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A CRITICAL REVIEW OF THE RESEARCH LITERATURE CONCERNING SOME BIOLOGICAL AND PSYCHOLOGICAL EFFECTS OF CANNABIS
Dr. Peter L. Nelson
Nelson, P. L. (1993). A critical review of the research literature concerning some
biological and psychological effects of cannabis. In Advisory Committee on Illicit Drugs
(Eds.), Cannabis and the law in Queensland: A discussion paper (pp. 113-152). Brisbane:
Criminal Justice Commission of Queensland.
An electronic search of the published research literature through computerised on-line
services, such as DIALOG Information Services, reveals that since the mid 1960's over 4000
papers, monographs and books on medical, psychological and social aspects of cannabis use
and abuse have been published.1 These studies cut across a wide range of disciplines
including: the potential teratogenicity of D-9-tetrahydrocannabinol and related compounds
(Cohen, 1986; Fried, 1989; Fried and O'Connell, 1987; Hill and Tennyson, 1986; Stern,
1981; Qazi, Mariano, Milman, Beller and Crombleholme, 1985); histopathology and functional
occlusion of the pulmonary system (Henderson, Tennant and Guerry 1972; Tashkin, Shapiro,
Ramanna, Taplin, Lee, and Harper, 1976; Tashkin, Shapiro, Lee, and Harper, 1976; Tennant,
Guerry, and Henderson, 1980); cardiovascular changes (Aronow and Cassidy, 1974; Benowitz
and Jones, 1975; Stimmel, 1979); possible permanent neurological effects (Campbell, Evans,
Thomson, and Williams, 1971; Co, Goodwin, Gado, Mikhael, and Hill, 1977; Feinberg, Jones,
Walker, Cavness, and Floyd, 1976; Fried, 1989; Grant, Rochford, Fleming, and Stunkard,
1973; Grant, Rochford, Fleming, and Stunkard, 1973; Hannerz and Hindmarsh, 1983; Heath,
1972; Heath, 1973; Heath, Fitzjarrell, Garey, and Myers, 1979; Kuehnle, Mendelson, Davis,
and New, 1977; Tassinari, Amrosetto, Peraita-Adrados, and Gastaut, 1976); the likelihood
of the existence of a psychological complex of behaviours and attitudes collectively
referred to as the "amotivational syndrome" (Creason and Goldman 1981;
McGlothlin and West, 1968; Smith, 1968; Weller, 1985); the possible effects on learning
and behaviour (DSM-III-R.; Fabian and Fishkin, 1981; Fried, 1977; Johnston, O'Malley, and
Bachman, 1986; Jones, 1975, 1980; Kolansky and Moore, 1971; McBay, 1986; Mullins, Vitola,
and Abellera, 1974; Weller, 1985); and the possibility of a relationship between cannabis
use and major psychiatric disorders (DSM-III-R, 1987; Andreasson, Allebeck, and Rydberg,
1989; Imade and Ebie, 1991; Lavik and Onstad, 1986; Meyer, 1975; Negrete, Knapp, Douglas,
and Smith, 1986; Thacore and Shukla, 1976; Thornicroft, 1990; Tunving, 1985). Amongst
these papers are a number of fairly thorough review articles and books which attempt an
overview of most areas of cannabis research (Cohen, 1986; Hollister, 1988; Jones, 1980;
Nahas, 1984; Nahas and Latour, 1992; Petersen, 1980).
Although the total volume of this literature is somewhat daunting at first glance, a
sampling of the material soon reveals that much is repetitive and a relatively small
number of papers are continually referred to by most authors. Therefore, this review will
concentrate on a selective group of these articles (90+), which represent the core of this
research, but in doing so, we proceed with a high degree of confidence in the
representative nature of those papers chosen for review and critique. Nonetheless, no
review can be assumed to be free of bias and this one is no exception. The quality of much
of this literature reviewed, however, is confounded by the political and social debate
surrounding illicit drug use in general and cannabis in particular. There seems to be few
neutral parties in the debate and some reports barely hide the prejudices which drive for
particular conclusions, no matter what the empirical data appears to indicate.
In commenting on the problems of research into the effects of cannabis on humans Jones
This large and rapidly growing literature demonstrates that all relevant information on
all effects of cannabis will probably never be available. Because of the nature of
science, usually facts change as experience accumulates. As more people use any drug for
more time, as analytic instruments become more sensitive, and as researchers ask more
focused questions, new facts appear and the significance of older facts is continually
revised (pp. 54-55).
And, we might add, the interpretation of these 'scientific facts' appears to change
with the changing political climate.
Of course, this growth of knowledge and evolving interpretation of the empirical data
can be seen in the alcohol and cigarette literature as well. Like these two licit drugs,
the effects of cannabis must be taken in relation to its frequency of usage and hence dose
rate. Thus, it is still an issue of debate whether the moderate use of alcohol, as claimed
by some, is beneficial to cardiovascular health. However, there is little disagreement
that intense, prolonged use of alcohol is deleterious to both physical and psychological
well being. In the case of cannabis, on the other hand, no one appears to be able to
define what constitutes heavy use and in field research of illicit users the results
become highly uncertain because of the inability of scientists to ascertain actual dose
rates and hence life-time intake of cannabinoids. This is due to the wide range of
concentrations of THC and related compounds in smoked marijuana and differences of smoking
habits from one individual to another. A 'fifth' of single-malt whisky at a given percent
strength is a very precise amount of ethyl alcohol, but a kilogram of marijuana can vary
widely in its content of bioactive and psychoactive compounds.
Further, when reading the scientific literature on the effects of cannabis, it is
important to put the emerging evidence into perspective. Very often statements are made
about the effects of its use which, when taken out of context, appear to be somewhat
exaggerated in their supposed effect on human health. For example, infant birth weight is
considered an important indicator of later rates of cognitive and psychological maturation
and thus taken to be a significant risk-factor in the use of any drug by pregnant women.
Some studies relate cannabis usage to reduced birth weight, but neglect to put this
finding in the context of other, more commonly used substances such as tobacco, which
cause even greater effects on birth weights of the infants of using mothers (Hill and
Tennyson, 1986; Fried and O'Connell, 1987).
Behavioural studies also have attempted to address the issue of the relative effect of
cannabis, as compared to other licit drugs such as alcohol, in performance tasks -
particularly for its effect on driving an automobile. One of the more recent of these
studies by Chesher et al (1985) concludes that "duration of impairment produced by
all three drugs (cannabis was taken in two ways) at the doses used was very similar"
(p. 624). A report issued in February, 1990 by the United States National Transportation
Safety Board indicated that 12.8% of those involved in fatal truck accidents showed signs
of cannabis ingestion in post mortem examination (cited in Nahas and Latour, 1992, p.
496). However, these published rates are usually confounded by multiple use of
psychoactive substances in the majority of cases, particularly alcohol, which is believed
to increase the deleterious effects on behaviour and judgement induced by cannabis alone.
However, in an earlier and larger study drivers using cannabis only were involved in only
2.2% of recorded fatal accidents and Hollister (1988) concludes from the data that
"at present, THC plays a relatively minor role in fatal traffic accidents as compared
with alcohol" (p. 113). Apart from the direct neuropsychological effects of both
drugs, the problems caused by alcohol and cannabis in relation to motor vehicle accidents,
in particular, are more due to the methods and circumstances of their use by a minority of
individuals rather than the fact that these substances both cause, in the main, reversible
As indicated in the opening remarks, this review of the effects of cannabis on humans
will not attempt to be exhaustive and will be divided into two broad categories -
physiological and psychological. The physiological classification will include discussions
of effects on the cardio-pulmonary system, teratogenicity and the central nervous system.
The psychological grouping, on the other hand, will discuss the relationship of cannabis
use to social adjustment, driving behaviour, toxic psychoses and schizophrenia. Of course,
the psychological and neurological are inextricably intertwined, but for heuristic
purposes they will be kept separate, being cross-referenced only where necessary.
Since most cannabis users smoke either marijuana or hashish, it is reasonable to
examine the effect of smoking cannabis on the occurrence of lung disease. Nahas (1984)
reminds us that smoking cannabis releases plant constituents such as tars, carbon
monoxide, acids, aldehydes, pyrobenzenes and particulate irritant substances, so any
toxilogical or pharmacological studies must consider these by-products of smoking in
addition to the delta-9-THC content of the smoke, especially in the case of chronic use.
The reader should also take note that many reporters on the effects of cannabis ingestion
do not always make clear conceptual discriminations between the effects of smoke
by-products (which are very similar to tobacco except for the presence or absence of
nicotine or THC) and those specifically related to the pharmacology of THC. Of course,
users primarily smoke cannabis, but it can also be ingested orally giving similar
psychoactive effects. Thus, any reasonable discussion of the physiological effects of
cannabis must take into account that it is illegally used primarily for its psychoactive
properties and if THC were to be provided in an easily ingested rapid acting oral form,
the problems due to smoking could be obviated.
When taken, delta-9-tetrahydrocannabinol rapidly disappears from the blood plasma and
is taken up in fat where it remains with a half life decay rate of 5-7 days. This means
that after a single dose of THC, less than 1% of the primary active ingredient remains in
fatty tissue after approximately 35-50 days (Nahas, 1984). THC's oil solubility and thus
high affinity for fatty tissue probably accounts for its attraction to neural tissue with
its high lipid content in myelin and other components of the neurone. Herkenham et al
(1990) used quantitative autoradiography to map the distribution of THC in mammalian
brains in which they demonstrated that:
...in all species very dense binding was found in the globus pallidus, substantia nigra
pars reticulata (SNr), and the molecular layers of the cerebellum and hippocampal dentate
gyrus. Dense binding was also found in the cerebral cortex, other parts of the hippocampal
formation, and striatum. In rat, rhesus monkey, and human, the SNr contained the highest
level of binding. Neocortex in all species had moderate binding across fields, with peaks
in superficial and deep layers. Very low and homogeneous binding characterised the
thalamus and most of the brainstem, including all of the monoamine-containing cell groups,
reticular formation, primary sensory, visceromotor and cranial motor nuclei, and the area
postrema. The exceptions—hypothalamus, basal amygdala, central gray, nucleus of the
solitary tract, and laminae I-III and X of the spinal cord—showed slightly higher but
still sparse binding (p. 1935).
They conclude that the structure activity profile defined by the binding of the THC
analogue used in the study is consistent with "the same receptor that mediates all of
the behavioural and pharmacological effects of cannabinoids, ...including the subjective
experience termed the human 'high'" (Herkenham et al, 1990, p. 1935). These binding
sites are also consistent with THC's effects on loosening of associations, fragmentation
of thought and short-term memory deficits. Further, dense bindings found in the basal
ganglia and cerebellum suggest a role for cannabinoids in effecting motor control while
involvement with the ventromedial striatum suggests connections to dopamine circuits.
However, the expected reinforcing properties usually associated with these dopamine
pathways is difficult to demonstrate in the case of THC.
There are over 60 other cannabinoids and cannabidiols present in cannabis smoke, most
of which have very little psychoactivity and do not bind to these same sites. The effect
of these substances is largely unknown, nor is the level of psychoactivity for any THC
remaining in fatty tissue on the days subsequent to the original ingestion known.
Although, in the case of light to moderate cannabis users, THC can be detected in body
fluids for approximately 30 days after the last consumption, it is quite difficult to
detect perceptuo-motor effects this long after a given average single dose (1-3 mg THC in
cannabis to be smoked). This is unlike alcohol where a clear dose/response curve is
demonstrable in which effects of ethanol on behaviour and judgement can be demonstrated at
blood levels below 0.05%. In their comparative study Chesher et al (1985) have estimated
that a dose of cannabis originally containing 1 to 2 mg THC produced a decrement in
performance on a battery of psychological tests which was approximately the same as that
produced by alcohol at a concentration of 0.05% (at peak) (p. 627).
The results of this last study suggest that many of the behavioural studies to be
examined later in this paper may be seriously flawed. The high dose rates of the typical
chronic cannabis user recruited for these behavioural studies, when taken in the context
of the relatively long half-life of THC, suggest that behavioural and psychological tests
conducted on chronic users who are supposedly no longer using cannabis are, in fact, being
carried out on individuals still highly intoxicated. If, as Chesher et al (1985) suggest,
the ingestion of 1-2 mg of THC to be smoked is the equivalent, in a behavioural sense, of
achieving a 0.05% blood alcohol, then typical dose rates of 150 mg per day (to be smoked)
are the intoxication equivalent of drinking more than fifteen 10 oz schooners of standard
beer per hour. Cannabis users at this level of consumption will still have very
significant accumulations of THC in their fatty tissue, and hence a serum equivalent of
more than 0.05% blood alcohol, several weeks after their last ingestion of cannabis. Thus,
any studies conducted to examine the permanent effects of THC on behaviour for heavy
cannabis users must be sure that their subject sample has not used any cannabis whatsoever
for several months prior to examination.
