a response to dr. barrett

7
RICHARD WARNER A RESPONSE TO DR. BARRETT To his eternal glory, the British naval hero Lord Nelson (when he was still a mere vice-admiral) was guilty of an act of intentional blindness in the defense of his country. When signaled to withdraw at the Battle of Copenhagen by a commanding officer who was doubtful of the outcome, Nelson clapped his telescope to his blind eye (lost in an earlier naval encounter), reported to an aide, "I really do not see the signal" and fought on to victory. While I appreciate Dr. Barrett's many generous remarks about my book, I fear that, in defense of his vision of schizophrenia, he is guilty of Nelson's offense -- deliberate blindness. WHAT IS SCHIZOPHRENIA? It takes a special outlook, for example, to read Kendler and Robinette's (1983) twin registry study, which shows that schizophrenia is sixteen times more common in identical twin siblings of schizophrenics than in fraternal twin siblings, and to see -- not what many would see, powerful evidence for a genetic influence in the etiology of schizophrenia -- but instead evidence against genetic transmission in the finding that a majority of identical twin pairs were not concordant for the condition. Confronted with the observation (in the same paper) that the role of genetic factors in predisposing to schizophrenia is somewhat stronger than in hypertension, diabetes or peptic ulcer, would Dr. Barrett argue that a multifactorial- genetic model for these medical conditions would be even more "mys- terious" or "enigmatic" than he believes it to be in schizophrenia? The other articles which Barrett cites to sustain his case for the weakness of the genetic factor in predisposing to schizophrenia are equally questionable. I have described elsewhere (Warner 1983) some of the problems with Abrams and Taylor's (1983) article to which Barrett attaches importance. In brief, their study is flawed by their applying narrow "modern criteria" to a family study of schizophrenia, finding a low prevalence of the disorder (as one would predict from the use of narrow criteria) among first-degree relatives, comparing this familial prevalence (16.1 per 1,000 adults) with a "generally accepted population prevalence" of 8 per 1,000 not narrowly defined and then drawing the unwarranted conclusion "that the case for familial transmission of narrowly defined schizophrenia is weak." Without knowing the population prevalence of narrowly defined schizophrenia, of course, they can draw no useful conclusion about familial transmission at all. Culture, Medicine and Psychiatry 12 (1988) 389--395. © 1988 by KluwerAcademic Publishers.

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Page 1: A response to Dr. Barrett

RICHARD WARNER

A R E S P O N S E T O DR. B A R R E T T

To his eternal glory, the British naval hero Lord Nelson (when he was still a mere vice-admiral) was guilty of an act of intentional blindness in the defense of his country. When signaled to withdraw at the Battle of Copenhagen by a commanding officer who was doubtful of the outcome, Nelson clapped his telescope to his blind eye (lost in an earlier naval encounter), reported to an aide, "I really do not see the signal" and fought on to victory. While I appreciate Dr. Barrett's many generous remarks about my book, I fear that, in defense of his vision of schizophrenia, he is guilty of Nelson's offense -- deliberate blindness.

WHAT IS SCHIZOPHRENIA?

It takes a special outlook, for example, to read Kendler and Robinette's (1983) twin registry study, which shows that schizophrenia is sixteen t imes

more common in identical twin siblings of schizophrenics than in fraternal twin siblings, and to see -- not what many would see, powerful evidence for a genetic influence in the etiology of schizophrenia -- but instead evidence against genetic transmission in the finding that a majority of identical twin pairs were not concordant for the condition. Confronted with the observation (in the same paper) that the role of genetic factors in predisposing to schizophrenia is somewhat stronger than in hypertension, diabetes or peptic ulcer, would Dr. Barrett argue that a multifactorial- genetic model for these medical conditions would be even more "mys- terious" or "enigmatic" than he believes it to be in schizophrenia?

The other articles which Barrett cites to sustain his case for the weakness of the genetic factor in predisposing to schizophrenia are equally questionable. I have described elsewhere (Warner 1983) some of the problems with Abrams and Taylor's (1983) article to which Barrett attaches importance. In brief, their study is flawed by their applying narrow "modern criteria" to a family study of schizophrenia, finding a low prevalence of the disorder (as one would predict from the use of narrow criteria) among first-degree relatives, comparing this familial prevalence (16.1 per 1,000 adults) with a "generally accepted population prevalence" of 8 per 1,000 not narrowly defined and then drawing the unwarranted conclusion "that the case for familial transmission of narrowly defined schizophrenia is weak." Without knowing the population prevalence of narrowly defined schizophrenia, of course, they can draw no useful conclusion about familial transmission at all.

