Biological Explanations For Schizophrenia Flashcards
Schizophrenia may be inherited. What do contemporary views suggest?
That heredity explains at least 50% of the cause of schizophrenia
What does the biological theory suggest?
That it is very unlikely that there is no one gene which causes schizophrenia but possessing a certain combination of genes makes you more susceptible to developing the disorder
Where does evidence for the biological explanation come from?
Twin studies
Family studies
Adoption studies
What evidence do twin studies give?
As MZ twins share 100% of their genes but DZ twins only share 50%, if schizophrenia was a genetic disorder we would expect that the concordance rate for MZ would be much greater then go DZ twins
Explain Gottesman and Shields (1982) meta-analysis study
Meta-analysis of 5 twin studies
Found that average concordance rate for MZ twins was 46% and for DZ twins 14%
What did Gottesman and Shields conclude from their 1982 study?
As MZ twins have greater concordance rates than DZ twins this supports a genetic explanation of schizophrenia, because MZ twins share 100% of their genes, compared to DZ twins who only share 50% of their genes
MZ twins are often treated more similarly. Why is this a weakness of twin studies?
As they tend to grow up in MORE SIMILAR ENVIRONMENTS (Lytton, 1977) than DZ twins, this suggests that it may be this which causes higher levels of concordance between them
What is the aim of family studies?
Family studies find individuals who have schizophrenia and determine whether their biological relatives are similarly affected more often than non-biological relatives.
What is the main point of family studies?
Schizophrenia tends to run in families
What have family studies found?
That schizophrenia is more common among biological relatives of a person with schizophrenia
What did Gottesman (1991) find? (Family studies)
That children with 2 schizophrenic parents have a concordance rate of 46%, children of one schizophrenic parent 13% and siblings 9%
(General pop 1%)
Does Gottesman’s family study support a genetic explanation?
YES because it shows that compared to the general pop, you are significantly more likely to develop schizophrenia the more genes you share with someone who has schizophrenia
NO, would be 100% if completely caused by genes
What is an alternative explanation as to why schizophrenia may run in families?
Nurture - similar/same upbringing
Family studies do not remove environmental influences. Why is this a weakness?
members of the same family share a SIMILAR ENVIRONMENT so the higher risk of close family members could reflect elements of a common environment such as STRESS or SOCIAL LEARNING rather than genetic factors
Why are adoption studies unique?
They are able to separate the effects of environment and genes
What did Heston (1966) find in his early adoption study of 47 mothers with schizophrenia whose children were adopted within days by psychiatrically well mothers?
An incidence of schizophrenia in the group to be 16% (well above the 1% chance level)
How many adoptees were in Heston’s control group, and what was their common history?
50
No history of schizophrenia in either their biological or adoptive family
How many of Heston’s control group went on to develop schizophrenia?
None
What can Heston conclude from his adoption study?
Supports the genetic explanation, because group who shared genes (with schizophrenic mother) 16% developed schizophrenia
Why does Heston’s adoption study not fully support a genetic explanation?
The concordance rate would be 50% if schizophrenia was solely caused by genes
What are the limitations of adoption studies?
An assumption of adoption studies is that ADOPTEES are NOT ‘SELECTIVELY PLACED’ - I.e. Adoptive parents whose adopt children with a schizophrenic biological parent are no different from adoptive parents who adopt children whose background is normal
Adoption studies are not definitive. Why is this a weakness?
This means that they are not he most reliable or complete as it assumes that ADOPTEES are NOT SELECTIVELY PLACED
A broader definition of schizophrenia could be looked at. Why would this be a strength?
Taking into account people who GO ON TO DEVELOP DISORDERS then CONCORDANCE RATE are EVEN HIGHER than those seen in the studies
Research evidence clearly supports the role of a genetic predisposition for schizophrenia. Why is this a strength?
(eg Heston) more likely to be correct
Twin studies are incomplete. Why is this a weakness of genetic explanations?
The data shows that schizophrenia can only be in part genetic. If the disorder were purely genetic, then MZ TWINS would show a 100% concordance rate as they are GENERICALLY IDENTICAL
No single gene for schizophrenia had been identified. Why is this a limitation if the genetic explanation?
The present view is that multiple genes located on different places on the chromosome are involved - each gene is innocent in itself but that people who inherit a no. of them are at a high risk of developing schizophrenia
It is unclear whether increased concordance rates are due to nature or nurture. Why is this a weakness of he genetic explanation?
The higher MZ than DZ rates would be predicted by environmentalists, as MZ pairs have a MORE SHARED ENVIRONMENT than DZ pairs and are often treated more similarly.
Conclusion - does a genetic explanation give a complete explanation?
