bio explanations of schizophrenia Flashcards
What are the genetic explanations of schizophrenia
- Genetics
- Family Studies
- Twin Studies
- Adoption studies
- genetic origin in the absence of family
How do genetics cause schizo
One possible cause of schizophrenia may be heredity, i.e. genetics. The risk of developing the disorder among individuals who have family members with schizophrenia is higher than it is for those who do not. No one gene is thought to be responsible for this disorder; it is more likely that a number of different genes are involved i.e. it is polygenic. Candidate genes associated with increased risk include those coding for the functioning of a number of neurotransmitters, including dopamine. Schizophrenia is also aetiologically heterogeneous, i.e. different genetic variations can lead to the condition.
What is the evidence from families to demonstrate schizo is genetic
Evidence from family studies:
Schizophrenia is more common among biological relatives of a person with schizophrenia, and the closer the degree of genetic relatedness, the greater the risk.
e.g. Gottesman found children from two parents who had schizophrenia has a concordance rate of 46%, compared with 13% from one parent and only 6% where a sibling had schizophrenia
What is the evidence from twin studies to demonstrate schizo is genetic
Evidence from twin studies:
Studies support genetic explanation as they show higher concordance rates for MZ twins than DZ twins.
e.g. Joseph (2004) found a concordance rate of 40.4% for MZ twins and 7.4% for DZ twins.
What is the evidence from adoption studies to demonstrate schizo is genetic
Evidence from adoption studies:
Studies of genetically related individuals who have been reared apart allow genetics and the environment to be separated.
e.g. Tienari (2000) found 6.7% of adoptees whose biological mothers had schizophrenia compared to 2% of adoptees whose biological mothers did not have schizophrenia
How else can schizo be genetically obtained?
However, schizophrenia can also have a genetic origin in the absence of a family history. This is because the parental DNA may have become mutated by radiation, poison or viral infection for example. Evidence for mutation comes from positive correlations between paternal age (associated with increased risk of sperm mutation) and risk of schizophrenia, increasing from around 0.7% with Fathers under 25 to over 2% in Fathers over 50 (Brown, 2002).
Evaluation of genetic
Twin studies - limitation
P - One limitation with using twin studies as genetic evidence is the assumption of equal environments.
E - It is assumed by researchers studying twins that environmental factors are held constant because twins are brought up together and therefore must experience similar environments. However, this ‘shared environment assumption’ may apply much more to MZ twins than DZ twins because MZ twins look identical and people tend to treat them more similarly, which in turn may provide reasons for why concordance rates of developing schizophrenia are higher with monozygotic twins.
E - This is a limitation as it suggests that the closer genetic relatedness of monozygotic twins as support for the genetic explanation for schizophrenia may actually be solely because they are more likely to experience the same triggers for schizophrenia than dizygotic twins.
Practical application
P - A strength of the increased understanding of the genetics of schizophrenia is that it has been used to inform genetic counselling.
E - One practical application of the genetic explanation of schizophrenia is genetic counselling as if schizophrenia is known in the family then there is a risk that it will be passed to any future children. However, this does not really reflect the probability of a child developing schizophrenia as they also need to experience certain environmental risk factors.
E - Therefore, this service can provide support during difficult times and enable people to make smart decisions around family planning, however the extent to which genetic counselling is effective is limited as it does not take into account the nature element, solely the nurture.
Environmental factors
P - One limitation of the genetic explanation is there is clear evidence to show that environmental factors also increase the risk of developing schizophrenia.
E - These environmental factors include birth complications and smoking THC-rich cannabis in teenage years. Psychological risk factors include childhood trauma which leaves people more vulnerable to adult mental health problems in general but there is now evidence for a particular link with schizophrenia. In one study by Mørkved et al., 67% of people with schizophrenia and related psychotic disorders reported at least one childhood trauma as opposed to 38% of a matched group with non-psychotic mental health issues.
E - This means that genetic factors alone cannot provide a complete explanation for schizophrenia.
What are neural correlates
Neural correlates are measurements of the structure or function of the brain that correlate with an experience, in this case schizophrenia.
The best-known neural correlate is the neurotransmitter dopamine. It is important in the functioning of several brain systems related to the symptoms of schizophrenia.
Dopamine hypothesis
THE DOPAMINE HYPOTHESIS
Hyperdopaminergia in the Subcortex:
The original version of the dopamine hypothesis focused on the possible role of high levels of activity of dopamine in the subcortex (central area) of the brain
e.g. an excess of dopamine receptors in Broca’s area may be associated with poverty of speech and/or the experience of auditory hallucinations
Hypodopaminergia in the Cortex:
More recent versions of the dopamine hypothesis have focused instead on abnormally low dopamine systems in the brain’s cortex
e.g. low levels of dopamine have been found in the prefrontal cortex which have been associated with the negative symptoms of schizophrenia
It may be that both hyper- and hypo-dopaminergia are correct explanations as it has been suggested that cortical hypodopaminergia leads to subcortical hyperdopaminergia, so both high and low levels of dopamine in different brain regions contribute to schizophrenia.
Neural correlates and symptoms
Neural correlates of positive symptoms:
Allen et al (2007) scanned patients’ brains that were experiencing hallucinations and compared them to a control group.
Lower activity levels in the superior temporal gyrus and anterior cingulate gyrus were found in schizophrenia group
Reduced brain activity in these two parts of the brain correlates negatively with positive symptoms (hallucinations)
Neural correlates evaluation
P - One strength is support for the idea that dopamine is involved in schizophrenia.
E - Amphetamines increase dopamine and worsen symptoms in people with schizophrenia and induce symptoms in people without. Additionally, antipsychotic drugs reduce dopamine activity, with atypical antipsychotics completely blocking dopamine receptors in the synapses of the brain, reducing the action of dopamine, and typical antipsychotics that temporarily occupy the dopamine receptors which have been found to reduce the intensity of symptoms. Moreover, some candidate genes act on the production of dopamine or dopamine receptors.
E - This strongly suggests that dopamine is involved in the symptoms of schizophrenia.
P - one limitation of the dopamine hypothesis is evidence for a central role of glutamate
E - Post-mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions of people with schizophrenia. In addition, several candidate genes for schizophrenia are believed to be involved in glutamate production or processing.
E - This means an equally strong case can be made for a role for other neurotransmitters
