‘Psychiatry and the dominance of the bio-medical model.’ Brilliant article from a psychiatric nurse’s view. Sums up the disease/bio-medical model approach. International Critical Psychiatry Network.
Psychiatry and the dominance of bio-medical model
Recent years have seen enormous changes in the provision of services and therapies for people suffering from ‘schizophrenia’ (hearing voices) in the UK. The move away from large-scale institutional care and towards community-based care has been accompanied by a growth in the research and practice of psychosocial approaches to serious mental illness.
Given the progress in these areas it seems pertinent to ask why mental health services are still dominated by the bio-medical model.
Whilst willing to recognise the value of social and psychological factors, psychiatry often does so in a way that relegates them to an order below that of biological factors. Yet this happens in the absence of any clear evidence for a biological cause of schizophrenia.
As a psychiatric nurse and a member of a community mental health team I am particularly interested in the impact that bio-medical research and thinking has on how we try to help those who use our service. In this essay I intend to briefly examine the historical development of biological psychiatry and critically examine some issues and arguments regarding current practice.
Controversy regarding approaches to mental and emotional distress is nothing new. Sedgwick (1982) notes that differing approaches can be traced back to ancient Rome. These varied from crude physical interventions such as drilling through a person’s skull to allow evil spirits out, to the providing of “good counsel”.
The eighteenth century saw a revolutionising of the way society dealt with the mentally ill which accompanied other revolutionary social changes that the beginnings of modern industrial society brought. Arguments about the nature of madness took place in the context of mass urbanisation and impoverishment on a scale never seen before.
At this time a humane tradition of care known as moral treatment briefly flourished in Europe. The method claimed excellent recovery rates. Typical of the kind of institution to practice moral treatment was the York Retreat. It provided a safe non-medical environment where self-control and self-esteem were fostered. The approach was in stark contrast to the cruel and squalid conditions of the new madhouses. (Warner 1994).
In 1845 the whole approach to insanity changed forever with the introduction of the Lunatics Act. This consolidated a shift from parochial, privatised and non-institutionalised approaches to a segregated, custodial approach, dominated by the new sub-speciality of medicine, psychiatry. (Rogers and Pilgrim 1996).
One of the motivating beliefs of the reformers was that medicine would be able to cure insanity. (Rogers and Pilgrim, 1996). Eager to live up to this expectation and to hold on to their new status not only as “responsible guardian of the lunatic” but also as valid practitioners of medicine, the early psychiatrists sought to improve their knowledge as a matter of urgency. McCrone (1996) demonstrates that some doctors asserted a physiological basis for mental illness as early as 1812, quoting Dr. Benjamin Rush: ‘The cause of madness is seated primarily in the blood vessels of the brain and that it depends upon the same kind of morbid and irregular actions that constitute other arterial diseases’.
By the end of the nineteenth century different researchers proposed various taxonomies of mental disorders but it was the ideas of Emil Kraepelin which first gained widespread acceptance (Bentall, 1998). He proposed that there were only two types of mental disorder: dementia praecox and manic-depressive illness.
Kraepelin systematically collected data on the course and outcome of disorders, with the intention of developing a diagnostic system. In 1911 Eugene Bleuler went on to revise some of his forerunner’s findings and to suggest the term schizophrenia instead of dementia praecox. Interestingly, neither doctor regarded hallucinations or delusions as core symptoms of madness.
Some writers have argued that on close examination, the methods of both doctors were scientifically flawed. Boyle (1990) suggests that both Kraepelin and Bleuler took the concept of schizophrenia for granted. They failed to provide any convincing evidence of having observed any symptom patterns that would justify such a construct and didn’t find valid diagnostic criteria. Boyle goes on to point out that the kind of cases seen by Kraepelin & Bleuler are rarely seen today and raises the possibility that the population that they were observing could have been entirely different from that described as schizophrenic today.*
The century that has passed since Kraepelin’s work has seen a great variety of competing theories regarding the aetiology of schizophrenia. Technological innovation has advanced our understanding of brain structure, genetics and brain chemistry.
Kevin Gournay has reported research findings in these areas in an article boldly titled ‘New facts on schizophrenia’ (Gournay 1995). He asserts that although social and psychological factors are important in determining outcome and quality of life for people with schizophrenia, the condition is essentially a brain disease.
This is presumably one of the ‘new facts’ referred to in the article’s title. Others include: recent studies into brain structure ‘provide compelling evidence of a reduction in grey matter or nerve cell loss’, ‘schizophrenia contains a very strong genetic component’, and more tentatively with regard to biochemical factors, ‘the growing body of knowledge…should lead to more effective drug treatments’ (Gournay 1995).
