Methods and Morals in the Life Sciences: A Guide for Analyzing and Writing Texts

Methods and Morals in the Life Sciences

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Methods and Morals in the Life Sciences A GUIDE FOR ANALYZING AND WRITING TEXTS Wim J. van der Steen and Vincent K.Y. Ho With Contributions by Harry Cook, Dorine Bax, and Arjen Groen

PR AEGER

Westport, Connecticut London

Library of Congress Cataloging-in-Publication Data van der Steen, Wim J., 1940Methods and morals in the life sciences : a guide for analyzing and writing texts / Wim J. van der Steen and Vincent K.Y. Ho. p. cm. Includes bibliographical references and index. ISBN 0-275-97119-S (alk. paper) 1. Medical literature—Evaluation. 2. Life sciences literature—Evaluation. 3. Logic. 4. Medical logic. I. Ho, Vincent K.Y, 1978- II. Title. R118.6.S84 2001 808'.06657—dc21 00-052869 British Library Cataloguing in Publication Data is available. Copyright © 2001 by Wim J. van der Steen and Vincent K.Y Ho All rights reserved. No portion of this book may be reproduced, by any process or technique, without the express written consent of the publisher. Library of Congress Catalog Card Number: 00-052869 ISBN: 0-275-97119-S First published in 2001 Praeger Publishers, 88 Post Road West, Westport, CT 06881 An imprint of Greenwood Publishing Group, Inc. www.praeger.com Printed in the United States of America

@r The paper used in this book complies with the Permanent Paper Standard issued by the National Information Standards Organization (Z39.48-1984). 10

9 8 7 6 5 4 3 2 1

Contents

Introduction to This Book

1

PART I. METHODOLOGY AS PRACTICAL PHIILOSOPHY

7

1. Introduction

9

2. Concepts, Statements, and Arguments 113 2.1 Introduction 13 2.2 Concepts 14 2.3 Statements 19 2.4 Arguments 25 3. Hypotheses, Theories, and Explanations 3.1 Introduction 3.2 Hypotheses 3.3 Theories and Explanations

35 35 35 41

4. Facts and Values

45

PART II. PUTTING SCIENCE IN CONTEXT

49

1. Introduction

51

2. A Survey of Guidelines

55

Contents

VI

PART HI. APPLICATIONS: TEXTS WITH COMMENTS

71

1. Introduction

73

2. Altruism and Egoism Text 1 Evolution: No Place for Altruism?

75 76

Text 2 Cooperation in Animals and Man

79

Text 3 A Philosopher Looks at Evolution and Altruism Text 4 No Moral Merit for Altruism? Text 5 How Not to Think about Evolution: Murder within the Family Text 6 Against Pervasive Self-interest Text 7 A Methodological Eye-Opener for Altruism Text 8 Ethics: Oddities of Self-interest Text 9 Ethics: A Vacuous Theory of Self-interest

81 86

Text 10 A Philosophical Lesson for Ethicists Text 11 Ethics: Discarding a Spurious Puzzle of Self-Interest

96

Text 12 A Lesson from History: More about Self-interest Text 13 Marriage, Self-interest, and Psychotherapy

98 99

3. Genes, Behavior, and Psychopathology Text 14 Psychopathology: A Matter of Genes? Text 15 Toward a Full Explanation of Psychopathology by Genetics? Text 16 Biology for Deviant Forms of Human Behavior Text 17 The Genetics of Separation Anxiety

88 90 92 93 95

97

101 101 103 105 106

Text 18 A Simplistic View of Genes and Human Behavior Text 19 Psychopathology and Biology: A Report for Those in Power

108 110

Text 20 Concentration Camps and Psychopathology Text 21 Should Biology Engulf Psychiatry? Text 22 Mental Health and Food

111 113 116

Text 23 Psychopathology and Neurotransmitters Text 24 How Not to Think about Evolution and Depression Text 25 Biological Abnormality and Psychopathology

117 119 121

Contents Text 26 The Puzzle of Attention Deficit Hyperactivity Disorder Text.27 Evolutionary Biology Distorted Text 28 Evolution and Psychopathology: A Methodological Riddle Text 29 Evolutionary Biology as a Profitable Source for Medicine

vii

122 125 126 128

4. Medication Text 30 Osteoporosis, Menopause, and the Pharmaceutical Industry Text 31 Medical Journals and the Pharmaceutical Industry Text 32 Drugs and Placebos: Methodological Bias in Research Text 33 Placebos, Animals, and Man Text 34 Should We Do Away with Biological Psychiatry?

131

5. Stress Text 35 Life Events: Stress for Medicine from Psychology Text 36 A Conceptual Pitfall Text 37 The Fate of Pigs in Husbandry

143 143 146 147

6. Genetic Engineering Text 38 Against Genetic Engineering Text 39 GMOs in the Field: A Misleading Call for Moderation Text 40 GMOs in the Field: A Staunch Defense

151 151

7. Miscellaneous Subjects Text 41 Genetics as Our Future Savior? Text 42 Make Room for Molecular Cell Biology Text 43 Stress in Plants Text 44 Population Bomb or Pernicious Politics? Text 45 Shortcomings of Biomedicine: The Chronic Fatigue Syndrome

161 161 162 163 165

131 134 137 138 139

154 157

167

PART IV. A TALE OF NONSTEROID ANTI-INFLAMMATORY DRUGS

171

1. Introduction

173

Vlll

Contents

2. Biased Promotion of Drugs: The Case of NSAIDs Wim J. van der Steen

177

3. Responses Response 1 Private Drug Research, Harry Cook Response 2 Diet Therapy as a Viable Alternative for NSAIDs, Dorine Bax Response 3 NSAIDS in the Netherlands: The View of a General Practitioner, Arjen Groen

185 185

Appendix to Part IV: Improving Style

193

Postlude

203

Bibliography: A Note Concerning Sources

205

Index

207

188 190

Introduction to This Book

Few theories in biology provoke as heated a debate as the notion that human behavior in general, and mental disorders in particular, have a genetic basis. While there would be no more potent evidence of a biological basis than the identification of causative genes, none have been found; on the other hand, opponents of this theory characterize it as deterministic, casting behavioral genetics as the enemy of free will. —The Biology of Mental Disorders, Washington, DC: Government Printing Office 1992, p. 101)

This is how a report of the OTA (the Office of Technology Assessment in the United States) introduces genetic aspects of mental disorders. At issue is a controversy over the causation of the disorders, and of behavior in general. Considering normalities and abnormalities in human behavior, some see and applaud a pervasively influential genetic basis of human behavior, whereas others voice loud protests against the view that man of all species should be victimized by the new genetics. These are the extremes, of course, from a range with many intermediate positions. If the issue interests you, for example, because you happen to be a student of biology or biomedicine, we would like to ask you: "Which side would you take?" Our teaching experience has us anticipate that answers come in three kinds. First, you take sides with the opposition that militates against the genetic determination of human behavior. Second, you take sides with the defense. Third, you hope for a hung jury, since you know that both sides

2

Introduction to This Book

must be wrong: genes and the environment are both important in the explanation of human behavior. The relative frequencies of answers are not as easy to anticipate: They vary with cultures and subcultures—at times in a rapid fashion. Allow us to come up with an additional anticipation. In reading the foregoing paragraph, your response has been that, with our classification of possibilities, we merely state the obvious: Behaviors, be they normal or abnormal, are either genetically determined, or environmentally determined, or something in between. We would anticipate this response on the ground that we were told that much, over and over again—during optional courses for small groups of students in the Netherlands, our country. We mostly managed to convince our students that, however odd it may seem, this issue of classification is not obvious at all, but getting to this point typically took many sessions. The problem here is this: All features of organisms, mental disorders in human beings not excluded, are subject to influences from genes and from the environment. That is a matter of elementary biology that appears to imply that our classification of possible views had better be discarded in favor of a single view: all behaviors are "determined" by genetic factors and also by environmental factors; hence, no fact of the matter remains to be investigated, the classification represents nonsense, and we had better put an end to all the disputes since they have no substance. However, the clamor continues from science down to the popular press. We have to envisage that this paradoxical situation should not resolve itself by means of being ignored. (Notice the implied additional paradox.) We postpone presentations of our own views of the matter. The remarks about our experiences during courses for students make clear why we do that: Since brief oral contacts did not suffice for us to convey fundamentals to other persons, then all the more so would a brief preview in an introduction invite and even strengthen the idea that views of ours should be put into into the garbage can for superfluity. (We know, the burden of proof is ours; wait with a verdict until you have seen much more about this in the book.) For now, the themes of mental illness and genetic determination only serve to indicate what the approaches in our book are like. These themes, and many others from biology and biomedicine, recur throughout the book so as to unite in stages a variety of approaches. We present two collections of tools that may foster capabilities and opportunities for the analysis of existing views of the themes, and indirectly in this way for the writing of new texts. The collections are labeled here as methodological criteria and guidelines.

Introduction to This Book

3

Part I of the book introduces the criteria from methodology. This is the most elementary part of the book. It is self-sustaining, so that it can be used for teaching at an elementary level. Since many students, and some researchers also, from the life sciences—unlike, for example, those from psychology—are not familiar with methodology applied to live science, Part I fills a lacuna; the book market is unfortunately unhelpful in this area. In addition to this, the entire book, with a modest beginning in Part I, represents a novel approach of science, society, and morality. Considering the example of mental illness, you may think here, for example, of influences that the pharmaceutical industry exerts on scientific tests of psychoactive drugs. Part II introduces our guidelines, which put biology and biomedicine in a broader setting. The guidelines represent a new approach. Before putting them together, we had long brooded over a well-known problem: Science is affected by a great variety of factors that are jointly covered many different disciplines. However, nowhere has the coverage matured into an exhaustive coherence that satisfies some significant purpose. Nobody has the capability for dealing with all the significant factors that bear on particular undertakings. This situation generates much bias, tension, and confusion in biology and biomedicine. Our guidelines are meant to help ease this problematic situation by evoking the necessity of modesty and goodness in the moral sense. Salient elements of our approach include: awareness of context-dependence, and avoidance of overgeneral theories paradoxically but feasibly combined with a generalist research strategy. The guidelines would only suit advanced level teaching. They may be helpful also for researchers who search for new approaches of interdisciplinarity. In Part III, we present case studies in which methodological criteria from Part I and guidelines from Part II are applied to published articles and books. The case studies comprise elements from forty-five texts about socially important themes, together with comments based on the criteria and the guidelines. The texts are loosely grouped around a limited number of themes to prevent incoherence. This part of the book has many potential uses, for example: teaching at several levels (elementary, moderately advanced, advanced), with aims such as training in applied logic, training in interdisciplinary thinking; additional training for researchers in interdisciplinary thinking; locating new source materials for lectures; and so forth. Part IV deals with a single theme, in greater detail: one of us has prepared a text on nonsteroid anti-inflammatory drugs in a social setting. The text is reproduced in Part IV together with invited responses, so as to unite themes from the entire book.

4

Introduction to This Book

Lastly, the Appendix is a guide in miniature for improving style in the preparation of texts. Our contribution here is minor since many good style manuals are on the market. However, we felt that it would be improper to leave out style entirely in a book such as ours. TOOLS FACILITATING ACCESSIBILITY Cross-references effectuated by a numbering system make the book more accessible. In part I, methodological criteria are numbered Ml, M2, . . . (for an overall survey, see Part I, 1.1), and in part II, guidelines are numbered Gl, G2, . . . (for an overall survey, see Part II, 1.1). Methodological criteria and guidelines are listed with each text in Part III. Conversely, some significant texts are listed with each criterion in Part I and with each guideline in Part II. Boxes facilitate the assimilation of new materials throughout Part I, since is is the most elementary part of the book. Furthermore, we use in Part I, with the exception of Chapter 5—which is a transition to Part II—at section headings, lists with keywords from science and from methodology. We have refrained from doing this also in Parts II and III—that would have led to dysfunctional lists, since our book has various functions that aim at different potential readerships. Finally, the level (elementary, moderately advanced, advanced) of each text in Part III is indicated at the text heading, together with the source discipline if it is outside the life sciences proper, to ease optional selections for different purposes of the book. For example, students or teachers who wish to stay with Part I, and to ignore Part II because it is too advanced, are advised to consider only elementary texts from Part III. Against common convention, we use much italics in Part I. This calls for some justification. The italicized words and phrases correspond with keywords in lists at section headings; this facilitates the search for salient points. Furthermore, we had to strike a balance between the aim of optimal readability and the aim of optimal learnabiliy. If we had reduced the quantity of words and phrases in italics, the text would have become a more easy read. However, from experience we know that many students and researchers in the life sciences are unaware of much methodology—in the sense of philosophy made practical for scientists—whereas methodology has a prominent role, for example, in psychology. Since we are convinced that this situation detracts from optimal science, we privileged learnability over readability. To achieve coherence, we have chosen from science themes that recur in the book in several places. As you proceed, you will notice that criteria and

Introduction to This Book

5

guidelines presented as separate items—how else could we introduce them?—are in many ways interconnected. The lists of criteria and and of texts provided by us to ease cross-reference, are therefore somewhat arbitrary: You may come to recognize items that are not in a list as more significant in the area you are considering. In any case, attempts to evaluate texts by the mere use of criteria and guidelines should be fruitless. The point is to develop a feeling for how all things hang together. That comes close to art.

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PARTI Methodology as Practical Philosophy

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Chapter 1

Introduction

Keywordsfrom methodology, methodological criterion, methodology. Suppose that a friend you are dining with, after eating a shrimp cocktail, suddenly starts vomiting—your own choice having been melon and bacon. Your hunch may be that something was wrong with the shrimps; perhaps they contained poison. Alternatively, your friend may have a shrimp allergy. To get at the right explanation, you need facts. An analysis of the shrimp cocktail could, for example, uncover the fact that the cocktail does contain a particular poison. That would provide a reasonable explanation. Facts, however, are not the only things you need. You also need to interconnect facts by a process of reasoning. Why suspect the shrimps in the first place? The answer is obvious. Your friend consumed shrimps, and he did the vomiting, whereas you had no shrimps and you did not vomit. Your reasoning about this amounts to an inference that belongs to logic. If a poison were detected afterward, you would have evidence that confirms the idea that the shrimps were to blame, and this evidence would provide a reasonable explanation. Logical inference, evidence, confirmation and explanation do not belong to the world where shrimps and vomiting belong. They indicate how science provides perspectives on things such as shrimps and phenomena such as vomiting. Naturally, in doing science, we want to know about proper and improper perspectives. We need for that criteria to evaluate the correctness of logical

Methodology as Practical Philosophy

10

inferences, the quality of evidence, and so forth. Such criteria are called methodological criteria. The development and the application of the criteria is a task of methodology—philosophy of science made practical for scientists. Part I introduces methodological criteria. Chapter 2 concerns logic, and Chapter 3 shows how logic is implemented in structuring science. Chapter 4 charts from a more extensive methodological perspective the territories of science and ethics. As indicated in the Introduction to This Book, we use a numbering system for cross-references. The methodological criteria of Part I are numberedMl, M2, . . . . We use boxes to introduce new criteria and themes. All the criteria are illustrated with brief examples. Applications of the criteria to live science are to be found in Part III; text numbers in boxes refer to part III of the book. The box that follows contains the overall list of the criteria, in the order of consecutive presentation. Methodological criteria for concepts Ml

clarity

M2 operationally Principles of classification M3 exclusiveness M4 exhaustiveness M5 consistency Methodological criteria for empirical statements See criteria for hypotheses Methodological criteria for arguments about empirical matters M6 clarity M7 validity or inductive support M8 noncircularity M9 truth or confirmation of premises M10 empirical content of premises M i l relevance of premises

Introduction

Methodological criteria for hypotheses/theories M12 clarity M13 simplicity M14 empirical content M15 testability/survival of tests M16 generality M17 universality M18 explanatory power M19 predictive power Methodological criteria for explanations M20 identification of causes See also criteria for arguments/hypotheses/theories

11

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Chapter 2

Concepts, Statements, and Arguments

2.1

INTRODUCTION Keywords from methodology: argument, language, logic, reconstruction, statement, thing. Keywords from science: altruism, etiological factor, genetic determination, Gross National Product (GNP), stress.

