High Alcohol Intake and Smoking Linked to Age-Related Epigenetic Changes
Philibert and his collaborators showed that the DNA methylation state at two specific locations in the genome, was a more accurate indicator of an individual’s substance use than a person’s self-reported estimates.
October 13, 2015 | by Sarah Massey
Recent research presented at the American Society of Human Genetics (ASHG) 2015 Annual Meeting in Baltimore, identified a link between epigenetic DNA modifications associated with aging, and heavy use of alcohol and cigarettes. These epigenetic changes were linked with hastened aging, which researchers were able to distinctly quantify and measure.
Dr. Robert A. Philibert and his team at the University of Iowa – in collaboration with other institutions – used publically-available data from the Gene Expression Omnibus, to conduct their research. The researchers used the genetic data to determine the DNA methylation state – a modification made outside of the genetic sequence which alters expression of the gene – of various sequences.
Previous research in this field has revealed that changes in DNA methylation state occur predictably as people age, and environmental factors – such as consumption of alcohol and cigarette smoke – can also have an epigenetic effect. Prior research performed by Philibert and his team, identified two distinct loci – base pairs cg05575921 in the AHRR gene and cg23193759 on chromosome 10 – which show variation in methylation levels, dependent on cigarette smoking and alcohol consumption, respectively.
Philibert and his collaborators even showed that the DNA methylation state at these two specific locations in the genome, was a more accurate indicator of an individual’s substance use than a person’s self-reported estimates. In using these previously-established links between DNA methylation and age, Meeshanthini Dogan – a researcher in Philibert’s lab – estimated a participants’ biological age using methylation state alone.
Dogan and other researchers analyzed 71 regions within the human genome, based upon previous studies which designed and tested an epigenetic ‘clock’ based on methylation. The methylation state of each region was identified using an Infinium HumanMethylation450 BeadChip.
The biological age – estimated using the methylation state – was compared with a person’s chronological age, and the difference was used to determine whether there was a link between substance use and accelerated aging.
The results were surprising: high and low consumption of alcohol were linked to premature aging, however those that drank one to two drinks per day were show to have epigenetic changes associated with the healthiest type of aging. Regardless of the level of exposure to cigarette smoke, it was highly correlated with accelerated aging.
According to Dogan, “These new tools allow us to monitor smoking and alcohol use in an objective way, and to understand their effects quantitatively. Furthermore, our methods could be used to analyze any set of 450 BeadChip data, which means that existing data can be used to identify new patterns and that all such results can be easily compared.”
“Being able to objectively identify future smokers and heavy alcohol users when they are young – before major health issues arise – can help providers and public health practitioners prevent future problems, improve quality of life, and reduce later medical costs,” said Philibert. Their next study will aim to determine what changes occur in DNA methylation following various environmental factor fluctuations, over the course of an individual’s life.
“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,” said Dogan. “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.”
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Keywords:Epigenetic, Aging, DNA Methylation
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