Cover image for The unbalanced mind
Title:
The unbalanced mind
Author:
Leff, Julian P.
Personal Author:
Publication Information:
New York : Columbia University Press, [2001]

©2001
Physical Description:
168 pages : illustrations ; 24 cm.
Language:
English
ISBN:
9780231120265
Format :
Book

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Summary

Summary

Do defective genes give rise to defective thought? The revolution in molecular genetics has indeed given rise to the increasing optimism that advancements in biotechnology will soon uncover the causes of all disturbances of mind and behavior. In this book, leading psychiatrist Julian Leff counters this reductionist claim and emphasizes what is known about the psychological, social, and cultural factors underlying mental illness. In doing so, he addresses many serious and urgent questions. What exactly is the difference between sadness and depression? What are the difficulties in categorizing psychiatric conditions? How are psychiatric diagnoses made in the first place? Are international attempts to standardize diagnosis flawed? Can doctors ever hope to disentangle cause and effect in the treatment of mental illness? What is the influence of emotional relationships on psychiatric conditions? How do public attitudes to mental illness affect choices of treatment? And, finally, what does all this tell us about the cultural causes of mental illness?

Throughout the book Leff also takes stock of the origins and effects of many medications used to treat mental illnesses, from antidepressants such as Prozac to Thorazine, a drug used to treat patients with delusions and hallucinations. Showing how broad social and community forces play into human development, he highlights the importance of life events and external forces in the origin and treatment of depression and schizophrenia. Leff acknowledges the biological basis of mental activity, but underscores the vital role of the social environment.

The Unbalanced Mind addresses such questions as:

* Why was there a lower rate of diagnosis of schizophrenia in Great Britain than in the United States?

* Why do people with schizophrenia in developing countries have a better rate of recovery?

* How did the USSR use the diagnosis of schizophrenia for political ends?

Full of engaging examples, The Unbalanced Mind provides a clear picture of how mental illnesses are diagnosed and treated--and what is at the root of the cause. As Leff explains, "My vision for the future of psychiatry is one that depends not on technical advances in making images of the brain or replacing bad genes with good ones, but on increasing our understanding of relationships between people."


Author Notes

Julian Leff is professor of social and cultural psychiatry at the Institute of Psychiatry in London. He has published more than two hundred articles and contributes regularly to television and radio broadcasts. He is the author and coauthor of ten books, one of which won the Starkey Prize of the Royal Society of Medicine, UK. In 1999 he became the first winner of the Burgholzli Prize for outstanding contributions to psychiatry.


Reviews 3

Publisher's Weekly Review

The roles of genetics and personal experiences in the development of mental disorders has long been debated in psychiatry. Freud argued that although hereditary factors predisposed certain individuals to "anxiety neuroses," they could not completely account for the symptoms he observed in his patients. With the advances in today's genetic research, many believe that the symptoms seen in disorders such as schizophrenia and manic depression will ultimately be attributed to DNA and the brain's biochemistry. Yet Leff, a psychiatrist at the Institute of Psychiatry in London, convincingly argues that genetics alone cannot completely explain the cause of psychiatric disorders and that there is good evidence supporting the role of the "social environment" in the genesis of mental illnesses. He cites studies, and while the results of one analysis cannot be taken as "proof," Leff's review of the evidence concerning the role of city life and socioeconomic status in the epidemiology of schizophrenia shows, in a balanced fashion that does not discredit biological-based research, how taking account of social relationships is essential to understanding and healing mental illness. First published in the U.K., this book is accessible to a general American audience. Although it does not explain which social factors contribute most to the onset of mental illnesses, it provides a striking counterpoint to biological determinism. Those with an interest in the relationship between the social world, genetics and the problems of mental life will enjoy this. (Nov.) (c) Copyright PWxyz, LLC. All rights reserved