You cannot do science without considering language. It is therefore natural for methodology to take off from the logic of scientific language. Logic considers how we should reason. Reasoning goes by way of arguments consisting of statements as building blocks, and statements contain concepts as building blocks. Thus we should deal with three levels of language: Concepts expressed by words Statements expressed by sentences Arguments', statements combined in patterns of reasoning Note. Quotation marks indicate items of language. For example: "horse" is a word or concept, a horse is an animal. Before introducing the three levels, we briefly mention a theme that—in the writing and in the analysis of texts—should always be remembered. The

Methodology as Practical Philosophy

14

language used in texts seldom exhibits its logic in an explicit way. Meanings of words are often presupposed instead of being mentioned, and the status of statements must often be inferred from the context. "Squirrels are animals" stands for "All squirrels are animals," but "Americans like fast food" does—in most contexts—not refer to all Americans. Arguments, lastly, may be formulated in succinct ways, as statements taken for granted are omitted. The statement "Antibiotics will not cure your sore throat, because it is caused by a virus," for example, takes for granted a premise not formulated: "Antibiotics do not cure diseases caused by a virus." From this premise, together with the premise that a virus caused your sore throat, we can infer the conclusion: "Antibiotics will not cure your sore throat." These things show that we have to reconstruct texts in order to understand and to evaluate them. Reconstruction should be a natural activity throughout science. Unfortunately, both in science itself and in writings about science, reconstruction is seldom discussed in an explicit way. 2.2

CONCEPTS Keywords from methodology: accompanying feature, ambiguity, clarity, classification, consistency, defining feature, definition, dichotomy, exclusiveness, exhaustiveness, operationality, principle of classification, property, relation, vagueness. Keywords from science: altruism, context, determination (genetic, environmental), egoism, ethics, etiological factor, evolution, genetic determination, Gross National Product (GNP), stress, stressor.

We focus in this section on two crucial methodological criteria for concepts, as indicated in the box. Ml

Clarity = lack of vagueness and ambiguity

Texts: 1,3,4, 5, 6, 8, 11,14,15,24 M2 Operationality = possibility to determine applicability Texts: 24, 28

Concepts, Statements, and Arguments

15

Clarity is achieved by definitions, which elucidate the meaning of a concept by other concepts that are clear in themselves. Example "Identical twins" =df "twins deriving from one zygote." The sign in the middle stands for "is defined as." Being derived from one zygote is a defining feature of identical twins. Striking resemblance is an accompanying feature of identical twins—a feature not belonging to the definition. Operationality amounts to the possibility of observing or inferring the presence of defining or accompanying features. Considering twins, we can observe striking resemblances indicating that we are dealing with identical twins. However, we cannot be entirely sure of this. Operationality is seldom a matter of absolute certainty. In addition to being operational, concepts must be made operational in the right way. Example In economics, the so-called Gross National Product (GNP) is often used as an index for economic conditions in countries. The GNP covers processes in the marketplace; it does not cover environmental detoriation due to economic activity. Representatives of governments are often heard to say: "We must strike a balance between economic well-being and protection of the environment from pollution." Modern economic theories show that this line of reasoning is deeply flawed since environmental detoriation generates economic costs. In classic economic models used to calculate the GNP, these costs are disregarded. The costs are conceptualized in the models as so-called externalities. However, if we wish to remedy the detoriation, then we have to pay for it, and that is a matter for economics. Therefore, the GNP is an inappropriate operational index for economic conditions. Concepts come in different kinds. They may represent things—in a broad sense including, for example, persons and substances—or properties of things, or relations among things. A tree is a thing with the property of having a particular height. In the statement "The tree stands near the river," "stands near" represents a relation between two things. Concepts are linked up with classifications. If we say that something is green, we implicitly classify objects into green and nongreen things. We

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Methodology as Practical Philosophy

thereby get a dichotomy—a classification with two classes. Classifications may also contain more classes. In many contexts, appropriate classifications should satisfy three elementary principles, as indicated in the box. M3 Exclusiveness: No thing should belong to more than one class. Texts: 1, 2, 3 M4 Exhaustiveness: Each thing in the domain of a classification should belong to some class. Texts: 1,2,3,7,8,16,21,29,35 M5 Consistency: The criteria of classification must apply to all classes. Texts: 1,2,29

Example Suppose that we define the concept of altruism as "any act that benefits another person whereas it harms the actor," and the concept of egoism as "any act that harms another person whereas it benefits the actor." If these definitions were presented as a classification of all acts, then we should not accept it. It is true that the classification is exclusive, and that it uses the benefit—harm criterion in a consistent way. But the classification is not exhaustive: Many more types of acts are possible.

Intricacies of Live Science: More Difficult Examples 1. The example of altruism and egoism is on the face of it simple. If we probe more deeply, the simplicity evaporates. Do the definitions really provide clarity? What meaning should we attach, for example, to the notions "benefit" and "harm"? Benefits come in many forms. Suppose that I give you money, without getting anything in return. That would make you get richer—a benefit—whereas I would become poorer—a harm. However, I may feel good in giving you money, and we could surely count that as a benefit for myself.

Concepts, Statements, and Arguments

17

This kind of reasoning has caused much confusion in the literature, particularly in ethics, because different authors construe benefits in different ways. "Altruism" and "egoism," in ordinary language as well as in ethics, are indeed highly ambiguous notions. Furthermore, much confusion exists concerning the implications of evolutionary biology for ethics. Evolutionary biologists reckon with a particular benefit: fitness in the sense of reproductive success. Evolution tends to promote the maximization of fitness. Hence, altruism in this sense should not be expected to exist in organisms. Many researchers have concluded from this that altruism should be rare in human beings. Some of them have overlooked that uevolutionary altruism" is a different concept than "altruism" in ordinary language and in ethics. Having equalized the two concepts, they easily slide to the inference that evolutionary biology has substantive implications for ethics. Unfortunately, this fallacious mode of reasoning has become common among researchers outside biology who aim at evolutionary footholds for their own discipline. This illustrates that a methodologically improper use of concepts may have profound implications for views of human nature. 2. The concept of stress, however familiar, is also a source of confusion. Adverse conditions may cause a state of stress in you. If the stress is severe enough, then you may become ill. Scientists in many disciplines have done research about stress. In animals and in human beings, factors representing stress—so-called stressors—are thought to affect hormones and the immune system, so as to impair health in the long run. You may be tempted to conclude from this that the thesis "Stressors cause stress responses or states of stress in organisms," is a general truth. But you had better avoid the temptation. What conditions should count as stressors? Obvious candidates are extreme temperatures, extreme humidity, a boring job, and so forth. However, some organisms thrive in particular extreme situations, for example, extreme cold. For organisms that withstand extreme cold, this factor is not a stressor. The notion of stressor obviously requires specifications for particular situations and particular organisms. That leaves us with restrictive claims associated with contexts of interest. We should claim at most that particular factors should count as a stressor for particular organisms. This is not to deny that the notions of stress and stressor are useful labels to unite information on responses of organisms to all sorts of extreme

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Methodology as Practical Philosophy

conditions. Our intention here is merely to stress that useful labels must not be confused with important general concepts. 3. The color of your eyes represents an example of genetic determination. The way you brush your teeth is not genetically determined. Examples such as these suggest that the concept "genetic determination" is unproblematic. If we probe more deeply, however, awkward methodological problems come to the surface. From conception onward, organisms—humans not excepted—can only develop in particular environments. Genes and the environment jointly cause you to have a particular eye color. The same is true for the way you brush your teeth. Indeed, all features of organisms are both genetically determined and environmentally determined. We are apparently forced to conclude from this, that the statements concerning eye color and tooth brushing, are boring trivialities. However, this flies in the face of common sense. In fact, common sense is right. But to see this, we need subtle concepts of determination. What we should mean by the thesis "The color of your eyes is genetically determined" is this: If your friend's eye color is different from yours, this difference between the two of you is the result of a genetic difference, and not, in addition to this, to an environmental difference. The same is true for all comparisons with other persons who do not share eye color with you. According to a similar mode of reasoning, teeth brushing is environmentally determined. Other features are in part genetically determined, and in part environmentally determined. This should be taken to mean: These features result from genetic differences in some comparisons of one person (or organism) with another person (or organism), whereas an environmental difference is relevant in different comparisons. The concepts discussed here apparently represent relations among persons in the features considered. For this reason, the attribution of genetic or

Concepts, Statements, and Arguments

19

environmental determination to features of individuals makes no sense if the intended comparisons are unclear. 4. In various areas of medicine and psychiatry, etiological factors (= factors causing disease) are often classified into two major categories: biological factors and psychosocial factors. Biological factors are subdivided according to disciplines, for example as anatomical, physiological, and genetic factors. Missing in many classifications is the category of ecological factors—factors of the biological or of the physical environment. This means that the dichotomy of biological versus psychosocial factors is conflated with the dichotomy of internal versus external factors. The ensuing classification is inappropriate, since it is not exhaustive. The classification is often associated with research that disregards particular etiological factors in a biased way. For example, many research programs have no place for findings outside mainstreams that indicate that improper diets may cause all sorts of diseases. 2.3

STATEMENTS Keywords from methodology: classification, cognitive statement, empirical content, empirical statement, existential statement, fact, falsity, generality, logical form, logical statement, meaning, noncognitive statement, normative statement, probabilistic statement, singular statement, truth, universality, universal statement. Keywords from science: AIDS, altruism, disease symptom, egoism, function, HIV, identical twin, stress, stressor, stress response, virus infection.

Statements come in different kinds. We present three different ways to classify statements in successive boxes; succinct examples are included in the boxes here to avoid loss of coherence. The first classification concerns the content of statements from the perspective of logic.

20

Methodology as Practical Philosophy A Cognitive statements = statements that are true or false Al

Empirical statements = statements with empirical content The truth or falsity of these statements is determined by facts: states of affairs in the real world.

Examples. "Identical twins show a striking resemblance" (true); "Identical twins do not show a striking resemblance" (false); "Radioactive materials can produce mutations" (true). A2 Logical statements = statements without empirical content Statements with truth or falsity determined by the meaning of words or by logical form. Examples. "Identical twins are twins derived from one zygote" (truth determined by meaning of "identical twin"); "It is raining or it is not raining" (truth determined by logical form, "p or not-p"); "It is raining and it is not raining" (falsity determined by logical form, "p and not-p"). B Noncognitive statements = statements which are not true or false Example. "Shut the door." Special case: Normative statements = statements expressing norms or values. Example. "Murder is bad." This statement is acceptable, but is it true? Some people believe that the terms "truth" and "falsity" do not apply here. As the classification in the box indicates, facts play a salient role in the characterization of logical form. Some statements present factual issues, whereas other statements concern issues of logic or of ethics, for example. The terms i(true"and 'false" play important roles in the classification. Philosophers have developed many difficult, controversial theories about truth and falsity; we ignore these theories because we regard them as unhelpful. We would presuppose that you know what "truth " and "falsity" mean when you use these terms—but you should be aware here of possible problems with normative statements.

Concepts, Statements, and Arguments

21

The term "fact," which is also salient in the classification, does call for comments. The term "fact" must not be taken here in the broad sense of ordinary language. We normally use the term for many different things: 2 + 2 = 4; murder is bad; we wrote this text; all metals expand when heated; all bachelors are unmarried; and so forth. In science and in philosophy, the concept of fact mostly has a narrower meaning. It stands for things covered by statements that describe situations or events at particular times and particular places. The statement "We wrote this text" is true because it expresses a fact. So it has empirical content. The statement "We did not write this text" similarly has empirical content; it is false, because what it expresses is at odds with a fact. The general statement "All metals expand when heated" describes a multitude of facts. It obviously has empirical content. If you overlooked the distinction between these kinds of statements in your research, you would run the risk that some scientific doings of yours would not make sense: Research to determine the truth or falsity of claims that are in fact logical statements, is futile. Example The thesis "Measles are caused by a virus" is a logical statement. Being caused by a virus is part of what the concept "measles" means. Therefore, it is futile to do research on the thesis. Suppose that you discover a patient with the usual symptoms of measles, but the patient later turns out not to have a virus infection. Would that indicate that the thesis is not true after all? No, it would not. Instead, you would have discovered a type of disease that shares symptoms with measles, whereas it has different causes. It is true that, to accommodate the new finding, you have the liberty of changing the definition of measles. If you opted for this, you would have the right to conclude: "Measles are not always caused by a virus." However, this would not invalidate the original thesis. We would instead be dealing with two different theses that through similarities of wording create ambiguity—and a spurious contradiction in the wake of this. The second classification concerns logical form, which here concerns expressions such as "all" and "there is."

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Methodology as Practical Philosophy

1. Universal statements = statements referring to all things in some category Example. "All fish are vertebrates" (= "There is no fish which is not a vertebrate"). 2. Existential statements = statements that refer to a limited number of things in some category Example. "Some fish are not vertebrates (= "Not all fish are vertebrates") 3. Probabilistic statements = statements that specify the probability that particular situations exist Example. 'The probability that a coin after being tossed will land tails is 0.5." 4. Singular statements = statements that refer to a specific thing Example. 'The fish I am eating cannot swim." Note. Positive universal statements can be transformed into negative existential statements, and vice versa. The precise status of statements is seldom explicit in written and spoken language. For example, "Fish are vertebrates" usually means "All fish are vertebrates." The third classification concerns the content of statements from the perspective of science. This classification calls for special scrutiny, since it is often confused with the second classification. We should distinguish here between generality and universality. Generality is a matter of scope: general statements refer to many things, whereas specific statements have a narrower scope. General statements need not be universal, and vice versa.

1. Relatively general statements 2. Relatively specific statements

Concepts, Statements, and Arguments

23

Example Consider the statement: "Environments with extreme values for some physical factor represent stress for organisms." If we managed to define "stress" without referring to the extreme situation, then this statement would be a relatively general empirical statement. However, irrespective of the way we define "stress," the statement is probably false, since many organisms are adapted to extreme situations. If we wish to lay our hands on true empirical statements about stress, we have to make the statement more specific by reference to particular organisms. To do that, we also need to specify physical factors for the context considered, as different species are adapted to different conditions.

Methodological Criteria for Statements Statements of science can have all sorts of functions. Hence different methodological criteria may apply to different statements. All statements, however, should only contain concepts that are clear and operational. Clarity of concepts does not guarantee that statements containing the concept are clear. Unclear statements are in any case unacceptable. The substance of (empirical) science also calls for statements with empirical content—preferably simple statements—that are testable. Scientific research aims at the elaboration of theories. Theories are compounds of interrelated sets of statements—preferably general statements—that are accepted as true. Theories result from tests of hypotheses. Because the role of hypotheses and theories is pivotal, methodological criteria for statements receive detailed treatment in Chapter 3, which deals with hypotheses and theories. As a prelude, we present, in the examples that follow, connections between clarity of concepts and empirical content of statements. Ambiguous concepts may mislead us into thinking that particular general statements have empirical content, whereas—from some interpretations—they are in fact true by definition. This situation would not represent good science. The examples help us see relations among different methodological criteria: clarity, generality and empirical content.

