LSD and schizophrenia

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LSD is an acronym for the German chemical name Lysergsäure-Diethylamide (English: Lysergic Acid Diethylamide), a powerful semi-synthetic hallucinogen derived from the ergot fungus that infects grains of rye. Early in its history, various medical workers observed some schizophrenics had used LSD.[1] The early work thought that LSD-induced hallucinations or psychosis resembled schizophrenic hallucinations, and "LSD psychotics" resembled schizophrenics.[2] Surveys of schizophrenics found apparently high LSD usage rates. This led to the hypothesis that LSD is one of the causes of schizophrenia, with the mechanism being related to the serotonin neurotransmitter.[3][4]

Research into any connection between schizophrenia and LSD (or hallucinogenics) has been largely eliminated by the banning of LSD and no straightforward experimental test has been done.[5]

Objections

Difficulties with the hypothesis include:

  1. schizophrenics use many stimulants as well as hallucinogenics, some to cope, self-medicate, and for other reasons;[6] it seems unlikely that, say, nicotine or alcohol cause schizophrenia. Similarly, amphetamines can produce similar symptoms without apparently causing schizophrenia.[7]
  2. this use of many drugs introduces considerable confounds - even if a chemical is harmless, the lifestyle and impurities can cause issues
  3. the suggested serotonergic abnormalities did not pan out[8]
  4. the similarity of symptoms may have been overstated[9]
  5. no apparent epidemiological correlations
    1. One would predict changes in schizophrenia diagnosis rates with changes in LSD usage, and one would predict seeing shocks like the US (and quickly, international) LSD ban reflected. This does not seem to have occurred; none of the papers mention any such "coincidence", nor any anomalies in age cohorts (e.g. an unexpected drop in diagnoses for "40 year-olds" when this drop is observed 20 years after the LSD ban)
    2. A gender imbalance in favor of men, whereas lifetime rate of schizophrenia are equal for the genders once late-onset victims are included (Hafner & Heiden 1997)
    3. An economic imbalance in favor of the wealthy, who can afford recreational drugs such as LSD
    4. And many other such factors, whereas the true incidence rates seem smoothly varying over a small range over most times & places, leading Hafner & Heiden to write (emphasis added):

The transnational variability of the incidence rates decreases as the stringency of studies increases. The national studies show the greatest variation in methodology, for example, diagnostic definitions and case findings. In the intermediate section, annual incidence rates for a broadly defined diagnosis of schizophrenia (ICD 295 or CATEGO S, P, and O), based on the same sample as in section III, show less but still considerable variation, whereas in section III, based on a restrictive and highly reliable diagnosis of nuclear schizophrenia (CATEGO S), no significant differences can be seen, the annual rates varying around 10/100,000.
Incidence rates of the same size in all populations and cultures studied render a substantial role of cultural, social, or climatic factors in the morbidity risk for schizophrenia inconceivable.
Zubin (38) tried to explain this unusual epidemiological pattern by assuming that schizophrenia is the common final pathway arising from a great number of causes. Another common disorder with an almost identical age-corrected incidence throughout the world is dementia in old age (39,40), which shows a clear-cut causal heterogeneity, but largely identical symptoms.


For example, Australia with some of the lowest rates is not famous for LSD absence, and Indonesia is not famous for its high consumption of LSD (as opposed to opiates or amphetamines).

Undecided

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These objections do not rule out the possibilities that

  1. LSD increases risk by a small amount,
    One perspective is to compare rates of lifetime LSD use with lifetime schizophrenia diagnoses. Hafner & Heiden list lifetime risk estimates from 0.6-1.6%; US estimates of lifetime rate of LSD use fall in the 10-20% decile.[10] Clearly, it is impossible for LSD to have more than a ~10% lifetime risk of schizophrenia; the lack of epidemiological correlates suggests that tighter upper bounds could be derived.
  2. or that it does not increase risk but does hasten the onset
    This is difficult to support or reject, but it is the negative possibility most consistent with the overall picture.[11]

[1]

[6]

[3]

[4]

[8]

[2]

[7]

[9]

[10]

[11]

References

  1. ↑ 1.0 1.1 For example, "Untoward Reactions to Lysergic Acid Diethylamide (LSD) Resulting in Hospitalization":

    ...A sudden surge of admissions to the Bellevue Psychiatric Division after ingestion of d-lysergic acid diethylamide (LSD) prompted us to review the history . . . The 3 patients in whom an extended psychosis followed a single ingestion of LSD clearly had long standing schizophrenia...

