In a recent study published in Drug and Alcohol Dependence, researchers explored the connections between substance use and epigenetic age acceleration. The study involved 2,276 adults from Indiana, who participated in the Person-to-Person Health Interview Study. Participants provided saliva samples for DNA methylation profiling and completed validated assessments of substance use disorder (SUD) severity, alcohol use, and nicotine consumption.
Key Findings
The researchers utilized two measures of biological aging: AgeAccelGrim2 and DunedinPACE. They found that:
- Illicit opioid use was positively associated with both AgeAccelGrim2 and DunedinPACE, indicating a link between opioid use and accelerated biological aging.
- Non-prescription opioid use also showed a positive association with both measures of biological aging.
- Clinically significant alcohol use correlated positively with AgeAccelGrim2, but not with DunedinPACE.
- Cigarette smoking was associated with accelerated biological aging at all levels of consumption.
- Interestingly, hookah use was negatively associated with AgeAccelGrim2, while vaping did not show any association when analyzed alongside cigarette smoking.
These findings suggest that certain forms of substance use, particularly cigarette smoking and opioid use, may contribute to accelerated biological aging. The authors emphasize the need for further research to understand the mechanisms behind these associations.
What this study does not show
This study does not establish causation between substance use and biological aging, nor does it provide insights into the long-term health outcomes related to these associations.
Evidence scorecard
- Analytic validity: Established
- Clinical validity: Partial
- Clinical utility: Not established
The evidence is based on primary research involving human participants.