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An evaluation of risk applied to marijuana products for recreational or medical purposes concludes that advanced mitigation strategies and new protective delivery protocols are necessary to adequately protect the public from harm. In Canada a controlled distribution program is in place called the RevAid®.1,2    This program assures consumers are monitored to prevent or minimize major side effects and or reactions. Under this program only prescribers and pharmacists who are registered or patients who are enrolled and who have agreed to meet all the conditions of the program are given access to these drugs.

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Cannabidiol (CBD) and cannabidivarin (CBDV) are natural cannabinoids which are consumed in increasing amounts worldwide in cannabis extracts, as they prevent epilepsy, anxiety, and seizures. It was claimed that they may be useful in cancer therapy and have anti-inflammatory properties. Adverse long-term effects of these drugs (induction of cancer and infertility) which are related to damage of the genetic material have not been investigated. Therefore, we studied their DNA-damaging properties in human-derived cell lines under conditions which reflect the exposure of consumers. Both compounds induced DNA damage in single cell gel electrophoresis (SCGE) experiments in a human liver cell line (HepG2) and in buccal-derived cells (TR146) at low levels (≥ 0.2 µM). Results of micronucleus (MN) cytome assays showed that the damage leads to formation of MNi which reflect chromosomal aberrations and leads to nuclear buds and bridges which are a consequence of gene amplifications and dicentric chromosomes. Additional experiments indicate that these effects are caused by oxidative base damage and that liver enzymes (S9) increase the genotoxic activity of both compounds. Our findings show that low concentrations of CBD and CBDV cause damage of the genetic material in human-derived cells. Furthermore, earlier studies showed that they cause chromosomal aberrations and MN in bone marrow of mice. Fixation of damage of the DNA in the form of chromosomal damage is generally considered to be essential in the multistep process of malignancy, therefore the currently available data are indicative for potential carcinogenic properties of the cannabinoids.

PMID: 30341733  DOI: 10.1007/s00204-018-2322-9

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  • • Pre-existing mental disorders increases the risk of developing SUD.
  • • Prior SUD increases the risk of transitioning from use to use disorder.
  • • Highest rates of transition to SUD occurred among stimulant and opioid users.
  • • Mood and anxiety disorders increased the risk of transitioning to AUD and CUD.
  • • The rapidity of transition to SUD emphasizes the narrow opportunity to intervene.

Conclusion: The relative speed associated with the transition from use to SUD emphasizes the narrow window of time available to intervene, underscoring the urgency of early identification of mental health conditions and the timely provision of appropriate evidence-based interventions, which could potentially prevent the development of secondary SUDs.

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Cannabis is the most commonly used illicit drug worldwide and its use is associated with multiple adverse health effect including the risk of addiction. Identifying factors involved in cannabis use and abuse is critical for optimizing evidence-based prevention and treatment protocols. Similarly to other drugs of abuse, the prevalence of cannabis use and addiction differs between males and females, suggesting that sex is an important modulator of cannabinoid sensitivity. Accumulating evidence shows that the endocannabinoid system is sexually dimorphic and that sex hormones play a key role. Hormone-driven differentiation of the endocannabinoid system seems to provide a biological basis for sex differences in endocannabinoid-related behaviors, including reward-related behaviors. While sex differences in cannabinoid action are being increasingly studied in animals, controlled human studies are still limited. The endocannabinoid system is, for its intrinsic characteristics, a privileged target of the actions of both sex and anabolic-androgenic steroid hormones at different levels and, in turn, it can modulate the activity of sex hormones (Table 1). The observation that exposure to AAS causes dysfunction of the brain reward pathway in rats points to a potential risk factor for initiation of cannabis use, maintenance of regular use and development of CUD. The cross talk between endocannabinoid signaling and steroid hormones can occur differently in males and females, and many questions about underlying mechanisms remain unanswered, demanding further research in the field in an attempt to elucidate the basis of the sex differences often observed in cannabinoid sensitivity.

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