1. 8. The interactionist approach to Schizophrenia

2. Answer the following….
1. What is the diathesis-stress model of schizophrenia?
2. What is Meehl’s traditional diathesis-stress model exactly?
3. What is the more modern understanding of diathesis-stress?
4. Explain how Tienari’s study supports the diathesis-stress model.
5. What exactly are the treatment applications of the diathesis-stress model?

3. Explaining the interactionist approach: the diathesis-stress model
This approach acknowledges that there are biological, psychological and societal factors in the development of schizophrenia.
Diathesis means vulnerability. In this context stress means a negative psychological experience. The diathesis stress model suggests that both a vulnerability to sz and a stress trigger are necessary in order to develop the condition. One or more underlying factors make a person particularly vulnerable to developing sz but the onset of the condition is triggered by stress.

4. Meehl’s model
In the original diathesis stress model (Meehl 1962) diathesis (vulnerability) was entirely genetic, the result of a singe schizogene. This led to the development of a biologically based schizotypic personality, characterised by sensitivity to stress.
According to Meehl however if a person does not have the gene then no amount of stress would lead to schizophrenia.
However, in carriers of the gene, chronic stress and the presence in particular of a schizophrenogenic mother could result in the development of the condition.

5. How our understanding of diathesis-stress has changed.
Many genes each appear to increase genetic vulnerability slightly, there is no single gene (Ripke).
Diathesis may include factors beyond the genetic. Psychological trauma could be diathesis rather than stressor. Read et al. proposed a neurodevelopmental model in which early trauma alters the developing brain. Such trauma and abuse can seriously affect many aspects of brain development, for example the hypothalamic pituitary adrenal system may become overactive making the person more vulnerable to stress.
Stress in the traditional model was seen as psychological in nature, related to parenting. A more modern definition includes anything that risks triggering sz. Recent research has concerned cannabis use . Cannabis is a stressor because it increases the risk of sz by up to seven times according to dose. This may be because cannabis interferes with the dopamine system. However most people do not develop sz after smoking cannabis obviously.
Urban environments, poverty and discrimination are also potential stressors. Vassos et al. (2012) the risk for sz in the most urban environments was estimated to be 2.37 times higher that in the most rural environments. Adverse living conditions in densely populated areas may be contributory factor.

6. Tienari et al.
Children adopted from Finnish mothers with schizophrenia between and 1979 were followed up. Their adoptive parents were assessed for childrearing style and the rates of schizophrenia were compared to those in a control group of adoptees without any genetic risk. A child-rearing style characterised by high levels of criticism and conflict and low levels of empathy was implicated in the development of schizophrenia but only for the children with high generic risk but not in the control group. This suggests that both genetic vulnerability and family related stress are important in the development of schizophrenia – genetically vulnerable children are more sensitive to parenting behaviour.
This is strong support for the importance of adopting an interactionist approach to schizophrenia, including hanging on the to the idea that poor parenting is a possible source of stress.
Problems with this study? Could the family problems be caused by a child who already demonstrates symptoms of the disorder?

7. Problems (some already mentioned) with traditional diathesis-stress model
Classic model of a single schizogene and schizophrenic parenting style as major stressor is now known to be over simple.
Multiple genes increase risk of schizophrenia, each having a small effect on its own, there is no single schizogene.
Also stress can come in many forms, including but not limited to dysfunctional parenting.
Vulnerability and stress do not have one single source.
Vulnerability (diathesis) can be the result of early trauma as well as genetic make up and stress can come in many forms. Houston et al. (2008) childhood sexual trauma emerged as a vulnerability factor whilst cannabis use was a trigger. The old idea of diathesis as biological and stress as psychological is over simple.
However, does cannabis CAUSE schizophrenia?

8. Treatment according to the interactionist model
The model is associated with combining antipsychotic medication and psychological therapies – most commonly CBT.
Turkington et al. (2006) it is perfectly possible to believe in biological causes of sz but still practise CBT to relieve psychological symptoms. However, this requires adopting an interactionist model; it is not possible to adopt a purely biological approach and tell patients that their condition is purely biological and that there is no psychological significance to symptoms yet to simultaneously treat them with CBT.
In Britain – standard practice to treat patients with a combination of antipsychotic drugs and CBT. In the USA though there is more of a conflict between psychological and biological models of sz and this may have led to slower adoption of an interactionist approach. Thus medication without an accompanying psychological treatment is more common than in the UK.
It is extremely unusual however to treat sz using psychological therapies alone.

9. Support for interactionist treatments
There is support for the usefulness of adopting an interactionist approach from studies comparing the effectiveness of combinations of biological and psychological treatments for schizophrenia versus biological treatments alone.
Studies show an advantage to using combinations of treatments for sz.
Tarrier et al. 315 patients were randomly allocated to a medication and CBT group, mediation and supported counselling or a control group. Patients in the two combination groups showed lower symptom levels than those in the control group (medication only), although there was no difference in hospital readmission rates.
Studies such as this then suggest there is a clear practical advantage to adopting an interactionist approach in the form of superior treatment outcomes and therefore this highlights the importance of this approach.

10. Still unclear how diathesis-stress works/ the treatment-causation fallacy
Strong evidence to suggest that some sort of underlying vulnerability coupled with stress can lead to sz. However we do not yet fully understand the mechanisms by which the symptoms of schizophrenia appear and how both vulnerability and stress produce them.
Turkington et al. argue there is a good fit between interactionist approach and combination treatments. However, the fat that combined biological and psychological treatments are more effective than either on their own does not necessarily mean the interactionist approach is correct. Similarly the fact that drugs help does not mean that sz is biological in origin. This error of logic is the treatment causation fallacy. Just because a treatment helps doesn’t mean the mechanisms involved in that treatment caused the disorder. (Lack of aspirin doesn’t cause headaches.)