    "Effects of mescaline and lysergic acid (d-LSD-25)", Cattell et al 1952:

    The effects of mescaline and lysergic acid were studied in schizophrenic patients. It was found that physiological changes were produced in these patients and that their mental symptomatology was markedly aggravated. The observations made with the above-mentioned drugs on normal individuals were compared with those seen in schizophrenic patients. Mescaline and lysergic acid are drugs that disorganize the psychic integration of a person. This disorganization is much more apparent in schizophrenics than in normals.

    Abraham et al 1996:

    Other reports describe post-LSD psychotics appearing as schizophrenic (Blumenfield and Glickman 1967; Vardy and Kay 1983). Heikimian and Gershon (1968) likewise noted that a majority of their 47 inpatients with a drug abuse history were diagnosed as schizophrenics, with half describing psychosis prior to drug use. Four additional studies found post-LSD psychotics with prior psychosis but also patients in whom the drug precipitated psychosis without a prodrome (Public Health Committee 1966; Ungerleider et al. 1966; Smart and Bateman 1967; Frosch 1969). One group reported cases of psychosis following a single dose, suggesting a peculiar vulnerability to the drug in certain individuals. A review of this problem concluded that prior illness was evident in many, but not all, psychoses following LSD (Kornblith 1981).

    • Blumenfield M, Glickman L (1967): Ten month’s experience with LSD users admitted to county psychiatric receiving hospital. N Y State J Med 67:1849-1853
    • Vardy MM, Kay SR (1983): LSD psychosis or LSD-induced schizophrenia? A multimethod inquiry. Arch Gen Psychiatr 40:877-883
    • Hekimian LJ, Gershon S (1968): Characteristics of drug abusers admitted to a psychiatric hospital. JAMA 205:125-130
    • Public Health Committee, Subcommittee on Narcotics Addiction, Medical Society of the County New York Medicine 22, pp. 241
    • Ungerleider JT, Fisher DD, Fuller M (1966): The dangers of LSD. Analysis of seven months’ experience in a university hospital’s psychiatric service. JAMA 197:389-392
    • Smart RG, Bateman K (1967): Unfavourable reactions to LSD: A review and analysis of the available case reports [Review]. Can Med Assoc J 97:121&1221
    • Frosch W (1969): Adverse reactions to hallucinogenic drugs. In Meyer RE (ed), NIMH PHS Pub 1910, Bethesda, MD, National Institute of Mental Health
    • Kornblith AB (1981): Multiple drug abuse involving nonopiate, nonalcoholic substances. II. Physical damage, long-term psychological effects and treatment approaches and success [Review]. Int J Addictions 16:527-540
  2. ↑ 2.0 2.1 Vardy & Kay 1983, "LSD Psychosis or LSD-Induced Schizophrenia? A Multimethod Inquiry":

    The family histories, manifest symptoms, premorbid adjustment, and profiles on an extensive test battery were analyzed for 52 LSD psychotics and 29 matched first-break schizophrenics. The LSD patients did not differ from schizophrenics in incidence of psychosis or suicide among the parents. However, the rate of parental alcoholism for LSD psychotics far exceeded that for schizophrenics and the general population. The two groups were distinguished on some clinical features but were equivalent in premorbid adjustment, on most cognitive measures when initially hospitalized or reassessed three to five years later, and in number of subsequent rehospitalizations. Thus, in most respects the LSD psychotics were fundamentally similar to schizophrenics in genealogy, phenomenology, and course of illness.

    Turner & Tsuang 1990:

    Cole and Katz (1964) examined the psychotomimetic properties of d-lysergic acid diethylamide (LSD), concluding that it produces a "state which is similar but not identical to naturally occurring schizophrenia" (p. 758).


