- diathesis was entirely genetic caused by a single 'schizogene'
- this led to a schizotypicpersonality characterised by sensitivity to stress
- this is what causes schizophrenia; if a person doesn't have this gene no amount of stress can cause schizophrenia
- if carriers of the gene experience chronic stress throughout childhood and adolescence (particularly a schizophrenogenic mother) can cause the disorder
- as the model acknowledges biological and psychological factors it combines both types of treatment
- the model is associated with combing anti-psychotic drugs and psychological therapies e.g. CBT
- in Britain it is increasingly standard practice to use a combination of antipsychotic drugs and CBT
- in the US there is more conflict between the biological and psychological models of schizophrenia which has led to a slower adoption of the interactionist model
- this means that drug treatment without psychological therapy is more common in the US
- (Tienari et al, 2004) investigated the impact of both genetic vulnerability and a psychological trigger (dysfunctional parenting)
- 19,000 Finnish children whose biological mother shad schizophrenia were monitored
- the genetic risk group was compared to the control group of adoptees who didn't have a family history of schizophrenia
- adoptive parents were assessed for child-rearing style and it was found that high levels of criticism, hostility and low levels of empathy were associated with the development of schizophrenia
- (Jarvis & Okami, 2019) point of saying successful treatment for a mental disorder justifies a particular treatment is the logical equivalent of saying because alcohol reduces shyness, shyness is caused by lack of alcohol
- this logical error is called the treatment-causationfallacy
- we cannot automatically assume the success of combinedtherapies means interactionistexplanations are correct