There have been a number of anecdotal reports and uncontrolled clinical observations
which link cannabis smoking to the risk of pulmonary pathology (Cohen, 1986). However,
this evidence is much less conclusive than a controlled study of lung function tests
carried out by Tashkin and colleagues (1980) in which 74 habitual cannabis smokers were
compared to non-users. The results indicated no substantive difference between users and
non-users but Cohen (1986) criticises these results as being skewed by the fact that all
the participants were initially screened and those showing any respiratory pathology were
removed from the study. In addition, Tashkin et al's (1980) findings somewhat contradict
their earlier (1976) report in which they conclude that very heavy marijuana smoking for 6
to 8 weeks appears to cause mild but significant airway obstruction.
Earlier studies of U.S. servicemen hashish smokers conducted by Henderson and Tennant
(1972), however, make a more damaging case against cannabis in relation to lung disorders.
These researchers found frequent and severe nose and throat inflammation often accompanied
by X-ray findings which included sinusitis and lower airway diseases such as bronchitis
and asthma. As part of these studies patients with chronic cough were subjected to
bronchoscopy and biopsy of the epithelial lining of the posterior wall of the trachea.
Microscopic examination of the biopsy samples revealed a number of cellular abnormalities
which are associated with the later development of lung cancer and chronic obstructive
pulmonary disease. These include the loss of cilia, basal epithelial cell proliferation
and proliferation atypical cells.
The authors acknowledge that most of these men smoked tobacco along with hashish, but
insist that the development of the abnormalities observed significantly pre-dates their
usual appearance in those who are tobacco smokers only. The problem with ascribing these
pathological changes to cannabis alone is obvious. The later attempts of Tennant and
associates to disconfound tobacco effects from those of cannabis tended to show that
either smoking tobacco alone or use of hashish on its own is less deleterious than
combining the two (Tennant, Guerry, and Henderson, 1980). However, the sample size used in
this later study was much too small to allow any clear-cut conclusions to be drawn. Cohen
summarises these findings.
Although not a single case of lung cancer has yet been attributed to chronic marijuana
smoking in this country (U.S.), the possibility cannot be ignored that chronic, heavy
marijuana smoking, like chronic tobacco smoking, may be a risk factor for the development
of lung cancer and that the risks of developing lung cancer as the result of combined
marijuana and tobacco smoking could be additive or even synergistic (parentheses mine)
(Cohen, 1986, p. 156).
Finally, it should be borne in mind that cannabis produces similar carcinogenic 'tars'
to that of tobacco, but in greater quantities than for an equal weight of tobacco, and the
deep inhalation techniques employed by marijuana and hashish smokers tends to deposit that
tar more deeply in the lungs. It has been calculated that 70% of the particulate matter is
retained in the lungs and it thus can be assumed that in the case of cannabis this
percentage is even greater (Jones, 1980). Again, in contrasting pulmonary effects of
cannabis smoking with that of tobacco it should be recalled that most tobacco smokers are
now using products which have been modified to reduce the 'tar' content and which are
often filtered to that same end. Therefore, the comparison of illicit cannabis with legal,
processed tobacco, in terms of health effects, is somewhat spurious.
When cannabis is first smoked one of its most prominent immediate effects is
tachycardia which tends to be proportional to the ingested dose (Stimmel, 1979). The rate
increase varies from 50-100% of resting pulse with an accompanying decrease in orthostatic
blood pressure. It was observed by Aronow and Cassidy that the consumption of one
marijuana cigarette containing 19 mg of THC decreased exercise time until angina by 48% as
compared to a marijuana placebo which only reduced time to angina by 9%. The authors of
this study concluded that cannabis smoking increased myocardial oxygen demand while
decreasing myocardial oxygen delivery (Aronow and Cassidy, 1974). Hollister (1988)
concludes from these results that, although smoking is not recommended for anyone with
angina, the shorter time until angina seen with cannabis combined with its induction of
tachycardia makes it particularly deleterious for those suffering from arteriosclerosis of
the coronary arteries or congestive heart failure. Nahas (1984) summarises what he
believes to be the cardiovascular threat of cannabis ingestion based on the above
The smoking of marihuana increases the work of the heart by increasing heart rate, and
in some cases by increasing blood pressure. This increase in work load poses a threat to
patients with hypertension, cerebro-vascular disease, and coronary atherosclerosis.
Marihuana can also cause postural hypotension. The drop in blood pressure could be
hazardous in those individuals with compromised blood flow to heart or brain, especially
if they are volume-depleted or if other drugs have impaired reflex control of their blood
vessels. In older patients treated by delta-9-THC or who had smoked marihuana for
glaucoma, orthostatic hypotension has been disabling and a risk factor of cardiovascular
Marihuana appears to intensify the effects of the sympathetic nervous system on the
heart, an undesirable consequence in patients with coronary artery disease and in those
susceptible to arrythmias (p. 127).
Jones (1980) admits that distinguishing chronic from acute effects of cannabis on the
cardiovascular system is problematic. Chronic, long term oral administration of THC can
result in mildly depressed heart rate and slight lowering of blood pressure (Benowitz and
Jones, 1975). Although these changes appear to be of little biological significance, Jones
feels that long term use might be associated with lasting health consequences, drawing his
argument from the accumulated data now existent on tobacco use and heart disease. It was,
he argues, years before the connection was made between smoking and coronary artery
disease. Jones claims that THC has "far more profound effects on the cardiovascular
system than does nicotine," but fails to tell us how. In fact, the findings of
Benowitz and Jones he presents on long term oral administration of THC (above) shows an
effect which could be construed as potentially useful in combating the negative
cardiovascular effects of long term stress. As is often the case in THC research,
interpretation is in the eye of the beholder.
Jones' prediction concerning the effect of long term cannabis use as having potentially
more serious effects than nicotine ingestion is somewhat peremptory. Until the effects of
the "tars," particulates, carbon monoxide and differing smoking styles involved
in marijuana smoking are disconfounded from the effects of the cannabinols (THC in
particular), prognostications about the future effects of cannabis on the cardiovascular
system are somewhat precipitous. His statement comparing nicotine with THC is particularly
ill founded. Most studies have not looked at comparisons between THC and nicotine, per se,
but have made comparisons between smoked cannabis and tobacco cigarettes. The actions of
both compounds are no doubt altered by the method of delivery (smoking) as well as by the
combination of responses caused by other constituents of the smoke such as carbon
monoxide, for example. Nicotine itself is known to be a strong activator of sympathetic
pathways of the autonomic nervous system thereby having a direct, stimulating effect on
the heart (Kalat, 1988). No such direct action has been demonstrated for THC or its other
Again, as in the case of possible pulmonary action of THC, conjecture seems to far
outweigh empirical evidence. What evidence there is appears to be flawed by studies which
are either uncontrolled, anecdotal, or based on small, idiosyncratic cases. Even more
importantly, the research cited above does not control for the effect of psychological
factors on cardiovascular activity. As will be described later in this paper, cannabis
intoxication is well known for producing mild to severe panic reactions in naive users
(Cohen, 1986; Hollister, 1988; Jones, 1980; Nahas, 1984; Weil, 1970). The level of stress
produced by such states, and by altered consciousness experiences in general, often may be
responsible for the clinical signs of stress syndrome such as shortness of breath,
tachycardia, etc. There is little doubt that any individual with incipient cardiopathology
may show symptoms of cardiac distress when so psychologically taxed.
Central to the issue of teratogenicity and THC is the possibility that there is a
direct action of the cannabinoids on chromosomes. In studies by Stenchever, Kunysz, and
Allen (1974) and Herha and Obe (1974) a significant increase in chromosomal abnormalities
was observed in marijuana users as opposed to non-users. These changes consisted largely
of breaks or translocations of chromosomes and more of the latter were found in chronic
users than non-users. However, when breaks were included in the count, the effect was
drowned and the differences were lost. A later study, however, found that after 72 days of
chronic marijuana smoking, no increase in chromosomal breakage rate could be found when
compared to the base level existing before the study (Hollister, 1988; Matsuyama, Jarvik,
Fu, and Yen, 1976). The pre-test, post-test design of this last study can be considered
superior to the previous two clinical investigations because of the built-in controls of a
within-subject statistical design. Studies not using this particular design usually cannot
approximate the dose rate received by their subjects nor are they able to rule out other
causes of chromosome anomalies, which may be related to differences in life-style between
users and non-users and/or the effects of other drugs rather than being due to the action
of THC alone.
In addition, one must take any chromosome studies in the proper context. Many commonly
used licit drugs are capable of causing chromosome abnormalities as well. For example, in
a recent in vitro study it was demonstrated that Paracetamol is capable of producing
concentration-dependent chromosomal aberrations in primary rat hepatocytes (Muller,
Kasper, and Madle, 1991). Although these clastogenic effects in vitro were observed only
at very high concentrations, pharmacokinetic data and other published mutagenicity data
suggest that there might be a risk for human use. According to the authors, in vivo
studies suggest Paracetamol is also weakly clastogenic in human lymphocytes when used at
the maximum human therapeutic dose range. However, there appears to be no public alarm
regarding this and earlier studies which made similar observations about the effects of
aspirin. For both THC and Paracetamol the long-term effects of induced chromosomal
abnormalities remains unknown and thus we must be cautious in extrapolating to any
possible teratogenic consequences without considerably more controlled research.
One of the more contentious areas of cannabis research concerns the effect on foetal
development of the mother's use of THC containing preparations during pregnancy. As Cohen
(1986) suggests, these effects can be highly confounded by other factors such as
nutrition, alcohol, tobacco, other drug use and socioeconomic status. He further suggests
that fairly large numbers of matched-pair subject would be required for the maintenance of
external validity in such studies. Hingston et al (1982) studied 1,690 mother/child pairs
in which 234 mothers used marijuana in varying amounts during the course of their
pregnancies. The outcome of this study revealed that cannabis use was associated with
lower infant birth weight and length for the babies of users. This results revealed a
proportional effect for the level of consumption of THC, with higher use rates delivering
greater birth weight deficits. Zuckerman et al (1989) obtained similar results in which
they found a statistically significant average 79 gram decrement in foetal weight and a
0.5 cm reduction in body length for maternal THC users as opposed to non-users. In this
study they further raise the issue of the importance of biological markers in
differentiating users from non-users. When analysing the results of their subjects on
verbal reports alone, the significant differences disappeared in contrast to a
differentiation made by urinanalysis for THC metabolites.
Cohen (1986) states in his interpretation of the results of Hingston et al (1982) that
maternal marijuana use was the strongest independent predictor of the occurrence of
features compatible with foetal alcohol syndrome (FAS) and was better than alcohol as a
predictor of FAS. In a later study Hingston et al (1984) clarified their earlier study and
concluded that some adverse effects attributed to maternal drinking and smoking may be the
result of an interaction with marijuana. In other words, there may be an additive effect
of drug combinations on the foetus.
In a related study Gibson, Bayhurst, and Colley (1983) found that, of the 7,301 births
sampled for abnormal infant characteristics, mothers using marijuana were significantly
more likely to deliver premature babies of low birth weight. However, the largest study
reported in Cohen's (1986) review of the literature is that of Linn, Schoenbaum, Monson,
Stubblefield, and Ryan (1983). In this study 10 independent variables were analysed for
12,718 women who gave birth at the Boston Hospital. Marijuana was the most highly
predictive of congenital malformation above alcohol and tobacco. Further, Qazi et al
(1985) studied the infants of five regular marijuana only users and found that each infant
had low birth weight, small head circumference, tremors at birth, abnormal epicanthic
folds, posteriorly rotated ears, a long philtrum, a high arched palate and abnormal palm
creases which are all considered signs of FAS. Cohen suggests the cause of these
morphological anomalies can be found in the results of research conducted by Morishima
(1984) in which he found that 5% of ova are damaged by exposure to THC.
Cohen (1986) admits that gross malformations in human infants have not yet been
conclusively linked to THC exposure. Fried (1985), on the other hand, observed that any
possible neonatal nervous system effects occurring from the result of regular marijuana
use by mothers during pregnancy do not manifest in poorer performance on cognitive and
motor tests at one and one half and two years of age. In addition, a later study by Fried
(1989) found that, by age three, a dose response relationship between lower language
scores, lowered cognitive scores and prenatal cigarette (tobacco) exposure is observable.
