The diathesis-stress model sees schizophrenia as the result of an interaction between biological and environmental influences. The genetic role for schizophrenia is supported by the findings that the identical twins, one with schizophrenia, is at greater risk than a sibling. However, 50% of identical twins where one twin is diagnosed with schizophrenia, the other never meets the diagnostic criteria. This discordance indicates that environmental factors must also play a role in determining whether the vulnerability for schizophrenia actually develops into the disorder.
Stressful life events that can trigger schizophrenia take a variety of forms such as childhood trauma. Varese found children who experienced severe trauma before 16 were 3x as likely to develop schizophrenia compared to the general population. Research also suggested that a high level of urbanisation is associated with increased risk of psychoses, including schizophrenia. A meta-analysis by Vassos found the risk for schizophrenia in the most urban environments was estimated to be 2.37x higher than in the most rural environments.
The urbanisation and schizophrenia link isn’t clear, but many people live in densely populated urban areas, but only a minority will develop schizophrenia. The relationship between urban stress and schizophrenia is conditional on some other factor, i.e. a genetic risk for the disorder. There are several ways in which a combination of diathesis and stress can lead to schizophrenia. For example, relatively minor stressors may lead to the onset of the disorder for an individual who is highly vulnerable, or a major stressful event might cause a similar reaction in a low vulnerability.
Tienari 2004 reviewed hospital records for nearly 20,000 women admitted to Finnish psychiatric hospitals between identifying those who had been diagnosed with schizophrenic or paranoid psychoses. They checked to find mothers who gave away their children. The sample was 145 adopted-away offspring was then matched with a sample of 158 adoptees without the genetic risk. Both groups were independently assessed after 12 years, with a follow-up after 21 years. Psychiatrists also assessed family functioning in the adoptive families using the OPAS scale.
This measures families on various aspects of functioning such as lack of empathy. The interviewing psychiatrists were kept blind as to the status of the biological mother. Of the 303 adoptees, 14 had developed schizophrenia. Of these, 11 were from the high-risk group and three were from the low-risk group. The low OPAS ratings appeared to have a protective effect even for those at high genetic risk. High-genetic-risk adoptees were more likely to develop schizophrenia in families with high OPAS ratings compared to low.
Most diatesis stress models emphasise vulnerability in terms of genetic influences alone.
However, an increased ‘vulnerability’ in schizophrenia can come from more environmental factors such as obstetric complications at birth (prolonged oxygen deprivation) which makes the risk of developing conditions 4 times greater than no such complications.
These findings suggest that brain damage can play a role in the development of schizophrenia.
The diathesis stress model makes reference to stressful events the occur to the onset of schizophrenia, however stressors in earlier life can also influence how they respond to them later in life and increase the susceptibility to the disorder.
Hammen argues that maladaptive methods of coping with stress in childhood and in development, the individual fails to develop effective coping skills which can reduce resilience and increase vulnerability.
Ineffective coping skills may therefore make life generally more stressful for the individual and trigger a mental illness.
Researchers in the tienari study identified a number of limitations.
For example, when psychiatrists assessed the stress in adoptive families using the UPAS scale, they were only assessing it at one point in time. Tienari acknowledged that this fails to reflect development changes in family function over time.
Observing reciprocal interactions between the adoptive family and adoptees makes it impossible to determine how much of the stress observed it assigned to the family and how much caused by adoptees themselves.