Prospective cohort study of cannabis use, predisposition for psychosis
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《英国医生杂志》
1 Department of Psychiatry and Neuropsychology, South Limburg Mental Health Research and Teaching Network, EURON, Maastricht University, PO BOX 616, 6200 MD Maastricht, Netherlands, 2 Max Planck Institute of Psychiatry, Clinical Psychology and Epidemiology Unit, Kraepelinstrasse 2, D-80804 Munich, Germany, 3 Institute of Clinical Psychology and Psychotherapy, Technical University ofDresden, Chemnitzerstrasse 48, D-01187 Dresden, Germany
Correspondence to: J van Os j.vanos@sp.unimaas.nl
Abstract
There is accumulating and converging evidence that cannabis use may be a risk factor for psychotic symptoms.1 2 The possible causal nature of the association between cannabis and psychosis, however, is still a matter of debate, the main discussion revolving around the role of predisposition for psychosis and adjustment for confounders.3 4 According to the self medication hypothesis,5 individuals may start using cannabis because of predisposition for psychosis, rather than cannabis use causing expression of psychosis. To our knowledge, no prospective study to date has tested this hypothesis using information on predisposition for psychosis in relation to later cannabis use. Recent research, however, has suggested that rather than being the cause of cannabis use, such predisposition interacts synergistically with cannabis use. Two studies suggested that the joint effect of cannabis use and predisposition for psychosis on the emergence of psychotic symptoms was greater than the sum of their individual effects.2 6
We investigated prospectively whether cannabis use at baseline increases the risk of subsequent development of psychotic symptoms, whether any such increase in risk is higher in individuals with a predisposition for psychosis, and whether baseline expression predisposition increases the risk for subsequent use of cannabis. We adjusted for possible confounding factors in a large population-based sample of adolescents and young adults.
Methods
We followed up 2437 participants, of which 1251 (51.3%) were men. The mean age was 18.3 years (SD 3.3 years) at baseline and 21.8 years (3.4 years) at follow up. At four year follow up the cumulative lifetime incidence of at least one psychotic symptom was 424 (17.4%), irrespective of severity and impairment probe criteria, and 174 (7.1%) participants reported two or more psychotic symptoms. At baseline 320 (13.1%) admitted to any use of cannabis (five times or more) and 361 (14.8 %) did so at follow up.
Any cannabis use at baseline increased the risk of psychotic symptoms according to the M-CIDI at follow up four years later in a dose-response fashion (tables 1, 2, 3), regardless of confounders, and with larger effect sizes for the narrowly defined psychosis outcome.
Table 1 Patterns of cannabis use at baseline and psychotic symptoms at follow up. Figures are numbers (percentages) of participants
Table 2 Associations between any cannabis use at baseline and psychotic symptoms at follow up. Figures are odds ratios (95% confidence intervals)
Table 3 Associations between frequency of cannabis use at baseline and any psychotic symptoms. Figures are odds ratios (95% confidence intervals)
The effect of baseline cannabis use on the psychosis outcome according to the M-CIDI at follow up four years later was much stronger in those with predisposition for psychosis at baseline (23.8% adjusted difference in risk) than in those without (5.6% adjusted difference in risk, table 4). The population attributable fraction was 6.2% for the total group and more than twice as large (14.2%) for the group with predisposition for psychosis at baseline.
Table 4 Interactions between any cannabis use and predisposition for psychosis
Predisposition for psychosis at baseline did not significantly predict cannabis use at follow up four years later (odds ratio 1.42, 95% confidence interval 0.94 to 2.15, for the whole sample and 1.42, 0.88 to 2.31, for the subgroup with no cannabis use at baseline).
Based on 1000 imputation sequences in which we stochastically imputed missing values of cannabis use at baseline and psychotic symptoms according to the M-CIDI at four year follow up in the whole sample, the estimated average additive interaction between predisposition for psychosis at baseline and cannabis use at baseline remained significant (19.5% difference in risk, 95% confidence interval 0.3 to 38.6, P = 0.039).
