biological explanations

• Family studies

  The risk of schizophrenia increases in line with genetic similarity
• Family studies

  • Gottesman (1991) carried out a large-scale family study
• Family studies are quite weak evidence for a genetic basis because family members also share the same or similar environment as well as genetics
• Candidate genes

  There seems to be a number of genes that increase the risk of a person getting schizophrenia, this means that schizophrenia is polygenic
• Different studies have identified different candidate genes, it also appears that schizophrenia is aetiologically heterogeneous, i.e. different combinations of factors can lead to the condition
• Candidate genes

  • Ripke et al (2014) carried out a huge study comparing the genetic make-up of 37,000 patients to 113,000 controls, 108 separate genetic variations were associated with increased risk of schizophrenia
• Mutation

  Another genetic explanation, in the absence of family history, is mutation in parental DNA caused by radiation, poison or viral infection
• Mutation

  • Positive correlations between paternal age (associated with increased risk of sperm mutation) and risk of schizophrenia, increasing from 0.7% with fathers under 25 to over 2% in fathers over 50 (Brown et al 2002)
• There is strong evidence to support the genetic explanation of schizophrenia
• Evidence for genetic explanation

  • Gottesman (1991) shows how genetic similarity and the shared risk of getting schizophrenia are related
  • Adoption studies such as the one by Tienari et al (2004) show that children of schizophrenia sufferers are still at heightened risk of schizophrenia if adopted into families with no history of schizophrenia
  • Ripke et al (2014) found that particular genetic variations significantly increase the risk of schizophrenia
• Although there is substantial evidence, it does not mean that schizophrenia is entirely genetic – there are also environmental factors
• Environmental factors

  • Biological risk factors (birth complications, smoking THC-rich cannabis in teenage years)
  • Psychological risk factors (childhood trauma)
• Research shows that 67% of people with schizophrenia and related psychotic disorders reported at least one childhood trauma, opposed to 38% of a matched group with non-psychotic mental health issues
• Genetic factors alone cannot provide a complete explanation for schizophrenia
• Genetic counselling

  If one or more potential parents have a relative with schizophrenia, they risk having a child with the condition
• The risk estimate is just an average figure, it will not really reflect the probability of a particular child going on to develop schizophrenia because they will experience a particular environment which also has risk factors
• Neural correlates

  Brain structure/function and schizophrenia
• Dopamine hypothesis (original)

  Schizophrenia might be linked to high levels of dopamine (hyperdopaminergia) in the subcortical areas of the brain
• Dopamine hypothesis (updated)

  Abnormal dopamine systems in the brain's cortex, with low levels of dopamine (hypodopaminergia) in the prefrontal cortex being linked to the negative symptoms of schizophrenia
• Evidence for dopamine

  • Dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia like symptoms in non-sufferers (Curren et al 2004)
  • Antipsychotic drugs work by reducing dopamine activity (Tauscher et al 2014)
• There is also evidence that suggests that dopamine does not provide a complete explanation for schizophrenia, as some of the genes identified code for the production of other neurotransmitters
• Evidence for the dopamine hypothesis is mixed, it may be that both hyper and hypodopaminergia are correct explanations, both high and low levels of dopamine in different brain regions are involved in schizophrenia – different for different people
• Glutamate


  Live brain scans and post-mortems have consistently found raised levels of glutamate in several areas of the brain in people with schizophrenia, and several candidate genes are thought to be responsible for glutamate production or processing
• Glutamate seems to be equally important as the role of other neurotransmitters
• Amphetamine psychosis


  • Tenn et al (2003) induced schizophrenia-like symptoms in rats using amphetamines and then relieved symptoms using drugs that reduce DA action
  • However, other drugs that increase DA do not cause schizophrenia like symptoms, and Garson (2017) has challenged the idea that amphetamine psychosis closely mimics schizophrenia