At this age, some cognitive and language deficits are also observable with prenatal
marijuana exposure. In summary, although Fried observed that at one, two and three years
of age, there are persistent effects of prenatal exposure to cigarettes, the effects of
prenatal marijuana exposure, if present, are not as readily ascertained.
If, as noted in the introductory section of this paper, neonatal weight, length and
head circumference are critical variables predictive of later psycho-motor development,
there is good reason for concern based on the results of most of the studies cited above.
However, Fried's (1985, 1989) work appears to contradict the conventional wisdom in the
case of the THC users he studied vis--vis reduction in foetal body size and its
relation to later learning and behavioural deficits. These contradictory findings would
tend to indicate either that the research into birth effects is somewhat confounded, or
there is not a simple relationship between foetal body size and behavioural development.
Again, as in other areas of research into the effects of THC on humans, the disentangling
of these issues awaits more exacting and controlled studies in the future (Nahas and
In many ways the existence or not of permanent, harmful changes to the nervous system
caused by the use of cannabis is central to the debate on the drug's long-term effects.
Obviously, any substance which has definite psychoactivity must, ipso facto, be
neurologically active. That cannabis alters brain function there is no doubt. The
questions addressed by most research is how and to what degree. Jones (1980) summarises
the nature of cannabis intoxication and its relation to neurological clinical signs.
Acute cannabis intoxication includes not only the pleasant state of relaxation,
euphoria, and sought-after sensory alterations, but also impairs judgments of distance and
time, memory for recent events, ability to learn new information, and physical
coordination. At slightly higher doses the acute intoxication includes tremor, transient
muscular rigidity, or myoclonic muscle activity. The subjective feelings of muscular
"weakness" or stiffness can be measured objectively. Low doses produce no
changes in tendon reflexes, but high doses cause hyperexcitability of knee jerks with
clonus. At even higher doses a full blown acute brain syndrome is possible (p. 67).
Jones (1980) goes on to add that some researchers would argue that such altered and
impaired brain function represents a prima facie case of temporary neurological damage
during the period of acute intoxication. The health issue which arises from this is
whether these neurological alterations last only a few hours or whether they persist with
deleterious cumulative effects. As will be seen below, the data is by no means consistent
and conclusions are difficult to draw.
In the early 1970's press reports appeared which claimed that scientists had found that
cannabis use caused 'shrinking of the brain'. These claims were based on the work of
Campbell (1971), who used pneumoencephalography to examine a small sample (10) of cannabis
users by examining the size of their neural ventricles. These measurements appeared to
reveal that the ventricles were enlarged, a finding consistent with cerebral atrophy. The
problem with this early research is that it was conducted on a population of patients who
were suffering from various neurological disorders. This fact, together with the
inaccuracy of the earlier air-volume measurement technique, is deemed by Jones (1980) to
render the work invalid. Later, similar, small-scale studies conducted by Co et al (1977)
and Kuehnle et al (1977) using computerised transaxial tomography (CAT scans) found no
evidence of anatomic changes. In the latter research the subjects were preselected for
being healthy, normal cannabis users. However, these last two studies beg the research
question by, in effect, choosing subjects who have not yet developed any pathology for an
examination of possible permanent neurological effects of cannabis use.
Electroencephalographic (EEG) changes in humans using cannabis usually entail an
increase in mean-square alpha energy levels and a slight slowing of alpha frequency. In
general, only very minor changes tend to appear in the surface EEG's of cannabis users and
those that do, such as increases in alpha wave activity, tend to be synonymous with
drowsiness and relaxation (Jones, 1980; Cohen, 1986; Klonoff, Low, and Marcus, 1973).
Although scalp EEG changes are minimal, Heath (1973) and Heath et al (1979) report
significant alterations in electrical activity recorded in mid-brain structures of
primates, most notably in the septal and amygdala areas. Although the focal EEG changes
reported in this research have been seen only in the brains of monkeys which were exposed
to marijuana smoke or given THC intravenously, the research of these authors has been
quoted widely in both scientific review articles as well as in various anti-cannabis
tracts. Therefore, a closer examination of some of this work is in order.
Heath et al (1979) found that continuous, daily exposure to the equivalent of the smoke
from about 3 marijuana cigarettes per day produced abnormal electrical alterations after 2
to 3 months. Additional exposure of up to 3 to 6 months produced electrical abnormalities
which persisted for up to 8 months. Heath also conducted histological examinations on
brain tissue from the monkeys and found anatomic changes were apparent in the
electronmicrographs, suggesting long-lasting changes related to the THC exposure. These
changes included widening of the synaptic cleft, clumping of synaptic vesicles and other
unspecified changes in morphology of neurones which occurred in monkeys after 6 months of
forced cannabis intake and were still evident 6 months after cessation of cannabis use.
However, it is unclear from his report whether a methodical evaluation of the supposed
histopathology was made which included an independent panel of judges or whether these
were his own personal judgements.
The deep sites from which abnormal EEG recordings were recorded are generally believed
to be involved in emotional expression and hence affect disorders.2 Heath's earlier work
remains somewhat problematic when his experimental setup is examined in more detail.
Although his monkeys included controls who were exposed to both very low THC containing
marijuana and tobacco smoke alone,3 this research remains highly confounded. The monkeys
were strapped into chairs with transparent, sealed plastic boxes surrounding their heads.
The smoke, together with oxygen, was pumped into the box for a pre-determined period while
EEG recordings were made through permanently implanted deep electrodes. Given that in
humans THC can induce panic anxiety attacks and given that monkeys do not like to be
restrained, it is impossible to tell whether the abnormal electrical activity recorded in
limbic areas was directly induced in the brain by the action of THC or whether this
activity was what one would observe when panic is induced in restrained monkeys
intoxicated by THC.
Heath describes the monkeys' behaviour.
All displayed dilated pupils and sharp reduction in level of awareness. The monkeys
would stare blankly into space, sometimes displaying spontaneous nystagmus, and would
become much less attentive or completely unresponsive to environmental stimuli. When their
hands or feet were grasped, the clasping response, which was consistently elicited on
baseline examinations, was absent. Responses to pain (pinprick) and to sound (hand claps)
were minimal to absent. Although the monkeys were not particularly drowsy, spontaneous
motor movements were notably slowed, and passive tests of muscle tone suggested a degree
of catatonia, although true waxy flexibility never developed (Heath, 1973, p. 4).
This certainly is not the way that the vast majority of human beings react to cannabis
intoxication. The behaviour Heath describes appears to be more in line with an animal
frozen in panic or manifesting what used to be called 'animal hypnosis'. Hunt (1984), a
cognitive psychologist, has called this the "negative capability" and it appears
to be part of a neurophysiological mechanism for behavioural and cognitive shutdown when
an animal is overwhelmed by, for example, a predator.
Another major problem with Heath's 1973 study was the control of O2 partial pressure
(PP) in the head chamber. From tables in his paper one can see that the PP of O2 inside
the monkey's "breathing chamber" was 75% greater than room PP in the marijuana
run but only 9% above for the control tobacco sequence. The measured serum PP of O2 was
143% above pre-exposure levels as seen in his data for the marijuana sequence as opposed
to a rise of only 22.4% in the case of the tobacco run. There is little doubt that high
partial pressures of serum O2 will affect brain function and hence the EEG recordings (p.
9). Thus, any comparisons between THC exposure and tobacco exposure in this study are at
best spurious. Finally, Heath states that, as the choice of subjects for cannabis studies
moves up the phylogenetic scale, it is observed that THC produces a more localised effect
in the brain involving fewer areas. In other words, humans show the least generalised
reactions to THC. In summary, apart from the confounding factors of behavioural variables
and O2 partial pressures in this research, any attempt to generalise from monkeys to
humans is fraught with the possibility of committing a logical category error.
As mentioned above, the research of Heath and his colleagues has been widely reported
and appears to have been accepted somewhat uncritically by a number of serious researchers
as seen in two of the review articles being reported on here (Cohen, 1986; Jones, 1980).
This seems to be a recurring theme in much of the cannabis research today. In most
research into psychopharmacological effects on EEG reliable conclusions are rarely drawn
from so small a number of studies. The interaction of pharmacological agents with brain
and behaviour is complex and even the simplest relationships require many experiments in
order to delineate the causal connections with any degree of reliability. It appears as
though any findings in cannabis research are immediately set upon by the those opposed to
it use for the purpose of adding power to already pre-drawn conclusions.
Sleep EEG recordings sometimes can be more sensitive indicators of drug effects than
waking EEG (Jonew, 1980). Reduction in rapid eye movement (REM) sleep accompanied by
increases in total sleep time have been reported in humans together with considerable
changes in surface EEG recordings as effects of cannabis use (Feinberg , 1976). The
cessation of cannabis intake after prolonged use will then lead to a rebound effect in
which REM sleep stages and eye movements rise above baseline levels. This rebound is not
unlike those seen after the cessation of other sedative hypnotic drugs. In addition to
these EEG changes, cortically evoked potentials consistent with altered central nervous
system (CNS) function have been recorded from scalp electrodes of waking subjects
(Herning, Jones, and Peltzman, 1979). However, as is often the case in cannabis research,
"the pattern of change varies with dose and measurement technique, and between
laboratories. The biological or functional significance of these alterations remains
obscure" (Jones, 1980, p. 69).
Jones (1980) summarises the difficulties and uncertainty which must be accepted as part
of cannabis research into its neurological effects.
Many survey and laboratory studies comparing user and nonuser populations have reported
no differences in cognitive, intellectual, or perceptual function between these two
groups....Many of the studies reporting no neurological differences between users and
nonusers have compared very selected people using 1, 2, or 3 marijuana cigarettes per week
to those using none. It may well be that lasting impairment will be evident only at a
greater dosage level or that the marijuana use interacts with some other unrecognised
factor to produce lasting effects. The impairment will thus be missed in such limited
studies. On the other hand, when deleterious, possibly marijuana-related, effects on
function have been noted in groups of cannabis users, it is very difficult to determine
whether the cannabis use caused the impairment, or was simply associated with it, or
If one considers neurochemical data from test tubes, animal data, clinical case
reports, survey data, controlled laboratory data, and semicontrolled field studies, the
weight of the evidence so far is that lasting neuropsychological impairments are possibly
but not inevitably associated with some undetermined level of heavy, prolonged cannabis
use. However, the many factors that would determine the appearance of clinically evident
cannabis-induced neuropsychological changes in any given user are so complex as to make
any simple pronouncement of risk almost meaningless (pp. 70-71).
The research paradoxes revealed in the above section on physiological effects of
cannabis can only be adequately resolved through the application of controlled
experimental research techniques on large groups of humans. It is obvious that this is
neither ethical nor practical. Of course, the tautological trap created by subject choice,
as described in most of the above clinical research into cannabis, applies to all
epidemiological studies, not just cannabis research. As we have seen with both tobacco and
alcohol research in the past, reliable conclusions can only be pieced together slowly
through large-scale and methodical data collection. So, it must be recognised that
decisions probably cannot wait for the final datum to be collected because it is unlikely
that all the data will ever be 'in'.
As with many decisions in other aspects of life, we must examine the apparent 'facts',
while attempting to understand their context and accuracy, and then make the best possible
choice based on the pragmatics of the circumstances rather than on absolutist principles
posing as facts. One might well argue that if there is any doubt, whatsoever, that
cannabis is safe to use, then it should be permanently banned. However, there may be
useful social purposes served by allowing controlled use of cannabis which outweigh any
possible deleterious effects it may have on the human organism. This is obviously the kind
of thinking behind the current freedom we have to use analgesics, such as aspirin and
Paracetamol, in spite of their well documented negative side-effects.
In any review of the psychological effects of cannabis, a clear distinction should be
drawn between cannabis use, abuse and dependency. Because of the problems involved in
determining potency, as delineated in the opening section of this paper, it is often
difficult to distinguish casual users from those who are abusers or dependent on the drug.
The standard reference for differential diagnosis of psychiatric disorders, the Diagnostic
and Statistical Manual of the American Psychiatric Association (1987), defines cannabis
Cannabis Dependence is usually characterised by daily, or almost daily, use of the
substance. In Cannabis Abuse, the person uses the substance episodically, but shows
evidence of maladaptive behaviour, such as driving while impaired by Cannabis Intoxication
The DSM-IIIR asserts that the impairment of occupational and social functioning and the
resultant physical pathologies associated with cannabis dependence tend to be less than
those seen in other psychoactive intoxicants, such as heroin, cocaine and alcohol. As a
result, people showing signs of cannabis abuse or dependency are less often seen by
medical doctors and psychiatrists. This fact further clouds any attempts at delineating an
accurate definition or symptomatology of cannabis abuse and/or dependency.
