And so begins a new series entitled “The consensus on”. In this series of articles, I will attempt to give the best current information all the major drugs and try and clear up the common misconceptions about them. The main focus of this series will be on the implications for recreational use, rather than medical use or treatment. As the title suggests, the first drug is marijuana.
The psychoactive drug ‘marijuana’ refers to the flowers or buds that are picked from a group of plants in the genus Cannabis. These flowers can be smoked, or infused into food, to release the psychoactive ingredients (cannabinoids) that these plants are known for. Tetrahydrocannabinol (THC) is the most important of these, it binds to CB1 receptors in the brain to cause the feeling of being ‘high’. The strength of marijuana is often associated with the amount of THC present. Cannabidiol (CBD) is the other main psychoactive ingredient, however it does not cause the ‘high’ that THC does, it binds to CB1 receptors but does not activate them, acting as an inhibitor to THC. It also binds to several other receptors in the brain, including the FAAH enzyme which regulates the levels of one of the body’s natural cannabinoids (anandamide), for this reason it can be used as an anti-anxiety medication and is legal in many places throughout the world.
The long term risks:
Marijuana is a relatively non-addictive drug. Nine percent of people that try marijuana will end up addicted, this rises significantly if first use is before the age of 18 (Lopez-Quintero et al., 2011). For reference, smoking is currently at 64%.
Effects on the brain:
When used as a teenager attention, memory and learning ability are often hindered. It impacts the way the brain builds connections, mainly varying on the amount of THC consumed. These effects are magnified when age of onset is earlier (Filbey et al., 2014). However, when the brain is fully developed, these issues are far less impactful, and there is little evidence for their existence in light users due to no signs of structural damage being present, although long term heavy smokers are likely to have neuropsychological deficits (Gonzalez, 2007).
On top of this, regular consumption often results in disorientation and feelings of anxiety. Users are also significantly more likely to develop temporary psychosis and long-term disorders such as schizophrenia, with these risks being magnified for individuals with a genetic history of the disease (Pasman et al, 2018. Volkow et al., 2016).
Marijuana smoke contains many similar substances as tobacco smoke, but the way marijuana is often smoked, with several deep inhalations, is even more harmful at causing chronic bronchitis and emphysema (Wu et al, 1988). The evidence, however, points towards the fact that cannabis smoking is very comparable to smoking tobacco, with the mild effects of marijuana due to the decreased total volume of smoke inhaled by marijuana smokers (Taylor et al., 2000). However, there is no link between marijuana intake and blocked arteries (COPD*). Furthermore, lung cancer and upper airway cancer appear to have mixed findings with most studies have either been confounded by tobacco use or hindered by the lack of heavy, long term users (Tashkin, 2013). The general consensus is that studies have found very few reasons to suggest that there is an increase in lung cancer risk for light smokers. However, heavy smokers had an increased risk (still significantly less harmful than tobacco smoking), and findings for this risk are not entirely certain (Sidney et al., 1997).
Overall, the smoke from Marijuana is harmful to the lungs and if smoked regularly, will likely have a similar negative effect on lung functioning as tobacco smoke. However, there are differences, risks of lung cancer are significantly less in marijuana smoke and there is no risk of COPD*.
*Chronic Obtrusive Pulmonary Disease
Edibles offer the same risks with regard to brain function in adolescents and similar risks of anxiety and schizophrenia, provided dosage of THC is similar. They also take far longer to take effect and it is difficult to measure the dosage, leading to unintentional excessive dosages.
Given the evidence, the main takeaways from this review are:
- Heavy long term marijuana use can cause a decrease in psychological performance and an increased risk of schizophrenia and psychosis
- The risks of marijuana smoke should be considered as comparable to the risks of tobacco.
- Light usage significantly decreases the risks of all health concerns.
- Marijuana use before full brain development should be heavily advised against.
It is for all these reasons that light edible use after full brain development is the most preferable in terms of reducing negative health side effects, if using marijuana is unpreventable. Addiction must be avoided at all costs as this has compounding negative effects on the user’s wellbeing. Those with pre-existing risks of psychosis or schizophrenia should also avoid marijuana entirely.
As a final note, it must be stated that these facts are only true if the marijuana product used is exactly what is advertised. Marijuana is illegal in many countries around the globe and therefore is highly unregulated. A study was completed in the USA which found that even from legal dispensaries, only 17% of edible marijuana products tested were accurately labelled, with most products having significantly less cannabinoid product that advertised (Vandrey et al., 2015). It is doubtful that the illegal markets, consistently offer a higher standard of product.
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Filbey, F. M., Aslan, S., Calhoun, V. D., Spence, J. S., Damaraju, E., Caprihan, A., & Segall, J. (2014). Long-term effects of marijuana use on the brain. Proceedings of the National Academy of Sciences, 111(47), 16913-16918.
Gonzalez, R. (2007). Acute and non-acute effects of cannabis on brain functioning and neuropsychological performance. Neuropsychology review, 17(3), 347-361.
Lopez-Quintero, C., de los Cobos, J. P., Hasin, D. S., Okuda, M., Wang, S., Grant, B. F., & Blanco, C. (2011). Probability and predictors of transition from first use to dependence on nicotine, alcohol, cannabis, and cocaine: Results of the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC). Drug and alcohol dependence, 115(1-2), 120-130.
Pasman, J. A., Verweij, K., Gerring, Z., Stringer, S., Sanchez-Roige, S., Treur, J. L., Abdellaoui, A., Nivard, M. G., Baselmans, B., Ong, J. S., Ip, H. F., van der Zee, M. D., Bartels, M., Day, F. R., Fontanillas, P., Elson, S. L., 23andMe Research Team, de Wit, H., Davis, L. K., MacKillop, J., … Vink, J. M. (2018). GWAS of lifetime cannabis use reveals new risk loci, genetic overlap with psychiatric traits, and a causal influence of schizophrenia. Nature neuroscience, 21(9), 1161–1170.
Sidney, S., Quesenberry, C.P., Friedman, G.D. and Tekawa, I.S. (1997). Marijuana use and cancer incidence (California, United States). Cancer Causes & Control, 8(5), 722-728.
Taylor, D. R., Poulton, R., Moffitt, T. E., Ramankutty, P., & Sears, M. R. (2000). The respiratory effects of cannabis dependence in young adults. Addiction, 95(11), 1669-1677.
Vandrey, R., Raber, J. C., Raber, M. E., Douglass, B., Miller, C., & Bonn-Miller, M. O. (2015). Cannabinoid dose and label accuracy in edible medical cannabis products. Jama, 313(24), 2491-2493.
Volkow ND, Swanson JM, Evins AE, et al. (2016). Effects of cannabis use on human behavior, including cognition, motivation, and psychosis: a review. JAMA Psychiatry. 73(3):292-297.
Wu, T. C., Tashkin, D. P., Djahed, B., & Rose, J. E. (1988). Pulmonary hazards of smoking marijuana as compared with tobacco. New England Journal of Medicine, 318(6), 347-351.