The effects of cannabis and cannabinoids on the endocrine system

Meah, Farah; Lundholm, Michelle D.; Emanuele, Nicholas V.; Amjed, Hafsa; Poku, Caroline; Agrawal, Lily; Emanuele, Mary Ann

doi:10.1007/s11154-021-09682-w

Cited by 24 publications

(25 citation statements)

References 189 publications

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“…Many mechanisms of genotoxicity from cannabinoids are described including altered sperm morphology [ 26 , 27 ], disruption of oocyte division [ 28 , 29 , 30 , 31 ], chromosomal breaks [ 32 , 33 ], chromosomal fusions [ 26 , 29 , 30 , 31 ], chromosomal bridges [ 29 , 30 , 31 ], disruption of histone synthesis [ 34 , 35 , 36 , 37 , 38 ] and post-translational modification [ 35 ], impaired histone-protamine exchange in sperm [ 39 ], oxidation of DNA bases [ 40 ], single- and double- stranded DNA breaks [ 40 ], and major changes to the DNA methylome and histone post-translational modifications which are heritable to subsequent generations [ 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 ]. Changes in the genital tracts in both sexes [ 50 , 51 ] and alteration of the male and female endocrine milieu is also reported [ 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 ] which is known to rapidly modulate the epigenome generally [ 62 ].…”

Section: Introductionmentioning

confidence: 99%

Cannabis- and Substance-Related Epidemiological Patterns of Chromosomal Congenital Anomalies in Europe: Geospatiotemporal and Causal Inferential Study

Reece

Hulse

2022

IJERPH

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Introduction: Laboratory data link cannabinoid exposure to chromosomal mis-segregation errors. Recent epidemiological reports confirm this link and raise concern that elevated chromosomal congenital anomaly rates (CCAR) may be occurring in Europe which is experiencing increased cannabis use, daily intensity of use and cannabinoid potency. Methods: CCAR data from Eurocat. Drug use data from the European Monitoring Centre for Drugs and Drug Addiction. Income from World Bank. Bivariate, multivariate, panel and geotemporospatial regressions analyzed. Inverse probability weighting of panel models and E-values used as major quantitative causal inferential methodologies. Results: In countries where daily cannabis use was rising the trend for CCA’s was upwards whereas in those where daily use was declining it was usually downwards (p = 0.0002). In inverse probability weighted panel models terms for cannabis metrics were significant for chromosomal disorders, trisomies 21 and 13 and Klinefelters syndrome from p < 2.2 × 10−16. In spatiotemporal models cannabis terms were positive and significant for chromosomal disorders, genetic disorders, trisomies 21, 18 and 13, Turners and Klinefelters syndromes from 4.28 × 10−6, 5.79 × 10−12, 1.26 × 10−11, 1.12 × 10−7, 7.52 × 10−9, 7.19 × 10−7 and 7.27 × 10−7. 83.7% of E-value estimates and 74.4% of minimum E-values (mEV) > 9 including four values each at infinity. Considering E-values: the sensitivity of the individual disorders was trisomy 13 > trisomy 21 > Klinefelters > chromosomal disorders > Turners > genetic syndromes > trisomy 18 with mEV’s 1.91 × 1025 to 59.31; and daily cannabis use was the most powerful covariate (median mEV = 1.91 × 1025). Conclusion: Data indicate that, consistent with reports from Hawaii, Canada, Colorado, Australia and USA, CCARs are causally and spatiotemporally related to metrics and intensity of cannabis exposure, directly impact 645 MB (21.5%) of the human genome and may implicate epigenomic-centrosomal mechanisms.

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Section: Introductionmentioning

confidence: 99%

Cannabis- and Substance-Related Epidemiological Patterns of Chromosomal Congenital Anomalies in Europe: Geospatiotemporal and Causal Inferential Study

Reece

Hulse

2022

IJERPH

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“…Long-term cannabis dependence is characterized by a cluster of syndromes which are themselves age defining illnesses including: neuroinflammation from the many mental illnesses [ 123 , 124 , 125 , 126 , 127 , 128 , 129 , 130 , 131 , 132 ]; steatohepatitis and cirrhosis progression [ 133 , 134 , 135 , 136 ]; myocardial infarction, cerebrovascular disorders and cardiac arrythmia [ 17 , 137 , 138 , 139 ]; immunomodulation [ 35 , 36 , 37 , 38 , 39 ]; endocrine suppression [ 67 , 68 , 69 , 70 , 71 , 72 , 73 ]; impaired male and female fertility [ 67 , 71 , 74 ]; cancers [ 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 , 63 , 64 , 65 , 66 ]; congenital anomalies [ 66 , 103 ...…”

Section: Resultsmentioning

confidence: 99%

“…Widespread suppression of many key endocrine systems including luteinizing hormone (in males and females), testosterone, prolactin (chronic effect), growth hormone, estradiol and progesterone, Graafian follicle maturation, vasopressin and pregnancy including reduced fertility have been demonstrated in association with chronic cannabis use [ 67 , 68 , 69 , 70 , 71 , 72 , 73 ]. It has also been demonstrated in combined opioid-cannabinoid-dependent patients that the reversal of the FSH/LH ratio, a key clinical biomarker of the perimenopause, happened 20 years earlier [ 197 ].…”