    ...The work of Janowsky and Davis (1976) provides some justification for the use of stimulants as psychodiagnostic agents in view of their ability to enhance psychotic symptoms under controlled conditions, although these authors also advocate more conservative strategies for obtaining similar information about schizophrenic symptomatology.
  3. ↑ 3.0 3.1 "Molecular pathology of schizophrenia: more than one disease process?", T J Crow:

    On the basis of the LSD psychosis and the pharmacological antagonism by LSD of some effects of serotonin Gaddum19 suggested that serotonergic transmission might be deficient. Tryptophan metabolism (by way of the serotonin and other pathways), however, is not abnormal in the schizophrenic brain,21 and serotonin receptors (assessed by binding of LSD and 5-hydroxytryptamine) are unchanged.17 Reports have been conflicting on possible changes in the monoamine oxidase activity in platelets24 in schizophrenia, but interest in this question has been diminished by the finding25 that enzyme activity, assessed with several different substrates, is normal in the brain of schizophrenics. [see also Whitaker et al 1981]

    • 17: Owen F, Gross AJ, Crow TJ, Loftnouse R, Poulter M. Neurotransmitter receptors in brain in schizophrenia. Acta Psychiatr Scand (Suppl) (in press).
    • 19: Gaddum JH. Drugs antagonistic to 5-hydroxytryptamine. In: Wolstenholme GW, ed. Ciba Foundation symposium on hypertension. Boston: Little Brown, 1954:75-7.
    • 20: Woolley DW, Shaw E. A biochemical and pharmacological suggestion about certain mental disorders. Proc Natl Acad Sci USA 1954;40: 228-31.
    • 21: Joseph MH, Baker HF, Crow TJ, Riley GJ, Risby D. Brain tryptophan metabolism in schizophrenia: a post-mortem study of metabolites on the serotonin and kynurenine pathways in schizophrenic and control subjects. Psychopharmacology 1979 ;62 :279-85
    • 24: Murphy DL, Wyatt RJ. Reduced monoamine oxidase activity in blood platelets from schizophrenic patients. Nature 1972;238:225-6
    • 25: Crow TJ, Baker HF, Cross AJ, et al. Monoamine mechanisms in chronic schizophrenia: post-mortem neurochemical findings. Br 7 Psychiatry 1979 ;134 :249-56
  4. ↑ 4.0 4.1 From Snyder et al 1974:

    ...Psychotomimetic drugs such as LSD and mescaline are thought to exert their behavioral effects primarily by way of serotonin in the brain (77). While serotonin is largely 0-methylated, tryptamine, which also occurs naturally in the brain (78), is N-methylated. One of the products of this reaction, N,N-dimethyltryptamine (Fig. 3), is a potent psychotomimetic drug. The fact that serotonin and tryptamine have been definitively shown to be converted to psychedelic-like compounds in the normal brain provokes speculation that variations in the activity of the amine-methylating enzyme play a role in mental disturbances such as schizophrenia.

    • 77: G. K. Aghajanian, W. E. Foote, M. H. Sheard, J. Pharmacol. Exp. Ther. 171, 178 (1970); N. J. Giarman and D. X. Freedman, Pharmacol. Rev. 17, 1 (1965).
    • 78: S. R. Snodgrass and A. S. Horn, J. Neurochem. 21, 687 (1973); J. M. Saavedra and J. J. Pharmacol. Axelrod, Exp. Ther. 182, 363 (1972).
  5. ↑ Lua error in package.lua at line 80: module 'strict' not found.
  6. ↑ 6.0 6.1 "Substance Use Disorders in Schizophrenia—Clinical Implications of Comorbidity" discusses nicotine, cannabis/marijuana, alcohol, and cocaine. From "Hallucinogenic drugs as precipitants of schizophrenia", Breakey et al 1974:

    The authors have examined the drug-taking histories of 46 schizophrenics and 46 matched controls. They have found that the schizophrenics on average used a wider variety of drugs, in greater amounts. Schizophrenics who had used drugs experienced the onset of symptoms on average four years earlier than non-users and were also admitted to hospital four years earlier, on average. Those schizophrenics who had used drugs had had better premorbid personalities than the non drug-users. These results are indicative of some precipitating role of drug abuse in the onset of schizophrenia.

    Abraham et al 1996:

    Studies examining the association of specific psychiatric diagnoses to specific classes of drugs found schizophrenia most frequently tied to amphetamine and hallucinogen abuse (McLellan and Durley 1977; McLellan et al. 1979). A chart review of 176 inpatients found that more psychotic patients abused hallucinogens than did a comparable group of drug abusers without psychosis. The drug-abusing psychosis were also differentiated from drug-abstinent psychotics by earlier ages of onset, more visual hallucinations, depression, and families with affective disorder. These workers concluded that the data were consistent with the hypothesis that the drug abuse had precipitated a psychosis (Tsuang et al. 1982)...O'Brien et al. (1984) reported high frequencies of psychiatric diagnoses among opioid users in treatment, but relatively low levels of psychosis or schizophrenia. McLellan et al. (1979) found psychosis was much more prominent among stimulant users...Similarly, Tsuang et al. (1982) reported a significantly earlier onset of psychiatric illness and first psychiatric hospitalizations among long-term drug-abusing psychotic patients when compared to non-drug-abusing schizophrenic or atypical schizophrenic patients.