It appears that INHERITANCE DOES PLAY A PART in schizophrenia but CANNOT offer a COMPLETE EXPLANATION
Explain the Diathesis-Stress model
Suggests individuals may be BIOLOGICALLY PREDISPOSED to DEVELOP the DISORDER, but it is not certain that they will. ENVIRONMENTAL FACTORS are required to TRIGGER off this predisposition such as STRESS
Describe the early dopamine hypothesis
Excess levels of the neurotransmitter dopamine in the brain was the cause of schizophrenic symptoms
What does dopamine do?
Acts to INCREASE the RATE of FIRING at the SYNAPSE, ENHANCING COMMUNICATION between NEURONS and leads to the characteristic symptoms of schizophrenia
Where does evidence for the dopamine hypothesis comes from?
Post mortems
Amphetamine
Parkinson’s disease
Antipsychotic drugs
What is the evidence from amphetamine?
When taken by healthy individuals, drugs that INCREASE DOPAMINERGIC ACTIVITY in the brain result in PSYCHOTIC SYMPTOMS like those experienced by schizophrenics (eg hallucinations)
What are the two different biological explanations for schizophrenia?
Genetics
Neurochemical
What is the evidence from post mortem for the old dopamine hypothesis?
Post mortem of schizophrenia sufferers tend to show high levels of dopamine (Iverson 1979)
What is the evidence from Parkinson’s disease for the old dopamine hypothesis?
Low levels of dopamine are found in people with Parkinson’s disease. When they are treated with amphetamine type drugs, which increase dopamine levels, often report hallucinations as a side effect
What is the evidence from antipsychotic drugs for the old dopamine hypothesis?
Such as Chlorpromazine, block dopamine activity in the brain. They are a dopamine antagonist. By reducing stimulation of dopamine, these drugs eliminate positive symptoms such as hallucinations and delusions
Evidence for the old dopamine hypothesis was inconsistent. Why was this a weakness?
eg post mortem studies did not show how consistent evidence for increased dopamine levels in the brains of schizophrenics
Less likely to be true
What is the new dopamine hypothesis?
That the cause is not just an INCREASE in DOPAMINE but is the RESULT of HEIGHTENED SENSITIVITY of RECEPTORS OF DOPAMINE in the brain. Schizophrenics have ABNORMALLY HIGH NO. OF D2 RECEPTORS on receiving neurons, resulting in more dopamine binding and therefore more neurons firing. This then leads to EXCESSIVE DOPAMINE and resulting schizophrenic symptoms
Where does evidence for the new dopamine hypothesis come from?
PET scans
Post-mortem studies
Phenothiazine and Chlorpromazine are neuroleptic drugs which block the D2 receptor sites. Why is this a strength of the dopamine hypothesis?
Therefore they prevent the normal neurotransmission carried out by dopamine, resulting in decreased dopamine activity. Schizophrenics taking these drugs have fewer and less severe positive symptoms
The dopamine hypothesis is incomplete due to cause and effect. Why is this a weakness of he hypothesis?
As with any correlation, it is not possible to identify CAUSE and EFFECT
It may well be that raised levels of dopamine/D2 receptors are an effect of schizophrenia NOT the cause
Pearlson et al (1993) used neuroimaging studies to rule out cause and effect problem. Explain this strength
Neuroimaging studies were carried out on schizophrenic patients who had not been exposed to neuroleptic drugs, thus ruling out the cause and effect problem
Clozapine, a drug which is effective at reducing psychosis, does not affect levels of dopamine. Why is this a limitation of the dopamine hypothesis?
Suggesting there has to be more to schizophrenia than excess dopamine - INCOMPLETE
Animals injected with amphetamine type drugs show catatonia like states. Why is this a strength of the dopamine hypothesis?
Increase dopamine activity
Affects movement
More evidence
Dopamine levels (and D2 receptor no.) vary in different parts of the brain. Why is this a weakness of the dopamine hypothesis?
It is unclear what effect this may have on schizophrenia
Does the dopamine hypothesis provide a clear explanation?
OVERSIMPLIFIED
It is now clear that the neurotransmitter systems interact and other neurotransmitters such as serotonin have been associated with schizophrenia (Breier, 1995).
CANNOT explain the NEGATIVE SYMPTOMS
Twin studies have small sample sizes. Why is this a weakness?
ONE twin pair will have a LARGE EFFECT on concordance rates
GENERALISABILITY
Older twin studies may be unreliable. Why is this a weakness?
Due to CHANGES in the DIAGNOSTIC CRITERIA
Some people diagnosed with schizophrenia 40 years ago may not have been diagnosed today
Equally, some people not diagnosed 40 years ago may be diagnosed today