Intricacies of Live Science: More Difficult Examples 1. In Section 2.2, we argued that altruism and egoism are difficult, ambiguous concepts. It should not come as a surprise, therefore, that

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statements about altruism and egoism are often problematic. If I feel good in giving you money, that may be considered a benefit, as I am then serving not only your interests, but also an interest of mine. In a way, therefore, I am not an altruist in this situation. Indeed, if I feel bad about having less money as a result of my generosity, that may also be considered a benefit—if feeling bad is what I want. If we consistently took this kind of approach, then all acts would become a matter of self-interest. The notion of self-interest would then be extended so as to make altruism impossible per definition. In this kind of situation, the thesis "Altruism is impossible" represents bad science, because it is then a logical statement. Such statements are worthless scientifically, because they do not represent any facts. If we aim at interesting, empirical theses about altruism and egoism, we need to come up with a narrower definition of self-interest. Interests come in many different forms. Overarching notions of altruism and egoism could therefore be defined in many different ways. The choice of particular definitions is to some extent arbitrary. No definition would cover all the behavioral exchanges we may wish to consider. Overarching notions of altruism and egoism are therefore useless. Instead, we need a more extensive, varied vocabulary for different contexts of interest. 2. The notions of stressor and stress response—which we also considered in Section 2.2—may similarly cause methodological trouble. "Stressor" is a concept that represents complex relations: A factor may be a stressor for one organism whereas it causes no trouble for a different organism. This may preclude the formulation of generalities about stress. We should never define "stressor," without qualifications, as any factor that causes stress responses. The problem is here that the most obvious general way to define "stress response" would entail reference to stressors as a cause. However, that would transform the claim "Stressors cause stress responses" into a boring logical statement. If you browse through literature about stress, you should be aware that conceptual trouble may be waiting for you. 3. The classification that comprises universal, existential, probabilistic, and singular statements is not exclusive. For example, the thesis "All features of organisms have a, function" is on the face of it a plain universal statement. However, grammatical appearances are deceptive. From a logical point of view, the thesis also has an existential component. We can rephrase it as: "For all features of all organisms: there is a function such that the

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feature has this function." As shown later, this has important implications for testability. 4. To some extent, the distinction between empirical statements and logical statements is a matter of convention. To illustrate this, we consider here research on AIDS. AIDS was initially defined through particular symptoms. The statement that a person with AIDS had these symptoms, was in this situation a logical statement. The discovery of the Humane Immunodeficiency Virus (HIV) as a cause of AIDS resulted in a new definition of the disease: AIDS is caused by HIV. The original definition was thereby transformed into an empirical statement. Some people may wish to stick to the original definition. If so, then the thesis that AIDS is characterized by particular symptoms is a logical statement for some persons, and at the same time an empirical statement for other persons. The thesis that AIDS is caused by HIV, would then be ambiguous as well. The ambiguity dissolves once we realize that a given word may express different concepts for different persons. Nothing much hinges on this. We must take care, however, not to define AIDS as a disease caused by the virus, when our aim is to find out by research whether the HIV does in fact cause AIDS. 2.4 ARGUMENTS Keywordsfrom methodology: argument, ceteris paribus, circularity, clarity, conclusion, confirmation, deductive, empirical content, explanation, fallacy of affirming the consequent, falsity, function (of argument), hypothetical syllogism, inductive, inductive generalization, inductive support, modus ponens, modus tollens, premise, reductio ad absurdum, relevance, truth, (in)validity. Keywordsfrom science: altruism, disease, double-blind experiment, drug, evolution, genetic determination, homosexuality, medication, method of agreement, method of concomitant variation,method of difference, noncircularity, placebo, virus. If we argue for something, we infer a particular statement called conclusion from other statements called premises. This is how logicians use the term argument. Take care to distinguish this usage from colloquial meanings. For example, the word "argument" is often used for "premises" in the sense of logic, which is confusing. We begin here with the most fundamental classification from logic of arguments, which concerns the strength of inferences from premises to conclusions.

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Methodology as Practical Philosophy Deductive arguments: premises are assumed to make the conclusion inevitable. More accurately: it is assumed that the conclusion cannot be false if the premises are true. The argument is valid if the assumption is true, it is invalid if the assumption is false. Inductive arguments: premises are assumed to make the conclusion probable.

The distinction for arguments between validity and invalidity is subtle. Validity is often confused with truth. The two notions are interrelated, though. An argument is valid if and only if it is impossible that the premises are true whereas the conclusion is false. The survey that follows presents a few valid argument forms and one invalid argument form, together with examples. Valid D e d u c t i v e A r g u m e n t Forms Note. We use conventional symbols of formal logic: p, q, . . . variables for statements; x, y, .. . variables for things; a, b,. . . constants representing particular things; P, Q, . . . constants representing particular features.

Modus ponens Premise 1: If/?, then q Premise 2:p Conclusion: q

Example of modus ponens Premise 1: If human populations will keep growing, then environments on the earth will detoriate further. Premise 2: Human populations will keep growing. Conclusion: Environments on the earth will detoriate further.

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Variant of modus ponens Premise 1: For all x, if x has feature P, then x has feature QPremise 2: a has feature P. Conclusion: a has feature Q.

We get the modus ponens if we replace Premise 1 by its implication "If a has feature P, then a has feature Q." Example of variant of modus ponens Premise 1: Amphibians are unable to live in deserts (= for all x, if x is an amphibian, then x is unable to live in deserts). Premise 2: Frogs are amphibians. Conclusion: Frogs are unable to live in deserts.

Modus tollens Premise 1: If/?, then q Premise 2: Not-g Conclusion: Not-/?

Example of modus tollens Premise 1: If a person suffers from an infection with a bacterial pathogen, then he or she runs a fever. Premise 2: Mary does not run a fever. Conclusion: Mary does not suffer from an infection with a bacterial pathogen. This example is slightly more complex than the ordinary modus tollens; see modus ponens, second box.

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Methodology as Practical Philosophy Hypothetical syllogism Premise 1: If/?, then q Premise 2: If q, then r Conclusion: If/?, then r

Example of hypothetical syllogism Premise 1: If the emission of greenhouse gases is not curbed, then ultraviolet radiation will intensify worldwide. Premise 2: If ultraviolet radiation will intensify worldwide, then the incidence of skin cancer will increase worldwide. Conclusion: If the emission of greenhouse gases is not curbed, then the incidence of skin cancer will increase worldwide. Note. A previous example, about amphibians, frogs, and deserts, can also be reconstructed as a hypothetical syllogism. An Invalid A r g u m e n t Form

Fallacy of affirming the consequent Premise 1: If/?, then q Premise 2: q Conclusion: /?

Example of fallacy of affirming the consequent Premise 1: If a person suffers from an infection with a bacterial pathogen, then he or she runs a fever. Premise 2: Mary runs a fever. Conclusion: Mary suffers from an infection with a bacterial pathogen.

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The example is slightly more complex than the ordinary fallacy of affirming the consequent; see modus ponens, second example. You can find many more uncontroversial examples of deductive arguments in any elementary logic text. Inductive arguments are more elusive, and logicians often quarrel about them. However, common sense will often help you a lot in inductive reasoning. We present here some well-known patterns of inductive argumentation. The most important pattern concerns inductive generalization, which moves from a sample of cases to a broader category. In other words, we infer here a relatively general conclusion from a more specific premise. Example We note that in many cases certain disease symptoms occur in people harboring a particular virus. We infer that the virus is always a cause when the symptoms occur. Several other methods exist to infer from data the causes of phenomena through inductive reasoning. For example, if particular plants in the desert always produce flowers after it has rained, it is reasonable to infer that rain is the cause of the phenomenon. This example represents the so-called method of agreement, which stipulates that a factor that is always present when a particular phenomenon occurs, is presumably a cause of the phenomenon. It is also possible that we observe the phenomenon once, and that a particular factor was present on this occasion, whereas it was absent on occasions when the phenomenon did not occur. The attribution of a causal role to the factor would then amount to application of the so-called method of difference. Finally, the covariation of a factor with a phenomenon allows causal inferences, according to the so-called method of concomitant variation. All these methods—though useful—do not yield certainty. In comparison with concepts and statements, arguments are complex entities. It is by no means easy, therefore, to assess them with methodological criteria. The next box lists criteria for the assessment of arguments about empirical matters:

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M6 Clarity Texts: 3,23,31,39 M7

Validity or inductive support

Texts: 2, 13, 14, 15, 17,23,26, 28, 30, 37, 38, 39,40 M8 Noncircularity Texts 3,21,23,26,37 M9 Truth or confirmation of premises Texts 2, 3, 28, 29, 37, 38, 39, 40 M10 Empirical content of premises Texts 30 Mil

Relevance of premises

Texts: 1,14,15,17,38,39

The criterion of validity only applies to deductive arguments. Considering inductive arguments, we should replace it by inductive support, the requirement that the premises must provide good enough grounds for accepting the conclusion. The criterion of truth must also be qualified. It is in many cases impossible to be sure that a particular statement is true. We should then be content with the weaker criterion of confirmation, which says that good grounds exist for assuming that the statement is true. In the next section, this point is analyzed in more detail. The criteria of clarity, empirical content, and relevance are straightforward, and the criterion of noncircularity is virtually self-evident. Circular reasoning exists when premises of an argument already contain in some way the conclusion. This is unacceptable, as the premises are meant to support the conclusion. Self-support is not genuine support. Examples a. Premise I: All predators live from preys. Premise 2: Cats are predators. Conclusion: Cats live from preys. This argument is clear

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and valid, and the premises are true. However, it is not acceptable because Premise 1 has no empirical content. This premise is a logical statement: Its being true or false depends on the definition of "cat." Therefore Premise 2 is in fact identical to the conclusion. The argument is circular: it does not have the feature of noncircularity. b. Mary has a particular disease. She is treated with a drug, and recovers within a week. Her recovery could be explained on the basis of two premises: People with the disease who take the drug always get well; Mary took the drug. If it turned out that people who do not take the drug recover as well, then this explanation would not be acceptable. In that situation, the first premise would become irrelevant: It disregards crucial information. Recovery, in this situation, would have nothing to do with the drug. Notice that the argument may satisfy the other criteria we considered. Arguments may serve many functions. We distinguish two major categories of function. The presence of absence of prior knowldege concerning the phenomenon described in the conclusion, is here the criterion of classification.

1. Inference of new information from known premises 2. Inference of known information from premises that enhance explanation

Examples Weather prediction would belong to the first category. It is easy to get this point. The second category is more difficult. The explanation of a known disease by the discovery of a virus causing it, would belong to the second category. Information about the virus would in the second situation belong to the premises. The conclusion would portray the existence of a known disease. The assumption that logical inference always moves from the known to the unknown is intuitively plausible, but it is false. It may be difficult to criticize some arguments that are unacceptable on the basis of methodological criteria. In such a situation, a special technique called reductio ad absurdum may be helpful. The technique uses the modus

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tollens format. It departs from the insight: if the argument were acceptable, a different argument known to be unacceptable should also be acceptable. This implies that the original argument cannot be acceptable. The first example that follows is an illustration.

Intricacies of Live Science: More Difficult Examples 1. Some people, scientists among them, have argued as follows that homosexuality is a disease: Premise 1: If homosexuality is genetically determined, then homosexuality is a disease. Premise 2: Homosexuality is genetically determined. Conclusion: Homosexuality is a disease. As we have argued several times, the concept of genetic determination is tricky. The argument could be problematic for this reason. Let us assume for the sake of argument that this is not so. We then still have to face that Premise 1 is unacceptable. If it were acceptable, then we could argue as well that being male or being female should count as diseases, as these features are genetically determined. 2. Consider the following argument. Premise 1: If evolutionary theory is true, then it is impossible for animals—including humans—to perform altruistic behaviors. Premise 2: Evolutionary theory is true. Conclusion: It is impossible for humans to perform altruistic behaviors. On the face of it, this is a valid argument. However, as we have already argued, the notion of altruism is ambiguous. In evolutionary theory, it is defined as behavior that benefits another organism by way of reproductive success, whereas it harms the actor on the same count. If "altruism" in the conclusion represents the ordinary notion, then the conclusion does not follow from the premises. The argument has the modus ponens form so that it is on the face of it valid. However, it is in fact invalid, as altruism is ambiguous. If meanings of altruism were spelled out, we would get a more intricate argument that does not conform to the modus ponens. 3. Drugs in the sense of medications play increasingly important roles in attempts to cure diseases. The marketing of new drugs is only allowed after tests have shown that they work and have no unacceptable side effects. A test that shows that patients get well after taking a drug will not suffice to show this, because it is conceivable that patients should have done equally well if they had not taken the drug. Therefore, we must rely on experiments

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in which we compare patients receiving a drug under investigation to patients who do not get the drug. An apparently sensible starting point would be to rely on this general thesis: A drug works well if patients receiving the drug experience more relief than patients not receiving the drug. This thesis, combined with the additional premise that the drug under investigation has effects in conformity with the thesis, would deductively imply that the drug works well. The thesis is only acceptable, however, if the treatment group and the control group do not differ in other relevant factors. In technical language: we need to be confident that a ceteris paribus clause is satisfied; ceteris paribus means "other things being equal." Unfortunately, it is hard to realize a set up in which this clause is satisfied. Merely the knowledge of receiving a drug, may allow patients to experience an alleviation of symptoms. A proper control group should therefore consist of patients receiving a pseudo-drug: a so-called placebo. Furthermore, neither the doctors nor the patients should be told which patients get the real thing; an experiment set up in conformity with this is called a doubleblind experiment (both doctors and patients are "blind"). However, this set up is still inadequate. Drugs, unlike ordinary placebos, have side effects. Research has indeed shown that doctors and patients are able to guess correctly whether a true drug or a placebo is being provided. We therefore need so-called active placebos: substances with side effects but without pharmacological effects on symptoms. The problems encountered in drug testing plague much research in science. If we want to know whether some factor has a particular effect, then we need to compare situations in which the factor is present to situations in which the factor is absent, and the two situations should not differ in other respects. Experimental set ups seldom ensure this in a fool-proof way. For that matter, if they are feasible at all, they would consume much time and money.

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Chapter 3

Hypotheses, Theories, and Explanations

3.1

INTRODUCTION Keywords from methodology: explanation, hypothesis, theory, test.

In science, we aim at general theories that help us explain phenomena. A theory—in a common sense of the term—is a set of interrelated general statements assumed to be true. We arrive at such statements through hypothesis testing. Hypotheses are new ideas of a general kind. We are hardly constrained in the invention of hypotheses, but we must be willing to test them critically. A hypothesis that survives tests may get a place in a theory and serve as a basis for explanation. 3.2

HYPOTHESES Keywords from methodology: ad hoc, assumption, clarity, (dis)confirmability, deductive argument, disturbing factor, empirical content, evidence, explanatory power, falsifiability, falsification, falsity, generality, hypothesis, logic of test, modus tollens, predictive power, simplicity, testability, test implication, theory, trade-off, truth, universality, universal statement, verifiablility, well-confirmed hypothesis (theory). Keywords from science: altruism, biological abnormality, calcium, dinosaur, disease, extinction, health, land snail, lung cancer, psychiatric disorder, smoking, stress, stressor.

