The study published in Drug and Alcohol Dependence explores the relationship between substance use and epigenetic age acceleration. Conducted by researchers from the Irsay Institute for Sociomedical Sciences Research and the University of Michigan, the research analyzed data from 2,276 adults participating in the Person-to-Person Health Interview Study in Indiana.
Participants provided saliva samples for DNA methylation profiling and completed validated assessments regarding their substance use, including alcohol, nicotine, and opioid use, as well as overall substance use disorder (SUD) severity. The researchers utilized two measures of biological aging: AgeAccelGrim2 and DunedinPACE.
Key findings indicated that binary measures of illicit opioid use and non-prescription opioid use were positively associated with both AgeAccelGrim2 and DunedinPACE. Additionally, clinically significant alcohol use was positively associated with AgeAccelGrim2 but not with DunedinPACE. Cigarette smoking was also found to be positively associated with both aging measures, while hookah use showed a negative association with AgeAccelGrim2.
The results suggest that substance use, particularly cigarette smoking and opioid use, is strongly linked to accelerated biological aging. The authors emphasize the need for further research to understand the mechanisms through which these substances may contribute to biological aging.
What this study does not show
This study does not establish causation between substance use and epigenetic age acceleration, nor does it explore the underlying biological mechanisms involved.
Evidence scorecard
- Analytic validity: Established
- Clinical validity: Partial
- Clinical utility: Not established
The evidence is based on primary research involving human participants.