eval biological schizs Flashcards
Research support
One strength of the genetic explanation Is the strong evidence base.
Family studies such as Gottesman (facing page) show that risk increases with genetic similarity to a family member with schizophrenia. Adoption studies such as Pekka Tienari et al. (2004), show that biological children of parents with schizophrenia are at heightened risk even if they grow up in an adoptive family. A recent twin study by Rikke Hilker et al. (2018) showed a concordance rate of 33% for identical twins and 7% for non-identical twins.
This shows that some people are more vulnerable to schizophrenia as a result of their genetic make-up.
Environmental factors
One limitation of the genetic explanation is there is clear evidence to show that environmental factors also crease the risk of developing schizophrenia.
These environmental factors include both biological and psychological influences. Biological risk factors include birth complications (Morgan et al. 2017) and smoking THC-rich cannabis in teenage years (Di Forti et al. 2015). 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 Nina Merkved et al. (2017), 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.
This means that genetic factors alone cannot provide a complete explanation for schizophrenia.
Evidence for dopamine
One strength is support for the idea that dopamine/The (DA) is involved in schizophrenia.
First, amphetamines increase DA and worsen symptoms in people with schizophrenia and induce symptoms in people without (Curran et al. 2004). Second, antipsychotic drugs reduce DA activity and also reduce the intensity of symptoms (Tauscher et al. 2014). Third, some candidate genes act on the production of DA or DA receptors.
This strongly suggests that dopamine is involved in the symptoms of schizophrenia.
Glutamate
One limitation of the dopamine hypothesis is evidence for a central role of glutamate.
Post-mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions of people with schizophrenia (McCutcheon er al. 2020). in addition, several candidate genes lor schizophrenia are Delieved to be involved in glutamate production or processing.
This means that an equally strong case can be made for a role for other neurotransmitters.
Genetic counselling
One application of our understanding of the likely role of genes in schizophrenia is genetic counselling. If one or more potential parents have a relative with schizophrenia, they risk having a child who would go on to develop the condition. For example, based on Gottesman’s study they will have a 2% probability if they have an uncle or aunt with schizophrenia, and a 6% probability if they have a half-sibling with it. Genetic counselling involves informing potential parents of these probabilities so that they can make informed choices about whether to have children who risk having a poor quality of life if they develop schizophrenia.
However, the risk estimate provided by genetic counselling is just an average figure based on risk across the whole population. It will not really reflect the probability of a particular child going on to develop schizophrenia because any given child will experience a particular environment which also exposes the child to risk factors. For example, a child’s risk of going on to develop schizophrenia will be much higher than is suggested by their genetic probability if they go on to experience a childhood trauma and then smoke cannabis in their teens. However their risk will be less than the average if they do not experience these environmental risks because the average includes those who do experience them.
This means that genetic counselling only provides a crude estimate of the risk of an unborn child going on to develop schizophrenia.
Amphetamine psychosis
Amphetamines (speed) can reproduce symptoms of schizophrenia. Catherine Tenn et al. (2003) induced schizophrenia-like symptoms in rats using amphetamines and then relieved symptoms using drugs that reduce DA action. It might be an issue that this data is from animal studies because cognitive systems are quite different. In other research amphetamines have been found to raise DA levels (Curran et al. 2004) so evidence of a link between amphetamines and schizophrenia symptoms supports the dopamine hypothesis. Amphetamines in high doses can produce auditory hallucinations that resemble those often seen in schizophrenia.
However, other drugs that also increase DA levels (e.g. apomorphine) do not cause schizophrenia-like symptoms (Dépatie and Lal 2001). Also, Justin Garson (2017) has challenged the idea that the symptoms of amphetamine psychosis closely mimic schizophrenia. Also, we should bear in mind that some of the evidence linking amphetamine psychosis to dopamine levels comes from animal studies (e.g. Tenn et al. 2003), which may not generalise well to humans. So the link between amphetamine psychosis and schizophrenia may not be as close as some people have suggested.
This means that amphetamine psychosis is not particularly strong evidence to support the dopamine hypothesis.
