The alleged connection between mental illness and cannabis derives from Africa, the Middle East and India. These areas are currently developing economically and scientifically, but for many years medical care and especially psychiatric care were given low priority. Many chronic illnesses still persist in these countries which may affect mental functioning. Furthermore, well-trained psychiatrists and methodologists are very rare in mental hospitals in these countries. Consequently, the findings of earlier studies are questionable due to lack of controls, biased sampling and poor data collection and failure to account for variables like nutrition, living standard, cultural factors and socioeconomic status.

India's mental institutions were widely quoted to support the, connection between excessive cannabis consumption and insanity. The Indian Hemp Commission performed a thorough and objective investigation of this question, although methodologically it was not up to modern standards. The Commission was unconvinced of the reliability of hospital statistics, where often the diagnosis was not made by a psychiatrist but by a referring policeman.

Therefore, the Commission examined all admissions to Indian mental hospitals for one year. They found that cannabis rise could not be considered a factor in more than seven to 13% of all cases of both acute and chronic psychosis.

Chopra et al. (1942) carefully performed the same examination of admission to Indian mental hospitals from 1928 through 1939 when cannabis use was extremely high. They found 600 cases of acute and chronic psychosis which could be traced to cannabis use. Other reports from India have produced varying estimates of the incidence of cannabis psychosis (Peebles and Mann, 1914; Chopra, 1971; Dhunjibhoy, 1930 Evens, 1904). In Egypt 27% to 33% of mental hospital admissions were cannabis related (Ireland, 1893; Warnock, 1903).

Benabud (1957) reported that cannabis users comprised 68% of all mental hospital admissions in Morocco but only 25% of these admissions could be called cannabis psychosis. Watt (1936 and 1961) reported that 2% to 3% of mental hospital admissions in South Africa were due to the use of dagga (cannabis).

Boroffka (1966) and Asuni (1964) reported that 14% of psychiatric admissions in Nigeria used cannabis. Toxic psychosis accounted for half of these and cannabis was felt to aggravate underlying schizophrenia in the remainder.

Several statistical studies from other countries including Jamaica, Colombia, Algeria, Panama and Tunisia support this type of data (Prince et al., 1970; Beaubrun, 1971 Allentuck and Bowman, 1942; Bouquet, 1951; Chevers, 1870; Defer and Dielil, 1968; Fraser, 1949; Freedman and Rockmore, 1946; Porst, 1942; Siler et al., 1933; Reales-Aroyco, 1953; Medical Staff, 1938).

Very little information is available on the prevalence of psychosis in the overall population of cannabis users. Chopra and Chopra (1939) classified 2% of the ganja and charas smokers and 0.5% of the bhang drinkers in their sample of 1,200 as psychotic.

Roland and Teste (1958) estimated that no more than 0.5% of kif (cannabis) smokers in Morocco suffer from recurrent mental conditions.

Prince et al. (1970), in a study in Jamaica, noted that about 20 patients per year are admitted to mental or general hospitals with acute psychotic reactions allegedly precipitated by ganja. In one general and one mental hospital the, ganja smokers comprised 20% of the psychiatric admissions. Furthermore, the percentage of heavy ganja smokers in the community was significantly higher than 20%. Thus, a larger percentage of psychiatric admissions were, derived from non-ganja smokers in a comparable lower socioeconomic segment of the population.

This finding contrasts with the 68% prevalence of cannabis use among psychiatric admissions reported by Roland and Teste (1958) which is considerably higher than the prevalence of cannabis use in the general population of Morocco.

Studies based on several hundred cases indicate that the large majority of individuals hospitalized in mental institutions for "cannabis psychosis" have suffered acute toxic psychoses associated with a sharp toxic overdose or massive excesses among habitual users. Occasional smokers and moderate habitual users seldom had psychotic reactions and then only when there were substantial predisposing factors.

The acute clinical picture seen in these delirium with confusion, disorientation, terror, and subsequent amnesia is that of a severe exogenous psychosis. It does not typically involve the type of thought disorder characteristic of schizophrenia. Short recovery times ranging from a few days to six weeks are uniformly reported in sharp contrast to the lengthy recovery period of functional psychoses (Chopra et al., 1942; Roland, and Teste, 1958; Defer and Diehl, 1968; Beaubrun , 1971; Stringaris, 1939).

Consequently, the psychiatric literature on cannabis-induced chronic psychosis is quite confused. In general, it appears that cannabis use probably produces a specific psychosis, but this must be quite rare, since the prevalence of psychosis in heavy cannabis users, world-wide, is only doubtfully higher than the prevalence in general populations (Murphy, 1963). However, incidence and prevalence data for these countries on psychosis of users and non-users of cannabis does not exist.

A Morroccan investigator, Christozov (1965), studied 140 chronic heavy hashish users hospitalized in a mental hospital. Their behavior was characterized by a confusional state of consciousness, an impulsivity, an irresponsible attitude, and an instability of mood and character. The patients were often psychotic with persistent hallucinations. Intellectual functions were reduced in over half the cases although this was related to a low intellect prior to drug use. Electroencephalography showed no specific changes. In addition, it was noted that half of the patients were also alcoholics.

