Gone are the times of having a life full of hardships, rough days, arguments with loved ones, teary eyed moments, job losses, being scared, mourning for lost ones, being a child, talking to yourself, saying what you feel and saying "No thank you, I don’t like it." What it means to be human, to act as we do in such wonderful, extravagant and at times eccentric ways to a variety of situations has been medicalised. In placing an emphasis on diagnosing human distress and misery as a medical problem treatable by medical intervention, psychiatry has opened Pandora’s Box. The daemons that escape are science and philosophy. My aim in this essay is to establish what these daemons have to say and how they have, or more correctly have not been addressed by the guilty party.

All individuals who seek psychiatric assistance for help will be viewed through the medical model. As such biology tends to take precedence over social and psychological factors. Double (2000) states the basic assumption of biological psychiatry as being ‘that mental illness is due to a biochemical imbalance…the implication is that personal conflict and responsibility are avoided’. Leifer (2000) extends this basic premise in saying that psychiatry views mental illnesses as being ‘caused by "pathological" changes in the chemistry, structure, or organisation of the brain’. It is clear from this that psychiatry has established itself with a strong biological perspective. However, the major problem with this is that the scientific evidence currently available does not adequately support it. In fact after nearly two hundred years nothing has ever been found to be wrong with the brains of individuals that have been diagnosed as having a mental disorder/illness (Newnes, 2002).

Further to this problem is our own difficulty in understanding how the brain produces consciousness at all. We have no model of what is considered ‘normal’ therefore how can we begin to suggest what is ‘abnormal’ (Dawson, 1997). A question that Leifer (2000) proposes is ‘if neurochemistry can cause undesirable thoughts, feelings and actions can it also cause desirable ones?’ If this is the case then which is cause and which is effect? If the death of a loved one involves feelings of depression, is this unhappiness due to low serotonin levels or the loss of the loved one? In treating what psychiatry believes to be lower-than-normal serotonin levels does it bring back the loved one so that happiness can ‘return to normal’? Of course it doesn’t. Such a thought is delusional, which is yet another ‘symptom’ of mental illness. In light of inconclusive evidence to support biochemical imbalances and biological dysfunctions, this unproved hypothesis is seemingly used in day to day psychiatric practise to inform its clients that the reasons for their unhappiness, bar the fact that they have just lost their partner, are due to a biochemical imbalance in the brain which can be treated by medication.

Now such a situation finds itself with quite a problem. In common medical diagnosis of true medical conditions such as ‘diabetes,’ certain tests are undertaken to ensure correct diagnosis and subsequent treatment. The patient will present with various symptoms such as persistent thirst, constant urination, fatigue and dizziness. From these alone it is not possible to diagnose any complaint and doing so would be extremely hazardous business (Boyle, 1999).

In her chapter on diagnosis, Boyle (1999) states that the basic task of medical and scientific research is to find relationships between phenomena. In medicine the most basic phenomena are bodily complaints; fatigue, dizziness, constant urination, headache, pain etc. These are known as symptoms. Such complaints have three very important characteristics. Firstly they rely on personal report and are thus subjective, unbearable pain to one may be bearable to another yet neither are measurable; secondly, symptoms are quite common, many people experience headaches in their life; and finally these symptoms are generally not specific to any one cause. That is they may have many antecedents. As such further information is required for the correct diagnosis to be made. This comes in the form of blood tests, hair analysis, skin biopsies etc. to ascertain true deviances from normality. These tests look for what are known as signs. They are less common than symptoms, generally have fewer antecedents but most importantly they are measurable. It is this set of symptoms and sign(s) that needs to be observed for the notion of disease to be implied. This however can only occur when and if a previously discovered pattern of signs and associated symptoms have been established.

