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Major Studies of Drugs and Drug Policy
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Volume I - General Orientation

Chapter 7 - Cannabis: Effects and Consequences

Cognitive and psychological consequences

The main cognitive and psychological consequences of chronic cannabis use concern brain functions involved in memory and verbal and math skills; motivation; and psychiatric disorders.


Brain functions

We have seen that cannabis has acute effects on short-term memory, attention and concentration. Does chronic use eventually result in effects on cognitive function that may be irreversible? These questions first raise the question of the neurotoxicity of cannabis, defined as “a reversible or irreversible impairment of the structure and/or functions of the central (and/or peripheral) nervous system by physical, chemical or biological agents”[1][56] [translation]

According to professor Roques:


[translation] Cannabis dependence does not result in neurotoxicity (…). Thus old results suggesting anatomical changes in the brain of chronic cannabis users, as measured by tomography, have not been confirmed by precise modern techniques of neuro-imaging. Similarly, morphological changes in the hippocampus of the rat following administration of very high doses of THC (Landfield et al., 1988) have not been repeated (Slikker et al., 1992). (…) Several studies have been devoted to the effects of cannabis on evoked responses and on electroencephalograms of humans. Intermittent use produces reversible changes in a wave patterns in the frontal cortex, probably with respect to the state of drowsiness induced by THC. In the very long term (more than fifteen years) and with heavy daily use, d hyperfrontality and an increase in q frontal activity have been observed (Struve et al., 1990, 1994). The possible connection with behavioural changes and changes in neuropsychological tests is not in question, nor moreover is that which is possible with the anticonvulsive effects of THC. [2][57]


The results of studies reported by the collective expertise of INSERM are contradictory as some observe changes while others do not. Even when changes are observed, they are often of minor amplitude and are reversible after a period of abstinence. The INSERM report observes that studies using neuro-imaging techniques have not confirmed the neurotoxicity of cannabis in either man or baboon.[3][58] Therefore it is through observing functioning and behaviour that we are still best able to examine the question of the neurological effects of cannabis.

Unfortunately, studies are just as contradictory here and the results are inconclusive. Studies performed in the 1970s in countries where cannabis use is traditional (Jamaica, Costa Rica, India) did not point out any significant differences in cognitive functions of users and non-users, whereas more recent studies, in particular in Costa Rica in the 1980s, did show differences: [translation] “In particular, long-term users recalled fewer words on a list they had been shown earlier and response time was longer.[4][59] In the United States, studies conducted in the 1970s found contradictory results for memory functions, whereas more recent studies reported subtle deficits in cognitive functions of heavy users after a brief period of abstinence. Some studies also showed continued memory impairment in adolescents after six weeks of abstinence.[5][60]

Most studies tend to show that overall, ex-users recover all cognitive functions, but depending on the length of use, subtle impairments can persist, in particular with regard to the ability to process complex information.

Still according to the collective expertise of INSERM, the age when use begins can be a determining factor. Thus, a recent study shows the persistence of some visual scanning impairments (related to attention) in young people who began to use cannabis before age 16, whereas those who began use after age 16 show no difference from non-users.[6][61]

In all, we cannot really establish that cannabis use has negative consequences for brain functions, even in chronic users, unless use begins before age 16.


Some studies suggest the presence of an amotivational syndrome in chronic cannabis users, a syndrome that could affect the performance of young people at school and employees in a professional environment in particular. In its 1997 report, the WHO pointed out that our knowledge has not advanced since its previous report in 1981: the amotivational syndrome has still not been clearly defined, its effects have still not been clearly distinguished from the effects of intoxication itself, and the data available comes from clinical case reports with no control group.[7][62]

In order to evaluate the impact of cannabis on motivation, Canadian researchers developed a study where subjects received cannabis in exchange for work performed. Even though it is not recent, the study is no less interesting. They observed that subjects worked less efficiently immediately after using cannabis. However, their level of productivity then increased rapidly and exceeded levels achieved during periods of abstinence. Although working fewer hours, the subjects using cannabis were not less productive because they worked harder. Furthermore, over the course of the period of heaviest use, the subjects organized a strike and successfully negotiated a “salary” increase, after which they worked even harder.[8][63] [9][64]

