Cannabis: Friend or Foe?


“Historically, some societies have idealized cannabis whereas others have demonized it and, recently, Western society has tended to oscillate between the two. In reality, as cannabis derivatives have the potential for causing both good and harm, the important question for society is how to maximize the former and minimize the latter” (cited from “Cannabis, the mind and society: the harsh realities” by Murray and colleagues).

Cannabis and Mental Illness

The majority of recreational cannabis users does not experience serious adverse reactions and is able to regulate their use. However, a minority of frequent or long-term users will develop problems. Abuse and dependence have already been discussed, as well as potential long-term consequences of chronic use for cognitive brain function. But another problem that drew much attention in recent years is the steady increase in mental health problems associated with cannabis use. As other chapters in this book deal with this topic in more detail, I will only give a short overview here.

Most of the interest concerning cannabis and mental health issues has focused on psychosis and schizophrenia. Here, the core question is whether cannabis plays an etiological role in schizophrenia, i. e., does cannabis use cause schizophrenia. A causal relationship between cannabis and schizophrenia is qualitatively different from an association acting in two directions, that is, cannabis use is a risk factor for as well as a consequence of schizophrenia. Nowadays, the association between cannabis use and psychosis and schizophrenia is well-established. For one, epidemiological studies have shown that frequent cannabis use is associated with a greater risk of suffering from psychotic symptoms or of developing schizophrenia and this is particularly prominent in those who started cannabis use at an early age. Once the disease has manifested itself, continued cannabis use can trigger more severe psychotic symptoms and relapse, and is associated with poorer clinical outcome. Second, the proportion of schizophrenic patients that abuses cannabis is much higher than in the general population. Overall, the available evidence strongly suggests that cannabis use may precipitate the development of schizophrenia in vulnerable people, increases the symptoms, and reduces the likelihood to recover from the disease. But the hypothesis that cannabis use causes schizophrenia has not been proven yet. Moreover, we should keep in mind that schizophrenia is a very complex multifactor condition with multiple causes in which a great number of environmental factors interact with (genetic) predispositions to cause this disease.

Compared with schizophrenia, there is less evidence of cannabis playing a role in the etiology of other mental disorders, including depression, bipolar disorder, and anxiety disorder. Similar to schizophrenia, there seems to be a link between affective disorders and elevated rates of cannabis use, but the number of studies investigating the exact nature of this relationship is still limited and until now, has not resulted in a consistent picture.

Cannabinoids as a Medicine

The focus of this chapter is on the potential negative consequences of cannabis use, i. e., abuse, dependence and addiction, persistent effects on mood, behavior, brain and brain function, and increased mental health problems. With this in mind, it seems odd to include a paragraph on the therapeutic properties of cannabinoids. Yet, this is an issue that should not be ignored, as cannabinoid pharmacology in medicine is a rapidly expanding and exciting field of research. I will not go into detail about the apparent paradoxical mechanisms by which cannabinoids may induce both detrimental and therapeutic effects, but for the interested reader there are some excellent reviews on this topic from Sarne and colleagues.

Cannabis as a therapeutic drug is not new. It has been of medicinal and social significance for millennia, and it even was listed on the US Pharmacopeia until 1944. Then, it was removed owing to political pressure to ban its social use in the USA. It has never been reinstated since, but in 1986 the Food and Drug Administration authorized the use of THC for specific medical purposes. Legislation of medical use of THC and some other cannabinoids has followed, also in other countries. Now, several cannabinoids are commercially available, such as Marinol ® (dronabinol; a pure isomer from THC), Cesamet ® (nabilone; a synthetic form of THC), and Sativex ® (containing THC and cannabidiol (CBD), a nonpsychoactive component from Cannabis sativa). Approved indications are treatment for nausea and vomiting induced by chemotherapy in cancer patients, to relieve AIDS-associated anorexia and physical wasting, and pain reduction in patients with neuropathic and multiple sclerosis-related pain. However, the therapeutic potential of cannabinoids has been recognized for many other medical conditions and includes muscle relaxation in diseases causing muscle spasms, anti-inflammatory and anti-allergic effects, improvement of mood, lowering of intraocular pressure (treatment of glaucoma), bronchodilatation, anticonvulsive, and neuroprotective effects. Many of these potential applications are still tested in the preclinical stage (animal research) or in the stage of experimental clinical trials in humans.

One major drawback of cannabinoids that hampers their clinical use is the unavoidable psychotropic effects exhibited by many of them. In most conditions, these effects are considered as unwanted side-effects. In this context, much attention is currently focused on cannabidiol (CBD) that is, like THC, a main constituent of C. sativa. Due to its lack of any cognitive and psychoactive side-effects, CBD is a promising future candidate for clinical utilization. Finally, interest is growing in the role of the body’s own (endogenous) cannabinoid brain system and the role this system may play in the pathophysiology of several psychiatric disorders. For example, in rodents it has been shown that administration of a chemical denoted URB597, which inhibits the breakdown of the endocannabinoid anandamide, resulted in amplification of the effects of anandamide on neuronal signaling. This produced antidepressant-like effects in mice. It will probably take several years of additional pre-clinical and clinical research, but these studies show that cannabidiol and the endocannabinoids may provide valuable lead compounds for development of future psychopharmacological interventions for many psychiatric and CNS disorders.


Selections from the book: Joris C. Verster • Kathleen Brady Marc Galanter • Patricia Conrod Editors “Drug Abuse and Addiction in Medical Illness: Causes, Consequences and Treatment”, 2012.