Interactionist Approach in Explanation and Treatment

• Evidence to support role of genetic vulnerability and stress in the development of schizophrenia (original D-S model). Tienari et al (2014) found children who knew an environment with high levels of criticism and low levels of empathy were more likely to develop Scz, but only if there was a high genetic risk of Scz. This shows that a genetic vulnerability which is then triggered leads to Scz, supporting the idea of an interaction between genetics and environmental factors. This could be used to help make a treatment that tackles both genetic and environmental factors of Scz.  
• There is evidence to support the role of genetic vulnerability and stress in the development of schizophrenia (updated D-S model). Houston et al (2008) found that childhood sexual trauma emerged as a vulnerability factor whilst cannabis use was a trigger. This shows that vulnerability does not just have to be biological, supporting the updated model.  
• We do not fully understand how the combination of a vulnerability and stress can lead to schizophrenia. There is evidence to suggest that there is a link between the two but there is no explanation of how the symptoms of schizophrenia are produced. This reduces the validity of the interactionist approach as the model is purely descriptive and not explanatory. This means that we cannot develop effective treatments if we do not know why symptoms occur.  
• The interactionist explanation of schizophrenia is a more holistic explanation. It considers both biological and psychological factors such as genetics, trauma, and smoking habits that can be implicated in the development of schizophrenia. This shows this explanation takes a more holistic approach as it does not disregard possible causes, meaning it is a more effective explanation.  
• There is support from studies using combos of treatments of Scz. Tarrier et al (2004) randomly allocated 315 patients to a meds and CBT group, meds and support counselling, or a control (meds only). Patients in the 2 combon groups showed less symptoms than those in the meds only group. This supports the int. approach as it provides evidence that combined treatment options are more effective than individual. This means patients have a better Q of life when multiple treatments are provided. However, this is more expensive for the NHS so may put strain on the economy.  
• Interactionist treatments for schizophrenia may have flawed logic. Turkington et al (2004) argue just because there's a good logical fit between the int. approach and combo treatments doesn't mean the int. approach is correct. Although combined treatments are more effective, this doesn’t support the interactionist approach as the treatments do not necessarily dictate the causes. It does not explain the origins of schizophrenia as combined treatments simply cover all bases. As it does not explain the disorder, this may lead to patient confusion or even mistrust in the NHS.  
• Although there is evidence to support interactionist treatments of schizophrenia, they are not cost effective. For example, giving a sufferer biological and psychological treatment is much more costly than giving them antipsychotic drugs alone and Tarrier et al found that although combination therapies reduced symptom levels in sufferers, it did not reduce their readmission to hospital. This may mean that money and resources are wasted on combined treatments when, despite less symptoms, it does not prevent hospital readmission so there is pressure on the NHS anyway.