It is hard to tell what the PACE research really indicates without details of symptoms, treatment, and transition to psychosis for individual patients. The most benign interpretation would be that about 50 per cent of their patients had false positive diagnoses and were therefore treated without the normal level of evidence for mental illness. However, it is entirely possible that all or most of their patients had false diagnoses and that any transitions to psychosis were only adverse reactions to treatment.
Despite the honourable intentions of many of the researchers in this field, problems with symptomatology and treatment make it unlikely that pre-psychosis detection and intervention programmes will ever deliver the kind of unequivocal social and community health advantages that are generally expected from preventive medicine campaigns. This means that the extension of the definition of schizophrenia into a prodromal phase is unlikely to further enhance the plausibility of the medical model of schizophrenia.
In fact, it is quite likely that in the long run pre-psychotic programmes will damage the credibility of the medical model. When psychiatrists openly refer to pre-psychotic indicators as being ‘putative’, and then proceed to intervene in the lives of people who are thought to manifest them, treating them with the same potent neuroleptics that are used on supposedly full-blown schizophrenia, the argument that schizophrenia is just a psychiatric myth looks ever more persuasive.
This point is further emphasised by the blatant commercial opportunism by pharmaceutical companies evident in this area. A preventive medicine campaign based on the type of prodromal symptoms and risk factors specified in the Australian Clinical Guidelines for Early Psychosis potentially defines a whole generation of young people as being at-risk and in need of treatment. If pharmaceutical marketing strategies are eventually exposed as the primary motivating force behind the concept, it will make it a lot easier to argue that the whole medical model for schizophrenia is a psychiatric myth invented to serve special interests.
The use of magical thinking as the pre-eminent symptom by leading researchers is particularly damaging. This is because the researchers clearly had prior knowledge from their own surveys that magical thinking is experienced by the majority of normal young people. The researchers simply ignored evidence they had themselves collected and published that magical thinking is not a sign of mental pathology at all. Detection and treatment of magically-thinking adolescents provides evidence for those who might want to argue that pre-psychotic treatment is no more than a crude attempt by medical scientists to nip mystical/religious experience in the bud.
The pseudo-authoritativeness characterising much of the literature in this field regularly demonstrates a lack of reflection on the part of early-psychosis researchers about the superficial nature of their claims. A good example of this can be found in the Early Psychosis Training Pack. Under the heading of ‘How to achieve early recognition—triggers for considering psychosis or pre-psychosis’, the Training Pack advises doctors dealing with adolescents and young people to be sure of ‘[m]aintaining a high index of suspicion—signs to look out for’.[48] This advice is followed by the sixteen-item list of ‘Signs and Symptoms’ adopted by the Australian Clinical Guidelines for Early Psychosis. The first item on this list is ‘suspiciousness’. This juxtapositioning of the idea of suspicion, first as an efficiency measure for diagnosticians and then as a sign of pathology in patients, begs the question: Is it credible for psychiatrists to claim that ‘suspiciousness’ in young people is a sign of serious mental illness when the same psychiatrists argue that clinicians should cultivate an attitude of suspicion in themselves as an efficiency measure?
There is a certain degree of irony here, where suspicion is encouraged to uncover suspicion, which apparently escapes the authors of the Training Pack. But the contrariness raises an important question as to whether suspiciousness and the other putative signs and symptoms are correctly judged to be indications of an underlying serious mental illness. The authors seem to be claiming that suspicion is a worthy quality when it is used as a tool of efficiency by a person with authority but it becomes a sign of pathology when it is found in a person of low status, or in a person who is challenging authority.
The EPPIC researchers have cited a 1938 article by D. Ewen Cameron as their original source of authority for believing that ‘suspiciousness may predict subsequent psychosis’.[49] This is itself a decidedly suspicious source. Cameron is the Canadian psychiatrist who gained notoriety in the 1980s after it was revealed he had undertaken cruel and unethical experiments on his patients during the 1950s and 1960s with funding from the CIA.[50]
Using a deep sleep technique combined with multiple daily assaults of ECT, Cameron attempted to cure schizophrenia by erasing all memory of self from his patients’ minds. The CIA was apparently interested in utilising these techniques in espionage work. In 1988 the CIA acknowledged complicity in Cameron’s work when they arranged to pay $750,000 in compensation to some of the victims.[51] Cameron’s exploits were the subject of a 1979 book by John Marks entitled The Search for the Manchurian Candidate.[52]
Cameron is perhaps the most widely discredited psychiatrist of all time, and contemporary psychiatric researchers who cite him as a source of authority for their own work demonstrate, at the very least, a deficiency of judgement. Nevertheless, the Cameron-inspired symptomatology has been incorporated into the Australian Clinical Guidelines for Early Psychosis, in which suspiciousness is given as the leading symptom of pre-psychotic schizophrenia.[53] The linking of Cameron’s name with a government-sponsored preventive medicine campaign for schizophrenia is a fairly extraordinary development.
