Schizophrenia and civilization 9780876683804

Table of contents :
Frontmatter
Chapter 1 Introduction (page 1)
Chapter 2 Is Schizophrenia of Recent Origin? (page 19)
Chapter 3 Is Schizophrenia a Disease of Civilization? (page 43)
Chapter 4 The Distribution of Schizophrenia in the Americas (page 77)
Chapter 5 The Prevalence of Schizophrenia in Europe and Israel (page 97)
Chapter 6 Croatia and Western Ireland: Two Special Cases (page 115)
Chapter 7 Schizophrenia in Asia, Australia, and Africa (page 137)
Chapter 8 Clinical Similarities and Differences in Schizophrenia Across Cultures (page 149)
Chapter 9 Synthesis (page 169)
References (page 189)
Index (page 223)

Citation preview

Schizophrenia anol Civilization

Upon this gifted age, in its dark hour, Rains from the sky a meteoric shower Of facts... they lie unquestioned, uncombined, Wisdom enough to leech us of our ill [s daily spun, but there exists no loom To weave it into fabric. —Kdna St. Vincent Millay, Sonnet 137

Scinizopharenia andl Civilization

E. Fuller Torrey, M. D.

pa Jason Aronson New York @ London

Copyright © 1980 by Jason Aronson, Inc.

All rights reserved. Printed in Canada. No part of this book may be used or

reproduced in any manner whatsoever without written permission from Jason Aronson, Inc. except in the case of brief quotations in reviews for inclusion in a magazine, newspaper or broadcast. ISBN: 0-87668-80-4

Library of Congress Catalog Number: 79-5193]

Manufactured in Canada.

for Rhoda and her friends, who must suffer through our ignorance

Acknowledgments Portions of chapter 3 are taken from E. F. Torrey, B. B. Torrey, and B. G. Burton-Bradley, “The Epidemiology of Schizophrenia in Papua New Guinea,” American Journal of Psychiatry 131:567-573, 1974. A brief portion of chapter 8 is also found in E. F. Torrey, ‘‘Epidemiology, in The Disorders of the Schizophrenic Syndrome, edited by L. Bellak,

New York, Basic Books, 1979. Ms. Barbara Torrey and Dr. Dermot

Walsh provided valuable criticism, and Ms. Mary Adams did an excellent job of typing the manuscript.

Contents

Chapter | Introduction l What Is Schizophrenia? On Incidence and Prevalence

What Causes Schizophrenia? | Cultural Studies of Schizophrenia Schizophrenia as a Badge of Civilization What Is Civilization? Summary

Chapter 2. Is Schizophrenia of Recent Origin? 19 Ancient Texts Rx: One Roasted Mouse Enter Schizophrenia Was Schizophrenia Increasing? The Curious Case of the Missing Disease Summary

Chapter 3 Is Schizophrenia a Disease of Civilization? A3 Karly Impressions and Some Myths Dispelled From Cherokees to Kalmucks and the Achinese Studies in Africa The South Pacifie The Making of “Sheer Folklore” Studies since 1960 Schizophrenia That May Not Be Schizophrenia Summary

in the Americas vl

Chapter 4 The Distribution of Schizophrenia Schizophrenia among Minority Groups and Lower Socioeconomic Classes

Vili Schizophrenia and Civilization Prevalence Rates of Schizophrenia in the United States Prevalence Rates of Schizophrenia in Canada and South America Summary

Europe and Israel 97

Chapter 5 The Prevalence of Schizophrenia in Northern Europe Schizophrenia among European Emigrants Western and Southern Europe Eastern Europe Israel Summary

Chapter 6 Croatia and Western Ireland: Croatia

Two Special Cases 15

Western Ireland: The Early Story Studies of Irish Immigrants Recent Irish Findings What Are the Causes? Summary

Chapter 7 Schizophrenia in Asia, Australia, and Africa 137 Japan Taiwan

India, Ceylon, and Iran Australia Africa Summary

Chapter 8 Clinical Similarities and Differences of

Schizophrenia Across Cultures 149

Symptoms and Subtypes Onset, Sex, and Course Month of Birth Treatment Summary

Contents 1X Chapter 9 Synthesis 169 Psychosocial Theories Biological Theories Conclusion

References 189

Index 223

BLANK PAGE

Introduction

We are the hollow men We are the stuffed men Leaning together Headpiece filled with straw. Alas! Our dried voices, when We whisper together Are quiet and meaningless As wind in dry grass Or rats’ feet over broken glass In our dry cellar Shape without form, shade without colour, Paralysed force, gesture without motion; Those who have crossed With direct eyes, to death’s other Kingdom Remember us—if at all—not as lost Violent souls, but only As the hollow men The stuffed men. —T. 5S. Eliot, “The Hollow Men” (1925)

Schizophrenia is the cruelest disease of the Western world. It afflicts

young adults, often beginning insidiously and progressing until the ambitions, potentials, and hopes of early years are discarded in disar-

ray. In their place lie broken thoughts, inappropriate or stunted emotions, and internal voices or other misperce”'tions that can make existance a living hell. Cancer at least has the decency to kill the body after it has devastated it; schizophrenia rarely does so. Schizophrenia is a common disease. One out of every 100 Americans will be diagnosed as having it during their lifetime. In other countries the incidence can be much higher; in parts of Western Ireland | out of 25 people will be afflicted. The cost of schizophrenia is incalculable,

and includes the expenses of mental hospitals, boarding and halfway houses, educations never used, lost wages, and compensatory welfare payments for those who cannot support themselves. To this must be

added the anguish of relatives and friends, helpless to change the situation or make the person well. It is indeed a disease worthy of Dante’s Inferno.

This book will explore the relationship between schizophrenia and civilization. Although many people have assumed that schizophrenia

has always been with us and exists universally at about the same prevalence rate, the evidence is to the contrary. In all ages and countries a few cases of schizophrenia have existed. These cases can be viewed as the baseline prevalence of the disease, and probably consist largely of organic diseases such as pellagra, trypanosomiasis, temporal

lobe epilepsy, and brain tumors masquerading as the disease. In developing nations the few cases of schizophrenia which do exist are probably of this type; the fact that most such cases have a rapid onset (chapter 3) and a good prognosis (chapter 8) supports this view. Beyond this baseline prevalence, however, there appear to be wide

differences in the distribution of schizophrenia. The disease was apparently rare before 1800, then increased rapidly during the nineteenth century in both Europe and the United States (chapter 2). It

4 Schizophrenia and Civilization continues to be rare in most developing countries although as such countries move toward development a sharp increase in schizophrenia is sometimes seen (chapters 3 and 7). Because of this schizophrenia has become a badge of civilization for some, and its existance pointed to as proof that the country is indeed “‘civilized”’ (chapter 1). In developed countries there is at least an eightfold difference in the

prevalence of schizophrenia. Areas with the highest rates include Ireland, Scandinavia (especially an area in northern Sweden), and astern Kurope (especially part of Croatia) (chapters 5 and 6). Areas with an intermediate prevalence are England, Germany, the United States, and Japan (chapters 4, 5, and 7). Southern European countries

appear to have a low prevalence rate (chapter 5), and developing countries the lowest of all (chapter 3). Schizophrenia occurs more commonly among lower socioeconomic

groups in the United States, England, Japan, Norway, Ireland, and Iceland; in India and possibly Italy the opposite is true (chapters 4-7). The disease is also more prevalent among urban dwellers and among blacks in the United States; northeastern states in particular have been

noted to have a high rate of schizophrenia (chapter 4). In many countries there is also known to bea definite seasonality to the births of people who become schizophrenic, with many more of them born in the

winter and spring months than in summer and fall (chapter 8). The most likely explanations for the epidemiological patterns of schizophrenia are biological, not psychosocial (chapter 9). This coincides with other emerging clinical and laboratory data strongly suggest-

ing that schizophrenia is a collection of brain diseases. Within the biological realm viruses combined with familial or genetic factors explain the data best, although dietary factors and environmental contaminants must be kept in mind. Schizophrenia and civilization, then, are correlated, and the relationship is probably controlled by biological factors. Such is the thesis of this book.

What is Schizophrenia? It is most unfortunate that in the United States the term schizo- —

phrenia is used so broadly—often completely erroneously. The imprecision that surrounds the term impairs our ability to see the disease clearly and thereby probably hinders research on it. Schizophrenia is not, for example, a ‘‘split personality” in the sense of “‘Sybil”’

Introduction 3 or “The Three Faces of Eve,” even though the vast majority of Americans believe this to be so. These “split personalities,” a very rare psychiatric occurrence, are properly called dissociative reactions, and they usually occur in people who do not have schizophrenia.

Rather, schizophrenia is a symptom complex of abnormal brain function consisting of some combination of the following: Disorders of the thinking process. The person may pick up a rubber band and tell you that it is a musical instrument because it is a “‘band”’ and that reminds him of the instruments used in the hospital emergency room where the FBI implanted electrodes in his brain. This thinking pattern demonstrates both loose associations and delusions. Disorders of emotions. The person may have blunted or flattened

emotions or may respond with very inappropriate emotions. For example, he or she may laugh when told something most people would find sad. Disorders of perception and sensory stimuli. The person hears nonexis-

tant voices. These auditory hallucinations are a hallmark of schizo-

phrenia, although they are not found in every patient and are occasionally found in other diseases.

Because of these disorders, the person with schizophrenia may behave in very strange ways or may say very strange things. (For example, he may take off his clothes in public because of a belief that it

will stop the sun from melting.) Thus, the schizophrenic is labeled “crazy.” The disease usually begins in early adulthood and progresses

either steadily or intermittently until middle age, when it becomes | quieter. By then, however, the person manifests residual brain damage

from the disease. Asasymptom complex of disordered thinking, emotions, and perception, there is much agreement worldwide on who should be labeled schizophrenic. A World Health Organization study of schizophrenia

found that psychiatrists in participating centers in nine separate countries could agree on a “concordant” group with schizophrenic symptoms (World Health Organization 1973). This symptom complex is also referred to as “process” schizophrenia by many (Garmezy 1968) and coincides with the usual use of the term schizophrenia in Western European nations, especially Scandinavia. It is also closely allied with

“poor prognosis” schizophrenia as described in studies in Sweden, Norway, England, and the United States (Robins and Guze 1970). It is in this narrow sense of the term that schizophrenia will be used in this book.

6 Schizophrenia and Civilization It would be nice if all the studies to be described in this book utilized a

similarly narrow definition of schizophrenia. The truth, of course, is that many of the studies do not specify what they mean by the term.

Others appear to adopt a broader definition which includes some combination of pseudoneurotic, borderline, latent, atypical, and schizo-affective varieties. Many others apparently include, under the schizophrenia label, acute transient psychotic states that resemble

schizophrenia. The latter condition is often called “reactive” (as opposed to “process’’) schizophrenia (Garmezy 1968) or “good prognosis’ (as opposed to “poor prognosis’’) schizophrenia (Robins and Guze 1970). These acute transient psychoses appear to be especially common in the developing countries of the world and will be discussed in more detail in chapter 3. Such lack of precision in defining schizophrenia has been a major impediment to epidemiologic research and has compromised the most virtuous cross-cultural intentions. Another source of confusion in defining schizophrenia is its separation from manic-depressive psychosis. In the latter disease, the affect is disordered, with either periodic manic episodes or depressive episodes or both. Manic-depressive psychosis is much less common than schizophrenia, and the person having it often is quite normal between attacks. In its early stages, manic-depressive psychosis may be misdiagnosed as schizophrenia, although as time progresses the correct diagnosis usually becomes evident. A small intermediate group of patients who have symptoms of both diseases, usually called schizo-affectives, compounds diagnostic confusion. This confusion often may result in chaos when

diagnosis is considered in a cross-cultural context: separating a schizo- i phrenic from an early manic-depressive patient in one’s own culture | may be difficult, but attempting to do so in another culture or in another language may be impossible. In most Western countries, three schizophrenic patients are admitted to mental hospitals for every one manic-depressive. What can be

said about studies in India (Rao 1966a) or Japan (Seligman 1930) showing ratios of 5:1 or studies in China (Woods 1929) showing a ratio

of 6:1? Are there genuinely more schizophrenic patients or fewer manic-depressive patients, or are these simply differences in diagnosis?

Alternatively, do these differences coincide with claims that schizophrenia is more common in lower socioeconomic populations and manic-depressive psychosis more common in higher socioeconomic classes (Tietz, Lemkau, and Cooper 1941, Odegaard 1956)? What are we to make of a ratio of 8:1 in Nigeria (Lambo 1960) or even 17:1 in South

Introduction 7 Africa (Lamont and Blignault 1953)? At least some of these are due to differences in diagnosis. In the case of South Africa, for instance, we can analyze the relevant studies and find that “‘schizophrenic’”’ patients who were noisy and excited had a better prognosis (Moffson 1954); we

may therefore tentatively conclude that many manic-depressive patients were being categorized as schizophrenic, thus leading to the high

ratio reported for that country. Another apparent example of this mislabeling of manic-depressive patients as schizophrenics is seen when Malays are described as having a high percentage of atypical schizophrenics and schizo-affectives “with a marked depressive or, more often, hypomanic coloring’ (Schmidt 1961b). The manic-depressive picture becomes even more confusing when studies showing a reversed ratio are considered—that is, more manic-

depressive patients than schizophrenic patients. There have been claims that such a pattern is the case in Mediterranean countries such as Morocco, Tunisia, Portugal (Gold 1951) and parts of Italy (Rose 1964). It has also been described for a group of Formosan aborigines (Rin and Lin 1962), among the Maoris of New Zealand (Beaglehole 1950), and most prominently in the Hutterite study in the United States (Eaton and Weil 1955) which will be discussed in detail in chapter 4. If these ratios are really accurate, they may offer important clues about causative factors in manic-depressive psychosis and schizophrenia. This book will not include an analysis of manic-depressive psychosis

in different cultures, as the task of sorting through the literature on schizophrenia appeared sufficiently overwhelming. A discussion of manic-depressive psychosis will be included whenever it will throw light on the true prevalence of schizophrenia—especially in those cases where schizophrenia appears to be either very sparse or very abundant, giving rise to the question of whether cases of schizophrenia have been erroneously called manic-depressive psychosis or vice versa. In a few

studies, the authors fail to separate these two major psychoses and simply lump them together; such instances will be so indicated.