Culture, Medicine and Psychiatry 12 (1988) 389--395. © 1988 by KluwerAcademic Publishers.

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390 R I C H A R D W A R N E R

The study by Pope and co-workers (1982), in which indirect data on fewer than 200 relatives of group of patients with narrowly defined schizophrenia was examined, can scarcely be considered rigorous enough for us to rethink the whole question of the heritability of schizophrenia, nor yet to claim that I have misled the reading public by withholding key facts. This is particularly true since I made it clear that I am not using a narrow definition of schizophrenia in my book, but the broader, British classification, which is most commonly used around the world.

I have a similar problem in accepting Barrett's criticism that my references to the dopamine hypothesis and other biochemical theories of schizophrenia endorse current beliefs and simplify the issues "by failing to mention important areas of contention." What I actually wrote was: "The large number of such theories is perhaps an indication of the inadequacy of any one hypothesis and of our relative ignorance. . , of the biochemis- try of the brain" (Warner 1985, p. 26). Nor do I see how my handling of the dopamine hypothesis legitimizes the use of antipsychotic drugs, as Barrett suggests, when the entire thrust of the discussion in the relevant chapter is aimed at demonstrating that such drugs may, in fact, worsen the hypothesized biochemical defect in schizophrenia.

Barrett's blindness to what I actually wrote, in defending of his claim that I have been "mischievous" in presenting "highly questionable hypo- theses as the facts of schizophrenia," becomes very evident when he implies that I see CT scan abnormalities as specific to schizophrenia. Again, my actual words are: "Perhaps the most probable explanation is that the cerebral atrophy found in some schizophrenics is an indicator of some earlier brain injury which is n o t specific to schizophrenia . . . " (p. 27, italics added).

Barrett seems so keen to de-emphasize the biology of schizophrenia that he has uncritically accepted the limited evidence against the herita- bility of the condition and has seen specters in my writing which are not there. Why should he have made such errors? The answer seems to lie in his assumption that a condition in which familial transmission plays a role and which has a demonstrable biochemical abnormality must somehow be "permanent." If I shared that belief, I too would be at pains to question the biological aspects of schizophrenia, for my book is an assault on the notion of the inevitable permanence of schizophrenia. It pulls together a good deal of evidence which suggests that complete recovery from schizophrenia is not uncommon and is, indeed, frequent under certain social conditions. I cannot conceive, though, how any mental process (such as experiencing pleasure or learning a language) can fail to have a biochemical correlate, or how any abnormal mental condition, permanent

Page 3: A response to Dr. Barrett

RESPONSE TO DR. BARRETT 391

or transitory, can occur without some associated biochemical anomaly. Nor do I understand why a condition with an inherited vulnerability must

needs be permanent - - peptic ulcer, porphyria and asthma are all examples of illnesses which are often intermittent or transitory in nature, and in which biological or psychological stresses interact with an inherited vulnerability to produce episodes of disorder.

"VULGAR" MATERIALISM

From Barrett 's criticisms of the background information I presented on schizophrenia we should move to his critique of my materialist theoretical approach. Dialectical materialists since Marx have routinely referred to a non-dialectical materialist approach as "vulgar" materialism. The use of this epithet implies that the dialectical approach will always be superior in its analytical power. I make no apologies, however, for the fact that I use a purely non-dialectical form of infrastructural determinism in my work. I prefer a research strategy which allows me to generate ideas about how the circumstances of our material existence affect the course of mental disorder and which allows those ideas to be empirically tested. The dialectical approach does not lend itself to analysis by the scientific method. As the Marxist scholar Isaiah Berlin (1978 :115- -116) writes:

The Marxist doctrine of movement in dialectical collisions is not a hypothesis liable to be made less or more probable by the evidence of facts, but a pattern, uncovered by a non- empirical, historical method, the validity of which is not questioned. To deny this would be tantamount, according to Marx, to a return to "vulgar" materialism . . . .

Anthropologist Marvin Harris (1979:145) clarifies this issue further:

The central weakness of dialectical epistemology is the lack of operational instructions for identifying causally decisive "negations".... Since there are no instructions for identifying the properties or components that are the crucial negations, dialectical relationships can never be falsified.

