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Substance Use Linked to Epigenetic Age Acceleration

Substance use has long been a topic of interest in public health, particularly regarding its effects on physical and mental well-being. A recent study published in Drug and Alcohol Dependence investigates the connections between various forms of substance use and epigenetic age acceleration, a biological marker that may indicate the aging process at a cellular level.

The research 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 and completed validated assessments of substance use disorder (SUD) severity, alcohol use, and nicotine consumption. The study specifically looked at measures of biological aging, including AgeAccelGrim2 and DunedinPACE.

Key Findings

  • Binary measures of illicit opioid use and non-prescription opioid use were positively associated with both AgeAccelGrim2 and DunedinPACE.
  • Clinically significant alcohol use showed a positive association with AgeAccelGrim2 but not with DunedinPACE.
  • Cigarette smoking was positively associated with both measures of biological aging, while hookah use showed a negative association with AgeAccelGrim2.
  • Vaping did not show a significant association with accelerated biological aging when cigarette smoking was also considered.

These findings suggest that certain substances, particularly opioids and cigarettes, may contribute to accelerated biological aging. The study emphasizes the need for further research to explore the mechanisms behind these associations and their implications for public health.

What this study does not show

This study does not establish causation between substance use and accelerated biological aging, nor does it address the potential effects of other lifestyle factors.

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