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Substance Use Linked to Accelerated Biological Aging

Recent research has explored the relationship between substance use and biological aging, specifically focusing on how alcohol, tobacco, and illicit drugs may contribute to accelerated epigenetic age. This study, published in Drug and Alcohol Dependence, analyzed data from 2,276 adults participating in the Person-to-Person Health Interview Study in Indiana.

Background

Prior studies have not adequately assessed the impact of clinically significant alcohol use, nicotine consumption, and opioid use on biological aging. The authors aimed to fill this gap by examining population-based data to determine if these substances are linked to accelerated biological aging.

Methods

Participants in the study completed validated assessments of substance use disorder (SUD) severity, alcohol use, and nicotine use, while also providing saliva samples for DNA methylation profiling. The researchers employed measures of biological aging, specifically AgeAccelGrim2 and DunedinPACE, to evaluate associations with substance use indicators.

Results

The findings revealed several significant associations:

  • Binary measures of illicit opioid use showed a strong positive correlation 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 was positively associated with both aging metrics at all levels of consumption.
  • Interestingly, hookah use was negatively associated with AgeAccelGrim2, while vaping did not show any significant association when analyzed alongside cigarette smoking.

Overall, the study suggests that substance use, particularly opioid use and cigarette smoking, is strongly linked to accelerated 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 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.

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Evidence classes are taken from source metadata — publication type and trial registration — never from opinion. How we classify · Corrections