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Executive Summary
Cannabis can be both addictive and harmful.
Our understanding of the precise extent and nature of the health implications of recreational cannabis use is developing but, at this stage, there is a great deal of uncertainty. On the eve of the first legal retail sales of recreational cannabis in Canada, the Canadian Medical Association Journal published an editorial which referred to legalisation as: a national, uncontrolled experiment in which the profits of cannabis producers and tax revenues are squarely pitched against the health of Canadians.1
The World Health Organisation recognises addiction rates of 1 in every 9 adults that uses cannabis. This rate of addiction is significantly higher in teenagers, the very age group most susceptible to its harmful effects. Currently, there is scientific uncertainty regarding the causality between cannabis use and the onset of conditions such as psychosis or diminished cognitive function. Nevertheless, there is a compelling body of correlational evidence, spanning 20 years and multiple jurisdictions, that heavily suggests that there is a such relationship. This is particularly pronounced in frequent and younger users. The existing law does mitigate the risk that cannabis poses. Although there has been a slight up-lift in recent years, cannabis consumption has been falling for nearly 20 years in the UK. A great many people do take the law seriously and, to many, the law continues to deter them from using a harmful substance.
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Abstract
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