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Science aims at theories that provide knowledge of the world, but not any old bit of knowledge will qualify. What we know about particular plants in our gardens is not scientifically interesting. To count as science, knowledge should satisfy particular methodological criteria, for example, generality. However, as we shall see, no hard-and-fast array of methodological requirements exists, because it may not be possible to satisfy in any particular situation all criteria that are reasonable in themselves. We have to face trade-offs among methodological criteria. Of course we want the statements in our theories to be true. As long as we do not feel sure about this, we are dealing with hypotheses that remain to be tested for truth. Let us begin, then, with hypotheses. A statement is only a proper hypothesis, if we are able in principle to gather information about its being true or false: Hypotheses must be testable. Statements in theories must have survived tests: They must be well-confirmed. For the rest, methodological criteria applying to statements in theories apply in principle also to hypotheses. The next box lists the criteria for hypotheses. I"

M12

Clarity

Texts: 3, 9, 10,24, 39 Ml 3 Simplicity Texts: 21, 26, 39 M14 Empirical content Texts: 3, 9, 10, 11,21 Ml 5 Testability/survival of tests Texts: 2, 3, 23, 24, 26, 31, 32, 33, 34, 37, 38 Ml 6 Generality Texts: 1,3,4,9,21,36,39 Ml 7 Universality Texts: 3, 9, 21,36, 39 M18 Explanatory power Texts: 1,5, 14, 15, 17,26,35 Ml9 Predictive power Texts: 1,14,15,17,26,38,40

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The importance of clarity is obvious. The rationale of simplicity is that it would be unwise to endorse a complex hypothesis if a simpler one is possible. Hypotheses should be empirical statements. Logical statements will not do, because they do not provide information about the real world. Intuitively, generality and universality are appealing criteria, but scientists regard some hypotheses as appropriate even though they do not satisfy these criteria. Examples The thesis that the dinosaurs went extinct during a particular period of the Earth's history is not general, because it only concerns one particular group of organisms. Yet the impact of the extinction event was so marked, that we regard it as scientifically important. The same is true for the statement "The Earth has a particular quantity of plant species," which is neither general nor universal. Explanation is perhaps the most important function of theories. Therefore, hypotheses must have the potential of explanatory power: We should expect them to get explanatory power once they are properly confirmed. For that matter, a hypothesis that satisfies the criteria already mentioned, is unlikely to lack explanatory power. Predictive power, finally, is a natural corollary of testability: We typically test hypotheses by way of predictive inferences. ' Prediction'' in this case need not concern the future. "Predictive power" means here that hypotheses must help us infer new information about the past, or the present, or the future. Examples a. "Stress is caused by stressors" looks like a nice general hypothesis, but it will not do if "stressor" is defined as "factor that causes stress." In that situation we are dealing with a logical statement. b. The hypothesis "Altruism among human beings is impossible" would be an example of a hypothesis that needs much unpacking. It is not sufficiently clear: The notion of altruism can take on many different meanings. An act is altruistic if it benefits another person at a cost to the actor. As we have already argued (see Chapter 2, Sections 2.2 and 2.3), the collection of potential benefits—and the collection of potential costs—can be defined in different ways ranging from very narrow—as in evolutionary altruism: "benefits" defined by reproductive success—to highly inclusive. From a highly inclusive interpretation, the hypotheses is useless as it becomes a logical statement. More

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Methodology as Practical Philosophy narrow interpretations come in different forms. Therefore, we had better replace the hypothesis by more specific statements. c. The hypothesis "Severe psychiatric disorders, such as schizophrenia, are caused by biological abnormalities" is in psychiatry almost taken for granted. Many researchers regard it as well-confirmed as the brains of patients suffering from such disorders are supposed to differ in some respects from the brains of healthy persons. Specific differences noted are controversial. Even if consistent differences were found, for the hypothesis to be acceptable we would need to test whether features of the brain in patients are abnormal. By no means would this be easy. Mere difference need not implicate biological abnormality. We could instead have a mental abnormality accompanied with a biological feature. As far as we know, researchers accepting the hypothesis have seldom bothered to formulate independent criteria of biological abnormality—"independent" meaning "not inferred from mental phenomena." Failing this, the hypothesis violates the criterion of clarity. It also invites circular reasoning.

We consider testability in more detail, as it is a subtle criterion. As the box indicates, three potential kinds of testability are usually distinguished. Verifiability: Truth can be demonstrated //the hypothesis is true. Falsifiability: Falsity can be demonstrated //the hypothesis is false. (Dis)confirmability: Evidence (not necessarily conclusive evidence) for or against the hypothesis can be found. Hypotheses are often universal statements. Such statements cannot be verified, because negative evidence may turn up in the future. As the logic of tests also precludes strictfalsification, we have to be content with a weak form of testability: (dis)confirmability. Absolute certainty is seldom possible in live science. The Logic of Tests: The Simple Case If hypotheses have implications that can be checked—test implications—we have a means to test them. If the implication is false, then the hypothesis is falsified. However, a true implication would not verify the hypothesis, but only confirm it. The logical pattern of falsification is as follows:

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Premise 1: If H, then / Premise 2: Not-/ Conclusion: Not-// This is a deductive argument form, the modus tollens', H stands for the hypothesis, /for the test implication. Example Hypothesis: "Persons injected with—a particular amount of—sodium pentothal will always speak the truth." From this hypothesis we can infer: "John, if he gets the pentothal, will speak the truth." If we discover that he lies after taking the pentothal, then the hypothesis is falsified. The Logic of Tests: The Normal Case In reality tests are seldom that simple, since assumptions play an important role in hypothesis testing. The normal scheme is: Premise 1: If H and A, then / Premise 2: Not-/ Conclusion: Not-//or not-^ A stands for assumptions. We can reject //with complete certainty only if we know that the assumptions are true. A typical assumption is this: ccNo disturbing factor played a role." It is impossible to prove such a thing conclusively. At best, evidence will show that A is well confirmed. If so, then it is reasonable to reject //, but this amounts only to disconfirmation; it is not strict falsification. If hypotheses survive a fair and varied quantity of tests, then we accept them as well-confirmed. Strict verification is impossible if we are dealing with universal statements: Such statements cover infinitely many instances. Example The hypothesis "Smoking causes lung cancer" is currently regarded as well-confirmed. Initially, the evidence was limited to epidemiological data: The incidence of lung cancer among smokers vastly exceeds the incidence among nonsmokers. That amounts to confirmation of a test implication. However, one could still argue that an assumption,

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Methodology as Practical Philosophy "Smokers and nonsmokers do not differ in other relevant factors," might be false. Some have indeed argued in the past, for example, that smokers have a genetic predisposition that is responsible both for the tendency to smoke and for the liability to develop lung cancer. Afterward, entirely different test implications have been confirmed. For example, tar, an important component of tobacco, has been shown to cause lung cancer in animals. All in all, it is now reasonable to accept the hypothesis.

Ad Hoc Assumptions Assumptions that are invented in the face of negative evidence are called ad hoc assumptions. Researchers should aim to minimize the role of such assumptions. Example Dr. Johnson, a general practitioner, elaborated the hypothesis "Diseases of internal organs are associated with pains in particular fingers." In particular, he thought, malfunctions of the heart lead to pain in the little finger of the left hand. The theory is an example of "projection theories" that are endorsed in some areas of alternative medicine. According to some researchers, for example, the body is projected onto the foot sole and onto the ear. To test the hypothesis, Johnson gives a number of patients a routine check-up. He asks them to spread their fingers on a table. The fingers are gently struck with a little hammer to detect abnormal sensitivities. In this way, Johnson diagnoses a malfunction of the heart in many patients. The afflicted persons are sent to a cardiologist. After a while, the cardiologist gets fed up with this. "What do you think you are doing?" he says to Johnson, "these people are all in good health." Johnson replies that his method is obviously very sensitive, since it helps practitioners diagnose heart disease in an early stage, when orthodox methods fail. Johnson's hypothesis is testable and empirical. However, he treats it as if it were a logical statement, as he regards pain in a particular finger as an overriding criterion of heart failure. In this way, he makes the hypothesis untestable in practice. If he is confronted with negative evidence, Johnson saves the hypothesis by the ad hoc assumption that orthodox methods of diagnosis fail to reveal all cases of heart malfunction. This procedure is unacceptable.

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Test implications are not the only source of evidence. If a hypothesis follows from a well-confirmed theory, then the theory is also a source of evidence. Example Consider the hypothesis "Land snails are absent in areas with little free calcium in the soil." We can test this hypothesis by observations on calcium and on snails in various areas. But the hypothesis can also be tested by deducing it from available theoretical knowledge. The shells— or internal skeletons—of land snails are rich in calcium. They can therefore develop only in environments where calcium isfreelyavailable. 3.3 THEORIES AND EXPLANATIONS Keywords from methodology: cause, deductive argument, explanation, generality, idealization, inductive argument, inference, necessary condition, necessary-and-sufficient condition, simplicity, salience, sufficient condition, theory, validity. Keywords from science: AIDS, air pollution, altruism, context of interest, disease, drug, etiological factor, egoism, HIV, immune system, lichen, lung cancer, mud slide, safe concentration, smoking, stressor, stress response, toxic chemical, unsafe sex, virus. Theories come in many different forms. We characterize here a situation that is often regarded as the ideal we should aim at, and contrast it with a more realistic portrayal. The Nature of Theories: The Ideal Case Ideal theories are collections of interrelated hypotheses that satisfy the methodological criteria formulated for hypotheses. In addition to this, we want theories to be well-confirmed. The N a t u r e of Theories: The Normal Case Highly general, well-confirmed theories are seldom possible. Many allegedly general theories are idealizations that apply only to a limited variety of actual situations. Scientists have to concentrate on things regarded

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as important and/or manageable, and they disregard other things. If this one-sidedness is misleading, we are dealing with bias. Furthermore, some subjects simply do not allow of theorizing at highly general levels. Examples a. Toxic chemicals are mostly tested separately on a limited number of species—for example, rats, earthworms—in the laboratory. A ' 'safe concentration" is here defined as some concentration much below the lowest concentration causing mortality. This may lead to biased theories of safe concentrations in food or in the environment: for example, accumulation of chemicals in food chains and interactions among chemicals increasing toxicity are disregarded. b. We have repeatedly considered the concepts of altruism and egoism, and the concepts of stressors and stress responses. These concepts cover heterogeneous collections of situations. Therefore, they hardly allow of generalizations; we should be content here with theorizing at low levels of generality. Research can but focus on particular forms of altruism and egoism, and on particular negative responses—considered to be "stress responses"—in particular to particular extreme conditions—considered to represent "stressors."

The Nature of Explanations: The Ideal Case Explanations are a mixed lot. Explanations can ideally be cast as arguments. Then the methodological criteria applying to them will be like those of arguments in general. In addition to this, we would like to use elements from an ideal theory—resulting from confirmed hypotheses—in the premises. All in all, methodological criteria for arguments, hypotheses, and theories carry over to explanations. There is one important additional criterion—explanations are deemed to uncover causes:

M20 Identification of causes Texts: 23, 25, 26, 29 Example We want to explain the low diversity of lichens—a group of lower plants—on trees in some area. Since we know that most lichens cannot survive air pollution, and that the area has much air pollution, it is

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reasonable to infer that air pollution is the cause. This explanation can be formulated as a deductive argument: Premise 1: For all x, if x is an area with air pollution, then x has a low diversity of lichens on trees. Premise 2: a is an area with air pollution. Conclusion: a has a low diversity of lichens on trees. This explanation satisfies the methodological criteria that we have formulated. The Nature of Explanations: The Normal Case Ideal situations are rare. The example just given contains a valid deductive argument in which the reasoning goes from causes to effects. In many cases of explanation, we can only reason from effects to some cause and not the other way round as we do not know enough about all the relevant causes to infer effects from them. Explanations with the form of a deductive argument are then impossible. Example Consider the following hypothetical situation. A doctor is faced with a patient who has a disease that is always fatal if no treatment is given. Only one treatment with a drug is known. Unfortunately, the drug leads to recovery in only 10 percent of the cases. Other factors that play a role in recovery are unknown. The doctor prescribes the drug, and the patient recovers. It is then reasonable to endorse the statement "The treatment was the cause of recovery" in this situation, and to assume that this statement explains the recovery. Notice that the cause is here inferred from the effect. We could not deductively infer the effect from the cause. We can reconstruct the explanation as an inductive argument that moves from cause to effect. But the inductive support of this argument would be weak as the premises do not make the conclusion probable. The concept of cause can have various meanings. As indicated in the next box, four meanings are usually distinguished. Necessary conditions Sufficient conditions Necessary and sufficient conditions Conditions that are neither necessary nor sufficient

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If a cause is sufficient for an effect, then we can infer the effect from the cause. If a cause is necessary for an effect, then we can infer the cause from the effect. The examples just given illustrate these possibilities. (Both possibilities are realized if a cause is both necessary and sufficient.) In many cases, we are dealing with causal factors that are neither necessary nor sufficient for the effect. Knockdown inferences in either direction are then impossible. We often maintain that we know the cause of a phenomenon. That may be misleading. Every phenomenon has an infinite number of causes. In ordinary parlance as well as in science, we regard particular factors that are salient in the context of interest as causes; other factors have to ignored to avoid excessive deviations from simplicity. Examples a. In the lichen example considered in this chapter, air pollution was mentioned as a cause (a sufficient condition) of trees having a low diversity of lichens. Of course, air pollution also has causes, and these are at the same time—indirect—causes of trees having a low diversity of lichens. b. It is not unreasonable to regard smoking as the cause of lung cancer, because smoking is here the most salient etiologicalfactor of this disease. However, some smokers do not develop lung cancer, and some nonsmokers develop it. Smoking is important etiologically, but it is neither necessary nor sufficient as a cause. c. HIV is the cause that explains AIDS. The virus causes the immune system to detoriate. Therefore, the detoriation of the immune system might also be considered as the cause. Other causes also exist: We may, for example, regard unsafe sex resulting in the spread of the virus as a salient cause. The context of interest determines what factor is best regarded as causally salient. Virologists will focus on the virus. Professionals concerned with prevention will focus on other factors: unsafe sex and so on. d. Mudslides are common in mountainous areas. It is reasonable to attribute mudslides to heavy rains. But we may also explain them as caused by deforestation. In this case as well, the context of interest determines what factor is best regarded as a salient cause.

Chapter 4

Facts and Values

Many researchers have argued that science should be value free, but no researcher would maintain that values—in the sense of ethical norms and values—should not play any role at all in science. Ethical concerns, for example, do limit the permissibility of experiments on animals and human beings. Values play many different roles in science. We provide an inventory of roles, and we defend the thesis that value freedom, however narrowly construed, is impossible. 1. Methodological values are indispensable in science. This thesis needs no defense. The subject of value freedom concerns ethical rather than methodological values. "Values" in the sequel will stand for "ethical norms and values." 2. Priorities in research depend on values. Biomedical research and military research—and research in other areas—compete for funds. It is obvious that resource allocation is ultimately a matter of ethics here. 3. Values guide applications of scientific research. The human genome project, according to some—by no means all—researchers, should enhance possibilities for treating all sorts of diseases. This sort of application, if feasible, is to be welcomed. The project may also generate knowledge that enables us to chart risks for individuals to develop particular diseases. Insurance companies may wish to know about this, so that they can fix

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premiums accordingly. Many would regard this application as morally problematic. 4. Values restrict the admissibility of research on animals and human beings. Research that causes extreme harm or discomfort in human beings is out of the question. More moderate forms of harm or discomfort may be acceptable, provided that the research benefits others and that subjects participating in research give informed consent. By and large, proper regulation of research on humans exists. It is more difficult in the case of animals. We have to weigh here advantages for humans against disadvantages for experimental animals. Regulation in this area exists, but it is elusive for several reasons. Animals should not be subjected to extreme suffering, and advantages for humans must involve fundamental values, such as health. However, the assessment of suffering in animals is difficult since we do not know much about animal consciousness. Future advantages concerning human health may also be difficult to assess. 5. Facts about values can be investigated by ordinary scientific means. Psychology and social science have much to say about values endorsed by people, and about the motives they have for endorsing them. The life sciences also have information to contribute about these themes. Some forms of immoral behavior, for example, may result from psychopathology, so that evolutionary biology may help to explain the origin of our values. However controversial these issues are at present, we are dealing with legitimate subjects of research. The role of values in science is also a proper subject of empirical research. For example, biomedical research supposedly aims to enhance human health, but research about this research indicates that funding by the pharmaceutical industry does not invariably contribute to human health. 6. Scientific research can helpjustify values. A straightforward derivation of values from scientific theories is logically impossible. Such a derivation would amount to a so-called naturalistic fallacy. However, the derivation of particular values from other values together with empirical premises, may be entirely legitimate. If particular residues of pesticides in food endanger human health (an empirical issue), and we endorse the view that food endangering human health should not be marketed (a normative issue: a matter of values), then we can infer that food containing these residues should not be marketed (again a normative issue).

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7. Methodological choices depend on values. Suppose, you have the opportunity to do research on biological diversity in a particular forest. You can do that in many different ways. For example, you may decide to focus on species numbers of particular groups of organisms, such as insects and birds. You may find that species numbers depend on particular features of the forest, such as environmental heterogeneity. This may fit in with a general theory that connects diversity with environmental heterogeneity. Alternatively, you may decide to identify particular species with a large ecological impact and to seek explanations of why these species inhabit the forest. That would call for relatively specific information that does not sit well with theorizing at a highly general level. Which approach should you follow? The issue here would not merely be the choice of research subject. You would also have to opt for a particular methodology: generality, no explanatory power with respect to individual species versus specificity, explanatory power with respect to individual species. Notice that different methodological criteria may be at odds with each other: In the example, the criteria envisaged cannot at the same time be satisfied. If this is indeed true, then you have to prioritize the methodological criteria. Neither the substance nor the methodology of science would provide the means to do this. We therefore have to rely on criteria from outside science—not least ethical criteria—to make a choice. Considering the forest, for example, you may decide that the second approach is preferable because it serves preservation purposes better. Thesis 7 indicates that science cannot even be value free in the most restrictive sense of the term: Values should find a place at the core of science as they determine what methodology is proper. If methodology is part and parcel of science, then so are values from the domain of ethics. This thesis can also be defended through a focus on causal explanation. As we argued in Chapter 3, phenomena always result from an unlimited number of causes, if only because any particular cause of a phenomenon has causes of its own that thereby causally influence the phenomenon, albeit in an indirect way. For this reason, explanations that identify all causes of a phenomenon are not feasible. We have to focus on particular causal factors that are deemed relevant for some reason. Relevance depends on contextual factors implicating values. We conclude again: Values cannot be missed even at the heart of science.