    • McLellan AT, Durley KA (1977): Non-random relation between drugs of abuse and psychiatric diagnosis. J Psychiatr Res13:179-184
    • McLellan AT, Woody GE, O’Brien Cl’ (1979): Development of psychiatric illness in drug abusers. Possible role of drug preference. New Eng J Med 301:1310-1314
    • Tsuang MT, Simpson JC, Kronfol Z (1982): Subtypes of drug abuse with psychosis. Demographic characteristics, clinical features, and family history. Arch Gen Psychiatr 39:141-147

    "Impact of Substance Abuse on the Course and Outcome of Schizophrenia", Turner & Tsuang 1990, Turner & Tsuang 1990:

    McLellan and Druley (1977) reported high rates of drug problems among schizophrenic patients (48 percent of paranoid patients and 43 percent of chronic patients), with alcohol being the drug of choice among 31 percent of the sample. Similarly, Alterman et al. (1980) reported that 50 percent of their schizophrenic sample who had a secondary alcoholism diagnosis continued to consume alcohol in the hospital.


    In contrast, Rimmer and Jacobson (1977) encountered no greater rates of alcoholism among schizophrenic patients and their relatives than among the general population. Richard et al. (1985) also found relatively low rates of drug abuse (21 percent) in their sample. O'Tarrell et al. (1983) examined addictive behaviors in hospitalized male veterans and found lower rates of alcohol abuse among schizophrenic patients than among all other psychiatric patients. Tsuang et al. (1982) compared substance abuse, along with other variables, among schizophrenic and non-schizophrenic patients and found more hallucinogen use but less sedative-hypnotic use in schizophrenic patients and no differences in the use of alcohol.
  7. ↑ 7.0 7.1 "Drugs, Neurotransmitters, and Schizophrenia", Snyder et al 1974

    While confusion about diagnosis has been a major stumbling block, one must invoke other explanations for the many false hopes and subsequent disappointments in biochemical studies of schizophrenia. Innumerable "discoveries" of the biochemical abnormality in one or another body fluid of schizophrenics have relentlessly been followed by failures of confirmation in other laboratories. Reported abnormalities in parameters as diverse as carbohydrate, protein, amino acid, and lipid metabolism have been advanced, only to be shown by more careful studies to derive from factors such as drug ingestion, diet, muscular activity, and the effects of chronic hospitalization.


    ...However, in controlled studies in which large doses of amphetamine were administered to subjects who had no evidence of preexisting schizophrenia or schizoid tendency, psychosis was uniformly produced within 1 to 4 days (9, 10). Thus, amphetamine psychosis is not likely to be simply a precipitation of latent schizophrenia . Since some patients became psychotic in about 24 hours, there could not have been sufficient deprivation of sleep to account for the psychosis. As for the question of overexcitement, after some initial moderate euphoria, most subjects were sullen rather than excited, although it is conceivable that there was "internal" hyperexcitement,which might not be evident to observers.
    • 9: J. D. Griffith, J. Cavanaugh, J. Held, J. A. Oates, Arch. Gen. Psychiatr. 26, 97 (1972)
    • 10: B. M. Angrist and S. Gershon, Biol. Psychiatr. 2, 95 (1970); B. Angrist, G. Sathananthan, S. Wilk, S. Gershon, J. Psychiatr. Res., in press; B. Angrist, B. Shopsin, S. Gershon, Nat. New Biol. 239, 152 (1971).

    Amphetamines and related stimulants of the central nervous system can, in small doses, exacerbate symptoms of schizophrenia (11) rather than superimpose a distinctive psychosis upon the illness. Patients themselves perceive that their illness is worsening under the influence of the drug. By contrast, when schizophrenics are treated with other psychotomimetic drugs, such as LSD (D-lysergic acid diethylamide), they recognize that the superimposed psychosis differs from their own mental disturbance (12).

