- There are more than two biological explanations but you only need to know two in great detail. However, acknowledge that others exist (such as viral infections and the neuroanatomical explanation) as you can use them for comparison/evaluation.
- Neurochemical:
- The dopamine hypothesis is based on the role of chemical messages between nerve cells called neurotransmitters.
- Early 1950’s – the anti-schizophrenic effects of chlorpromazine and reserpine (drugs) were documented and related to their side effects of Parkinson’s disease.
- Late 1950’s – the brains of recently deceased Parkinson’s patients were found to be depleted of dopamine.
- Early 1960’s – it was hypothesised that schizophrenia was associated with excessive dopamine activity in the brain.
- This led to the theory that excessive dopamine neurotransmitters are the cause schizophrenia.
- Post mortems of schizophrenics have shown high levels of dopamine.
- Anti-psychotic drugs bind to dopamine receptor sites (D2) and block them so that they can no longer respond to the dopamine neurotransmitters.
Evaluations:
- An excess of dopamine located in the MLP seems to be most relevant to understanding schizophrenia. Antipsychotic drugs have therapeutic effects on the positive symptoms by blocking the D2 receptors here.
- The hypothesis has been refined – improved technologies for studying neurochemical factors have led to the claim that schizophrenics have an excess of dopamine receptors or oversensitive D2 receptors. This refined hypothesis is based on several post-mortem and PET scan studies.
- Supporting studies – Early 1950’s – antipsychotic drugs (blocking dopamine receptors) linked to Parkinson’s disease. Late 1950’s – Parkinson’s patients brains found to be depleted of dopamine. Early 1960’s – Schizophrenia associated with excessive levels of dopamine activity in the brain.
- Cause and effect – it is possible that the high levels of dopamine are a result of having the disorder, rather than the other way round.
- Dopamine = an indirect causative factor.
- Inconclusive evidence – There is no consistent difference in dopamine levels between those who have schizophrenia (drug free) and those who do not.
- The dopamine hypothesis cannot explain all cases because it is unlikely that problems with dopamine production/receptivity will prove to be the basic biochemical abnormality underlying all forms of schizophrenia.
- The dopamine hypothesis is not a complete explanation because it can take several weeks for antipsychotic drugs to gradually reduce symptoms even though they begin blocking D2 receptors very quickly.
- The action of neurotransmitters is complex and not fully understood meaning other neurotransmitters could be implicated.
- Genetics:
- This is based on the idea that the development of the body, including the brain, is heavily determined by genetics.
- It assumes that most behaviours, whether seen as ‘normal’ or not, are considered to be inherited from the genes or the parents.
- This suggests that relatives of people with schizophrenia have a greater chance of developing schizophrenia themselves due to their genetics.
Twin studies are used to show concordance rates for developing schizophrenia. If schizophrenia was totally genetically determined we would expect monozygotic twins to have a 100% concordance rate because they are genetically identical. Dizygotic twins would have a 50% concordance rate.
However, this is not the case:
- Kallman, USA (1946) – used 174 Mz twins and 296 Dz twins and found one of the highest concordance rates for Mz twins – 69%, only 14% for Dz twins.
- This study is criticised because Kallman used a ‘broad’ set of criteria to diagnose the disorder and he was not strict so mis-diagnosis may have occurred.
Gottesman and Shields, England (1966):
- 24 Mz twins and 33 Dz twins that were reared apart.
- Concordance rates – Mz = 48% and Dz = 17%
- Small sample size and the use of the ICD-10 means it is culturally bias.
They concluded that genes appear to play an important role in the development of schizophrenia because the concordance rate is higher in Mz twins than Dz twins. However, there must be another important factor (environmental?) that effects whether a genetically predisposed person will develop it or not.
Family resemblance studies have shown that there is a link between environmental and genetic factors. There is no way of telling whether the correlation between developing schizophrenia and degree of family resemblance is caused by genetic or environmental factors. Adoption studies are used by researchers because they allow the separation of genetic and environmental influences in order to determine whether genetics plays a role in the development of schizophrenia.
Heston (1966) – 47 adopted children whose biological mothers had schizophrenia compared to a group of children from the same foster home whose mothers did not have schizophrenia. 5 of the children in the experimental group developed Sz when they were adults compared to none in the control group.
Heston concluded that even though none of the children were raised by schizophrenic parents, those with a schizophrenic in their biological family were more likely to develop it themselves.
Evaluations:
- There is a lot of supporting evidence for the theory from multiple sources, all suggesting that genetics play a key role in causing schizophrenia.
- The explanation has allowed those with schizophrenic relatives to be tested and treated early due to the knowledge of a genetic predisposition.
- Twins that weren’t reared apart may have both developed schizophrenia due to their shared environment – same house, same family etc. We cannot eliminate environmental factors.
- Even adoption studies (twins reared apart) do not show that genetics is the complete cause of schizophrenia because not all of them develop it.
- Concordance rate is never 100% – even with Mz twins it is never higher than 50% – so we cannot conclude that genetics is a complete explanation.
- Without knowing the exact gene it is impossible to isolate the underlying mechanisms that lead to a genetic risk of developing the symptoms of schizophrenia, therefore we cannot develop an effective treatment.