The majority of the patients were, sedated and showed a rapid improvement, allowing them to be discharged and be employed, Although it appeared that these characteristics are reversible, the patient often returned to heavy drug use again causing return of the syndrome.

Thus, the existence of a more long lasting cannabis-related psychosis is poorly defined. Some evidence indicates the existence, of a, quite rare slow-recovery, residual cannabis-psychosis following heavy chronic use. Patients often exhibit schizophrenic-like withdrawal, mental confusion and mild residual hallucinations; but there is little tendency for the, symptoms to become organized or proliferate. The symptoms develop gradually and then subside gradually before proceeding to full-blown psychotic symptoms. These may produce gradual psychic deterioration in the habitual excessive user after prolonged periods of time. Several authors theorized that the chronic psychosis consists of recurrent acute attacks with gradual deterioration in habitual excessive users (Roland and Teste, 1958; Chopra, et al., 1942; Stringaris, 1939; Sigg , 1963).

Most investigators, therefore, find it exceedingly difficult to distinguish a psychosis due to cannabis from other acute and chronic psychoses because, few, if any symptoms, are uniquely found in it and not observed in other psychoses. Often the diagnosis of cannabis psychosis is made because of the history of heavy marihuana or hashish use. Several have suggested that a characteristic cannabis psychosis does not exist and that marihuana will not produce a psychosis in a well-integrated, stable person (Allentuck and Bowman, 1942; Reales-Aroyco, 1953).

In addition, alcohol often played a part in producing the mental derangement (Medical Staff, 1938; Porst, 1942). Most data refers to any form of psychosis in marihuana users; not specifically cannabis psychosis.

Although it is fairly well-established that cannabis use attracts the mentally unstable, the prevalence of major mental disorder among cannabis users appears to be little if any higher than that in the general population. Therefore, true cannabis psychosis must be earlier, very rare or it must substitute for other forms of psychosis. Perhaps, cannabis use alternatively is protecting some less stable individuals from a psychosis (Murphy, 1963).

Because of these many difficulties, the role of cannabis use in acute and especially chronic psychoses in these countries is impossible to determine with certainty.

Finally, the Eastern literature often mentions the existence of a characteristic psychic degeneration among older habitues after prolonged excessive use (Chopra et al., 1942; Christozov, 1965; Indian Hemp Commission, 1893; Roland and Teste, 1958; Stringaris, 1939; Warnock, 1903). They are frequently described as showing a single minded, carefree state, such as "Kif-happy vagabonds."

Soueif (1967) administered psychomotor and cognitive performance tests to imprisoned hashish users and non-hashish users in Egypt. Preliminary results indicate that, on most of the tests, the hashish sample scored 10% to 20% below the control, and differences were larger for those with higher educational levels. These results do not necessarily indicate a causal relationship. Assessment of the significance of these findings must await further description of the samples utilized.

Experience in the U.S. and Western Europe has not involved a level of marihuana use comparable to the above-mentioned countries. Consequently, the associated chronic psychotic disturbances have not been seen.

In Western countries, Bromberg (1939) and Allentuck and Bowman (1952) reported on acute psychotic episodes with clear-cut onset during the marihuana intoxication. Most symptoms cleared within a few days although several had a, prolonged illness. These rare acute psychotic episodes, discussed earlier, have been described recently by a variety of authors in scattered countries (Smith, 1968; Weil, 1970; Bialos, 1970; Keeler, 1967; Milman, 1971; Pesyko, 1970 Kaplan, 1971; Prince et al., 1970; Baker and Lucas, 1969; Grossman, 1969; Beaubrim, 1971; Spencer, 1970).

Some of these reported cases are quite transient and clear rapidly with support of others and may be more like acute panic reaction than psychosis. Still others appear to fit the picture of transient toxic psychosis.

A few cases of marihuana psychosis reported by Kaplan (1971) recovered very slowly after extensive psychotherapy. However, the high incidence of schizophrenia and borderline states described in these patients and their families may indicate that marihuana use merely aggravated or precipitated an underlying psychosis in these individuals.

George (1970) reported a case in Britain in which an acute episode of confusion, disorientation, hallucination, anxiety, paranoia, agitation and memory loss related to cannabis use was followed by a more chronic schizophrenic-like syndrome with thought disorder, incongruous affect and hallucinations. This individual was experiencing considerable financial and marital stress prior to these two separate acute episodes. The chronic condition eventually responded to psychotherapy.

Bernhardson. (1969) reported aggravation by cannabis of schizophrenic conditions in several Scandinavian patients. Perna (1969) reported a case in which marihuana appeared to aggravate an extended psychosis for which the patient had required psychiatric treatment prior to the use of marihuana.

Keup (1970) reported 14 cases of prolonged psychotic symptoms requiring hospitalization associated with the use of marihuana. He noted evidence for the existence of a, high level of psychopathology in many of them which predated their marihuana use.

Kolansky and Moore (1971) in a widely publicized report of cases of individuals ages 13-to-24 has claimed profound adverse psychological effects from smoking marihuana two or more times a week.

