Biological explanation

• Family studies have confirmed that risk of schizophrenia increases in line with genetic similarity to a relative with the disorder.
• Recent research has found schizophrenia to be polygenic. The most likely genes involved would be those coding for neurotransmitters including dopamine.
• Ripke et al. studied the genetic makeup of 37,000 people with schizophrenia and 113,000 controls. 108 separate genetic variations were associated with slightly increased risk of schizophrenia.
• Because different studies have identified different candidate genes it also appears that schizophrenia is aetiologically heterogenous, i.e. different combinations of factors, including genetic variation, can lead to the condition.
• Another explanation of schizophrenia is mutation in parental DNA which can be caused by radiation, poison or viral infection.
• Evidence for mutation comes from 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.
• The original dopamine hypothesis was based on the discovery that drugs used to treat schizophrenia (antipsychotics which reduce dopamine) caused symptoms similar to those in people with Parkinson’s disease, a condition associated with lower dopamine levels. Therefore schizophrenia might be the result of high levels of DA (hyperdopamimergia) in subcortical areas of the brain.
• For example, an excess of DA receptors in pathways from the subcortex to Broca's area may explain symptoms of schizophrenia such as speech poverty.
• Davis et al. proposed the addition of cortical hypodopaminergia i.e. abnormally low DA in the brain's cortex. Low DA in the prefrontal cortex (responsible for thinking) could explain cognitive problems (negative symptoms of schizophrenia).
• It has also been suggested that cortical hypodopaminergia leads to subcortical hyperdopaminergia (so both high and low levels of DA in different brain regions are part of the updated version).
• Current versions of the dopamine hypothesis also try to explain the origins of this abnormal DA function. It seems that both genetic variations and early experiences of stress, both psychological and physical, make some people more sensitive to cortical hypodopaminergia and hence subcortical hyperdopaminergia (Howes et al.).
• There is a strong evidence base for the genetic explanation. Gottesman's study shows that risk increases with genetic similarity to a family member with schizophrenia. Adoption studies such as Tienari et al. show that biological children of parents with schizophrenia are at heightened risk even if they grow up in an adoptive family. Hilker et al. showed a concordance rate of 33% for identical twins and 7% for non-identical twins. This shows some people are more vulnerable to schizophrenia as a result of their genetic make-up.
• However, there's evidence to show that environmental factors also increase the risk of developing schizophrenia. These environmental factors include both biological and psychological influences. Biological risk factors include birth complications (Morgan et al.) and smoking THC-rich cannabis in teenage years (Di Forti et al.). Psychological risk factors include childhood trauma. Mørkved et al. found that 67% of people with schizophrenia and related psychotic disorders reported at least one childhood trauma as opposed to 38% of a matched group with non-psychotic mental health issues.
• There is support for the idea that dopamine is involved in schizophrenia. First, amphetamines increase DA and worsen symptoms in people with schizophrenia and induce symptoms in people without (Curran et al.). Second, antipsychotic drugs reduce DA and reduce the intensity of symptoms (Tauscher et al). Third, some candidate genes act on the production of DA or DA receptors. This strongly suggests dopamine is involved in the symptoms of schizophrenia.
• A limitation of the dopamine hypothesis is evidence for a central role of glutamate. Post-mortem and live scanning studies have consistently found raised levels of glutamate in several brain regions of people with schizophrenia (McCutcheon et al). In addition, several candidate genes for schizophrenia are believed to be involved in glutamate production of processing. This means that an equally strong case can be made for a role for other neurotransmitters.
• Gottesman found that risk of schizophrenia increases with genetic similarity to a family member with schizophrenia. For example, someone with an aunt with schizophrenia has a 2% chance of developing it increasing to 9% if the individual is a sibling and 48% if they are an identical twin.