Psychiatry however does not follow this premise even though it claims to be medical. Unlike all other branches of medicine, psychiatry does not do any form of physical test to confirm that there is this sign of a biochemical imbalance or biological dysfunction because there is no accurate test (Newnes, 2002; Leifer, 2000). It is merely inferred that such exists from the sets of ‘symptoms’ that their patient talks of. This symptomatic approach to psychiatric diagnosis is appalling as it relies on external observation and self-report both of which have been shown to be unreliable in psychological research (Haslam & McGarty, 1998). Further to this is that there has never been a previously reliably demonstrated pattern of signs and symptoms from which current diagnosis is based, thus diagnosis is flawed (Boyle, 1999). This has been argued as existing for many ‘mental disorders’ including schizophrenia (Boyle, 2002), agoraphobia (Hallam, 1983), panic disorder and depression (Boyle, 1999). Currently it seems that psychiatry is frantically searching for the signs to tie in with the ‘symptoms’ to allow for a more valid diagnosis. As Szasz (1960) puts it ‘All problems in living are attributed to physicochemical processes which in due time will be discovered by medical research’.

To date, the quantity of resources that have been devoted to this medical research are enormous. The result has been many studies searching for genetic, physiological and biochemical causes of mental illness. However investigation into these as causes has produced no conclusive evidence. In fact there is a disappointing lack of consistency with results and as such most can not be deemed reliable. Aside from the lack of consistency there are extreme flaws in the methodology of these studies.

Psychiatry’s claim that depression is caused by a serotonin deficiency has been ‘discovered’ through participants response to SSRI antidepressant medication and not through significant differences between control and experimental groups serotonin levels (Leifer, 2000). Thus the only deficiency evident is that of the proof of any serotonin problem. The response to antidepressant medication remains the strongest support for depression being a physiological condition (Moncrieff, 1997). Yet this is not proof, but rather the effects of ingesting a psychoactive substance.

Molecular genetic studies looking to identify possible genes as the underlying cause of what is known as schizophrenia have identified a gene, dysbindin, which is believed to be involved in the pathogenesis of the disorder (Straub, R. E., Jiang, Y., MacLean, C. J., Ma, Y & Webb, B. T., 2002). The researchers state that ‘It remains a formal possibility that dysbindin itself is not aberrant in schizophrenia’. So which is it? It either is or it is not. These results can only be put down to chance until they are reliably replicated numerous times. This has yet to happen. Aside from the clear lack of clarity as to whether or not the gene is responsible these results are inconclusive as they fail a vital component of scientific research, replication.

Further studies interested in the lateral ventricle size in the brains of those diagnosed as schizophrenic have found differences; however there is substantial overlap with the ‘normal’ population (Andreasen, N. C., Swayze, V. W., Flaum, M., Yates, W. R., Arndt, S. & McChesney, C, 1990). Also most of these studies have used participants that have a long history of drug treatment with neuroleptics which have been shown to produce serious brain damage (Lehmann, 2001; Breggin, 1990). All these studies really demonstrate is that no direct evidence of a reliable nature has been found, and that their scientific method is poor.

What all this is suggesting is that in a vain attempt to find the biological cause/s of human misery and distress psychiatry has failed miserably. The evidence for all theories relating to biological causation is inconsistent and therefore only proves that no such cause exists. But why is this so? It can be argued that mental illness does not exist in the literal sense, that is, as a disease of the brain. Thus biological factors can never be found. Szasz (2000) argues that mental diseases are not diseases in the pathological sense, rather the mind, not being a material object, can only be diseased in the metaphorical sense. Leifer (2000) states that ‘the medical model portrays the mind as object, it equates mind with brain and uses this assumption to justify certain thoughts, feelings and behaviour as medical diseases’. Yet a person’s beliefs, be it that there is a god or that someone is out to get them, can not be explained by a defect or disease of the brain (Szasz, 1960). No such evidence exists for the idea. Therefore treating an individual for depression caused by a (non-proven) diseased brain does not make much sense. Portraying the mind as object also makes little sense. It is clear that mental illness is a metaphor that has been made literal by psychiatry in an attempt to validate the medical model. After all, it would seem quite unusual prescribing a drug for a metaphoric illness (Leifer, 2000).