Studies do not enable us to establish if motivational problems, when observed, preceded or followed cannabis use, or if other emotional or psychosocial factors played a greater role, or were even determining factors in the chronic use or abuse of cannabis in young people in particular. These conclusions are shared by the collective expertise of INSERM and by the authors of the report submitted to the International Scientific Conference on Cannabis in March 2002.[10][65]


Psychiatric disorders

Various psychiatric disorders have been associated with chronic cannabis use: mood disorders and depressive episodes, anxiety disorders, personality disorders, as well as more severe conditions, such as psychoses and schizophrenia. For each of these situations, the conclusion drawn by the authors of the report on mental health and cannabis prepared for the International Scientific Conference on Cannabis generally applies:


There are three possible ways to account for the relationship between cannabis and mood disorders. First, both may share common risk factors, so that their relationship is not causal. Second, mood disorders may predispose people to use cannabis. Third, cannabis use may trigger or increase depressive symptoms. As yet, there is no clear answer to this question of “which comes first”. [11][66]


Specifically with regard to mood disorders, depressive states and anxiety disorders, it seems probable that they precede chronic use. However, study results are extremely disparate: for mood disorders in so-called dependent people, the prevalence varies (depending on study methods), from 10% to almost 50%; with respect to major depressive episodes in clinical populations, studies report percentages varying from 4% to almost 20%. INSERM’s report presents a review that we feel is much more enlightening with regard to the situation for adolescents:


[Translation] Acquiring new knowledge has allowed for a better assessment of the burden of “early onset depression” in terms of individual suffering and public health. Its prevalence, around 5% in adolescence, makes it one of the most common pathologies for this period. The risk of suicide is high, and the functional deficits inherent in depressive syndromes are a source of school and family problems, and cause withdrawal from peers, for which the psychosocial consequences can be severe, especially if the disorder is prolonged. Additionally, depression is rarely an isolated disorder in a young subject: anxiety or behavioural disorders often precede or accompany depressive episodes and can survive them; moreover, the existence of a depressive disorder is a risk factor for addiction (alcohol or any other psychoactive substance) and eating disorders. [12][67]


With respect to psychotic disorders and schizophrenia, the two subjects are controversial, the methodologies weak, the data contradictory and the interpretations are often based on simplistic models of causality. If, in certain circumstances, cannabis can trigger psychotic episodes, they are most often short and resolve rapidly. As for schizophrenia, if it is true that cannabis use is more prevalent in these subjects than in the general population, some feel that it is self-medicating behaviour while others feel that the chronic use of cannabis is a trigger for the schizophrenic process. We feel that the conclusion of professor Roques’ report agrees best with current data:


[Translation] No mental pathology directly related to the overuse of cannabis has been reported, which distinguishes this substance from psychostimulants such as MDNA, cocaine or alcohol, heavy and repeated use of which can give rise to characteristic psychotic syndromes. Similarly, cannabis does not seem to precipitate the onset of pre-existing mental dysfunctions (schizophrenia, bipolar depression, etc.). [13][68]


As it is, most scientific reports come to the same conclusion: more research is needed, with more rigorous protocols, allowing in particular for comparison with other populations and other substances.


[1][56]  Roques, B., (1999) op. cit., page 73.

[2][57]  Roques, B., (1999) op. cit., page 187.

[3][58]  INSERM, op. cit., page 206.

[4][59]  Ibid., page 204.

[5][60]  Ibid., page 205.

[6][61]  Ibid., page 206.

[7][62]  WHO (1997), op. cit., page 18.

[8][63]  Miles G.C. et al., (1974) An Experimental Study of the Effects of Daily Cannabis Smoking on Behavioural Patterns, Toronto: Addiction Research Foundation, Toronto.

[9][64]  Campbell, I. (1976) The Amotivational Syndrome and Cannabis Use With Emphasis on the Canadian Scene, Annals of the New York Academy of Sciences 282, 33-36.

[10][65]  INSERM, op. cit.; Hanak, C. et al., (2002) “Cannabis, mental health and dependence”, Pelc, I. (ed.), International Scientific Conference on Cannabis, op. cit., page 61.

[11][66]  Hanak, C. et al. (2002), op. cit., page 62.

[12][67]  INSERM (2001), op. cit., page 98.

[13][68]  Roques, B., (1999) op. cit., page 186.

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