The Manual does list a set of general symptoms characteristic of dependency, however.
These include lethargy, anhedonia, and attentional and memory problems. This dependency
syndrome usually develops with repeated use over a considerable period of time with rapid
development following initial use being rare. Although there has been considerable debate
over the issue of the development of tolerance in cannabis users, the DSM-IIIR asserts
that "tolerance may develop to some of the substance's psychoactive effects and thus
promote increased levels of consumption" (p. 177). This increase is not very great,
according to the Manual, and if levels of consumption become very high, there may be a
decrease in pleasurable effects with a concomitant increase in the number of dysphoric
effects experienced by users. Jones (1980) summarises.
Tolerance, that is, a diminished response to a repeated cannabis dose, is clearly
associated with repeated use...It appears now, both in animals and in humans, that
tolerance develops quite rapidly to many of the effects of THC. The more frequent the
administration and the higher the dose the more rapidly it develops, but even subjects
smoking as little as one marijuana cigarette per day in a laboratory experiment
demonstrate tolerance on some behavioural and physiologic dimensions when they are
carefully measured....Most of the tolerance seems to be lost rapidly, but this rate may
vary with the sensitivity of the measures used (p. 74).
Other researchers, on the other hand, argue from both clinical and personal experience
that one must learn to get 'high' and, therefore, it takes less cannabis for experienced
users to obtain the desired effect than for neophytes (Tart, 1971; Weil, 1975). However,
Weller, Halikas, and Moorse (1984) found, in a five-year follow-up study of regular
marijuana users, that continuous use was associated with decreasing pleasurable effects.
Cohen (1986) summarises their results.
Users who had earlier reported positive feelings of relaxation, peacefulness, enhanced
sensitivity, floating sensations, self-confidence, subjective impressions of heightened
mental power, and other sought-after effects now said that these effects had significantly
diminished. The undesirable aspects of the experience, however, persisted essentially
unchanged (p. 158).
Nahas (1984), a major contributor to the cannabis literature, takes a strongly
proscriptive stand towards cannabis use and underscores the potential psychological
dangers inherent in cannabis intoxication when he argues that exposure during the key
developmental periods of foetal growth and adolescence may produce long-term, permanent
psychopathological changes in individuals thus exposed. In order to further emphasise the
allegedly unseen threat of cannabis use, Brill and Nahas (1984) address the issue of the
paradox of the apparent minimal physiological effects recorded in most cannabis users
warning us that
The discrepancy between the marked psychological alterations and the slight physical
symptoms associated with Cannabis intoxication represents another aspect of its deceptive
nature. Many people today believe that since no apparent gross physical damage results
from the absorption of Cannabis derivatives, there is little or no danger associated with
their use. They are mistaken: Cannabis and all other hallucinogens have a common
characteristic, their psychotoxicity and their ability to disintegrate mental function,
which is not accompanied by any major alterations of the vital physiological functions.
Mental illness, especially in the young, is also characterised by a similar discrepancy
between the functions of the mind, which are markedly impaired, and those of the body,
which are well preserved (p. 263).
This strongly held position, only loosely based on empirical data, often characterises
the quality of discussion seen in the research literature concerning the psychological
effects of cannabis. In the work of Brill and Nahas (1984) the unclear relationship
between the physiological cause and psychological effect of cannabis intoxication is used
to insinuate an almost 'devious' and/or 'sneaky' action for ∆-9-tetrahydrocannabinol. On
the other hand, the actual argument given in the last section of the above quote, aimed at
establishing a potent relationship between the minimal physiological causes arising from
cannabis ingestion and its apparent strong psychological effects, is, again, typical of
the cannabis debate and, in this case, spurious on at least two counts.
The first is the obvious logical category error of arguing from the class of mental
illness to the psychological effects of cannabis intoxication without any evidence that
these two phenomena are in any way the same category of event, physiologically or
psychologically. The second, the argument as to the universality of deleterious
psychological consequences of cannabis use, is based on a small minority of cases who have
demonstrated some psychopathological effects directly attributable to cannabis use and
thus have come to the attention of medical authorities. However, it should be remembered
that the vast majority of users, whether occasionally experiencing some negative states or
not, manage the use of cannabis and are able to integrate it into productive life-styles
without developing any apparent psychopathology (Weil, 1975). The size of this majority is
in the many millions whereas the minority from which most of the pathological data is
drawn is a non-representative (statistically) few hundred.
In contrast to the view of cannabis as psychologically dangerous in itself, Weil (1975)
has argued that it should be understood to be what he calls an "active placebo."
Weil describes an "active placebo" as "a substance whose apparent effects
on the mind are actually placebo effects in response to minimal physiological action"
rather than being a direct cause of the psychological changes seen in users (p. 95). This
effect is attested to, empirically, by the wide variety of responses individuals make to
similar batches of cannabis in similar situations. Weil's conclusions, based on hundreds
of clinical observations, led him to argue that it was highly unlikely that cannabis alone
could be responsible for the very varied psychological responses and effects which he
From the recent work of Herkenham et al (1990), cited earlier in this paper, there is
no doubt that the cannabinols have affinities for specific brain structures. However, it
is as yet unclear as to whether cannabis has any predictable specific behavioural,
cognitive, and/or affective effects resulting from the particular receptor site bindings
mapped in their study. To date it is not possible to describe a unique and repeatable
constellation of psychological responses to the action of the cannabinols as is possible
for the opiate derivatives or the neuroleptic compounds used in the treatment of
schizophrenia. This observation alone must cast some considerable doubt on most
psychopharmacological ascriptions made for the actions of the cannabinols in humans.
There have been numerous attributions made about the psychological effects of cannabis.
In the sections below a number of areas which have had considerable attention in the
research literature will be reviewed. However, before embarking on issues, such as
"panic reaction" and "toxic psychosis" amongst cannabis users, at
least one popular misconception concerning cannabis intoxication requires clarification.
As a result of press and electronic media coverage there is a widely held belief by the
community-at-large that those intoxicated by cannabis are more prone to show aggressive
and violent behaviour. This idea also has found its way into scientific discourse (Brill
and Nahas, 1984; Imade and Ebie, 1991). In their exploration of this issue, Brill and
Nahas attempt to distil a phenomenology of cannabis intoxication based, to a large extent,
on the idiosyncratic reportage of Jacques-Joseph Moreau who recorded observations about
himself and other hashish users in the mid-Nineteenth Century. Moreau describes the
quality of affect experienced during the mood swings he encountered while intoxicated on
With hashish, the emotions display the same degree of overexcitement as the
intellectual faculties. They have the mobility and also the despotism of the ideas. The
more one feels incapable of directing his thoughts, the more one loses the power to resist
the emotions they create. The violence of these emotions is boundless when the disorder of
the intellect has reached the point of incoherence (Brill and Nahas, 1984, p. 270).
Not only is this description contexualised in Nineteenth Century cultural values and
convictions, and thus not applicable as a direct comparison with late Twentieth Century
experience, but the language itself is not easily interpretable from current contexts. The
culturally embedded beliefs regarding the nature of emotions and mind have changed
radically since Moreau's time as have the way individuals understand their relationship
with their subjective lives. Therefore, using such a source in order to understand
cannabis intoxication in the present is dubious at best. Claims concerning violence thus
appear to be somewhat confounded and in summarising this issue Jones (1980) reports that
Most commissions and review groups that have specifically studied the relationship
between cannabis and violence have concluded that the use of marijuana is not a major
cause of aggression. There is little new that would change that conclusion (p. 73).
In fact, it is most often the case that chronic cannabis users have a depressed
demeanour, a lack of drive and rarely show signs of violent behaviour (Tennant and
Groesbeck, 1972). In contrast to the myth of 'hashishim' running amok, is the often
witnessed syndrome referred to as "panic reaction", which has likely been
confused with aggression and violence in many cases.
One of the most common dysphoric responses to cannabis intoxication is what has been
called the "panic reaction." "Panic reaction" most often appears as
part of an anxiety reaction in relatively inexperienced users, or in those ingesting a
higher than expected dose, and is characterised by the appearance of an acute fear
reaction sometimes associated with panic connected to the experient's possible, imminent
death (Tennant and Groesbeck, 1972). This "panic reaction" typically follows or
is followed by an acute paranoid state characterised by mistrust of others and a belief
that others have malintent towards the intoxicant. These reactions are generally acute and
disappear with the loss of intoxication within hours (Cohen, 1986; Hollister, 1988).
Of this acute panic syndrome, Jones (1980) delineates the possible psychological
This reaction, which usually starts off with an exaggeration of normal cannabis
effects, can range from mild anxiety and restlessness to panic with paranoid delusions, to
a full-blown acute toxic psychosis with loss of contact with reality, delusions,
hallucinations, and agitated and inappropriate behaviour. The reaction is more likely to
occur in inexperienced users or in the user who unknowingly consumes more potent cannabis
material than is anticipated. Preexisting psychological difficulties may also contribute.
The symptoms usually diminish over a few hours and are somewhat alleviated by reassurance,
a quiet environment, and generally supportive atmosphere (p. 71).
Kolansky and Moore (1971) studied a group of 38 subjects who had smoked marihuana twice
per week or more, consuming two or more marijuana cigarettes per session. They found that
their subjects consistently demonstrated poor "social judgement", poor
"attention span", poor concentration associated with confusion, anxiety,
depression, apathy, passivity and indifference. These changes appeared to be part of an
alteration of consciousness characterised by: 1) a bifurcation of the ego into observing
and experiencing selves; 2) an apparent inability of the subjects to bring their thoughts
together; 3) a paranoid suspiciousness of others; and 4) a seeming regression to a more
infantile state (p. 487). They summarise using a mixture of psychoanalytic and
physiological metaphors, which appear to owe more to speculation than to good scientific
It was our impression in these cases that the use of cannabis derivatives caused such
severe decompensation of the ego that it became necessary for the ego to develop a
delusional system in an attempt to restore a new form of reality. It would appear that
this type of paranoid reaction is a direct result of the toxic effects of cannabis upon
the ego organisation of those patients described in this study (p. 489).
However, in this paper Kolansky and Moore (1971) appear to indulge in generalisations
concerning the effects of THC which are based on a tiny, psychiatrically referred sample.
Any conclusions thus drawn concerning the action of cannabis on the general population
commit the logical error of inferring a universal from an existential instantiation. In
addition, value judgements are made about their patients throughout which reflect a strong
cultural bias in favour of American middle-class professional standards.
There was marked interference with personal cleanliness, grooming, dressing, and study
habits or work or both. These latter characteristics were at times present in some
patients prior to smoking marihuana, but were always markedly accentuated following the
onset of smoking (pp. 487-488).
There seems to be little introspective awareness on the part of the authors regarding
their strong prejudices and value judgements. If science is supposed to be a value-free
activity, then this current report does not begin to represent science in either spirit or
praxis. These two psychiatrists appear to be blissfully unaware of the cultural changes
taking place around them at the time (1968 - 1971) and thus much of their criticism is
confounded by their cultural blinkeredness. Further, the appearance of opposite and
contradictory symptomologies (some became apathetic while other became hyperactive) in
their study group suggests that THC is not a strictly a causal agent of the observed
psychopathology, as argued by Weil (1975), but, rather, a facilitator of predisposed
Negrete et al (1986) offers a conceptual description of what might be the underlying
psychological mechanisms of the panic, ego decompensation and paranoid ideation sometimes
seen in cannabis users. He states that it has been
...observed that tetrahydrocannabinol (THC) impairs the rate, sequence and goal
directness of thinking; that under the influence of cannabis the individual experiences an
intermittent loss of information; that the feed-back and feed-forward perceptive
mechanisms - which are essential in the process of reality testing - are upset. In
addition, there is a distortion in the sense of time which leads to a telescoping of past,
present and future. Unrelated events become peculiarly connected in the user's own
'psychological time'. All these phenomena foster projection and stimulate paranoid
ideation (pp. 515-516).
