In the study, all levels of exposure to smoke were associated with significantly premature ageing, the scientists found.
Moderate alcohol use -about one to two drinks per day - was correlated with the healthiest ageing, while very low and high consumption were linked to accelerated ageing, the study found.
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Prior research had shown that methylation patterns change in predictable ways as people age, as well as in response to environmental exposures, such as cigarette smoke and alcohol.
In these earlier studies, Philibert's laboratory identified two specific locations in the genome, base pairs cg05575921 on the AHRR gene and cg23193759 on chromosome 10, at which methylation levels were highly associated with smoking and alcohol consumption, respectively.
They showed that DNA methylation levels at these two locations was a better measure of substance use than people's self-reported estimates.
Thus, in this follow-up study, Meeshanthini Dogan and Philibert used methylation levels as a proxy for tobacco and alcohol consumption.
They estimated each person's biological age using a previously validated epigenetic "clock" based on methylation levels at 71 locations in the genome, as measured by the widely used Infinium HumanMethylation450 BeadChip.
Then, they calculated the difference between biological age and chronological age, and assessed the relationship between tobacco and alcohol use and premature ageing.
They found that all levels of exposure to smoke were associated with significantly premature ageing. Moderate alcohol use was correlated with the healthiest ageing, while very low and high consumption were linked to accelerated ageing.
The researchers' next step is to unravel the details of how methylation patterns change in response to lifestyle changes during the life course.
"For example, we want to study how the intensity of current tobacco and alcohol use and cumulative levels of use throughout a lifetime affect methylation, including what happens when a person quits smoking or drinking," Dogan said. "By clarifying at what point the epigenetic changes become tougher to stop or reverse, we can inform decisions about how best to use the limited public health resources we have," Dogan said.
The research was presented at the American Society of Human Genetics 2015 Annual Meeting in Baltimore.
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