Biological explanations of schizophrenia

• Family studies

  The risk of schizophrenia increases with genetic similarity to a relative with the condition. For example, Gottesman found if your aunt has it there's a 2% chance, 9% if it’s a sibling, 48% if it’s an identical twin.
• Candidate genes for Schizophrenia

  Sz is polygenetic. Most likely the genes would be those coding for neurotransmitters including dopamine. Ripke et al. (2014) combined all previous data from genome-wide studies of Sz. 108 separate variations were associated with slightly increased risk of Sz. Different studies have identified different candidate genes so Sz is aetiologically heterogenous (different combinations of factors including genetic variation, can lead to the condition)
• The role of mutation

  Sz can also have a genetic origin without the presence of a family member with the disorder.

  This may be explained by a mutation in parent DNA which can be caused by radiation, poison or viral infection. Evidence for mutation comes from positive correlations between paternal age (associated in increased risk of sperm mutation) and risk of Sz, increasing from around 0.7% with fathers under 25 to over 2% in fathers over 50 (Brown et al. 2002)
• The original dopamine hypothesis

  Based on the discovery of anti-psychotic drugs used to treat Sz that reduce dopamine caused symptoms similar to Parkinson's, a disease associated with low dopamine levels. Therefore Sz may be a result of high dopamine levels (hyperdoperminergia) in subcortical (involved in complex activities such as memory, emotion, pleasure and hormone production) areas of the brain. E.g. in the Broca's area. This may explain specific symptoms such as speech poverty and/ or auditory hallucinations.
• Updated dopamine hypothesis

   Kenneth Davis et al. (1991) proposed the addition of cortical hypodopaminergia  (abnormally low dopamine in the brain cortex) to explain negative symptoms e.g. how low dopamine in the prefrontal cortex could cause cognitive problems. It has also been suggested low dopamine in the cortex leads to high dopamine levels in subcortex-both high and low levels of dopamine in different areas are involved.
• Vulnerability to cortical hypodopaminersia

  It seems genetic variations and early experiences of stress, both psychological and physical, make some people more sensitive to cortical hypodopaminergia and therefore subcortical hyperdopaminergia. (Howes et al. 2017)
• Strength of genetic explaination

  A strength is there is a strong evidence base. Family studies like Gottesman's show that risk increases with genetic similarity to a family member with Sz. Adoption studies such as Tienari et al (2004), show biological children of parents with Sz are at heightened risk even if they grow u in an adoptive family. A twin study by Hilker et al. (2018) found a concordance rate of 33% for identical twins and 7% for non-identical twins. Showing people are more vulnerable to schizophrenia as a result of genetics.
• Limitation of the genetic explanation

  There is clear evidence for an environmental influence. Biological risk factors include birth complications and smoking THC-rich cannabis in teenage years. Psychological factors include childhood traumas, leaving people vulnerable to adult mental health problems. Morkved et al. (2017) found 67% of people with Sz and related psychotic conditions reported at least one childhood trauma opposed to 38% of a matched group with non-psychotic mental health issues. This means genetic factors alone cannot provide a complete explanation for Sz.
• Support for the dopamine hypothesis

  There is support for the idea dopamine is involved in Sz. Amphetamines increase dopamine and worsen symptoms in people with Sz and can induce symptoms in people without Sz. Second, antipsychotic drugs reduce dopamine and also reduce the intensity of symptoms. Third, some candidate genes act on the production of dopamine or dopamine receptors. This strongly suggests that dopamine is involved in the symptoms of schizophrenia.
• Limitation of the dopamine hypothesis

  A limitation is there is evidence for a central role of glutamate. Post-mortem and live scanning studies have consistently found raised levels of neurotransmitter glutamate in several brain regions of people with Sz. In addition, several candidate genes for Sz are believed to be involved in producing glutamate or processing. This means that an equally strong case can be made for the role of other neurotransmitters.
• Amphetamine psychosis and the dopamine hypothesis

  Tenn et al (2003) induced Sz like symptoms in rats using amphetamines and the relived symptoms using drugs that reduces dopamine action. This supports the dopamine hypothesis. However, other drugs also increased dopamine levels do not cause Sz like symptoms.
• Limitation of genetic explanations application

  If one or more parents has a relative with Sz, they risk having a child that may develop Sz. However, the risk estimate provided by genetic counselling 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 with also has risk factors.