Drinking alcohol can definitely speed up the ageing process, researchers have found. The more alcohol you drink, the more your cells appear to age.
In the study shared at the ongoing 40th annual scientific meeting of the Research Society on Alcoholism (RSA) in Denver that concludes on Tuesday, researchers found that alcoholic patients had shortened telomere lengths, placing them at greater risk for age-related illnesses, such as cardiovascular disease, diabetes, cancer and dementia.
''Telomeres, the protein caps on the ends of human chromosomes, are markers of aging and overall health,'' said Naruhisa Yamaki of the Kobe University Graduate School of Medicine.
Yamaki explained that every time a cell replicates, a tiny bit of telomere is lost, so they get shorter with age. But some groups may have shorter telomeres for reasons other than ageing.
''Our study showed that alcoholic patients have a shortened telomere length, which means that heavy drinking causes biological aging at a cellular level,'' he said. ''It is alcohol rather than acetaldehyde that is associated with a shortened telomere length.''
Another report by the same group found that "Chronic alcohol consumption, as well as chronic glucocorticoid exposure, can result in premature and/or exaggerated ageing."
Specifically, alcohol activates the HPA axis in the body, causing glucocorticoid secretion and thus elevating levels of stress hormones in the body. Chronic exposure to these hormones results in an acceleration of the ageing process, which is associated with "gradual, but often dramatic, changes over time in almost every physiological system in the human body. Combined, these changes result in decreased efficiency and resiliency of physiological function."
Chronic stress and chronic heavy alcohol use cause a similar premature ageing effect, including nerve cell degeneration in the hippocampus.
"There is growing evidence that moderate alcohol intake may be a risk factor for atrial fibrillation, the most common heart rhythm disturbance in the world, but the mechanism by which alcohol may lead to atrial fibrillation is unknown," Gregory Marcus, researcher at the University of California, San Francisco, told the conference.
Yamaki and his co-authors recruited 255 study participants from alcoholism treatment services at Kurihama National Hospital in Yokosuka, Japan: 134 alcoholic patients and 121 age-matched controls or non-alcoholics, ranging in age from 41 to 85 years old. DNA samples, as well as drinking histories and habits, were collected from all participants.
''We also found an association between telomere shortening and thiamine deficiency (TD),'' said Yamaki. ''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''.