4.3.5 - Interactionism and schizophrenia

Why interactionism matters

Most explanations and treatments of schizophrenia can sound as if they belong to separate camps. Biological explanations focus on genes, dopamine and neural correlates. Psychological explanations focus on family stress, cognitive processes, trauma and the meanings attached to symptoms. The interactionist approach says this split is too neat for a disorder as complex as schizophrenia.

For AQA, the key point is not simply "biology plus psychology". It is interaction. A person may have a genetic vulnerability and never develop schizophrenia. Another person may experience severe stress and never develop schizophrenia. The risk rises when vulnerability and stress occur together in a particular person at a particular time.

This matters for explaining schizophrenia because it avoids two weak single-factor claims:

It also matters for treating schizophrenia. If symptoms involve biological processes and psychological meanings, then treatment may need both antipsychotic medication and psychological therapies such as CBT or family intervention. Medication may reduce symptom intensity; therapy may help the person cope with voices, challenge distressing beliefs, reduce stress at home and plan for relapse.

A strong answer keeps all three assessment objectives visible:

The diathesis-stress model

The main interactionist explanation of schizophrenia is the diathesis-stress model.

Meehl's original model

Meehl (1962) proposed a single inherited "schizogene" producing an underlying neural vulnerability, termed schizotaxia. Development and social learning could lead to a schizotypic personality organisation; only some vulnerable people would then develop clinical schizophrenia under stress. In this historical account the genetic vulnerability was necessary, while stress helped determine the outcome. It is a proposed model, not an established fact about one gene or a reason to blame a particular parent.

That original version is useful historically, but it is too simple for modern Psychology. It treated the diathesis as one gene and treated the stressor mainly as psychological parenting stress.

Modern versions

Modern diathesis-stress accounts are broader.

Ripke and the Schizophrenia Working Group (2014) are useful for AO3 because they found 128 independent associations across 108 genetic loci in a very large genome-wide association study. That supports a polygenic view: schizophrenia is not explained by one "schizogene".

Psychological trauma can also be treated as part of the diathesis, not only as a later stressor. Early severe trauma may alter stress responses and make later stress harder to manage. Cannabis use is often used as an example of a biological stressor because frequent or early use is associated with increased risk of psychosis, especially in vulnerable people. However, most cannabis users do not develop schizophrenia, which is exactly why the interactionist idea matters.

Consider Alison, who has a family history of schizophrenia and experienced severe childhood adversity. Later she encounters a major stressful event. A modern account might treat genetic liability and stress-system changes as vulnerabilities and the recent event as a trigger. The distinction depends partly on timing and mechanism: trauma can contribute to longer-term vulnerability as well as be an immediate stressor. Listing two risks is not yet an interaction explanation; the next step is to explain why one may change sensitivity to the other. These details do not allow prediction of Alison's individual diagnosis.

Evidence for interaction

The best AQA evidence for the diathesis-stress model shows that vulnerability and environment interact. The classic study is Tienari et al.'s Finnish adoption research.

Tienari et al. (2004) used a Finnish adoption design. This is valuable because adopted children are raised away from their biological parents, helping researchers separate genetic risk from rearing environment. The study compared adoptees whose biological mothers had schizophrenia-spectrum disorders with adoptees whose biological mothers did not have this genetic risk. Adoptive families were observed and rated using the OPAS family rating scale, and adoptees were followed up over many years.

The key sample for the 2004 paper was 303 adoptees with adoptive-family ratings: 145 at high genetic risk and 158 at low genetic risk. The researchers found that adverse adoptive-family patterns predicted schizophrenia-spectrum outcomes in the high-genetic-risk group, but not in the low-genetic-risk group. Healthy adoptive families also appeared protective for high-risk adoptees.

This supports the diathesis-stress model because neither factor worked well as a complete explanation on its own:

There is also evidence for more complex stressors. Houston et al. (2008) analysed National Comorbidity Survey data and found a statistically significant interaction between childhood sexual trauma and cannabis use under 16 in predicting psychosis diagnosis. The retrospective survey concerned psychosis diagnoses, not schizophrenia alone. Recall error, small subgroups and unmeasured confounding limit causal inference; the finding suggests interacting risks but does not prove that cannabis or trauma caused an individual diagnosis.