A genetic study has provided new evidence that alcohol accelerates biological aging. This is based on experimental data, where the participants who recorded higher weekly intakes of alcohol were found to have significantly shorter telomeres. This is indicative of direct DNA damage.
In more extreme cases of alcohol intake, it was found by the University of Oxford researchers that having an alcohol-use disorder was associated with up to six years of age-related DNA damage. Overall, the findings could implicate alcohol with age-related diseases such as Alzheimer’s disease.
While the short-term harm that excessive drinking causes is well established. However, data about whether alcohol accelerates the aging process is less well-defined. One reason for this is because ageing may relate to other factors, like socio-economic status.
These other variables have been controlled through new research which uses a genetic-based analysis. This research finds alcohol directly accelerates aging by damaging DNA in telomeres.
Telomeres are repetitive DNA sequences that cap the end of chromosomes, protecting them from damage. Telomere length is considered an indicator of biological aging, since 50-100 DNA bases are lost each time a cell replicates. Once telomeres become too short, cells can no longer divide and may even die.
Shorter telomere lengths have been connected with other aging-related diseases like Alzheimer’s disease, cancer, and coronary artery disease.
The association between alcohol intake and telomere length was examined for 245,000 participants, drawing data from the UK Biobank. A genetic method called Mendelian Randomisation (MR) was deployed, where ‘genetic proxies’ were used to predict the level of exposure for each participant. These were genetic variants that have previously been associated with alcohol consumption and alcohol use disorders in large-scale genome-wide association studies.
The researchers also performed an observational assessment, based on the participants’ self-reported weekly alcohol intake at recruitment.
The data showed there was a significant association between high alcohol intake and shorter telomere length. As an example, compared with drinking less than 6 units of alcohol a week (about two large 250ml glasses of wine), drinking more than 29 units weekly (about ten 250ml glasses of 14 percent alcohol by volume wine) was associated with between one and two years of age-related change on telomere length.
With a second example, an increase from 10 units to 32 units per week was associated with the equivalent of 3 years of aging. The association between genetically-predicted alcohol consumption and telomere length was only significant for those drinking more than 17 units per week. This suggests that a minimum amount of alcohol consumption may be required to damage telomeres.
For people with an alcohol-use disorder, these individuals had significantly shorter telomere lengths compared with controls. This was equivalent to between 3 and 6 years of age-related change.
The research appears in the journal Molecular Psychiatry. The study is titled “Alcohol consumption and telomere length: Mendelian randomization clarifies alcohol’s effects.”