Therefore, the evidence that new or inexperienced cannabis users are prone to panic,
paranoid, or anxiety attacks must be seen from the perspective of this effect being
largely a function of particular personality types (psychological 'set') and the quality
of the 'setting' in which these personalities find themselves when intoxicated. Any
substance or situation which is capable of facilitating (directly or as an "active
placebo") a fairly radical change in cognitive sequencing and affective states and,
hence, an individual's relationship to and understanding of social reality, has the
potential of generating panic, anxiety and paranoid states as a response to loss of
control and attendant feelings of uncertainty. No doubt this is a danger in the use of
cannabis as well as being a danger when one leaves home for the first time, marries, gives
birth for the first time, or starts a new job.
When this type of psychological response does occur, there is, of course, a real
possibility of it escalating into a fully fledged psychotic reaction. The literature on
cannabis is, in fact, replete with cases and discussions of the relationship of cannabis
use and abuse to the formation of toxic psychoses, a subject to which we will now turn.
CANNABIS TOXIC PSYCHOSIS
In 1944 the New York La Guardia study concluded that given a suitably oriented
personality, marijuana use could lead, in the right time and environment, to a true
psychotic state.4 Even earlier, however, a physician from British Guyana in 1893 described
the symptoms of what he believed to be a cannabis psychosis.
The cannabis psychosis gives the impression of acute mania or melancholia. Most often
the patient is in a state of mania, suffering from delusions and visual and auditory
hallucinations. He moves incessantly, waving his arms, throwing himself from one side to
another, running up and down in the room, crying and singing. The psychosis might be
associated with violent behaviour. Sometimes the patient refuses to eat, sometimes he gets
an intense hunger. The state may change rapidly and very soon the patient will recover and
seem quite normal again. - But after two or three recurrences, every time triggered by
relapses into cannabis abuse, the patient runs the risk of becoming apathetic and blunt.
The cases of melancholia triggered by cannabis abuse are more rare. I have, however,
observed such cases where the patients have become deeply depressed - to the limit of
committing suicide (Tunving, 1985, p. 209).
Imade and Ebie (1991), working in Nigeria, assert that cannabis psychosis "has
gained recognition as a nosological entity" (p. 134). According to these authors
cannabis psychosis is categorised by the ICD-9 and DSM-III as either a form of drug
dependence or an induced organic mental disorder. The diagnostic criteria given include
intoxication marked by delusional disorder. The delusional behaviour appears to be caused
solely by the ingestion of cannabis and persists for about 2 - 3 hours. Both social and
occupational functioning are claimed to show impairment and these reactions, argue Imade
and Ebie, "vary according to the socioeconomic class, personality and attitude of the
users" (p. 134).
These authors claim that members of lower socioeconomic classes derive feelings of
power and self-engrandisement from cannabis use whereas members of the higher status
classes perceive cannabis as a relaxant and thus take it to achieve greater calm. In
contrast to Imade's and Ebie's position, Brill and Nahas (1984) maintain that "at the
present time there seems to be insufficient evidence to state that a purely
cannabis-induced psychosis exists as a separate clinical entity" (p. 294). However,
the latter two authors do argue strongly that cannabis is psycho-toxic and may precipitate
a psychotic reaction.
Whether or not the dysphoric, psychotic-like response of some cannabis users is a
"nosological entity", the work of the Nigerian researchers may be
over-generalising from the special conditions of their cultural and economic circumstances
since there do not appear to be similar sociodemographic differences in response to
cannabis reported by researchers in economically more developed countries. In fact, Brill
and Nahas (1984) point out that most reports of 'cannabis psychosis' have their origins in
the Third World which may reflect a special vulnerability of those people to any toxic
substance due to malnutrition with its attendant low body fat and plasma protein
concentration in affected individuals.
In addition to the cultural, social and economic mismatches of many reports concerning
cannabis induced psychosis, the problem with most of the data reported in these studies is
that they are highly confounded and hence not scientifically sound. There is rarely any
clear, clinical data on the psychiatric condition of these individuals pre-dating their
cannabis 'psychosis' and, hence, no way of assigning cause or any other relationship
between use and psychopathology. In addition, the age range in most of these studies is
that of young adults which is a common time for the onset of psychotic disorders for
non-drug takers as well.
Thornicroft (1990) summarises the possible relationships which may exist between
psychosis and cannabis use.
Previous reviews of the possible association between cannabis and psychosis have
proposed six types of association. Cannabis may cause psychoses de novo. It may reveal a
previously latent psychosis. Cannabis may precipitate a relapse of a pre-existing
psychosis. Established psychotic mental disorder may lead to an increased intake of
cannabis. There may be a spurious relationship. Finally, there may be no relationship
between psychosis and cannabis.
These views have, however, failed to make three vital distinctions. Firstly, they have
not adequately separated organic from functional psychotic reactions to cannabis.
Secondly, they have insufficiently discriminated between psychotic symptoms and the
syndromes of psychosis. Thirdly, they have not balanced the weight of evidence for and
against the category of 'cannabis psychosis' (p. 25).
Further, the symptomatology of the hypothesised 'cannabis psychosis' is very varied and
often contradictory, indicating a lack of a true and coherent constellation of symptoms
one would expect with an actual definable disorder. The only consistent set of responses
appears to be those associated with any toxic brain syndrome whether caused by cannabis or
any other neurologically active substance (DSM-IIIR; Weil, 1975). This lack of specificity
is underscored by the following sample of symptom constellations given by various modern
cannabis researchers including: a) shyness, irritability, hypersensitivity and arrogance
with chronic cannabis users being more often alienated from the environment and indulging
in day dreams (Stringaris, a Greek psychiatrist described in Tunving ); b) loss of
contact with reality, delusions, and hallucinations as well as agitated and inappropriate
behaviour (Jones, 1980); c) depression and agitation (Cohen, 1986); d) the occurrence of
extravagant ideas such as being 'ageless' (Brill and Nahas, 1984);5 e) the delirium
similar to that of high fever (in its acute toxic phase) which includes confusion,
prostration, disorientation, derealisation, and, at times, auditory and visual
hallucinations (Brill and Nahas); and f) paranoia and depersonalisation occurring in a
manner indistinguishable from acute brain syndrome and a belief on the part of the subject
that s/he is going mad in spite of remaining oriented with unimpaired consciousness
(Kaplan, 1971). The above group of symptoms taken with the descriptions given earlier
could, in fact, constitute a wide range of conditions ranging from severe anxiety neurosis
to true psychotic bipolar affect disorder.
Thacore and Shukla (1976) indicate that patients with 'cannabis psychosis' show panicky
and violent behaviour with greater frequency, but they do "not consider this
behaviour psychotic, because reality contact is maintained" (p. 385). Further, from
my own clinical and personal observations it often appears that many users who are having
extreme dysphoric reactions are suffering from the fear of 'going crazy' rather than
actually becoming truly psychotic. Thus, it is possible to interpret many of the so-called
psychotic responses to cannabis use as extreme panic reactions which have escalated out of
control. The force of this argument derives from the fact that a) the vast majority of
these cases recover fully when the acute phase of intoxication is past and b)
interpersonal support during this process is most often positively and constructively
received by the victim in a non-psychotic manner, viz., consciousness is unimpaired thus
allowing self-reflection and understanding in rational and non-delusional ways.
Individuals suffering from clinically diagnosed organic or psychodynamically
identifiable psychoses do not respond in this manner. The acute phase of psychosis, for
the majority of cases, moves into a chronic phase with life-long consequences. With these
psychotics the clinician finds it almost impossible to penetrate the patient's delusional,
referential thought process and, similarly, positive support appears not to be capable of
penetrating the psychotic's world when in this acute phase. This is not to say that such a
psychotic episode never happens in association with cannabis. However, it has not been
possible, to date, to disconfound the role of cannabis as a conceivable facilitator of
psychosis from its other possible roles as self-medication used to treat an impending
psychosis or its coincidental use as part of a syndrome of disturbed behaviour in an
already troubled individual.
Jones (1980) suggests that the toxic psychotic-like reaction sometimes associated with
cannabis intoxication is often caused by unexpectedly high doses in experienced users, the
reaction to intoxication by neophyte users, and/or the response of individuals with a
pre-existing psychopathology. It has been observed that this "toxic" response is
not consistent with cannabis type or potency suggesting no direct, predictable
pharmacological link. He summarises the overall state of research into 'cannabis
As is often the case with clinical reports, studies describing cannabis psychosis
rarely present data in a way that would withstand rigorous scientific scrutiny. A number
of reports finding no evidence of links between cannabis use and psychoses unfortunately
have the same methodologic problems as studies claiming drug-related associations, making
it very difficult to draw unequivocal conclusions (p. 72).
Moreau, in his mid-Nineteenth Century writings, seems to recognise that there is a
difference between delusional psychosis and "hashish fantasy" which suggests
that researchers, today, may have to delineate, with some precision, this difference
before any definable and consistent 'nosology' of extreme cannabis dysphoria can be found.
One possible suggestion is that there is no such clinical entity as a 'cannabis psychosis'
but, rather, a series of fear and panic reactions which sometimes achieve the intensity of
a psychotic-like state. This extreme but temporary response should be understood more as a
result of the user's inability to cope with the cognitive and affective reorganisation
caused by THC rather than as a direct and permanent "poisoning" of the CNS
leading to a permanent psychosis.
There have been a number of studies which make a connection between cannabis and
schizophrenia. As in the case of reports on toxic psychosis and cannabis, the relationship
between cannabis use and onset of pathology is unclear. Again, cause and effect are
difficult to establish because of the fact that most cases studied are the result of
psychiatric referrals from which only post hoc attributions can be made.
In one of the very few longitudinal studies of cannabis and psychopathology designed to
disconfound the aetiology of schizophrenia in relation to cannabis use Andreasson et al
(1987) studied Swedish military conscripts. Commencing in 1969-70 this investigation used
a pre/post research design, which, in its first stage, included obtaining a history of
drug use, social background, psychiatric history, a current psychological assessment and,
where necessary, a psychiatric interview. In their current paper, reviewing follow-up
assessment made fifteen years later, Andreasson et al state that, in addition to cannabis
consumption, increased occurrence of schizophrenia in the conscripts was strongly
correlated with diagnosis of psychiatric disease other than schizophrenia at the time of
conscription; indicators of a disturbed childhood; abuse of solvents; and poor adjustment
at school. However, in this study no relationship was observed between the increase in
schizophrenic occurrences and alcohol consumption, smoking, or socioeconomics.
Although the authors suggest that the association of cannabis usage with schizophrenic
onset may possibly be a result of an "emerging schizophrenia", they argue for
the interpretation that cannabis is a likely a precipitating factor in schizophrenic onset
for "vulnerable" individuals. This conclusion was drawn as a result of the
observation of an increasing risk for development of schizophrenia being associated with
increasing cannabis consumption in individuals with previous psychiatric symptoms. For the
authors, this conclusion is underscored with the additional finding that conscripts with
no psychiatric symptoms initially also demonstrate an increased risk of schizophrenia with
increasing cannabis consumption. In conclusion, Andreasson et al (1987) state
...an individual might be vulnerable to schizophrenia but not get the disease unless it
is triggered by some life-event stressor. The findings in this study suggest that cannabis
may be such a stressor. The effect of cannabis on the central nervous system support this
hypothesis (p. 1485).
The effect of THC on the nervous system, they argue, is localised in the hippocampus
and is accompanied by a lowered turnover of acetylcholine. However, the more recent and
comprehensive study of Herkenham et al (1990) reported earlier in this paper appears to
contradict this hypothesis of Andreasson et al (1987). The distribution of THC in the
human CNS is much more diffuse than these authors suggest and, to date, there is no
definite evidence that acetylcholine systems in the hippocampus are associated with
schizophrenogenesis. In fact, it is more strongly argued that dopamine pathways in the
ventral medial brain are more directly involved in some of the 'schizophrenias' (Helmchen
and Henn, 1987).
Another problem with the Andreasson et al (1987) study is that the causal relationship
of cannabis to the onset of schizophrenia still remains equivocal. Although the data
appears to be suggestive of a possible link between cannabis and the precipitation of a
schizophrenia in vulnerable individuals, the authors go beyond their data by strongly
suggesting that cannabis is, nonetheless, another clue to the cause of schizophrenia.
However, even a cursory examination of the literature on schizophrenia (which is beyond
the scope of this paper) reveals that the stresses of late adolescence and early adulthood
appear to be one of the major precipitating factors in the development of schizophrenia in
vulnerable individuals - with or without the use of cannabis. Since this study examined
young men of this age group, the relationship of increasing cannabis use with increasing
incidence of schizophrenia may be an artefact related to the overall range of deviant
behaviours adopted by young men suffering from the stresses of life change for which they
And finally, of the 55,000 conscripts entering the initial phase of the Andreasson et
al (1987) study, only 274 schizophrenics emerged of which 21 were in the high cannabis
consuming group with a total of 49 having ever consumed THC at all. Thus, taken together
with the fact that the causal connection between cannabis use and the onset of
schizophrenia was still left unclarified, these results should be considered insufficient
for drawing any scientifically sound conclusions concerning a meaningful link between
cannabis and schizophrenia.
