Biological Explanations Of Schizophrenia Essay
How do the four biological explanations fit together to explain schizophrenia or are they mutually exclusive?
The biological explanation can be divided into subcategories to explain schizophrenia; genetic, biochemistry (dopamine hypothesis), brain structure and season of birth explanation.
Firstly there’s genetics. This view says some people posses certain genes that predispose them to schizophrenia. However, if schizophrenia was totally and always inherited then concordance rates between MZ twins (identical) and DZ twins (non identical) would be 100%. If on the other hand genetic inheritance had nothing to do with schizophrenia, the concordance rates would be close to 0%. Gottesman found there was a concordance rate of 48% for MZ twins as opposed to 17% for DZ twins. Kendler supported this, finding there was a concordance rate of 50% …show more content…
for MZ twins compared to a 15% rate doe DZ twins. Gottesman also looked at concordance rates within families finding if both parents had schizophrenia, then there was a 46% chance the offspring would suffer from it, and if one parent had schizophrenia there was 16% chance offspring would have it.
Gottesman’s research supports the idea of genetics playing a role, however, concordance rates are not 100% so it can’t be said that genetics are the only cause. Also, twin studies don’t account for the fact that twins are often brought up in the same environment and treated similarly, especially MZ twins, therefore the concordance rates could be due to environmental factors rather than genetics.
All these studies support each other and this therefore shows there is a predisposition to schizophrenia. However, concordance rates are not 100%, so it cannot be said that genetics is the only cause. There is further support from adoption studies for the genetic explanation of schizophrenia. Tienari found that children who had been adopted away from a schizophrenic biological mother were still more likely to get it than children adopted from non-schizophrenic parents, despite being raised in a different environment. However, not all high risk cases (where parent had schizophrenia) got the disorder so evidence is not conclusive.
The second genetic explanation is to do with brain biochemistry focusing on the idea that schizophrenia arises from an excess of dopamine in the brain. Dopamine is a neurotransmitter causing neurons to fire, so too much dopamine makes neurons fire too often and transmit too many messages which produces many of the symptoms of schizophrenia.
It has been found through post mortems that people diagnosed with schizophrenia have higher dopamine levels in the brain that non-suffers. However, it cannot be certain whether high dopamine is a cause for schizophrenia, or an effect from the disorder and it is difficult to actually monitor the brain levels of dopamine in suffers to find conclusions as this can only be done through post-mortems after death. On the other hand, research as shown that taking amphetamines causes symptoms similar to schizophrenia for example, hallucinations and delusions, and they are known to increase levels of dopamine in the brain. This would suggest that high dopamine is more a cause of the disorder than an effect. However, not all people who take amphetamines develop schizophrenic symptoms; this suggests there are other factors which make people more susceptible. Also, Randrup et al. studied rats by giving them amphetamines and they developed schizophrenic symptoms. However, rats and humans are different physiologically and therefore research can’t be applied to humans. Also this experiment was highly unethical as the animals underwent unnecessary abuse. Clozapine, a drug for schizophrenia has been researched and it actually decreases dopamine levels less than some other drugs, so surely if schizophrenia was because of high dopamine levels, then logically Clozapine should be less effective, yet it’s not. This suggests that it is not dopamine controlling schizophrenia.
The evidence for the dopamine hypothesis is correlational, therefore it cannot be concluded that schizophrenia is caused by an excess of dopamine.
The third explanation is brain structure which says schizophrenia is the result of abnormal brain structure and there are differences in the brains of schizophrenics and non-schizophrenics. Brown said that many schizophrenics have lighter brains with enlarged ventricles. However, a study by Pearlson has failed to replicate these findings. It is also possible that the ventricular enlargement could be the result rather than the cause of schizophrenia. Suddath et al’s twin study supports this as he found MZ twins where one twin has schizophrenia does actually have larger ventricles than the other.
The biological explanation is a reductionism explanation because it explains complex behaviour by the simplest terms, genetics, inheritance, neurotransmitters, neuroanatomy and the flu virus.
The biological approach emphasizes nature and ignores nurture; this approach therefore ignores the stress part of the diathesis stress model and so ignores psychological and environmental
triggers.
High expressed emotion in families has been linked with schizophrenia. Brown found that schizophrenic patients returning to high expressed emotion homes were more likely to relapse then those returning to low expressed emotion homes. This is supported by Vaughn and Leff who found a 51% relapse rate in high expressed emotion homes compared to 13% in low expressed emotion homes. It is important to remember however that high expressed emotion does not cause schizophrenia but explains how it is maintained and why the symptoms may reappear.
The social causation hypothesis states that schizophrenia is caused by factors to do with social class. Hollingshead and Redlich found that schizophrenia was twice as likely to be found in the lower social classes especially those living in densely populated and inner city areas. A study by Farris supports this. Farris found a higher rate of schizophrenia in working class areas with poor housing, overcrowding and high crime rates, than in the more middle class areas. They also found that the schizophrenics had always lived in these areas and had not drifted into them because of their disorder.
From this we can conclude that the biological approach does not explain everything. The biological approach is deterministic in that it believes all behaviour is caused by factors other then one’s on will.
The biological approach does not tell us all we need to know about schizophrenia. The biological approach is reductionistic, deterministic, emphasizes nature and ignores nurture. Therefore it ignores psychology and environmental triggers such as high expressed emotion and social causation. However, the biological approach explains a genetic predisposition to schizophrenia but for a full understanding the diathesis stress model needs to be used.
