Substance use has been a topic of extensive research, particularly regarding its impact on health and longevity. A recent study published in the journal Drug and Alcohol Dependence explores the associations between various forms of substance use and biological aging, specifically through the lens of epigenetic age acceleration.
Background
Previous research has not thoroughly investigated whether clinically significant measures of substance use disorders (SUD), such as alcohol consumption, nicotine use, and opioid use, are linked to biological aging. This study aims to fill that gap by analyzing data from a large population-based sample.
Methods
The researchers analyzed data from 2,276 adults who participated in the Person-to-Person Health Interview Study in Indiana. Participants completed validated assessments of SUD severity, alcohol use, opioid use, and nicotine consumption. Additionally, they provided saliva samples for DNA methylation profiling to measure biological aging using the AgeAccelGrim2 and DunedinPACE metrics.
Results
The findings revealed several significant associations:
- Binary measures of illicit opioid use were positively associated with both AgeAccelGrim2 and DunedinPACE.
- Non-prescription opioid use also showed a positive correlation with biological aging metrics.
- Clinically significant alcohol use was positively associated with AgeAccelGrim2.
- Cigarette smoking was linked to accelerated biological aging across all levels of use.
- Interestingly, hookah use was negatively associated with AgeAccelGrim2, while vaping did not show a 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. The study emphasizes the need for further research to explore the mechanisms underlying these associations.
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.