Of 38 individuals reported, all had decompensated personalities, eight had psychoses (four attempted suicide) and 13, according to the authors became sexually promiscuous due to marihuana. These clinical impressions were, all based on, at most, a few interviews with the, individuals who were referred to these psychiatrists for consultation for problems (including one-third by legal authorities after arrest for possession of marihuana).

Unfortunately, the authors made sweeping generalizations to all young adolescent marihuana users from this biased and non-representative sample. No attempt was made to interview other young marihuana users who have not been referred for psychiatric help, and the high prevalence of promiscuity and psychopathology in comparable adolescent populations was totally disregarded. In addition, case histories of previous mental health were obtained introspectively from the patient, their families or the referral source.

Thus, it is impossible, to state unequivocally, as the authors do, that since marihuana use and psychiatric problems occurred at the same time the former is causative of the latter.

Several authors have reported acute toxic psychosis following marihuana use by soldiers in Vietnam (Talbott and Teague, 1969; Colbach and Crowe, 1970, Bey and Zecchinelli, 1971).

All these cases represented transient reactions and cleared rapidly with treatment. In many cases, personality disorders or borderline personality states appeared to be predisposing factors in the development of the psychotic state. Often revealed were problems of identify diffusion, ego weakness, low self-esteem and inability to form close interpersonal relationships. Also the stressful conditions of the setting in which the drug was used deserves emphasis.

Halikas et. al. (1971, 1972) performed intensive psychiatric interviews on a population of 100 regular marihuana users and a control group of 50 of their non-using or casually using friends. Half of each group met the criteria for some psychiatric diagnosis. Psychiatric illness and antisocial behavior most often preceded marihuana use.

Some attempts have been made to estimate the incidence, of psychosis and other adverse reactions to marihuana in Western countries. Obviously, such estimates depend on how these reactions are defined-one questionnaire study of 2,700 psychiatrists, psychologists, internists and general practitioners in the Los Angeles area reported 1,887 "adverse reactions" to marihuana in an 18-month period (Ungerleider et al., 1968). Adverse reactions were not defined by the authors in the survey. Those reported ranged from mildly unpleasant parental objections to use to severe anxiety or acute psychosis.

Keeler (1967) reported on "adverse reactions" to marihuana (paranoid feelings, etc.) which are limited to the immediate period of intoxication. These phenomena occasionally occur in such a light proportion of regular users that they are of little interest in the present discussion, e.g., 80% of users report they sometimes have paranoid reactions during the marihuana intoxication (Tart, 1970).

Other estimates have been based on hospital admissions in which marihuana use was the recognized precipitating cause. Lundberg et al. (1971) reviewed the admission records for the Los Angeles County General Hospital for the period 1961-1969 and found marihuana use was listed as the reason for admission in only nine out of 700,000 cases, and five of these were for intravenous injections.

Keup (1970) reports that 0.9 per 1,000 of the 1968 admissions to a Brooklyn psychiatric hospital were directly related to cannabis use, and in another 1.9 per 1,000 it was found to be a contributory factor.

In 1966, psychiatric hospitals in England listed 82 admissions for which cannabis use was considered a factor (Baker and Lucas, 1969) in 1967, the number was 140 (George, 1970). For the 1966 data, further analysis revealed that eight of the 82 cases were acute psychotic reactions to cannabis, 20 were related to "cannabis addiction as a way of life," and cannabis could not be established as a definite factor in the remainder (Baker and Lucas, 1969).

Colbach and Crowe (1971) estimate that among a population of 45,000 U.S. soldiers in Vietnam in 1969, some 40 to 50 per month were hospitalized for psychiatric reasons and about five of these were associated with (usually heavy) marihuana use.

Among college populations, Pillard (1970) estimates five to seven marihuana-associated anxiety reactions are, seen per year by the Boston University Health Service which cares for a student population of 20,000; and Bialos (1970) reported 11 cases during a one-year period (1968-1969) for a student population of 8,500.

If it is assumed that about one-third of the Vietnam and college populations are using marihuana to some degree, the annual incidence of hospitalized cases in Vietnam would be about four per 1,000 users; the rate for student-health cases, 0.3 to 1.3 per 1,000 users.

The 1972 Secretary of Health, Education and Welfare's report on Marihuana and Health prepared by the National Institute of Mental Health noted in summary that marihuana can clearly precipitate certain less serious adverse psychiatric reactions, such as simple depression and panic, particularly in inexperienced users.

In these reactions, non-drug factors may be the most important determinants. Psychotic episodes may also be precipitated in persons with a preexisting borderline personality or psychotic disorder or those persons under excessively stressful conditions. These acute psychoses appear to share considerable clinical similarities with the acute toxic psychoses noted in the Eastern literature. Both these psychoses resemble an acute brain syndrome in that they occur primarily after heavier than usual usage and are self-limited and short-lived after the drug is removed from the body.

Some reports describing a prolonged psychotic course after an initial acute episode cannot rule out the role of pre-existing psychopathology. At the present time evidence that marihuana is a suf ficient or contributory cause of chronic psychosis is weak and rests primarily on temporal association. This issue may be clarified by extensive epidemiological and controlled clinical studies. (Secretary, HEW, 1972)