biological explanations for schizophrenia: ao3

Question 1

Strength - research support for genetic vulnerability

Answer 1

P: There is now very strong evidence for genetic vulnerability to schizophrenia from a variety of sources.
E: Gottesman (1991) shows how genetic similarity and shared risk of schizophrenia are closely related. Adoption studies (Tienari et al. 2004) shows that children of schizophrenia sufferers are still at heightened risk of schizophrenia if adopted into families with no history of the condition.
E: There is also evidence from studies conducted at the molecular level showing 108 gene variations that increase the risk of schizophrenia (Ripke et al. 2014).
L: These findings don’t mean that schizophrenia is entirely genetic, however it does suggest that genetic factors make some people more vulnerable to developing schizophrenia than others.

Question 2

Weakness - issues and debates - biological reductionism

Answer 2

P: One limitation of the genetic explanation is there is clear evidence to show that environmental factors also increase the risk of developing schizophrenia.
E: These environmental factors include both biological and psychological influences. Biological risk factors include birth complications (Morgan et al. 2017) and smoking THC-rich cannabis in teenage years.
Psychological risk factors include childhood trauma which leaves people more vulnerable to adult mental health problems in general but there is now evidence for a particular link with schizophrenia.
E: In one study by Morkved et al. (2017), researchers found 67% of people with schizophrenia and related psychotic conditions reported at least one childhood trauma as opposed to 38% of a match group with non-psychotic mental health problems.
L: This means that genetic factors alone cannot provide a complete explanation for schizophrenia.

Question 3

Strength of Dopamine hypothesis - evidence from drug studies

Answer 3

P: There is support from a number of sources for abnormal dopamine functioning in schizophrenia.
E: Dopamine agonists like amphetamines that increase the levels of dopamine makes schizophrenia worse and can produce schizophrenia like symptoms in non-sufferers (Curran et al. 2004). Antipsychotic drugs, on the other hand, work by reducing dopamine activity (Tauscher et al. 2014) and are used effectively with many schizophrenic patients.
E: Furthermore, research has suggested that a number of candidate genes implicated in schizophrenia act on the production of DA or DA receptors
L: All of this strongly suggests that dopamine is involved in the symptoms of schizophrenia.

Question 4

Weakness of dopamine hypothesis - the role of glutamate

Answer 4

P: One limitation of the dopamine hypothesis is evidence for a central role glutamate.
EE: Post-mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions of peopl with schizophrenia (McCutcheon et al. 2020). In addition, several candidate genes for schizophrenia are believed to be involved in glutamal production or processing.
L: This means that an equally strong case can be made for a role for other neurotransmitters