The biological approach assumes that schizophrenia is a real and discrete illness, just like any physical illness.
What are genes?
Genes are sections of DNA that code for the proteins that make up our bodies and brains.
We inherit our genes from our parents, and will look at how schizophrenia runs in families, and what genes might cause vulnerability to psychosis.
Genetic inheritance is the single biggest risk factor for schizophrenia.
People have different versions (known as alleles) of the same genes. These arise from random mutation, and are passed on from parent to child.
There are two components to the genetic explanation:
Heredity
Candidate genes
Heredity explanation:
Heredity is defined as the manner in which characteristics and traits are passed on from parent to offspring.
Research into heredity traits of schizophrenia look at degree of relatives: parents are first degree and share around 50% of their genetic variation. Second degree relatives share 25% of their genetic variation such as uncles
Heredity explanation:
If a condition is hereditary, the closer the degree of relatives the more likely they are to share the same condition.
Family studies are used to compare rates of schizophrenia in relatives of people with a diagnosis - it has found that the risk rises with the degree of relatedness to an affected individual.
Heredity explanation: study
The Copenhagen high-risk study was a longitudinal study that identified 207 offspring of schizophrenic mothers and compared them with a match group of 104 offspring of non-schizophrenic mothers.
They found that 16.2% of the high-risk group had been diagnosed with schizophrenia compared with just 1.9% of the low-risk group.
This concludes that theres a substantial genetic component for schizophrenia.
Heredity explanation: evaluation
Gottesmans study 1982:
They used 57 twin pairs where at least one twin had an existing diagnosis of schizophrenia.
They assessed the concordance rates for schizophrenia using multiple data collection methods.
They found a concordance rate of 75% for monozygotic twins with 'severe' schizophrenia compared to only 22% of dizygotic twins.
MZ twin share 100% DNA and so the concordance rates should be 100%, but the concordance rates in this study isn't 100% suggesting other influential factors.
Heredity explanation: evaluation
Adoption studies are used to asses heritability of schizophrenia.
The Finnish adoption study identifies 112 adopted children whose biological mothers had been diagnosed with schizophrenia.
They found that the children had all been adopted by age 4 and 7% of the offspring from a biological mother had been diagnosed with schizophrenia.
Candidate genes explanation:
A 2016 genome sequencing study involved 65,000 people's DNA found that genes involved in synaptic pruning were linked to schizophrenia.
The scientists suggested that a variant of the complement 4 (C4) gene may cause schizophrenia by promoting excessive synaptic pruning during brain development.
They also found other genes involved in synaptic pruning 0 schizophrenia is polygenetic.
Dopamine Hypothesis:
The dopamine hypothesis says that people with schizophrenia have abnormalities in dopamine neurotransmissions.
Dopamine is a neurotransmitter that is particularly active in the limbic system which controls basic emotions and drives.
The hypothesis says that excess dopamine activity in this area (the mesolimbic pathway) could cause the symptoms of schizophrenia such as hallucinations.
Dopamine hypothesis: evidence
Brain imaging:
Using PET scansWong et al 1986 found two-fold increase in the density of postsynaptic dopamine receptors in a group of schizophrenic patients who had never been treated with drugs.
Wong's study isn't reliable as no one has replicated it.
Dopamine hypothesis: evidence
Post-mortem studies
Analysis of the brains of schizophrenic patients after death show increased dopamine receptor density in parts of the limbic system of the brain of schizophrenic patients.
A limitation of post mortem studies is that the patients were usually receiving dopaminergic drugs in their lifetime which may amount for the receptor changes.
Neural correlates of schizophrenia
Neural correlates refers to the search for brain areas and pathways involved in schizophrenia.
Enlarged ventricles are characteristics of schizophrenia, as the ventricles are simply fluid-filled cavities in the brain, this suggest that the surrounding grey matter of the brain has shrunk.
This suggests that schizophrenia has damaged the brain tissues.
Neural correlates: Superior temporal gyrus
This area is thought to control the process of speech and has been linked to positive symptoms of schizophrenia such as hallucinations.
Schizophrenic patients showed reduced volume of grey matter in the superior temporal gyrus suggesting that those who are schizophrenia have an abnormal superior temporal gyrus.
Neural correlates: Auditory hallucinations
When a person experiences auditory hallucinations, there is increased activity in brain areas responsible for auditory perceptions and speech production.
This has been demonstrated in many PET and fMRI studies.
Neural correlates: evaluation
The dopamine hypothesis may be an oversimplification - while dopamine abnormalities in the mesolimbic and prefrontal lobe do exist, recent research indicates that glutamate, GABA and serotonin alterations are involved in the acquisition of schizophrenia.
Neural correlates: evaluation
many schizophrenic psychologists and researchers have argued that biological explanation are too reductionistic. It reduces the illness down to the basic units of genes and neurotransmitters.
it ignores other explanation and inferences such as personal experiences and environmental as well as cognitive influences.
Neural correlates: evaluation
Even though there is plenty of evidence to support the dopamine theory and genetic explanation, it cannot be the whole picture. Other biological influences might also implicate the vulnerability to schizophrenia such as brain structures.