Biological explanations for schizophrenia Flashcards
Genetic explanation
Schizophrenia is inherited and results from a biological process driven by the activity of certain genes, such as for brain structure development and neurotransmitter levels
There is no one ‘schizophrenia gene’, however a collection of gene locations have been located that are associated with a higher risk of developing schizophrenia. This means schizophrenia is thought to be a polygenetic disorder
If schizophrenia is genetic then we expect to see the more closely related two people are, if one person has the disorder the more likely the other person is to have the disorder (concordance rate)
Family studies
- example
The closer a person is related to someone with schizophrenia, the greater the chance that they too will develop the disorder
Gottesman reviewed cases of schizophrenia in families and found a concordance rate of 48% for identical twins and 17% for non identical twins (DZ). This compares to the general population rate of 1%. This suggests schizophrenia has a genetic aspect as there is such a large difference between the two sets of twins. Both DZ and MZ twins should share similar environments. However concordance not 100% in MZ so not fully genetic
EVAL: Nature and nurture debate
Twin studies
- example
Identical twins (MZ) share 100% of each other’s DNA
Non identical twins (DZ) are no more genetically similar than any other sibling
Schizophrenia were a genetic disorder, we would expect to see a higher concordance rate for MZ twins than DZ twins
Kendler et al
50% concordance rate in MZ twins
15% concordance in DZ twins
- In addition to this they studied the unusual case of MZ twins who thought they were DZ twins and vice versa
Genetic status had more of an impact on the development of schizophrenia than believed status
- Believing that they were identical to their twin did not make make more likely to develop the disorder
- The MZ’s who thought they were DZ’s were still more likely to develop Schizophrenia
Adoption studies
-example
Identify the influence of genetic factors by studying children of schizophrenic biological parents who are brought up in alternative environments
Tienari et al - 155 schizophrenic mothers who had given up their child for adoption
- Compared to 155 children adopted from non schizophrenic parents
-10.3% of those with schizophrenic mother developed schizophrenia
- 1.1% of those with non schizophrenic parents developed schizophrenia
Candidate genes
- example
Individual genes that have been found to be associated with schizophrenia
- However early research looked unsuccessfully for a single genetic variation to explain schizophrenia
- Schizophrenia is polygenic (multiple genes working together)
It is also aetiologically heterogenous i.e risk is affected by different combinations
Ripke et al - combined all previous data from genome wide studies and found 108 separate genes associated with slightly increased risk of schizophrenia
Mutation
Schizophrenia can also have genetic origin in the absence of a family history because of mutation in parental DNA
Evidence comes from the correlation between parental age (associated with increased risk of sperm mutation) and risk of schizophrenia - Brown et al
EVALUATION: Three points regarding genetic basic of schizophrenia
- Research support/support for genetic vulnerability
- Biological reductionism (environmental factors)
- Genetic counselling
EVALUATION: Research support
P - Schizophrenia’s biological and genetic basis is supported by evidence.
E - For instance, Brown et al. (2002) discovered that if the father was older than 50 as opposed to younger than 25, the likelihood of having children with SZ increased by more than 1.3%.
E - This implies that SZ is likely to have a high heritability coefficient and biological basis due to mutations in the regions of DNA containing the potential genes, such as those coding for the production of serotonin and dopamine particularly.
L - This reinforces the use of neural correlates and family studies to look into and clarify SZ incidence rates.
EVALUATION: Support for genetic vulnerability
P - Numerous sources now provide extremely strong evidence that people are genetically vulnerable to schizophrenia. Gottesman demonstrates the close connection between genetic similarities and shared risk of schizophrenia.
E - According to adoption research (Tienari et al.), adopted children of people with schizophrenia are still more likely to develop the disorder than children from adoptive families without a history of it.
E - Additionally, research at the molecular level has demonstrated that 108 variations in genes raise the risk of schizophrenia (Ripke et al).
L - These results imply that certain people are more vulnerable to developing schizophrenia than others due to genetic factors, but they do not prove that schizophrenia is solely genetic.
EVALUATION: Biological reductionism
P - One limitation of 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.
E - Biological risk factors include using cannabis with a high THC content when you areteenager and birth abnormalities (Morgan et al.). Childhood trauma is one psychological risk factor that makes people more vulnerable to adult mental health issues generally, but there is also evidence linking it specifically to schizophrenia.
E - Morkveddiscovered that 67% of patients with schizophrenia and similar psychotic disorders had experienced at least one childhood trauma, compared to 38% of a control group with mental health problems that were not psychotic.
L - This implies that a full explanation cannot be given by genetic factors alone
EVALUATION: Genetic counselling
If potential parents have a relative with schizophrenia, they can be advised of risk of having a child with the condition
However the risk estimate is just an average figure based on genetic similarity to relatives, doesn’t take account of the future child’s development
This means that genetic counselling only provides a crude idea of vulnerability and is of limited use
Dopamine hypothesis
Schizophrenia may be caused by excessive levels of dopamine due to:
- Overproduction of the neurotransmitter
- Faulty regulation of the update mechanism (through which the dopamine returns to, and is stored by vesicles in the pre-synaptic neurons)
- It may also be due to over-sensitive or too many dopamine receptors
Original DA hypothesis
High dopamine activity in subcortex (central areas of the brain) associated with hallucinations and poverty of speech e.g excess of DA receptors in pathways linking from subcortex to Broca’s area
May explain specific symptoms e.g poverty of speech and auditory hallucinations
Updated DA hypothesis
Added low levels of DA in the prefrontal cortex (responsible for thinking), could explain negative symptoms
Explains origins of abnormal DA - genetic variations and early experiences of stress make some people more sensitive to cortical hypodopaminergia and hence subcortical hyperdopamingeria (Howes et al)
EVALUATION: Three points regarding neural correlates of schizophrenia
Dopamine hypothesis - evidence from drug studies
Limitation - evidence for a central role of glutamate
Evidence for dopamine hypothesis can be mixed
