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Abstract - Aims: This study was designed to assess links between lifetime levels of marijuana use and accelerated epigenetic aging.
Design: Prospective longitudinal study, following participants annually from age 13 to age 30.
Findings: Lifetime marijuana use predicted accelerated epigenetic aging, with effects remaining even after covarying cell counts, demographic factors and chronological age (β's = 0.32 & 0.27, p's < 0.001, 95% CI's = 0.21-0.43 & 0.16-0.39 for DNAmGrimAge and DunedinPoAm, respectively). Predictions remained after accounting for cigarette smoking (β's = 0.25 & 0.21, respectively, p's < 0.001, 95% CI's = 0.14-0.37 & 0.09-0.32 for DNAmGrimAge and DunedinPoAm, respectively). A dose-response effect was observed and there was also evidence that effects were dependent upon recency of use. Effects of marijuana use appeared to be fully mediated by hypomethylation of a site linked to effects of hydrocarbon inhalation (cg05575921).
Conclusions: Marijuana use predicted epigenetic changes linked to accelerated aging, with evidence suggesting that effects may be primarily due to hydrocarbon inhalation among marijuana smokers. Further research is warranted to explore mechanisms underlying this linkage.
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- Cannabis Causing Cancer Part 1 - Epidemiological overview and survey of USA cannabis, cannabidiol and cannabinoid genotoxicity expressed in cancer incidence 2003–2017: Part 1: Complete Research here https://rdcu.be/cKfKp
Conclusion: Data suggest that cannabinoids including THC and cannabidiol are important community carcinogens exceeding the effects of tobacco or alcohol. Testicular, (prostatic) and ovarian tumours indicate mutagenic corruption of the germline in both sexes; pediatric tumourigenesis confirms transgenerational oncogenesis; quantitative criteria implying causality are fulfilled.
- Cannabis Causing Cancer Part 2 - Epidemiological overview and survey of USA cannabis, cannabidiol and cannabinoid genotoxicity expressed in cancer incidence 2003–2017: Part 2: Complete Research here https://rdcu.be/cKfKq
Conclusion: Data implicate 23/28 cancers as being linked with THC or cannabidiol exposure with epidemiologically causal relationships comparable to those for tobacco. AFE-attributable cases for cannabinoids (91,677 and 48,510) compare with PAR-attributable cases for tobacco (36,450). Cannabinoids constitute an important multivalent community carcinogen.
- Cannabis Causing Cancer Part 3 - Epidemiological overview and survey of USA cannabis, cannabidiol and cannabinoid genotoxicity expressed in cancer incidence 2003–2017: Part 3: Complete Research here https://rdcu.be/cKfOH
Conclusion: Cannabinoids including THC and cannabidiol are therefore important community carcinogens additive to the effects of tobacco and greatly exceeding those of alcohol. Reproductive tract carcinogenesis necessarily implies genotoxicity and epigenotoxicity of the germ line with transgenerational potential. Pseudoexponential and causal dose-response power functions are demonstrated.
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(Published in Neurology)
TAKE-HOME MESSAGE
- In this AHA Scientific Statement, numerous effects of marijuana on brain health are described. These include the effects of:
1) prenatal cannabinoid exposure as well as abnormal fetal neurotransmission in preclinical models and its impact on neuroanatomic areas associated with cognition and emotional regulation;
2) marijuana use on human cognition focusing on possible structural and functional changes in areas involved in cognition, potential detrimental effects of early cannabis exposure on cognition, and multidomain impact of acute marijuana intoxication; and
3) marijuana use on cerebrovascular disease risk, highlighting an association between cannabis use and increased risk of stroke.
- Overall, cumulative evidence suggests that consumption of marijuana may have detrimental effects on brain health, challenging widely accepted beliefs that marijuana is innocuous.
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Aims: This study was designed to assess links between lifetime levels of marijuana use and accelerated epigenetic aging. Design: Prospective longitudinal study, following participants annually from age 13 to age 30. Setting and participants: A community sample of 154 participants recruited from a small city in the Southeastern United States.
Measurements: Participants completed annual assessments of marijuana use from age 13 to age 29 and provided blood samples that yielded two indices of epigenetic aging (DNAmGrimAge and DunedinPoAm) at age 30. Additional covariates examined included history of cigarette smoking, anxiety and depressive symptoms, childhood illness, gender, adolescent-era family income, and racial/ethnic minority status.
Conclusions: Marijuana use predicted epigenetic changes linked to accelerated aging, with evidence suggesting that effects may be primarily due to hydrocarbon inhalation among marijuana smokers. Further research is warranted to explore mechanisms underlying this linkage.
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