Discussion
Andreasson S, Allebeck P, Engstrom A, Rydberg U. Cannabis and schizophrenia. A longitudinal study of Swedish conscripts. Lancet 1987;ii: 1483-6.
van Os J, Bak M, Hanssen M, Bijl RV, de Graaf R, Verdoux H. Cannabis use and psychosis: a longitudinal population-based study. Am J Epidemiol 2002;156: 319-27.
Degenhardt L, Hall W. The association between psychosis and problematical drug use among Australian adults: findings from the national survey of mental health and well-being. Psychol Med 2001;31: 659-68.
Macleod J, Oakes R, Copello A, Crome I, Egger M, Hickman M, et al. Psychological and social sequelae of cannabis and other illicit drug use by young people: a systematic review of longitudinal, general population studies. Lancet 2004;363: 1579-88.
Khantzian EJ. The self-medication hypothesis of addictive disorders: focus on heroin and cocaine dependence. Am J Psychiatry 1985;142: 1259-64.
Verdoux H, Gindre C, Sorbara F, Tournier M, Swendsen JD. Effects of cannabis and psychosis vulnerability in daily life: an experience sampling test study. Psychol Med 2003;33: 23-32.
Lieb R, Isensee B, von Sydow K, Wittchen HU. The early developmental stages of psychopathology study (EDSP): a methodological update. Eur Addict Res 2000;6: 170-82.
Poulton R, Caspi A, Moffitt TE, Cannon M, Murray R, Harrington H. Children's self-reported psychotic symptoms and adult schizophreniform disorder: a 15-year longitudinal study. Arch Gen Psychiatry 2000;57: 1053-8.
Breslow NE, Day NE. Statistical methods in cancer research. Vol 2. The design and analysis of cohort studies. New York: Oxford University Press, 1994.
Wittchen HU, Lachner G, Wunderlich U, Pfister H. Test-retest reliability of the computerized DSM-IV version of the Munich-Composite International Diagnostic Interview (M-CIDI). Soc Psychiatry Psychiatr Epidemiol 1998;33: 568-78.
Derogatis JR. SCL-90-R: administration, scoring, and procedures manual—II. Towson: Clinical Psychometric Research, 1983.
Sharpley MS, Hutchinson G, Murray RM, McKenzie K. Understanding the excess of psychosis among the African-Caribbean population in England: review of current hypotheses. Br J Psychiatry 2001;178(suppl 40): S60-8.
Read J, Ross CA. Psychological trauma and psychosis: another reason why people diagnosed schizophrenic must be offered psychological therapies. J Am Acad Psychoanal Dyn Psychiatry 2003;31: 247-68.
Darroch J. Biologic synergism and parallelism. Am J Epidemiol 1997;145: 661-8.
Van Os J, Hanssen M, Bak M, Bijl RV, Vollebergh W. Do urbanicity and familial liability coparticipate in causing psychosis? Am J Psychiatry 2003;160: 477-82.
Johns LC, van Os J. The continuity of psychotic experiences in the general population. Clin Psychol Rev 2001;21: 1125-41.
Kendler KS, Thacker L, Walsh D. Self-report measures of schizotypy as indices of familial vulnerability to schizophrenia. Schizophr Bull 1996;22: 511-20.
Verdoux H, Sorbara F, Gindre C, Swendsen JD, van Os J. Cannabis use and dimensions of psychosis in a nonclinical population of female subjects. Schizophr Res 2003;59: 77-84.
Chen J, Paredes W, Lowinson JH, Gardner EL. Delta 9-tetrahydrocannabinol enhances presynaptic dopamine efflux in medial prefrontal cortex. Eur J Pharmacol 1990;190: 259-62.
Dean B, Sundram S, Bradbury R, Scarr E, Copolov D. Studies on CP-55940 binding in the human central nervous system: regional specific changes in density of cannabinoid-1 receptors associated with schizophrenia and cannabis use. Neuroscience 2001;103: 9-15.
Leweke FM, Giuffrida A, Wurster U, Emrich HM, Piomelli D. Elevated endogenous cannabinoids in schizophrenia. Neuroreport 1999;10: 1665-9.
