Biological explanation

• The dopamine hypothesis is supported by evidence from drug treatments such as antipsychotics
• Schizophrenia tends to run in families who are genetically related
• The risk of developing the simpler among individuals who have family members with schizophrenia is higher than those who don’t
• family studies have confirmed that risk of schizophrenia increases in line with genetic similarity to a relative with the disorder

  • the closer the degree of genetic relatedness the greater the risk
• Family study

  Gottesman (1991)

  • large scale family study
  • children with 2 schizophrenic parents had a concordance rate of 46%, children with 1 schizophrenic parent a concordance rate of 13% and siblings a concordance rate of 9%
• Disadvantages of family studies

  Family members tend to share aspects of their environment as well so correlation presents both genetics and environment

  If genes were the only caus of schizophrenia the concordance rate should be 100%

  Many researchers now accept that schizophrenia concordance rates in families may be more to fo with common rearing patterns or other environmental factors which have nothing to do with heredity
• If MZ twins are more concordant than DZ twins then this suggests that the greater similarity is due to genetic factors
• Twin studies

  Gottesman and Shields (1972)

  • found that the concordance rate for schizophrenia in MZ twins was 48% compared ti 17% for DZ twins

  Joseph (2004)

  • calculated that the pooled data for all schizophrenia twin studies carried out prior to 2001
  • Showed a concordance rate for MZ twins of 40.4% and 7.4% for DZ twins
• Adoption studies are studies of genetically related individuals who have been reared apart due to being adopted
• Adoption studies allow researchers to overcome the problem of disentangling genetic and environmental influences
• Heston (1966) compared 47 adopted children whose biological mother had schizophrenia with a control group of adopted children with no history of schizophrenia in their biological family
• None of the control group was diagnosed with schizophrenia compared to 16% of the offspring with schizophrenic mothers
• Tienari (2000) study in Finland of 164 adoptees whose biological mothers had been diagnosed with schizophrenia
• 11 (6.7%) were diagnosed with schizophrenia compared to just 4 (2%) of the 197 control group
• Investigators concluded that these findings show the genetic liability to schizophrenia had been decisively confirmed
• Aetologically heterogeneous


  A number of different combinations of genes can cause the condition
• Candidate genes

  Appears that a number of different genes are involved in schizophrenia
• Polygenic


  Schizophrenia can be caused by many different genes
• Most likely genes would be coding for neurotransmitters including dopamine
• Ripke et al. (2014)

  • large study combining all previous data from genome wide studies of schizophrenia
  • genetic make up of 37000 people with a diagnosis of schizophrenia was compared to 113000 controls
  • 108 seperate genetic variations were associated with slightly increased risk of schizophrenia
• The role of mutation

  schizophrenia can have a genetic origin even without family history

  one explanation for this is mutation in parental DNA which can be caused by radiation, poison or viral infection

  Brown et al. (2002)

  • found positive correlations between parental age (associated with increased risk of sperm mutation) and risk of schizophrenia
  • increasing from around 0.7% with fathers under 25 to over 2% in fathers over 50
• Research support for genetic basis- A03

  Strong evidence base for genetic explanation

  Family studies such as Gottesman show that risk increases with genetic similarity to a family member with schizophrenia

  Adoptions studies like Tiernari et al. (2000) show that biological children of parents with schizophrenia are at heightened risk even if they had been adopted

  A recent twin study by Hilker et al. (2018) showed a concordance rate of 33% for MZ twins and 7% fro DZ twins

  Shows that some people are more vulnerable to schizophrenia due to their genes
• Environmental factors-A03

  There’s clear evidnce to show that environmental factors increase the risk of developing schizophrenia

  • like birth complications and smoking THC-rich cannabis in teenage years

  Psychological risk factors include childhood trauma which leaves people more vulberable to schizophrenia

  Morkved et al. (2017)

  • 67% of people with schizophrenia and related psychotic disorders reported at least 1 childhood trauma compared to 38% of a matched control group

  means that genetic factors alone can’t provide a complete explanation for schizophrenia
• Genetic counselling- A03

  • if onbe or more potential parents have a relative with schizophrenia they risk having a child who would go on to develop the condition

  the risk estimate provided by genetic counselling is just an average figure

  • it won;t reflect the probability of a particular chiuld going on to develop schizophrenia becuase they’ll experience a particular environment which also has risk factors

  One application of understanding the role of genes is genetic counselling
• Dopamine hypothesis

  Claims that an excess of dopamine in certain regoins of the brain is associated with the positive symptoms of schizophrenia

  schizophrenics have abnormally high numbers of D2 recptors resulting in more dopaine binging and so more neurons firing.

  It’s important in the functioning of several brain systems related to the symptoms of schizophrenia
• Dopamine

  Generally has an excitatory effect and is linked to the sensation of pleasrue

  • unusually high levels associated with schizophrenia
• Original dopamine hypiothesis

  Based on the discovery that antipsychotics (which reduce dopamine) caused symptoms similar to Parkinsons
• Hyperdopaminergia


  High levels of dopamine
• Schizophrenia might be the result of hyperdopaminergia in the subcortical areas of the brain

  • e.g an excess of dopamine receptors in pathways from the subcortex to Broca’s area may explain specific symptoms of schizophrebua like speech poverty or auditory hallucinations
• Updated versions of the dopamine hypothesis

  Hyperdoaminergia cause positive symptoms

  • particularly in the sub cortical areas of the brain like the mesolimbic pathway

  Addition of cortical hypodopaminergia can cause the negative symptoms

  • abnormally low dopamine in the brains cortex
• Hypodopaminergia


  low levels of dopamine

  Cause negative symptoms
• Low dopamine in the prefronatl cortex could explain cognitive problems
• Suggested that cotical hypodopaminergia leads to subcortical hyperdopaminergia

  • so both high and low levels of dopamine in different brain regions are part of the updated version
• Patel et al. (2010)

  • using PET scans to assess dopamine levels in schizophrenic and normal individuals
  • found lower levels of dopamine in the dorsolateral prefrontal cortec of schizophrenic patients compared to their normal controls
• Howes et al. (2017)

  • seems that both genetic variations and early experiences of stress make some people more sensitive to cortical hypodopaminergia and as a result subcortical hyperdopaminergia
• Evidence for dopmaine- A03

  Curran et al. (2004)

  • Amphetamines increase dopamine and worsen symptoms in schizophrenics and induce symptoms in people without

  Tauscher et al. (2014)

  • antipsychotic drugs reduce dopamine activity and intensity of symptoms

  Some candidate genes act on the production of dopamine or dopamine receptors

  Strongly suggets that dopamine is involved in the symptoms of schizophrenia
• Ineffectiveness of anti-psychotics- A03


  Anti-psychotics fon’t work for everyone

  Anti-psychotics work better for positive symptoms than negative symptoms

  Suggesting other neurotransmitters may have an effect
• Glutamate- A03

  Central role of glutamate goes against dopamine hypothesis

  Post mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regoins of people with schizophrenia

  also several candidate enes for schizophrenia are believed to be involved in glutamate production or processing

  Means there’s a strong case for a role of other neurotransmitters
• Amphetamine psychosis- A03

  Tenn et al. (2003)

  • induced schizophrenia like symptoms in rats using amphetamines and then relieved symptoms using drugs that reduce dopamine action
• Contradictory findings- A03

  Departie and Lal (2001)

  • other drugs that increase dopamine levels (e.g. apomorphine) don’t cause schizophrenia like symptoms

  Garson (2017) challenges the idea that amphetamine psychosis mimics schizophrenia