Library Journal Review

This year has already seen the publication of two unusually fine books on biopsychosocial complexity (J. Allan Hobson and Jonathan A. Leonard's Out of Its Mind, LJ 6/15/01, and Elio Frattaroli's Healing the Soul in the Age of the Brain, LJ 8/01), and here is another. In this little gem, Leff (social and cultural psychiatry, Inst. of Psychiatry, London; Psychiatry Around the Globe) brings together material essential for health and mental health workers but too important for lay readers to miss. The author's intent is not to discount biological determinism but to show how it can be "integrated with our understanding of social environment." For example, to treat such mental illnesses as schizophrenia successfully, he suggests taking into account a patient's environment and socioeconomic status. Elements of psychiatric diagnosis, cross-cultural comparisons, epidemiology, genetic and environmental factors, the influence of pharmaceuticals on our perceptions of disease, and the limitations of brain science are all made crystal-clear. Leff's humane, hard-nosed social science attests that "our minds can be unbalanced by disturbances in our social environment, and the balance can be restored by actively reshaping our relationships with the people [who] matter to us." Highly recommended for all libraries. E. James Lieberman, George Washington Univ. Sch. of Medicine, Washington, DC (c) Copyright 2010. Library Journals LLC, a wholly owned subsidiary of Media Source, Inc. No redistribution permitted.


Choice Review

Leff's excellent study forces readers to assess the pendulum swings that have dominated attempts to understand mental illness. According to Leff (Institute of Psychiatry, London), those who move from a Freudian perspective of unconscious conflicts and urges and succumb to contemporary psychiatry's push to define all aspects of mental illness as biological may miss important points. Leff encourages the reader to explore the combined influences that may determine who will and who will not develop a mental illness. Any faculty member who has taught a course in abnormal psychology course can probably relate well to Leff s point. How can one describe and understand an illness (any illness, be it "mental" or more recognizably physical like diabetes) if one does not understand its physical, emotional, social, and cognitive components? This reviewer found Leff's book to be enlightening, the writing to be crisp and clear, and the comparison of what is labeled as "abnormal" to what many "normal" people do (at least at some level) refreshing and on the mark. Recommended for all readers. R. E. Osborne Southwest Texas State University