In another large-scale military study of cannabis use carried out on American soldiers
Tennant and Groesbeck (1972) found that for the 720 hashish users culled from the 36,000
subjects of the research sample direct medical and psychiatric observation revealed
that the casual smoking of less than 10 to 12 gm of hashish monthly resulted in no
ostensible adverse effects other than minor respiratory ailments. Panic reactions, toxic
psychosis, and schizophrenic reactions were infrequent occurrences except when hashish was
simultaneously consumed with alcohol or other psychoactive drugs (p. 133).
The authors found 115 cases of acute psychosis analogous to schizophrenia amongst
hashish smokers but only 3 were of hashish users only. The remainder were multiple drug
users which included amphetamines, hallucinogens and alcohol taken together with hashish.
In these cases treatment with chlorpromazine did not entirely resolve the symptoms in
these cases and most appeared to move into a stage which resembled chronic schizophrenia.
However, Tennant and Groesbeck (1972) argue that because of the nature of such a soldier
sample, they had good access to premorbid records for the entire group. "In each case
there was considerable evidence that latent schizophrenia probably preexisted" (p.
134). However, no indication is given in this paper as to how the pre-trial screening was
carried out nor is there any evidence of how the criteria for determining pre-morbid
latent psychosis was established.
Jones (1980) argues for a partial causal relationship between the onset of
schizophrenia and cannabis use. He believes that patients with schizophrenia, or with a
genotype for schizophrenia "may be more prone to develop schizophrenic-like psychoses
after consuming only modest amounts of cannabis" (p. 72). However, his use of the
term "schizophrenic-like" may indicate, as in the case of toxic psychoses, that
some of these more extreme but transient negative responses to cannabis have
characteristics in common with schizophrenic disorders but are not fully constitutive of
the pathology itself. Imade and Ebie (1991), on the other hand, in an empirical
statistical study comparing schizophrenic and cannabis psychosis symptomologies, conclude
that there is no significant difference between the two groups leading them to speculate
that cannabis may be a possible additional risk factor in the development of
schizophrenia. Surprisingly, this conclusion of no statistically significant difference in
symptoms is contradicted by Table 2 (p. 135) in their published results which shows a
statistically significant difference in 9 of the 13 symptom categories presented. One can
only speculate as to why the authors draw conclusions in direct contradiction to their
Other researchers appearing to agree with Imade's and Ebie's conclusions concerning the
similarity of cannabis psychosis and schizophrenia are Thacore and Shukla (1976). Their
study of chronic cannabis abusers in India found a constellation of symptoms some of which
are similar to schizophrenia while other are not. Their work indicates that the special
characteristics of schizophrenic thought disorder (loosening of association, thought
blockage, disturbance in conceptual thinking, alienation of thought) occur statistically
significantly more frequently in schizophrenic patients than in cannabis intoxicants
suffering psychotic-like reactions. Hallucinations were experienced equally in both
conditions but "all (cannabis) patients had predominant persecutory delusions in a
setting of clear sensorium" (p. 384) in contrast to schizophrenics who do not show
any capacity for rational self-reflection while in an acute phase. Although these findings
suggest some fundamental differences between the two conditions, caution must be applied
in accepting these results because of the small sample involved and the culturally
idiosyncratic method of scoring and interpreting patients' symptoms.
In conjunction with Jones (1980) Hollister (1988) asserts, based on research conducted
by Knudsen and Vilmar (1984) as well as by Tunving (1985), that cannabis use may aggravate
an already existing schizophrenia, and this would be true whether the pathology was as yet
unmanifest, but he is not convinced that THC can cause schizophrenia or depressive
disorders on its own. Moreover, referring to Rottanburg et al (1982), he declares that
cannabis use may lead to "a self-limiting hypomanic-schizophrenic-like
psychosis" (Hollister, 1988, p. 112). Again, this statement suggests that the
relationship between drug use and pathology may be linked through an as yet unidentified
third factor involving the preference by schizophrenics for particular classes of drugs in
their attempts at self-medication and thus control of frightening delusional states.
Consequently, there appears to be an association between cannabis use by diagnosed
schizophrenics which confounds the interpretations of a causal link between cannabis and
schizophrenia. Needless to say, the connection is problematic and unresolved and certainly
needs considerably more and better controlled research before any firm conclusions can be
BEHAVIOUR AND SOCIAL ADJUSTMENT
Weller (1985) summarises a number of findings across a variety of studies aimed at
establishing a profile of cannabis users.
One study found that marijuana users were more impulsive and nonconforming than
nonusers. Another study discovered more "psychiatric impairment" in users based
on personality tests. A self-administered drug survey conducted at two colleges found that
users were less likely to be at the top of their class, had looser religious ties, and
were more dissatisfied with school. They were also more likely to be bored, anxious,
cynical, disgusted, moody, impulsive, rebellious, or restless. In still another study,
marijuana users were more opposed than nonusers to external control and likely to use the
drug to relieve tension (p.101).7
He criticises much of this characterisation by arguing that little effort was made to
determine the personality types and differences before subjects became involved in a
cannabis 'lifestyle'. Thus, it is arguable that any ascription of personality type for
cannabis users must be seen as not scientifically grounded and hence somewhat spurious.
This logical error of explanations given post hoc propter hoc appears to be a commonly
repeated one throughout the cannabis literature. However, Weil's (1975) argument that
cannabis is an "active placebo" (p. 95) which facilitates already existent
covert behaviours and pathologies offers an equally credible explanation for most
observations made concerning pathological syndromes and cannabis use with the added
benefit of accounting, in part, for the great variation seen from individual to
individual. One such constellation of behaviours which has been repeatedly claimed as
unique to chronic cannabis users is the so-called "amotivational syndrome" to
which we now turn.
McGlothlin and West (1968) first reported that regular cannabis use can lead to the
development of passive, inward-turning, amotivational personality characteristics. At
about the same time, Smith (1968) made a similar observation, based on several young
marijuana users, that regular cannabis ingestion leads to a loss of desire to compete and
work which, like McGlothlin and West, he labelled the "amotivational syndrome".
Weller (1985) describes the characteristics associated with this hypothesised syndrome.
This contention was based on clinical observation of middle-class, heavy marijuana
users referred to them for treatment. Conforming, achievement-oriented behaviour had
changed to relaxed and careless drifting. Inability to concentrate for long periods,
endure frustration, follow routines, and carry out complex, long-term plans, as well as
apathy and loss of effectiveness, were noted. Such individuals became totally involved
with the present at the expense of future goals. They had less objective productivity and
seemed to withdraw subtly from the challenge of life (pp. 95, 98).
He reminds us, however, that no specific studies or case reports were cited to support
McGlothlin's and West's (1968) observations. Other descriptors which supposedly
characterise this syndrome include: shift or decline in ambition; unproductive, aimless
life; poor class attendance; lack of goals; poor school performance; apathy;
disorientation; and depression (Weller, 1985). Nevertheless, in most cases symptoms
disappeared if marijuana was discontinued suggesting not so much as a syndrome but
behaviour of chronically intoxicated individuals using their intoxicated state as a way of
focusing their resentment of social and parental pressure.
In addition, Weller (1985) cites a number of studies which report lowered levels of
sperm and testosterone. The latter change was observed in a closed ward situation with
subjects at first showing no alteration in testosterone levels for about four weeks,
followed by a subsequent and gradual drop in testosterone level which continued until
cannabis intake stopped. This situation reversed itself on cessation of cannabis intake
with levels beginning to rise after one week's abstinence. Weller concludes that "if
testosterone affects aggression and drive, low testosterone might affect motivation.
However, this relationship must be considered hypothetical without additional research (p.
Cohen (1986) reminds us that the syndrome is so variable in presentation and influenced
by the magnitude and type of premorbid pathology, the very existence of such a syndrome
remains quite controversial. On the other hand, lethargy and loss of ambition and goal
orientation persist during intervals of withdrawal from cannabis. In many cases this
anergic condition is apparently reversed after months of abstinence, but Cohen indicates
that some clinicians report what they believe to be the occurrence of permanent brain
dysfunction in some subjects. Again, as in reports of other psychopathologies being
connected to cannabis usage, the constellation of symptoms tends not to constitute a
definite syndrome with great variation being observed in each case.
The symptoms of what is being called "amotivational syndrome" could be
understood as a facilitated endogenous depressive disorder which is brought to the fore by
chronic cannabis use in a minority of individuals. Halikas et al (1978) reported a high
incidence of depressive disorder in regular cannabis users who had smoked at least fifty
times in the past six months before the commencement of the study. Weller (1985) indicates
that an examination of the subjects of that study reveals that most were young (mean age =
22 years), middle-class and had been smoking cannabis for an average of 2 years.
"Systematic evaluation revealed that most of their psychiatric problems predated
marijuana use. About 18% had a history of definite or probable depression before
significant marijuana use (p. 102)."
It should be borne in mind, once again, that the subjects of many of these studies are
referred for treatment and hence do not represent the population of cannabis users. In
fact, from the numbers given in many sources, those presenting with psychopathologies of
any kind represent a very small minority indeed. For example, the 1991 NCADA survey of
drug use in Australia reveals that 30+% of all Australians have tried cannabis at least
once. 13.1% have used it within the past year and 5.4% within the last week. Thus, there
are hundreds of thousands of cannabis users who apparently function well enough so that
they do not come to the attention of medical or legal authorities. If "amotivational
syndrome" was a fact of cannabis use, Australian society would unmistakably feel its
impact. One can only conclude that this supposed 'syndrome' is, in actuality, the
mis-labelling of a latent affect disorder which, in a small minority of unfortunate
individuals, becomes manifest when facilitated by chronic cannabis use.
It is not surprising to find repeated assertions in the literature of reduced
performance on learning and memory tasks in a population of cannabis users who are
available for evaluation largely through psychiatric referral. The pathological symptoms
leading to referral most often include agitation (panic disorders) and/or lethargy
(amotivation). These symptoms are often primary manifestations of on-going affect
disorders and, in the case of depression, are frequently accompanied by feelings of
alienation, depersonalisation, flattened affect, memory and other cognitive impairments. A
large-scale study by Mullins et al (1974) conducted for the United States Air Force on
recent conscripts who were, for the most part, young, healthy and not psychiatrically
morbid, reveals a different picture regarding performance among cannabis users.
The authors compared 2,842 US Air Force trainees who had used only cannabis with 1,843
who had used cannabis and/or other drugs and with a control sample of 9,368 on whom no
drug-using information was available. Comparisons were made on five separate aptitude
measures, on educational level attained prior to enlistment, and on three measures of
performance of Air Force duties. These aptitude measures are the Armed Forces
Qualification Test (AFQT) and four aptitude indexes of the Airman Qualifying Examination
(AQE); Mechanical (M), Administrative (A), General (G), and Electronic (E). Comparisons of
scores were made between those who used only cannabis; those who used cannabis in
conjunction with some other drug; those who used other drugs singly, but not cannabis;
those who used other drugs in combination, but not cannabis; and the control group. It was
found that every mean score for the drug using groups was significantly different from the
control group at p = 0.01 or better. The most interesting finding, however, is that for
level of performance "all means are significantly lower than the control mean except
the means for the cannabis-only group, which are significantly higher than the control
means" (Mullins et al, 1974, p. 4)
Mullins et al (1974) argue that the differences between the cannabis-only group and the
other drug groups in relation to the controls may be the result of the degree of drug use.
In other words, multiple drug users are seen by the authors as likely heavy users as
opposed to cannabis-only user group. Thus, the lower means for the multiple drug groups
are interpreted as resulting from the total overall consumption of drugs rather than the
mixing of mind-altering substances. In addition, when controlling for total ingestion of
cannabis, the authors conclude that the cannabis-only group is more talented on average
(according to the operational definition of talent embedded in the Air Force aptitude
tests) than any of the other groups tested. Although the authors argue that the lower
scores of the multiple group are likely due to the degree of overall consumption of drugs,
they conclude that one of the more notable dangers of cannabis is in coupling it with
The authors attempt to explain the results by first observing that the use of other
drugs, with or without cannabis, is correlated with lower overall educational attainment
in the study's subject group. They continue by noting that there are significantly more
cannabis-only users who have graduated from high school (76.4%) than there are in the
control group (70.7%), which is offered in partial explanation of the higher aptitude
scores achieved by the cannabis-only group. In light of our earlier discussion concerning
motivation, both achievement scores and educational level tend to be good indicators of
higher motivation in the cannabis-only users than in the other experimental groups and the
controls. On the other hand, of those controls and cannabis-only users who entered
university, Mullins et al found a significantly higher percentage of control subjects
(37.5%) than of cannabis-only subjects (24.9%) completed their studies.