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PARTII Putting Science in Context

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Chapter 1

Introduction

In Part I, we introduced methodological criteria that scientific texts should satisfy. Ideal texts, one could be tempted to think, are those that satisfy all the criteria. Unfortunately, such texts do not exist. Methodological criteria can be at odds with each other: A text that satisfies one criterion may thereby violate a different criterion. Here is a simple example. Suppose that you want to do research about causes of schizophrenia—a common "disease." One way to approach the subject would be to focus on genetics and on biological variables affected by genetic factors. Many researchers have done just this. They have shown, for example, that in schizophrenia identical twins exhibit a high concordance (50 percent according to some), whereas nonidentical twins exhibit a much lower concordance. This appears to suggest that genetic factors are among the salient causes of schizophrenia. It also demonstrates that environmental factors must be implicated. However, we must realize that this approach concerns the level of populations, and that it entails few things about the level of individuals. The following fictitious example illustrates this. A group of identical twins and nonidentical twins is on a trip on a coastal plain. The trip is wrecked by a flood that causes short individuals to drown, whereas tall individuals survive. Identical twins will be concordant with respect to the drowning, which in this situation is caused by their having identical body lengths. Since some of the nonidentical twins have dissimilar lengths, they reveal a lower concordance. From the assumption "Variation in body length

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is fully explained by genetic variation," we are entitled to infer that variation with respect to drowning in this population (group) is explained by genetic variation. However, it would be odd to claim that the individual cases of drowning have been caused by genetic factors rather than the flood. This example does by analogy demonstrate for schizophrenia that mere twin data cannot generate a theory about individuals. Such data only help us formulate a theory for populations. If we wished to expand such a theory to explain fates of individuals, we would have to uncover links between genetic factors and disease symptoms. Such links would represent an analogy of links between genes and body length in the fictitious example. They would have to comprise all sorts of processes within the human body as well as roles of the environment, and the environment should cover ecological factors in addition to the psychosocial setting. No general theory can accommodate all this. In our research, we have to aim at a theory that covers populations only, or a theory that says much about few features of many individuals, or a theory that says little about many features of many individuals, and so forth. What kind of theory should we prefer? That question cannot be answered from the substance and the methodology of science. The merits of a theory depend on how we want to use the theory. If our aim is, for example, to understand individual patients suffering from schizophrenia, and to provide them with an adequate treatment, then a theory centering on the population level is useless. However, such a theory may suit the purpose of charting the epidemiology of schizophrenia. In brief, contextual considerations, including ethical concerns, determine what methodological balance is proper in theorizing. Such considerations also determine how particular methodological criteria are best fleshed out. The methodological criterion of explanatory value, for example, presupposes the context-dependent identification of salient causes. Mere methodology obviously does not suffice to determine the scientific quality of a text. Scientific quality is context-dependent. It therefore cannot be divorced from moral quality. The guidelines presented here indicate how domains beyond methodology can help us assess the merits of scientific texts. In addition to this, the guidelines cover more mundane matters of presentation as well. Guidelines to be considered in Part II are listed in the box that follows.

Introduction Gl

Context-dependence

G2 Generalist backing G3 Charity G4 Source check G5 No dirty hands G6 Reconstruction |

G7 No excessive generality G8 No causal selectivism G9 Proper levels of organization G10 Implications of descriptions G i l Salient points G12 Explicit relations G13 Consistency G14 No heterogeneity G15 Ordinary language

General Remarks 1. The guidelines apply both to the interpretation of texts and to the writing of texts. 2. The guidelines involve two levels: presentation and content. Representative texts of science seldom distinguish explicitly between these levels. 3. It is convenient to distinguish between internal criticism and external criticism of a text. For internal criticism, we only need materials inside the text. External criticism relies on outside sources. Internal criticism is a convenient point of departure. If internal criticism uncovers a profound inconsistency, then no need may exist for external criticism—which tends to be more time consuming.

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Chapter 2

A Survey of Guidelines

In other books devoted to the writing of texts or to the analysis of literature, you will not come across a collection of guidelines as brought together in our survey. You will therefore need some time to get the idea of our approach. Note. All sorts of relations between guidelines exist. Some of the relations are listed here by notes. Relations also exist between the methodological criteria in Part I and the guidelines. These relations are occasionaly mentioned in our survey, but they are not separately listed. You will be aware of them after having studied Part I. The presentation of each guideline is headed by a list of illustrative texts to be found in Part III. Gl

CONTEXT-DEPENDENCE Texts: 1, 4, 14, 15, 17, 18, 20, 22, 30, 35, 36, 39, 40, 44, 45 Note. Gl is associated with several other guidelines.

Be aware of context-dependence. We regard this as the most important guideline. Scientific claims are often presented as universal, even if they are true only for particular contexts within science.

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More fundamentally, the attribution of quality to scientific work should depend on contexts beyond science. Scientific quality depends on numerous methodological criteria, and the choice of proper criteria ultimately depends on the social context. Intrinsic relations therefore exist between scientific quality and moral quality. Example Suppose that 10 percent of the persons who regularly eat fast food develop a nasty disease. Let us assume the following things: Research indicates that fast food affects a neurotransmitter in persons with a particular predisposition, and impaired neurotransmitter function is a cause of the disease symptoms. Researchers paid by the pharmaceutical industry unravel all the biochemical details. They formulate this theory: "Impaired neurotransmitter function is the factor that causes the disease." The theory portrays how this factor produces the symptoms. The industry develops a drug without nasty side effects that improves neurotransmitter function and thereby alleviates symptoms. That is apparently a great thing. However, researchers elsewhere point out: Fast food is the ultimate culprit, with the implication that patients should alter their eating habits. Their work is ignored in mainstream research. What about the scientific quality of the theory generated through the industry? We would answer that the theory is entirely appropriate in some contexts: No theory can chart all the causes for the phenomena covered by it. The industry is faced with the moral imperative to benefit patients, and also with the moral imperative to make money. Without the money, it could not benefit patients. The industry acts in this example in accordance with acceptable moral imperatives. It would be unreasonable to require, in theory or in practice, that it should consider diets in addition to drugs. Diet should be causally relevant, of course, in a broader context. A theory that merely uncovered, without specifying any biochemical detail, the causal link between diet and the disease, would presumably not satisfy as many methodological criteria as the industry's theory would. However, the diet theory would have the merit of pointing to a causal factor that is disregarded in the industry's theory. In some contexts, for example, health management or behavioral medicine, the diet theory would be the most meritorious option. In other contexts, a focus on the industry's theory would be more appropriate.

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In closing, we note that our hypothetical example might be unrepresentative within the context of the pharmaceutical industry. G2 GENERALIST BACKING Texts: 16, 18, 24, 27, 28, 30, 31, 35, 44, 45 Note. This guideline tends to be associated with many other guidelines. Aim at a generalist backing of specialist work. Numbers of disciplines have rapidly proliferated during the last few decades. Researchers need not be aware that their subjects of research are investigated in many disciplines beyond their area of expertise. Take care, in any research you undertake—in the analysis of literature or in writing—to search for relevant disciplines outside your primary area of work. Read some representative reviews in these disciplines. The results of this activity may well shock you. An ideal understanding of subjects calls for some knowledge from many sources. The discovery of a novel source may have profound implications. Example Source: Fairhead, J., and M. Leach. Misreading the African Land scape: Society and Ecology in a Forest-Savanna Mosaic. Cambridge: Cambridge UP, 1996. Many regions in Africa have a mosaic landscape of forest patches interspersed with savanna. The common view is: this type of landscape represents land degradation due to bad agricultural practices of local peasants. The savannas, in this view, result from deforestation that is now taking place at alarming rates. The mosaic landscape is present, for example, in Kissidougou, an area in Guinea. That is where Fairhead and Leach (1996) did an in-depth study comprising of ecological, anthropological, climatological, and historical approaches. Fairhead and Leach show, for example, that the common ecological interpretation of the landscape is problematic, whereas ecological studies outside mainstream research offer better interpretations. Their evidence shows that local agricultural practice does not lead to deforestation. The quantity of forest has in fact increased during the last few decades, due to sophisticated agricultural practices of local farm-

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ers. Aerial photographs confirm the increased extension of the forests. The generalist approach of Fairhead and Leach has produced convincing evidence against commonly accepted views, which presuppose that deforestation is rampant in the area. It is to be hoped that their book will change policies toward local farmers, who have been branded as stupid and irresponsible. To the detriment of the peasants, huge amounts of money have been wasted by the government, and by development agencies, in attempts to "reform" an agriculture that hardly needed improvement. G3 CHARITY Texts: 25, 30 Note. This guideline is often associated with G8. Exercise charity in criticizing texts. This guideline is known as the principle of charity. At first sight, this is an odd principle: Charity appears to invite a mitigation of criticism that protects the person criticized rather than the critic. However, charity is in fact necessary for self-protection. Suppose that you criticize an argument that allows of two interpretations, that you opt for one of these interpretations, and that you demonstrate that the argument is invalid from this interpretation. This may backfire if the other interpretation yields a valid argument. The person criticized by you would simply point out that your interpretation is wrong, as it generates an invalid argument. Example Source: Van der Steen, W.J. Bias in behaviour genetics: An ecological perspective. Acta Biotheoretica 46: 369-377, 1999. Behavior geneticists have done much twin research on schizophrenia. Replicated studies have shown that concordance for the disorder is much higher in identical twins than in nonidentical twins. This implies that variation of schizophrenia at the population level is explained in part by genetic variation. Researchers often summarize this by the thesis "Schizophrenia has an important genetic component." We could object that this thesis is a fallacy, because it suggests that twin research has implications for etiology at the level of indi-

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viduals. As we argued in Part II, Chapter 1, nothing of the kind can be inferred from twin data. I (WJS) have repeatedly voiced this objection in discussions with behavior geneticists. Invariably, I got the reply that they are fully aware that inferences from the population level to the level of individuals are invalid, and that such inferences are indeed criticized in behavior genetics. In this way, I was accused of violating the principle of charity. The behavior geneticists would be right if they mostly avoided the fallacy in their writings. In fact, the fallacy is not uncommon in behavior genetics. G4 SOURCE CHECK Texts: 24, 27, 28, 30, 31, 38, 44, 45 Note. This guideline is characteristically associated with Gl, G2, G4,G8,G9,andGll. Take care to check sources provided in texts. The existing "publish or perish" culture and conciseness of writing may enhance false claims not supported by sources cited. False claims are also fostered by concepts and statements that have different meanings in different disciplines. Example We have a beautiful example, but the source describing it is no longer available to us. One of us (WJS) came across it some thirty years ago. An article then reviewed research about the generally accepted hypothesis 'The number of neurons in the brain can but decrease in the course of our lives." Cell division in the brain is impossible according to the hypothesis. The author of the article had done an exhaustive historical study of all the sources mentioned in the literature. As it turned out, the hypothesis had been published for the first time in a sloppy article concerning a histological study of a single specimen of human brain conserved in a museum in the United Kingdom. The original article was approvingly quoted by many authors, and each of them was quoted by many others. After a few decades, the hypothesis developed into standard textbook wisdom. The authors would state that the hypothesis is confirmed by much research, and they would

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Putting Science in Context provide many references in support of this. However, no additional research had in fact taken place after the sloppy article appeared. Later research showed that the hypothesis is false.

G5 NO DIRTY HANDS 7^:30,31,41,44 Note. This guideline is often associated with G8, G9, G i l , and G13. Avoid dirty hands. Many researchers, and persons concerned with research policy, have voiced to us their conviction that scientific work is impossible without dirty hands. This conviction comes down to the thesis "To make funding of research possible at all, one should be willing to violate to some extent both moral and methodological norms." We entertain the conviction that dirty hands must be avoided at all costs. However, we do not have the capability for deriving this conviction from an adequate knowledge base, since the issue is complicated. We can but plead for more studies aiming to expose unacceptable bias in research due to vested interests. In any case, we feel that hands can become somewhat cleaner in many contexts. Example If in doing biomedical research, you are funded by the pharmaceutical industry, the chances are that funding will cease if you consistently come up with a negative verdict about the efficacy of the drugs you study. So the chances that you will be able to continue with useful research may be remote, unless you are willing to "cheat" a little bit, if only by selective reporting. Existing literature that addresses this issue, in line with personal communications, suggests that this kind of situation has become a serious problem. G6

RECONSTRUCTION Texts: 2, 11, 17, 19, 20, 23, 26, 28, 30, 31, 37, 38, 39, 40 Note. This guideline is associated with G12.

Use reconstruction to evaluate texts.

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Do not underestimate the efforts required for a proper reconstruction of texts. Almost all texts in science are extremely complicated nowadays, because editors want authors to be succinct. Much reconstruction should therefore precede the evaluation of texts. Reconstructions should aim to make implicit presuppositions explicit. Reconstruction can never bring all presuppositions out into the open. The notion of a collection of all presuppositions is indeed meaningless, since presuppositions in texts depend on contexts of interest. Reconstruction in a broader sense should also aim to discover important subjects that are missing in a text. Example Consider the thesis "The theory of evolution is problematic because it has no predictive value." This thesis is best reconstructed as an argument: Premise 1: Theories without predictive value are problematic. Premise 2: The theory of evolution has no predictive value. Conclusion: The theory of evolution is problematic. This is, on the face of it, a valid deductive argument. However, appearances are deceptive. The methodological criterion of predictive value in Premise 1 should be taken to mean: Theories must allow of the inference of new information. We can predict in this sense, for example, that particular life forms should have existed in particular geological eras. If we find fossils representing these life forms, then the prediction is borne out; this may confirm the theory of evolution. From this interpretation of prediction, Premise 2 is false. However, someone who comes up with the argument presumably has in mind that future evolutionary changes cannot be inferred from the theory. From this interpretation of Premise 1, the argument would not be valid after all, as the notion of "prediction" would have been used in two different senses. We are dealing here with two possible reconstructions. On the basis of one reconstruction, we have a valid argument with a false premise. On the basis of a different reconstruction, we have an invalid argument. In either case, the argument we get is unacceptable. To be adequate, reconstructions should often be as complicated as this. G7 NO EXCESSIVE GENERALITY Texts: 3, 4, 6, 12, 17, 29, 35, 36, 39, 43, 44 Note. This guideline is often associated with G6.

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Avoid excessive generality of concepts and statements. Texts are easily misunderstood due to unrecognized implicit contexts. When such contexts are made explicit, theses formulated as general claims may turn out to be fairly specific. Example Consider relations between stressors and stress responses. Stressors come in so many different kinds, that we cannot define the notion of stressor through features shared by all stressors. We may therefore choose to define this notion through particular responses. However, if we did this, then the common idea that stress responses are caused by stressors would become empty, as it is then true by definition. Meaningful theories of stress are possible only for lower levels of generality. G8 NO CAUSAL SELECTIVISM Texts: 4, 5, 14, 15, 16, 17, 18, 21, 22, 23,26,28, 30, 34, 38, 39,41, 42, 44, 45 Note. This guideline is associated with Gl, G9, and G i l . Avoid causal selectivism. In Part I, Section 3.3, we indicated that phenomena always result from numerous causes. In opting for a causal explanation of some phenomenon, researchers can but regard particular operative factors as salient, at the cost of a focus on other factors. The context of interest determines what factors are salient so as to count as causes. We use the term "selectivism" for improper selectivity. Example If a particular diet resulted in impaired neurotransmitter function, and thereby generated psychopathology, we would—in the context of medical practice—brand a pervasive focus on the transmitters and on drugs affecting them, as causal selectivism. A focus with diets in a salient position would in this situation be more appropriate. As we have indicated in considering Gl, the emphasis on neurotransmitters and drugs may all the same be appropriate in a different context: research done by the pharmaceutical industry.

