Substance use has been a topic of extensive research, particularly regarding its effects on health and longevity. A recent study published in the journal Drug and Alcohol Dependence investigates the relationship between various forms of substance use and epigenetic age acceleration. The research focuses on clinically significant alcohol use, nicotine consumption, opioid use, and overall substance use disorder (SUD) severity.
Study Overview
The study 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, which is a method used to assess biological aging through epigenetic markers. The researchers employed regression models to evaluate the associations between substance use indicators and biological aging, adjusting for various covariates.
Key Findings
The results indicated several significant associations:
- Binary measures of illicit opioid use were positively associated with both AgeAccelGrim2 and DunedinPACE, two measures of biological aging.
- Non-prescription opioid use also showed a positive association with biological aging indicators.
- Clinically significant alcohol use was positively associated with AgeAccelGrim2 but did not show a significant association with DunedinPACE.
- Cigarette smoking was positively associated with both measures of biological aging at all levels of consumption.
- Interestingly, hookah use was negatively associated with AgeAccelGrim2, while vaping did not show a significant association when considered alongside cigarette smoking.
These findings suggest that certain forms of substance use, particularly cigarette smoking and opioid use, are strongly linked to accelerated biological aging. The study emphasizes the need for further research to explore the underlying mechanisms that connect these substances to biological aging.
What this study does not show
While the study identifies associations between substance use and biological aging, it does not establish causation or the specific mechanisms through which these substances may influence epigenetic age acceleration.
Evidence scorecard
- Analytic validity: established
- Clinical validity: partial
- Clinical utility: not established
The evidence is based on primary research involving human participants.