Biological Explanations of schizophrenia

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  • Created by: sia sundu
  • Created on: 13-06-13 12:16

Genetic Influences

Twin studies:

  • Rosenthal (1963) - Genain quadruplets all developed SZ but they differed in age of onset and the precise symtoms. However, they had a dreadful childhood (including neglect and abuse) so it isn't clear that only genetics factors were involved.
  • Concordance means when a disorder is found in both twins; researchers look at the probability that in twins both will develop SZ.
  • Gottesman (1991) - summarised 40 studies that included considerable differences in severity of the symptoms of SZ. In MZ twins the concordance rate was 48%, but only 17% in DZ twins. Also the concordance rate for MZ twins brought together was similar for those brought up apart. This suggests that the high concordance rate isn't due to them being treated in a similar way in the family.  
  • Torrey (1992) - twin studies were inadequate. Found that the concordance rate for MZ twins was 28% compared with only 6% for DZ twins. Joseph (2003) found similar results MZ = 22.4% and DZ = 4.6%.

However, we need to take into account the fact that the lifetime risk of SZ in the general population is only 1%. Even on the figures of Torrey and of Joseph, you have an increased chance of SZ if you have a twin with the condition.

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Family studies:

Concordance rate:

  • Both parents have SZ = 46%
  • One parent has SZ = 16%
  • Sibling with Sz = 8%

First degree relatives share 50% of their genes and second degree around 25% To investigate the genetic links studies compare rates of schizophrenia in relatives with diagnosed cases with relatives of controls The closer the biological relationship, the greater the chance of developing schizophrenia KENDLER first degree relatives of those with schizophrenia are 18x more at risk than the population

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Adoption studies:

Tenari (1991)Identified adopted-away offspring of biological mothers who had been diagnosed with schizophrenia (155) plus a matched control group of adopted-away children (155) whose mothers had no mental disorder. Adoptees aged from 5-7 at the start of the study, all separated from their mother by the age of 4. In all, 10.3% of those children with schizophrenic mothers developed SZ, compared with only 1.1% of children without schozophrenic mothers. 

Wahlberg et al. (1997) - studied the evironment provided by the adopted families in terms of whether it was low or high in communication deviance (a tendecy to communicate in unclear and confusing ways). Children at genetic risk because thier mothers had SZ had very good psychological health if raised by adopted families low in communication deviance. Children who were at genetic risk and were raised by adopted familiesthat were high in communication deviance showed high levels of though disorder.

The chances of developing SZ depended on an interaction or combination of genetic factors and environmental ones.

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 Despite large differences in concordance rates across studies 2 findings were constient:

  • MZ and DZ twins who have a co-twin with SZ are much more likely than random members of the population to suffer from SZ.
  • Among twins having a co-twin with SZ, MZ twins are at significantly greater risk than DZ twins.

These 2 findings strongly suggesst that genetic factors play a role in the development of SZ.


  • The diagnostic criteria for schizophrenia is constantly changing which is a problem for longitudinal studies Even MZ twins reared apart share a womb so environmental factors cannot be discounted
  • Retrospective family studies involve people already diagnosed – problems with diagnosis?
  • Children adopted into families with poor communication were more likely to be schizophrenic – environmental again?
  • Genetics is not a complete explanation – 89% of people with schizophrenia have no family member diagnosed We still haven’t isolated the relevant gene
  • What about the diathesis stress arguement?
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The Dopamine hypothesis:

Dopamine is a neurotransmitter found in the limbic system of the brain SZ is thought to develop as a result of over-activity in parts of the brain controlled by dopamine It was discovered when people realised that phenothiazine antipsychotic drugs can reduce symptoms of schizophrenia as they inhibit dopamine activity .


  • Amphetamines and cocaine increase the effects of dopamine in the brain.
  • L-Dopa (a chemical that increases the levels of dopamine) can produce schizophrenic symptoms.
  • Chlorpromazine, (an anti-psychotic drug frequently used in the treatment of schizophrenia), blocks dopamine receptor sites.  This makes the brain less sensitive to dopamine. 
  • Post mortems carried out on schizophrenics, show that they have up to six times the number of dopamine receptors than normal.  Again this suggests that their brains are more sensitive than usual to the neurotransmitter.
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Randrup and Munkvad -

Induced behaviour similar to that of those suffering from schizophrenia into rats by giving them amphetamines. Effects were then reversed using neuroleptic drugs.

PET scans and post mortems - 

These have shown excess dopamine in the brains of schizophrenics.


Dopamine metabolism is abnormal in patients with schizophrenia. BUT is this a cause or a result of schizophrenia?

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It's hard to assess brain levels of dopamine in patients with SZ.

Directly by post-mortems. Indirectly which involves inserting a needle into the spine, which can be dangerous.

Findings have generally been negative - patients with SZ don't seem ti produce more dopamine than other people.

A strength of the research into SZ is that it has practical applications.

From the research using schizophrenics new drugs have been developed e.g. Clozapine, which is more effective than neuroleptics at relieving schizophrenic behaviour.

This suggests that psychoatrists and GP's can understand the role played by different drugs when treating different types of SZ and thus improve the patients quality of life.

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The chicken or the egg - Is the raised dopamine levels the cause of SZ, or is it the raised dopamine levels result of SZ? It isn't clear which comes first. This suggests that one needs to be careful when establishing cause and effect.

There is contradictory evidence for the biochemical explanation from Kasper et al (1999) - There are a no. of problems with the dopamin hypothesis: antipsychotics drugs are effective for only positive symptoms, therefore, excessive dopamine can at best explain some types of SZ. Newer atypical antipsychotic drugs have proved more effective than traditional ones in successfully treating the symptoms of SZ despite blocking fewer dopamine receptors, this suggests that there is refuting evidence for the notion of dopamine being the main contributing factor associated with SZ.

The dopamine hypothesis is biologically deterministic because if the individual does have excess amounts of dopamine then does it really mean that they will develop SZ? This suggests that the dopamine hypothesis doesn't account for freewill.

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