Conclusions
Our findings add to the growing literature on cannabis as a risk factor for schizophrenia and, in addition, suggest that methamphetamine use sufficient to warrant a hospital diagnosis may also be a risk factor. We do have some skepticism about the suggestion in our data that the risk of subsequent development of schizophrenia is elevated in all of the major drug-of-abuse groups. This finding, which requires replication, was unanticipated, in large part because of the apparent absence in the literature of largescale longitudinal studies (except those examining cannabis
users) sufficiently powered to have addressed this issue (27). In the context of the stress-vulnerability (7) and dopamine sensitization (34) hypotheses of schizophrenia,
it could in fact be argued that the propensity for development of a persistent psychosis could be elevated after significant use of any drug of abuse, given that all such drugs
are “stressors” and that most act on the dopamine system. It has also been proposed, for example, that drugs of abuse(e.g., alcohol) might cause brain structural abnormalities
that could increase the risk of schizophrenia in genetically susceptible individuals (35). The relationship between methamphetamine use and schizophrenia could involve
a common etiology, shared genetic and environmental(e.g., low socioeconomic status) vulnerability factors (36),or a premorbid state (e.g., depression, anxiety, and poor
cognitive functioning) prompting substance use (as an attempt at self-medication) and pathological drug-induced sensitization (34), in which repeated exposure to a dopaminergic stimulant induces a hyperdopaminergic state sufficient to induce psychosis in vulnerable individuals.
Conclusions
Our findings add to the growing literature on cannabis as a risk factor for schizophrenia and, in addition, suggest that methamphetamine use sufficient to warrant a hospital diagnosis may also be a risk factor. We do have some skepticism about the suggestion in our data that the risk of subsequent development of schizophrenia is elevated in all of the major drug-of-abuse groups. This finding, which requires replication, was unanticipated, in large part because of the apparent absence in the literature of largescale longitudinal studies (except those examining cannabis
users) sufficiently powered to have addressed this issue (27). In the context of the stress-vulnerability (7) and dopamine sensitization (34) hypotheses of schizophrenia,
it could in fact be argued that the propensity for development of a persistent psychosis could be elevated after significant use of any drug of abuse, given that all such drugs
are “stressors” and that most act on the dopamine system. It has also been proposed, for example, that drugs of abuse(e.g., alcohol) might cause brain structural abnormalities
that could increase the risk of schizophrenia in genetically susceptible individuals (35). The relationship between methamphetamine use and schizophrenia could involve
a common etiology, shared genetic and environmental(e.g., low socioeconomic status) vulnerability factors (36),or a premorbid state (e.g., depression, anxiety, and poor
cognitive functioning) prompting substance use (as an attempt at self-medication) and pathological drug-induced sensitization (34), in which repeated exposure to a dopaminergic stimulant induces a hyperdopaminergic state sufficient to induce psychosis in vulnerable individuals.
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