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.
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.
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
Three studies in rodents suggest prenatal exposure to the drug may pose risks for infants
DANA G. SMITH NOVEMBER 18, 2018
This article was originally published by Scientific American.
One recent study revealed that in 2016 7 percent of pregnant women in California used marijuana, with rates as high as 22 percent among teenage mothers. In Colorado 69 percent of dispensariesrecommended the drug to pregnant women to help with morning sickness.
… prenatal drug exposure can be harmful to unborn babies. Previous research has shown infants exposed to cannabis in the womb are 50 percent more likely to have a lower birth weight. Now three new studies presented Tuesday at the Society for Neuroscience annual meeting here suggest prenatal cannabis exposure—at least in rodents—could have serious consequences for fetal brain development.
In one study researchers at Washington State University in Pullman showed rat pups born to mothers exposed to high amounts of cannabis vapor during pregnancy had trouble with cognitive flexibility. Twice a day the scientists filled the pregnant rats’ containers with marijuana vapor from an e-cigarette, elevating levels of the psychoactive chemical THC (tetrahydrocannabinol) in the rats’ blood to roughly the human equivalent of smoking a joint. After the pups grew up the researchers trained them on a task that measured their ability to think flexibly and learn new rules. The young rats first learned to follow a light cue to push one of two levers in order to receive a sugary treat. The next day, pushing only the left lever would deliver the reward, regardless of which side the light had been on.
The rats exposed to cannabis in utero learned the first rule (following the light cue) without a problem, but they took significantly longer to learn the new rule (pushing the left lever) than did rats not exposed to the drug. The cannabis-exposed rats also made many more mistakes on the second day.
In a similar study, scientists at Auburn University in Alabama found rats born to mothers that had been injected with a low, continuous dose of synthetic cannabis during pregnancy were significantly impaired on several different memory tasks involving mazes…“There was a gap in the acquisition of the memory and the consolidation of the memory.”
The young rats whose mothers were dosed with the drug also had abnormalities in the hippocampus, the brain’s primary memory center. Specifically, they had difficulty creating new connections between neurons—the basis for forming new memories. The researchers think the differences in the hippocampus stem from changes in levels of glutamate, the brain’s main excitatory neurochemical involved in learning and memory..