Lifetime marijuana use and epigenetic age acceleration: A 17-year prospective examination

Allen, Joseph P.; Danoff, Joshua S.; Costello, Meghan; Hunt, Gabrielle; Hellwig, Amanda F.; Krol, Kathleen M.; Gregory, Simon; Giamberardino, Stephanie N; Sugden, Karen; Connelly, Jessica J.

doi:10.1016/j.drugalcdep.2022.109363

Cited by 21 publications

(17 citation statements)

References 33 publications

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“…Since DNA methylation was shown to be a key determinant of the progressive decline of the function which characterizes the aging process, and since cannabis dependence and withdrawal was shown to widely disrupt both DNA methylation and demethylation and the histone code with which it is coordinated, the disruption of the aging process itself is not unexpected. As noted above, this was confirmed in somatic tissues experimentally and found to be of high magnitude at 30% at 30 years of age [ 54 ].…”

Section: Mechanisms Of Cannabinoid Genotoxicitysupporting

confidence: 57%

“…This important study was followed by another pivotal study, which demonstrated a dramatic 30% increase in cellular aging at a median chronological age of 30 years using a late-generation epigenomic clock based on DNA methylation, demonstrating the acceleration of the aging process from cannabinoid exposure in somatic (non-germ cell) tissues utilizing ‘state-of-the-art’ technologies [ 54 ].…”

Section: Cannabinoid Genotoxic Phenomenologymentioning

confidence: 99%

“…There are various strengths and limitations to the present conceptualization. The strengths include the remarkable consistency across the many epidemiological studies, which clearly demonstrates the genotoxic harms of cannabis exposure in several different international jurisdictions, in relation to both the congenital anomalies [ 28 , 36 , 37 , 40 , 45 , 46 , 49 , 51 , 71 , 73 , 74 , 75 , 76 , 77 , 78 , 79 , 80 , 81 , 82 ] and cancer [ 22 , 23 , 24 , 25 , 26 , 30 , 41 , 232 ], and, indeed, now also in aging [ 53 , 54 ]. Similar results in many different studies are clearly mutually supportive and strengthen the overall quality of the body of evidence.…”

Section: Mechanisms Of Cannabinoid Genotoxicitymentioning

confidence: 99%

“…Contrariwise, strong epidemiological evidence from many jurisdictions showed the likely involvement of cannabinoids in many cancers, dozens of serious birth defects and cellular and organismal aging [ 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 ]. Moreover, there is a remarkably close uniformity between the findings from different jurisdictions [ 38 , 39 ], which not only confirms the findings of single studies but also, according to the established Hill criteria of causality, lends formal credence to the likely causal relationship between epidemiologically assessed cannabis exposure and the observed morbidity.…”

Section: Introductionmentioning

confidence: 99%

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Clinical Epigenomic Explanation of the Epidemiology of Cannabinoid Genotoxicity Manifesting as Transgenerational Teratogenesis, Cancerogenesis and Aging Acceleration

Reece

Hulse

2023

IJERPH

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As global interest in the therapeutic potential of cannabis and its’ derivatives for the management of selected diseases increases, it is increasingly imperative that the toxic profile of cannabinoids be thoroughly understood in order to correctly assess the balance between the therapeutic risks and benefits. Modern studies across a number of jurisdictions, including Canada, Australia, the US and Europe have confirmed that some of the most worrying and severe historical reports of both congenital anomalies and cancer induction following cannabis exposure actually underestimate the multisystem thousand megabase-scale transgenerational genetic damage. These findings from teratogenic and carcinogenic literature are supported by recent data showing the accelerated patterns of chronic disease and the advanced DNA methylation epigenomic clock age in cannabis exposed patients. Together, the increased multisystem carcinogenesis, teratogenesis and accelerated aging point strongly to cannabinoid-related genotoxicity being much more clinically significant than it is widely supposed and, thus, of very considerable public health and multigenerational impact. Recently reported longitudinal epigenome-wide association studies elegantly explain many of these observed effects with considerable methodological sophistication, including multiple pathways for the inhibition of the normal chromosomal segregation and DNA repair, the inhibition of the basic epigenetic machinery for DNA methylation and the demethylation and telomerase acceleration of the epigenomic promoter hypermethylation characterizing aging. For cancer, 810 hits were also noted. The types of malignancy which were observed have all been documented epidemiologically. Detailed epigenomic explications of the brain, heart, face, uronephrological, gastrointestinal and limb development were provided, which amply explained the observed teratological patterns, including the inhibition of the key morphogenic gradients. Hence, these major epigenomic insights constituted a powerful new series of arguments which advanced both our understanding of the downstream sequalae of multisystem multigenerational cannabinoid genotoxicity and also, since mechanisms are key to the causal argument, inveighed strongly in favor of the causal nature of the relationship. In this introductory conceptual overview, we present the various aspects of this novel synthetic paradigmatic framework. Such concepts suggest and, indeed, indicate numerous fields for further investigation and basic science research to advance the exploration of many important issues in biology, clinical medicine and population health. Given this, it is imperative we correctly appraise the risk–benefit ratio for each potential cannabis application, considering the potency, severity of disease, stage of human development and duration of use.

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Section: Mechanisms Of Cannabinoid Genotoxicitysupporting

confidence: 57%

Section: Cannabinoid Genotoxic Phenomenologymentioning

confidence: 99%

Section: Mechanisms Of Cannabinoid Genotoxicitymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Clinical Epigenomic Explanation of the Epidemiology of Cannabinoid Genotoxicity Manifesting as Transgenerational Teratogenesis, Cancerogenesis and Aging Acceleration

Reece

Hulse

2023

IJERPH

View full text Add to dashboard Cite

show abstract

“…15 We also focused on biological ageing and midlife health, financial, and social preparedness for older age because each of these domains is related to health span ( appendix pp 1–8 ). Moreover, evidence from cannabis studies of adolescents and younger adults, 2 , 16 – 19 and the few cannabis studies of adults in midlife and older adults ( appendix pp 9–12 ), 20 – 24 support cannabis use associations with these domains.…”

Section: Introductionmentioning

confidence: 95%

Preparedness for healthy ageing and polysubstance use in long-term cannabis users: a population-representative longitudinal study

Meier

Caspi²,

Ambler³

et al. 2022

The Lancet Healthy Longevity

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Examining Health Behaviors as Mechanisms Linking Earlier Pubertal Timing with Accelerated Epigenetic Aging in Late Adolescence

Goering,

Tiwari,

Patki

et al. 2024

J. Youth Adolescence

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Lifetime marijuana use and epigenetic age acceleration: A 17-year prospective examination

Cited by 21 publications

References 33 publications

Clinical Epigenomic Explanation of the Epidemiology of Cannabinoid Genotoxicity Manifesting as Transgenerational Teratogenesis, Cancerogenesis and Aging Acceleration

Clinical Epigenomic Explanation of the Epidemiology of Cannabinoid Genotoxicity Manifesting as Transgenerational Teratogenesis, Cancerogenesis and Aging Acceleration

Preparedness for healthy ageing and polysubstance use in long-term cannabis users: a population-representative longitudinal study

Examining Health Behaviors as Mechanisms Linking Earlier Pubertal Timing with Accelerated Epigenetic Aging in Late Adolescence

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