But the deficiency of judgement regarding Cameron extends beyond merely adopting his suggestion about the use of suspiciousness as a symptom. Proponents of early psychosis repeatedly cite Cameron as the originator of the whole concept of early detection and intervention programmes for schizophrenia.[54] Patrick McGorry, the Director of EPPIC, even quoted an extract of Cameron’s article to lead his introductory essay to a June 1998 early-psychosis supplement he edited of the British Journal of Psychiatry:
"Very early schizophrenia still constitutes a relatively unexplored territory. Entry into this territory calls for new ideas on the social problems involved in bringing the early schizophrenic promptly under treatment, or where the treatment should be carried out and in what it should consist. D. Ewen Cameron (1938)"[55]
In his 1938 article Cameron wrote enthusiastically about the effectiveness of ‘the newer therapeutic techniques used in schizophrenia’. But apparently unnoticed by McGorry, in its original publication form, Cameron’s article was immediately followed with a commentary by the leading authority on schizophrenia at the time, Harry Stack Sullivan. Unlike McGorry, and without foreknowledge of Cameron’s future notoriety, Sullivan demonstrated disgust with Cameron’s proposal and issued a strong rebuttal.
"I would be very deeply disturbed if, as is implied by the last speaker [Cameron], people who show signs of personality disorders, early mental disorder of an indeterminate kind, were to be rushed through treatment with insulin, metrazol and camphor on the chance that they might otherwise have developed schizophrenia. I privately have a suspicion that might have a distinctly unfavourable effect on the general intelligence level and so on of the community.
What does it mean that a person will have schizophrenia which can be detected by the intelligent layman months to years before the schizophrenia appears? In seven and half years of exclusive preoccupation with the schizophrenia problem I was unable to put my finger on anything sufficiently simple and obvious to service this purpose."[56]
Sullivan’s scorn in 1938 apparently helped to knock out the idea of schizophrenia prevention for almost sixty years. But what are we to make of its recent resurrection? If it is now feasible to use the latest form of pharmacological shock—atypical neuroleptics—perhaps it is only because there is no longer any figure in the psychiatric profession, such as Sullivan, with both high stature and a highly developed social conscience, to mount the necessary protest.
There are several fundamental knowledge gaps in the pre-psychosis concept that a Sullivan-like figure could exploit. Firstly, no firm consensus exists about what psychosis actually is. DSM-IV introduces the spectrum of psychotic disorders by stating: 'The term psychosis has historically received a number of different definitions, none of which has achieved universal acceptance'.[57] The manual goes on to discuss various narrower and broader definitions of psychosis.
Is it a narrower or a broader form of psychosis that is to be prevented with pre-psychotic treatment? This question is not discussed by pre-psychosis researchers. But how can pre-psychotic detection criteria even be considered until a consensus is reached about how to define the psychosis that is to be prevented? If a broader definition of psychosis is agreed upon then this will inevitably mean that a broader range of pre-psychotic symptoms are required to predict it. The opposite is true for a narrower definition.
Closely associated with this is the problem of establishing a baseline for the lifetime prevalence of psychosis in the general community. Once again this issue does not arise in the pre-psychosis literature. But if a baseline of prevalence has not been calculated before pre-psychotic detection and treatment begins it will be impossible to determine whether pre-psychotic treatment reduces or increases the rate of psychosis in the general community.
Another closely-related unresolved problem is the imprecision in determining the threshold of psychosis. This is particularly important when people are being given pre-psychotic treatment. Without a precise definition of the threshold it is impossible to compare the efficacy of preventive treatments. This problem has been discussed in the literature and the EPPIC researchers have admitted they are forced to make determinations of psychosis 'arbitrarily'.
