Biological Explanations Flashcards
Outline the role of family studies of Schizophrenia for the biological explanation for Schizophrenia
Gottesmann (1991) found someone had a:
2% chance if aunt/uncle
9% chance if sibling
48% if identical twin
Had Schizophrenia
Family members tend to share aspects of environment as well as genes, so correlation represents both but family studies still give good support for importance of genes
Outline the role of candidate genes for the biological explanation for Schizophrenia
-Early research looked for single genetic variation in belief one faulty gene could explain Schiz
-Number of genes involved (polygenic), most likely genes are coding for neurotransmitters including dopamine
-Ripke et al. (2014) combined from genome-wide studies of Schiz
-Genetic make up of 37,000 Schizos compared to 113,000 controls, 108 separate genetic variations associated with slightly increased risk of Schiz
-Bc different studies identified different candidate genes it appears Schiz is aetiologically heterogenous
Outline the role of mutation in the biological explanation for Schizophrenia
-Schiz can also have genetic origin in absence of family history of disorder
-One explanation is mutation in parental DNA, caused by radiation, poison or viral infection
-Evidence for mutation comes from positive correlations between paternal age & risk of Schiz
-Increases from around 0.7% with fathers under 25 to over 2% in father over 50
Outline the dopamine hypothesis for the neural correlates of Schizophrenia for the biological explanations for Schizophrenia
-Based on discovery drugs treating Schiz caused similar symptoms to Parkinson’s - condition with low levels of dopamine
-Thus, Schiz may be result of high dopamine levels in subcortical areas of brain
-E.g. excess of DA receptors in pathways from subcortex to Broca’s area may explain specific symptoms of Schiz like speech poverty
Outline the updated versions of dopamine hypothesis for the neural correlates of Schizophrenia for the biological explanations for Schizophrenia
-Davis et al. (1991) proposed addition of low DA in brain’s cortex (hypodopaminergia)
-Low DA in prefrontal cortex could explain cognitive problems (negative symptoms)
-Been suggested cortical hypodopaminergia leads to subcortial hyperdopaminergia, so both high & low levels of DA in different brain regions part of updated version
Evaluate the genetic basis for Schizophrenia as an explanation for Schizophrenia
STRENGTH - Research Support
E.g. -Family studies like Gottesmann (1991) Show risk increases with genetic similarity to family member with Schiz
Adoption studies like Tienari et al. (2004) show bio children of parents with Schiz at higher risk even if growing up in adoptive family
Twin study by Hilmer et al. (2018) showed concordance rate of 33% for identical twins & 7% for non-identical
Ex. - Shows some more vulnerable to Schiz as result of genetic make up
LIMITATION - Environmental included bio & psych factors
E.g. - Bio = birth complications & smoking THC-rich cannabis in teenage
Pysch = childhood trauma, leaving high vulnerability to adult mental health issues, linked with Schiz
Mørkved et al. (2017) found 67% of Schizos & related psychotic conditions reported min. 1 childhood trauma opposed to 38% of matched group with non-psychotic mental health issues
Ex. - Genetic factors alone isn’t complete explanation
STRENGTH - Genetic counselling
E.g. -If 1+ potential parents have relative with Schiz, they risk having child developing condition
HOWEVER: Risk estimate provided by genetic counselling just average figure
Ex. - Won’t really reflect probability of particular child developing as they’ll experience particular environment
Evaluate the dopamine hypothesis
STRENGTH - Evidence for dopamine
-Amphetamines increase DA & worsen symptoms with Schizos & induce symptoms in people without
-Antipsychotics drugs reduce DA activity & reduce intensity of symptoms
-Some candidate genes act on production of DA or DA receptors
-Suggests DA involved in symptoms of Schiz
LIMITATION - Evidence for glutamate role
-Post-mortem & live scanning studies consistently found raised levels of neurotransmitter glutamate in several brain regions of Schizos
-Several candidate genes for Schiz believed to be involved in glutamate production/processing
-Means equally strong case can be made for role for other neurotransmitters
