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Published Online: 6 May 2019

Prediction of Onset of Substance-Induced Psychotic Disorder and Its Progression to Schizophrenia in a Swedish National Sample

Abstract

Objective:

The objective of this study was to clarify the etiology of substance-induced psychotic disorder and its progression to schizophrenia in a Swedish national sample.

Methods:

Individuals with a registration of substance-induced psychotic disorder between 1997 and 2015 in national medical registries (N=7,606) were followed up for a mean of 84 months. Data from medical, criminal, and pharmacy registries on first-degree through third-degree relatives were used to calculate familial risk scores for nonaffective psychosis, drug abuse, and alcohol use disorder.

Results:

Individuals with substance-induced psychotic disorder had large elevations in standardized familial risk scores for drug abuse (+1.09, 95% CI=1.02, 1.15) and alcohol use disorder (+0.98, 95% CI=0.93, 1.03) and modest elevations for nonaffective psychosis (+0.35, 95% CI=0.30, 0.41). The cumulative risk for progression to schizophrenia was 11.3%; it was lowest for alcohol-induced and highest for cannabis-induced psychotic disorder, and it was predicted by early age at diagnosis of substance-induced psychotic disorder, male sex, and further registrations for episodes of drug abuse, alcohol use disorder, and substance-induced psychotic disorder. A risk prediction model found that 47% of individuals who converted to schizophrenia were in the upper 20% of risk. Familial risk scores for drug abuse and alcohol use disorder did not significantly discriminate those who converted to schizophrenia from those who did not, while familial risk score for nonaffective psychosis did (0.67, 95% CI=0.40, 0.95, versus 0.33, 95% CI=0.28, 0.39). Familial risk scores for nonaffective psychosis were indistinguishable between individuals with schizophrenia with and without prior substance-induced psychosis. Assignment of early retirement by the Swedish Social Insurance Agency strongly discriminated between individuals with substance-induced psychotic disorder with and without later schizophrenia.

Conclusions:

Substance-induced psychotic disorder appears to result from substantial drug exposure in individuals at high familial risk for substance abuse and moderately elevated familial risk for psychosis. Familial risk for psychosis, but not substance abuse, predicts progression from substance-induced psychosis to schizophrenia. Schizophrenia following substance-induced psychosis is likely a drug-precipitated disorder in highly vulnerable individuals, not a syndrome predominantly caused by drug exposure.

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Information & Authors

Information

Published In

Go to American Journal of Psychiatry
Go to American Journal of Psychiatry
American Journal of Psychiatry
Pages: 711 - 719
PubMed: 31055966

History

Received: 29 October 2018
Revision received: 26 January 2019
Accepted: 4 March 2019
Published online: 6 May 2019
Published in print: September 01, 2019

Keywords

  1. Schizophrenia
  2. Psychoses-Substance-Induced

Authors

Details

Kenneth S. Kendler, M.D. [email protected]
The Virginia Institute for Psychiatric and Behavioral Genetics and the Department of Psychiatry, Virginia Commonwealth University, Richmond (Kendler); the Center for Primary Health Care Research, Lund University, Malmö, Sweden (Ohlsson, J. Sundquist, K. Sundquist); the Department of Family Medicine and Community Health, Department of Population Health Science and Policy, Icahn School of Medicine at Mount Sinai, New York (J. Sundquist, K. Sundquist); the Center for Community-Based Health Care Research and Education, Department of Functional Pathology, School of Medicine, Shimane University, Japan (J. Sundquist, K. Sundquist).
Henrik Ohlsson, Ph.D.
The Virginia Institute for Psychiatric and Behavioral Genetics and the Department of Psychiatry, Virginia Commonwealth University, Richmond (Kendler); the Center for Primary Health Care Research, Lund University, Malmö, Sweden (Ohlsson, J. Sundquist, K. Sundquist); the Department of Family Medicine and Community Health, Department of Population Health Science and Policy, Icahn School of Medicine at Mount Sinai, New York (J. Sundquist, K. Sundquist); the Center for Community-Based Health Care Research and Education, Department of Functional Pathology, School of Medicine, Shimane University, Japan (J. Sundquist, K. Sundquist).
Jan Sundquist, M.D., Ph.D.
The Virginia Institute for Psychiatric and Behavioral Genetics and the Department of Psychiatry, Virginia Commonwealth University, Richmond (Kendler); the Center for Primary Health Care Research, Lund University, Malmö, Sweden (Ohlsson, J. Sundquist, K. Sundquist); the Department of Family Medicine and Community Health, Department of Population Health Science and Policy, Icahn School of Medicine at Mount Sinai, New York (J. Sundquist, K. Sundquist); the Center for Community-Based Health Care Research and Education, Department of Functional Pathology, School of Medicine, Shimane University, Japan (J. Sundquist, K. Sundquist).
Kristina Sundquist, M.D., Ph.D.
The Virginia Institute for Psychiatric and Behavioral Genetics and the Department of Psychiatry, Virginia Commonwealth University, Richmond (Kendler); the Center for Primary Health Care Research, Lund University, Malmö, Sweden (Ohlsson, J. Sundquist, K. Sundquist); the Department of Family Medicine and Community Health, Department of Population Health Science and Policy, Icahn School of Medicine at Mount Sinai, New York (J. Sundquist, K. Sundquist); the Center for Community-Based Health Care Research and Education, Department of Functional Pathology, School of Medicine, Shimane University, Japan (J. Sundquist, K. Sundquist).

Notes

Send correspondence to Dr. Kendler ([email protected]).

Competing Interests

The authors report no financial relationships with commercial interests.

Funding Information

National Institute on Alcohol Abuse and Alcoholism10.13039/100000027: R01AA023534
National Institute on Drug Abuse10.13039/100000026: R01DA030005
Supported by NIH grants R01-DA030005 and R01-AA023534, the National Institute on Alcohol Abuse and Alcoholism, the Swedish Research Council (K2012-70X-15428-08-3), the Swedish Research Council for Health, Working Life, and Welfare (Forte; reg. nr. 2013-1836), the Swedish Research Council (2012-2378, 2014-10134), and Forte 2014-0804, as well as Avtal om Läkarutbildning och Forskning (ALF) funding from Region Skåne.

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