A serious deficit in the concept of pre-psychotic detection is the failure to compare the prevalence rate of supposed pre-psychotic indicators with the prevalence rate for psychosis. The prevalence rate is the percentage of the general community who exhibit the symptoms. If the two rates do not correspond fairly closely the pre-psychotic indicators are unlikely to be accurate. A common assumption is that psychotic disorders have a lifetime prevalence of about 2 to 3 per cent.[58] For argument’s sake let us choose the higher figure and use it to test the prodromal symptoms used by the EPPIC researchers.
The EPPIC researchers experimented with a couple of different sets of prodromal symptoms to select the people they thought were pre-psychotic. Both of these sets used 'magical thinking' as a symptom, and each time it was used magical thinking alone could indicate a pre-psychotic condition. This means that the prevalence rate of magical thinking in the general community represents the minimum prevalence rates for these sets of prodromal symptoms. In other words, since we know that 51 per cent of adolescents experience magical thinking, then we also know that EPPIC's pre-psychotic indicators identify at least 51 per cent of the general population of young people.
If we compare the 50 per cent prevalence rate for the pre-psychotic selection criteria, with the 3 per cent prevalence rate for psychosis, we can begin to see the scale of the problem that will emerge with wide-scale implementation of pre-psychotic treatment programs. Something like 50 percent of young people could be targeted and treated when only 3 percent are really at-risk. On top of this it is not even certain the selection criteria identify the 3 percent who are actually at-risk. Perhaps the 50 percent target group is wholly comprised of people who, if left alone, would never experience psychosis.
But the outcome of the PACE research tells an even worse story than that. It was claimed that 40 per cent of the patients selected by these means became psychotic after six months of treatment, and 48 per cent became psychotic within twelve months. Assuming the 50 per cent prevalence rate for the selection criteria, this means that if this program were adopted on a large scale the rate of psychosis in the general community would be increased, by the application of six months prophylactic treatment, from the baseline of 3 per cent to something like 20 per cent. Not only that, but the longer the treatment is given, the higher the psychosis rate goes. The EPPIC research indicates that a full year of prophylactic treatment for all the young people in the community who are symptomatic would raise the prevalence rate of psychosis from 3 per cent to about 25 per cent.
As Harry Stack Sullivan so rightly observed 60 years ago attempts to implement preventive medicine programs for schizophrenia are likely to have a "distinctly unfavourable effect on the general intelligence level and so on of the community".
Subjective opinions about people, across generations, involving concepts like 'odd beliefs or magical thinking', 'odd thinking' and 'odd appearance' are never going to lend themselves to genuine scientific research. Indeed, it would be decidedly odd if psychiatric researchers actually believed that they would. So what is going on with pre-psychotic research? Breggin and Cohen have explained the anomalous nature of much psychiatric research this way: 'The sad truth is that, in the field of psychiatry, it is impossible to "trust in research". Nearly all the research in this field is paid for by drug companies and conducted by people who "deliver" in the best way possible for those companies'.[59]
Next: 10. Conclusion
[48] McGorry and Edwards, Early Psychosis Training Pack, p. .9.
[49] Yung et al., ‘Monitoring and Care of Young People at Incipient Risk of Psychosis’, p. 286.
[50] Report of the Royal Commission Into Deep Sleep Therapy, Volume 2, pp. 48–58.
[51] Peter Breggin, Toxic Psychiatry, p. 250.
[52] John Marks, The Search for the Manchurian Candidate.
[53] National Early Psychosis Project, Australian Clinical Guidelines for Early Psychosis, p. 13.
[54] See for example, Alison R. Yung et al., ‘Prediction of psychosis: A step towards indicated prevention of schizophrenia’, British Journal of Psychiatry, pp. 14–20. and Richard Jed Wyatt et al., ‘First-episode schizophrenia: Early intervention and medication discontinuation in the context of course and treatment’, pp. 77–83.
[55] D. E. Cameron, ‘Early schizophrenia’. Quoted in Patrick McGorry, ‘Preventive strategies in early psychosis’, pp. 1–2.
[56] Harry Stack Sullivan, ‘Discussion’, in D. Ewen Cameron, ‘Early schizophrenia’, p. 579.
[57] American Psychiatric Association, op. cit., 1994, p. 273.
[58] T. J. Crow, 'Sexual selection, Machiavellian intelligence, and the origins of psychosis', Lancet, 342, 1993, 594-599.
[59] Peter R Breggin and David Cohen, Your drug may be your problem, Perseus, Reading, 1999, p. 189.