Researchers say that the more a person drinks, the greater the chance of doing damage at the biological level to their cells.

Drinking alcohol is widely accepted in the Western world, but few people are probably aware of the damage that alcohol can do on a biological level.

New research shows how drinking can affect the health of our cells, causing them to age prematurely.

The National Institute on Alcohol Abuse and Alcoholism (NIAAA) reports that in the United States, alcohol is the fourth leading preventable cause of death. Every year, approximately 88,000 U.S. adults die from alcohol-related causes.

And yet, according to recent estimates, more than half of U.S. individuals have drank in the past month and almost 27 percent of adults report binge drinking in the past month.

New research – presented at the 40th annual scientific meeting of the Research Society on Alcoholism (RSA), held in Colorado – suggests that the more people drink, the older their cells get.

The findings were presented by Dr. Naruhisa Yamaki, a clinical fellow at the Kobe University Graduate School of Medicine in Japan.

The study focused on the effects of alcohol on telomere length.

“Telomeres, the protein caps on the ends of human chromosomes, are markers of aging and overall health,” explained Yamaki.

Telomeres are repetitive segments of DNA found at the end of chromosomes. As explained in U.S. National Library of Medicine, their role is to protect the ends of chromosomes, just like “the tips of shoelaces keep them from unraveling.”

Every time a cell divides, telomeres lose a part of their DNA. As we age, our telomeres get shorter and shorter, until all of the DNA in the telomere is lost and the cells can no longer replicate, causing them to die.

Some people, however, may have shorter telomere length for other reasons than aging. This puts them at risk of illnesses that are normally associated with growing older, such as cardiovascular disease, diabetes, dementia, and some forms of cancer.

Shorter telomeres, thiamine deficiency

Yamaki and colleagues examined 255 people.

Some of them were enrolled in treatment programs for alcoholism at the Kurihama National Hospital in Japan.

Of the study participants, 134 had alcoholism and 121 did not. The participants’ age ranged between 41 and 85 years old.

The researchers examined the drinking patterns and drinking history of the participants, as well as collected DNA samples from all of them.

“Our study showed that alcoholic patients have a shortened telomere length, which means that heavy drinking causes biological aging at a cellular level [...] It is alcohol rather than acetaldehyde that is associated with a shortened telomere length,” said Yamaki.

Acetaldehyde is a toxic byproduct that occurs when the human body metabolizes alcohol.

The researchers also found that shorter telomeres correlated with thiamine, or vitamin B-1, deficiency.

Thiamine is a vitamin that the human body needs in order to metabolize carbohydrates, amino acids, and fatty acids.

A severe deficiency of thiamine can cause a disease called “beriberi” that affects several organs, and it can also lead to neurological disorders such as Wernicke's encephalopathy or the Wernicke-Korsakoff syndrome.

Yamaki explains, “Although how exactly TD [thiamine deficiency] can cause neural impairments is unclear, it is well known that oxidation stress cause[s] telomere shortening and, thus, it is possible that oxidation stress may also cause neuron death.”

He also emphasizes the importance of the findings for public health. People must know that heavy alcohol use and binge drinking can lead to the premature shortening of the telomeres, Yamaki says, because “awawareness of this fact provides important information necessary for people to live healthier.”