Perhaps it is easier for psychiatry to say that unwanted behaviours, thoughts etc are caused by abnormalities in the brain rather than to try and understand why individuals express themselves accordingly. More likely though it is in the self-interest of psychiatrists to promote the medical model to retain psychiatric identity as real doctors treating real medical problems (Leifer, 2000). However in labelling biology as to blame for behaviour/s they become caused and not chosen. Therefore under this model individuals are no longer responsible for their actions. But where is the distinction between cause and choice in ‘healthy’ and ‘unhealthy’ behaviours? Are pleasant thoughts and behaviours chosen or caused? Is giving a rose to a loved one a conscious decision or a result of balanced biochemistry? Is killing your loved one a conscious decision or a result of imbalanced biochemistry? Surely they are both choices yet one is deemed socially desirable to be responsible for, the other is not.

By taking responsibility out of action, psychiatry is not allowing humans to be just that, human. By medicalising distress, misery and ‘madness’ psychiatry has opened itself up to scrutiny from science and philosophy, some of which have been discussed in this essay. Pandora’s box has been opened and the daemons are out. But what is psychiatry doing about it? In a sense psychiatry is practising what it preaches. The little voices that say "scientifically invalid", "mental illness is a myth", "flawed methodology" and "no evidence to support biology" are all being ignored. This is exactly what psychiatry tells its ‘schizophrenics’ to do, to ignore the voices they hear (if they hear them). Unfortunately, ignoring the voices is not the best answer in either case.

Leifer (2000) describes one of the basic principles of the scientific method as being ‘free, critical enquiry and debate’. That is to criticise scientific procedure, theory and supposed knowledge. This just doesn’t happen it psychiatry. The minority that do criticise are labelled as ‘anti-psychiatrists’ and then ignored by saying that they clearly don’t acknowledge the true nature of distress (Double, 2001). Worse still it seems that in the past psychiatry has exercised its power of social control over its own. After Thomas Szasz’s paper The Myth of Mental Illness was published the response was to restrict and repress him. He was forbidden to teach in the department of psychiatry at Syracuse State Psychiatric Hospital and further attempts were made to remove him as professor of psychiatry (Leifer, 2000).

Various psychiatric journals have rejected articles that criticise the discipline. Psychiatry’s response has been "Todschweigen," death by silence (Leifer, 2000). Such repression violates that basic principle of the scientific method namely, free, critical enquiry and debate. In doing so psychiatry is attempting to make all its statements impossible to falsify which again violates another important aspect of scientific method, the null hypothesis, the result of no significant difference. By dismissing such all results will point to some minute difference and clearly this has been the case with psychiatric research to date. In silencing its critics and not allowing it to be subject to critical evaluation, psychiatry can not claim itself to be scientific (Leifer, 2000). As Double (2001) states ‘How much faith should we have in a psychiatry that is so easily threatened by any challenge to its basis?’

In this essay I have attempted to highlight the main arguments against the medicalisation of behaviour. The insufficient evidence, the poor scientific method and the mythic nature of it all. By labelling human experience, the highs and lows of life, as being of medical in nature, psychiatry is suggesting a simple answer to a complex array of problems. Little white pills don’t bring families back together and they don’t heal grief. Electro Convulsive Therapy can not make you loveable and it won’t stop voices but most importantly a prefrontal lobotomy will not help you deal with your life.

If only psychiatry would answer the critics, open its eyes and see how disqualifying and excluding it is being. Maybe, just maybe they might learn something that is worth knowing about how we all deal with adversity in our world. But in order to do this they must accept these voices as being real and not delusions.

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Straub, R. E., Jiang, Y., MacLean, C. J., Ma, Y & Webb, B. T. (2002). Genetic variation in the 6p22.3 gene DTNBP1, the human ortholog of the mouse dysbindin gene, is associated with schizophrenia. American Journal of Human Genetics 71, 2, pp. 337 – 349.

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Brook Durling 19807152