    • 11: D. S. Janowsky, M. K. El-Yousef, J. M. Davis, Compr. Psychiatr. 13, 83 (1972); -, H. J. Sekerke, Arch. Gen. Psychiatr. 28, 185 (1973)
    • 12: L. E. Hollister, Ann. N.Y. Acad. Sci. 96, 80 (1962); L. W. Chloden, A. Kurland, C. Savage, J. Nerv. Ment. Dis. 122, 211 (1955)
  8. ↑ 8.0 8.1 Whitaker et al 1981, "Tritiated LSD Binding in Frontal Cortex in Schizophrenia":

    The present study, however, reveals in a Scatchard analysis of tritiated LSD binding in frontal cortex in the brains of 13 schizophrenic patients that there was no decrease in binding by comparison with eight control brains. Quantities of neuroleptic remaining in the brain after death cannot be readily washed out and could have led to the previous report of reduced LSD binding.

  9. ↑ 9.0 9.1 From Snyder et al 1974:

    They were impressed by the fact that LSD reproducibly evoked a psychotic state which differed from toxic drug psychoses in that subjects were always alert and reasonably well oriented to time, place, and person. However, detailed comparisons of the mental states produced by LSD and related psychedelic drugs such as mescaline, dimethyltryptamine (DMT), and psilocybin with the typical functioning of most schizophrenics in mental hospitals revealed many differences (12). Psychedelic drugs tend to alter visual perception, with few changes in auditory perception. By contrast, although schizophrenics can experience visual hallucinations, these are much less frequent than auditory hallucinations. The psychedelic drug experience is frequently pleasurable, while for most schizophrenics their psychosis presumably is an unpleasant experience. Whether or not a -typically schizophrenic disturbance of thinking and feeling takes place in psychedelic drug-induced psychosis is a matter of controversy. Moreover, unlike the case with amphetamine psychosis, individuals under the influence of drugs such as LSD can be readily distinguished from schizophrenics in mental institutions. Schizophrenics receiving psychedelic drugs report that the drug experience is unlike their endogenous psychosis; it seems like something "different" superimposed upon their fundamental disease (12).
    However, one should be cautious before rejecting out of hand any possibility of a relationship between psychedelic drug psychosis and schizophrenia. Even if a drug acted by disturbing the same site in the brain that is affected in schizophrenia, one would still not expect the effects of the drug to be identical to those displayed by schizophrenic patients. Patients with schizophrenia have been suffering from their disturbance for many years, probably long before overt symptoms were manifested, whereas the drug experience is acute and short-lived. Moreover, an individual receiving a psychedelic drug knows exactly what is happening to him and can anticipate speedy restitution to normality, while the schizophrenic is afflicted with an unknown and unpredictable long-term process.
    ...This line of reasoning suggests that one should compare drug psychosis to the clinical state displayed by schizophrenic patients during their earliest acute breakdown. There seem to be some striking similarities between the subjective states of some early schizophrenic patients and the effects of psychedelic drugs. Psychedelic drugs elicit feelings of enhanced self-awareness, awe, and ecstasy, with sensations of increased acuity and profundity of all sensory perception. Similarly, in case histories of patients suffering acute schizophrenic breakdowns, Bowers and Freedman (15) frequently encountered apparent psychedelic experiences. Perceptual modes were heightened, the patients feeling that they had broken through conventional modes of perceiving, thinking, and feeling to attain a "new creativity." Instead of the flattened affect of chronic schizophrenics, these patients experienced intense joy or dread, which is of interest since with psychedelic drugs one often sees an alternation between extremes of elation and abject terror. Although their thinking was altered, these patients often did not display the typical schizophrenic disturbance of thought or feeling. Moreover, in these acute schizophrenics, changes in visual perception were much more frequent than they were in chronic patients. Snyder and Lamparella (16) quantified the presence of various "psychedeli" behaviors in schizophrenia and observed that these were much more frequent in acute patients.