On Incidence and Prevalence Most diseases known to mankind are distributed unevenly around

the world. Some, like cholera and typhoid fever, are distributed unevenly because of differences in sanitation. Others—dental caries,

for instance—vary according to such dietary factors as the use of

8 Schizophrenia and Civilization refined sugars in candy and soft drinks. And still others, such as multiple sclerosis and many cancers, vary for unknown reasons; if we knew the reasons we would probably understand what causes them. Schizophrenia falls into the latter group.

| The measurement of the distribution of a disease is done by measuring either its incidence or its prevalence. Incidence is the number of new cases occurring within a specified time period, whereas prevalence

is the total number of cases in a given population at any one time (Kramer 1957). Both are expressed as a rate per total population, and for the sake of uniformity, most rates in this book have been converted to rates per thousand population. Attempting to ascertain the distribution of schizophrenia is fraught with difficulties, not the least of which is the definition of the disease. As discussed previously, this book uses the term schizophrenia in the narrower sense. However, many of the studies to be discussed use the term more broadly, and, even more regrettably, some fail to say how they are using it. Another problem is finding all the cases. Mental hospitals are of course the most logical place to look, and admissions (especially first

admissions) to mental hospitals have been used in many studies of schizophrenia in the United States. The problem is that hospitalization rates are partly determined by the availability of hospital beds; as the beds increase so do the number of patients (Page and Landis 1943). The discharge rate and the death rate of patients in the hospital also affects the hospitalized rate. And some schizophrenic patients can be found in other community institutions, such as prisons and alcohol treatment facilities. Some schizophrenic patients are never hospitalized at all. Different cultures and subcultures define the limits of deviancy differently, anda patient that one group may tolerate and humor the next may insist on

hospitalizing. These limits may vary even within subcultures in the

United States. For example, one recent study showed that Irish Americans have a high tolerance for thought disorder but will readily

hospitalize a person with overt emotional disturbance. Jews in the United States, on the other hand, are said to tolerate emotionally disturbed individuals but to be more likely to hospitalize a person witha

thought disorder (Wylan and Mintz 1976).

Varying amounts of stigma are attached to mental disorders in different cultures, leading some groups to hospitalize patients more quickly, others to hide affected members in the hall closet when

[Introduction 9 company comes to visit, and still others to simply tolerate the deviant member with gentle good humor. A good example of the last situation was cited by H. B. M. Murphy when he was trying to identify all the schizophrenic patients in a Canadian village: One of our other informants learnt first of another case in a fashion which still less suggests shame or embarrassment. To use his own words, it happened that my wife had been making a social visit to them and she noticed a blanket over the parlour sofa as if some stuff had been covered up there. After a time, while they were having tea, it moved. She must have seemed a little startled, for they said: “Oh, that’s just Hector. He always hides himself like that.”’ Then they went on with tea! [1964, p. 169]

The age distribution of the population may also be a source of error. Since schizophrenia is an age-specific disease, usually beginning after the age of 15, and prevalence rates are expressed as a rate per thousand population, populations with greater numbers of children will appear to have lower schizophrenia prevalence rates than in fact they have. For

this reason, it is desirable to correct schizophrenia rates for the age distribution of the population, and this will be done wherever possible by citing the rate for the age-susceptible group. The advantage of using incidence rates over prevalence rates is that age factors are less important. However, the use of incidence presupposes that it is possible to determine, with some certainty, when in each case the disease began. For cholera or typhoid fever, ascertaining the ‘date of origin may be possible, but for schizophrenia it is notoriously difficult. Did the schizophrenia begin when the patient first had to be hospitalized? When the high school teacher noticed that the person was different from the other children? Or when the mother noticed that the

child never wanted to play with other children? Because of this problem, incidence studies have not been used very much to study schizophrenia.

The exceptions to this statement are a series of three lifetime incidence studies that took a group of people born during certain years and followed them for life to ascertain how many developed schizophrenia. Klemperer’s 1933 study in Munich was the first, and he found

that 1.4 percent of the population ultimately developed the disease. Fremming (1947) followed up all persons born on Bornholm Island (Denmark) between 1883 and 1887 and found that just under | percent ultimately were affected. And Helgason (1964) replicated Fremming’s

10 Schizophrenia and Civilization study in Iceland, following up all persons born from 1895 to 1897 and

finding an incidence of schizophrenia only slightly less than what Fremming found. Parenthetically, it is interesting that Helgason found in Iceland an incidence of manic-depressive psychosis twice that of

schizophrenia; in most places in the world, schizophrenia is more common by a ratio of approximately 3:1. As nice as the three studies just discussed are methodologically, they stand alone in the field of schizophrenia epidemiology and cannot be compared with others. As the vast majority of studies are prevalence studies, it is to them we must turn for clues. Despite their limitations,

they provide the best information available. Because of the many problems with prevalence studies, however, we should not expect to be able to make precise conclusions regarding the distribution of schizophrenia.

What Causes Schizophrenia? Until the last decade little was known about the causes of schizophrenia. The leading theories of twenty and thirty years ago have led nowhere. For example, it was once said that stress can cause schizophrenia (and many laymen still hold that assumption). This belief arose because a person can be made to appear transiently schizophrenic if he or she is subjected to overwhelming stress. This syndrome is seen in military personnel under fire, in immigrants cut off from their native language, and occasionally in others under extreme personal stress. It is usually called acute reactive psychosis, and its hallmark is that the person gets better very rapidly when the stress is removed. Research on true schizophrenia has not uncovered any evidence that it is caused by

stress, and in fact the person who gets the disease cannot be distinguished in any significant way from other people in terms of previous life experience. Similarly, research attempting to show that schizophrenia is caused

by pathological interactions between parent and child in the early years, or by faulty intrafamily communications, has borne little fruit. Both theories have been abandoned by many contemporary schizophrenia researchers, though they linger on in the public image of the disease.

Within the last decade, however, there has been an outpouring of promising biological research on the causes of schizophrenia. A familial

Introduction 11 or genetic factor has been further clarified, biochemical abnormalities have been described, and neurological, physiological, pathological, radiological, and immunological abnormalities in schizophrenic patients have been established; these will be briefly reviewed in chapter 9. The biological bases of this disease are beginning to emerge, making it a particularly auspicious time to review the epidemiology of the disease.

There is one fact about schizophrenia that has become virtually certain in recent years: It is not a single disease. Schizophrenia is probably no more precise a term than is cancer or mental retardation; we now know that in all three cases there are many different subtypes and causes. Some people have therefore suggested that schizophrenia be referred to as ‘‘the schizophrenias’’; although the plural is undoubtedly more semantically correct, in this volume schizophrenia will be used in the singular in conformity with common usage. It should be understood, however, that schizophrenia used in the singular, just like cancer and mental retardation, refers to a group of diseases with clinical similarities and not to a single disease.

Because there is still so little known about the causes of schizo-

phrenia, it is important to use all available clues. Studies of the distribution and prevalence of diseases have yielded invaluable clues to causation in most diseases known to mankind. To use the two diseases mentioned above, for example, the prevalence of lung cancers among

smokers and the prevalence of mental retardation in children of mothers exposed to the rubella virus during pregnancy both pointed strongly to one of the causes of these diseases. Whereas epidemiologic studies can rarely prove cause and effect, they can lay the groundwork for laboratory studies which may do so. They also, of course, often open

up the road to prevention of the disease. It is the main thesis of this book that epidemiologic and cross-cultural studies will yield similarly valuable clues to the causes of schizophrenia.

Cultural Studies of Schizophrenia The history of cross-cultural approaches to schizophrenia is a curi-

ous one, beset with premature convictions and prematurely closed minds. As will become apparent in chapters to come, this isa field witha paucity of methodologically sound studies, yet with a plethora of firm

conclusions drawn from the inadequate studies which exist. “One of the striking characteristics of the field is the fact of a small amount of

12 Schizophrenia and Civilization inadequate research combined with a large amount of adequate criticism,’ according to one review of it (Mishler and Scotch 1963).

Cross-cultural studies of schizophrenia began in earnest with Kraepelin. Shortly after the turn of the century, Kraepelin traveled to Singapore and Indonesia and subsequently corresponded with physicians in many parts of the world. He found patients who appeared to have schizophrenia in his travels, and concluded that it has been shown that in all civilized nations it comes under observations

in approximately the same forms and everywhere accounts for the greatest number of the permanent inhabitants of institutions. [Kraepelin 1919]

Kraepelin’s conclusions, frequently quoted in textbooks of psychiatry, appear to have put a damper on further research in this area. Scandinavian researchers pursued epidemiologic studies of incidence and prevalence, but only a handful of others (for example, Lin 1953 and Eaton and Weil 1955) made serious attempts to determine whether schizophrenia really did exist in different proportions in different cultures.

The lack of development of cross-cultural approaches to schizophrenia reflected the difficulty of the methodological problems in this field—language, definition of schizophrenia, and accuracy of census data needed for such studies. Another reason was the “‘politicization”’ of schizophrenia, which will be discussed later. Still another reason was the dominance of psychoanalytic concepts in psychiatry until recent years. These concepts stressed the in-depth analysis of a few cases of the disease rather than a broad analysis of many cases. Since the causes of the disease were thought to be rooted in the early experiences of the individual, there was little incentive to look at epidemiologic or crosscultural data on large populations. This led to a paucity of psychiatrists going into the field to study its incidence and prevalence and also toa

psychoanalytic orientation in many anthropologists who did related fieldwork (for example, Spiro 1950 and Roheim 1939) who might otherwise have looked at the prevalence of the disease. The consequence of these problems has been a benign neglect of epidemiologic and cultural approaches to schizophrenia which has continued to the present. When contemporary textbooks of psychiatry deal with the question at all, it is usually in a tone of brief dismissal: Sociocultural studies have demonstrated that schizophrenia occurs in both primitive and civilized societies and that incidence rates, when properly evaluated, do not vary significantly. [Knox and Tourney 1965]

Introduction 13 Schizophrenia is said to “occur in all known cultures” (Crocetti and Lemkau 1967) and “‘to have a world-wide distribution’ (Henderson and Batchelor 1969). Such ideas develop a life of their own, enshrined and sanctified as truth by the printing press and passed on from textbook to

textbook. Notice, for example, the following statement from a 1963 text: The schizophrenic psychoses are recognized in all cultures in which mental disorders have been subjected to thorough study. [Noyes and Kolb 1963]

This view was passed on eleven years later virtually intact: Schizophrenia reactions have been observed in all parts of the world and in all societies subjected to careful study. [Solomon and Patch 1974]

As shall become clear in succeeding chapters, many qualifications of such a statement had developed during those eleven intervening years. In retrospect, it is curious that there has not been more interest in epidemiologic and cross-cultural studies of schizophrenia. Virtually all current theories of the disease would lead one to expect moderate or even marked differences in prevalence in different population groups through differences in rates of inbreeding, exposure to psychosocial stress, child-rearing patterns, and theoretical environmental agents. Furthermore, nearly all the important diseases known to man show major differences in prevalence in different population groups. The current situation is summarized by Stewart Wolf in a volume on the biology of schizophrenia: We are accustomed to such variability in the case of many diseases, cancer of the stomach for example and many others. So it is very startling and striking, that the incidence and prevalence of schizophrenia appears to be monotonously uniform from geographical area to geographical area, and from time to time through turbulent differences in social structure. [1976]

Schizophrenia as a Badge of Civilization There is another generic problem that winds among the studies of

this book like a thread, weaving in and out but only occasionally

14 Schizophrenia and Civilization becoming visible. As the association of schizophrenia with civilization became increasingly clear over the years, schizophrenia became known as a badge of civilization. The presence of the disease was put forth by

some people as proof that their particular culture was no longer uncivilized. Psychiatrists from developing countries occasionally claimed a high prevalence rate and were indignant when it was suggested that theirs might be lower than that of England or the United States. Conversely, psychiatrists from developed countries occasionally went to developing countries and said that there was little schizophrenia because the inhabitants were not “‘civilized’’ enough for it. Like lung cancer and auto fatalities, which are also associated with developed countries, the claiming of a disease like schizophrenia as a badge of civilization seems irrational. The important point, however, 1s

that it did indeed become such a badge, and this fact must be kept in mind when evaluating field studies. The motives of the researcher must be considered. Schizophrenia was not always considered a badge of civilization. For

example in 1850, Groddeck submitted a thesis, “On the Democratic Disease, a New Form of Insanity,” to the University of Berlin in which

he attempted to prove that the apparent increase in insanity in the United States was a consequence of independence. He argued that democracy was bad because it produced insanity (Rosen 1959). Two decades later, another view of insanity in America was put forward by

W. A. F. Browne, the superintendent of the Montrose Asylum in England: By the calculations of Sir A. Halliday, . . . which, although perhaps merely approximations to the truth, have the merit of being the only data

we possess, it appears that the proportion of the insane to the sane population of Europe, is 1 to 1,000. In Wales, the proportion is | to 800, in

Scotland | to 574. The Americans, so closely allied to us by descent, language, national character, and customs, it is computed by Dr. Brigham, present | lunatic in every 262 inhabitants. This disparity probably depends on the rapid acquisition of wealth, and the luxurious social

habits to which the good fortune of our transatlantic brethren has exposed them. With luxury, indeed, insanity appears to keep equal pace. [Rosen 1959]

The Sir A. Halliday referred to in the Browne quotation was Andrew Halliday, a physician who in 1828 had also claimed that insanity was caused by increasing technology in civilization and “over-exertion of

Introduction ld the bodily powers”’ (1828). George Rosen, in his fascinating overview of

this development, summarizes it as follows: Ackerknecht has made the provocative suggestion that the belief in a progressive increase of insanity during the 19th century is an aspect of the belief in progress, that the belief was firmly held even when there was no firm basis in fact because the greater prevalence of mental illness was evidence of more advanced civilization, since civilization was considered

a basic element in its causation. As Jarvis put it, insanity was the price

paid for the high level of civilization attained by the 19th century Western European culture as a consequence of the Industrial Revolution. In this sense, the problem of mental illness was no different than the contemporary problems of physical disease. [Rosen 1959]

Once the link had been made it was solid. Although Groddeck and Browne would probably have liked to see the United States fall on its collective ear, it did not, and democracy and technology became envied. Insanity was a small price to pay for such things, and a certain amount

of insanity proved that people were on the right track and were becoming civilized.

The argument sharpened as more and more explorers opened up “primitive” lands for the use of European nations. Did the natives have insanity, or were they free from it? Rousseauean romantics, many of whom opposed the Industrial Revolution, found that the “natives”’ were free of insanity, thus further indicting advances in technology. Conversely, the small educated elites of the “primitive” lands often claimed that they did indeed have insanity, realizing the implication that they were therefore somehow advancing. Mixed with these ideas was a fundamental racism prevalent among some cross-cultural researchers. For example, Carothers (1948) attempted to show that the brains of Africans were inferior to those of Europeans, specifically that the frontal lobes of the former were underdeveloped. The very low prevalence of schizophrenia which Carothers recorded in Kenya at the time was implicitly attributed to the Kenyan brain not being developed enough to acquire such advanced diseases. Smartt found a low prevalence of schizophrenia in what is now Tanzania, and partly explained this by postulating that Africans were inferior: “The African seems, in some way, to be lacking the higher moral sense which is the heritage of more advanced civilizations” (1956). On the other side of the African

continent, a young African psychiatrist, Thomas Lambo, correctly labeled Carothers a racist and proceeded to demonstrate that his

16 Schizophrenia and Civilization Nigerian countrymen did indeed present some classical cases of para-

noid schizophrenia and that therefore they were civilized (Lambo 1955).

