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Substance Use Linked to Accelerated Biological Aging in Adults

Substance use has long been a topic of interest in understanding its effects on health and longevity. Recent research 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

The study, conducted by Fekete et al., involved a comprehensive analysis of data from 2,276 adults participating in the Person-to-Person Health Interview Study in Indiana. The researchers aimed to determine whether clinically significant alcohol use, nicotine consumption, opioid use, and overall substance use disorder (SUD) severity are linked to accelerated biological aging.

Methods

Participants completed validated assessments regarding their substance use and provided saliva samples for DNA methylation profiling. Two measures of biological aging were employed: AgeAccelGrim2 and DunedinPACE. The researchers utilized regression models to estimate associations between substance use indicators and biological aging while adjusting for various covariates.

Results

The findings revealed several noteworthy associations:

  • Illicit opioid use and non-prescription opioid use were positively associated with both AgeAccelGrim2 and DunedinPACE.
  • Clinically significant alcohol use was positively associated with AgeAccelGrim2 but did not show a similar association with DunedinPACE.
  • Cigarette smoking was linked to accelerated biological aging across all levels of use, while hookah use showed a negative association with AgeAccelGrim2.
  • Vaping did not demonstrate a significant association with biological aging when analyzed alongside cigarette smoking.

Overall, the study underscores the strong link between substance use, particularly cigarette smoking and opioid use, and accelerated biological aging.

What this study does not show

While the study identifies associations between substance use and biological aging, it does not establish causation or the underlying mechanisms driving these relationships.

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