In a recent study published in Drug and Alcohol Dependence, researchers explored the relationship between substance use and epigenetic age acceleration. The study analyzed data from 2,276 adults participating in the Person-to-Person Health Interview Study in Indiana, focusing on various substances, including alcohol, tobacco, and opioids.
Background
Prior research had not adequately assessed the connections between clinically significant alcohol use, nicotine consumption, opioid use, and overall substance use disorder (SUD) severity with biological aging. This study aimed to fill that gap by utilizing validated assessments of SUD severity and biological aging measures.
Methods
Participants provided saliva samples for DNA methylation profiling, which were used to measure biological aging through AgeAccelGrim2 and DunedinPACE metrics. Regression models were employed to estimate the associations between substance use indicators and biological aging, adjusting for various covariates.
Results
The findings revealed several significant associations:
- Illicit opioid use and non-prescription opioid use were positively associated with both AgeAccelGrim2 and DunedinPACE.
- Clinically significant alcohol use showed a positive association with AgeAccelGrim2 but not with DunedinPACE.
- Cigarette smoking was positively associated with both biological aging measures, while hookah use showed a negative association with AgeAccelGrim2.
- Vaping did not demonstrate a significant association with accelerated biological aging when analyzed alongside cigarette smoking.
Conclusions
The study concluded that substance use, particularly cigarette smoking and opioid use, is strongly linked to accelerated biological aging. These findings highlight the need for further research into the mechanisms connecting opioid use and vaping to biological aging.
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.