The research strategy which I have found valuable in my work is Harris 's cultural materialism. This theoretical approach proposes that modes of product ion and reproduction will probabilistically determine domestic and political economy which will in turn probabilistically determine the ideological superstructure (Harris 1979). It by no means eliminates the possibility of feedback from the cultural superstructure influencing the economy, product ion and reproduction or, to use the phrase Barrett quotes, the consideration of the way "in which man actively shapes the world he lives in at the same time as it shapes him" (Giddens

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392 R I C H A R D W A R N E R

1971:21). Barrett, very properly, eschews a unidirectional infrastructural determinism. Cultural materialism, I believe, avoids this flaw but without weighing itself down with the Hegelian baggage of the untestable dialectical approach.

Does my "vulgar" materialist analysis turn out to be as fettered as Barrett fears? I believe not. In fact, the chapter of Recovery from Schizo- phrenia entitled "Madness and the Industrial Revolution" expresses many arguments similar in scope and content to those of Foucault for which Barrett has praise. I outline there the relationships between the capitalist transformation of production, Enlightenment ideals of individualism and progressive rationalism, and the development of moral treatment ap- proaches which helped legitimize the development of institutions for the insane (pp. 103--6). I point out how the development and management of asylums were influenced by the growth of wage labor and by the Poor Laws designed to shape the new industrial work force (pp. 106--9). I stress how psychiatric ideology, then and now, switches to the direct opposite of its original intent, under the influence of changes in the economy and labor force requirements, while retaining the original name. Moral treatment was still "moral treatment" when it became unenlivened confinement, overcrowding and mechanical restraint; community treat- ment remains "community treatment" when it encompasses the abandon- ment of the mentally ill to hunger, victimization, disease and death on Skid Row (pp. 109--11).

In other words, I argue precisely the point which Barrett can see in Foucault but is unable to perceive in Recovery from Schizophrenia -- "not only that the capitalist mode of production makes possible the develop- ment of sites of discipline and an ideology of individualism, but also that these practices and ideas organize the accumulation of men which fuels capitalism." Then I take the further step of showing how readily profes- sional ideology in these "sites of discipline" adapts to changes in political economy.

B A R R E T T ' S P E R S P E C T I V E ON S C H I Z O P H R E N I A

I doubt that my "thesis could be expanded considerably" if I adopted Barrett's approach to schizophrenia. Rather, it might be restricted to a series of blank pages following some such title as "Recovery from Schizophrenia -- If There is Such a Condition, Which Seems Doubtful." Barrett's adherence to an extreme form of cultural relativism leads him to the conclusion that schizophrenia is an invention of the industrial age -- that the condition did not exist before the nineteenth century and that the

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R E S P O N S E TO DR. B A R R E T T 393

label is irrelevant to the categorization of psychosis in the Third World. What we call psychosis could be divided up any number of ways, it is true. "Schizophrenia" is a relatively arbitrary category, in that sense, and I personally doubt that it will survive long after we gain substantial insights into the neurophysiology of mental disorder. Given that we do categorize some psychoses as schizophrenia, however, I believe that Barrett's view is incorrect. The same conditions did exist before the industrial age and can profitably be studied in Third World cultures.

I would argue that Kraepelin's formulation of dementia praecox, with poor outcome as the central feature, only became possible when recovery rates in the psychoses he was studying declined with the advance of industrialization. This does not mean that these psychoses did not exist before Kraepelin, but looking back on earlier periods of history, we might well have difficulty in recognizing descriptions of the conditions if we expect chronicity to be a prominent feature (Warner 1987). I am more impressed than Barrett, apparently, by the evidence that schizophrenia existed before the eighteenth century. He reserves only a footnote and a mocking tone for an article which presents information contrary to his view, and which indicates, for example, that the categorization of mental disorder in ancient India and Rome distinguished schizophrenia-like conditions from those resembling mania, depression, catatonic stupor and delirium (Jeste et al. 1985). Other recent work has pointed to evidence for schizophrenia among the patients consulting Richard Napier, a seven- teenth-century English specialist in the treatment of mental disorders (MacDonald 1981, Ellard 1987). The interesting question which remains open, and will no doubt continue to remain open, since the concept of schizophrenia is peculiar to our own time, is whether schizophrenia was at all c o m m o n before Kraepelin's day.

