Biological Explanations

• inheritance of schizophrenia

  • Evidence in favour of a genetic link, comes from family studies which indicate that the closer the genetic relationship to someone with schizophrenia, the greater the chance of developing the disorder.
  • Gottesman (1978) reports that while the rate of schizophrenia in the general population is 1%, the chances of first degree relatives (for example parent and child or sibling) developing the disorder is 12%, furthermore if both parents have schizophrenia, there is a 40% likelihood that a child of theirs will develop the disorder.
• candidate genes and schizophrenia

  • schizophrenia is polygenic and there are many candidate genes involved
  • For example, Miyakawa et al. (2003) studied DNA from families affected by schizophrenia, and found that those with the disease were more likely to have a defective version of a gene, called PPP3CC. This gene is associated with the production of calcineurin, which regulates the immune system.
• evaluation of genetic explanation of schizophrenia (1)

  • genetics cannot be the sole factor since the concordance rates for MZ twins are between 40-60%. As the concordance rates are not 100% it means that genes cannot fully explain schizophrenia. It could be that an individual is genetically pre-disposed to schizophrenia, making them more at risk. adopted a biologically reductionist approach. Using this very narrow approach has led to an explanation which cannot explain why if one MZ twin has schizophrenia why the other twin only has a 40-60% risk of getting it too.
• evaluation of genetic explanation of schizophrenia (2)

  • difficult to separate the impact of nature and nurture. For example, both family and twin studies investigate individuals who are sharing the same environment, which could be increasing the concordance rates, irrespective of the genes. Possibly the high concordance rates between MZ twins is actually due to them being treated more similarly than DZ twins or ordinary siblings and not in fact due to their genetics. The shared environment could be a confounding variable as we can’t differentiate between genetic and environmental influences.
• evaluation of genetic explanation of schizophrenia (3)

  • Family studies are conducted retrospectively when they are comparing a cross section of people who have already been diagnosed. Retrospective data can be unreliable as problems in memory and records are likely. Prospective studies provide more reliable data as they follow people over time and can make comparisons before and after their condition occurs.
• what is dopamine?

  • Dopamine is one of the chemicals i.e. a neurotransmitter in the brain, which causes neurons to fire; it is one of the chemicals that is responsible for transmitting signals between the neurons in the brain.
• what was the original dopamine hypothesis?

  • schizophrenia was caused by excessive activity of dopamine.
  • This causes the neurons that respond to dopamine to fire too often and transmit too many messages.
  • This message ‘over load’ may produce many symptoms of schizophrenia.
  • The dopamine hypothesis suggests that schizophrenia is caused by a high density of dopamine receptors, and by a high level of sensitivity in dopamine receptors.
  • This causes the messages from neurons that transmit dopamine to fire too easily or too often.
• what affect does hyperdopaminergia have in the subcortex?

  • It focuses on the possible role of high levels or activity of dopamine in the subcortex i.e. the central areas of the brain. For example, an excess of dopamine receptors in Broca’s area might be associated with poverty of speech and/or the experience of auditory hallucinations (Broca’s area is responsible for speech production).
• what affect does hyperdopaminergia have in the cortex?

  • more recent version of the hypothesis
  • Focused on abnormal dopamine systems in the brain’s cortex- particularly the pre-frontal cortex, which is responsible for thinking and decision making- this could explain negative symptoms.
• evaluation of the dopamine hypothesis (1)

  • A weakness of the hypothesis is that newer drugs such as clozapine, are more effective than traditional ones. These new drugs affect dopamine as well as other neurotransmitters, such as serotonin. It appears that several neurotransmitters may be involved in the development of schizophrenia and therefore the hypothesis is too simplistic. Along with dopamine and serotonin, some research has implicated glutamate.
• evaluation of the dopamine hypothesis (2)

  • A strength of the research into the dopamine hypothesis is that it has practical applications as it has led to the development of an effective treatment. From the research using schizophrenics, new drugs have been developed such as Clozapine, which is much more effective than neuroleptics at relieving schizophrenic behaviour. This suggests that psychiatrists can understand the role played by neurotransmitters when treating different types of schizophrenia and thus improve the patient’s quality of life
• evaluation of the dopamine hypothesis (3)

  • Dopamine abnormalities are not present in all schizophrenics, especially those with negative symptoms. Problems with dopamine seem to be associated more with positive symptoms, so it may only explain certain aspects or types of the illness. Davis et al. (1991) argue that the diversity of types and symptoms in schizophrenia implies that there are several neurotransmitters involved and not just dopamine.
• evaluation of the dopamine hypothesis (4)

  • Research evidence shows that schizophrenia sufferers have more receptors which may lead to more neural firing and therefore an over production of messages. Autopsies have found that there are generally a larger number of dopamine receptors in schizophrenics (Owen et al. 1987) and an increased amount of dopamine in the left amygdala (Falkai et al. 1988) and increased dopamine in the caudate nucleus and putamen (Owen et al. 1978) in patients suffering from schizophrenia.
• evaluation of the dopamine hypothesis (5)

  • One criticism of the dopamine hypothesis is there is a problem with the cause and effect. Lloyd et al. believe that if dopamine is a causative factor, it may be in indirect one mediated through environmental factors, because abnormal family circumstances can lead to high levels of dopamine, which in turn triggers the schizophrenia symptoms. This suggests that one needs to be careful when establishing cause and effect relationships in schizophrenic patients.
• neural correlates in schizophrenia

  • schizophrenia is caused by enlarged ventricles.
  • These are the fluid-filled gaps between brain areas. Enlarged ventricles are especially associated with damage to central brain areas and the prefrontal cortex.
  • Such damage is often associated with negative symptoms. For example, Johnstone et al. (1976) found that schizophrenics had enlarged ventricles while non-sufferers did not, which suggests schizophrenia is related to a loss of brain tissue.
• evaluation of neural correlates (1)

  • Research indicates the enlarged ventricles may only explain certain schizophrenia symptoms. Weyandt (2006) reported that enlarged ventricles are associated with negative symptoms only. This implies that this explanation cannot explain all symptoms and types of the illness.
• evaluation of neural correlates (2)

  • Research into the role of enlarged ventricles is inconclusive. Some non schizophrenics have enlarged ventricles, while not all schizophrenics do. This goes against the ideas of schizophrenia being linked to a loss of brain tissue. If it were the sole cause every person with enlarged ventricles would suffer from the illness.
• evaluation of neural correlates (3)

  • Evidence suggests that schizophrenics that do not respond to medication are those with enlarged ventricles. This could mean that it is an effect of suffering from schizophrenia over a long period of time i.e. it is the schizophrenia causing long term physical brain damaged rather than the brain damage causing the schizophrenia. Therefore, the enlarged ventricles could be a consequence of the illness rather than the cause.
• evaluation of neural correlates (4)

  • there is research that does indicate that structural brain damage is often evident at first onset of schizophrenia. But only by performing longitudinal studies would it be possible to assess whether the damage progressively worsens as the schizophrenia continues. Ho et al. (2003) performed MRI scans on recent-onset schizophrenics and then re-scanned them 3 years later. They found evidence of brain damage in the recent-onset patients, which worsened over time (even though they were on medication).