Biological explanations Flashcards
Genetics
Heredity (genetics) is one possible cause of schizophrenia. Schizophrenia tends to run in families and the risk of an individual developing schizophrenia is higher for those with biological relatives with schizophrenia than those without. It is thought that different combinations of genes make a person more vulnerable to schizophrenia.
There are three main ways of studying the genetic explanation of schizophrenia:
Family studies
Twin studies
Adoption studies
Genetic Explanations
Candidate genes are ones which, through research, have been implicated in the development of schizophrenia.
Schizophrenia is thought to be polygenic – this means that its development is not determined by a single gene but a few (maybe as many as 108 genes) – this means that there is little predictive power from this explanation.
Genes associated with the increased risk included those coding for the functioning of a number of neurotransmitters including dopamine, e.g. PCMI / PPPC3 / NRG1 vs NRG3
Dopamine is a neurotransmitter that generally has an excitatory effect and is associated with the sensation of pleasure
Each individual gene confers a small increased risk of SZ (it is polygenic).
Different combinations can lead to SZ (it is aetiologically heterogeneous).
Family Studies
This shows that genes do play an important factor, however if genes were the only cause of schizophrenia then the percentages surely should be 100%,
The theory could be seen as deterministic; just because we are ‘predisposed’ by our genes cannot mean we necessarily get the disorder schizophrenia.
Many researchers now accept that schizophrenia concordance rates in families may be more to do with common rearing patterns or other environmental factors that have nothing to do with heredity.
Family Studies 2
Studies show that schizophrenia is more common in biological relatives than non-biological relatives, and that the closer degree of genetic relatedness, the greater the risk of developing schizophrenia.
Gottesman (1991) found that children with two biological parents with schizophrenia had a concordance rate of 46%, children with one schizophrenic parent had a rate of 13% and siblings had a concordance rate of 9%. (compared to a 1% chance for the general population).
Twin Studies
If Monozygotic (MZ) twins are more concordant than Dyzygotic (DZ) twins, then this suggests that the greater similarity is due to genetics.
Joseph (2004) points out that MZ twins are treated much more similarly, encounter more similar environments and experience more ‘identity confusion’ (frequently being treated as ‘the twins’ rather than as individuals) than DZ twins.
Twin Studies A03
Twin studies seem to indicate that there is a strong genetic component to the disorder
Twin studies demonstrate that there may be a predisposition to develop schizophrenia, however, the fact that both twins do not always develop schizophrenia means that environmental factors must also play a part
The fact that the concordance rate for twins is not 100% means that schizophrenia cannot be accounted for by genetics alone
Sample sizes of such twin studies is always going to be very small so therefore it is difficult to generalise to the general population
Adoption Studies
Are a way of truly separating the influence of genetics and environment, by investigating individuals who are genetically related by reared apart.
Tienari et al. (2000) found that of 164 adoptees whose biological mothers had been diagnosed with Schizophrenia, 6.7% also received a diagnosis, compared to just 2% of the 197 control adoptees (born to non-schizophrenic mothers).
Adoption Studies A03
As the results of adoption studies only reveal small percentages, they nonetheless support the idea that genes must play a role within schizophrenia.
However, Tienari conducted his study within Finland, therefore we are not able to generalise this study to the rest of the world.
Evaluation of Genetics
Research Support (family / twin)
Nature
Biological determinism
Biological reductionism (fails to acknowledge nurture)
Dopamine Hypothesis
claims that an excess of the neurotransmitter dopamine in certain regions of the brain is associated with the positive symptoms of the schizophrenia.
Messages from neurons that transmit dopamine fire too easily or too often, leading to hallucinations and delusions.
Schizophrenics are said to have too many D2 receptors on receiving neurons, resulting in more dopamine binding and, therefore, more neurons firing.
Hyperdopaminergia in the Subcortex
The original version of the dopamine hypothesis focused on the high levels of dopamine in the subcortex i.e. central areas of the brain.
An excess of dopamine receptors in Broca’s area (speech production) may be associated with auditory hallucinations.
Hypodopaminergia in the Cortex
More recent versions of the dopamine hypothesis have focussed on dopamine in the cortex.
Goldman-Rakic 2004 found that low levels of dopamine in the prefrontal cortex (thinking and decision making) was linked to negative symptoms of schizophrenia.
So which one is correct? Hyperdopaminergia or Hypodopaminergia
It may be that both hyper and hypodopaminergia are correct.
It could be that high levels in some parts of the brain are linked to positive symptoms and low levels in other parts of the brain are linked to negative symptoms.
Two sources of evidence highlight the key role of dopamine:
Drugs that increase dopaminergic activity
Drugs that decrease dopaminergic activity
Drugs that increase dopaminergic activity:
amphetamine is a dopamine agonist (it stimulates nerve cells containing dopamine, causing the synapse to be flooded with dopamine).
Non-schizophrenics who are exposed to large doses of dopamine can develop hallucinations and delusions, and these disappear with abstinence from the drug.
Likewise, people with Parkinson’s disease (who have low dopamine levels) who take the drug L-dopa to raise their levels of dopamine have been found to develop schizophrenic-type symptoms.