Barrett's claim that "the fundamental constitutive components of schi- zophrenia may not necessarily be found in some non-Western cultural settings" is particularly difficult to accept in the light of a large body of literature indicating that clinical and research psychiatrists in the Third World have no difficulty in identifying schizophrenia, even when defined by rigorous standards (WHO 1973). The "fundamental" component which is often lacking in these settings is poor outcome: but unless we are willing to accept that schizophrenia c a n be a benign condition, we can never draw the important conclusion that it /s a benign condition under certain circumstances. Even if Barrett cannot accept this argument, he should confront the evidence that there are chronic schizophrenics in the Third World (Westermeyer 1980) -- but fewer of them.

What holds Barrett back from applying the Western concept of "schi-

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zophrenia" to Third World psychotics is his failure to grasp the important distinction between what anthropologists term emic and etic types of data. The emic approach relies on the native informant's description and analysis of events: the etic approach uses the outside observer's categories and concepts in its analysis of cultural phenomena. A research strategy which fails to make use of both types of data cannot achieve the explana- tory power of one that does use both (Harris 1979). Barrett is arguing that we may only use emic data in studying psychosis in the Third World: he is disturbed because my analysis incorporates both approaches -- Western diagnostic concepts as well as folk categories of illness. His approach would yield insights into the social meaning of psychosis in pre-industrial cultures; mine allows us to progress from there to draw conclusions about why schizophrenia assumes the dimensions it does in Western society.

T H E F I N A L R E C O M M E N D A T I O N S

Barrett is concerned because I have made recommendations for the treatment of schizophrenia within our current economic system. As a community psychiatrist who confronts such issues daily, I cannot regard this segment of my book as a weakness. In fact, I am hopeful that other mental health practitioners will find in the book the stimulus for ideas for humane and effective systems of care, just as my analysis of the factors shaping the course of schizophrenia has had a direct effect on my own program development philosophy. As for Barrett's claim that I have fougl, shy of macrosocial interventions, I can only redirect him to my discussion of psychiatric care in centrally planned societies, my review of proposals for a return to a full-employment economy and to the conclud- ing remark in my book (p. 307): "To render schizophrenia benign we may, in essence, have to restructure Western society."

R E F E R E N C E S

Abrams, R. and M. A. Taylor 1983 The Genetics of Schizophrenia: A Reassessment Using Modem Criteria.

American Journal of Psychiatry 140:171-- 175. Berlin, I.

1978

Ellard, J. 1987

Karl Marx: His Life and Environment. Fourth Edition. Oxford: Oxford Uni- versity Press.

Did Schizophrenia Exist before the Eighteenth Century? Australian and New Zealand Journal of Psychiatry 21: 306--314.

Giddens, A. 1971 Capitalism and Modern Social Theory: An Analysis of the Writings of Marx,

Durkheim and Mex Weber. Cambridge: Cambridge University Press.

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Harris, M. 1979 Cultural Materialism: The Struggle for a Science of Culture. New York:

Random House. Jeste, D. V., R. Carmen, J. B. Lohr and R. J. Wyatt

1985 Did Schizophrenia Exist before the Eighteenth Century? Comprehensive Psy- chiatry 26: 493--503.

Kendler, K. S. and C. D. Robinette 1983 Schizophrenia in the National Academy of Sciences -- National Research

Council Twin Registry: A 16-Year Update. American Jounal of Psychiatry 140: 1551--1563.

MacDonald, M. 1981 Mystical Bedlam: Madness, Anxiety, and Healing in Seventeenth-Century

England. Cambridge: Cambridge University Press. Pope, H. D., J. M. Jonas, B. M. Cohen and J. F. Lipinski

1982 Failure to Find Evidence of Schizophrenia in First-degree Relatives of Schi- zophrenic Probands. American Journal of Psychiatry 139: 826--828.

Warner, R. 1983 Modern prevalence rates of schizophrenia. (Letter to the editor.) American

Journal of Psychiatry 140:1108. 1985 Recovery from Schizophrenia: Psychiatry and Political Economy. London:

Routledge and Kegan Paul. 1987 Commentary on "Did Schizophrenia Exist before the Eighteenth Century?"

Australian and New Zealand Journal of Psychiatry 21: 317--318. Westermeyer, J.

1980 Psychosis in a Peasant Society: Social Outcomes. American Journal of Psychia- try 137: 1390--1394.

World Health Organization 1973 The International Pilot Study of Schizophrenia. Volume 1. Geneva: World

Health Organization.