Schneider M, Koch M. Chronic pubertal, but not adult chronic cannabinoid treatment impairs sensorimotor gating, recognition memory, and the performance in a progressive ratio task in adult rats. Neuropsychopharmacology 2003;28: 1760-9.(Cécile Henquet, research psychologist1, )
Correspondence to: J van Os j.vanos@sp.unimaas.nl
Abstract
There is accumulating and converging evidence that cannabis use may be a risk factor for psychotic symptoms.1 2 The possible causal nature of the association between cannabis and psychosis, however, is still a matter of debate, the main discussion revolving around the role of predisposition for psychosis and adjustment for confounders.3 4 According to the self medication hypothesis,5 individuals may start using cannabis because of predisposition for psychosis, rather than cannabis use causing expression of psychosis. To our knowledge, no prospective study to date has tested this hypothesis using information on predisposition for psychosis in relation to later cannabis use. Recent research, however, has suggested that rather than being the cause of cannabis use, such predisposition interacts synergistically with cannabis use. Two studies suggested that the joint effect of cannabis use and predisposition for psychosis on the emergence of psychotic symptoms was greater than the sum of their individual effects.2 6
We investigated prospectively whether cannabis use at baseline increases the risk of subsequent development of psychotic symptoms, whether any such increase in risk is higher in individuals with a predisposition for psychosis, and whether baseline expression predisposition increases the risk for subsequent use of cannabis. We adjusted for possible confounding factors in a large population-based sample of adolescents and young adults.
Methods
We followed up 2437 participants, of which 1251 (51.3%) were men. The mean age was 18.3 years (SD 3.3 years) at baseline and 21.8 years (3.4 years) at follow up. At four year follow up the cumulative lifetime incidence of at least one psychotic symptom was 424 (17.4%), irrespective of severity and impairment probe criteria, and 174 (7.1%) participants reported two or more psychotic symptoms. At baseline 320 (13.1%) admitted to any use of cannabis (five times or more) and 361 (14.8 %) did so at follow up.
Any cannabis use at baseline increased the risk of psychotic symptoms according to the M-CIDI at follow up four years later in a dose-response fashion (tables 1, 2, 3), regardless of confounders, and with larger effect sizes for the narrowly defined psychosis outcome.
Table 1 Patterns of cannabis use at baseline and psychotic symptoms at follow up. Figures are numbers (percentages) of participants
Table 2 Associations between any cannabis use at baseline and psychotic symptoms at follow up. Figures are odds ratios (95% confidence intervals)
Table 3 Associations between frequency of cannabis use at baseline and any psychotic symptoms. Figures are odds ratios (95% confidence intervals)
The effect of baseline cannabis use on the psychosis outcome according to the M-CIDI at follow up four years later was much stronger in those with predisposition for psychosis at baseline (23.8% adjusted difference in risk) than in those without (5.6% adjusted difference in risk, table 4). The population attributable fraction was 6.2% for the total group and more than twice as large (14.2%) for the group with predisposition for psychosis at baseline.
Table 4 Interactions between any cannabis use and predisposition for psychosis
Predisposition for psychosis at baseline did not significantly predict cannabis use at follow up four years later (odds ratio 1.42, 95% confidence interval 0.94 to 2.15, for the whole sample and 1.42, 0.88 to 2.31, for the subgroup with no cannabis use at baseline).
Based on 1000 imputation sequences in which we stochastically imputed missing values of cannabis use at baseline and psychotic symptoms according to the M-CIDI at four year follow up in the whole sample, the estimated average additive interaction between predisposition for psychosis at baseline and cannabis use at baseline remained significant (19.5% difference in risk, 95% confidence interval 0.3 to 38.6, P = 0.039).
Discussion
Andreasson S, Allebeck P, Engstrom A, Rydberg U. Cannabis and schizophrenia. A longitudinal study of Swedish conscripts. Lancet 1987;ii: 1483-6.
van Os J, Bak M, Hanssen M, Bijl RV, de Graaf R, Verdoux H. Cannabis use and psychosis: a longitudinal population-based study. Am J Epidemiol 2002;156: 319-27.
