Substance use has been a topic of extensive research, particularly regarding its impact on health and longevity. A recent study published in Drug and Alcohol Dependence investigates the relationship between various forms of substance use and epigenetic age acceleration. The research highlights significant associations between substance use and biological aging, particularly focusing on alcohol, tobacco, and opioid use.
What this study does not show
This study does not establish causation between substance use and epigenetic age acceleration, nor does it provide insight into 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.
The study analyzed data from 2,276 adults participating in the Person-to-Person Health Interview Study in Indiana. Participants provided saliva samples for DNA methylation profiling, which were used to measure biological aging through two specific metrics: AgeAccelGrim2 and DunedinPACE. The study employed regression models to assess the associations between substance use indicators and biological aging while controlling for various covariates.
Key findings indicate that binary measures of illicit opioid use and non-prescription opioid use were positively associated with both AgeAccelGrim2 and DunedinPACE. Specifically, illicit opioid use showed a strong association (β=0.417, p=5.913e-11) with AgeAccelGrim2, while non-prescription opioid use also demonstrated significant associations (β=0.264, p=1.744e-09). Furthermore, a continuous measure of substance use disorder (SUD) severity was positively linked to biological aging metrics, suggesting that greater severity of SUD correlates with accelerated aging (β=0.061, p=6.608e-06).
Alcohol use was found to have a positive association with AgeAccelGrim2 (β=0.177, p=2.111e-08), although it did not show a significant relationship with DunedinPACE. Interestingly, cigarette smoking was positively associated with both biological aging measures across all levels of smoking. Conversely, hookah use was negatively associated with AgeAccelGrim2 but did not show a significant relationship with DunedinPACE. Vaping, when analyzed alongside cigarette smoking, did not demonstrate an association with accelerated biological aging.
The findings of this study underscore the potential impact of substance use, particularly cigarette smoking and opioid use, on biological aging. These results highlight the importance of further research into the mechanisms that may link substance use to accelerated biological aging, particularly in the context of public health and preventive strategies.
Conclusion
In summary, this study provides valuable insights into the associations between substance use and epigenetic age acceleration. While the findings suggest a strong link between certain substances and biological aging, further research is necessary to explore the underlying mechanisms and establish causation.