    This "psychedelic" phase of schizophrenia seems not to be tolerated for long. Either the acute state subsides and normal mental function is restored, or the bewildering experience is resolved by encapsulation into fixed delusional systems, or restricted modes of interacting, including autistic behavior, altered affect, and a formal thought disorder.
    • 15: M. J. Bowers, Jr., and D. X. Freedman, Arch. Gen. Psychiatr. 15, 240 (1966)
    • 16: S. H. Snyder and V. Lamparella, Commun. Behav. Biol. Part A Orig. Artic. 3, 85 (1969)

    From "The Psychopharmacology of Hallucinogens", Abraham et al 1996

    In a classic study of altered states of consciousness, Langs and Barr (1968) observed similar patterns of paranoia in schizophrenics and about a fourth of normal subjects receiving LSD....Hollister (1962), however, concluded that symptoms from a group of 59 experimental subjects receiving hallucinogens were discriminable from those in schizophrenics....In 1968 Freedman surveyed the dangers of a casual view towards hallucinogens in a pivotal paper that concluded that the harms of using LSD outweighed the apparent benefits...It is noteworthy that the years 1960-1968 constituted a preponderance of favorable reports, which subsequently reversed from that point to the present. The absolute number of publications, as well as the number of favorable reports, fell off coinciding with the passage of federal regulations limiting research with this drug.

    • Langs and Barr (1968) Langs RJ, Barr HL (1968): Lysergic acid diethylamide (LSD-25) and schizophrenic reactions. A comparative study. J Nerv Ment Dis 147:163-172
    • Hollister LE (1962): Drug induced psychoses and schizophrenic reactions: A critical comparison. Ann N Y Acad Sci 96:80-88
    • Freedman DX (1968): On the use and abuse of LSD. Arch Gen Psychiatr I&330-347

    ...Stoll (1947) noted a much higher incidence of acute adverse effects in subjects who were unaware of its administration....Schizophrenics may developed tolerance in 2 to 3 days (Cholden et al 1955)

    • Stoll W (1947): LSD-Ein Phantasticum aus der Mutterkorn-gruppe (LSD-a phantasticum of the ergot group). Schweizer Archiv fiir Neurologie und Psychiatric 60: 279-323
    • Cholden IS, Kurland A, Savage C (1955): Clinical reactions and tolerance to LSD in chronic schizophrenia. J Nerv Ment Dis 122:211-221

    The clinical nature of psychoses following LSD appears to resemble schizoaffective disorders with the not-infrequent addition of visual disturbances. Fink et al. (1966) noted in an early experiment with chronic psychotic patients that, “the hazard of LSD administration appears not to be in the precipitation of a schizophrenic-like state but rather in decreasing emotional and affective controls and inducing a persistent state of altered consciousness.“ from a psychiatric outpatient department as described: 23% had diagnoses of schizophrenia characterized by visual disturbances, good relatedness, mild thought disorder, and mystical preoccupations suggestive of temporal lobe disorder (Abraham 1980). Bowers found that schizophrenic drug users had healthier premorbid personalities than nondrug-using schizophrenics and an earlier age of onset (Bowers 1972a), a finding confirmed by Breakey et al. (1974).

    • Fink M, Simeon J, Haque W, Itil T (1966): Prolonged adverse reactions to LSD in psychotic subjects. Arch Gen Psychiatry 15:450-454
    • Abraham HD (1980):Psychiatric illness in drug abusers[letter]. New Eng J Med 302:868-869
    • Bowers M Jr (1972a): Acute psychosis induced by psychotomimetic drug abuse. I. Cllmcal findings. Arch Gen Psychiatr 27:437440
    • Breakey WR, Goode11 H, Lorenz PC, McHugh PR (1974): Hallucinogenic drugs as precipitants of schizophrenia. Psycho1 Med 4255-261

    The clearest description of post-LSD psychotic disorder comes from 75 case reports in which clinical features were described in detail (Table 2). What emerges is that the commonest symptoms reported include mood swings, visual hallucinations, mania, grandiosity, and religiosity. The most effective treatments were electroconvulsive therapy (ECT) and lithium. Bowers's longitudinal study of 15 patients with LSD psychosis prompted him to conclude that a major affective component was present (Bowers 1977).