Section: Resultsmentioning

confidence: 99%

Epigenomic and Other Evidence for Cannabis-Induced Aging Contextualized in a Synthetic Epidemiologic Overview of Cannabinoid-Related Teratogenesis and Cannabinoid-Related Carcinogenesis

Reece

Hulse

2022

IJERPH

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Background: Twelve separate streams of empirical data make a strong case for cannabis-induced accelerated aging including hormonal, mitochondriopathic, cardiovascular, hepatotoxic, immunological, genotoxic, epigenotoxic, disruption of chromosomal physiology, congenital anomalies, cancers including inheritable tumorigenesis, telomerase inhibition and elevated mortality. Methods: Results from a recently published longitudinal epigenomic screen were analyzed with regard to the results of recent large epidemiological studies of the causal impacts of cannabis. We also integrate theoretical syntheses with prior studies into these combined epigenomic and epidemiological results. Results: Cannabis dependence not only recapitulates many of the key features of aging, but is characterized by both age-defining and age-generating illnesses including immunomodulation, hepatic inflammation, many psychiatric syndromes with a neuroinflammatory basis, genotoxicity and epigenotoxicity. DNA breaks, chromosomal breakage-fusion-bridge morphologies and likely cycles, and altered intergenerational DNA methylation and disruption of both the histone and tubulin codes in the context of increased clinical congenital anomalies, cancers and heritable tumors imply widespread disruption of the genome and epigenome. Modern epigenomic clocks indicate that, in cannabis-dependent patients, cannabis advances cellular DNA methylation age by 25–30% at age 30 years. Data have implications not only for somatic but also stem cell and germ line tissues including post-fertilization zygotes. This effect is likely increases with the square of chronological age. Conclusion: Recent epigenomic studies of cannabis exposure provide many explanations for the broad spectrum of cannabis-related teratogenicity and carcinogenicity and appear to account for many epidemiologically observed findings. Further research is indicated on the role of cannabinoids in the aging process both developmentally and longitudinally, from stem cell to germ cell to blastocystoids to embryoid bodies and beyond.

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“…More specifically, a growing body of research, including observational, preclinical, and clinical data, suggests that phytocannabinoids may play a role in the prevention or treatment of hepatic steatosis (Berk et al 2021 ; Barré et al 2021b ). As modulators of the endocannabinoid system, which is a main therapeutic target for treating diabetes mellitus (Veilleux et al 2019 ), cannabis compounds may exert a beneficial role on the development of diabetes in different populations (Bielawiec et al 2020 ; Wargent et al 2013 ; Jadoon et al 2016 ; Meah et al 2021 ), including HCV-infected people (Barré et al 2020 ). Observational studies have also highlighted a potential role of cannabis compounds in liver disease prevention in this population (Adejumo et al 2018 ; Santos et al 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Cannabis use as a factor of lower corpulence in hepatitis C-infected patients: results from the ANRS CO22 Hepather cohort

et al. 2022

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Background Patients with chronic hepatitis C virus (HCV) infection are at greater risk of developing metabolic disorders. Obesity is a major risk factor for these disorders, and therefore, managing body weight is crucial. Cannabis use, which is common in these patients, has been associated with lower corpulence in various populations. However, this relationship has not yet been studied in persons with chronic HCV infection. Methods Using baseline data from the French ANRS CO22 Hepather cohort, we used binary logistic and multinomial logistic regression models to test for an inverse relationship between cannabis use (former/current) and (i) central obesity (i.e., large waist circumference) and (ii) overweight and obesity (i.e., elevated body mass index (BMI)) in patients from the cohort who had chronic HCV infection. We also tested for relationships between cannabis use and both waist circumference and BMI as continuous variables, using linear regression models. Results Among the 6348 participants in the study population, 55% had central obesity, 13.7% had obesity according to their BMI, and 12.4% were current cannabis users. After multivariable adjustment, current cannabis use was associated with lower risk of central obesity (adjusted odds ratio, aOR [95% confidence interval, CI]: 0.45 [0.37–0.55]), BMI-based obesity (adjusted relative risk ratio (aRRR) [95% CI]: 0.27 [0.19–0.39]), and overweight (aRRR [95% CI]: 0.47 [0.38–0.59]). This was also true for former use, but to a lesser extent. Former and current cannabis use were inversely associated with waist circumference and BMI. Conclusions We found that former and, to a greater extent, current cannabis use were consistently associated with smaller waist circumference, lower BMI, and lower risks of overweight, obesity, and central obesity in patients with chronic HCV infection. Longitudinal studies are needed to confirm these relationships and to assess the effect of cannabis use on corpulence and liver outcomes after HCV cure. Trial registration ClinicalTrials.gov identifier: NCT01953458.

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The effects of cannabis and cannabinoids on the endocrine system

Cited by 24 publications

References 189 publications

Cannabis- and Substance-Related Epidemiological Patterns of Chromosomal Congenital Anomalies in Europe: Geospatiotemporal and Causal Inferential Study

Cannabis- and Substance-Related Epidemiological Patterns of Chromosomal Congenital Anomalies in Europe: Geospatiotemporal and Causal Inferential Study

Epigenomic and Other Evidence for Cannabis-Induced Aging Contextualized in a Synthetic Epidemiologic Overview of Cannabinoid-Related Teratogenesis and Cannabinoid-Related Carcinogenesis

Cannabis use as a factor of lower corpulence in hepatitis C-infected patients: results from the ANRS CO22 Hepather cohort

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