One fact that Gourney misses out is that a biological marker for schizophrenia has yet to be found (Szymanski et al 1991). Dawson (1997) points out that what Gournay fails to take into account is how little is understood about how the brain produces consciousness at all: ‘we do not have a viable model of normal thought processes, let alone a model of ‘abnormal’ processes’.
The evidence that Gournay refers to is far less conclusive than he claims. For instance, in the area of brain structure, the studies found that differences were very small and fell within normal limits. Furthermore the differences were not found in all schizophrenic subjects, and did appear in normal brains. Dawson argues that there is a tendency common within the literature cited by Gournay ‘to reject any evidence that disproves the dearly held hypothesis and to accept anything that might prove that same hypothesis. Gournay, like many of the researchers he admires, is a biological determinist (Dawson 1997).
Regarding genetic factors, Bentall (1998) points out that early tests on identical twins which indicated a very high genetic loading have been discredited in recent years by more methodologically rigorous studies which significantly relegated the contribution that genes make to schizophrenia.
Likewise, modern research into bio-chemical factors has so far failed to produce any conclusive findings (Warner 1997). Even the Association of the British Pharmaceutical Industry suggests (with predictable optimism) that our knowledge from biological research is far less advanced than Gournay suggests. Discussing research findings over the last 25 years they say: ‘If just one or two of these discoveries live up to early expectations, the prospects for many people with schizophrenia…will be greatly improved’ (ABPI 1997).
Gournay states that one of the reasons he is so keen to re-assert the principals of bio-psychiatry is his concern that the ‘antipsychiatrists’ who’s ideas came to prominence thirty years ago still have some influence amongst professionals (Gournay,1995). He seems unaware however, of more rigorous research into non-medical approaches to mental distress that has taken place in recent years. For instance Bebbington et al (1993) found a significant increase in the incidence of life events prior to the onset of psychosis. They concluded that ‘the excess of events is related aetiologically to the emergence of psychosis’
The British psychologist Richard Bentall has suggested a radical re-appraisal of the problem. He argues that since schizophrenia was first ‘discovered’ no one has succeeded in demonstrating it to be a reliable or valid diagnosis. Not only has no particular cause been identified, but no real progress has been made to show that it has any specific symptoms, outcome or that it responds to any particular treatment. In light of these considerations he proposes complete abandonment of the diagnosis. Instead he suggests helping and studying people according to the actual problems and symptoms they present with, rather than grouping them into broad diagnostic categories.
As well as refuting the traditional approach of dividing severe mental distress into a small number of disease entities, Bentall’s research undermines a basic tenet of the disease model – that psychotic symptoms are meaningless. Bentall claims that unlike people suffering brain damage, the symptoms of people diagnosed with schizophrenia nearly always concern ‘the patient’s position in the social universe, or wider existential themes’ (Bentall 1998).
To question the dominant ideology of psychiatry too vigorously can prompt the question, ‘why work in the field at all?’ The group of people however, who are most consistently critical of services we provide are the people who use them. The growth of the users movement in Britain has significantly raised the profile of users, but many of the difficulties that gave rise to the movement remain.
A recent survey of 500 mental health service users commissioned by MIND suggested that the majority of people receiving psychiatric treatment are not offered a choice of alternative, do not get enough information to understand what they are agreeing to and are not always given the opportunity to agree or not. (Rogers et al, 1993).
Most community and hospital teams are stretched by demand for services and are under-resourced but drug treatments are unlikely to be affected by financial restrictions. This contrasts with psychological approaches such as psychotherapy and cognitive behavioural therapy that are often in short supply.
If schizophrenia is a biological disease however, then it makes sense that its treatment should be primarily biological. Thus any modern ward round or case conference is likely to be dominated by discussion of diagnosis and treatment, and psychological and social considerations are at best considered secondary. A bio-medical approach dictates that physical treatment is paramount.
A frequent problem that psychiatrists face however is that the people that they are trying to treat may not necessarily be willing participants. This might be attributed to a ‘lack of insight’, itself a further indicator of illness. But the decision to refuse medication can seem rational in the light of their potentially devastating iatrogenic effects, and with conflicting evidence of their efficacy.
The list of side effects of major tranquillisers makes for worrying reading for anyone so it is perhaps not surprising that many users feel they are not given sufficient information about treatments that they may be reluctant to try anyway (Rogers et al 1993). The list includes Parkinsonism, restlessness and sluggishness, tardive dyskinesia (a potentially irreversible brain disorder involving abnormal and uncontrollable muscular movements), and a massive range of other effects including anticholinergic, cardio-vascular, sensitivity reactions, weight gain and sexual dysfunction. (Cobb 1993).