Excerpts

Excerpts

Chapter One How Blue is Blue? We all have times when we feel miserable, often for no apparent reason. We talk of feeling `blue', of being `down in the dumps', or `under the weather'. We proffer explanations which have no plausibility, such as `I got out of bed the wrong side this morning'. Sometimes a low mood is an obvious consequence of a major disruption in our life, such as the break-up of a relationship or the death of someone we love. Our friends and relatives would be concerned for us if we became sad following such an event, but would not think of us as ill. Andrew held a responsible job in a wines and spirits firm in which he had worked for twenty years. He had another fifteen years before retirement and enjoyed his work. The firm was taken over by a large corporation and he was declared redundant without notice. He was shocked and could not believe it had happened to him. He lay awake at night experiencing a mixture of misery and rage. He went off his food and moped around all day doing nothing. His wife and friends rallied round and encouraged him to think of alternative jobs. After a few weeks of being paralysed by his situation, he began to look for a position and realised that there were a number of options open to him. How intense does our misery have to become before a doctor would consider it to be an illness and diagnose depression? Should Andrew have been treated with antidepressants? The problem facing the doctor is that there is no test that will reveal whether the person is suffering from a depressive illness. In fact this problem affects the whole of psychiatry. There are no distinctive abnormalities of the blood, the body chemistry, the electrical activity of the brain or its appearance that can serve to diagnose any of the common psychiatric disorders. Numerous studies have identified changes in the structure of the brain and in the form of the brain waves in people with schizophrenia, while depressed people have been found to have abnormalities in the amounts of certain chemical transmitters in the brain. However, many people with these illnesses do not differ from healthy people in their brain structure and function, while some people with no psychiatric symptoms show the same abnormalities as the patients. This large overlap between healthy and ill people makes it impossible for the psychiatrist to use these brain changes to make a diagnosis.     Exciting new methods continue to be developed to visualise the structure and function of the brain. Although beautiful pictures are produced by these techniques, they have not advanced to the stage where they can be used to back up a diagnosis. There is a widespread belief among psychiatrists and researchers that this goal is not far off, but no one can be sure that it will ever be achieved. Serendipity and psychiatric treatments We can ask how far depression might be explained by changes in the functioning of the brain. Our thoughts, feelings and actions are obviously the result of brain activity at one level; but it does not follow that depression can be explained by changes in the way the brain works, or that reversing these changes would necessarily cure the depression. Antidepressant drugs were introduced in the 1950s and have become one of the most widely prescribed class of psychiatric treatments. But they were not designer drugs, chemically crafted to correct a known abnormality in the brain. Far from it: one of the first groups of antidepressants was developed from isoniazid, an antibiotic used for tuberculosis, because it was noticed that patients treated with this medication appeared to gain relief from the depressing effects of their chronic ill-health. Many of the treatments introduced into psychiatry have their origins in serendipity, including another frequently prescribed group of drugs, the tricyclic antidepressants. The first representative of this group, imipramine (UK trade name Tofranil), was synthesised in the 1940s as one of a series of antihistamines, sedatives and painkillers. It was recommended as a treatment to calm agitated psychotic patients, but in 1958 it was found to do little for these patients, but to have effects in relieving depression. How the brain sends messages A recent development in the drug treatment of depression is the introduction of a family of drugs called specific serotonin reuptake inhibitors (SSRIs). Signals are sent between brain cells (neurons)by chemicals known as transmitters. One of the most common chemical messengers in the brain is serotonin, the chemical name of which is 5-hydroxytryptamine. Serotonin is also found in the gut, and in bananas as well! One theory is that depression is caused by an inherited lack of serotonin in the brain.     The brain is an efficient organ and does not waste chemicals. When a transmitter has been released and has activated a receptor on the adjacent brain cell, any excess is transferred back into the nerve ending ('reuptake'), to be recirculated later. There is a specific serotonin reuptake process which works through a transporter molecule. The use of an SSRI to prevent this molecule transporting the excess serotonin back into the nerve ending results in an increase in the amount of serotonin washing around the neurons. Since serotonin activates a particular class of brain cells, this increase is believed to counteract the sluggishness of these neurons in depression. The drug fluoxetine, better known as Prozac, is an SSRI, but is only one of a whole family of antidepressants with similar effects on the level of serotonin in the brain. Although these drugs specifically block the reuptake of serotonin, they are not like so-called `smart' bombs which pinpoint targets, since they affect the chemical process wherever it occurs in the body. As there are many serotonin receptors in the gut, `collateral damage' occurs in the form of unpleasant intestinal side-effects, such as nausea and diarrhoea. Maternity blues One of the pieces of evidence put forward for a biochemical origin for depression is the occurrence of `maternity blues' in the mother immediately after the birth of a