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G9 PROPER LEVELS OF ORGANIZATION Texts: 14,15,18,24,26,42 Note. This guideline is associated with G8 and G i l . Cherish higher levels of organization. Reductionism—the idea that phenomena at higher levels of organization are always best explained by processes at lower levels—is a pernicious myth. Example If an employee gets depressed due to excessive workloads and harassment, the chances are that he or she will then suffer also from impairments of neurotransmitter function. However, such impairments would in this situation be an odd item to explain the depression. Explaining depression in this way would amount to a form of causal selectivism that overemphasizes lower levels of organization. The salient cause should in this situation be sought at a higher level. This example shows that causal arrows may point in many different directions. G10 IMPLICATIONS OF DESCRIPTIONS Texts: 5, 14, 15, 18, 24, 26, 30, 42, 44, 45 Note. This guideline is associated with G8. Chart implications of descriptions for theorizing. Example Suppose that an acre of a particular type of farmland on average harbors the following numbers of insect species: with ecological farming, 500; with spraying by pesticide A, 10; and with spraying by pesticide B, 5. We could here describe the effects of spraying by stating: "Spraying with A promotes diversity." Indeed, with A, insect diversity is twice as high as with B. However, this description represents a misleading bias, in particular if it would serve to defend theories that suggest that particular forms of spraying are biologically beneficial.

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Gil

SALIENT POINTS Texts: 6, 8, 23, 37, 39 Note. This guideline is associated with Gl, G8, and G9.

Take care to make salient points visible. Many texts do not properly distinguish between major and minor issues. Furthermore, salient points in a text may not be salient at all in other texts that deal with similar subjects. Example Source: Shrader-Frechette, K. Science Policy, Ethics, and Economic Methodology. Dordrecht: Reidel, 1985. The passage quoted from the book by Shrader-Frechette (1985) concerns contexts of research. Contextual (social and cultural) values also influence research because they often are part of the assumptions required to mediate between hypotheses and theories of observations and experiments. A good example of the mediating influence of contextual values occurs in the case of using differential distribution of hormones between males and females to explain behavior differences between the sexes. Since testosterone has been observed to bring about aggressive behavior in laboratory animals, many scholars jump from this observation to the theory that testosterone can explain male-female behavioral and status differences. Often mediating the gap between the observation of laboratory animals and the theory about humans, however, is the cultural or contextual norm that aggressivity is biologically determined in humans, or that male social dominance is natural and inevitable. Although such contextual valuesfrequentlyplay a role in the allegedly scientific explanation of behavior, often scientists fail to recognize their nonempirical character. Shrader-Frechette is here dealing with methodological and moral aspects of science, and relations between methodological quality and moral quality. She suggests that her example illustrates (negative) influences of contextual values on research. However, her diagnosis is incorrect. The thesis "Aggressivity is biologically determined" is not a contextual norm, but a problematic empirical thesis. The thesis is indeed problematic because of a one-sided emphasis on biology.

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Furthermore, the notion of "biological determination" is unclear (see Part I: many examples; Part II, Chapter 1). The issue in the situation she describes is in fact that researchers often accept this thesis on the basis of poor evidence. Why would they do that? The answer could be: The researchers envisaged by the author are ultimately motivated to justify male dominance in our society, and to assume that the thesis provides the justification. The salient point is here that a covert value, "Male dominance is desirable," promotes biased research, so as to foster the acceptance of a problematic empirical thesis "Male dominance is natural." Conversely, the thesis may covertly justify this value, which amounts to a naturalistic fallacy and to circular reasoning. Shrader-Frechette broaches many different issues in one stroke. That hampers the identification of salient points, and it also promotes improper reasoning. G12 EXPLICIT RELATIONS Texts: 19, 23 Note. This guideline is associated with G6. Take care to make explicit the relations between different items in a text. This guideline speaks for itself. It is by no means easy to implement it. To the extent that implementation is impossible, relations between items in a text should be conveyed to the reader by implicit means. That calls for high quality writing. Example Source: Vander, A.J., J.H. Sherman and D.S. Luciano. Human Physiology: The Mechanisms of Body Function. 6th ed. New York: McGraw-Hill, 1994. Consider the following quotation from the book by Vander and colleagues. In humans and other primates there are no inherent male-female differences in the ability of the hypothalamus to secrete GnRH [gonadotropin releasing hormone] in response to neuronal or hormonal inputs. For example, administration of large amounts of estrogen to

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Putting Science in Context castrated male monkeys elicits LH [luteinizing hormone] indistinguishablefromthose shown by females. The situation may be different for sexual behavior, however, in that differences in the brain may be formed during development. For example, genetic female monkeys given testosterone during late fetal life manifest evidence of masculine sex behavior . . . as adults. In this regard, a potentially important difference in brain anatomy has recently been reported for people: The size of a particular nucleus (neuronal cluster) in the hypothalamus is more that twice as large in men as in women, (p. 695) [A similar area in rats is involved in male sexual behavior. It is influenced by testosterone.] The first and the second paragraph in this passage are entirely clear. Unclear is how they are related. The first paragraph states: males and females do not differ in particular physiological responses of the hypothalamus. The second and the third paragraph state: males and females differ in sexual behavior regulated by a nucleus in the hypothalamus; males and females differ in the size of the nucleus. The first paragraph is contrasted in the text with the second paragraph, but the nature of the contrast is unclear. The suggestion is, at first sight: Differences in sexual behavior between males and females are caused by differences in anatomy, and not by differences in physiology. However, that would seem odd. It is implausible biologically that behaviors could be different without physiological differences in the brain. Perhaps the intended point is this: males and females differ in some physiological brain processes, whereas other brain processes are similar in males and females. The similarities reported for females and castrated males may not apply to females versus normal males, and the differences in normal situations may account for differences in behavior. Yet, this cannot be the entire story that the authors have in mind: Anatomical differences in the brain also play a role. We are unable to reconstruct the intended story, because the authors do not clearly state what they have in mind.

G13

CONSISTENCY Texts: 5, 8, 19,20,30,44 Note. This guideline is associated with G6.

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Search for inconsistencies within and among texts. We should aim to recognize inconsistencies in texts, but that is not always easy. Many inconsistencies are visible only after an extensive reconstruction of texts. Furthermore, items generating inconsistencies may occur in text units that are far apart from each other. Example Source: Blackmore, S. Dying to Live: Science and the Near-Death Experience. London: Grafton, 1995. Attempts to solve fundamental problems of science and philosophy easily generate inconsistencies. Skepticism is a famous example. This view assumes that we cannot be sure of anything. Skepticism gets into trouble as it implies: if we cannot be sure of anything, we cannot be sure of skepticism itself either. In brief, if you are sure that you cannot be sure of anything, then you are endorsing inconsistent views. We think that Blackmore has succumbed to this kind of inconsistency in a skeptical approach of parapsychology and mystical interpretations of near-death experiences. Blackmore thinks that our brains build mental models of the world and of ourselves, and thereby make our "reality." So my proposal is quite simple: that the system takes the most stable of its models and attributes to it the status of 'real.' Our 'reality' at any time is the brain's collection of stable mental models built largely out of sensory input and integrated to form a model of self in the world.... And it there a real world out there? Well, if we adopt this view we can never know. We assume there is in the way we talk about brains and what they do. But it is only an assumption—a useful working model. It is just another of those ubiquitous mental models. Indeed everything we experience ... is a mental model, (p. 161) To be consistent, Blackmore would have to say that the thesis "Everything we experience is a mental model" is itself just another mental model. However, this thesis would tend to undermine her own view. Blackmore defends, for example, the "I" or "self of our ordinary experience is an illusion; it is merely a mental model. That is also her view of "ultimate" realities experienced by mystics. Her defense is based on evidence from neurobiology and from cognitive science. These disciplines explain how we construct mental

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Putting Science in Context models. However, why should we assume that the explanations are acceptable? If they represent mere (stable) mental models, then it is unclear why they should represent superior knowledge. Blackmore extensively discusses visual illusions to substantiate her view. However, the very notion of visual illusion presupposes that we are able to find out how appearances distort reality. Here Blackmore comes full circle! We do not see how she could leave the circle.

G14 NO HETEROGENEITY Texts: 1,2, 12, 19,23 Note. This guideline is often associated with Gl 1 and G12. Avoid heterogeneous items or excessive numbers of items in a single text unit. It is often difficult to implement this guideline, as editors ofjournals exert much pressure on authors to be succinct. If you cannot implement the guideline to the extent of your wishes, then it may be wise in some situations to elaborate one item by way of an example—to convey your approach to the reader, and to convince him or her that you know what you are doing. Example Source: MacLean, P.D. A Triune Concept of the Brain and Behaviour. Toronto: University of Toronto Press, 1973. The passage quoted here is from the book by MacLean (p. 10), who defends the view that human brains are a loose mixture of parts with different ancestries. The reptilian brain seems to be hidebound by precedent. Behaviourally, this is illustrated by the reptile's tendency to follow roundabout, but proven, pathways, or operating according to some rigid schedule. Customs of this kind appear to have some survival value and raise the question as to what extent the reptilian counterpart of man's brain may determine his obeisance to precedent in ceremonial rituals, religious convictions, legal actions, and political persuasions.... In his essay Beyond the Pleasure Principle, Freud (1922) refers again and again to man's compulsion to repetition.... Obeisance to precedent is the first step to obsessive-compulsive behaviour, and this is well illustrated by the sea turtle's returning to the

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same place year after year to lay her eggs. It has been shown in recent studies on mammals that they are also like the reptile in their tendency to return to home grounds.... Man, too, may harbour a continuous yearning to return home after moving to a distant land. MacLean defends in his book a provacative thesis: "Our brains are composed of regions that are not well-integrated since they represent different stages of our evolutionary history." One region, according to him, derives from our reptilian ancestry. In the passage quoted, he defends this thesis by postulating links between a heterogeneous collection of items that share the theme of repetition. We would suggest that stronger links are needed to make plausible his assumption that religious convictions and the tendency to return to home are both explained by particular features of the brain. Mere features shared by things that are qualitatively very different do not suffice for a common explanatory framework. G15 ORDINARY LANGUAGE Texts: 1, 2, 3, 4 Note. This guideline is associated with G6. Scrutinize ordinary words as much as technical words, and avoid technicism, the use of technical words where ordinary language would suffice. Science aims to cover the real world in a methodologically rigorous way. This creates tension. The real world is complex and messy. We reduce complexity and messiness, for example, by causal selectivity. In this way we cover the real world by a process of abstraction that distorts it—if only by omissions. This is indeed unavoidable, and we had better be aware of it as much as we can, to avoid all sorts of pitfalls. In our view, common sense and ordinary language are indispensable for maintaining a sensible connection between sophisticated scientific theories and the real world. Scientific texts without ordinary language are in fact impossible. Since ordinary language is part and parcel of science, it merits our attention to the same degree as technical language. Common sense and ordinary language are often undervalued.

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Putting Science in Context Example Source: Wilkes, K. Yishi, duh, um, and consciousness. In AJ. Marcel and E. Bisiach (eds). Consciousness in Contemporary Science, pp. 16-41. Oxford: Clarendon Press, 1988. Scientists and philosophers have not been able to explain—in a satisfactory way—the relationship between mind and body. This failure is known as the mind-body problem. Some researchers assume that the problem can only be solved through the elimination from science of ordinary language, regarded by them as misleading. The following passage from Wilkes (1988) illustrates this view. There are encouraging signs today that the [mind-body] dichotomy— in other words 'the mind'—is losing its grips. Consider the very label 'neuropsychology.' Neuropsychologists studying the hippocampus, or the amygdala, see no need to defend their ascription of 'mental' terms, such as 'classifying,' 'analysing,' 'comparing,' to these brain masses.... Instead of asking how two levels—mental and physical—interrelate and interact, there is, increasingly, the admission that there are 'dozens' of levelsfromabstract ratiocination to cell membrane and beyond. Wilkes is trading on ambiguities. The mental terms she mentions are indeed used, metaphorically, to describe neurophysiological processes in the brain. In this way, the mentalistic connotations associated with ordinary meanings are lost. The ensuing approach cannot explain mental phenomena, since the mental has been defined out of existence. Wilkes is right in that ordinary language describing mental phenomena is at times be misleading. Perhaps we can improve on it in some respects by technical notions. However, nowhere could we get rid of ordinary notions entirely.

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Chapter 1

Introduction

The methodological criteria from Part I, and the guidelines from Part III, are jointly applied in Part II to texts, from the life sciences and from other significant areas. To promote coherence, the texts are grouped into six chapters on particular subjects: Altruism and Egoism Genes, Behavior, and Psychopathology Medication Stress Genetic Engineering Miscellaneous Subjects Each text is from one book or article. We first describe views of the author(s) by paraphrase and quotation. After that, we present comments, with implicit or explicit reference to methodological criteria and guidelines. Note. Our readership is heterogeneous. Different readers will be acquainted with different subjects and ideas. Do not expect that all the texts will be an easy read for you. We suggest that you make a selection of texts for yourself, and that you disregard texts not selected. Levels—elementary, moderately advanced,

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Chapter 2

Altruism and Egoism

Altruism has long kept biologists pondering about the adequacy of evolutionary theory. On the face of it, altruism does not sit well with evolutionary thinking: natural selection should promote egoism rather than altruism. That is indeed how common wisdom would have it—in biology and in many other disciplines. However, we should take heed to avoid rash conclusions. Before taking for granted that altruism is an anomaly, we should pause to reflect on conceptual puzzles. The literature on altruism is confusing for lack of conceptual clarity. The meanings of "altruism"—and of "egoism"— are context-dependent: these terms represent different concepts in different areas of research. The texts in this chapter reveal a great variety of conceptual differences. In the wake of this, they indicate that puzzles concerning altruism dissolve if we avoid aiming at general theories of altruism and egoism. Note. We include here texts from biology and also texts from some other disciplines—particularly ethics and philosophy. Altruism and egoism are indeed subjects that receive entirely different treatments in the life sciences on the one hand, and ethics and philosophy on the other hand. Students of the life sciences may not feel at ease with texts by professional ethicists and philosophers. We suggest that you first read the collection of texts in a superficial way, and then decide what texts are appropriate for you to be studied in greater detail. Other themes in Part III do

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TEXT 1 EVOLUTION: NO PLACE FOR ALTRUISM? Source: Trivers, R. Social Evolution. Menlo Park, CA: Benjamin/Cummings Publishing Company, 1985. Level: elementary, but requires knowledge of evolutionary biology Criteria and guidelines: Ml, M3, M4, M5, Ml 1, M16, M18, M19, G1,G14,G15 Related texts: 2, 3, 6, 7, 13 Most explanations of altruism in evolutionary biology are not in fact explanations of altruism. Instead, they explain apparent altruism away by unmasking it as sophisticated egoism. The book by Trivers is a good, representative source that articulates the tendency to explain altruism away. "An altruistic act is one that confers a benefit on someone at a cost to the other. Since cost is measured by a decrease in reproductive success, we know that altruistic acts are opposed by natural selection's working on the actor" (p. 41). Trivers argues that natural selection may favor the spread of altruistic traits in three ways: kinship, reciprocity, and parasitism. The best way to understand the importance of kinship it to take a gene's eye view of social interactions. . . . Consider an altruistic interaction in which an actor, at a cost of C, confers on a recipient a benefit of B. Imagine, for simplicity, that there is a single gene in an altruist directing the altruistic action. The gene suffers a cost in reduced copies in offspring of magnitude C. If the recipient is unrelated to the altruist, then the altruistic gene only suffers a cost, and decreases in frequency, but if the recipient is related to the actor, then there is some probability that the recipient also has a copy of the altruistic gene, by direct descent from a common ancestor, (p. 45) Therefore, altruism toward kin—in some situations, as determined by costs, benefits, and degree of relatedness—is not really altruism: It serves the genetic self-interest of the actor. This form of apparent altruism, which

