biological explanations for schizophrenia Flashcards
genetic explanations
• Schizophrenia is heritable / inherited through the generations through transmission of genes → runs in families
• Studied in a variety of different ways.
studying genetic explanations
Family studies find individuals with schizophrenia and determine whether their biological relatives are similarly affected more often than non-relatives.
• Gottesman (1991) found that children with two schizophrenic parents had a concordance rate of 46% and those with 1 schizophrenic parent 13% and siblings had 9%.
Twin Studies: If MZ twins are more concordant than DZ twins it suggests that the similarity is due to genes.
• A meta-analysis of twin studies conducted before 2001 found a combined concordance rate of 40% for MZ twins and 7% for DZ twins (Joseph, 2004).
Adoption Studies: Studies of genetically related individuals who have been reared separately.
• Tienari et al. (2000), found that of 164 adoptees with schizophrenic mothers, 11 (6.7%) also received a diagnosis, compared to just 2% of the 197 control adoptees.
neural correlates
Patterns of structure or activity in the brain that occur in conjunction with an experience and may be implicated in the origins of that experience.
-Dopamine hypothesis
The original dopamine hypothesis claims that an excess of the neurotransmitter dopamine in certain regions of the brain is associated with the positive symptoms of schizophrenia.
• Further research has suggested that schizophrenics are thought to have abnormally high numbers of D2 receptors on receiving neurons, resulting in more dopamine binding and therefore more neurons firing.
The revised dopamine hypothesis
Davis et al. (1991)
• Excess of dopamine in the mesolimbic pathway.
• Positive symptoms
• Deficit of dopamine in areas of the prefrontal cortex.
• Area responsible for thinking, decision making etc.
• Negative symptoms
Evidence
• Neural Imaging - Patel et al. (2010)
• Used PET scans and found lower dopamine levels in dorsolateral prefrontal cortex of schizophrenics compared to normal controls.
strength- support for genetic vulnerability
There is now very strong evidence for genetic vulnerability to schizophrenia from a variety of sources.
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.
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).
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.
issues and debates-biological reductionism
One limitation of the genetic explanation is there is clear evidence to show that environmental factors also increase the risk of developing schizophrenia.
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.
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.
This means that genetic factors alone cannot provide a complete explanation for schizophrenia.
strength-dopamine hypothesis
There is support from a number of sources for abnormal dopamine functioning in schizophrenia.
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.
Furthermore, research has suggested that a number of candidate genes implicated in schizophrenia act on the production of DA or DA receptors
All of this strongly suggests that dopamine is involved in the symptoms of schizophrenia.
limitation-rose of glutamate
One limitation of the dopamine hypothesis is evidence for a central role of glutamate.
Post-mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions of people with schizophrenia (McCutcheon et al. 2020). In addition, several candidate genes for schizophrenia are believed to be involved in glutamate production or processing.
This means that an equally strong case can be made for a role for other neurotransmitters
