SCHIZOPHRENIA explanations Flashcards
(25 cards)
biological explanations
genetic
biochemical
psychological explanations
cognitive
genetic explanations
classic research
contemporary research
digeorge and the COMT gene
classic research
heritability of the disorder
eg…the concordance rate for monozygotic twins is 42% but dizygotic is 9% (gottesman and shields 1966)
since MZ and DZ were raised in the same household the higher concordance rate in MZ twins was thought to be due to greater shared DNA
contemporary research
genome-wide association studies (GWAS)
some genes are polymorphic meaning they come in different forms
GWAS studies have helped to identify which versions (alleles) are more common in people with schizophrenia
however the genetics of schizo is extremely complex; thousands of gene variant have been linked to this complex condition (smeland et al 2020)
therefore it is referred to as polygenic
often the affected genes are linked to the many different proteins associated with the development (synthesis), transportations and breakdown of neurotransmitters such as dopamine
this means the inheritance of certain alleles may be responsible for neurochemical imbalances associated with schizophrenia
digeorge and the COMT gene
aside from the inheritance of less than favourable alleles sometimes problems arise during cell division and whole strands of DNA become duplicated or even deleted
causes a printing error in the biological manual
can increase a person’s risk of developing schizophrenia
eg…in digeorge syndrome a strand of DNA containing 30-40 genes is deleted from chromosome 22
1 in 4 people with this condition develop schizo
compared with less than 1 in 100 without digeorge syndrome
this has been linked to the deletion of a specific gene called COMT (kim et al 2020)
this gene codes for an enzyme which breaks down neurotransmitters such as dopamine
this suggests that the absence of this gene could be partially responsible for the complex neurochemical imbalances that seem to underpin the symptoms of schizophrenia
some researchers believe the ‘disrupted in schizo’ or the DISC1 gene increases the risk of schizo due to its association with neurotransmitter GABA
GABA is an inhibitory neurotransmitter which helps to regulate activity in neural circuits that communicate via dopamine and glutamate
an abnormality of this gene could therefore increase vulnerability to excess dopaminergic activity
and subsequent symptoms of schizo
genetic EVAL strengths
supported by research and evidence
two versions of COMT gene called MET and VAL
VAL allele is associated with decreased dopamine activity in the prefrontal cortex, decreased cognitive performance and a slightly elevated risk of schizo (egan et al 2001)
important evidence to support both the role of genetic factors and the dopamine deficiency hypothesis
some evidence to suggest the effect of the VAL allele on cognition may be stronger in men than women w schizo (wang et al 2020)
also research evidence to support the role of the DISC1 gene variant in schizo
a large scottish family with an unusually high rate of schizo
34 family members carried this gene (st claire et al 1990)
more recently a meta analysis of the findings of 14 animal experiments suggests that this may be linked to the impact of DISC1 on presynaptic dopamine dysregulation (dahoun et al 2017)
this is an important finding as animal experiments are tightly controlled
meaning the findings have greater internal validity
contribution of DISC1 is highly contested and has been linked to other mental health conditions in addition to schizo (sullivan 2013)
genetic EVAL issues and debates
nature vs nurture
although there are a wealth of twin studies to support the role of genetics/nature in schizo
validity of these findings is questionable
assumed that MZ twin pairs living in the same household will be exposed to environmental factors that are similar to pairs of DZ twins
but this is highly unlikely
as MZ twins are always the same gender, look similar than DZ twins and more likely to share similar temperaments, they’re more likely to be parented more similarly than DZ twins
this means that the degree of both genetic and environmental similarity differs between MZ and DZ twins
making it impossible to infer that the higher concordance rate for schizo in MZ twins is due to them sharing 100% of their DNA
suggests nurture might play a greater role in schizo than prev thought
reductionism vs holism
overly reductionist
limit awareness of the range of treatment options
genome may impact the way we process info and experience the world, research suggests it’s possible to train ourselves to interpret our thoughts in more beneficial ways
CBT as a way for managing both pos and neg symptoms
demonstrates that nurture can override nature when environmental experiences are carefully curated
biochemical explanations
excess dopamine
dopamine deficiency hypothesis
excess dopamine
in the 1960s arvid carlsson and margot lindqvist proposed schizo was caused by an excess of the neurotransmitter dopamine
deep in the brain’s limbic system and mesolimbic pathways (carlsson and lindqvist 1963)
this excess can be caused by many factors such as excess L-Dopa the substance dopamine is made from
synapses that use dopamine may also be overactive due to diff in the number of receptors in the postsynaptic cell
over time new evidence caused scientists to update this explanations
for example many people who were taking dopamine antagonists like chlorpromazine still suffered w neg symptoms
and some experienced no improvement in symptoms at all
dopamine deficiency hypothesis
kenneth davis and colleagues suggested that a lack of dopamine in the prefrontal cortex and mesocortical pathways may explain the negative and cognitive symptoms (davis et al 1991)
symptoms such as disorganised thinking and speech could result from problems with dopamine regulation
neurotransmitter is important for shifting and directing attention
over the years, further contradictory evidence revealed that updated hypothesis still oversimplified
overactivity in the mesolimbic pathways thought to result from excess D2 dopamine
2006 arvid and maria carlsson proposed the dopamine deficiency hypothesis
brain compensates for low levels of dopamine by increasing the number of receptors in the postsynaptic cell
upregulation
biochemical EVAL issues and debates
nature vs nurture
reductionism vs holism
determinism vs free will
biochemical NATURE NURTURE
