Schizophrenia: An interactionist approach Flashcards
What is the diathesis-stress model?
Explains mental disorders as a result of an interaction between biological and the environmental influences.
What is diathesis?
We have seen that SZ has a genetic component in terms of vulnerability. What supports the idea of a genetic role for SZ are the findings that the identical sibling or fraternal twin, and that adoptive relatives do not share the increased risk of biological relatives. However, in about 50% of identical twins in which one twin is diagnosed with SZ, the other never meets the diagnostic criteria for the disorder. This discordance among identical twins indicates the environmental factors must also play a role in determining whether a biological vulnerability for SZ actually develops into the disorder.
What is stress?
The sort of stressful life events that can trigger SZ take a variety of forms such as childhood trauma or the stresses associated with living in a highly urbanised environment. For example, Varese et al (2012 found that children who experienced severe trauma before the age of 16 were three times as likely to develop SZ in later life compared to the general population. There was a relationship between the level of trauma and the likelihood of developing SZ, with those severely traumatised as children being at greater risk.
What is the addictive nature of diathesis and stress?
There are several ways in which a combination of diathesis and stress can lead to SZ. 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 person low in vulnerability. Whatever the combination, the idea pre-supposes additivity.
What was Tienari at al (2004) aim?
To study the hypothesis is that genetic factors moderate susceptibility to environment risks associated with adoptive family functioning.
What was Tienari’s procedure?
Hospital records were reviewed for nearly 20,000 women admitted to Finnish psychiatric hospitals between 1960 and 1979, identifying those who had been diagnosed at least once with schizophrenic or paranoid psychoses. The list was checked to find those mothers who had one or more of their offspring adopted away. The resulting sample of 145 adopted-away offspring was then matched with a sample of 158 adoptees without the genetic risk.
What is Tienari’s findings?
Of the 303 adoptees, 14 had developed SZ over the course of the study. Of these 14, 11 were from the high risk group and 3 were from the low risk group. However, being reared into a healthy adoptive family appeared to have a protective effect even for those at high genetic risks for SZ. High-genetic risk adoptees reared in families with low OPAS ratings were significantly less likely to have developed SZ than high-genetic risk of SZ, but not in those at low-genetic risk, adoptive family stress was a significant predictor of the development of SZ.
A03:
- Diatheses may not be exclusively genetic
- Limitations of the Tienari et al study
- Difficulties in determining casual stress.
- Implications for treatment
A03: Diatheses may not be exclusively genetic
Most diathesis-stress models emphasise vulnerability in terms of genetic influences alone, which seemed to cause neurochemical abnormalities that, in turn, result in increased risk for schizophrenia. However, this increases risk and also results from brain damage caused by environmental factors. For example, individuals may also develop a vulnerability to schizophrenia if they experience both complications. Verdoux (1998) estimated that the risk of developing schizophrenia late in life in individuals who have experienced obstetric complications at birth is four times greater than in those who experience no such complication.
A03: Limitations of the Tienari et al study
Researchers in the Tienari et al study identified a number of limitations of the study, particularly in the assessment of adoptive family functioning. For example, when psychiatric assessed stress in the adoptive family using the OPAS scale, they assessed family functioning at only one given time. Tienari acknowledges that the stress reflects the developmental stages in family functioning over time. They also acknowledge that observing reciprocal interactions between the adopted family and the adoptees makes it impossible to determine how much of the stress observed is assigned to the family and how much is actually caused by the adopted him or herself.
A03: Difficulties in determining casual stress.
Diathesis stress models reference stressful events that occur close to the onset of schizophrenia. However, it is possible that stress early in life can also influence how people respond to later stressful events and increase their future susceptibility to the disorder. For example, Hammen (1992) argues that maladaptive methods of coping with stress in childhood and throughout development mean that the individual fails to develop effective coping skills, compromising resilience and increasing vulnerability. Ineffective coping skills may make life generally more stressful for the individual and trigger mental illness.
A03: Implications for treatment
If the onset of schizophrenia is a result of the addictive effects of genetic vulnerability and environmental stress, then this has implications for the treatment of the disorder. Although the generic vulnerability is, as yet, difficult to control, certain other important factors known to interact with genetic vulnerability can be addressed with current knowledge, for example, Borglum et al (2014) found that women infected with cytomegalovirus during pregnancy were more likely to have a child who develops schizophrenia, but only if both mother and children carried a particular gene defect. This suggests that anti-viral medication during pregnancy may prevent the onset of schizophrenia and the offspring of the woman known to have this gene defect.
