The study titled ‘Substance use and epigenetic age acceleration: Associations with alcohol, tobacco, illicit drugs, and SUD severity’ explores the relationship between various forms of substance use and biological aging. Conducted by Fekete et al., the research analyzes data from 2,276 adults participating in the Person-to-Person Health Interview Study in Indiana.
Background
Prior research has not thoroughly examined whether clinically significant measures of substance use disorders (SUD), including alcohol and opioid use, correlate with accelerated biological aging. This study aims 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 analyzed using two biological aging measures: AgeAccelGrim2 and DunedinPACE. The researchers employed regression models to estimate the associations between substance use indicators and biological aging, adjusting for various covariates.
Results
The findings revealed that:
- Binary measures of illicit opioid use showed a strong positive association with both AgeAccelGrim2 and DunedinPACE.
- Non-prescription opioid use was similarly linked to accelerated biological aging.
- Clinically significant alcohol use was positively associated with AgeAccelGrim2 but not with DunedinPACE.
- Cigarette smoking correlated positively with both biological aging measures, while hookah use showed a negative association with AgeAccelGrim2.
- Interestingly, vaping did not show an association with accelerated biological aging when analyzed alongside cigarette smoking.
Conclusions
The study concludes 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 connecting these substances to 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 of these associations.
Evidence scorecard
- Analytic validity: Established
- Clinical validity: Not established
- Clinical utility: Not established
The evidence is based on primary research involving human participants.