Strangely, in summarising their study the authors conclude that this last difference
indicates the possible existence of an "amotivational syndrome" in cannabis-only
users and, in their final remarks, strongly suggest that cannabis has definite serious,
negative effects on behaviour. However, in summarising their findings they state
...in general, the use of cannabis-only appears to be associated with a much less
serious performance deficiency than the use of other drugs, singly or in combination"
(Mullins et al, 1974, p. 11)
This statement can only be seen as a distortion of the empirical findings of these
researchers. Except for the issue of university completion rates for the various groups,
cannabis-only users in their study appear to be superior in performance on every measure
used by the United States Air Force. The authors' conclusion, on the other hand, stresses
that the performance of the cannabis-only group is merely less worse than the multiple
drug groups rather than better than all other groups. Again, this is an good example of
the problems which occur with value-driven research in the investigation of cannabis. No
doubt this method of interpretation of the empirical findings arises because it is very
unlikely that positive conclusions concerning cannabis use in young airmen would lead to
career advancement for members of the military who conduct social science research on
their own organisation.
Of course, there have been a number of other studies which have obtained very different
results when measuring performance. It should be noted, however, that most of these have
been conducted on a more select population than the Mullins et al investigation, with
considerably smaller sample sizes and often on individuals who have been psychiatrically
referred. Cohen's (1986) general review of these issues in relation to cannabis leads him
to conclude that
A wide range of intellectual performance impairment due to marijuana intoxication is
known. Cognitive tasks, such as digit symbol substitution, complex reaction time, recent
memory and serial subtractions, are all performed with an increased error rate as compared
to the sober state. These abilities are all generally recognised to be necessary to
perform skilled tasks. Marijuana interferes with the transfer of information from
immediate to short-term storage. Less demanding tasks such as simple reaction time are
performed as well during the non-drug condition. A major unresolved question is whether
long-term use produces irreversible effects (p. 157).
Two confounding issues are generally not critically addressed in the literature on
cannabis and performance summarised by Cohen (1986) above. The first is proper control for
the role of motivational levels in the outcome of performance tests conducted on cannabis
intoxicated individuals. THC may have differential effects on motivation depending on the
type of task to be completed. Cohen acknowledges that the apparent attenuation of the
ability to learn while intoxicated with cannabis may be due to possible perceptual and
motivational changes experienced by intoxicants. He speculates that the concomitant
impairment of immediate recall associated with these changes is linked to a lack of
motivation to learn and to the related attenuation of logical thinking abilities which
makes the acquisition of new information more difficult.
Simply stated from a more phenomenological perspective, while intoxicated, "right
brain" activities appear to be preferred by those using cannabis. Logico-deductive
cognitions tend to be usurped by metaphoric imaging arising as a result of an intensified
'absorptive state'. "Absorption", a personality characteristic often studied in
relation to hypnosis and other altered state of consciousness experiences, appears to
deploy attention in ways antithetical to the more usual linguistically ordered information
processing of daily life activities (Tellegen and Atkinson, 1974; Tellegen, 1982). Since
the majority of memory and performance tasks used in many of the studies on cannabis and
performance are dependent on language processing ("left brain") for recall, it
is not surprising that most cannabis users do less well on these tests when intoxicated.
The second issue is, naturally, the notion of 'long' and 'short' term memory employed
by Cohen (1986) and others. If we recognise that different styles of cognition and
learning are associated with different states of consciousness (Tart, 1972), then the
model of memory storage and transfer deployed by Cohen is likely to be inapplicable to the
study of individuals in an "Absorptive" state of consciousness. In addition, the
statement about information "transfer" as used by Cohen is, at this stage of
learning and memory research, more metaphor than fact since the actual neuropsychological
substrates and mechanisms of this hypothetical construct have yet to be located and their
Creason et al (1981), on the other hand, do attempt to control for motivation in
relation to cannabis consumption levels in their study of 55 high school adolescents. From
this group four sub-groups were identified consisting of nonusers ("Never"),
casual users ("less than once a week" or "once or twice a week"),
heavy users ("three or more times a week" or "daily"), and heavy users
who are now ex-users (p. 449). Motivation was operationally defined as
...the difference between the subject's performance on a task when working for a reward
and when the subject is not externally motivated. A subject who performed better working
for a reward than when not was considered more motivated than a subject who performed at
the same level regardless of whether there was a reward at stake (p. 448).
"The dependent variable was the difference in the number of solved single-solution
anagrams between the first and second trials," the assumption being the first trial
measured actual ability and the second measured performance level when motivated, with the
difference showing the effect of motivation (p. 449). From this research design the
authors found that heavy users and heavy ex-users were significantly (statistically) lower
in motivation than non-users or casual users, the latter two groups showing no significant
difference. The authors thus conclude that the effect of heavy use on motivation is not
dependent on the presence of the drug in the user's system. To account for this they
hypothesise the existence of an intervening variable, such as a personality factor, which
distinguishes those who are high users from low or non-users. In conclusion they argue
that there is good evidence in the research literature to suggest that "heavy
marijuana use is limited to those who are already inclined to low motivation and
depression" ( p. 452) Unfortunately, Creason et al were not able to assess for any
possible pre-existing psychiatric morbidity or personality differences which may have
indicated any prior conditions in heavy users before the commencement of their cannabis
habit. Thus, there is no empirical evidence arising from this study which is able to
support their explanatory hypothesis.
Although there have been suggestions regarding brain damage in cannabis users, as cited
earlier in this paper, Varma et al (1988) find no evidence of a real difference between
users and controls on measures of intelligence and memory. These findings are consistent
with two United States Government studies (National Institute of Mental Health, 1972,
cited in Rubin and Comitas, 1975; National Institute on Drug Abuse,1980) in which the
authors suggest that any differences found between cannabis users and non-users in
cognitive functioning pertain more to perceptuo-motor tasks. However, Varma et al (1988)
observed that in Indian cannabis users who are not part of a deviant sub-culture, the
users still appear to be significantly more disabled in "personal, social and
vocational functioning" (p. 151). However, the higher rating of disability in this
group of cannabis users did not, in the opinion of the authors, amount to a noticeable
In assessing the work of Varma et al (1988) it is necessary to understand that the
group studied is the equivalent, in the West, of heavy, chronic drinkers of alcohol. This
is underscored by the authors' recruitment of subjects amongst a known group of heavy
users whose life-style revolves around congregating together specifically for the purpose
of consuming cannabis. In addition, findings of higher 'neuroticism' and 'psychoticism'
test scores for these individuals also indicates that they are not average members of the
society being studied (Eysenck, 1960).
In effect, this research is confused by the usual problems of personality disorder and
psychopathology almost certainly existing in the study group prior to cannabis addiction
as indicated by membership in and adherence to a cannabis-based sub-group in the context
of a country (India) in which this substance is widely accepted and probably broadly used
in other social circles as well. If pathology was not present prior, then such extreme use
could be regarded as a cause of the psychological problems (as in the case of severe
alcohol abuse). Nevertheless, this cannabis sub-culture is an inappropriate group to
estimate the long-term effects of social cannabis ingestion, just as it would be
inappropriate to estimate the social, physiological and psychological effects of alcohol
by studying chronic, intractable drunks.
In contrast to Varma et al (1988), a study by Schwartz et al (1989) claims to
demonstrate definite adverse effects of cannabis on memory. The latter researchers
evaluated the auditory/verbal and visual/spatial memory for groups matched on age, IQ, and
absence of previous learning disabilities. The study used 10 cannabis-dependent
adolescents and compared them with the performance two control groups consisting of 8
adolescent drug abusers, who had not been long-term users of cannabis, and 9 adolescents
who had never used any drug. Significant differences between the cannabis-dependent group
and the two control groups were demonstrated on the Benton Visual Retention Test and the
Wechsler Memory Scale Prose Passages. The authors also found that, after 6 weeks of
supervised abstention from intoxicants, those in the cannabis-dependent group demonstrated
some improvement on the Wechsler Memory Prose Passages score and on the Benton Visual
Retention Test. This improvement, however, failed to achieve statistical significance
leading the authors to conclude that cannabis-dependent adolescents develop selective
short-term memory deficits which appear to continue for at least 6 weeks after the
complete cessation of cannabis intake.
This last study employs very small numbers of subjects in its experimental and control
groups, which makes the results somewhat weak in a statistical sense. Further, in this
research the experimental subjects consumed approximately 900mg/week of THC (18 grams of
high-potency marijuana @ 5% THC) which is about equivalent to 130 mg/day for a 4 month
period - considerably higher than most heavy users. This level of cannabis was consumed to
within a couple of days of end of the trial.
Heavy users, according to a recent survey conducted by the Criminal Justice Commission
of Queensland, Australia use about 10 grams of cannabis containing about 2-3% THC, or
300mg of THC/week.9 The ward study by Schwartz et al (1989) referred to here provided
subjects with about 900mg THC/week, or three times the amount of in vivo heavy users. If
the physiological half-life is taken as one week (Cf. Nahas, 1984), then at the end of a 6
week abstinence period following 12 weeks of cannabis ingestion at the rate of 900mg
THC/week, the lipid burden of THC will be approximately 28mg THC.10 Further, if, as
revealed in the work of Chesher et al (1985), 1-2 mg of ingested cannabis causes a similar
level of behavioural deficit as a 0.05 blood alcohol level, then the retest situation in
the Schwartz et al study is on subjects who are still in a highly THC affected state.
Unlike alcohol, THC is highly soluble in body lipids and it is this property which
causes it to remain systemically present much longer than water soluble alcohol. Thus, the
resultant levels of THC accumulated by participants in the Schwartz et al (1989) study
would be extremely high at the end of the first part of the study. With a half-life of 5-7
days it would be many weeks before the serum THC would be at an equivalent zero level for
these extremely high-dose subjects. It is quite conceivable, therefore, that the subjects
were, at re-test time, still at or above the intoxication equivalent of 0.05 blood
alcohol.11 This, of course, does not include an approximation for the effect of any
additional THC remaining in brain lipids which, conceivably, could still be quite high.
Therefore, low or zero measures of serum THC do not guarantee that participants in the
post-test section of the Schwartz et al study are cannabis-free and, hence, the test
subjects may still be affected by a low-level, background intoxication.
Returning to the issue of perceptuo-motor and cognitive performance, Chesher et al
(1985), using nine different tests, attempted to ascertain the effects of cannabis
consumption on performance in a controlled study employing individuals in a dose level by
time pre- post-drug experimental design. Employing the centroids of the combined test
scores for each condition, the authors compared the performance effects of smoked
cannabis, orally ingested cannabis, and alcohol with the resulting evidence suggesting
that "the duration of impairment produced by all three drugs at the doses used was
very similar" (p. 624). However, the earlier findings of Weil et al (1968), that some
dose-related impairment is observable on simple intellectual and psychomotor tests for
naive subjects but not for regular users, indicates a need for finer elucidation of the
observed effects, if the results of Chesher et al are to be taken at face value.
Chesher et al's (1985) results also suggest that orally administered THC is 4000 times
more potent than ethanol in its pharmacological action. Although exact comparisons could
not be made between smoked cannabis and imbibed alcohol, it was estimated that 1-2 mg of
THC in the marijuana-to-be-smoked produces a decrement in performance equivalent to 0.05
blood alcohol level (p. 627). This finding suggests that, since the average marijuana
cigarette contains approximately 1-3 mg of THC, similar restrictions would have to be
placed on cannabis consumption and driving as now exist for alcohol.
Hollister (1988) reports a summary of four separate studies in which the occurrence of
positive serum tests for drugs in dead drivers involving 2610 fatalities was estimated.
Alcohol was found in 1680 cases and THC in 351 with 294 of the latter involving alcohol as
well. Of those found with THC, 278 had serum concentrations less than 5mg/ml, suggesting
that "THC plays a relatively minor role in fatal traffic accidents as compared with
alcohol" (Hollister, 1988, p. 113; McBay, 1986). In other words, only 2.2% of
cannabis-only users were involved in these fatal accidents. Of course, the long half-life
of cannabinols in the body and the presence of them in blood long after acute intoxication
has ceased, as seen from the studies cited above, does not indicate whether or not those
individuals who tested positive in the quoted road fatalities were intoxicated.