In a recent editorial the British Journal of Psychiatry talked of the ‘rediscovery of negative symptoms of schizophrenia’ and lists; affective flattening, alogia, apathy, amotivation, anhedonia and asociality. (Taylor and Leberzon, 1999). A few years ago people may have been forgiven for interpreting this as a list of side effects of major tranquillisers. Thus damaging effects of treatment can be reframed as symptoms of the original illness.
The article goes on to suggest ‘the reduced range of facial expression remains a core feature of the negative symptom syndrome’. Another striking similarity between negative symptoms and drug side effects! Clearly deficits in functioning and mood problems were identified in patients long before the development of major tranquillisers, but given the near-universal use of these drugs now, the confidence with which psychiatrists attribute some of their patients deficits to negative symptoms seems misplaced.
Since the drugs were first introduced psychiatrists and pharmacologists alike have consistently made claims that major tranquillisers relieve psychotic symptoms. But renaming them ‘antipsychotics’ would have surprised the researchers who first investigated the effects of the new drugs.
One early researcher, Lehmann in 1954 commented: ‘we have not observed a direct influence of the drug on delusional symptoms or hallucinatory phenomena’ and, ‘chlorpromazine may prove to be a pharmacological substitute for lobotomy’ (cited in Breggin 1993). Breggin believes that the unstated intention of prescribing major tranquillisers is to actually induce brain dysfunction in the form of a ‘chemical lobotomy’ rather that to relieve symptoms.
Major tranquillisers are toxic to many brain functions but their most significant impact is on dopamine neurotransmitters, which provide the major nerve pathways from the deeper brain to the frontal lobes and limbic systems. These were the nerve connections most commonly affected in lobotomy. The result is ‘the production of a person who is emotionally blunted and more dependent, and hence more easily controlled’ (Breggin, 1993).
Breggin rejects any notion of benefit for the patient from the use of major tranquillisers. He argues that even without the production of brain dysfunction, the giving of drugs and other physical interventions tends to reinforce the doctor’s role as an authority and the patient’s role as a passive and helpless sick person. He terms this combination of authoritarian suggestion and drug induced brain damage ‘iatrogenic helplessness’ and sees this concept as key to understanding psychiatric treatments (Breggin, 1993).
But do the drugs actually work? Many impressive claims have been made about major tranquillisers by psychiatrists and pharmacologists alike. The Association of the British Pharmaceutical Industry states that the availability of modern medicines developed for schizophrenia is one factor that has greatly improved the quality of life for people with schizophrenia (ABPI 1997).
Doubts about the benefits of these drugs however, are revealed by the analysis of dozens of follow-up studies, from Kraepelin’s work through to the present day which suggest that the overall outcome in schizophrenia has not improved since the introduction of major tranquillisers in the 1950s (Warner 1994).
Furthermore, the ‘pharmacological revolution’ is frequently cited as a major factor in the mass discharges of the mentally ill from institutions in the fifties and sixties. A number of studies however reveal not only that the policy of discharge preceded the advent of major tranquillisers, but that their introduction did not accelerate the rate of discharges (Pilgrim and Rogers 1993).
The question of how effective major tranquillisers really are in treating schizophrenia is made harder to answer by the scarcity of examples of people being treated without their use. The Association of the British Pharmaceutical Industry themselves admit that between 10% and 30% of people experiencing acute episodes of schizophrenia do not respond to medication. (ABPI, 1997).
Warner (1994) suggests there are a further four distinct groups which should not be treated with major tranquillisers, whose existence has not been well recognised. These are misdiagnosed patients, patients who choose their psychotic symptoms over the disabling effects of medication, patients for whom tardive dyskinesia is a significant problem and patients who show signs of good prognosis.
Warner describes the findings of ten studies, most of which were follow up studies of groups of patients who were randomly assigned a major tranquilliser or a placebo. In all cases patients were assigned to drug or placebo treatments at the beginning of the study, rather than replacing drug treatment with a placebo half way through.
Generally the studies indicate that patients with good prognoses recovered quicker and relapsed less often when not receiving medication. For some, major tranquilliser use appeared to increase the possibility of relapse.
Warner (1997) claims that several studies support the possibility that this phenomena could be due to ‘drug induced dopamine super-sensitivity’ caused by long term use of major tranquillisers. Withdrawal of major tranquillisers could lead to rebound symptoms, worse than those that would have been present without treatment with medication.
How reliable are these findings? One of the problems with investigating drug free treatments is that they are so uncommon. Studies of the kind described above are rare compared to the thousands of papers researching conventional chemical approaches. These initial findings however seem encouraging enough to warrant further research.
