Cannabis has been legal in Canada since June 2012 and in the United States since November 6, 2012. The use of recreational marijuana has plummeted due to legal restrictions. The study follows participants prospectively from the age of 13 to the age of 30, allowing for the exploration over an extended period.
Design Methodology: Prospective longitudinal study with a community sample of 154 participants from a rural area in the United States who reported past marijuana use. Participants completed annual questionnaires on marijuana use, providing details on frequency, amounts, and duration of marijuana use. They also provided blood samples at baseline and after a follow-up period.
Epigenetic Age: The study assessed epigenetic aging through the analysis of DNA methylation, a technique that measures the methylation status of DNA. Participants' blood samples were analyzed using a high-throughput method to predict their epigenetic age, a measure of biological aging. The study used two indices of epigenetic aging: the GrimAge algorithm and the epigenetic clock based on DNA methylation patterns measured at base pair resolution.
Covariates: Covariates included age, sex, race/ethnicity, socioeconomic status, and history of cigarette smoking. The study adjusted for these factors to account for their potential impact on epigenetic aging.
Statistical Analysis: The study used linear mixed effects models to examine the relationships between marijuana use and epigenetic aging. Models were fitted with and without adjustment for covariates to determine the significance of the findings.
Findings: The study found that lifetime marijuana use predicted accelerated epigenetic aging, with an average increase of 32 centimeters (13 inches) in the GrimAge index and 27 centimeters (10.5 inches) in the epigenetic clock index. The effects remained after controlling for factors such as cell count, demographic characteristics, and chronological age. There was evidence of a dose-response relationship, meaning that the more marijuana participants used over their lifetimes, the greater the acceleration in epigenetic aging.
Mechanisms: The researchers propose that hydrocarbon inhalation, which is more common with smoking than vaping, may be responsible for the acceleration in epigenetic aging. This is suggested by the finding that methylation at a specific site, cg05575921, statistically mediated the relationship between marijuana use and epigenetic aging.
Strengths and Limitations: The strengths of this study include its prospective design, the large sample size, and the use of standardized measures of marijuana use and epigenetic aging. However, the study has limitations, such as its focus on recreational marijuana users in a rural area, the potential for self-report bias, and the lack of information on the specific compounds in marijuana that may influence epigenetic aging.
Implications: The findings have implications for public health interventions, particularly regarding the potential risks associated with recurrent exposure to marijuana. Given the growing body of evidence suggesting that marijuana use can affect aging processes, further research is necessary to better understand the long-term effects of different types of marijuana use on health.