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is not opposed by natural selection, is thus explained by unmasking it as self-interested behavior. "A second way in which selection may favor an altruistic act occurs when the act induces a return benefit to the actor larger that the initial cost" (p. 47). Trivers states (p. 48) that an important return benefit materializes by way of time lags: An individual may experience altruism from another individual and then return favors at a later date. This phenomenon is known as reciprocity or reciprocal altruism: two individuals are in this situation acting altruistically toward each other. Reciprocal altruism is not easily realized: Organisms have to guard against cheating. Organisms should therefore be able to distinguish between cheaters and noncheaters. That is most easily done among organisms that interact frequently. We should be aware that reciprocal altruism is apparently a misnomer: All concerned receive benefits. In social parasitism, lastly, a parasite induces altruism in another organism. Here is an example: Brood parasites among birds deposit eggs in the nests of different species of birds. The species receiving the egg may care for the young hatching from it. This amounts to forced altruism. Trivers also considers group selection as a mechanism that may favor apparent altruism. This mechanism—as elaborated by other authers— should work in the following way: Altruism may be individually disadvantageous within groups, but individuals in groups with many altruists are at an advantage in comparison with individuals in groups with few altruists. Therefore, in the view of some authors, selection at the group level could generate altruism by overriding selection among individuals. Trivers regards this as an implausible scenario: Individual selection easily overrides effects of group selection, since individual selection takes place at a relatively short time scale. [Comment. Some have argued more recently that group selection should be effective after all, because ephemeral groups may generate short-term selection. That could well explain some forms of altruism.] Finally, concerning spiteful behavior, Trivers argues that selection would oppose it as it does not pay. Trivers considers that reciprocal altruism is salient in human beings. The human altruistic system is a sensitive, unstable one. Often it will pay to cheat, namely, when the partner will not find out, when the partner will not discontinue his or her altruism even if he or she does find out, or when the partner is unlikely to survive long enough to

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The theories discussed by Trivers—which are accepted by most biologists—represent adequate portrayals of some categories of behavior. However, his classification of behaviors is not exhaustive. This is best illustrated by a focus on cheating—a salient issue in much theorizing. Considering reciprocal altruism, we should notice that cheating is being portrayed as the crucial problem. That is misleading. Trivers, just like many other biologists, should have allotted a more salient role to forms of cooperation in which cheating is impossible—for example, cooperative hunting. Failing this, we get a view of cooperation that has negative overtones. Furthermore, Trivers, in discussing the human case, overeasily moves from evolutionary altruism—in fact, cooperation by way of reciprocal "altruism"—to altruism in the normal sense, "psychological altruism." That is misleading: Premises concerning altruism from evolutionary biology should not be taken to support conclusions about altruism in the normal sense; that would result in an explanatory argument with irrelevant premises. Our comments indicate that the notion of altruism is highly ambiguous: The notion takes on different meanings in different contexts. It is by no means clear that a single general theory could cover connotations of evolutionary biology and of psychology, since the two kinds of connotations involve different criteria of classification. Evolutionary altruism concerns reproductive costs and benefits, whereas psychological altruism concerns entirely different sorts of costs and benefits. Furthermore, psychological altruism, unlike evolutionary altruism, is a matter of motivation.

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Therefore, the thesis "Evolutionary altruism, unless forced, is impossible" implies nothing whatsoever about psychological altruism. If we used a single term for altruism—and for egoism—in the two senses, then we would get a classification that is not exclusive, as evolutionary egoism is compatible with psychological altruism. The thesis "Evolutionary altruism is impossible" obviously has no explanatory power and no predictive power relative to altruism as commonly understood. Trivers' survey fosters an unduly bleak view of human nature. The ambiguity of the term "altruism" is, to a large extent, responsible for this. Trivers is mixing a technical notion of altruism in the evolutionary sense with "psychological altruism"—a notion deriving from ordinary language. We would argue that ordinary language and common sense—compared to the technical language of evolutionary biology—often provide superior means to understand psychological altruism. In any case, evolutionary altruism and psychological altruism are dissimilar categories of phenomena that should not be amalgamated. TEXT 2 COOPERATION IN ANIMALS AND MAN Source: Dugatkin, L. A. Cooperation Among Animals: An Evolutionary Perspective. Oxford: Oxford University Press, 1997. Level: elementary, but requires knowledge of evolutionary biology Criteria and guidelines: M3, M4, M5, M7, M9, G6, G14, G15 Related texts: 1, 3, 4, 6, 13 Trivers (see Text 1) presented a common classification of evolutionary explanations concerning altruism. Dugatkin argues that this classification is not exhaustive. Most authors, just like Trivers, would focus on kin selection, group selection, and reciprocal altruism as potential explainers. Considering reciprocal altruism, they would focus on the problem that cheating is possible. Dugatkin's views are conceptually a relief: He takes pains to allot a central role to "cooperation." That alone helps us get rid of pitfalls generated by confusion over "altruism." Dugatkin notes that cheating is often impossible in cooperation. For example, many predators cannot capture big preys on their own; they join efforts in hunting. In this situation, cooperation is obligatory for the participants to reap any benefits from their efforts. Such forms of cooperation,

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which are known as by-product mutualism, should be common in the animal world. In the view of Dugatkin, the emphasis in the literature is overmuch on reciprocity and on the problem cheating. One reason for this is probably that reciprocity represents a challenge for efforts at explanation: Cheating poses a deep theoretical problem. Another reason concerns the existing tendency to extrapolate from humans to animals. In our terminology, the result of all this is a classification with inconsistent criteria that is neither exclusive nor exhaustive. Part of the reason that the literature is so skewed may be that, despite all our attempts to avoid overlaying animal behavior with human sentiments, in the end we always do so, to one extent or another. Since cooperation is so fundamental to human behavior, and because humans are quite good "score keepers," reciprocity is the most salient form of human cooperation, and hence makes its way into the theoretical literature on this basis, (p. 167) Comments We applaud Dugatkin's emphasis on by-product mutualism as a form of cooperation in which cheating is not an issue: The common emphasis on cheating in the literature invites without justification a negative view of human nature. However, we would not side with Dugatkin's argument that reciprocal altruism—with possibilities of cheating implicated—is among human beings the most common variety of cooperation. His argument can be reconstructed as follows: Premise 1: If it is easy for an organism to perform a behavior, and the behavior is adaptive, then the behavior is relatively common in the organism. Premise 2: It is easy for human beings to perform reciprocity—because they are good score keepers and so can avoid cheating— and reciprocity is adaptive. Conclusion: Reciprocity is relatively common in human beings. This argument is valid. Yet, it is unacceptable because the first premise is false. Organisms may have capabilities for performing many kinds of adaptive behaviors; therefore, easiness need not entail commonness.

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If we replace "easy" by "relatively easy" in the two premises, we get a substantively different reconstruction of Dugatkin's view. In this reconstruction the first premise could be acceptable, but its second premise would be false. Dugatkin rightly notes that human beings are better score keepers than other animals because they are in some ways more intelligent than animals. We would comment here that intelligence enables human beings also to engage in all sorts of sophisticated "reciprocal altruism" that preclude cheating. To the extent that possibilities for reciprocity increase, possibilities for reciprocity without cheating should also increase. Therefore, it is by no means obvious that reciprocity that aims to avoid cheating should be the most salient form of cooperation in human beings. Furthermore, Dugatkin does not realize that "evolutionary altruism" and "psychological altruism" are different notions. He is mixing technical notions of evolutionary biology with notions deriving from ordinary language. We have critically focused here on one particular theme from Dugatkin's book. To avoid misunderstanding, we note in closing that the book is impressively innovative. TEXT 3 A PHILOSOPHER LOOKS AT EVOLUTION A N D ALTRUISM Source: Sesardic, N. Recent work on human altruism and evolution. Ethics 106: 128-157, 1995. Level: advanced; theme from theoretical ethics Criteria and guidelines: Ml, M3, M4, M6, M9, M12, M14, M16, M17,G7,G15 Related texts: 1, 2 In evolutionary biology, altruism is conceptualized as behavior of an organism that benefits at a cost to itself another species member, the "currency" for benefits and costs being degrees of reproductive success. Altruism in ethics and social science, and in daily life—psychological altruism for short—is a different phenomenon for two reasons. First, our acts represent psychological altruism only to the extent that our motive is to benefit another person at a cost to ourselves, whereas motives are not at issue from the evolutionary approach. Second, reproductive success would here be an odd currency for benefits and costs.

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The assumption that evolutionary altruism is rare, is compatible with the view that psychological altruism is common. It is unfortunate that many authors have suggested that evolutionary biology should entail psychological egoism. Sesardic is fully aware of this. However, he maintains through a sophisticated analysis that it may none the less be difficult to reconcile psychological altruism with evolutionary egoism. He first offers the following definitions of psychological altruism and evolutionary altruism: A is behaving altruisticallyp = dfA is acting with an intention to advance the interest of others at the expense of his own interests. A is behaving altruisticallye = df The effect of A's behavior is an increase of fitness of some other organisms at the expense of its own fitness. Sesardic argues next that psychological altruism is paradoxical in view of four apparently conflicting propositions: 1. Altruisme is a selectively disadvantageous trait. 2. Altruismp tends to lead to altruisme. 3. Altruismp exists. 4. Altruismp is a product of natural selection. Collectively, these propositions appear to imply that altruismp is both advantageous—because it is a product of selection—and disadvantageous—because it leads to altruisme, which is itself disadvantageous. In principle, two strategies for dealing with the paradox are possible: an eliminitavist strategy and a reconciliationist strategy. The eliminativist strategy is to deny one of the propositions. It comes in four variants: Each proposition could be denied. The reconciliationist strategy, which comprises three variants, aims to show that—contrary to the appearances—the set of propositions is coherent. Eliminativism 1. Considering the eliminativist strategy, Sesardic notes that altruism toward kin and reciprocal altruism, which are feasible under selection, are not really altruism. Group selection may favor altruism, but it is rare. Therefore, Proposition (1) is plausible in his view. Eliminativism 2. Proposition (2) might be rejected for two reasons: First, the intended effects of human actions may often not correspond with the actual effects. These possibilities, Sesardic argues, are not realistic. Second, the intended effects and the actual effects need not be linked with fitness.

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Sesardic rejects this possibility also. He states that important interests of ours do have links with fitness. Eliminativism 3. Considering Proposition (3), Sesardic analyzes two possible moves against it. First, according to psychological hedonism, our acts are motivated by the anticipation of our own pleasure. This would make Proposition (3) necessarily false—in our terminology, a false logical statement. However, philosophers have shown that hedonism is not a viable view. Second, we could maintain that Proposition (3) is empirically false on the ground that apparently altruistic acts are driven by unconscious, self-interested motives. Sesardic also rejects this possibility. Psychologists, according to him, have shown that this possibility is not generally true. Thus, no reason would exist to reject Proposition (3). Eliminativism 4. Proposition (4) is also plausible, according to Sesardic, because psychological altruism is sustained by powerful emotions that extend back to the period of hunter-gatherers. Let us move on to the reconciliationist strategy. Reconciliationism 1. The first variant, the vestige theory, assumes that altruism is a leftover from evolutionary history. Though maladaptive at present, it may have served useful functions in the Pleistocene. Nondiscriminatory altruism, for example, might have worked well for ancestors who lived in small kin-groups. Sesardic regards this as false: Our Pleistocene ancestors are supposed to have lived in large groups. Moreover, distinguishing between degrees of relatedness in small groups would have been adaptive. Reconciliationism 2. Next, we have the by-product theory, which regards altruism—itself nonadaptive—as linked to other features for which selection did occur. Sesardic considers two possibilities. First, altruism could be a by-product of rationality. This idea, says Sesardic, is implausible, among other things, on the ground that rationality is motivationally inert. Second, altruism could be a by-product of group conformity. This is according to Sesardic a reasonable idea. Reconciliationism 3. The last variant is the continuing adaptation theory, which sees psychological altruism as an adaptive product of natural selection. This is according to Sesardic a plausible variant: If you have a disposition to cooperate, others may recognize the disposition and so be willing to cooperate with you: since you do have the disposition, you will not cheat them, All in all, according to Sesardic, psychological altruism is feasible, but evolution strongly limits the possibilities for this type of behavior.

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In line with the views of many authors, Sesardic suggests that it is hard to find a place for altruism. This invites a rather bleak view of human nature. We disagree for many reasons. Let us review Sesardic's arguments in the order presented. Considering Proposition (1), we are not sure that it is obviously true. "Advantage" is a relative notion. Features of organisms can be advantageous compared to particular alternative features, against the background of the entire phenotype, in a particular environment. They can be advantageous in some respects and disadvantageous in other respects. Proposition (1) is therefore unclear for lack of details. For this reason, we would not regard it as either true or false. Without qualification, the notion of advantage is overly general. Proposition (1) is therefore problematic. Considering Proposition (2), Sesardic rejects it as a reasonable option: the intended effects of our acts may systematically differ from actual effects. However, we have also to consider here unintended effects; Sesardic merely comments on such effects in a footnote. Consider the following example of unintended effects. If you have a tendency to help other people, then an unenvisaged spin-off for you may be that you are well-liked. In such a situation, you may benefit from acting altruistically, so that your altruism is selectively advantageous. However, would not this make you a kind of egoist after all? That depends. We should notice here that "altruism" and "egoism" as labels without specification are overly general, vague, and uninformative. If benefits involved in Sesardic's definition of "psychological altruism" were restricted to intended benefits, then many acts that increase fitness would be altruistic in the psychological sense. From a broader definition, the acts should not necessarily count as altruistic. Furthermore, we have to specify here currencies. Should being liked be regarded as a proper currency? Indeed, feeling good about helping others might also be taken to represent a proper currency. On the basis of a highly inclusive conception of benefits, we would indeed get benefits for the actor in all apparently altruistic acts. Altruism would then become logically impossible. If so, then no facts of the matter would remain, and that would be unacceptable scientifically. Altruism without specification, in brief, can represent many different sorts of behavior. It is useless in view of referential heterogeneity. We are here dealing with a commonsense notion with context-dependent shades of meaning. If this notion is transplanted to the language of science, contexts get lost, so we are left with nonsense.

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Sesardic also rejects the possibility that interests involved in psychological altruism need not be linked with fitness. We would argue that links with fitness are the exception rather than the rule. Would you help another person if the price you pay for it is that you cannot have children? That surely sounds preposterous. We do not understand how Sesardic came to accept the idea that psychological altruism should entail a loss of fitness. Perhaps he had very strong forms of psychological altruism in mind that fit in with evolutionary theory. If so, then his argument would amount to circular reasoning. Proposition (3), as we already indicated, is altogether too vague to be useful. Sesardic regards it as true. For us, the issue of truth or falsity can only be decided after key terms have been given more precise meanings. Sesardic's acceptance of Proposition (4) presupposes that natural selection always maximizes fitness. He presents Proposition (4) as a universal statement that is true. A cursory inspection of any textbook of population genetics would reveal that Sesardic's presupposition is false. To test the vestige theory, we would have to reconstruct the phylogeny (evolutionary history) of human behavior, and we should not restrict our phylogenetic history to the Pleistocene. Sesardic's rejection of the theory is therefore problematic. {Note. The emphasis on the Pleistocene is common outside biology; many biologists would grind teeth in observing that.) Regarding the by-product theory, we should consider a possibility disregarded by Sesardic: It is conceivable that altruism toward kin and reciprocal altruism—neither of which counts as genuine altruism—would be fostered by a general disposition to help other persons, for example friends. From an evolutionary point of view, it may be difficult to develop a disposition that is more discriminative. So a genuine form of altruism may arise as a by-product of kin selection or as a by-product of selection for reciprocal altruism. We agree with Sesardic's positive view of the continuing adaptation theory, but we note that the theory concerns mutualism rather than altruism. Many possibilities for psychological altruism to arise obviously exist. Sesardic's view of human nature is biased in a negative way due to fundamental methodological shortcomings. In the first place, his classification of hypotheses and potential explanations is not exhaustive; he disregards the most plausible explanations. In the second place, he fails to notice that crucial concepts such as "psychological altruism" and "psychological egoism" are useless as they can take on many different meanings.

