The second source of evidence for the Dopamine Hypothesis has come from observations during drug therapies. It was discovered that phenothiazines (anti-psychotic drugs) were able to reduce the symptoms characteristic of schizophrenia through dopamine inhibition. Furthermore, L-Dopa (a synthetic source of dopamine) was able to induce acute symptoms in people who were not psychotic. These effects have been trialled on rats. Randrup and Munkuad (1966) found that rats took on schizophrenic behaviours after being administered amphetamines, and the effects could be reversed through neuroleptic drugs. This suggests that dopamine has a role in schizophrenia. However, there are significant differences in the neuroanatomy of rats and humans, which could lead to such effects being observed in rodent brains but not in human brains- these results cannot be generalised across species. The use of non-human animals in such studies raises questions of ethics as harm may come to animals in drug trials and animals are unable to give any form of consent. However, protection for non-human animals used in experiments was developed after this investigation took place (Medicines Act, 1968), so at the time it would have been more ethically appropriate.
Although these different studies appear to lend support to the Dopamine Hypothesis, the extent to which they can be used as evidence is limited. The role of dopamine has been noted; however these investigations cannot prove whether the presence of dopamine is a cause or a symptom of the disorder. In both cases higher levels of the neurotransmitter would be observed; therefore it would be important to measure the levels of a patient before onset and throughout development- this is of course difficult as it cannot be predicted with certainty who will develop schizophrenia or not.
It has also been argued that other neurotransmitters may play a significant role. For example, serotonin is now commonly used in anti-psychotic drugs and appears to have the same effect. This could either mean that both neurotransmitter work together, or one may have a direct impact on the other. (Such as serotonin acting by inhibiting dopamine, or vice versa).
The main criticism of the dopamine hypothesis is that it doesn’t take account of other explanations, and is therefore reductionist. It reduces the complex behaviours displayed in schizophrenia to simple biological terms, such as the imbalance of neurochemicals. Ideas represented through psychological theories are overlooked, although they too have supportive evidence. It is more likely that although dopamine levels may have some involvement in schizophrenia, this is not a complete explanation, and so will work in combination with other approaches.
The approach is also determinist, as it suggests that positive environmental factors will have no protective effect over a person who is “due” to develop schizophrenia. In other words, no preventative measures could be taken against the disorder. This may have good ethical implications though, as it means that the parents are released from blame, whereas in other approaches they may seem to be held accountable for causing the disorder. The fact that it is neurochemical also suggests that drug therapy may be successful in alleviating some symptoms by reducing levels of dopamine, which would allow some patients to live more “normal” and independent lives.
High levels of dopamine have been implicated in other disorders, such as Anorexia Nervosa; however these patients do not also exhibit schizophrenic symptoms, so it is unlikely that dopamine alone can cause this specific behavioural response.
A psychological theory that attempts to explain the development of schizophrenia is the behavioural approach. This uses the idea of operant conditioning as a way of causing the disorder. According to the behavioural approach, a sufferer of schizophrenia will not have received reinforcement for socially acceptable behaviours they displayed and so will stop attending to social cues. They will choose to focus on irrelevant cues instead. In turn this bizarre behaviour will elicit more attention from others, and will act as reinforcement, so the person will repeat such behaviours. This idea was put forward by Liberman (1982).
Belcher (1988) showed support for this through his study into teaching patients with schizophrenia appropriate behaviours. It was found that patients would act in a socially acceptable manner when they were rewarded in ways that were important to them (such as cigarettes or food). This sort of therapy is also based on operant conditioning, with their rewards acting as reinforcements for the positive behaviours.
However, this form of therapy has only proved successful on some patients. As mentioned earlier, it is thought that schizophrenia may be a series of disorders rather than just one. This may be demonstrated here, where patients suffering with one of these disorders diagnosed under the term ‘schizophrenia’ respond positively and are able to improve, whilst those with separate disorders (also diagnosed under the term ‘schizophrenia’) show no progress at all. The knowledge that this form of therapy has the potential to help some patients is positive as it will enable some people to gain a more ‘normal’ life and may make them less dependent on family or community support.
However, the basic theory of the behavioural approach could be described as flawed. It is over-simplistic in that it doesn’t account for patients who have received reinforcement in a normal way (hence they should develop normally) but who still develop schizophrenia. It also cannot explain how acute schizophrenia can occur- this is when the onset happens very suddenly following a particularly stressful event. The approach only accounts for chronic schizophrenia, where the development may happen over a period of months or years and the symptoms are not so immediately obvious. This could explain the progression as the process of reinforcement occurs over a long period of time, but not when a person has been functioning normally for their whole life and then suddenly experiences an episode. The theory would also suggest that schizophrenia would be developed in the earlier stages of life; however age of onset is known to be from 15 years to 45 years.
Behavioural theory could be seen to be unethical, as it implies that the parents are to blame for the development of this disorder. It suggests that they provided the child with a negative environment in which he/she received no reinforcement of normal behaviours, and hence caused the disorder. This blame could cause the parents to feel guilty and could have a negative psychological impact on them, when it is unlikely to be purely their fault. It is more likely, if the idea of operant condition is involved in the cause, that it coincides with other approaches such as a genetic predisposition or a chemical imbalance. If the cause could be entirely explained through the behavioural theory it is still possible that the parents would not be to blame. Kagan (1982) suggested the temperament hypothesis, which says that it could be possible for a child to be born with an innate personality or temperamental characteristics, so that no matter how much reinforcement the parents provided the child was unable to respond in a normal way.
Although both the dopamine hypothesis and behavioural approach have evidence supporting their roles in schizophrenia, it is unlikely that either would act as a causal factor alone. It is more probable that a number of different factors are involved in the development of schizophrenia, from both biological and psychological explanations. The way in which therapies have proved successful or theories proved fitting with some patients but not others further suggests that schizophrenia may in fact be a number of different disorders that have all been classed as one. This use of an overarching diagnosis may be hindering the progress in finding a cause or treatment for the disorders. Certain ethical issues may also arise in finding the causal factors, for example there may be guilt associated if parents are to be held accountable for bringing up children in a negative environment, or brain scans may become compulsory before job interviews or life insurance policies in order to eliminate those with the potential to develop schizophrenia.
Overall, these approaches over-simplify a complex disorder and try to explain it through basic mechanisms and terms. In order to fully understand schizophrenia it ought to be considered holistically and approaches may need to be combined.