Degenhardt L, Hall W. The association between psychosis and problematical drug use among Australian adults: findings from the national survey of mental health and well-being. Psychol Med 2001;31: 659-68.
Macleod J, Oakes R, Copello A, Crome I, Egger M, Hickman M, et al. Psychological and social sequelae of cannabis and other illicit drug use by young people: a systematic review of longitudinal, general population studies. Lancet 2004;363: 1579-88.
Khantzian EJ. The self-medication hypothesis of addictive disorders: focus on heroin and cocaine dependence. Am J Psychiatry 1985;142: 1259-64.
Verdoux H, Gindre C, Sorbara F, Tournier M, Swendsen JD. Effects of cannabis and psychosis vulnerability in daily life: an experience sampling test study. Psychol Med 2003;33: 23-32.
Lieb R, Isensee B, von Sydow K, Wittchen HU. The early developmental stages of psychopathology study (EDSP): a methodological update. Eur Addict Res 2000;6: 170-82.
Poulton R, Caspi A, Moffitt TE, Cannon M, Murray R, Harrington H. Children's self-reported psychotic symptoms and adult schizophreniform disorder: a 15-year longitudinal study. Arch Gen Psychiatry 2000;57: 1053-8.
Breslow NE, Day NE. Statistical methods in cancer research. Vol 2. The design and analysis of cohort studies. New York: Oxford University Press, 1994.
Wittchen HU, Lachner G, Wunderlich U, Pfister H. Test-retest reliability of the computerized DSM-IV version of the Munich-Composite International Diagnostic Interview (M-CIDI). Soc Psychiatry Psychiatr Epidemiol 1998;33: 568-78.
Derogatis JR. SCL-90-R: administration, scoring, and procedures manual—II. Towson: Clinical Psychometric Research, 1983.
Sharpley MS, Hutchinson G, Murray RM, McKenzie K. Understanding the excess of psychosis among the African-Caribbean population in England: review of current hypotheses. Br J Psychiatry 2001;178(suppl 40): S60-8.
Read J, Ross CA. Psychological trauma and psychosis: another reason why people diagnosed schizophrenic must be offered psychological therapies. J Am Acad Psychoanal Dyn Psychiatry 2003;31: 247-68.
Darroch J. Biologic synergism and parallelism. Am J Epidemiol 1997;145: 661-8.
Van Os J, Hanssen M, Bak M, Bijl RV, Vollebergh W. Do urbanicity and familial liability coparticipate in causing psychosis? Am J Psychiatry 2003;160: 477-82.
Johns LC, van Os J. The continuity of psychotic experiences in the general population. Clin Psychol Rev 2001;21: 1125-41.
Kendler KS, Thacker L, Walsh D. Self-report measures of schizotypy as indices of familial vulnerability to schizophrenia. Schizophr Bull 1996;22: 511-20.
Verdoux H, Sorbara F, Gindre C, Swendsen JD, van Os J. Cannabis use and dimensions of psychosis in a nonclinical population of female subjects. Schizophr Res 2003;59: 77-84.
Chen J, Paredes W, Lowinson JH, Gardner EL. Delta 9-tetrahydrocannabinol enhances presynaptic dopamine efflux in medial prefrontal cortex. Eur J Pharmacol 1990;190: 259-62.
Dean B, Sundram S, Bradbury R, Scarr E, Copolov D. Studies on CP-55940 binding in the human central nervous system: regional specific changes in density of cannabinoid-1 receptors associated with schizophrenia and cannabis use. Neuroscience 2001;103: 9-15.
Leweke FM, Giuffrida A, Wurster U, Emrich HM, Piomelli D. Elevated endogenous cannabinoids in schizophrenia. Neuroreport 1999;10: 1665-9.
Schneider M, Koch M. Chronic pubertal, but not adult chronic cannabinoid treatment impairs sensorimotor gating, recognition memory, and the performance in a progressive ratio task in adult rats. Neuropsychopharmacology 2003;28: 1760-9.(Cécile Henquet, research psychologist1, )