Interactionist approach to explaining Sz

Meehl suggested that the vulnerability is genetic (the result of a ‘schizogene’), causing someone to be sensitive to stress. Those who do not have the ‘schizogene’ would not develop schizophrenia, even if they experienced a stressful upbringing, such as having a schizophrenogenic mother.   

• It’s now believed that there’s no single ‘schizogene’ - but rather many genes that increase genetic vulnerability to Sz (polygenic genes) 

• It’s also believed that factors other than genes can be a diathesis such as psychological trauma. Early & severe enough trauma (such as child abuse) can seriously affect aspects of brain development & can make a person more vulnerable to stress.

A more modern definition of stress (trigger) incluses anything that risks triggering Sz, not just parenting, much of the recent research has concerned canabis use.

In terms of the diathesis stress model, canabis is the stressor because it increases the risk of Sz by up to seven times according to the dose, probably due to its interference with the dopamine system.

However, not everyone develops Sz after smoking canabis - suggesting there must also be one or more vulnerability factors.

The interactionist model considers both biological & psychological factors in the development of Sz & is therefore compatible with both biological & psychological treatments for Sz. In particular, the combination of antipsychotic medication & psychological therapies - i.e CBT. 

Turkkington et al (2006) argue that it is possible to believe in biological causes of Sz & still practice CBT to relieve psychological symptoms. However, this requires adopting an interactionist model. It is not possible to adopt a purely biological approach & tell the patient their condition is purely biological & that there is no psychological significance to symptoms & then treat them with CBT. 

In the UK, treatments such as CBT, family therapy & drug therapy are often combined

P - Research to support the interactionist approach in explaining schizophrenia comes from Tienari et al (2004). ​

E - They followed up 19,000 adopted children in Finland whose mothers had schizophrenia & compared them to a control group of adopted children without any genetic risk. The child-rearing styles of the adoptive parents were observed. ​

E - Those children who were brought up in families with a lot of conflicts & low empathy (family dysfunction) were much more likely to develop schizophrenia but only in the children who had a genetic vulnerability, not the control group. ​

L - This supports the interactionist approach because the genetic vulnerability only led to the children developing Sz when combined with a stress trigger - family dysfunction.

However, despite the research to support by Tarrier, the interactionist approach to treating and explaining schizophrenia may not be correct. 

• Jarvis and Okami (2019) point out that just because combining both biological and psychological treatments is more effective in treating schizophrenia, does not necessarily mean we can assume the interactionist approach to explaining schizophrenia is correct. 

• This is the equivalent of saying that because alcohol reduces shyness, shyness is caused by a lack of alcohol. This logical error is known as the ‘treatment-causation fallacy’ and is a limitation of the interactionist approach to explaining and treating schizophrenia.​