In a recent study published in the journal 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, which were analyzed to measure biological aging using the AgeAccelGrim2 and DunedinPACE metrics.
Background
Previous research has not adequately examined the links between clinically significant alcohol use, nicotine consumption, opioid use, and overall substance use disorder (SUD) severity with biological aging. This study aims to fill that gap by utilizing validated assessments of SUD severity and substance use.
Methods
The researchers employed regression models to estimate associations between various substance use indicators and biological aging, adjusting for relevant covariates. The measures of substance use included binary indicators for illicit and non-prescription opioid use, as well as assessments of alcohol use and smoking.
Results
The findings revealed several significant associations:
- Illicit opioid use was positively associated with both AgeAccelGrim2 and DunedinPACE, indicating a link to accelerated biological aging.
- Non-prescription opioid use also showed a positive association with biological aging metrics.
- Clinically significant alcohol use was positively associated with AgeAccelGrim2 but not 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 any significant association when analyzed alongside cigarette smoking.
These results suggest that substance use, particularly cigarette smoking and opioid use, is strongly linked to accelerated biological aging.
What this study does not show
This study does not establish causation between substance use and biological aging, nor does it explore the underlying mechanisms that may contribute 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.