baby. Dramatic hormonal changes occur in the mother's body with the expulsion of the placenta and the onset of lactation. The mother's mood swings up and down for the first few days after the birth and bouts of tearfulness are common, the lowest point being between the third and fifth postnatal day. There is, however, a great deal of individual variation: some mothers do not experience a low mood, and most of those who do level out in a few days, while a small group go on to develop a full-blown depressive illness. The proportions at each stage have been determined by a group of researchers working in a maternity hospital in Paris in 1997. They gave two questionnaires to 126 women who gave birth at their hospital. The first questionnaire was designed to detect maternity blues and was filled in by the mothers on the third or fourth day after delivery. The second was aimed at picking up depression of clinical severity and was completed eight months after the birth. The mothers were asked to respond to the questions according to their feelings in the previous eight days. Almost exactly half the women reported experiencing maternity blues: of those with moderate blues, sixteen per cent were diagnosed as depressed eight months later, whereas of those with severe blues, the proportion who became depressed reached twenty-eight per cent. Of the sixty-four women who escaped the blues, only one was rated as depressed at eight months. These figures establish a strong link between maternity blues and later depression, and suggest that there may be a common biochemical basis for the two conditions, but that is not the whole story.     In order to discover why some women were more likely than others to develop depression after a birth, in the 1980s Channi Kumar and Kay Robson in London investigated a number of factors that might be responsible. One of their findings was unexpected: women who had had an induced abortion were more prone to postnatal depression than those without this history. This was true even if the abortion had been many years earlier. It is inconceivable that the hormonal changes following an abortion could linger for years, so that the most plausible explanation is that the psychological impact of the abortion was reactivated by the birth of a baby, intensifying the biochemical changes occurring at that time. This is not the only environmental factor to be implicated in the origin of postnatal depression. Other researchers have stressed the importance of difficult living conditions, socioeconomic problems, and lack of emotional support from the child's father and the wider social network. These aspects of environmental stress have also been shown to contribute to the causation of depression unrelated to childbirth. Genes and the mind Research on the impact of the social environment on a person's feelings, thoughts and behaviour has been overshadowed in recent years by the conviction held by many brain scientists that all mental activity will sooner or later be explicable in terms of genes and molecules. It is undeniable that the infant science of molecular genetics has already led to huge leaps in our understanding of certain physical diseases, such as cystic fibrosis. Identification of the specific sequence of the particular gene that gives rise to the abnormality raises the exciting possibility of correcting the problem at source through genetic engineering. There have been extravagant claims to have found a gene for homosexuality and for child abuse, but these have not been replicated by other scientists. A number of different genes have been linked with schizophrenia, for which the evidence for an inherited basis is strong. However, no single gene has been identified as the prime cause of the illness and some research groups have failed to find the same links as others. It seems likely that a number of different genes acting in concert are risk factors for the brain problems underlying schizophrenia. The inheritance of height, for example, is known to depend on the interaction of a number of genes. We have to conclude that, so far, the bright promise of molecular genetics has failed to illuminate any psychiatric condition beyond identifying some genes as potential risk factors. Public attitudes It is intriguing that the scientists' love affair with biological determinism has not influenced the views of the public on the causes and treatment of mental illness. Numerous surveys of public opinion over the years have come up with the same finding: stress is held to be the prime cause of the entire range of psychiatric conditions from anxiety to schizophrenia. This belief has a long pedigree: Shakespeare in The Comedy of Errors has an abbess question the wife of a man deemed to be mad as follows: `Hath he not lost much wealth by wrack of sea? Buried some dear friend? Hath not else his eye stray'd his affection in unlawful love, a sin prevailing much in youthful men, who give their eyes the liberty of gazing? Which of these sorrows is he subject to?' When asked about the treatment of mental illnesses, the public favour social support and talking therapies over physical treatments, and are generally very wary of antidepressants, which they view as addictive. This mistaken conviction may well have been implanted by the widely disseminated information on the addictive nature of the minor tranquillisers, such as chlordiazepoxide (Librium) and diazepam (Valium), which for a time were extensively prescribed to depressed patients by primary care doctors.     