The research published in Drug and Alcohol Dependence investigates the relationship between substance use and epigenetic age acceleration. The study utilized data from 2,276 adults in Indiana who participated in the Person-to-Person Health Interview Study. Participants underwent assessments for substance use disorder (SUD) severity, clinically significant alcohol use, and various forms of nicotine consumption, alongside providing saliva samples for DNA methylation profiling.
Two primary measures of biological aging were employed: AgeAccelGrim2 and DunedinPACE. The findings indicate that certain forms of substance use are positively associated with accelerated biological aging. Specifically, binary measures of illicit opioid use and non-prescription opioid use showed significant positive correlations with both AgeAccelGrim2 and DunedinPACE.
Additionally, clinically significant alcohol use was positively associated with AgeAccelGrim2, although it did not show a similar relationship with DunedinPACE. The study also found that cigarette smoking was positively associated with both measures of biological aging across all levels of consumption. In contrast, hookah use was negatively associated with AgeAccelGrim2, while vaping did not demonstrate a significant association when considered alongside cigarette smoking.
The regression models used in the analysis were adjusted for various covariates, ensuring a robust examination of the associations between substance use and biological aging. The results underscore the strong link between substance use, particularly cigarette smoking and opioid use, and accelerated biological aging.
What this study does not show
This study does not establish a causal relationship between substance use and accelerated biological aging, nor does it explore the underlying mechanisms involved.
Evidence scorecard
- Analytic validity: established
- Clinical validity: partial
- Clinical utility: not established
The evidence is based on primary research involving human participants.