Using genomic data from up to 2.7 million people, researchers found that genetic predisposition to tobacco and problematic alcohol use causally accelerated biological aging, with mixed evidence for cannabis use disorder.
Researchers studying substance use and aging, public health officials, anyone interested in long-term health effects of cannabis
Causal evidence for CUD and accelerated aging was mixed but present
What the researchers found
Mendelian randomization analyses found significant causal effects of genetic predisposition to tobacco use disorder and smoking quantity on markers of biological, physical, and cognitive aging. Causal effects of problematic alcohol use and cannabis use disorder were also detected but with mixed results across different aging markers. Evidence of reverse causality (aging causing substance use) was minimal.
Why it matters
This study uses genetic methods to move beyond correlation and test whether substance use actually causes accelerated aging. The approach helps disentangle whether substance users age faster because of their use or because of shared underlying factors.
The numbers in context
GWAS data from 28,000 to 2.7 million participants. Widespread genetic correlations found between substance use/use disorders and aging metrics. Tobacco showed the strongest causal effects. Cannabis use disorder showed some causal effects but findings were mixed across aging markers.
How the study worked
Researchers used genome-wide association study data (sample sizes from 28K to 2.7M) to test genetic correlations between substance use and aging metrics using LDSC regression. Mendelian randomization was then used to assess causal relationships between genetic predisposition to substance use and various aging indices.
What this study cannot tell us
Mendelian randomization assumes genetic instruments affect aging only through substance use, which may not always hold. Cannabis use disorder GWAS sample sizes are smaller than for tobacco or alcohol. Most data comes from European ancestry populations.
How to read the evidence
Moderate: large-scale genomic analysis using rigorous Mendelian randomization methods, but cannabis-specific findings were inconsistent across aging markers
When this study was published
Published in 2025
The bigger picture
While tobacco's effect on aging is well established, this genetic approach provides some of the first causal evidence that cannabis use disorder may also contribute to accelerated biological aging, though the evidence is weaker and less consistent than for tobacco.
Questions still open
- Which specific aging pathways are affected by cannabis use disorder? Does the severity or duration of CUD matter for aging effects? Would larger cannabis-specific GWAS clarify the mixed findings?
Common questions
Does cannabis make you age faster?
What is Mendelian randomization?
Read the original research
Leveraging Genomic Data to Examine the Causal Impact of Alcohol, Tobacco, Cannabis, and Opioid Use on Biological and Cognitive Ageing.
Addiction biology, 30(7), e70066
Citation
Balbona, Jared V; Jeffries, Paul; Gorelik, Aaron J; Nelson, Elliot C; Bogdan, Ryan; Agrawal, Arpana; Johnson, Emma C. (2025). Leveraging Genomic Data to Examine the Causal Impact of Alcohol, Tobacco, Cannabis, and Opioid Use on Biological and Cognitive Ageing.. Addiction biology, 30(7), e70066. https://doi.org/10.1111/adb.70066
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