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Major Studies of Drugs and Drug Policy | ||||
Canadian Senate Special Committee on Illegal Drugs | ||||
Volume I - General Orientation |
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Chapter 7 - Cannabis: Effects and ConsequencesCognitive 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. Motivation
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. |