The important point to note in all the preceding discussion is not who was a racist or who was ethnocentric, but rather that many of the people

who have undertaken epidemiologic and cross-cultural studies on schizophrenia had preconceived ideas about what they wanted to find. Schizophrenia is not a neutral disease, but rather one intimately caught up in history and national self-esteem. ‘This factor makes evaluation of the research done to date doubly difficult.

What is Civilization? Up until this point we have been using “‘civilized”’ and “developed’”’

interchangeably. without examining their meaning. What is civilization? The dictionary defines it as a state of human society characterized by a high level of intellectual, social, and cultural development. Today

this would imply widespread systems of formal education, social groupings determined by economic advancement, and a broad distribution of technology and manufactured goods. As societies proceed from

“uncivilized” to ‘civilized’? conditions in the modern world, the following changes usually occur: breakdown in the extended family,

increased individual mobility, breakdown of traditional roles and values, changes in child-rearing patterns, industrialization, urbanization, job specialization, changes from a barter to amoney economy, and the increasingly wider distribution of new music, art, clothing, values, and technology which is adopted from “‘civilized”’ societies. It may be philosophically questioned whether the abandonment of breast feeding and adoption of transistor radios is good or not, but that is not the purpose of this book. The issue here is that schizophrenia is associated with civilization, and we therefore must examine all facets of what civilization is in order to learn why schizophrenia is a handmaiden of the civilized state. In concluding this overview, it might be legitimately argued, given the methodological problems referred to in this chapter, that the crosscultural studies of schizophrenia done to date are collectively worthless. The alternative view is that although many of the studies are methodologically poor, not all of them are. And given the state of the art in schizophrenia research, it is important that we utilize all the clues

Introduction 17 we have for whatever we can get out of them. You cannot make a silk purse out of asow’s ear it is true. But you can make a sow’s-ear purse out of it, and if you are spilling your money all over the ground the sow s-ear purse may do quite nicely until you can find a piece of silk.

Summary l. Schizophrenia is defined as a disease affecting the person’s thinking pattern, emotions, and perceptions. It usually begins in early adulthood and progresses either steadily or intermittently for a period of several years. 2. Until recently little was known about the causes of schizophrenia. It is now virtually certain, however, that the disease has a biological basis.

3. Schizophrenia is almost certainly not a single disease but is rather a symptom complex caused by several different agents. Thus, the term schizophrenia is similar to the terms mental retardation and cancer. 4. Epidemiologic and cross-cultural studies of schizophrenia have been lacking. Such studies may provide important clues to the causes of this disease. 3. Epidemiologic and cross-cultural studies are difficult to interpret for several reasons, one being that the presence of schizophrenia in a culture has come to be associated with the state of being civilized. It is often taken as a badge of civilization.

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2 Is Schizophrenia of Recent Origin?

Of the uncertainties of our present state, the most dreadful and alarming is the uncertain continuance of reason. —Dr. Samuel Johnson, Rasselas (1759)

It is generally assumed that schizophrenia is an ancient disease, probably as old as mankind. Kraepelin himself believed that it was: ‘Only so much may be said, that the disease is probably extremely old,

as indeed the descriptions of the old physicians often unmistakably point to the clinical pictures familiar to us” (1919, p. 232). Since Kraepelin, nobody has seriously challenged the assumption of the antiquity of schizophrenia, and it has been incorporated into psychiatric textbooks as fact. Suppose that Kraepelin was wrong and that schizophrenia is not an ancient disease but is instead of more recent origin. Since we are assuming that schizophrenia is a heterogenous condition, some (or most) of the biological conditions that cause it would be of more recent

origin. Thus schizophrenia would be like cancer, with multiple causes—some of which have been present for centuries but others (such as industrial carcinogens) being of more recent origin. What would we expect to find in looking at the history of schizophrenia if many or most of its causes were of more recent origin? We would expect to find some cases that sounded like schizophrenia, since many diseases of the brain known to mimic schizophrenia have presumably been around for a long time—for example, viral encephalitis, brain tumors, temporal lobe epilepsy, pellagra, trypanosomiasis, myxedema, and metabolic encephalopathy. These diseases by themselves

should produce a sprinkling of clinical conditions with historical description similar to what we call schizophrenia. In addition, we would expect some additional cases from those biological conditions currently

causing schizophrenia that also existed in the more distant past. So what do we actually find when we turn back the history pages and look for schizophrenia in previous centuries? First, we find a confusion

of words and psychiatric categories that makes the job enormously difficult. Not only is there the problem of whether the ‘“mania”’ of Celsus is the same condition as the “mania” of Soranus or that of Hippocrates, but also it is doubtful whether “mania” as any of them

22 Schizophrenia and Civilization used the term then is similar to the way it is used today. Furthermore, as we are dealing with words in translation, we must take account of the translators’ biases in choosing a word with which to convey the Greek or Latin meaning. To adequately answer the question posed, it would be necessary to analyze the texts in the original languages in which they were written. Since that task is well beyond the purview or ability of the present author, we must settle for less precise impressions.

Ancient Texts | _ Madness in the generic sense is definitely found in ancient texts. As ,

Se stated by Alexander in the opening line of his history of psychiatry, “the mentally ill have always been with us...” (1966). Early Indian texts on Ayurvedic medicine, the most ancient system of medicine in the world, prescribe strong purgatives and emetics as a treatment for madness (Whitewell 1936), and Deuteronomy in the Old Testament warns that ‘the Lord will smite you with madness and blindness and confusion of mind” if you disobey his commandments (Deuteronomy 28:28). Claims have been made that Saul was manic-depressive (Whit-

well 1936), and Karl Jaspers attempted to show that Ezekiel was a schizophrenic. According to medical historian George Rosen, however,

‘it cannot be said that the attempt was successful” (1968).

| The New Testament contains multiple references to madness, and also to seeing visions and hearing voices, although these are usually both attributed to the intervention of God. The most serious attempt to find schizophrenia per se in the New Testament was a series of four books published early in this century purporting to prove that Jesus was a paranoid schizophrenic. These books were subsequently analyzed and dissected by physician-theologian Albert Schweitzer in The Psychi-

atric Study of Jesus (1948); he found them to be of doubtful merit or scientific validity. Turning to ancient Greece and Rome, we find Horace describing a well-known man in Argos who sat daily in an empty theater claiming he

could hear actors talking on the empty stage and applauding the nonexistent theatrical performances (Meier 1970). The man, who was apparently experiencing auditory and perhaps visual hallucinations,

was subsequently said to have been cured. He then complained of having had his private productions taken away from him: ‘‘By Pollus! You’ve not done me a good turn. You’d far better have killed me than

Is Schizophrenia of Recent Origin? 23 take away the exquisite pleasure given me by my delusion |sic]”’ (Whitwell 1936). Another interesting ancient Greek case study was that of Alexarchos. On the basis of a single ietter Alexarchos is alleged to have written, he was said by Weinreich to have been schizophrenic. However, George Rosen (1968) disputes this conclusion by maintaining that Weinreich’s evidence was inadequate and that Alexarchos may not have even been mentally ill.

It is probable that clinical pictures ressembling schizophrenia in ancient Greece and Rome were subsumed under the category of “mania, a term used more broadly then than it is today. Aretaeus in the first century A.D. differentiated mania from “‘stupid, absent, mus-

ing,’ which may describe either mental retardation or organic brain disease (Lehmann 1967). Shortly thereafter, Celsus divided mania into those cases with hallucinations and those without (Menninger 1963).

In the second century, Soranus differentiated mania from delerium attributable to fevers and also described delusions of grandeur in those ‘““who believe themselves to be God’’ (Lehmann 1967).

The more one peruses these ancient sources, however, the more striking it becomes that nobody clearly described a case of schizophrenia with the initial break in late adolescence or early adulthood, the constellation of symptoms, and the chronic course. It may be that the syndrome was simply subsumed under mania, or it may be that it

was far less common than it is today. Its absence stands in sharp contrast to good clinical descriptions of many other psychiatric syndromes. Depression, subsumed under the broader category of melancholia, was differentiated into several subtypes, and senile dementia, acute brain syndrome, hysteria, hypochondriasis, and alcoholism were all clearly described (Menninger 1963). Even the astute eye of Hippocrates apparently missed schizophrenia if it existed, although he did describe such syndromes as postpartum psychosis, epilepsy with psychiatric symptoms, and transvestism (“the Scythian disease’) —all of which are much rarer than schizophrenia (Menninger 1963). And by the sixth century, Alexander Trallianus had provided the “earliest description of what later came to be called circular insanity” (Whitwell 1936), now known as manic-depressive psychosis and only approximately one-third as common as the schizophrenic syndrome is in most countries.

The Middle Ages contributed little of substance to psychiatric nosology or clinical description, the preoccupation of the observers being taken up with which incubi or succubi were afflicting which poor

24 Schizophrenia and Civilization soul. Referrals were for ecclesiastical rather than medical care. The only real advances during this period were Maimonides’ detailed descriptions of depression and the careful clinical observations of Rhazes and Avicenna among the Arab physicians. The latter, for example, described a young man with “melancholia” and delusions of being a cow: Every day he would low like a cow, causing annoyance to everyone, crying, ‘Kill me so that a good stew may be made of my flesh,” until he finally would eat nothing. Avicenna was called in. First of all he sent a message to the patient bidding him be of good cheer because the butcher was coming to slaughter him, whereat the sick man rejoiced. Some time afterwards Avicenna, holding a knife in-his hand, entered the sickroom saying, ‘Where is this cow that I may kill it?”’ The patient lowed like a cow to indicate where he was. By Avienna’s orders he was laid on the ground, bound hand and foot. Avicenna felt him all over and said, “He is

too lean, and not ready to be killed; he must be fattened.” The patient then took food eagerly, gradually gained strength, got rid of his delusion,

and was completely cured. [Whitwell 1936, pp. 96-97, quoting E. G. Brown, Arabian Medicine|

Rx: One Roasted Mouse It was not until the Renaissance was fully under way that physicians

returned to the task of describing and classifying mental disorders. Bethlem Hospital, the first mental hospital in England, began taking in mad people at the end of the fourteenth century, thereby providing the possibility of observing groups of mad people together and theoretically

multiplying the opportunities for a single observer to make clinical comparisons and describe syndromes (such as schizophrenia) that had not yet been described. In the four hundred years following the opening of Bethlem, some excellent clinical observations emerged, but not one provided a clear description of the schizophrenia syndrome as we know it. In the early sixteenth century, Bartholomaeus divided mental illness into melancholy (apparently including depression, anxiety, hypochondriasis, and some delusional states), mania or raving madness, forgetfulness or staring spells, delerium resulting from brain diseases, and delerium resulting from systemic diseases (Hunter and Macalpine 1963). Johann Weyer, a remarkably astute physician of this period, even attempted to

Is Schizophrenia of Recent Origin? 29 treat “witches” with psychotherapy rather than burning them at the stake, yet he did not describe schizophrenia (Galdston 1967). This era also witnessed experimental new therapies for the insane, including such gourmet specialties as “a roasted mouse eaten doth heal frantic [psychotic] persons’ (Hunter and Macalpine 1963). Good descriptions of delusions and hallucinations were published in

1570 by Ludwig Lavater in Zurich. Translated into English as “Of Ghosts” two years later, the author referred to previous historical descriptions of the same phenomena such as the man from Argos clapping in the empty theater (Hunter and Macalpine 1963). By the turn of the century, William Shakespeare was incorporating descriptions of delusions and hallucinations into his plays; for example, Macbeth and Hamlet experienced visual hallucinations. Madness is a prominent theme in Shakespeare, from the feigned lunacy of Hamlet to

the senile ravings of King Lear to the acute reactive psychosis of Ophelia when she discovered that her father had been killed by the man she loved (Anonymous 1844); but nowhere in Shakespeare’s works is

schizophrenia to be found. In 1621 Robert Burton published his classic The Anatomy of Melancholy. Reprinted five separate times during his lifetime, Burton’s book covered a broad range of mental disorders, including paranoid states,

but not schizophrenia per se. Shortly thereafter, Thomas Sydenham published an excellent description of hysteria, and in 1656 Felix Plater in Switzerland described a case of madness later shown to have been

caused by a brain tumor (Whitwell 1936). Also in 1656, an English minister named George Trosse published a self-account of his mental breakdown, with delusions and auditory hallucinations, at age 25. Some of his behavior appears catatonic: ‘‘for several days... I would neither open my eyes nor my lips” (Hunter and Macalpine 1963). Hospitalized for several months in a private asylum, Trosse subsequently recovered. This account may have been the first actual description in literature of what we now call schizophrenia.

Thomas Willis was another major contributor to psychiatric thinking in the seventeenth century. His work on cerebral anatomy isa classic (Willis 1683), and he was the first to describe the syndrome of general paresis, although its actual cause was not to be discovered for

another two hundred years (Hunter and Macalpine 1963). He also differentiated mental deficiency from ‘deteriorating illnesses’; the latter may have been a reference to schizophrenia. One passage is of particular interest to historians of schizophrenia:

26 Schizophrenia and Civilization ... apprehend simple things well enough, dextrously and swiftly, and retain them firm in their memory, but by reason of a defect of judgment, they compose or divide their notions evilly, and very badly inferr one thing from another; moreover, by their folly, and acting ackwardly and ridiculously, they move laughter in the bystanders. [Willis 1683]

One historian has claimed that Willis was describing loose associations

and that this description was the first of schizophrenia that can be identified in psychiatric literature (Cranefield 1961). However, it is also possible that Willis was describing thought processes in a person with

mental retardation, a chronic brain syndrome, or manic-depressive psychosis.

In the eighteenth century, there continued to be much interest in classifying diseases, yet schizophrenia is not to be found. Perhaps the closest approximation of schizophrenia was contained in a letter from Dr. David Kinneir of Edinburgh, published in 1727: A Gentlewoman of Nineteen Years of Age, from an obstinate Fasting for

Two Days, and Aversion to see Company, in a religious Turn before Easter, fell into a deep Melancholy, would not talk, nor answer any Questions for some Time, but moan’d and sigh’d continually; slept very little for Ten Days. This happen’d in the Decline of the Moon. The Night before the Change she spoke, and call’d for some Water to drink, which

being given her, she immediately fell a starting and laughing, and her Eyes got a Briskness in them somewhat uncommon, (as her Relations told me) then began to talk wildly, and continu’d so all that Night, She became next Morning very furious; whereupon a Physician was call’d, who bled her Four Times a Week the first Fourteen Days, vomited her, purg’d her, us’d the Cold Bath, and many other Methods common in such

Cases, all to no Purpose. In this Condition she continu’d for Nine Months; then I was apply’d to. [Hunter and Macalpine 1963, p. 333]

Kinneir went on to relate how he cured her with a camphor compound over a three-week period: “‘and tho’ nine years ago, at this time [she] is ina very good state of health, having no extraordinary ailing ever since

.... (Hunter and Macalpine 1963, p. 333). Thus it would appear to qualify as a single episode of a schizophrenia-like psychosis without recurrence over nine years. Dr. Samuel Johnson was a keen observer of the mid-eighteenth-

century London scene, from whom we have learned much about contemporary philosophy and politics. Johnson apparently had a special interest in madness and, as shown in the epigraph for this chapter,

Is Schizophrenia of Recent Origin? 27 described its occurrence as “dreadful and alarming” (1759). In 1763 Johnson told Boswell that insanity was increasing in frequency, which he attributed to a decrease in smoking, which was apparently becoming less fashionable. Smoking, reasoned Johnson, tranquilizes the mind,

and as smoking becomes less common insanity becomes more so (Anonymous 1847a). This reference is the first mention that | have found of the idea of a contemporary increase in insanity, a view that became widespread a hundred years later.