The term `addiction' is used loosely by the public, as in `addicted to shopping'. In medicine it covers both a psychological reliance on a drug, and also a physical need for it, which develops over time with certain drugs. Thus a person who is physically addicted to alcohol will develop the `shakes' after a day or so of not drinking, or even start to see small animals crawling over the walls and floor (delirium tremens or `the DTs'). The minor tranquillisers can produce a physical addiction even at small doses, so that a patient who stops taking them will experience very unpleasant sensations. Antidepressants never produce physical addiction, and most patients can stop them without ill effects, although a few find that their depression returns soon after. An educational campaign mounted recently in Britain by the Royal College of Psychiatrists and the Royal College of General Practitioners, which was partly aimed at lessening public prejudice against antidepressants, made only a small impact. We shall encounter this prejudice and its effects on compliance with drug prescriptions later, in our discussion of treatments for depression. Measuring depression across cultures Up to this point we have sidestepped the issue referred to in the title of this chapter, namely how miserable do you have to be before you cross the threshold into the domain of depression that requires treatment. We have to confront this question before discussing the social factors leading to depression, since it is fundamental to any comparison of results across studies. In 1988 I compiled a review of a large number of studies of the frequency of depression in the general population. These surveys had been carried out in many different countries, both developed, such as Britain, Greece and Argentina, and developing, such as Taiwan, India and Uganda. A variety of interview schedules and questionnaires had been used, making direct comparison of results very problematic. Imagine using a ruler marked in inches in one country and one marked in centimetres in another, and then attempting to compare the two sets of measurements without knowing how to convert from inches to centimetres. A more useful approach is to employ the same instrument for measuring depression in both countries, but unless the people speak the same language, it is necessary to translate it. This is not as straightforward as it might seem, since the accuracy of the translation has to be verified. The technique that has been developed for this purpose is called back-translation. One person translates the instrument from language A into language B. A second person, independent of the first, then translates the instrument back from language B to language A. The two versions in language A are then compared for discrepancies, revealing any faulty translations into B, which can then be corrected. Even this careful procedure is not foolproof, since it fails to detect problems with the usage of particular words. An example is provided by Lyn Gillis and his colleagues who translated a psychiatric assessment interview, the Present State Examination, from English into Xhosa, a South African language, in 1982. The Xhosa term for emotion, inimba , appeared to be correct when back-translated into English, but when the Xhosa version was used it emerged that the term denoted a feeling state that can only be experienced by women.     Very few of the studies I reviewed had used the same instrument plus the technique of back-translation. The frequency of depression and other neuroses ranged from a low of 0.8 per 1000 people in an aboriginal population on the island of Taiwan to a high of 287 per 1000 for women in Buenos Aires. It is unlikely that human populations differ so remarkably in their liability to neuroses, so that much of the variation can be attributed to problems of measurement. In support of this interpretation are the findings from a study conducted in 1979 in Uganda by John Orley and John Wing. John Orley has an unusual combination of training in both anthropology and psychiatry. He lived in a village in Uganda for eighteen months and learned the local language, Buganda. He then translated the Present State Examination interview into Buganda, following which his version was checked by back-translation. He surveyed two villages with this measuring instrument and then compared the rates of neuroses with those derived from a survey in London. The rate for Ugandan women was 269 per 1000 compared with 106 per 1000 for women in London. The rates for men were 174 and 58 per 1000 respectively. While the rates are two and a half to three times higher for Ugandan women and men, this is a credible difference compared with the 300-fold variation between the highest and lowest rates in my survey of the literature. Measuring symptoms We can learn a great deal about the measurement of depression by considering the construction of the Present State Examination (PSE). In the absence of laboratory tests, the only information available on which to base a diagnosis is the person's experiences and behaviour. Experience can be tapped only by questioning the person directly, while behaviour can be observed by the interviewer, supplemented by accounts given by people who know the person well (usually relatives). The techniques of exploring the person's experiences and classifying them derive from the science of phenomenology, and were applied definitively to psychiatry by the German psychiatrist, Karl Jaspers, whose textbook was published in 1913. The PSE provides the interviewer with a skeletal structure of questions which prompt a dialogue with the interviewee. The purpose of the dialogue is to explore and clarify the person's experiences in order to determine whether they fit the categories of symptoms built into the PSE.     Here is an example of a dialogue with a patient generated by the section of the PSE which covers anxiety: Interviewer: Have there been times lately when you've been very anxious or frightened? Patient: Yes, there have. Interviewer: Have you tended to get very anxious in certain special situations, such as travelling, or crossing the road? Patient: Yes, I find it hard to go out. Interviewer: Does it bother you to cross open spaces like parks or squares, or do you get anxious in shops or on buses? Patient: I can walk across a square if there aren't many people around, but I can't stand being in a shop with crowds of people. Interviewer: Is it the same problem with a crowded bus? Patient: Oh, yes. If a bus comes along that's full of people, I'll wait for the next one in the hope that it will be less crowded. Interviewer: Do you find it easier to go out at night? Patient: Yes, I do all my shopping at late-night supermarkets, because there aren't