The biological explanation can be divided into subcategories to explain schizophrenia; genetic, biochemistry (dopamine hypothesis), brain structure and season of birth explanation.
Firstly there’s genetics. This view says some people posses certain genes that predispose them to schizophrenia. However, if schizophrenia was totally and always inherited then concordance rates between MZ twins (identical) and DZ twins (non identical) would be 100%. If on the other hand genetic inheritance had nothing to do with schizophrenia, the concordance rates would be close to 0%. Gottesman found there was a concordance rate of 48% for MZ twins as opposed to 17% for DZ twins. Kendler supported this, finding there was a concordance rate of 50% …show more content…
for MZ twins compared to a 15% rate doe DZ twins. Gottesman also looked at concordance rates within families finding if both parents had schizophrenia, then there was a 46% chance the offspring would suffer from it, and if one parent had schizophrenia there was 16% chance offspring would have it.
Gottesman’s research supports the idea of genetics playing a role, however, concordance rates are not 100% so it can’t be said that genetics are the only cause. Also, twin studies don’t account for the fact that twins are often brought up in the same environment and treated similarly, especially MZ twins, therefore the concordance rates could be due to environmental factors rather than genetics.
All these studies support each other and this therefore shows there is a predisposition to schizophrenia. However, concordance rates are not 100%, so it cannot be said that genetics is the only cause. There is further support from adoption studies for the genetic explanation of schizophrenia. Tienari found that children who had been adopted away from a schizophrenic biological mother were still more likely to get it than children adopted from non-schizophrenic parents, despite being raised in a different environment. However, not all high risk cases (where parent had schizophrenia) got the disorder so evidence is not conclusive.
The second genetic explanation is to do with brain biochemistry focusing on the idea that schizophrenia arises from an excess of dopamine in the brain. Dopamine is a neurotransmitter causing neurons to fire, so too much dopamine makes neurons fire too often and transmit too many messages which produces many of the symptoms of schizophrenia.
It has been found through post mortems that people diagnosed with schizophrenia have higher dopamine levels in the brain that non-suffers. However, it cannot be certain whether high dopamine is a cause for schizophrenia, or an effect from the disorder and it is difficult to actually monitor the brain levels of dopamine in suffers to find conclusions as this can only be done through post-mortems after death. On the other hand, research as shown that taking amphetamines causes symptoms similar to schizophrenia for example, hallucinations and delusions, and they are known to increase levels of dopamine in the brain. This would suggest that high dopamine is more a cause of the disorder than an effect. However, not all people who take amphetamines develop schizophrenic symptoms; this suggests there are other factors which make people more susceptible. Also, Randrup et al. studied rats by giving them amphetamines and they developed schizophrenic symptoms. However, rats and humans are different physiologically and therefore research can’t be applied to humans. Also this experiment was highly unethical as the animals underwent unnecessary abuse. Clozapine, a drug for schizophrenia has been researched and it actually decreases dopamine levels less than some other drugs, so surely if schizophrenia was because of high dopamine levels, then logically Clozapine should be less effective, yet it’s not. This suggests that it is not dopamine controlling schizophrenia.
The evidence for the dopamine hypothesis is correlational, therefore it cannot be concluded that schizophrenia is caused by an excess of dopamine.
The third explanation is brain structure which says schizophrenia is the result of abnormal brain structure and there are differences in the brains of schizophrenics and non-schizophrenics. Brown said that many schizophrenics have lighter brains with enlarged ventricles. However, a study by Pearlson has failed to replicate these findings. It is also possible that the ventricular enlargement could be the result rather than the cause of schizophrenia. Suddath et al’s twin study supports this as he found MZ twins where one twin has schizophrenia does actually have larger ventricles than the other.
The biological explanation is a reductionism explanation because it explains complex behaviour by the simplest terms, genetics, inheritance, neurotransmitters, neuroanatomy and the flu virus.
The biological approach emphasizes nature and ignores nurture; this approach therefore ignores the stress part of the diathesis stress model and so ignores psychological and environmental
triggers.
High expressed emotion in families has been linked with schizophrenia. Brown found that schizophrenic patients returning to high expressed emotion homes were more likely to relapse then those returning to low expressed emotion homes. This is supported by Vaughn and Leff who found a 51% relapse rate in high expressed emotion homes compared to 13% in low expressed emotion homes. It is important to remember however that high expressed emotion does not cause schizophrenia but explains how it is maintained and why the symptoms may reappear.
The social causation hypothesis states that schizophrenia is caused by factors to do with social class. Hollingshead and Redlich found that schizophrenia was twice as likely to be found in the lower social classes especially those living in densely populated and inner city areas. A study by Farris supports this. Farris found a higher rate of schizophrenia in working class areas with poor housing, overcrowding and high crime rates, than in the more middle class areas. They also found that the schizophrenics had always lived in these areas and had not drifted into them because of their disorder.
From this we can conclude that the biological approach does not explain everything. The biological approach is deterministic in that it believes all behaviour is caused by factors other then one’s on will.
The biological approach does not tell us all we need to know about schizophrenia. The biological approach is reductionistic, deterministic, emphasizes nature and ignores nurture. Therefore it ignores psychology and environmental triggers such as high expressed emotion and social causation. However, the biological approach explains a genetic predisposition to schizophrenia but for a full understanding the diathesis stress model needs to be used.