In the literature of the eighteenth century, there are, of course, many other references to madness, but none appear to be to schizophrenia. William Cowper, a British poet who had recurrent depressions and fequired hospitalization for as much as a year at a time, immortalized psychotic ravings in his poem ‘‘Crazy Kate’ (Anonymous 1844). No longer were such people thought to be afflicted with devils; rather, the concept of brain disease was becoming more prevalent. Thus, at the

end of the eighteenth century, when a woman killed her infant as a result of a postpartum psychosis and was brought to trial, “the jury very justly found her not guilty of the murder” (Hunter and Macalpine 1963, p. 557). Interest in madness was also greatly stimulated at that time by the psychosis of King George III in England, whose mental illness is now thought by some to have been secondary to porphyria (Macalpine and Hunter 1966), though others disagree strongly with this position (Dean 1971).

Enter Schizophrenia It was as if somebody rang a bell precisely at the turn of the nineteenth century to herald the official entrance of schizophrenia.

Whereas up to that point there appear to have been at best a few scattered cases in the literature, classical schizophrenia was suddenly being described by different people in different places all at about the same time. Such an entrance for a disease is rather dramatic. The honors for the first clinical descriptions of schizophrenia belong to both Phillippe Pinel at Hospital Salpetriere in Paris and John Haslam at Bethlem Hospital in London; within the same year, in 1809, they both described classical examples of the disease with onset in early adulthood and progressive deterioration. Haslam’s 1809 publication was a second edition of his 1798 book, Observations on Insanity. In the earlier book he analyzed all admissions

28 Schizophrenia and Civilization to Bethlem Hospital from 1748 to 1794 and provided the following breakdown of age of admission:

Age Patients 10-20 113 20-30 488 30-40 O27 40-50 362 20-60 143 60-70 3]

The bulk of admissions were thus concentrated in the 20-40 age group, suggesting that many of these patients may have been schizophrenic. Haslam’s definition of insanity was similar to that of schizophrenia: an incorrect association of familiar ideas, which is independent of the prejudices of education and is always accompanied by implicit belief, and generally with either violent or depressing passions. [Haslam 1798, p. 10]

Haslam gave a good example of a delusion, stating that if a peasant says he is going to ride his horse to America he may just be ignorant, but if an

experienced seaman says the same thing he is insane. Haslam also seemed to describe the thought blocking commonly seen in schizophrenia: When patients of this description are asked a question, they appear as if

awakened from a profound sleep; they are searching, they know not where, for the proper materials for an answer, and in the painful and fruitless efforts of recollection generally lose sight of the question itself. [1798, pp. 19-20]

In other parts of the book, Haslem gave good descriptions of paranoid delusions and auditory hallucinations. The bulk of Haslam’s 1798 book, however, was devoted to descriptions of autopsy findings of the psychiatric patients who died and an

attempt to relate those findings to the patients’ previous clinical symptoms. Of special interest is the case of a 27-year-old woman who was hospitalized for “religious enthusiasm,” delusions, tactile hallucinations, suicidal thoughts, and periods of hyperactivity. Following an

intermittent course over nine months, she suddenly died, and an autopsy showed findings in the brain that sound like encephalitis: “The

[s Schizophrenia of Recent Origin? 29 medullary substance when cut into was full of bloody points” (Haslam 1798). Thus Haslam appears to have been the first researcher to recog-

nize that brain diseases such as subacute encephalitis (presumably viral) may produce the clinical picture that we now call schizophrenia. In terms of causation of insanity, Haslam included repeated intoxica-

tion, trauma, mercury ingestion (later to be immortalized by Lewis Carroll in the figure of the Mad Hatter, mercury being commonly used in the hat-making industry), and hereditary predisposition. Regarding

the latter factor, Haslam noted that insane persons with a positive family history were most likely to be admitted to the hospital between the ages of 30 and 40. He also made observations on the prognosis of different kinds of insanity—for example, that postpartum psychosis

had a high recovery rate of 63 percent. Finally, he recommended ‘gentleness of manner and kindness of treatment”’ in the management of these patients. Overall, Haslam’s 1798 study is a remarkable book, which has not been given adequate recognition by historians of psychiairy.

It was in the second edition of his book that Haslam fully gave himself over to clinical description. Although he was undoubtedly looking at schizophrenia in the earlier edition, it was not until the 1809 edition that case studies such as the following were presented: there is a form of insanity which occurs in young persons; and, as far as these cases have been the subject of my observation, they have been more

frequently noticed in females. Those whom I have seen, have been distinguished by prompt capacity and lively disposition: and in general

have become the favorites of parents and tutors, by their facility in acquiring knowledge, and by a prematurity of attainment. This disorder commences, about or shortly after, the period of menstruation, and in many instances has been unconnected with hereditary taint; as far as could be ascertained by minute enquiry. The attack is almost impercepti-

ble; some months usually elapse before it becomes the subject of particular notice; and fond relatives are frequently deceived by the hope that it is only an abatement of excessive vivacity, conducing to a prudent reserve, and steadiness of character. A degree of apparent thoughtfulness

and inactivity precede, together with a diminution of the ordinary curiosity, concerning that which is passing before them; and they therefore neglect those objects and pursuits which formerly proved sources of delight and instruction. The sensibility appears to be considerably blunted; they do not bear the same affection towards their parents

and relations; they become unfeeling to kindness, and careless of reproof. To their companions they shew a cold civility, but take no

30 Schizophrenia and Civilization interest whatever in their concerns. If they read a book, they are unable to give any account of its contents: sometimes, with steadfast eyes, they will dwell for an hour on one page, and then turn over a number ina few minutes. [tis very difficult to persuade them to write, which most readily develops their state of mind: much time is consumed and little produced.

The subject is repeatedly begun, but they seldom advance beyond a sentence or two: the orthography becomes puzzling, and by endeavouring to adjust the spelling the subject vanishes. As their apathy increases they are negligent of their dress, and inattentive to personal cleanliness. Frequently they seem to experience transient impulses of passion, but these have no source in sentiment; the tears, which trickle down at one time, are as unmeaning as the loud laugh which succeeds them; and it

often happens that a momentary gust of anger, with its attendant invectives, ceases before the threat can be concluded. As the disorder increases, the urine and feces are passed without restraint, and from the indolence which accompanies it, they generally become corpulent. Thus in the interval between puberty and manhood, I have painfully witnessed

this hopeless and degrading change, which in a short time has transformed the most promising and vigorous intellect into a slavering and bloated idiot. [Haslam 1809, pp. 64-67]

Here for the first time was true schizophrenia: a good premorbid personality, insidious onset in adolescence, classical signs and symptoms, and a chronic deteriorating course. At the same time as John Haslam was performing his autopsies in London, Phillipe Pinel in Paris was apparently examining a group of patients with the same symptoms. In 180) Pinel described patients with inappropriate or flattened affect, looseness of associations, and ‘‘dimin-

ished sensibility to external impressions” (Altschule 1967). Pinel called this condition demence, a term destined to stick to the syndrome

for more than a hundred years. He believed that the syndrome was primarily a disorder of thinking, and he distinguished it from melancholia and mania. Fight years later, in 1809, Pinel published more complete clinical descriptions of the démence syndrome in his Traite Medico-Philosophique sur L’Alientation Mentale (Altschule 1976). Be-

cause of the joint and almost simultaneous initial description of schizophrenia by Haslam and Pinel, it has been proposed that the term

schizophrenia be dropped altogether and replaced with the ‘‘PinelHaslam syndrome” (Altschule 1967). Pinel’s démence caught on quickly in Europe. In Germany in 1822, Neumann noted that when recovery from the syndrome did occur, it

was often incomplete. And in England in 1828, Burrows further

Is Schizophrenia of Recent Origin? 3] elaborated on the clinical manifestations of démence (Altschule 1967). In the United States Benjamin Rush published descriptions of “manalgia”’ in 1812, noting that it was a subgroup of general insanity in which patients had “‘taciturnity, downcast looks, a total neglect of dress and

person... indifference to surrounding objects . . . and sometimes a fixed position of the body” (Hunter and Macalpine 1963, p. 663). It is not certain whether Rush had read either Haslam or Pinel at the time he reported his findings.

In the early years of the nineteenth century, schizophrenia also began appearing in general literature. Madness in general still played a prominent role, as in Sir Walter Scott’s depiction of manic episodes in Madge Wildfire or of depression in Clara Mowbray (Anonymous 1844). But now classical schizophrenia appeared specifically, as in Balzac’s short story “Louis Lambert,” published in 1832. Not only did Balzac

provide an accurate description of a catatonic schizophrenic, but he even had his character go to Paris for treatment by Pinel’s famous pupil, Monsieur Esquirol. Unfortunately, Esquirol declared his patient incurable and sent him home to his chronic deteriorating fate. At the same time as Louis Lambert was undergoing his fictional schizophrenic psychosis, John Percivalin England was experiencing the same thing in real life, and in 1838 and 1840 he published a two-part autobiographical account of his psychosis (Bateson 1961). His illness, which began at age 27, sounds very much like schizophrenia; however, as little is known of

his later life, it is not possible to ascertain the ultimate outcome. From midcentury onward, the démence of Pinel was refined and expanded. In Belgium 1860, Morel emphasized that the onset occurred

in later adolescence, calling it démence précoce. Hecker described “hebephrenia”’ in 1871, and Kahlbaum added “‘catatonia”’ in 1874. By

1896 it merely remained for Kraepelin to relate the work of Morel, Hecker, and Kahlbaum to the symptoms of paranoia and to call the whole dementia praecox (Altschule 1967). Fifteen years later, Bleuler, apparently impressed by the splitting in thought processes and inappropriate affect, renamed it schizophrenia, a label the Pinel-Haslam syndrome has retained to this day.

Was Schizophrenia Increasing? Almost from the first historical suggestions of schizophrenia, an accompanying theme can be heard in the background: Insanity (and

32 Schizophrenia and Civilization schizophrenia) were rapidly increasing. The persistence of this idea throughout the nineteenth century and into the twentieth is one of the most striking facets of the short history of schizophrenia. As mentioned previously, Samuel Johnson introduced this idea as early as 1763, believing that the increase in insanity was the result of a decrease in the habit of smoking (Anonymous 1847a). John Haslam’s choice of Johnson for the epigraph of his 1798 book (the same quotation that appears as the epigraph for this chapter) suggests that Haslam too considered insanity to be on the rise, a suggestion he confirms in the preface to the 1809 edition: The alarming increase of insanity, as might naturally be expected, has incited many persons to an investigation of this disease. [Haslam 1809]

In England the newfound interest in insanity resulted in the County Asylums Act, which was passed by the House of Commons in 1808 and established asylums in many of the counties. As noted by one observer, “The period 1805-1817 saw a rapidly rising tide of interest in lunacy reform in the British Isles’ (Williamson 1969). Statistics were brought forth “which not only show that insanity, in all its forms, prevails to a most alarming extent in England, but that the numbers of the afflicted have become more than tripled during the last twenty years!” (Halliday 1829). In 1835 J. C. Prichard’s A Treatise on Insanity also recorded a strong impression of an increase in insanity: Yet the apparent increase is everywhere so striking that it leaves on the mind a strong suspicion that cases of insanity are far more numerous

than formerly. .. . [Prichard 1835, p. 350]

In Scotland W.A.F. Browne, writing in 1837, thought that insanity had also increased and that it was twice as common as it was in the rest of Europe. He admitted, however, that it was not an established fact and that “more careful examination is, without doubt, required to establish the proposition” (Rosen 1968, p. 185).

In France Pinel asserted early in the century that insanity was increasing, and he thought this was due to the stresses which followed the French Revolution (Rosen 1968). Prichard (1835) also believed that an increase in insanity had taken place in France between 1801 and 1823. By 1856 Renaudin had published an extensive analysis of the question, and cited figures indicating a rapid increase between 1835 and 1854 (Renaudin 1862). More important, the increase had been most

[s Schizophrenia of Recent Origin? 33 marked in the younger age groups, those in which schizophrenia is most

prevalent: ‘Formerly insanity of early age was a very rare exception; now, on the contrary, we observe a marked precocity. ... It happens in all ranks of society, and seems to be on the increase.”’ Renaudin said the

increase ‘ought to give rise to the most serious reflection’; he personally suspected that it was a consequence of the French Revolution but was unclear about the mechanism. Renaudin made another observation which is of interest. He showed that the incidence of insanity differed from one geographical region to

another, and that it was higher in urban areas than in rural: “this inequality is in proportion to the degree of agglomeration of the population, establishing a fundamental distinction between town and country.’ He showed that the incidence of insanity was three times as great for urban areas as for rural areas. We will return to a discussion of

this phenomenon in chapter 4. Meanwhile in England the debate was also continuing. By 1855 the question of an increase in insanity had become politicized and intertwined with debate over the merits of advancing technology and such things as smallpox vaccination. As a report to the House of Commons noted: It may be in place to notice the increase of another scourge—insanity— of which the J/lustrated London News of 17th February 1855 says, ‘In the city of London, without any increase of population the number of lunatic poor has doubled within the memory of some of the guardians, and the

cause has baffled their inquiries. Some are inclined to attribute this dreadful visitation to excess of eagerness and strife in commercial pursuits, or in mental exertions; others to diet, and some partially to the effects of railway travelling. Why not to vaccination?” [Gibbs 1855]

Two years later John Hawkes wrote a paper, “On the Increase of Insanity,” in which he said: “I doubt if ever the history of the world, or the experience of past ages, could showa larger amount of insanity than that of the present day’ (Hawkes 1857). In 1859 the American Journal of Insanity noted that the rapid rise in insane persons in England required the continuous building of new asylums: To meet the continual increase in the number of insane in England, the existing public asylums have recently been enlarged to an additional capacity of 2,481 patients. Besides this, eight new asylums [are] in course of erection. . . . [Anonymous 1859|

