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Very worthy report. Posted: Tue Jan 08, 2008 7:39 am
Have a read of this report , I could not copy and paste my copy but the 420 mag forum have posted it.
I consider it one of the best constructed papers on cannabis I have come across .. and a resource that needs more exposure..
Joined: Feb 19, 2004 Posts: 1347 Location: Nelson area
Posted: Tue Jan 08, 2008 7:55 am
Biological And Psychological Effects Of Cannabis
INTRODUCTION
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 (1980) states:
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 perceptuo-motor deficits.
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.
PHYSIOLOGICAL
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.
PULMONARY EFFECTS
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.
CARDIOVASCULAR EFFECTS
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 findings:
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 complications.
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 psychoactive derivatives.
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.
TERATOGENICITY
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-ˆ-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 Latour, 1992).
NEUROLOGICAL EFFECTS
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 followed it.
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.
PSYCHOLOGICAL
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 dependence.
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 (p. 176).
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).
PSYCHOPATHOLOGY
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 observed.
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 hashish.
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.
PANIC REACTION
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 progression.
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 inference.
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 conditions.
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 _________________ Regulation will set cannabis free
Joined: Nov 16, 2005 Posts: 464 Location: New Zealand
Posted: Tue Jan 08, 2008 9:00 am
Quite an impressive summary, however one quick read through it revealed two "nonperceptions" to me. Both relate to the dilatory affects of cannabis. Firstly, perhaps the dilatory affects of cannabis compared to the constricting ones of nicotine explain why the pulminary affects are not as deletorious. Secondly, perhaps the reason the heart rate increases is because flow resistance is decreased by the dilating of the blood vessels.
I enjoyed the following parts of the report -
steveoh wrote:
Biological And Psychological Effects Of Cannabis
INTRODUCTION
.....
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.
....
....
. 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.
....
It is one of the most comprehensive and balanced reports I have read.
A few things I would have a different take on but for the most part it really puts things into perspective..
Trouble is its a bit long , even the conclusion is comprehensive , it is going to be difficult to get those who should read it to actually do so..
Maybe someone like ROSS from the NZDF could reference it and as well do summary that would be user friendly??
I am sure there are bits and pieces which reflect some elements of truth regarding cannabis ingestion and its effects, but by and large it is a review of studies which are BULLSHIT.
Quite clearly, one thing this review of the literature does establish is how dominated by propoganda, mis-information and lies certain aspects of the alledged scientific community are.
In all my years of ingesteing cannabis, and having observed a great number of people having ingested cannabis, and I can honestly say that I have never seen even a miniscule percentage of people having presented some of these Frankenstein suppositions. Whether that be lung functioning impairment or any behavioral anomalies present in those who use cannabis as a result of their cannabis use. 99% of all cannabis use is non-problomatic. In a tiny portion of extremly heavy abusers there may be some lung/cardio-vascular impairment or even some psycological issues related to their cannabis abuse. However, cannabis is still one of the safest recreational drugs there is and by a huge margin is far safer than alcohol will ever be!
A great many of these alledged scientists who conducted such ridiculous studies in the interests of appeasing the war on people would make very interesting test subjects themselves. Of particular interest would be conducting some tests and interviewing the guy who forced cannabis smoke into restrained monkey's lungs via a bubble strapped over the monkey's head. Indeed, a great many of these supposed scientists would do well to recognise that they do not add to humanity, they takle away from it.
When we gone do a review of all the positive aspects of cannabis?
Take note too, of the origins of so many of these quasi-studies
This news just in: Prohibition is responsible for and creates a great deal of harm in users of cannabis who would other wise experience no problems. This includes an expected number of homocides every year and includes home invasions and extortion and facilitates the ease with which hard drugs like methamphetamine can be pushed on those seeking cannabis from their local gang distribution center. Lets not expand on that other wise we'd be simply repeating what is already known.
Make no mistake - cannabis prohibition is a disease. Should you find yourself subject to this disease, do not pander to the inequities perpetrated against you by the crown on behalf of the USA - NOT GUILTY all the way. And yes, I will be voting ALCP.
The reviewer in my view, did a great dis-service to the law reform community world wide by even attempting to 'review' so much nonsense and regurgitateing so much gutter science which should have been buried long ago never to see the light of day. Nahas and many others like him were dis-credited many years ago and by re-printing the lies and propoganda it just serves to further cloud the issue of cannabis law reform.
I did observe
"A few things I would have a different take on but for the most part it really puts things into perspective.."
But I would suggest even with those flaws it is more inclined than most neutral reports to give cause to those who read it to have a more open attitude.
Initially ,when I first read it I found all the bits I was uncomfortable with . They stuck out like dogs balls.. It was only when a associate (Medical) in another organization was given it to read , and as he was not very supportive prior I was not expecting a very positive take on it.. He had a very different view, unlike TEWNC and other material I have supplied in the past he took it on board and found it informative and was well swayed .I have sent it to other fence sitters for comment and have had some similar feed back.
It may well be more neutral than we would wish , but I would expect those with the opposite agenda to us ,might consider it biased the other way.
I could well have it wrong , maybe grabbing at straws .... I had intended to ensure those that matter actually got the opportunity to read it, was going to put it in a new presentation package i am doing .
Not so sure now , I respect both your views and may well have got it wrong ..
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.
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does establish is how dominated by 