    • Bowers M Jr (1977): Psychoses precipitated by psychotomimetic drugs. A follow-up study. Arch Gen Psychiatr 34:832-835
  10. ↑ 10.0 10.1 "Club Drug Use and Dependence Among Young Adults Recruited Through Time-Space Sampling", Parsons et al 2009:

    The National Survey on Drug Use and Health9 and the Monitoring the Future Study10 both assessed the prevalence of club drug use among young people. Although neither of these national studies assessed a complete range of club drugs, these data indicated high rates of lifetime exposure to MDMA/ecstasy (12.4% to 14.9%), cocaine (12.6% to 14.3%), and LSD/acid (7.9% to 11.2%) among young adults

    Abraham et al 1996:

    ...Hallucinogenic drugs are commonly abused. Data from the 1990 NIDA Household Survey (National Institute on Drug Abuse 1990) suggests that 7.6% of the U.S. population over the age of 12 years used hallucinogens at some time in their lives. The survey showed that in the previous 12 months 1.1% reported hallucinogen use. Comparative figures for other drugs were: 10.2% marijuana...In 1993 a survey of 18,054 householders over the age of 12 found a higher life use of hallucinogens of 8.7% (Substance Abuse and Mental Health Services Administration 1994). The Household Survey gives figures for lifetime exposure to individual hallucinogens, with 5.5% reporting having tried LSD...Demographic data indicate that LSD use is most prevalent between the ages of 18 to 25, with 4.9% reporting use in the past year, compared to 2.1% for the age group 12 to 18...High school seniors, while showing an inverse correlation between LSD use and college plans, demonstrate a strong positive one between LSD use and parents' education (Johnston et al 1990)...Since 1985 there has been a steady increase in hallucinogen use, reaching a decade long peak of 11.4% in 1994 (Johnston et al 1994).

    • National Institute of Drug Abuse (1990): National Household Survey on Drug Abuse, Main Findings. Pub. No. 91-1788, Washington, DC, U.S. Department of Health and Human Services; Alcohol, Drug Abuse, and Mental Health Administration
    • Substance Abuse and Mental Health Administration (1994): National Household Survey on Drug Abuse: Population Estimates 1993, Pub. No. (SMA) 94-3017, Washington, DC: Government Printing Office
    • Johnston L, Bachman J, O'Malley 1990: Monitoring the future. Ann Arbor, University of Michigan Institute for Social Research
    • Johnston L, O'Malley I', Bachman J (1994): National Survey Results on Drug Use from Monitoring the Future Study, 1975-1993. NIH Pub. No. 94-3809, Bethesda, MD, National Institute on Drug Abuse
  11. ↑ 11.0 11.1 Turner & Tsuang 1990:

    Researchers have stressed the increased vulnerability of drug abusers to psychotic episodes. For instance, Hensala et al. (1967) investigated the role of LSD in triggering psychotic episodes and hospitalizations. They examined a broad spectrum of variables, including demographic characteristics, family history, and psychosocial adjustment as well as drug involvement. They concluded that in only 25 percent of the cases investigated was LSD directly related to the index hospitalization. In the remaining cases, poor premorbid adjustment, high-risk family history, and extensive substance abuse were associated with an increased risk for hospitalization.


    Similarly, Alterman et al. (1980, 1981, 1982) found that a substantial number of patients had a history of drug abuse, and over half of them had used drugs in the hospital. Alcohol abuse appeared to be more prevalent among hospitalized patients with a diagnosis of paranoid schizophrenia than among patients with other diagnoses. Hasin et al. (1985) examined rates of alcohol and drug abuse among a large sample (n = 835) of inpatient subjects with affective disorders. Using relatively conservative ratings, they found nearly 23 percent of the subjects to have serious alcohol dependence problems, and 9 percent to have serious drug problems during their current affective episode. Unfortunately, their data did not differentiate rates among schizophrenic patients. Substance abuse has also been noted as a problem among psychiatric patients within rehabilitation treatment settings. Straussman (1985) noted significant alcohol problems among members of a psychosocial club, over half (7 of 13) of whom had schizophrenia.

    Schneier and Siris (1987) provided a more recent review of drug abuse patterns among schizophrenic patients. They concluded that drug choices cited in 18 articles they reviewed were not random. Schizophrenic patients appeared to prefer stimulants and hallucinogens, and to use less alcohol and fewer sedative-hypnotics than did other psychiatric patients. The authors noted that the choice of stimulants is counter-intuitive since schizophrenic patients suffer from an agitated mental state. They speculated that if the schizophrenic patients were attempting to self-medicate their symptoms, hypnotics or sedatives would seem to have been more effective. The authors concluded that the potential benefits of stimulant use could be relief of negative symptoms, counteracting side effects of their neuroleptic medications, or both. They further speculated that the drugs of choice may be related to the subtype of schizophrenia or severity of symptoms, although no studies have directly addressed that possibility to date.

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