Biological explanations Flashcards
Family studies
Strong relationship between the degree of genetic similarity and shared risk of schizophrenia. Gottesman’s (1991) large scale study found (for example) someone with an aunt with schizophrenia has a 2% chance of developing it, 9% for a sibling and 48% for an identical twin. Family members also share the environment but still indicate support for genetic views.
Candidate genes
Early research looked unsuccessfully for a single genetic variation to explain schizophrenia. Schizophrenia is polygenic - requires several genes. It is also aetiologically heterogeneous i.e. risk is affected by different combinations. Ripke et al (2014) combined all previous data from genome wide studies. Found 108 separate genes associated with slightly increased risk of schizophrenia.
Mutation
Schizophrenia can also have a genetic origin in the absence of a family history because of mutation in parental DNA. Evidence comes from the correlation between paternal age (associated with increased risk of sperm mutation) and risk of schizophrenia (Brown et al 2002).
Role of dopamine
Dopamine (DA) is widely believed to be involved in schizophrenia because it is featured in the functioning of brain systems related to the symptoms of schizophrenia.
Original DA hypothesis (Hyperdopaminergia linked to subcortex)
High dopamine activity in subcortex (central areas of the brain) associated with hallucinations and poverty of speech (e.g. excess of DA receptors in pathways linking from subcortex to Broca’s area). May explain specific symptoms e.g. poverty of speech and auditory hallucinations.
Updated version (hypodopaminergia linked to prefrontal cortex)
Updated hypothesis has added low levels of DA in the prefrontal cortex (responsible for thinking) could explain negative symptoms. Explain origins of abnormal DA - genetic variations and early experiences of stress make some people more sensitive to cortical hypodopaminergia and hence subcortical hyperdopaminergia (Howes et al).
A03:One strength of the genetic explanation is the strong evidence base.
Family studies (e.g. Gottesman) shows risk increases with genetic similarity. Twin studies found 33% concordance for MZ and 7% for DZ twins (Hilker et al 2018). Adoption studies (e.g. Tienari et al 2004) show that biological children of parents with schizophrenia are at greater risk even if they grow up in an adoptive family.
This shows that some people are more vulnerable to schizophrenia because of their genes.
A03:One limitation of the genetic explanation is evidence for environmental risk factors.
Biological risk factors include birth complications (Morgan et al 2017) and smoking THC-rich cannabis in teenage years (Di Forti et al 2015). Psychological risk factors include childhood trauma e.g. 67% with schizophrenia (38% matched controls) reported at least one childhood trauma (Morkved et al 2017).
This means genes alone cannot provide a complete explanation for schizophrenia.
A03:One strength is support for dopamine in the symptoms of schizophrenia.
Amphetamines (increase DA) mimic symptoms (Curran et al 2004). Antipsychotic drugs (reduce DA) reduce intensity of symptoms (Tauscher et al 2014). Candidate genes act on the production of DA or DA receptors.
This strongly suggests that dopamine is involved in the symptoms of schizophrenia.
A03 (counter):One limitation is evidence for the central role of glutamate.
Post-mortem and scanning studies found elevated glutamate in people with schizophrenia (McCutcheon et al 2020). Also, several candidate genes for schizophrenia are believed to be involved in glutamate production or processing.
This means that a strong case can be made for a role for other neurotransmitters in schizophrenia.
