Chapter 14 - Implications of research on comorbidity for the nature and management of substance misuse

Abstract

This chapter provides a critical evaluation of different models concerning the etiology of the high rate of substance use disorders (SUD) in patients with severe mental illnesses (SMI). Common factor models posit that high rates of comorbidity are the result of shared vulnerabilities to both disorders. Research shows that clients with comorbid disorders are more likely to have relatives with SUD than are similar patients with only SMI. It is suggested that genetic risk for dual disorders may be enacted through gene–environment interactions, whereby substance misuse acts as an environmental stressor on the developing brain. A variety of different models posit that SMI increases clients' vulnerability to developing SUD. These models can be broadly divided into three types, which include psychosocial risk factor models, the supersensitivity model, and the brain reward circuitry dysfunction model. Alleviation of dysphoria represents a more general model than self-medication that proposes people with SMI are prone to misuse substances in response to distress. Models proposing that psychotomimetic drug misuse can lead to long-term psychotic disorders typically build on the catecholamine hypothesis of schizophrenia or affective disorders, and are supported by basic animal research on drug effects. It is suggested that further significant advances in the basic science of addiction in people with SMI may be required before substantial leaps in effectiveness of interventions can be achieved.