34 Schizophrenia and Civilization Toward the end of the nineteenth century the debate became more sophisticated as reasons for the apparent increase were sought. D. H. Tuke showed that the number of insane rose in England between 1857 and 1877, and that part of the increase could be accounted for by an

increased number of mental hospital beds available. “At the same time,” he concludes, “we think that it is quite probable that there has been some real increase” (Tuke 1877). The 1892 edition of Tuke’s Dictionary of Psychological Medicine, on the other hand, analyzed specific admission figures for England and Wales for the years 1859 to 1885; the conclusion was that there had been an apparent increase but

that it was an artifact. Elsewhere on the Continent the story was much the same. In 186l Wilheim Griesinger said that insanity had increased in Germany, and six years later T. B. Belgrave asserted that in Denmark there had been ‘‘an increase in the proportion of lunatics to the general population”’ (Rosen 1968, p. 178). In France it was claimed that the Franco-Prussian War and the civil war that followed in 1871 had increased the number of insane (Rosen 1968, 1978). In Greece in 1893, it was noted that insanity was increasing (Sanborn 1893), and in Russia, Mierzejewsky made this

observation: ‘‘cases of insanity and nervous diseases increase enor-

mously in our days; they pertain mostly to a serious chronic and protracted character” (1888). The prize for the most extensive analysis of this question, however, must be awarded to Dr. G. A. Tucker, an Australian physician who undertook a three-year, 140,000-mile survey of more than 400 asylums from 1882 to 1885. Covering most of the United States and Europe, as well as scattered other countries, Tucker was a man whose zeal was only outstripped by his obsessive attention to detail; his trip report, Lunacy in Many Lands (1887), covered 1,564 large pages with small print. At

each asylum, Tucker asked the superintendent whether he believed that insanity was increasing Tucker than the general population. The superintendents replied that part of the apparent increase could be accounted for by a greater number of asylums and a greater readiness on the part of the population to use them. Tucker concluded, “Making every allowance on this score, however, it does not sufficiently account for the recorded increase in the number of the insane” (1887). The vast majority of superintendents believed that the increase in insanity was

real, and this “must be accepted as a fact” (Tucker 1887). Turning to the United States, there appears to have been considerably less interest than there was in Europe regarding the question of

Is Schizophrenia of Recent Origin? 30 whether insanity was increasing in the nineteenth century. Nevertheless, statistical data indicate that an increase was quite possible. For example, the first asylum for the insane in the United States opened in Williamsburg, Virginia in 1773. No other asylum opened until 1816, when suddenly there was an explosion of them: Baltimore in 1816; Philadelphia in 1817; McLean, Massachusetts, in 1818; Bloomingdale, New York, in 1821; Hartford and Lexington in 1824; South Carolina in 1827; and another in Virginia in 1828. Fourteen more asylums were opened by 1846; by that time, the superintendents of the asylums had organized themselves into what later became known as the American Psychiatric Association, and they had begun publishing the American Journal of Insanity (later renamed the American Journal of Psychiatry). Thus, the openings of asylums and the organization of the psychiatric profession took place in the United States during a period of only thirty years.

What statistical data are available suggest a concurrent rapid increase in numbers of insane patients. The first United States census that identified the “insane and idiotic” was that of 1840; ten years later, these two categories were separated and were reported individually. By the 1880 census, the identification of insane persons had become quite elaborate, and their numbers were even solicited by inquiries to private

physicians. Dr. Kurt Gorwitz (1966) has calculated the rise in the insane to be as follows:

1840 90.7 per 100,000 population 1850 67.3 per 100,000 population 1860 76.6 per 100,000 population 1870 97.1 per 100,000 population 1880 183.3 per 100,000 population

Thus there appears to have been a more than threefold increase in insanity over a forty-year period (Gorwitz 1966). During this same period the number of insane persons in asylums increased to 38,047 from 2,561 (Gorwitz 1966), and by 1904 this figure had skyrocketed to 150,151 (Pollock and Malzberg 1937).

Despite the dramatic statistical increases in the numbers of the insane there appears to have been much less public debate about them than there was in Britain. A few leaders, such as Dorothea Dix and Isaac Ray, said that insanity was on the increase in the United States, and nobody argued the contrary (Rothman 1971). The Report of the United States Commissioner of Education for 187] included the following statement:

36 Schizophrenia and Civilization The successive reports, upon whatever source or means of information procured, all tend to show an increasing number of the insane. In the United States, Great Britain, Ireland and other civilised nations, so far as known there has been a great increase of provision for the insane within forty years and a very rapid increase within twenty years. Hospitals have been built seemingly sufficient to accommodate all the lunatics within their respective States, counties, or districts. These have been filled, and then crowded and pressed to admit still more. They have been successively enlarged, and then other institutions created, and filled and crowded as the earlier houses were. [Corbet 1893]

Perhaps the massive increases and shifts in population in the United States during the years 1840-1880 were so great that the full effect of

the increasing insanity was not noticed. There was also a strong tendency to simply blame the increase on new immigrants, who were flooding in from Europe by the later years of the nineteenth century (Grob 1973).

The Curious Case of the Missing Disease The history of schizophrenia is, at best, an unusual one for a disease.

Prior to 1800, there were scattered bits and pieces of evidence but nothing to sink one’s teeth into and say that this was schizophrenia as

we know it. Virtually every other psychiatric syndrome was well described in ancient texts. Then, Haslam and Pinel independently provided clear and unequivocal descriptions in 1809. Simultaneously in both Europe and the United States, everyone began building asylums to house the insane, who appeared to increase faster than buildings could

be built for them. In Europe, the increase was the subject of much concern and speculation, which continued unabated for the entire nineteenth century. By the twentieth century, 1 out of every 100 people was being diagnosed with the disease. What are we to make of this history? Where was schizophrenia prior to 1800? Did it really increase during the nineteenth century, or is this

rise some kind of artifact? These questions are important, and the answers to them may provide clues to the disease’s causation. Some possible answers include the following: Schizophrenia was hiding behind mania. The most widespread expla-

nation for schizophrenia’s apparent absence in history is that it was there but just not described as such. We know that both “mania” and

Is Schizophrenia of Recent Origin? 37 ‘“‘melancholia” as they were used in the past were very broad terms,

much broader than we now know them. They could easily have subsumed the different varieties of schizophrenia, with the quieter forms being grouped with melancholia and the more agitated forms with mania. A correlative explanation is that the schizophrenia syndrome, as an

entity, consists of both clinical symptoms and its classical history: onset in early adulthood and chronic, often remitting and relapsing, course. Its full recognition, then, requires continuous observation over time, and it may be argued that ancient observers did not make such long-term connections. Thought disorders are more difficult to recognize. Schizophrenia is, first and foremost, a disorder of thinking. Dr. Mark D. Altschule of Harvard,

one of the few researchers who has focused on the peculiar history of schizophrenia, believes that this fact explains its apparent absence in

history. He argues that mood disorders with marked elation and depression are recognizable in all cultures and in all eras. Thought disorders, on the other hand, are much more relative to time and place

and “much harder to recognize unless extreme’ (Altschule 1976). Thus, manic-depressive psychosis was clearly described by the sixth century, whereas the recognition of schizophrenia was not forthcoming

for another fourteen hundred years. Recognition of the syndrome required the bringing together of a critical

mass of people. Prior to the nineteenth century, urbanization had been minimal. Life was still predominantly rural, and in such circumstances a delusional person here and there could go pretty much unnoticed. For schizophrenia to be recognized as a syndrome, it was necessary for large numbers of people afflicted with the disease to be seen by an observer within a reasonably short period of time. According to Cooper and Sartorius, this factor explains why schizophrenia was not recognized in

earlier centuries and why there was an apparent increase in the nineteenth century: During industrialization and rapid population increase, the increase in size of communities brings together schizophrenia in increasing numbers, resulting in their rejection by their community and a tendency to be gathered together in institutions. This happened on a large scale for the first time in Europe in the nineteenth century and resulted in psychiatrists having to deal with substantial numbers of patients. This made it much easier for common features to be recognized. The small towns and villages of non-industrial cultures will not generate sufficient numbers of

38 Schizophrenia and Civilization schizophrenic patients for them to become a very serious problem, since a few mentally ill persons can be managed on an individual basis. When

non-industrial communities become large, those with chronic mental illness tend to gather in small groups, recognized as odd by their peers and living in a social limbo, but yet half accepted. But with the much greater

increase in community size which accompanies industrialization the limits of local tolerance and support are exceeded, and the reaction of the community is to attempt to provide a special environment in the form of large institutions. Psychiatrists can then achieve an identity, and have to deal with large numbers of patients over a long period of time to be able to recognize common symptoms and develop new ideas about the subdivision of mental illness. [Cooper and Sartorius 1977]

Industrialization and rapid social change created the need for asylums. The crux of the argument based on industrialization and social change

is that the rapidly changing technological, social, and familial structures which accompanied industrialization in the nineteenth century created more insane (and presumably schizophrenic) patients because of psychological-social-family stress and that asylums were built to accommodate this need. This view is especially popular with those who

see schizophrenia as a psychosocial response rather than a biological disease. As explained by one proponent of this view: To summarize these points in terms of contrasting cultural stereotypes, an individual in a non-industrial culture who survives the hazards of a comparatively harsh physical environment, then experiences an interpersonal environment that is characterized by many relationships that are potentially supportive and flexible. There is a comparatively low level of pressure towards differentiation and specialization in work, and social

roles are more flexible. There is no intense expectation of social and financial advancement. For a person developing schizophrenia, this environment is more likely to be supportive and tolerant, and there will be little risk of prolonged rejection, isolation, segregation and institutionalization. [Cooper and Sartorius 1977]

D. J. Rothman brought this view to full fruition in The Discovery of

the Asylum (1971). Arguing that the rapid proliferation of insane asylums was simply part of a generalized proliferation of penitentiaries, orphanages, and almshouses for the poor in the nineteenth century, he

said that all of these were an attempt to control ‘“‘the frantic spirit at loose in the community” (p. 121) and “an effort to insure the cohesion of the community in newand changing circumstances’’ (p. xviii). ““The

Is Schizophrenia of Recent Origin? 39 epidemic of insanity, like the prevalence of crime, pointed to the most fundamental defects of the system, from mistaken economic, political, and intellectual practices to grave errors in school and family training” (Rothman 1971, p. 125). The rapid rise in the nineteenth century was just a consequence of adding hospital beds and the insane coming out of the closet. The medieval rule of

the Blue Cross was that patients would expand to fill whatever beds were built for them. The problem with this explanation is a confusion about cause and effect. Did the building of asylums occur independent of need, with the insane then emerging from their closets to fill them, or

was it the other way around? The hidden-in-the-closet theory is also flawed by the unsupported assumption that a great many people were probably living in closets for two thousand years or so. There really was no increase in insanity in the nineteenth century; it is

Just an artifact. This viewpoint was put forth by Goldhamer and Marshall in their Psychosis and Civilization (1949), a book widely cited

by textbooks of psychiatry as having proven that “there has been no increase in the frequency of the psychoses during the past one hundred years’ (p. 11). The authors compared first admissions to Massachusetts mental hospitals for five-year periods from 1840 to 1885 and then compared these figures with the rates for 1940. Interested readers are referred to the voluminous tables and footnotes to form their own conclusion, but it is difficult to understand how the authors arrived at their conclusions from the data they used. The first-admission rate per

100,000 population shows a progressive increase from 39.4 in 1840-1844 to 62.2 in 1885 (p. 28). The authors caution that such rates must be corrected for age of admission, and when they do this the rates for the 20-29 age of admission still climb progressively to 84.6 per 100,000 in 1885 from 50.1 in 1840-1844 (p. 49). Comparisons between 1885 and 1940 show a less dramatic rise, but it nonetheless appears to be real. For males in the 20-29 age group, the rise is to 124 from 96 and for females to 91 from 75. Goldhamer and Marshall appended a series of qualifiers to these figures, attempting to explain the differences as artifacts, and then concluded that “there has been no long-term increase during the last century in the incidence of the psychoses of early and middle life” (1949). This conclusion, they add, is compatible with psychoanalytic theories of the psychoses: Theories that view the functional psychoses as resulting from repressions of basic human drives and as the consequence of trauma developing

40 Schizophrenia and Civilization in early intimate personal and familial relationships, may possibly be thought of as being more especially consistent with our findings. [Goldhamer and Marshall 1949, p. 96] The late appearance of schizophrenia in history, and tts rapid increase in the nineteenth century, are real. In view of the historical data cited in this

chapter, this contention must be considered at least as seriously as the other explanations. When cases resembling schizophrenia from whatever cause (such as brain tumors) occurred in centuries past, as they

inevitably must have, they were almost certainly subsumed under mania or melancholia. Thought disorders are more difficult to recognize, and recognition of asyndrome increases when a critical number of patients are brought together. Industrialization made it more difficult for families to care for their schizophrenic members at home, and there was probably less of a tendency to hide them in closets than there had

been previously. And when comparing the rates for the different periods age factors must be taken into account. But these factors by themselves probably do not account satisfactorily for the relative absence of schizophrenia. It seems quite likely that this disease was far less common prior to the nineteenth century, and that it increased rapidly during that century. Schizophrenia as we know it is probably of recent origin, and the reasons for this have to do with the spread of civilization and its concomitants.

Summary 1. Schizophrenia appears to be of recent origin. While there were undoubtedly occasional cases of the disease in past centuries (as would

be expected from the baseline prevalence due to organic diseases mimicking schizophrenia), its widespread distribution appears to date to the beginning of the nineteenth century. 2. Descriptions of madness, including delusions and hallucinations,

date to ancient times. However, none of them appears to describe schizophrenia as we know it, with an onset in early adulthood and progressive deterioration.

3. The first probable description of schizophrenia in literature appeared in 1656.

4. The first clinical descriptions of schizophrenia were made by Haslam in London and Pinel in Paris, both in 1809.

Is Schizophrenia of Recent Origin? Al o. [hroughout the nineteenth century, there was evidence in Europe

that insanity (presumably including schizophrenia) was rapidly increasing. Evidence suggests that there was also a dramatic increase in insanity in the United States. 6. Several possible explanations for the late appearance of schizo-

phrenia and its apparent nineteenth-century increase have been offered. The explanation that the late appearance and increase are real phenomena is at least as persuasive as other explanations.

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Is Schizophrenia a Disease of Civilization?