a strength of the dopamine hypothesis and thus the role of nature is that there is wealth of evidence to support this explanation of schizo
in one study, rats were injected with amphetamines over a three week period, which is known to increase dopamine activity (tenn et al 2003)
the rats showed a range of schizo like behaviour including social withdrawal and strange movements
furthermore the rats’ symptoms were alleviated when they were given drugs to block their D1 dopamine receptors
this supports the role of bio factors/nature in schizo
but also underlines the importance of environmental factors/nurture such as taking drugs
despite many studies supporting the role of a dopamine dysfunction as a potential cause of schizo, depatie and lal 2001 found that apomorphine, a dopamine agonist, does not worsen symptoms in people who already have schizo
neither does it trigger symptoms in those that do not
findings such as these are harder to explain
may be more complicated
highlighting the role of nurture in predicting the impact of bio factors
biochemical REDUCTIONISM HOLISM
limitation of all the diff dopamine hypothesis is they are highly reductionist
the idea that a single neurotransmitter is responsible for schizo is no longer accepted
drugs such as clozapine which block dopamine and serotonin receptors are more effective than drugs that only block dopamine receptors
and the efficacy of new drugs such as glutamate agonists suggests that an exploration or the interactions between a wide range of neurotransmitters may prove more fruitful than studies that focus on single neurotransmitters
taking a holistic approach and recognising how neurotrasmitter levels are affected by experiences in the world and the ways in which we interpret them is also critical
prognosis of conditions like schizo can be affected by numerous individual and situational factors due to their impact on our biology
biochemical DETERMINISM VS FREE WILL
biological explanation of schizo is deterministic in that it suggests that the workings of the brain are responsible for the symptoms of schizo
research using PET brain imaging for eg demos that the people diagnosed with schizo have decreased binding on their prefrontal D1 dopamine receptors in comparison with matched controls without schizo (okubo et al 1997)
furthermore there were significant correlations between D1 binding, severity of neg symptoms and performance on the wisconsin card sorting test (a measure of cognitive ability)
this supports dopamine deficiency as an explanation of neg and cognitive symptoms and the role of biological determinism
cognitive explanations background
prof chris frith acknowledges that discussions about dopamine do not really explain the subjective experience of voice hearing
likewise as fascinating as up and down regulation may be, neither explains the development of bizarre false beliefs such as having one’s thoughts extracted by aliens or gov spies
in the 1990s he advanced one of the first cognitive explanations of schizo assuming both pos and neg symptoms result from faulty info processing
cognitive explanations
errors in self monitoring
difficulties with mentalising
thinking errors and biases
errors in self monitoring
internal monologue
can’t distinguish between them
may mistakenly perceive their sub vocal thoughts as coming from an external source
this is known as self monitoring error
helps explain auditory hallucinations
link between abnormal sensory experience/hallucinations and experiences of influence and the formation of delusions/false beliefs
difficulties with mentalising
baron cohen et al 2001 core
ASD process social info diff
schizo has some overlaps with autism and frith (1992) believes that difficulties in mentalising may result in persecutory delusions and paranoia
if people with schizo have difficulty understanding mental states/intentions
neutral states can be misinterpreted as hostility
under developed theory of mind may mean that people with schizo believe that others have the same opinion of them as they have of themselves
thus if a person with schizo believes they are a bad person they may believe others think the same
symptoms like social withdrawal neg symptoms may result from difficulties people with schizo have in the social work which may be perceived as a dangerous and threatening place
thinking errors and biases
discover new info in the world that confirms or refutes our beliefs
leads us to modify our views in light of new evidence
in schizo abnormal beliefs may be formed and maintained if people fail to update understanding based on new evidence
people with schizophrenia tend to draw conclusions based on insufficient evidence and show a bias against counter-evidence
info that disconfirms their delusions
these errors of judgement and biases explain why people with schizo hold bizarre beliefs even in the face of conflicting evidence
cognitive EVAL issues and debates
individual situational
reductionism holism
cultural differences
idiographic nomothetic
individual situational
INDIVIDUAL
Individual Explanation of Schizophrenia
Inner Speech Misattribution: Hallucinations may result from misattributing one’s own inner speech.
Allen et al (2007): Ps with schizophrenia who hear voices more likely to say their own words were spoken by someone else. Brain activity did not differ between own/others’ voices, unlike controls → suggests different info processing and biological basis.
Thinking Errors:
Garety et al (1991): In a beads task, people with schizophrenia made quicker, less accurate judgments based on fewer pieces of evidence (jumping to conclusions).
Interaction:
Cognitive deficits may predispose to psychosis, but situational factors (e.g., stress) trigger symptoms.
reductionism vs holism TOO REDUCTIONIST
Evidence supports cognitive deficits in delusions/hallucinations, but unclear why deficits occur.
Cognitive theories = reductionist; explain how symptoms develop but not why thinking differs.
Only a partial account — holistic approaches (biological, cognitive, social) offer fuller explanation.
cultural differences
Not everyone with cognitive deficits (e.g., poor mentalising) develops schizophrenia — similar deficits seen in autism/ADHD.
Sociocultural factors (beliefs, values, attitudes) shape how mental experiences are interpreted.
Cultural views on voice hearing affect distress levels and symptom severity.
Social attitudes impact wellbeing → importance of destigmatising mental health.
Schizophrenia best explained by interaction of genetics + environment (e.g., diathesis-stress model).
