Interactionist approach for explaining schizophrenia Flashcards
What is the interactionist approach?
It provides a more comprehensive framework for understanding SZ as it allows for the idea that both nature and nurture share responsibility for the development of SZ. This also implies that both biological and psychological therapies should be combined to help treat this disorder.
What is a diathesis?
Biological vulnerabilities - The 1st key proposal of this model is that certain factors make you more vulnerable to developing schizophrenia and create a predisposition (or increased likelihood) of developing the disorder. This is the diathesis part of the model. Many would suggest that this diathesis is biological (but modern explanations say it is more than this).
What is a stress?
Environmental factors - The 2nd key proposal is that certain situations, experiences, events, stressors etc. can trigger or activate this predisposition and cause the individual to develop schizophrenia, or cause an increase or relapse in symptoms if the individual is in remission. This is the stress part of the model.
What is Meehl’s original diathesis stress model?
In the original diathesis stress model (Meehl 1962) diathesis (vulnerability was entirely GENETIC- the result of a single ‘SCHIZOGENE’. This led to the development of a biologically based SCHIZOTYPIC PERSONALITY, one characteristic of which was sensitivity to stress. It was claimed that if a person does not have the schizogene then no amount of stress would lead to schizophrenia. However, in carriers of the gene, chronic stress through childhood and adolescence in particular the presence of a ‘schizophrenogenic mother’ could result in the development of the condition.
What is the modern understanding of diathesis?
One way in which our understanding of diathesis has changed is that it is now clear that MANY GENES each appear to increase genetic vulnerability slightly - there is NO single SCHIZOGENE (Ripke et al 2014) . Modern views of diathesis also include a range of factors beyond the genetic, including psychological trauma ( Ingram & Luxton 2005) - so trauma becomes the diathesis rather than the stressor. Read et al (2001) proposed a neurodevelopmental model in which early trauma alters the developing brain. Early & severe enough trauma, such as child abuse, can seriously affect many aspects of brain development e.g the HYPOTHALAMIC-PITUITARY- ADRENAL (HPA) system can become over-active, making the person much more vulnerable to later stress.
What is the modern understanding of stress?
In the original diathesis- stress model of schizophrenia, stress was seen as psychological in nature, in particular related to parenting. Although psychological stress, including that resulting from parenting, may still be considered important, as modern definition of stress (in relation to the diathesis stress model) includes anything that risks triggering schizophrenia (Houston et al 2008). Much of the recent research into factors triggering an episode of schizophrenia has concerned cannabis use. In terms of diathesis- stress model cannabis is a stressor because it increases the risk of schizophrenia by up to 7 times according to dose. This is probably because cannabis interferes with the DOPAMINE system. However, most people do not develop schizophrenia after smoking cannabis so it seems there must be one or more vulnerability factors.
What are uncontrollable stressors?
External forces outside a person’s control. They are seen to be a bigger trigger of biological vulnerabilities than perhaps controllable aspects. This implies early family factors or geographical location when young are highly implicated triggers in the diathesis stress model.
What is the additive nature of diathesis and stress?
These factors combine together and lead to SZ. For example, relatively minor stressors lead to the onset of SZ for those with high bio vulnerabilities, or a major stressor and chronic event may cause a similar reaction to someone who has a much lower bio vulnerability.
INTERACTIONIST EXPLANATION - Research support?
Tienari considered genetic risk and parenting style in a huge adoption study involving 19,000 Finnish mothers with SZ. Biological parents were assessed for rates of SZ and adoptive parents had their child-rearing styles analysed. Results showed styles that contained high levels of criticism and low empathy were implicated in the development of SZ, but only for those with a high genetic risk. Therefore both genetic risk and family related stress both cause SZ to some extent.
INTERACTIONIST EXPLANATION - Oversimplified?
Meehl’s original DT- 5 model suggested that diathesis was entirely genetic- due to a single schizogene. This led to a schizotype personality that was sensitive to stress. If a person was a carrier of this gene and experienced a chronic stress through childhood and adolescents, this could lead to SZ. This suggests that no other vulnerabilities or combination factors could lead to SZ which we now know is not the case.
INTERACTIONIST EXPLANATION - Practical applications?
Startup recruited 90 patients who were admitted to hospital due to an acute episode of SZ. 43 got the standard care of AP medication and nursing whilst the other 47 got the standard care plus up to 25 90 minute CBT sessions. They found that 60% of the CBT group showed clinical improvements compared to 40% of the control group. These benefits remained at 6 and 12 month follow ups compared to 17% for the control group.
INTERACTIONIST EXPLANATION - Methodological issues?
It is difficult to establish cause and effect. Stressors that contribute to the risk of developing SZ include biological, environmental and psychological factors. We cannot determine precisely how these factors contribute to the diathesis stress interaction for any single person because specific causes will vary. Therefore it is difficult to validate this explanation fully, as we are unable to isolate the cause.
INTERACTIONIST EXPLANATION - Further research evidence?
Murray reported how children born after the flu epidemic when the mother had contracted the disease whilst pregnant during the second trimester had an 88% increased chance of developing SZ compared to a control group. This exposure was suspected to cause neural defects which lead to an increased vulnerability to develop SZ. This suggests that SZ can result from an interaction of an environmental stressor and genetic vulnerability.