... Insanity belongs almost exclusively to civilized races of man: it scarcely exists among savages, and is rare in barbarous countries. —J. C. Prichard, A Treatise on Insanity (1835)

Vilhjalmur Stefansson was an explorer of Alaska and the Arctic who, shortly before his death, published a book entitled Cancer: Disease of Civilization? (1960). In it, he enumerated all of the explorers of Alaska

who had had the impression that cancer had been rare among the Alaskan natives before they had begun adopting the white man’s ways. The idea that cancer was a disease of civilization was not new, dating

back to at least the time of Napoleon, but Stefansson gave it new emphasis. By and large, his theory was dismissed in polite medical company because he had no hard data, only impressions. Since publication of Stefansson’s book less than two decades ago, there has been a dramatic shift in our understanding of cancer. We now assume that some cancers are indeed diseases of civilization, and red dye number two, asbestos, and various chemical carcinogens have

become household phrases if not pariahs. Statistical data are now available to substantiate Stefansson’s impressions that many cancers were rare among Alaskan natives prior to the influx of civilization and

that the prevalance and distribution of cancers began to change dramatically as the Eskimos traded in the sled team for the family snowmobile (Torrey 1962, Fortuine 1969, Schaefer et al. 1975). More-

over, the study of the prevalance of cancers in various areas of the world and among specific groups of workers has yielded important clues

to causation of the disease. Schizophrenia is, in many ways, like cancer. Both are singular terms for what we now suspect are multiple conditions. Both appear to have genetic and environmental components. Both are among the most common serious diseases of Western civilization. And both diseases have been said to be rare among people who have not been exposed to Western civilization. In the case of cancer, this observation led to important clues about the causation of the disease. In contemporary psychiatric textbooks, the idea that schizophrenia may be a disease of civilization receives virtually no mention whatsoever. Just as the idea that schizophrenia might have shown a dramatic

46 Schizophrenia and Civilization increase in the nineteenth century is said to have been disproved by the work of Goldhamer and Marshall (1949), so the idea that schizophrenia might be rare among people not exposed to Western technology is said to have been disproved. Dunham (1976) asserted that “schizophrenia is found in every culture of the world,” and Victor Sauna (1969), in an otherwise excellent review of the literature, concluded: One generalization which can be made is that schizophrenia is to be found

in all cultures. . . . The contention of Van Loon and Seligman that psychosis is almost nonexistent among primitives no longer has adherents today. [p. 291]

There is good reason for questioning Sauna’s conclusion. A careful examination of the literature suggests that schizophrenia is rare among people with minimal contact with Western civilization, and the conclu-

sion to the contrary is based on inadequate data.

Early Impressions and Some Myths Dispelled As the epigraph for this chapter indicates, the idea that “insanity belongs almost exclusively to civilized races of men”’ is an idea with a long history. The earliest reference to this idea is probably that of Sir Andrew Halliday in 1828: ““We seldom meet with insanity among the savage tribes of men; not one of our African travelers remark having seen a single madman”’ (Halliday 1828). Halliday’s statement was made shortly after Haslam and Pinel first clearly described cases of schizophrenia and during the period when a rapid rise in insanity was being noted in Europe.

Anecdotal accounts throughout the nineteenth century supported Halliday’s view. The commander of a United States expedition exploring South Pacific islands reported in 1846 that he had seen no cases of insanity and further concluded: “I am satisfied that insanity is a disease

incidental to civilized life’ (Anonymous 1846a). Two years later a missionary who had lived in China and Tibet for twelve years said that he had seen cases of mental retardation and epilepsy but virtually no cases of insanity: “there is no assignable reason why insanity should not also have come to the notice of the physicians in charge if cases had existed.” (Anonymous 1847c). In Australia it was noted that insanity had been rare among aborigines: ‘It appears that insanity, if we may

Is Schizophrenia a Disease of Civilization? 47 credit the accounts of early colonists, was very rare among the Aborigines of Australia” (Manning 1890). And in South Africa, Greenlees studied all admissions to the mental hospital from 1875 to 1894. and

concluded that the majority of cases came from those tribes with the greatest and longest contact with Europeans (Greenlees 1895). Already, however, it was being said that insanity was less common among less civilized groups because the insane were killed or simply left

to starve. Thus, when D. H. Tuke in 1877 published an account of the rarity of insanity among the natives of Madagascar, he felt compelled to

“add that they do not destroy the few insane and idiots which they have’ (Tuke 1877). His conclusion was unequivocally that “we have no doubt that in a civilized community there will always be found by far

the larger number of insane persons...” (Tuke 1877). There is no evidence that insane persons were systematically killed or left to starve in these cultures. No doubt some have been, especially if they became destructive or homicidal or if food was in short supply. But to postulate mistreatment of the insane as the primary reason that they are less common in less civilized cultures is contrary to known facts. Insane persons in most technologically undeveloped cultures are treated relatively humanely if they are harmless, usually being given food by the extended family or allowed to forage in other people’s gardens without sanctions. If they are belligerent or destructive, they are usually chained to a log or confined in huts or, as civilization makes inroads, jails. The other myth that must be dispelled is that insane persons in less developed cultures are esteemed, rewarded, and given special roles, so that they no longer appear as insane to the outside observer. As put forth by one proponent, “What is regarded as insane in our civilization

may be considered highly desirable in another culture” (Katz and Schanck 1938). The role most commonly thought to be assigned to insane persons in other cultures is that of shaman or medicine man. For example, an early twentieth-century study of Siberian shamans claimed that “not afew of them were half crazy’’ (Bogoras 1907). Anthropologist A. L. Kroeber even claimed that one of the points differentiating a ‘primitive’ from a “developed”’ society is that the former rewards its

psychotics with a socially sanctioned role as healer (Kroeber 1952). This view has persisted up to the present, as illustrated by a 1967 article in the American Anthropologist entitled “Shamans and Acute Schizophrenia”’ (Silverman 1967). I have elsewhere examined the history and

ramifications of this idea in more detail (Torrey 1972a,b).

48 Schizophrenia and Civilization The theory that the insane become shamans in other cultures is, ina word, nonsense. For us to sit comfortably in our ivory towers and say

that insane persons in less developed cultures are rewarded and sanctioned as healers indicates an extraordinary lack of contact with

these cultures. This myth has been refuted by several people, but perhaps most effectively by Ralph Linton: However, I am certain that there is no society in which the genuine psychotic occupies a favored social position. In order to exploit the advantages of abnormal behavior one must be capable of appraising situations in realistic terms and of devising behavior which would be advantageous to one. The inability to do this, to my mind, is the real test of psychosis. The medicine men, prophets and the like, who gain prestige

and acquire wealth and power through their abnormal behavior, are hysterics or neurotics, and not true psychotics. It is precisely this fact which enables them to exploit their own abnormality for purposes of gain, and to make it, so to speak, ‘‘pay dividends.” This is an ability which, to my mind, the psychotic does not possess. [Linton 1956]

An Eskimo summarizes the distinction between an insane person and a

shaman very nicely: ““When the Shaman is healing he is out of his mind, but he is not crazy” (J. M. Murphy 1976).

What can we say, then, about the role of insane people in less developed cultures? First, there is no evidence that such people are systematically killed or left to die. Second, the syndrome of insanity is indeed recognized in all known cultures, and it is distinguished from

mental retardation and hysterical behavior. And, finally, there is no evidence that insane persons are socially sanctioned or given roles as healers. There are occasional shamans who are insane, to be sure, but the same thing can be said about psychiatrists and other shamanequivalents in our own culture (Torrey 1972a,b). The important point is that we must not invoke such a mythical social role to explain why many have failed to find insane persons in less developed cultures.

From Cherokees to Kalmucks and the Achinese Following the turn of the twentieth century, reports of the infrequency of insanity among ‘primitive’ people became more numerous. American Indians were one such group. As far back as 1887 it was noted that “the small percentage of insane among the aborigines ... is fully in

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Is Schizophrenia a Disease of Civilization? 49 accord with the observations of writers upon the causes productive of

mental disease” (Rosen 1968, p. 191). In 1903 it was noted that “insanity is of rare occurrence among U.S. Indians” (White 1903). H. M. Hurd (1916) collected many of these impressions. For example: Dr. Lillybridge of Virginia, who was employed by the government to superintend the removal of the Cherokee Indians in 1827-8-9, and who saw more than 20,000 Indians and inquired much about their diseases, informs us he never saw or heard of a case of insanity among them. Dr. Butler, who has been a devoted missionary and physician among the Cherokees for about a quarter of a century, informs us in a recent letter that he has as yet seen them delirious when sick of other diseases; and adds that an intelligent chief, a man now 80 years old, told him that ‘he had never known a case of insanity among his people, such as he had seen in the hospital at Philadelphia.” [p. 381]

It was not claimed that insanity did not exist at all among primitive people, but rather that it occurred less commonly. Hurd (1916) offered the following example of insanity, which is very similar to what we now call schizophrenia: The story of Mark Jack, an insane Indian of the Tuscarora tribe, who was under treatment at the Utica State Hospital from 1851 to 1874 and at the Willard State Hospital from 1874 until his death there eight years later, is of interest, because it seems to show that insanity among Indians follows much the same course as among white persons. He was a farmer of common school education, but considered one of the most intelligent men of his tribe, of temperate habits and a church member. A maternal uncle was an imbecile and a maternal aunt was

‘singular’ and a half-brother by his mother’s former husband was insane. He first showed insanity at the age of 22 years, at a time when he was attempting to learn English and to study mathematics in 1843, and for two years he had periods of excitement, followed by intervals of quiet in which he was able to do farm work. About the third year he became so

violent and incoherent in his talk as to require to be kept in close confinement in a log hut, and remained there for six years. His excitement was called by his Indian associates “conreaya bonos,”’ or madness. Being a ward of the state, he was admitted on the order of Governor Washington Hunt. At the time of his admission his brother stated that two other members of the same tribe had been insane, one of whom

recovered and the other died. His condition during the 31 years of institutional treatment was one mostly of quiet dementia, with rare

50 Schizophrenia and Civilization intervals of noisy excitement. His habits became untidy and eventually convulsive seizures developed. He was probably in a stage of terminal dementia at the time of his admission to the hospital at Utica. It is evident that he had a strong hereditary tendency to insanity which was developed by his efforts to enter upon studies for which he was not fitted. [p. 383]

The impression of relative infrequency of this disorder among Amer-

ican Indians received some statistical validation in 1922 in U.S. government reports of all hospitalized mental patients. The firstadmission rate for Indians for dementia praecox was less than half that for white Americans (Rosenthal 1933). This difference may have partly reflected the more limited access of Indians to mental hospitals, but it is also possible that it was real. Similar reports were filed from many different corners of the world.

In China it was noted that “insanity of puberty and adolescence is seldom if ever met, and that ‘mania’ appeared to be more common” (Jeffreys and Maxwell 1910). This impression was substantiated in 1926

when an analysis of all hospitalized insane persons in China showed that 28 percent were diagnosed with manic-depressive psychosis, and only ll percent with dementia praecox (McCartney 1926). Such reports

fail, of course, to reveal whether manic-depressive psychosis was overdiagnosed, schizophrenia underdiagnosed, or both. A 1929 report in German from the Astrachow district of the USSR

noted that schizophrenia was rare among the ethnic Kalmucks and Kirghiz compared with the Russians and Armenians, and that it had been virtually nonexistent prior to “contact with civilization” about 1850 (Ackerknecht 1943). Another report said that Lopez in 1932 found no schizophrenia among ‘“‘true primitives” in the interior of Brazil but

that it did occur occasionaly among the urbanized “natives” on the coast (Demerath 1942). The vast majority of schizophrenic patients observed by Lopez were either whites or mulattoes (Roheim 1939). Twenty-five years later, this distribution of schizophrenia in Brazil was confirmed by Bastide (Sauna 1969). An especially interesting report citing a high prevalence of schizophrenia among the Achinese was Van Loon’s work in 1920, which was

published in German but was extensively summarized by H. B. M. Murphy (1968b, 1972). The Achinese live in northern Sumatra in Indonesia. These people were visited by a Dutch physician with an interest in anthropology, who noted that serious mental disorders were rare among them. According to Murphy:

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[s Schizophrenia a Disease of Civilization? ol Twenty years later, after a period of continuous war and attrition, a psychiatrist was commissioned to do a survey of mental illness in the same people, the reason for his commission being that the local governor

had been struck by the unusual frequency with which he encountered insane people during his local travels. The psychiatrist, Van Loon, found that in a neighboring, non-Achinese people that had taken little part in the war the prevalence of mental illness was very low, namely five cases in a population of twenty-six thousand, but that in the Achinese it was

very high, reaching twenty cases per thousand in places. Most of the mental illness which he found was schizophrenia of many years’ duration, and it affected men much more than women. When we ask what

changes had occurred between these two visits one answer is that venereal disease had become widespread thanks to the misuse of the Achinese women by the conquering soldiery, but the other thing is that the Achinese warriors had been defeated and now had little role in their own land, the women running most of the communal affairs. If the Achinese had had roughly the same level of schizophrenia as other Malaysian peoples in Sumatra before this war, as seems likely from the earlier report and from other clues, then one must think of at least a fivefold increase in the disease over the period. . . . [Murphy 1972]

Murphy explains the apparent rise in schizophrenia among the Achinese in terms of psychosocial factors. Whatever the cause, the case of the Achinese is an example of a group of people who had experienced a low prevalence of schizophrenia, with a rapidly rising rate following twenty years of continuous warfare.

Studies in Africa Beginning in the 1930s, there was a steady stream of studies from African countries noting the relative infrequency of schizophrenia.

Elisworth Faris, on an expedition in the Congo (now Zaire) in 1932-1933, reported no cases of schizophrenia, although there were some cases of “mania due to infectious disease”’ (Faris 1937). He even visited four large hospitals looking for cases of schizophrenia: No records of any such cases existed, nor was there any memory on the part of those of the staff of any such cases. In the villages attempts were made to describe the symptoms to the natives, but no comprehension of such disorders was found. [Faris 1937, p. 28]

a2 Schizophrenia and Civilization Twenty years later Vyncke reported that schizophrenia was more frequent among Westernized Congolese than among those not Westernized (Sauna 1969, quoting Vyncke 1957).

Across the African continent in Nyasaland (now Malawi), H. M. Shelley and W. H. Watson were undertaking the first of many studies of psychiatrically hospitalized Africans. Out of 84 inmates in the country’s only asylum, 30 were diagnosed as having schizophrenia. The

most striking finding in the analysis of these cases was the close correlation between the diagnosis and degree of Europeanization: “The tribal incidence indicated a definite predominance of the condition in natives who had been in close contact with European civilizing influence” (Shelley and Watson 1936). Eight of the 30 schizophrenics had been educated, and 6 had even traveled to other countries; the number of educated schizophrenics is high compared with the total number of

educated for the indigenous population of Nyasaland at that time (Shelley and Watson 1936). In Kenya, H. L. Gordon studied 120 consecutive admissions to the mental hospital. Nineteen cases were diagnosed with “‘simple adolescent psychosis,’ and the outstanding finding was that all 19 had been educated. Less than half of the admissions for other diagnoses had been educated. Gordon concluded that education caused the psychosis, a view which probably set education back in that country for several years (Gordon 1936). Gordon was followed in Kenya by J. C. Carothers (1948, 1951, 1953), who noted that a large percentage of hospitalized psychiatric patients

were detribalized” and had had more contact with Europeans. To clarify the question of prevalence in less Europeanized areas he initiated a “field study,’ which unfortunately consisted merely of asking the tribal chiefs to take a census of all their insane and mentally

defective persons. Not surprisingly, the lists were short. Carothers (1951) concluded that ‘‘there was probably a very low general incidence

of insanity among Africans living in their natural environment,’ although it is not clear what he bases his conclusion on. It is unfortunate that Carothers did not spend more time on research methodology and less time trying to prove that the brains of Africans were inferior. Two other East African studies found virtually the same paucity of schizophrenic patients in areas with minimal contact with Europeans. C. P. Donnison was a medical officer in rural Kenya for over two years in an area which “had only been under systematic government administration for less than twenty years at the time of my observations.” In

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Is Schizophrenia a Disease of Civilization? 93 the population of 200,000 people, he recalled seeing no cases of schizophrenia (Donnison 1937). And Smartt in Tanganyika (now Tanzania) studied hospitalized schizophrenic patients and found that a highly disproportionate percentage of them were from the towns and

not from the rural areas (Smartt 1956). The only African study which contradicts the several reported above was that conducted in South Africa by Laubscher (1938), who reported schizophrenia to be abundant among the ‘‘natives”’ there. This study

has been severely criticized, however, on several grounds. Lambo stated that Laubscher did not understand the culture and that he regarded sorcery as a phase of schizophrenia (Lambo 1955). Devereux (1939) called Laubscher’s schizophrenic diagnoses “debatable,” and Ackerknecht (1943) claimed that “Laubscher’s whole study [was] the result of a gigantic misunderstanding produced by his bias towards an exclusive hereditary theory of schizophrenia.’