So can it be said that service users benefit in any way from the domination of the bio-medical model? One potential benefit is the removal of individual liability for unacceptable behaviour. Evidence suggests however that users tend to see their problems overwhelmingly in social and psychological terms.
In the MIND survey few people identified their problem as an illness and were generally not prepared to internalise the bio-medical view. Instead they were more likely to see it as unhelpful and stigmatising. Social factors that psychiatrists might see as contributing to an illness were perceived as the actual problem (Rogers et al 1993). In medicalising the problem, the experience of the person in distress is reduced to deficits in such areas as cognition and perception rather than as meaningful within the context of their life experiences as Bentall (1998) would suggest.
Research conducted by Mechanic et al (1994) on the effect of illness attribution on quality of life revealed how attributing ones problems to mental illness significantly contributed to perceived stigma, lower self-esteem and a higher level of depression. Interestingly, the survey also demonstrated one possible advantage of a more physical approach; those who attributed their problems to a ‘physical, medical or biological’ problem reported more positive social relations and higher overall quality of life.*
One hundred and forty years ago an editorial in the forerunner of the British Journal of Psychiatry stated that ‘Insanity is purely a disease of the brain. The physician is now the responsible guardian of the lunatic and must ever remain so’. Only ten years ago an American psychiatrist writing in an editorial in the Journal Psychological Medicine stated ‘there can be no such thing as a psychiatry that is too biological’ (cited in Bentall, 1998). These two statements reflect a consistent commitment from psychiatrists to the theory that extremes of mental distress are manifestations of a disease process and require medical treatment.
It is unfortunate that such views have endured when, in the century and a half that has elapsed, little additional supporting evidence has been found. As a number of researchers and practitioners in the field have stated, what might be helpful is a more pluralistic approach to research and treatment which relocates biology as just one of many significant areas and places the human being back at the heart of the matter.
THE ASSOCIATION OF THE BRITISH PHARMACEUTICAL INDUSTRY (1997) Target Schizophrenia. London, ABPI.
BENTALL, R. (1998) Why There Will Never Be a Convincing Theory of Schizophrenia. In ROSE, S. (1998). From Brains to Consciousness? Essays on the New Sciences of the Mind. London, Penguin.
BEBBINGTON,P. WIKINS,S. JONES,P. FOERSTER,A. MURRAY,M. TOONE,B. LEWIS,S. (1993) Life Events and Psychosis. Initial Results from the Camberwell Collaberative Psychosis Study. British Journal of Psychiatry. No 162, pp72-79.
BOYLE, M (1990) The Non-discovery of schizophrenia in BENTALL, R.P. (1990) Reconstructing schizophrenia. London, Routledge.
BREGGIN, P.R. (1993) Toxic Psychiatry. London, Harper Collins.
COBB, A. (1993) Safe and Effective? MIND’s views on Psychiatric Drugs, ECT and Psychosurgery. London, MIND Publications.
DAWSON, P.J. (1997) A reply to Kevin Gournay’s “Schizophrenia: a review of the contemporary literature and implications for mental health nursing theory, practice and education”. Journal of Psychiatric and Mental Health Nursing. No.4, pp1-7.
GOURNAY K (1995) New facts on schizophrenia. Nursing Times, 91 (25), pp32-33.
MECHANIC, D. McALPINE, D. ROSENFIELD,S & DAVIS,S. (1994) Effects of illness attribution and depression on the quality of life among persons with serious mental illness. Social Science Medicine. Vol.39, No2, pp155-164
McCRONE, S (1996) The Impact of the Evolution of Biological Psychiatry on Psychiatric Nursing. Journal of Psychosocial Nursing, Vol. 34 (1), pp 38-46.
PILGRIM, D. & ROGERS, A. (1994) A Sociology of Mental health and Illness. Buckingham, Open University Press.
ROGERS, A & PILGRIM, D (1996) Mental Health Policy in Britain. A Critical Introduction. London, MacMillan.
ROGERS, A PILGRIM, D & LACEY, R (1993) Experiencing Psychiatry. Users Views of Services. London, MacMillan.
SEDGWICK, P (1982) Psychopolitics. London, Pluto Press.
SZYMANSKI S., KANE J.M. & LEIBERMAN JA. (1991) A selective review of biological markers in schizophrenia. Schizophrenia Bulletin. No.17, 99-101.
TAYLOR, S.F. & LIBERZON, I. (1999) Paying attention to emotion in schizophrenia. British Journal of Psychiatry. 174 pp6-8.
WARNER, R (1997) Recovery from Schizophrenia. Psychiatry and Political Economy. London, Routledge.