Discuss biological explanations of schizophrenia. (8+16) Flashcards
2 explanations
The Genetic Explanation, Biochemical Explanation
Genetic Explanation
The brain is the source of all mental states, schizophrenia is a disorder of mental states. If genes determine brain structure/neurochemistry, and these determine our thoughts and behaviours, then we can inherit psychological traits, including psychopathology
Liability threshold model
Most behavioural geneticists believe that there are a number of genes that each have a small effect, though some have more of an effect than others - the more of these genes you have, the higher is your risk of schizophrenia
Molecular genetics
Glatt - meta-analysis identifies an association between the dopamine D2 receptor gene and schizophrenia. The risk of developing schizophrenia was shown to increase by 30% in relation to a defect in the gene
Allen
showed 24 genetic variants in 16 different genes were strongly associated with an increased risk of schizophrenia - 4 of the top 10 variants are directly involved in dopaminergic pathways
Gottesman Review
based on the pooled results of about 40 studies - MZ twins reared together - 48%, DZ twins reared together - 17%, MZ twins reared apart - 58%
Kendler
based on pooled concordance estimate from a number of studies - MZ twins reared together - 53%, DZ twins reared together - 15%
Cardno et al
using the Maudsley twin register - MZ twins reared together - 50%, DZ twins reared together - 4.1%
Methodological Issues of Twin studies
Shared environment - raised similarly so unsure whether the environment was the cause of the schizophrenia
Tienari (1987)
Finnish adopted children who had schizophrenic mothers had a 7% chance of developing schizophrenia compared to 1.5% of the controls (who were also adopted children, with non-schizophrenic) mothers. Adoptees ranged from 5-7 years at the start of the study and had all been separated from their mother before the age of four
Tienari (2000)
the risk for developing schizophrenia was 4 times greater in adopted children with schizophrenic mothers compared to adopted children from biological mothers without schizophrenia
Kety et al
study of a national sample from Denmark - high rates of schizophrenia were found in adopted children whose biological parents were schizophrenic, even though they had been adopted by ‘healthy’ parents
Wahlberg
re-examined the Tienari et al data and found a strong effect of environmental factors where those at risk of developing schizophrenia were adopted into families with poor communication
Methodological issues in adoption studies
Selective placement - adoptive parents were likely to be aware of mental illness in genetic parents because the states where studies took place made such information available - adoptees with a mother with schizophrenia are more likely to be placed in more ‘psychologically harmful’ homes
The dopamine hypothesis
If genetic factors are important in the development of schizophrenia they might exert influence on brain hardware. Biochemical abnormalities might therefore be detectable in the brains of those diagnosed with schizophrenia. The biochemical interest has focused don the role of neurotransmitters
Dopamine
is a neurotransmitter found on the limbic system of the brain - the limbic system is involved in regulating and emotion so disturbances to dopamine levels might contribute to the agitation seen in schizophrenia
Basal Ganglia
(Dopamine is also found in the basal ganglia) - regulates movement and emotion. Abnormal levels might therefore contribute to the symptoms of paranoia and hallucinations
Psychotic symptoms are a result of:
super-sensitivity of dopamine receptors, excess of dopamine receptors, increased synthesis and release of dopamine from the pre-synanptic neuron
Antipsychotics work
if dopamine hypothesis is correct then anti-psychotics should work / they don’t always work for all patients, only on positive symptoms - low etiological validity
L-dopa produces symptoms of schizophrenia
(Parkinson’s patients) increases dopamine levels, can produce symptoms of schizophrenia in previously unaffected individuals / not always the case
Recreational use of amphetamines
stimulant drug which increases the availability of dopamine and noradrenaline in the brain, can induce symptoms of schizophrenia / do not always worsen symptoms in all people diagnosed with schizophrenia
Post mortem evidence
Seeman - reviewed a number of studies which found increases in dopamine receptor density between 60% and 110% compared to controls / post mortem examinations have usually been carried out on people who have taken neuroleptic drugs for years - difficult to tell whether dopamine levels are the result of drug therapy rather than the cause of schizophrenia
PET scan - Wong
Found a two-fold increase in the density of dopamine receptor sites in schizophrenic patients who had never been treated with drugs compared to patients who had been treated with drugs and to a control group / Farde - later PET scan studies have not replicated the results
Howes and Kapur
stated that the locus of dopamine dysfunction is pre-synaptic, involving increased synthesis and tendency to release the neurotransmitter. This might help to explain why drug treatment is not successful for all patients. Current drugs target dopamine receptors and are acting ‘downstream’ rather than ‘upstream’.
Diathesis-stress model
In the 1960s many researchers believed that schizophrenia was a wholly genetic disorder. However, most now think that genes increase your risk of schizophrenia, but that these interact with environmental factors. Schizophrenia will not develop in those without those genes, whatever the environmental factors, but those with the genes are affected by environmental stressors
Tienari (Diathesis-stress)
Adoptees high risk + disturbed family = schizophrenia
Adoptees high risk + healthy family = schizophrenia well below general population rates
Adoptees low risk + disturbed family = no schizophrenia
