Interactionist Explanations (AQA A-Level Psychology): Revision Notes
Interactionist Explanations
The interactionist approach represents a comprehensive way of understanding schizophrenia by considering how multiple factors work together rather than focusing on single causes. This approach acknowledges that schizophrenia develops through various interacting elements, viewing combinations of different therapies as the most effective form of treatment.
The diathesis-stress model
The diathesis-stress model forms the foundation of interactionist explanations. This model suggests that individuals possess varying genetic potentials for schizophrenia that combine with environmental stressors to determine their actual vulnerability to developing the disorder.
Under this model, schizophrenia emerges when environmental stressors trigger a worsening of symptoms in someone with an underlying biological predisposition (vulnerability). The biological component involves genetic factors that appear to increase susceptibility to the disorder, particularly through their effects on dopaminergic systems and other neurotransmitter functioning.
Importantly, genetic factors alone do not directly cause schizophrenia. Instead, they increase the likelihood that environmental stressors will trigger a schizophrenic episode. Research suggests that neural abnormalities associated with schizophrenia result from the disorder itself rather than genetic influences alone.
Psychological triggers for schizophrenia can include family dysfunction, substance abuse, critical life events, and other stressors. Those with the highest genetic risk for developing the disorder show the greatest vulnerability to such triggers. Additionally, cognitive deficits and dysfunctional thought processing are viewed as consequences of schizophrenia rather than direct causes or triggers.
Research evidence
Several studies provide support for the interactionist explanation of schizophrenia:
Research Example: Walker (1997) - Cortisol and Schizophrenia
Walker discovered that patients with schizophrenia exhibit higher cortisol levels compared to people without the condition. These elevated cortisol levels correlate with the severity of symptoms, and stress-related increases in cortisol heighten genetic-influenced abnormalities in dopamine transmission that contribute to schizophrenia vulnerability. This finding demonstrates the interaction between biological and environmental factors in line with the diathesis-stress model.
Research Example: Murray (1996) - Prenatal Flu Exposure
Murray examined children born after flu epidemics where their mothers had contracted the illness whilst pregnant, particularly during the second trimester (pregnancy months 4-6). These children showed an 88% increased chance of developing schizophrenia compared to children born during the same period whose mothers had not contracted flu. Exposure to flu during the second trimester is thought to cause neural development defects, leading to increased schizophrenia vulnerability due to brain damage with knock-on effects on dopamine functioning.
Research Example: Cannon et al. (2002) - Birth Complications
Cannon et al. reviewed available evidence and found a positive correlation between birth complications and later vulnerability to developing schizophrenia. Some evidence indicated damage to hormone and neurotransmitter systems, as well as the immune system. This research supports an interactionist explanation where biological vulnerabilities interact with later stressors to trigger the disorder.
Research Example: Barlow & Durand (2009) - Family History and Environment
Barlow & Durand reported that a family history of schizophrenia (indicating a genetic link), combined with being part of a dysfunctional stressor, elevated the risk of developing schizophrenia. This supports the diathesis-stress model, with the diathesis being the genetic tendency and the stress being the dysfunctional family environment.
Evaluation
Strengths
Research Validation Walker's (1997) research shows that cortisol levels are higher immediately before schizophrenia onset rather than during recovery, suggesting elevated cortisol levels trigger schizophrenia rather than being a consequence of it.
The differential susceptibility hypothesis extends the diathesis-stress model to include positive as well as negative environments - an individual with biological vulnerability combined with a stressor leads to schizophrenia, but the same individual in a positive environment (such as a loving family background) could have better outcomes that reduce their chances of becoming schizophrenic.
Genes Cannot Act Alone Genes cannot determine outcomes independently - they require particular environments to express themselves, so genes that predispose someone to increased schizophrenia vulnerability cannot cause the disorder alone but need particular stressors to trigger the genetic potential.
Limitations
Complex Interactions Stressors that may contribute to schizophrenia risk include biological, environmental, psychological and social factors, but it is not known precisely how these risks contribute to the diathesis-stress interaction for any individual, as specific causes may differ between people.
The complexity of multiple interacting factors makes it difficult to establish clear causal relationships or predict individual outcomes.
Interactionist treatments
Researchers evaluate the relative effectiveness of different schizophrenia treatments by comparing approaches. Although treatment effectiveness depends on factors such as cost, relapse rates, degree of side effects, and symptom reduction, research indicates that combination treatments (where multiple treatments are administered simultaneously) prove generally most effective.
The most suitable combination of treatments varies according to each patient's individual circumstances and needs. For example, family therapy particularly suits people with schizophrenia who experience problems with dysfunctional family relationships and require significant contact and interaction with their families.
Treatment Sequencing Generally, treatment with antipsychotics is administered first to reduce symptoms, allowing psychological treatments to have greater effect. However, antipsychotics are typically continued whilst these treatments are administered.
Research on treatment effectiveness
Research Example: Hogarty et al. (1986) - Treatment Combination Effectiveness
Hogarty et al. assessed relapse rates in 103 patients with schizophrenia from high expressed emotion families receiving various treatments. They found first-year relapse rates of:
- 19% for family therapy plus drugs
- 20% for social support therapy plus drugs
- 41% for drug treatment alone
- 0% for family therapy plus social support and drug therapies
This supports the idea of combining treatments to increase effectiveness. However, a follow-up study suggested the combined treatment only delayed relapse rather than prevented it.
Key Points to Remember:
- The interactionist approach views schizophrenia as resulting from a combination of biological, psychological and social factors working together
- The diathesis-stress model explains how genetic vulnerability combines with environmental triggers to cause schizophrenia episodes
- Research evidence from Walker, Murray, Cannon, and Barlow & Durand supports the interaction between biological predisposition and environmental stressors
- Combination treatments that address multiple factors simultaneously show greater effectiveness than single approaches
- Genes create vulnerability but require environmental stressors to trigger schizophrenia- they cannot cause the disorder independently