Presented over the weekend at the 40th annual scientific meeting of the Research Society on Alcoholism (RSA) in Denver, USA, the research was carried out by Naruhisa Yamaki and his team from the Kobe University Graduate School of Medicine, Japan.

The researchers recruited 255 study participants from alcoholism treatment services at Kurihama National Hospital in Yokosuka.

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Of these, 134 participants were alcoholic patients and 121 were age-matched controls or non-alcoholics, ranging in age from 41 to 85 years old. The team collected DNA samples from each participant as well as information on their drinking histories and habits.

The results showed that the alcoholic patients had shorter telomeres — the protein caps on the ends of human chromosomes, which are markers of aging and overall health. Yamaki explained that every time a cell replicates, a small piece of telomere is lost, so they naturally get shorter with age.

However, some people may have shorter telomeres for reasons other than aging, with the results of the study suggesting that heavy drinking can cause shorter telomeres and therefore biological aging at a cellular level.

“We also found an association between telomere shortening and thiamine deficiency (TD),” commented Yamaki, with alcoholics already known to be at a greater risk of TD. “TD is known to cause neuron impairments such as Wernicke-Korsakoff Syndrome.

Although how exactly TD can cause neural impairments is unclear, it is well known that oxidation stress cause telomere shortening and, thus, it is possible that oxidation stress may also cause neuron death.” Yamaki added that it’s important for the public to understand that heavy drinking causes telomere shortening because “awareness of this fact provides important information necessary for people to live healthier.”


This story first appeared on AFP Relax News 28th June 2017.