Introduction
Substance abuse and mental illness frequently occur together. The relationship between mental health and substance use is complex. Individuals may use substances both to self-medicate symptoms of mental illness and due to physiological impacts of substance use on brain chemistry. Improved understanding of this relationship could help enhance prevention and treatment efforts. This paper will review past research on the comorbidity of substance use disorders and other mental illnesses, investigate potential bidirectional relationships and causal pathways, and discuss implications for integrated treatment approaches.
Literature Review
Numerous epidemiological studies demonstrate high rates of comorbidity between substance use disorders and other psychiatric conditions (Kessler et al., 1996; Regier et al., 1990). One large national U.S. survey found that among individuals with a substance use disorder diagnosis in the past year, 47.0% also met criteria for at least one other DSM-III-R disorder (Kessler et al., 1996). Rates of comorbidity are even higher among clinical samples seeking substance abuse or mental health treatment (Flynn et al., 1996; Ross et al., 1988).
Different mental illnesses show varying levels of association with substance use. Mood and anxiety disorders commonly co-occur with alcohol and drug problems. Around one-third of individuals with major depressive disorder and over half of those with bipolar disorder also meet criteria for a substance use disorder at some point in their lives (Flynn et al., 1996; Merikangas et al., 1998; Regier et al., 1990). High rates of comorbidity are also seen between substance use disorders and post-traumatic stress disorder, generalized anxiety disorder, social anxiety disorder and panic disorder (Kessler et al., 1996; Kushner et al., 2000; Schneier et al., 1992).
Schizophrenia appears most strongly linked to nicotine, cannabis and alcohol use (Dixon, 1999; Ziedonis & Fisher, 1996). Nearly 50-70% of people with schizophrenia smoke cigarettes compared to 20-30% of the general population (De Leon & Diaz, 2005). Research suggests order of onset may impact the nature of relationship between schizophrenia and substance use. Secondary to emerging psychotic symptoms, individuals with schizophrenia are at elevated risk for substance abuse, possibly using drugs and alcohol to self-medicate negative symptoms or experiences of boredom (Dixon, 1999). At the same time, substances like cannabis may trigger or exacerbate psychotic episodes in vulnerable individuals (Henquet et al., 2005).
Bidirectional Relationships and Causal Pathways
The high rates of comorbidity observed between mental illnesses and substance use disorders beg the question: is one disorder causing the other, or are common underlying risk factors responsible for both conditions developing together? Support exists for bidirectional relationships as well as shared vulnerabilities that increase risk for dual diagnosis.
Self-Medication Model: The self-medication hypothesis proposes that individuals use psychoactive substances to alleviate symptoms, negative affective states or cognitive deficits associated with untreated mental illness (Khantzian, 1997). For example, alcohol may be used to reduce anxiety, depressants to relieve depression, stimulants to increase motivation or cope with attention deficit issues. Over time, substance use aimed at self-treatment can transition to abuse and dependence. This model is supported by findings that onset of psychiatric symptoms often precedes substance-related problems (Regier et al., 1990).
High-Risk Model: Genetic and environmental factors predisposing individuals to both substance use and mental illness account for their frequent co-occurrence (Merikangas & Gelernter, 1990; Swan et al., 1997). Shared vulnerabilities may include genes impacting impulsivity, reward processing or stress reactivity. Early life traumatic experiences, family history of substance abuse and parental psychopathology also increase risk for dual diagnosis (Breslau et al., 2006; Khoury et al., 2010). According to the high-risk model, the underlying liability is what leads to both conditions developing rather than one causing the other.
Self-Selection Model: Similar to shared vulnerabilities, this explanation considers mechanisms by which an individual’s pre-existing traits and personality draw them towards both substance use and at-risk lifestyles conducive to mental illness onset (Little & Clark, 2007). Impulsivity, sensation-seeking and tendency towards risky behaviors may “self-select” those at heightened probability for dual diagnosis.
Substance Effects on Brain Chemistry: Repeated use of addictive substances directly impacts circuitry and neurotransmitter balance involved in mood regulation and stress reactivity (Khantzian, 1997; Koob & Volkow, 2010). Altered dopamine, serotonin and cortisol signaling can cause or worsen symptoms of conditions like depression and anxiety, perpetuating a cycle of use to self-medicate emerging psychiatric dysfunction triggered by the physiological effects of substances.
Treatment Implications and Future Directions
Given complex bidirectional relationships, integrated treatment targeting substance abuse and mental illness together yields better outcomes than separate sequential or parallel approaches (Brunette et al., 2001; Watkins et al., 2001). Dual diagnosis programs teach coping skills for cravings, relapse prevention and psychiatric symptom management. Individualized treatment should consider order of onset and whether self-medication, high risk factors or substance-induced changes are driving comorbidity in each case. Coordinating pharmacological and psychosocial elements is also important since mental health medications may interact adversely with substances if not monitored closely during early recovery.
Future research should clarify specific genetic and environmental risk and protective factors conferring vulnerability or resilience to dual diagnosis. Longitudinal designs could provide insight into changing directionality of substance use and mental illness over the lifespan. Animal models hold promise for elucidating neurobiological mechanisms and potential new treatment targets based on brain regions and systems involved across disorders. Continued investigation into bidirectional relationships and how each condition uniquely or jointly impacts the other’s clinical course and prognosis will help optimize mental health and addiction services. With improved integration between substance abuse and psychiatric care settings, outcomes for dually diagnosed individuals have great potential for improvement.
Conclusion
Substance use disorders frequently co-occur with other mental illnesses at rates far exceeding chance. Both self-medication and high-risk models receive empirical support, suggesting underlying vulnerabilities may increase risk for dual diagnosis through multiple pathways. Direct physiological effects of substances on brain chemistry could also induce or exacerbate psychiatric symptoms over time. Integrated treatment targeting dual diagnosis concurrently yields the best prognosis. Further research unraveling genetic, neurobiological and environmental contributions to comorbidity can guide more targeted prevention and treatment innovations. Overall, improved understanding of relationships between mental health and addiction can enhance clinical care for dually diagnosed individuals.
Andrew Stroud