Substance use has been a topic of extensive research, particularly concerning its impact on health and biological aging. A recent study published in the journal Drug and Alcohol Dependence explores the associations between various forms of substance use—specifically alcohol, tobacco, and illicit drugs—and epigenetic age acceleration. The research, conducted by Fekete et al., analyzed data from 2,276 adults participating in the Person-to-Person Health Interview Study in Indiana.
Study Overview
The study aimed to assess whether clinically significant measures of alcohol use, nicotine consumption, opioid use, and overall substance use disorder (SUD) severity correlate with accelerated biological aging. Participants provided saliva samples for DNA methylation profiling, which were analyzed using two biological aging measures: AgeAccelGrim2 and DunedinPACE.
Key Findings
The results indicated that binary measures of illicit opioid use and non-prescription opioid use were positively associated with both AgeAccelGrim2 and DunedinPACE, suggesting that these substances may contribute to accelerated biological aging. Clinically significant alcohol use was also found to have a positive association with AgeAccelGrim2, although it did not show a similar effect on DunedinPACE.
Furthermore, the study highlighted that cigarette smoking was positively associated with both measures of biological aging across all levels of smoking. Interestingly, hookah use was negatively associated with AgeAccelGrim2, while vaping did not show any significant association when analyzed alongside cigarette smoking.
Implications of the Study
The findings underscore the potential impact of substance use, particularly cigarette smoking and opioid use, on biological aging. The authors emphasize the need for further research to explore the mechanisms that link these substances to accelerated aging processes.
What this study does not show
This study does not establish causation between substance use and biological aging, nor does it explore the long-term health outcomes associated with these associations.
Evidence scorecard
- Analytic validity: Established
- Clinical validity: Partial
- Clinical utility: Not established
The evidence is based on primary research involving human participants.