The South Pacific The South Pacific islands have also been fertile ground for studies of

schizophrenia. Margaret Mead initiated these studies when she appended to Coming of Age in Samoa (1928) a series of clinical descriptions of all mentally ill persons she observed among the 2,000 people with whom she was working. She recorded two people whom she said were Clearly mentally deficient, one man with delusions of grandeur,

and one 14-year-old boy whose “relatives insisted had always been stupid but only recently became demented” (Mead 1928). Mead stated that the boy gave the ‘external picture of catatonic dementia praecox.”’

She supplied no further information to allow us to differentiate this diagnosis from congenital or organic brain disease. Furthermore, this group of Samoans had undergone missionization for almost a century and, according to Mead, its members were exposed to both Western medicine and goods at the dispensary; thus they were not without exposure to Western technology. Mead’s Samoan study was a major part of the argument in Winston's

1934 paper, ‘The Alleged Lack of Mental Diseases among Primitive Groups.” Winston sought to show not only that functional psychosis existed among “‘primitive”’ people but also that its prevalence did not differ appreciably from that of the United States. Winston assumed that both Mead’s man with delusions of grandeur and the 14-year-old

4 Schizophrenia and Civilization “recently demented” boy qualified as functionally psychotic and then calculated the rate for Samoa as 1 per thousand. This rate was about the

same as that of admission to mental hospitals for rural Americans, thereby proving, in Winston’s view, that there was just as much psychosis in Samoa as in the United States. A prevalence study in a community, of course, cannot be compared with hospital admissions. The proper comparison would be with other prevalence studies, as are described in chapters 4-7; these studies show a prevalence rate in the United States and Europe of approximately 2-10 per thousand. Furthermore, Winston’s assumption that Mead’s two cases qualify as functional psychosis is, at least for the 14-year-old boy, highly questionable. It is important to analyze Winston’s study in detail, since it has been quoted frequently. And as is often the case, only the conclusions have passed from psychiatric textbook to textbook, with no reference to the quality of the data base or to its assumptions.

Ten years after Mead was on Samoa, Cora DuBois studied five villages on the island of Alor, just north of Timor. Out of the total population of 600 people, she cited two women she called “‘insane.”’ One was a woman who would frequently run off into the fields, stay for days at a time, and then return. The other woman married and then left her husband and returned to her village, where she eventually became

the village prostitute. DuBois stresses how both contravened the established social mores of the Alorese, but it cannot be said that there was sufficient evidence to diagnose either one as schizophrenic (DuBois 1944). Ernest Beaglehole, who is widely quoted by psychiatric epidemiologists, began studies of psychosis in both New Zealand and Hawaii in the

1930s. In New Zealand, he did not attempt to separate schizophrenia from the other psychoses, and he reported that the indigenous Maori population had a hospital-admission rate for psychosis only one-third the rate for the non-Maori (mostly European) population. The admis-

sion rate for non-Maoris was approximately the same as that for England. Beaglehole himself believed that the differences reflected the greater cohesiveness of Maori society and its ability to support psychot-

ic patients in the community without having to hospitalize them (Beaglehole 1950). More recently, there have been indications that the hospitalization rate for Maoris has risen as they have become more fully integrated into New Zealand society (Beaglehole 1969). Beaglehole’s data for Hawaii is very difficult to decipher (Beaglehole

1937). He reported the total resident cases of “insanity” by ethnic

Is Schizophrenia a Disease of Civilization? D0 population group in the state hospital from 1920 to 1936. However, he failed to take into account differences in age distribution, which varied

considerably among the ethnic groups. Beaglehole concluded that

Puerto Ricans (who had come to Hawaii around the turn of the twentieth century) and persons whose ancestry was part native Hawaiian showed a disproportionately high number of cases of schizophrenia; native Hawaiians of unmixed ancestry, who typically lived in

more rural settings than most other Hawaiians, had less than their share (Beaglehole 1937, 1969).

Shortly after World War II, three additional studies of schizophrenia were conducted on Pacific islands. McCartney (1947) found no cases of the disease among 10,000 people in a survey of the Marshall Islands, while on Ifaluck atoll in Micronesia Spiro (1950) found 2 cases

which he called schizophrenia among 250 people. He did not give us enough information about the cases to confirm the diagnosis, but does add, however, that both cases were men who had worked in forced Japanese labor gangs during the war. He notes that ‘‘the natives know of no instance of this kind [of illness] prior to the Japanese occupation.”’ On Saipan, Joseph and Murray (1951) identified 4 people who they said had schizophrenia out of a total population of 4,796, for a rate of

0.8 per thousand. One of the 4 experienced the onset of symptoms following a fever. Two other “possible’’ cases were discussed by the authors. One had regular “‘shaking spells’; the other was an old man who had come from outside (possibly Russia), and it is not possible to

tell from the data given whether he had schizophrenia or an organic brain syndrome. Most recently, Murphy (1979) conducted a survey of approximately 12,800 people on Truk, Tonga, the Solomons, the Cooks, and Niue in

the South Pacific, utilizing the same methodology as in his Quebec village study. Preliminary results revealed a prevalence of major mental disorder (including schizophrenia) on the Pacific islands of less

than one-third that found in the villages in Quebec.

The Making of “Sheer Folklore” By 1950, then, there had accumulated a hundred years of impressions from all over the globe. The striking feature of these impressions is the remarkable consensus that insanity (in the early literature) and schizophrenia (in later studies) were comparatively uncommon prior to

26 Schizophrenia and Civilization contact with European-American civilization. The opinion is not unanimous (for example, Laubscher’s 1938 study) but is very close to being

so. Few observers claimed that there was no schizophrenia in these more “‘primitive’’ societies, but rather that it simply was far less common, even rare. But around 1950 an interesting thing happened. At the same time as Goldhamer and Marshall (1949) were publishing their “proof” that psychoses had not increased in incidence over the previous hundred years, the idea became current in psychiatric literature that schizophrenia occurs in about the same prevalence in all cultures and is nota disease of civilization. As Knox and Tourney (1965) put it, “‘schizo-

phrenia occurs in both primitive and civilized societies and. . . incidence rates, when properly evaluated, do not vary significantly.” Most people today would accept the fact that a low prevalence of

schizophrenia is to be found in all cultures. This is because, as mentioned previously, there are a number of organic diseases (such as temporal lobe epilepsy, pellagra, trypanosomiasis, and brain tumors) which mimic schizophrenia. Thus a baseline prevalence of a disease appearing to be schizophrenia will be found virtually everywhere. This baseline existance of schizophrenia in all cultures got translated in psychiatric literature into a statement that schizophrenia was not a disease of civilization. To understand how this could have happened it is important to remember that schizophrenia was widely believed to be a

single disease around 1950. And if it was a single disease, then its occurrence at all in a culture was the important fact. Differences in prevalence were less important. And if it occurred at all in a culture with little contact with civilization, then schizophrenia obviously could not be a disease of civilization.

Now, three decades later, most people accept the fact that schizophrenia is probably a heterogeneous collection of several diseases. The mistake made in 1950 would not likely occur today. However, once an idea is printed in a textbook it tends to be transmitted from text to text without being reevaluated. Three papers are commonly cited in psychiatric texts as proof that schizophrenia is not a disease of civilization. Winston’s 1934 article, “The Alleged Lack of Mental Diseases among Primitive Groups,” has

already been discussed and has been found wanting. The second is Demereth’s “Schizophrenia among Primitives” (1942), in which he reviews many of the studies previously mentioned in this chapter. The

third and most influential paper, “Mental Illness in Primitive 5o-

Is Schizophrenia a Disease of Civilization? o7 cieties,’ was published by Benedict and Jacks in 1954. The authors cited the studies by Beaglehole in New Zealand and Hawaii, Laubscher’s study in South Africa, Carothers’s work in Kenya, and Tooth’s study in Ghana (which will be discussed in detail later in this chapter) and stated that they collectively “prove” that schizophrenia exists in “‘primitive”’ societies: It has been amply demonstrated by trained observers that the mental disorders known to Western psychiatry do occur among primitive peoples throughout the world despite the differences in incidence and symptomatology discussed above. [Benedict and Jacks 1954]

It should be noted that Benedict and Jacks realized that the incidence of these mental disorders may vary significantly between ‘primitive’ and

“civilized” cultures. However, this part of their conclusion was subsequently lost to view, and by 1963 it was said that Benedict and Jacks had

proved that the belief “that schizophrenia is a disease of civilization is sheer folklore” (Mishler and Scotch 1963). Since that time, virtually no writer in the psychiatric literature has put forth the proposition that schizophrenia is a disease of civilization.

Studies Since 1960 “Sheer folklore’? or not, evidence has continued to accumulate suggesting that schizophrenia is indeed a disease of civilization. No single piece of work has “‘proved” it once and for all, and it would be difficult to conceive of such a project. But several additional studies conducted in Taiwan, India, Ghana, and Papua New Guinea point in the same direction: the comparative rarity of the disease in societies with minimal contact with Western civilization and its increased prevalence

as such contact increases. Taiwan The Taiwanese study of Rin and Lin (1962) is perhaps the best known

of schizophrenic studies since 1960. It consisted of a survey of four tribes of Formosan aborigines who lived by themselves in remote mountain villages and who, compared with the Chinese on Taiwan, had

been much less influenced by Western technology. In all, 11,442

38 Schizophrenia and Civilization aborigines were surveyed. Case finding was accomplished by means of preliminary visits to local officials, headmen, elders, police, school-

teachers, and health officers; this work was followed by a house-tohouse survey in which two members of the trained survey team were accompanied by a local community leader. Mishler and Scotch (1963) cited this study as having had the best case finding methodology of any cross-cultural epidemiologic study (1963). Diagnosis of schizophrenia

was based on the patient’s history, premorbid personality, and the presence of such symptoms as dissociation of thinking, withdrawal, inappropriate emotional reactions, delusions, hallucinations, and hyperkinesis. Apparently, the long-term course was not considered part of the diagnostic criteria. Forty-five cases of past and present psychoses were found among this group; of these, 10 were diagnosed with schizophrenia, 10 with manic-

depressive psychosis, 3 with senile psychosis, and 22 with other psychoses (mostly of an acute transient variety). The 10 cases of schizophrenia produced a lifetime prevalence rate of 0.9 per thousand.

Of the 10 cases, 7 came on acutely, and only 3 insidiously. Furthermore, 2 of the cases had lasted less than three months, and only 2 of the 10 were chronic. Thus it may be questioned whether some of these cases

would have been considered schizophrenic had the long-term course been included in the diagnostic criteria. Most important, however, is the fact that this study of aborigines was

an exact replication of one conducted a decade earlier by the same research team on 19,931 Chinese emigrants to Taiwan (Lin 1953). This study group was a random sample of inhabitants of a city of 120,000, a town of 20,000, and five villages which were a few miles outside of the capital city of Taipei; thus, these Chinese emigrants were much more strongly influenced by Western technology and civilization than were the Formosan aborigines. Using the same criteria for schizophrenia, 43 cases were found, yielding a lifetime prevalence of 2.2 per thousand. There are, then, two studies using identical methodology and diag-

nostic criteria that were conducted on two groups of people with different degrees of exposure to Western technology and civilization. The high-exposure group has a schizophrenia prevalence rate of 2.2 per

thousand, whereas the low-exposure group has a rate of 0.9 per thousand. The researchers calculated that the difference is significant at a level of p < .O1. Rin and Lin’s explanation for this difference is an assumption that

World War II contributed to the deaths of some aborigine schizo-

Is Schizophrenia a Disease of Civilization? 29 phrenic patients “owing to their limited capacity for adjustment to the stresses and deprivation of war.’ Specifically, they said that malaria and malnutrition were prevalent. However, since the Chinese survey and the aborigine surveys were both done after the war, their explanation of the difference requires an assumption that the war decimated

more schizophrenic patients among the aborigines than among the Chinese on Taiwan. As no evidence is given to support the latter assumption, the authors’ own explanation of their findings remains merely an hypothesis. An equally plausible hypothesis is that the different prevalence rates represent real differences. India

Unique and fascinating findings in the epidemiology of schizophrenia have been generated in India. Since 1966, several separate studies have been published verifying earlier reports by Dhunjibhoy (1930) and Shaw (1930) that schizophrenia was found in greater prevalence among the more highly educated and/or Westernized castes. J. E. Dhunyibhoy, a British-trained Indian psychiatrist who ran

a mental hospital in Ranchi (Bihar State), noted that schizophrenia could be found in both sexes and among both educated and uneducated

Indians, but that “those Indian communities highly advanced in Western civilization and culture, such as the Anglo-Indians, Parsees, the educated section of the Bengalis etc. are more prone to this form of psychosis” (Dhunjibhoy 1930). He noted that paranoid and catatonic

subtypes were especially common among the educated, whereas hebephrenic and simple subtypes predominated among uneducated schizophrenic patients. In the same year that Dhunjibhoy published his papers, W. 5. J. Shaw independently reported the identical phenomenon at the mental hospital in Poona (Maharashtra State). Schizophrenia was noted to be prevalent among the Parsees, a comparatively wealthy group with much inbreeding and cross-cousin marriages (Shaw 1930). Among the Hindus, schizophrenia was said to be ‘rare’ and among the Moslems “rarer still’; for both groups Shaw reported, “I have seen the disease mainly among the more educated classes.”’ These early impressions were not confirmed for another thirty-six years. A study suggesting the same findings from Bangalore (Mysore

State) was published in 1960 but must be discarded because no breakdown in diagnostic categories was given (Hoenig and Sreenivasan 1960).

