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Aims To explore clinical features of methamphetamine-induced paranoia (MIP) and associations between MIP and a genetic polymorphism in dopamine β-hydroxylase (DBH −1021C→T). Design Retrospective analysis of clinical presentation and genetic association by chi-square test and logistic regression analysis. Setting A Thai substance abuse treatment center Participants 727 Methamphetamine-dependent (MD) individuals Measures Clinical: Semi-Structured Assessment for Drug Dependence and Alcoholism (SSADDA) and the Methamphetamine Experience Questionnaire (MEQ). Genetic: DBH −1021C→T. Findings Forty percent of individuals (289 of 727) with MD had MIP. Within-binge latency to MIP onset occurred more rapidly in the most recent compared with initial MIP episode (p=0.02), despite unchanging intake (p=0.89). Individuals with MIP were significantly less likely to carry lower (TT/CT) compared with higher (CC) activity genotypes (34% vs 43%; χ21=5, p=0.03). DBH effects were confirmed (OR=0.7, p=0.04) after controlling for associated clinical variables (MD severity, OR=3.4, p<0.001; antisocial personality disorder, OR=2.2, p<0.001; alcohol dependence, OR=1.4, p=0.05; and nicotine dependence, OR=1.4, p=0.06). TT/CT carriers were more likely to initiate cigarette smoking (OR=3.9, p=0.003) and probably less likely to be dependent on alcohol (OR=0.6, p=0.05). Conclusions Among methamphetamine-dependent individuals, paranoia appears to occur increasingly rapidly in the course of a session of methamphetamine use. Severity of methamphetamine dependence and antisocial personality disorder predicts methamphetamine-induced paranoia. The genetic polymorphism in dopamine β-hydroxylase is associated with methamphetamine-induced paranoia and influences smoking initiation.

Quetiapine may be used as an antipsychotic treatment for MAP with comparable therapeutic effects and adverse events to treatment with classical antipsychotic drugs.