Substance use, particularly cigarette smoking and opioid use, has been identified as a significant factor associated with accelerated biological aging. This article summarizes findings from a study that analyzed data from 2,276 adults participating in the Person-to-Person Health Interview Study in Indiana. The study aimed to explore whether clinically significant measures of substance use disorder (SUD) severity, alcohol use, nicotine consumption, and opioid use are linked to biological aging, as measured by DNA methylation profiling.
Background
Prior research has not extensively examined the connections between validated measures of substance use and biological aging. This study fills that gap by utilizing population-based data to assess the impact of various substances on epigenetic age acceleration.
Methods
Participants in the study completed validated assessments of SUD severity, clinically significant alcohol use, non-prescription and illicit opioid use, and nicotine use. They also provided saliva samples for DNA methylation profiling, which were analyzed using two biological aging measures: AgeAccelGrim2 and DunedinPACE. Regression models were employed to estimate associations between substance use indicators and biological aging while adjusting for relevant covariates.
Results
The findings revealed several significant associations:
- Binary measures of illicit opioid use showed a strong positive association with both AgeAccelGrim2 (β=0.417, p=5.913e-11) and DunedinPACE (β=0.180, p=0.010).
- Non-prescription opioid use also demonstrated a positive correlation with AgeAccelGrim2 (β=0.264, p=1.744e-09) and DunedinPACE (β=0.127, p=0.008).
- A continuous measure of SUD severity was positively associated with both AgeAccelGrim2 (β=0.061, p=6.608e-06) and DunedinPACE (β=0.039, p=0.008).
- Clinically significant alcohol use was positively associated with AgeAccelGrim2 (β=0.177, p=2.111e-08) but not with DunedinPACE.
- Cigarette smoking was positively associated with both AgeAccelGrim2 and DunedinPACE across all levels of use.
- Hookah use was negatively associated with AgeAccelGrim2 but did not show a significant relationship with DunedinPACE.
- Vaping was not associated 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. These findings highlight the need for further research to explore the mechanisms that connect opioid use and vaping to biological aging processes.
What this study does not show
This study does not establish causation between substance use and epigenetic age acceleration; it only identifies associations.
Evidence scorecard
- Analytic validity: Established
- Clinical validity: Partial
- Clinical utility: Not established
The evidence is based on primary research involving human participants.