many other people around and I don't have to stand in a queue with other customers. The interviewer's detective work establishes that the patient has anxiety that is provoked by being in crowds, which is classified as a phobia. The interview schedule is accompanied by a glossary which defines each symptom precisely and gives examples. People's experiences rarely fit neatly into predetermined categories, so the interviewer often has to judge whether an experience approximates closely enough to a definition to be rated as a symptom. In making this judgement, the interviewer needs to take into account both the intensity of the experience and its frequency. To take the pertinent example of depressed mood, the questions that need to be asked are: how often during the past month has the person felt depressed? Has it occurred every day or only once or twice a week? How long does it last? Does the person cry or feel like crying? Here I should comment that the interviewer must gauge the answer in the light of the person's gender and culture. It is more acceptable for women to cry than men, except on the football field, where the whole range of emotions gains much freer expression than in everyday life. Furthermore, people from northern Europe are less expressive than those from southern Europe.     Other questions that will help the interviewer decide on the degree of depression are: does the low mood fluctuate in intensity or remain at the same level? Can it be relieved by anything, for example, can a friend cheer the person up? Has all enjoyment of life ceased or are there still things that can be enjoyed? How bad is the feeling when it is at its worst? This last question differs in kind from the others as it is not factual, but requires the person to find their own words to describe their experience. Expressions such as `it feels like a dark cloud', `I feel paralysed by it', or, paradoxically, `it is an indescribable feeling', indicate a severity of mood that is well beyond ordinary sadness.     Here are some other descriptions by patients from interviews with the PSE which convey the experience of depression: `I just can't make myself do anything. My brain isn't working at all. My mind has gone dead. I've just become like this. I can't say to myself, "do this, do that". I'm just not how I used to be.' `I'm fighting the tiredness and the depression. Trying to organise my life. Everything's been such a muddle. I spent days lying in bed. The tiredness was getting me down. I have been crying incessantly.' `I get gloomy over anything I read in the newspapers. I dreamed about my father dying. I feel everyone would be better off without me.' `Sometimes I feel low and I cry quite a lot. I can see no future and I feel completely trapped. There's an emptiness inside me. Nothing means anything. I feel as if I'm sinking.'     The presence of depressed mood is obviously essential for a diagnosis of a depressive illness, but there are other symptoms that often accompany it and that contribute to the diagnosis. These include poor appetite and weight loss, difficulty in sleeping, loss of interest in sex, slowness in thinking and moving about, lack of energy, and poor concentration. The PSE requires the interviewer to enquire about each symptom in some detail to establish its presence, as in the example above. Consequently the interview is long and demanding for both interviewer and subject. Various short cuts have been developed in the form of self-report questionnaires, which do not require the presence of a professional person and can even be sent by post or be filled in on a computer. They cannot achieve the same degree of accuracy as an interview like the PSE, but they are practical alternatives for large-scale surveys. Some attempt to cover a wide range of symptoms of neurosis, such as the General Health Questionnaire developed by David Goldberg in 1970 while he was in Manchester, while others have a narrow focus on symptoms of depression and/or anxiety, such as the Hamilton Rating Scale for Depression and the Beck Depression Inventory. A couple of questions from the latter will convey the style of these questionnaires. B. 0 I am not particularly pessimistic or discouraged about the future. 1 I feel discouraged about the future. 2a I feel I have nothing to look forward to. 2b I feel that I won't ever get over my troubles. 3 I feel that the future is hopeless and that things cannot improve. H. 0 I don't feel I am any worse than anybody else. 1 I am critical of myself for my weaknesses or mistakes. 2 I blame myself for my faults. 3 I blame myself for everything bad that happens. Processing the data There is a major difference between self-report questionnaires and interview-based instruments in the way a diagnosis is derived from the answers. The PSE data are processed by a computer program which incorporates an algorithm, or set of rules. These assign greater weight to some symptoms than to others and attempt to reproduce the decisions a clinician makes in arriving at a diagnosis. A program of this nature not only standardises the process of diagnosis, which varies considerably from one psychiatrist to another, it makes the rules open to examination. By comparing the diagnoses of individual psychiatrists with the output of the program and discussing the differences, the diagnostic rules used by clinicians (which often remain unformulated) can be brought into the open and studied. As we shall see later, the opportunity to make this comparison internationally revealed striking differences between the Russians, the Americans, and the rest of the world in the rules governing the diagnosis of schizophrenia. (Continues...) Excerpted from The Unbalanced Mind by Julian Leff. Copyright © 2001 by Julian Leff. Excerpted by permission. All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.

Table of Contents

Introduction
1 How Blue is Blue?
2 Moscow and Washington vs. The Rest of the World
3 The Human Probe
4 A Couple of Pills or Couple Therapy?
5 I've Got You Under My Skin
6 The People vs. The Professionals
7 Do Cities Drive Us Mad?
8 A Black and White Issue
Epilogue: The Future