Cohen (1986) asserts, in his summary of the drug and driving research literature, that
70% of all fatal auto crashes involve alcohol. However, he reports that 37% of the fatal
crashes studied tested positive for the presence of serum cannabinols, but these were
found mainly in combination with alcohol and other psycho-active drugs with cannabis-only
users representing 12% of all those cases involving cannabis. Alcohol was mixed with
cannabis in 81% of the cannabis cases and, again, it is impossible to tell, unlike with
alcohol, whether those testing positive for cannabinols were in the acute phase of
intoxication rather than several days away from last cannabis usage. From his summary of
the statistics Cohen therefore argues that
Although alcohol is the prime cause of automotive accidents, marijuana and cocaine are
currently being found frequently enough to constitute potentially significant problems. It
is established that marijuana and alcohol have additive effects upon driving skills. Since
marijuana metabolites were found in more than a third of the drivers, impairment due to
marijuana is contributing to the problem (p. 158).
The above research likewise is confounded by the presence of alcohol in the majority of
cannabis cases. In order to support Cohen's contention, data would be required to show
that accidents are increasing, in any given demographic area, in direct proportion to the
increase in use of drugs such as marijuana and cocaine while simultaneously controlling
for alcohol use. Without such clear-cut quantitative relationships one must still conclude
that alcohol is the primary cause of fatal crashes even where other drugs are present.
Again, the findings of THC metabolites in 37% of the drivers involved in fatal crashes do
not indicate that these individuals were intoxicated with THC at the time. However, the
data may be suggesting that there is an increased danger when driving on alcohol for
cannabis users even post acute intoxication. Whether the hypothesised additive effect of
THC and alcohol is a fact and/or whether this effect happens post acute cannabis
intoxication remains to be elucidated through carefully controlled research which has not
yet been done.
Weil (1975), although writing in the early 1970s, still provides a useful and
insightful summary of research on cannabis and performance.
Because marihuana is such an unimpressive pharmacological agent, it is not a very
interesting drug to study in a laboratory. Pharmacologists cannot get a handle on it with
their methods, and because they cannot see the reality of the nonmaterial state of
consciousness that users experience, they are forced to design experimental situations
very far removed from the real world in order to get measurable effects. There are three
conditions under which marihuana can be shown to impair general psychological performance
in laboratory subjects. They are: (1) by giving it to people who have never had it before;
(2) by giving people very high doses that they are not used to (or giving it orally to
people used to smoking it); and (3) by giving people very hard things to do, especially
things that they have never had a chance to practise while under the influence of the
drug. Under any of these three conditions, pharmacologists can demonstrate that marihuana
impairs performance (p. 86).
Most altered states of consciousness, such as those produced in hypnosis, meditation
and ecstatic experiences, involve deployment of attention strongly in the present. This
'unreflected', unself-conscious attentional state, which is focused primarily in the
'now', will, whether induced by drugs or not, possibly interfere with the normal memory
processes associated with the 'reflected' conscious state required for discursive thought
and logico-temporal activities usually associated with memory and learning. Thus, any
discussion of memory and THC use must consider the possibility that THC facilitates a
free-floating 'absorptive' state which favours engagement in spatial-metaphoric cognitive
styles of the 'unreflected' state (Fabian and Fishkin, 1981). It is thus possible that the
apparent memory deficits seen in individuals intoxicated with THC, who are being required
to perform and attend to verbal, temporal, logico-deductive activities, is the result of
'time-sharing' between the two states. The effect is to interrupt the usual cognitive and
memory consolidation processes.
This 'time-sharing' process can be conceptualised as a temporary and rapid movement out
of the induced 'unreflected' state of consciousness into 'reflected' consciousness when
enough 'demand' is made to attend to a temporal, discursive information stream. As soon as
demand falls below some critical threshold required for attention, the 'unreflected' state
resumes thus disrupting any on-going learning process. The laying down of short-term
memory and the ability to attend accurately to objective (clock) time may require a
certain level of continuous background 'self-observation' - a primarily 'reflected' state
activity. Therefore, assigning the cause of memory deficits measured in THC intoxicated
individuals to the pharmacological action of cannabis may be an attribution error with
cannabis being primarily a catalyst for these altered states which are the actual cause
for a failure to process discursive information in the usual way.
Although this review has ranged over a rather broad area encompassing a number of different research disciplines, there appears to be a common concern linking most of the research reviewed - is cannabis a significant public health risk? It is the opinion of this author that this question is still, after almost thirty years of research effort, unclarified.
In the physiological domain there certainly appears to be reasonably strong evidence of the potential threat to the human respiratory system associated with chronic, heavy cannabis smoking. However, whether use amongst moderate, social cannabis smokers poses the same risk is a question as yet unanswered. This risk is, of course, from the combustion by-products of the cannabis leaves, stems, and flowers and is not directly associated with the active ingredient for which cannabis is sought and used, ∆-9-tetrahydrocannabinol. One method for obviating such a health risk would be to make pharmacologically pure forms of orally ingestible THC available to those who want it in a similar manner to the way in which governments now regulate the production and distribution of alcohol.
In general, the results of much of the research concerning the effects of THC on the CNS appears to be either negative or inconclusive. The work of Heath and colleagues is an exception, of course, but as was shown above, this research is highly confounded and cannot be considered to be reliable in spite of the fact that it is widely quoted in scientific and other literature on cannabis.
Turning to the psychological dimension, the "amotivational syndrome" appears to be a not very useful hypothetical construct which is poorly grounded in empirical psychological data. The populations studied in this type of research are often psychiatric referrals and it has been revealed in other, more methodologically thorough research, that supposed sufferers of cannabis-induced "amotivational syndrome" often had signs of clinical depression prior to their use of cannabis. As argued earlier in this paper, "amotivational syndrome" appears to be a category seeking content, especially when the profile of individuals studied is better understood through the more conventional psychiatric diagnostic category of depressive disorder. Nevertheless, there is little doubt that cannabis has some effect on behaviour and performance. Driving a motor vehicle while intoxicated with cannabis will certainly increase the risk of an accident. However, the apparent 'permanent' changes to memory and performance as demonstrated in some 'ward' studies are not entirely convincing considering the exaggerated dose levels used and the long half-life of THC in humans.
Studies in performance and aptitude such as that by Mullins et al (1974) highlight the
value-driven quality of much of the research reviewed here. When the effects of alcohol
and other drugs are controlled, cannabis-only users apparently show significantly greater
overall aptitude than any other group amongst U.S. Air Force recruits. Nevertheless, this
did not stop the authors from sounding alarms concerning the potential harmful effects of
cannabis on performance in young men. In fact, it appears as if most of the research
reviewed by this author commenced from an a priori position that cannabis is dangerous to
human health, physiological and psychological, it only remains to discover just how
dangerous. In pursuing these objectives authors such as Brill and Nahas (1984) breached
all current good scientific practice by using the writings of a Nineteenth Century
physician to make a supposed empirical case in the late Twentieth Century without any
apparent recognition on their part of the potential for misinterpretation or
It appears as though two possible hypotheses are available regarding cannabis and
public health. The first is that cannabis is a potential public health problem, it merely
remains to be discovered to what degree. The second states that cannabis represents no
significant or unreasonable threat to the general public well-being. According to the
physicist, James Jeans (1958), expanding on William of Occam's 'Razor'
When two hypotheses are possible, we provisionally choose that which our minds adjudge
to be the simpler, on the supposition that this is the more likely to lead in the
direction of the truth. It includes as a special case the principle of Occam's razor -
'entia non multiplicanda praeter necessitatem' (p.183).
From the position of this widely held scientific principle it is arguable that only the
second hypothesis is reasonable regarding the current debate on cannabis. From the use
levels observed in Australia (31.9% have ever tried cannabis and 7.1% (1.3 million
Australians) use it once a month or more [Department of Health, Housing and Community
Services, 1991]), when taken in conjunction with the very small number of cases who
actually come to the attention of medical authorities as a direct result of cannabis use,
one can only conclude that the simpler hypothesis which covers the facts is that cannabis
use does not pose a significantly increased risk to public health over and above many
other activities which are considered necessary and/or socially acceptable.
As suggested by Weil (1975) altered state experiences appear to be a natural human
capacity which can be facilitated by the ingestion of psychoactive substances such as THC.
The negative reporting, vis--vis cannabis and performance, may be understood as a
value judgement regarding what type of mental state and hence style of performance is
deemed useful by society. In other contexts, the present-centred altered state of
consciousness, which can be induced by cannabis, is highly prized in the contemplative
religious traditions of Christianity, Buddhism and Islam. The ability of this altered
state to open broader perspectives and, hence, new life meanings appears to be part of a
growth process which has the power to bring about personal renewal and relieve
psychological suffering. Although these religious traditions have developed methods for
achieving these altered states without the use of pharmacological facilitators, the need
for such experiences is probably innate to human personality. In the age of high-tech
medicine the use of chemical substances to achieve these ends should not be surprising.
The psychiatrist Arthur Deikman (1982) suggests that the bifurcation of consciousness
into "observing" (objective) and "experiencing" (receptive) selves is
the basis of mystical experience with the latter, 'unreflected' state, too often missing
in our lives. He further reminds us that without the cultivation of the "experiencing
self" we may fail to enter into mystical awareness and therefore be unable to heal
the psychopathology innate to our human condition. He thus argues for a return to
mysticism as both outlook and technique in the process of human growth.
The mystical tradition has been concerned with the very problems that modern
psychotherapy has been unable to resolve. It makes sense, therefore, to investigate
mysticism with a view to dealing more effectively with those problems and gaining wisdom
as human beings (p. 4).
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without the ability to enter wholly into these "experiencing" altered states, we
may fail to fully actualise our human creative and cultural potentials (James, 1936; Jung,
1960; Maslow, 1968; Wilber, 1977). Thus, we may understand the use of cannabis in society
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This work may not be reproduced, in whole or in part, by any means (printed or
electronic) without the written permission of the author.
1Searches were conducted in two data bases: Medline (Index Medicus) and PsychInfo
(Psychological Abstracts). The following inclusive 'or' statement was searched: MARIJUANA
OR THC OR CANNABIS OR TETRAHYDROCANNABINOL. Medline produced 2253 'hits' and PsychInfo
1935. One can assume that there is some overlap, hence the approximation of over 4000.
2The earlier, 1973, study of Heath, in addition to the septal area, included recording
sites in the cerebellum, postero ventral lateral thalamus, hippocampus, and orbital and
temporal cortices. The thalamic and hippocampal sites are major components of the limbic
system and hence intrinsically involved with emotional expression and would most likely
show unusual and significantly different activity in a situation of induced stress.
3The experimental group received exposure to marijuana smoke containing 2.29%
D-9-tetrahydrocannabinol and the controls were exposed to either marijuana smoke
containing 0.1% D-9-tetrahydrocannabinol or tobacco smoke.
4Mayor's Committee on Marihuana, 1944, cited in Nahas, 1984, p. 285.
5This idea, of course, is also the claim of many famous, historical mystics and
Cf. Happold (1963).
6A possible reason for this apparent contradiction may lie in the sources of funding
for cannabis research. Most money comes from government coffers and most governments are
in opposition to cannabis use. Therefore, one may conclude that researchers will attempt
to minimize findings which do not satisfy the views of their funders in order to insure
future support. This may seem harsh, if one accepts the myth of scientific objectivity,
but scientists are as competitive as any other group in their attempts to stay in the
"game" and to win.
7For his summary he draws extensively on Halikas, Shapiro, and Weller (1978).
8However, the authors qualify this statement later on by indicating that it is the
heavy use of cannabis in conjunction with other drugs which is most likely the cause of
the reduced scores. They fail to make the observation that heavy drug users of any kind,
particularly heavy multiple drug users, are very likely to be suffering from some other
psychiatric disorder which may affect motivation and/or performance.
9This was a preliminary report released in March, 1993 at a public forum held in
Brisbane. It will soon be published by the commission and copies are obtainable through
the Criminal Justice Commission, Coronation Drive, Toowong, QLD.
10This was calculated using a discrete approximation of a half-life decay.
11It should be remembered that 1-2 mg of THC to be consumed is the equivelant of an
alcohol blood level of 0.05 (Chesher et al, 1985).
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