60 Schizophrenia and Civilization In 1966 a study by Rao in Ranchi (Bihar State) provided a breakdown of first-admission schizophrenia patients by caste. Out of ten castes, the

highest numbers of schizophrenic patients came from the Brahmins (aristocracy), the Bania (traders), the Rajputs (landowners), and the Kayasthas (civil servants). The Brahmins and Kayasthas are the castes

with the highest literacy, and the Banias have the highest socloeconomic status and are the most urbanized (Rao 1966a,b). Rao’s work was confirmed by Saxena, Bhaskaran, and Anath in the same hospital in 1972 with the Brahmins and Kayasthas again found to be overrepresented among schizophrenic patients. In 1971, Rao participated in a psychiatric survey of a village in West Bengal State. Six cases of schizophrenia were found, all of which were

from the two highest castes. By contrast, other forms of mental disorders were found more prevalent among the lower castes. The authors concluded that “itis noteworthy that the highest prevalence of schizophrenia is in the socially and economically advanced groups”’ (Elnagar, Maitra, and Rao 197). Two other village surveys generated similar findings. Dube in Agra (Uttar Pradesh State) found 64 persons with schizophrenia in a survey of 29,468 Indians (Dube 1970, Dube and Kumar 1972). The highest prevalence rates by caste were among the Vaish (business or trade) and

the Brahmins (aristocracy and priests). This caste distribution for schizophrenia was not found for “other psychoses,” however; the Brahmins ranked fifth out of seven castes for this diagnosis. Thus, ‘‘the

distribution of schizophrenia according to caste is different from the distribution of other psychoses’’ (Dube and Kumar 1972). Another interesting finding is that although the schizophrenic patients as a group tend to come from castes that are more highly educated, the schizophrenics themselves are not. This trend contradicts the findings

of Dhunyibhoy, but it may be explained by postulating that early symptoms of the disease may force the preschizophrenic person to drop

out of the educational system. A final village survey is the work of Ravi Kapur, a British-trained psychiatrist and epidemiologist, in Kota (Karnataka State) in South India. Using an Indian Psychiatric Survey Schedule as an interview instrument, he sampled 1,233 villagers and found 9 chronic schizophrenic patients, one other with chronic persecutory delusions, and no manic-depressives. In terms of the distribution of cases by caste, he noted:

|

Is Schizophrenia a Disease of Civilization? 61] Even more peculiar was the fact that while the Brahmin males showed the

lowest ‘case’ rate, no fewer than six out of the seven male functional psychotics were Brahmins! Those numbers are too small for a satisfacto-

ry Statistical analysis but there is no doubt that the male Brahmins showed a psychosis rate much higher than could be expected. This excess was not associated with an excess of consanguineous marriages, which

occurred with similar frequency in the three castes. [Kapur 1975, Carstairs and Kapur 1976]

Kapur, now head of the Department of Psychiatry at the Indian National Institute of Mental Health and Neurosciences of Bangalore, added, “From my clinical work | am becoming more and more convinced of the thesis regarding a relationship between cultural sophistication and schizophrenia” (Kapur 1977). What do all these findings in India mean? Why should schizophrenic

patients be concentrated in more highly educated and/or wealthier castes? If only hospitalized schizophrenic patients were included in these studies, it would be reasonable to dismiss the results as a biased

sample of those who utilize the limited hospital facilities in India. However, with field studies of nonhospitalized schizophrenic patients finding the same thing—for example, Elnagar et al., Dube and Kapur— the findings cannot be so lightly dismissed. And the unanimity of them over almost forty years is impressive. Finally, it should be noted that India is not the only country in which schizophrenic patients are said to come disproportionately from the educated classes. In 1939, Kao, Ting, and Hsu studied parergastic (schizo-

phrenic) patients in China, comparing them with manic-depressive patients and those seen for general medical illnesses. They reported that “only one result came out clearly positive, namely, that educated and non-conservative families contributed significantly more to the parergastic group than to the (controls)”’ (Kao, Ting, and Hsu 1939). And in Kast Pakistan (now Bangaladesh), both Chowdhury (1966) and Rahman (1972) found a disproportionate number of literate persons among hospitalized schizophrenics; field studies are needed, however, to confirm that these findings are not merely a function of access to the

hospital. In the United States, it is generally thought that schizophrenic patients are disproportionately drawn from the lower socioeconomic classes, based on the work of Hollingshead and Redlich (1958) ; this conclusion is contrary to the findings in India and will be discussed in chapter 4.

62 Schizophrenia and Civilization Ghana Ghana (formerly the Gold Coast) has attracted three separate teams of psychiatric researchers who have produced data on the prevalence of schizophrenia in that country. In 1948, Dr. Geoffrey Tooth undertook a ‘census’ of patients by asking for lists of all “lunatics” in the different areas (Tooth 1950). His returns were very uneven, and the methodology of his study has been severely criticized (Mishler and Scotch 1963). The most interesting finding of Tooth’s study was a paucity of schizophrenic patients from the Northern Territories—the least missionized, least urbanized, and least developed part of the country—even though

he judged his case-finding techniques to have been most complete there. Schizophrenic patients were much more common in the southern part of the country, which had many more missions, schools, and towns. It was into this southern part of Ghana that Dr. Margaret Field came in 1955 to study the healing shrines. Trained in both anthropology and

medicine with some experience in clinical psychiatry, Field initially concentrated on the Ashanti area, studying their functions and the people (including schizophrenic patients) who were attracted to them.

Eventually she began to realize that there were a large number of psychotic persons in the district in which she was working: “It was clear that madness was common—commoner, most people thought, than in other districts’ (Field 1960). Although it was not part of her original plan to concern herself with chronic schizophrenia, she decid-

ed to undertake a survey of the twelve surrounding villages in an attempt to ascertain the prevalence. The method of Field’s survey was to use key informants and then interview all suspected cases. Field identified 41 cases of schizophrenia out of a population of 4,283. Some of these cases would clearly not have

been labeled as schizophrenia by other observers, however; 7 had an onset at the involution, 1 had an onset at age 60, and 8 were postpartum. Furthermore, at least | may have been organic (onset following a high fever), and some may have been manic-depressive psychosis— ‘among

the women the illness is most often schizo-affective and strongly depressive...” (Field 1960). It does appear, however, that Field identified an area in southern Ghana with a larger number of schizophrenic patients than surrounding areas: ‘“‘How far this applies to other parts of Ashanti [I do not know. As for non-Ashanti parts of Ghana, itis

likely that the situation is much less gloomy. I think I could count on

|

ls Schizophrenia a Disease of Civilization? 63 one hand the number of madmen I have met over the years elsewhere

...” (Field 1960). Field’s own explanation for this apparent pocket of schizophrenia is

genetic. She notes that the incidence of first-cousin marriage in the parents of schizophrenic patients was 40 percent, whereas it is only 10 percent in the general population. Furthermore, 13 of the 41 schizophrenic patients had schizophrenic siblings, parents, or first cousins. One other finding of Field’s study is significant: Although only 10

percent of the population of Ghana was literate, 40 percent of the schizophrenic patients who came to the shrines were literate. She suspected that it was because the literate ones were more likely to be able to afford to come to the shrines. However, in view of the previously

discussed findings in India, it is also possible that there is some relationship between higher levels of education and predisposition to schizophrenia in developing countries. The third study from Ghana is perhaps the most interesting. From 1934 to 1937, anthropologist Meyer Fortes, who had also been trained in

psychology, studied the Tallensi villages of northern Ghana. During that period he observed only one psychotic individual, a 22-year-old man who had become ill in adolescence, in the population of approximately 5,000. When talking to him, his attention “frequently wandered and a vacuous look spread over his face’’ (Fortes and Mayer 1969).

In 1963 Fortes returned to the Tallensi villages for two and a half months, this time accompanied by his wife, Doris Mayer, a boardcertified psychiatrist. In the same villages where twenty-seven years earlier there had been a single psychotic, there now were 17! Of these, Dr. Mayer diagnosed 13 as having schizophrenia, and | each as having manic-depressive psychosis, acute reactive psychosis, postpartum psychosis, and involutional depression. Borderline or doubtful cases were

excluded, a history was obtained from a family member, and each patient was interviewed in his own home. Of the 13 patients with schizophrenia, 9 were from the same Tallensi villages and 4 were Gorensi from nearby areas. The symptoms of the 9 Tallensi schizophrenic patients included thought disorder, flat or inappropriate affect, bizarre behavior, delusions, and hallucinations (present in all 9). Ages

of onset for the 9 were 14, 21, 22, 23, 27, 28, 31, 33, and 45. Trypanosomiasis (which may mimic schizophrenia) and neurological diseases were specifically examined: “and so far as I could tell by crude clinical methods it was not a factor in any of these cases”’ (Fortes and

64. Schizophrenia and Civilization Mayer 1969). Two cases had predominantly paranoid symptoms and

another was catatonic. Thus it seems likely that these patients did indeed have schizophrenia. Mayer and Fortes were themselves convinced that the dramatic rise in schizophrenia in the twenty-seven-year period was real, and that it could not be explained by population growth: What was quite startling, from my point of view, is that several of these cases occurred in families which were specially well known to me in 1934-37 and which were basically the same in structure in 1963 as in the early period. | knew some of the patients as young wives or youths or children. These were the families of my best friends and informants, some of whom are still living. Had such cases occurred among them in 1934-37 I could not have missed them. [Fortes and Mayer 1969]

Tallensi elders were also convinced that there had been a sharp rise in insanity. The authors rejected the possibility that cases of schizophrenia had simply been missed in the earlier study: “I doubt this, since sufferers are never hidden from public knowledge”’ (Fortes and Mayer 1969). Similarly, they rejected the explanation that schizophrenic patients in the earlier period had simply been allowed to starve: ‘This view is not tenable, for then, as now, food and shelter were always available to a

madman even if he was so violent as to require putting ‘in log’”’ (putting his foot through a log so that he could not run around and be destructive).

The villages under study had, of course, become much more developed and exposed to technology in the twenty-seven-year interim.

Schools, missions, bicycles, radios, canned goods, and gin had all become prevalent. In addition to this influx of technology into the Tallensi area, the authors noted that an unusual number of those who became psychiatrically ill had traveled to southern Ghana (the more urbanized and technologically advanced area) prior to the onset of their illness. Ten of the 17 who traveled “had become ill during or soon after a trip to southern Ghana for work.” H. B. M. Murphy, in discussing this study, believes that the psychosocial stresses encountered in this trip is

the key to understanding the rapid increase in schizophrenia among these people: On that trip they might have met new foods or new infections, but the one thing we know them to have met was a new social orientation which

Is Schizophrenia a Disease of Civilization? 65 severely challenged Tallensi traditional values. It seems likely that this trip to the coast was relevant to the development of the schizophrenia and that of the various environmental changes experienced there the social one was the most stressful. At the earlier period the Tallensi travelled less and met less challenging conditions when they did so. [1972]

Possible biological explanations for the increase in schizophrenia will be considered in chapter 9. One final observation by Mayer and Fortes is of interest. Despite the large number of schizophrenic patients observed among the Tallensi

people in 1963, it was their impression that they were even more numerous among the neighboring Gorensi. This group, according to the authors, had become even more Westernized than had the Tallensi.

Papua New Guinea Interest in Papua New Guinea was initiated by C. G. Seligman, a physician and anthropologist, who in 1929 reported no psychosis “‘in the villages among natives leading their own normal life.”” However, he did see 6 cases of psychosis among ‘‘natives’’ who were living along the coast in close contact with European settlers (Seligman 1929). General

paresis and neurosyphilis were also noted to be absent at that time. B. G. Burton-Bradley is a psychiatrist who has been in Papua New Guinea for over two decades, often as the only one to serve the nation’s 2.1 million people. In 1969 he published an analysis of the first 1,000

psychiatric patients who had been referred to him. Of the 1,000, 343 were said to have schizophrenia. Virtually all of them, however, were said to be individuals who had been living in the larger towns or who had recently migrated to the towns: ‘The person of limited cultural contact, the so-called bush individual, very rarely presents with the symptoms of schizophrenia’ (Burton-Bradley 1969). Those cases of ‘schizophrenia’ who did come from “the bush” do not sound like true schizophrenia but rather like acute reactive psychosis: Not uncommon is the acute schizophrenia of sudden onset coming on usually within three months of the patient’s leaving the village and working for the first time in a large town. Such patients readily recover and are returned to their village, at which level they can function without disturbance. [Burton-Bradley 1963]

Burton-Bradley also noted the rarity of general paresis of the insane

66 Schizophrenia and Civilization and the relative infrequency of psychosis among mixed-blood Papua New Guineans (1967). With these observations in mind, I undertook in 1973 a collaborative research project with Dr. Burton-Bradley and Barbara Boyle Torrey (Torrey, Torrey, and Burton-Bradley 1974). Papua New Guinea is an unusually good country in which to do epidemiologic research because census records for even the most remote villages are remarkably good

and the system of patrol officers, who visit all villages regularly, improves case finding. All psychiatric records for mainland Papua New Guinea were examined for the period January 1970 through May 1973, a total of 1,450 records. Only cases in which overtly psychotic signs and symptoms were present were selected. Psychoses with fever or organic disease,

postpartum psychoses, and mixed diagnoses (for example, schizophrenia with mental retardation, schizophrenia with epilepsy) were not included. Mixed-race individuals were excluded. The result was 478

individuals who had been admitted at least once during the study period. They were then divided into three groups: acute psychosis, schizophrenia, and manic-depressive psychosis. Acute psychosis (332 cases). One or two admissions, each lasting less than three months, with rapid and apparently complete recovery. A large percentage (one-third to one-half) of these cases of acute psychosis were in contract laborers brought from one part of the country to

another to work on plantations or in mines. The syndrome was so common that one psychologist simply diagnosed “plantation syndrome’ for such cases. Another unknown percentage of these cases undoubtedly included patients with brief organic psychosis for which the organic etiology was not detected. Some of these cases were culturebound syndromes like amok. Finally, some of these patients were true schizophrenics who would have been so had diagnosed their hospitalization been longer or had more information been available.

Schizophrenia (121 cases). Hospitalization for longer than three months, or more than two hospitalizations with signs and symptoms of schizophrenia (thought disorder, delusions and/or hallucinations, flat affect). The vast majority of these patients had had multiple admissions and classical signs and symptoms of schizophrenia. If there was any

substantial doubt about the diagnosis, the case was put in the acute psychosis group. Manic-depressive psychosis (25 cases). Multiple admissions for mania. Depressed periods had also been recorded for some patients, but there were no cases in which only multiple psychotic depressions occurred.

Is Schizophrenia a Disease of Civilization? 67 The 121] cases of schizophrenia were then grouped into their district of birth. The birthplace information was available on the records and was considered accurate, since it was the person’s primary identification. Mainland Papua New Guinea is divided into thirteen mainland

districts of which the nine coastal districts have had intermittent contact with Western influence and technology for approximately seventy-five years, and the four highland districts for only half that time. There are some areas of the highlands where the first contact between the inhabitants and Europeans has occurred only in the last ten years. The results of the divisions of schizophrenic patients by district revealed a greater-than-expected concentration of them in four coastal districts (Gulf, Central, Morobe, and Milne Bay), and approximately

the expected number in two other coastal districts (Western and Northern). Three other coastal districts (Madang, East Sepik, West Sepik) and the four highland districts all had a striking paucity of schizophrenic patients. In all of the seven the deficiency of schizophrenics compared with what was expected on the basis of population reached statistical significance (in four districts at a level of p< .Ol and in three districts at a level of p | vo oS 23 || =a 2a —_ S52 a“a

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