, those who enjoy an occasional tipple with dinner probably don’t need to worry too much: the association between alcohol consumption and telomere length was only significant among participants who drank more than 17 units (around six 250ml glasses at 12 percent ABV) per week.
Essentially, “telomeres play an important role in keeping our genes intact and genome stable,” explained Dr Wei Cui, from the Institute of Reproductive and Developmental Biology (IRDB) at Imperial College London. A bit like the ends of shoelaces, “you can think of telomeres like the protective ‘caps’ on the ends of our chromosomes,”said Matt Kaeberlein, PhD, professor of laboratory medicine and pathology at the University of Washington. “[These] are the structures into which our genetic material (our DNA) is organized in each cell.” “Chromosomes become slightly shorter with each cell division due to the way our DNA replicates, [and] the telomeres protect the important parts of our genome from being lost,” he continued. “But, eventually, the telomeres ‘run out’ and become so short that they give off a signal which causes the cells to stop dividing and become ‘senescent’ [biologically aged].” While Kaeberlein noted that discussion around the role of telomeres in aging “is still fairly controversial,” some studies have found associations between shorter telomeres with types of , , and .
Cells naturally divide in the body, which is the most common path to telomere shortening. However, other elements — such as , and chronic stress — have all been noted as possible influences. Another potential player — as highlighted by this research — is alcohol. Yet, how drinking booze directly influences telomeres isn’t entirely clear. “Our hypothesis is that, in the breakdown of ethanol (the main ingredient of alcohol), free radicals (unstable molecules that damage DNA) are produced,” shared Anya Topiwala, DPhil, a senior clinical researcher at Oxford Population Health and study lead. “As a double whammy, alcohol reduces antioxidants — the natural defense mechanism for free radicals.” Whatever the reason, it will likely be a while before the broader impacts are seen. “Telomere shortening does not affect normal cell physiological functions until one or more telomeres in a cell become very short,” said Cui. “In this aspect, I assume it is an accumulative effect.”
Knowing that shorter telomeres are linked to aging and certain diseases, you might wonder if you can ‘undo’ any damage that might have occurred. Cui stated the best approach to “slow down telomere shortening [is] by healthy living,” — and Kaeberlein agreed. “It’s likely that multiple lifestyle factors can impact telomere length in both a positive and negative direction,” he revealed. “Decreasing the amount of stress you experience correlates with longer blood telomeres. Sleep, exercise, and nutrition likely also influence blood telomere length.” For example, studies have found higher intakes of and may positively affect telomere length, while a suggested vitamins C and E may also be of benefit.
Telomeres help protect the body’s chromosomes, and shorter telomere length has been linked to accelerated biological aging and the development of diseases such as cancer. According to this study, drinking 29 or more units of alcohol per week could enhance telomere shortening at a rate parallel to up to three years of aging; but consuming less than 17 units weekly was associated with no effects. Researchers also highlighted an association between genetic disposition and AUD. However, while the study was the largest of its kind and the first to incorporate MR analysis, its results were not conclusive — and more research into alcohol’s direct effect on telomeres needs to be conducted. For instance, it might be beneficial to investigate telomeres in those previously diagnosed with AUD but who now no longer drink, said Kaeberlein. “If there is no effect there, that would suggest that the damage of heavy alcohol use, at least as measured by blood telomere length, is transient once you stop drinking,” he noted.