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TEXT 4 NO MORAL MERIT FOR ALTRUISM? Source: TuUberg, B.S., and J. TuUberg. On human altruism: The discrepancy between normative and factual conclusions. Oikos 75: 327-329, 1996. Level: elementary Criteria and guidelines: Ml, Ml 6, Gl, G7, G8, G15 Related texts: 2, 6, 13 Many people would regard altruism as morally commendable—but they would not limit the domain of morally appropriate behavior to altruism. The biologists TuUberg and TuUberg, who are inspired by evolutionary thinking, surprisingly defend a more negative view of altruism. [T]here is always a possibility to cheat and this possibility increases with a system that promotes unselfishness; in a system with a duty to serve others, there is no moral basis to expect or to claim a reward. Like the overwhelming majority, we think that human altruism exists, but we belong to the small majority who questions it worth. There is a general consensus that a gene for altruistic behaviour . . . cannot spread in a population, and theoretical analyses point at the importance of conditional behaviour for reciprocity to evolve.... Thus, a necessary condition for reciprocity is that individuals help reciprocators and avoid defectors.... In conclusion, altruistic strategies promote defector strategies and threaten reciprocal strategies. . . . As we see it, the principles for effective cooperation should be valid for humans . . ., that is, reciprocal strategies balance the self-interest of participating individuals and keep cheating in check. If this is so, a better advice than to teach altruism is to teach reciprocity, (p. 328) It is our firm belief that normative ethics has to be intellectualized to a higher degree than at present, and that evolutionary biology can be of great help in this effort. . . . [I]n order to be able to analyse ethics it is necessary to see that there is an antagonism between reciprocity and altruism. . . . Moreover, in accordance with evolutionary theory, if one goal is to reduce the opportunity for cheating, normative ethics would be better off to have reciprocity, not altruism, as the prime normative rule. (p. 329)

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Comments We agree with TuUberg and TuUberg that the emphasis in literature concerning evolution and morality has been overmuch on altruism. Regarding behavior in social species, it is more natural to have cooperation at center stage. However, we would not defend this view by appealing to evolutionary biology: By far the most social exchanges among human beings have nothing to do with reproductive interests. In addition to this, unlike TuUberg and TuUberg, we would not aim to substantiate any general thesis commending either altruism or reciprocity. Considering altruism we would think, for example, that surely nothing is wrong with helping behavior toward disadvantaged persons. Cheating is not an issue in this situation, because we do not expect such persons to reciprocate. Considering reciprocity, we would think that toward other persons it would be a natural thing. Attitudes of people toward other persons are context-dependent in many ways. TuUberg and TuUberg consider a limited context, as they selectively focus only on behaviors that involve reproductive interests and cheating. When reproductive interests are irrelevant, currencies for measuring costs and benefits in behavioral exchanges are a mixed lot. Should your feeling good in helping me count as a benefit? If so, then helping is not altruism in this situation. However, from a narrower conception of benefits, helping could count as altruism. Consider also this possibility: If you often helped other persons, then you could benefit from this through being liked. Should that indicate that your helping is not really altruistic? Common sense would deny that, unless being liked would be your motive. In brief, general notions of altruism and egoism—without qualification—are altogether too crude to describe human behavior. Considering possible tensions between altruism and reciprocity, we see no problem for normative ethics. If, in accordance with some moral principle, we help you in particular circumstances, you ought to help us in similar circumstances: Moral principles should not depend on the kind of person involved. Notice that this would have the following implication: Altruism as commonly conceived—psychological altruism—yields to reciprocity in virtue of the logic of moral discourse. Evolutionary altruism should be less common than reciprocity in an evolutionary sense. Should this have implications for the moral status of psychological altruism? Hardly so, we would say, because reproductive interests are seldom at stake in psychological altruism.

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Is altruism in the psychological sense less commendable than reciprocity? This question is altogether too general. It all depends on the persons involved and on the context. Once we specify what is involved, difficult theoretical problems tend to dissolve. Should we help needy persons, if this does not cost us much? Of course we should. Are we morally obliged to help persons who are likely to cheat? Of course we have no such obligation. Is helping behavior morally commendable if being liked is the sole motive underlying it? No, it is not. Few persons will quarrel with all this. We are dealing here with obvious matters that are often obscured by technicalities of science. Our comments do not imply that notions of altruism and reciprocity are entirely unproblematic. Hard problems do exist, but general problems discussed in theoretical literature are merely hard as a result of improper conceptualizations. TEXT 5 HOW NOT TO THINK ABOUT EVOLUTION: MURDER WITHIN THE FAMILY Source: Wilson, M., and M. Daly. Relationship-specific social psychological adaptations. In G.R. Bock and G. Cardew (eds). Characterizing Human Psychological Adaptations, pp. 253263. Chichester: Wiley, 1997. Level: elementary; theme from evolutionary psychology Criteria and guidelines: Ml, Ml 8, G8, G10, G13 Related texts: 12, 17, 26, 27, 28, 29 Researchers in many disciplines assume that human behavior reveals traces of our evolutionary past. Indeed, an entirely new discipline, evolutionary psychology, observes human behavior primarily through evolutionary spectacles. This discipline assumes that, to the extent that evolution is here important, we should expect traces of our history to be visible not least in behavior associated with reproduction. Wilson and Daly—both well-known evolutionary psychologists—aim to demonstrate this through the example of homicide. They argue for an intriguing thesis: Evolutionary theory entails that the risk for homicide to occur depends on the degree of relatedness between the culprit and the victim. Considering the attitude of mothers toward their offspring they write:

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This literature [in pediatrics] implicitly treats maternal attachments unidimensional, but an evolutionary perspective suggests instead that it is likely to involve at least three separable processes proceeding over different time courses: (1) assessment of the quality of the child and the situation; (2) rapid discriminative attachment to the baby as an individual; and (3) more gradual deepening of individual love. . . . The first hypothesized process functions as an immediate postpartum assessment of the reproductive episode's prospects. Adaptationist thinking suggests that present material and social circumstances, the baby's phenotypic quality and the mother's residual reproductive value will all be determinants of a 'decision' whether to follow through or opt out. The hypothesized effect of a mother's reproductive value is supported by age-specific infanticide rates (Fig. 2 ) . . . . [and other data] (p. 256) The figure shows that the level of infanticide is about 100 per million per year in mothers below the age of 20, and about 20 per million per year in older mothers. Homicide by stepparents, according to Wilson and Daly, also fit in with evolutionary theory: Step-relationship is like cuckoldry in that the child is a potential vehicle of fitness for one marriage partner but not the other. It is different, however, in that this asymmetry is out in the open, and has ideally entered into the negotiation of entitlements and reciprocities in the remarriage. Nevertheless, the presence of stepchildren is an important risk factor for marital disruption and violence, and the stepchildren themselves incur greatly elevated risk of violence too ( . . . Fig. 3). Step-parenthood is evidently the relevant risk factor, rather than some correlate or 'confound,' reinforcing the point that parental psychology is designed to channel affection and investment preferentially toward own offspring, (p. 260) The figure indicates that, in young children (0^1 years), filicide (that is, killing children of your own) by genetic parents occurs in about seven cases per million per year; in step-relationships the figure is between 50 and 60. Filicide in older children is, by comparison, rare.

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Explanation is a matter of comparison. Considering the homicide data, researchers may ask: why do young more often than older mothers kill their infant? Why do step-parents more often than genetic parents commit filicide? Why do stepparents commit filicide more often than genetic parents? These are the comparisons that Wilson and Daly focus on. However, researchers could also ask: Why do few young mothers kill their infant, whereas most of them do not commit this atrocity? Why do some stepparents commit filicide, whereas most of them do not succumb to acting in this way? We would argue here that evolutionary pressures—if present at all—are slight, as filicide is a rare event in all the categories of subjects. Wilson and Daily state that all sorts of factors associated with reproductive prospects are determinants for a "decision" of genetic mothers "considering" a future with their child either decide to opt out or to follow through. This is an odd form of causal selectivism. Considering a homicide rate of 1 in 10,000 per year in young children—less in older children—we can but conclude that the impact of such determinants is slight, and that other determinants have to be much more powerful. The "greatly elevated risk of violence" for stepchildren—in situations of murder—amounts to an elevation up to about 1 in 20,000 per year. That is indeed eight times as much as in genetic children, but the risk is still very low. Lions as a rule kill their stepcubs. This is commonly explained as an evolutionary adaptation that would suit Wilson and Daly. Data concerning humans, however, are entirely different. Humans typically behave in the opposite fashion: They seldom kill their children or stepchildren. Wilson and Daly choose to describe their data so as to confirm their evolutionary leanings. This description in fact has no explanatory value. We see here a mode of description chosen to support a biased theory. Indeed, a more proper description from common sense should lead to the rejection of the theory. TEXT 6 AGAINST PERVASIVE SELF-INTEREST Source: Frank, R.H. A theory of moral sentiments. In J.J. Mansbridge (ed). Beyond Self-interest, pp. 71-96. Chicago: University of Chicago Press, 1990. Level: elementary; theme from social psychology Criteria and guidelines: Ml, G7, Gil Related texts: 1, 2, 4, 7, 12

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Social psychology and social philosophy often allot a prominent role to self-interest, but protests against this role are also common in these disciplines. Frank is a staunch critic of the common view that human behavior is characteristically motivated by self-interest. Some people we feel we can trust, but of others we remain ever wary. Some we feel can be taken advantage of, others we know instinctively not to provoke. Being able to make such judgments accurately has always been an obvious advantage. But it may be no less an advantage than others be able to make similar assessments about our own propensities. A blush may reveal a lie and cause great embarrassment at the moment, but in circumstances that require trust, there can be great advantage in being known to be a blusher, (p. 78) Indeed, at first glance it may appear that the largest payoff of all goes to the shameless liar. In specific instances, this may well be true, but we must bear in mind the special contempt we reserve for such persons. Most of us will go to great trouble to inform others when we stumble upon someone who lies with apparent sincerity. Thus, even if such persons are caught only very rarely, it is far from clear that they command any special advantage. The ecological balance between more and less opportunistic strategies is in harmony with the view that self-interest underlies all action and with the opposing view that people often transcend their selfish tendencies. The key to resolving the tension between these views is to understand that the ruthless pursuit of self-interest is often self-defeating, (p. 80) Comments Frank's view of self-interest—and the implications of this view for views of altruism and egoism—should be welcomed. It uncovers conceptual pitfalls with substantial implications. He makes a profound point: Paradoxically but understandably, self-interested actions need not in fact serve our interests, as others may recognize them for what they are. He is right: "The ruthless pursuit of self-interest is often self-defeating." By implication, altruism and forms of cooperation not motivated by self-interest should be viable forms of human behavior. This way of looking at human beings is an

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antidote to more common views that manage to locate self-interest almost everywhere. The conceptual pitfalls considered by Frank are complicated. We may choose to regard acts that are motivated by interests of the actor as self-interested (egoistic). However, such acts may not in fact serve these interests. Alternatively, some interests envisaged by the actor may be served, even though the act works out against other interests not envisaged by the actor. I may, for example, aim to make much money and succeed in this by devious means, to the detriment of others. As a result, others may come to dislike me, which is not in my interests. In brief, we should distinguish between the effects intended and the actual effects of acts. In addition to this, we should distinguish between different kinds of effects. Many possible definitions of "egoism" and "altruism" should as a result from these considerations come to the surface. The paradox that the pursuit of self-interest may not be in our interest, is therefore not in fact a paradox, since it refers to different sorts of interest. Frank's analysis has the merit of dissolving undifferentiated, general notions of "egoism" and "altruism." Such notions are profoundly ambiguous. We need more specific concepts to characterize human behaviors. The notions "altruism" and "egoism" are ambiguous as we must distinguish between evolutionary notions and psychological notions. On top of this, we are plagued by ambiguities of general psychological notions. Once the proper distinctions are made, the pernicious view that acts always serve the interests of the actor (an empirical matter), and the idea that this is as it should be (a normative matter), can be put aside as meaningless generalities. TEXT 7 A METHODOLOGICAL EYE-OPENER FOR ALTRUISM Source: Blum, L.A. Altruism and the moral value of rescue: Resisting persecution, racism, and genocide. In P.M. Oliner, S.P. Oliner, L. Baron, L.A. Blum, D.L. Krebs, and M.Z. Smolenska (eds). Embracing the Other: Philosophical, Psychological, and Historical Perspectives on Altruism, pp. 30-^47. New York: New York University Press, 1992. Level: elementary; theme mainly from social psychology Criteria and guidelines: M4 Related texts: 2, 6

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Many researchers have voiced doubts about the feasability of altruism. Their views are often misleading since they argue from a narrow definition of "altruism." Blum militates against overly narrow definitions of "altruism": [B]uilding self-sacrifice into the very definition of altruism generally (heroic rescue being only one type of altruism) is misleading. For it masks the fact that it can be morally good or admirable to be genuinely concerned about the welfare of others even when there is no risk or loss to the self. The epithets "compassionate," "thoughtful," and "kind" all refer to admirable traits that involve altruism (in the sense of genuine concern for others), yet none of them actually requires loss or sacrifice to the agent. What altruism does require for the specific value that it has is an absence of concern for the self—a direct concern only for the other, (p. 32) Comments Blum usefully indicates that classifications of acts into egoism, altruism, cooperation, and spite are not exhaustive: One of the participants—the actor in the situation he considers—need not incur any costs (or, we may add, benefits). Oddly, this possibility is often disregarded in evolutionary biology, psychology, social science, and ethics. Blum adds to existing arguments for a thesis that has been pushed to margins of much science and philosophy: it is unreasonable to regard motives of persons to benefit others as outlandish. TEXT 8 ETHICS: ODDITIES OF SELF-INTEREST Source: Gauthier, D. Reason to be moral? Synthese 72: 5-27,1987. Level: moderately advanced, theme from philosophy Criteria and guidelines: Ml, M4, Gl 1, G13 Related texts: 9, 10, 11, 13 Many philosophers and ethicists have produced conceptual models in defence of self-interest. Gauthier appears to be one of them. Gauthier appears to cherish self-interest for theoretical reasons.

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Suppose that whether or not one accepts social requirements as overriding reasons [i.e., reasons to be moral] affects the regard one receives from others—in particular, their willingness to accept one as a partner or participant in mutually advantageous interactions. If one accepts social requirements as overriding one's self-anchored reasons, then one may be relied upon to do one's share in activities and practices that work for the good of everyone alike, even if one could benefit oneself even more by free-riding on the efforts of others. Whereas if one does not accept social requirements as overriding, then one may be expected to free-ride whenever this seems individually most beneficial. Those who may be relied upon not to free-ride are welcome partners; free-riders are not. . . . We must distinguish clearly between persons who act only on self-anchored reasons, and so adhere to social requirements only when it is beneficial for themselves to do so, and those who, for self-anchored reasons, dispose themselves to adhere to social requirements whether or not it is actually beneficial for them to do so. Which kind of person does one have better self-anchored reason to choose to be? Our present argument leads to the conclusion that one has better reason to choose to be the latter kind of person, who is disposed not to free-ride even though free-riding would of course benefit her. (pp. 19-20) Comments Gauthier's text is a representative example of ambiguities that in ethics pervade literature on egoism and altruism. At first, he writes about social requirements overriding self-anchored reasons. After that, he argues that we had better accept these requirements for self-anchored reasons. The expression "for self-anchored reasons" has in his text two entirely different meanings. In more accurate words: The expression is ambiguous, because it is implicitly associated with different criteria of classification. This seemingly generates an inconsistency. It is advantageous for us to free-ride, but it is also advantageous for us not to free-ride. The inconsistency disappears once the ambiguity is out in the open. Furthermore, we should notice that Gauthier's classification of acts is not exhaustive. He appears to presuppose that in either option described by him, we are motivated by self-interest. The possibility that we could be motivated primarily to serve the interests of others has no place in his philosophical scheme. As in much literature, self-interest is given here an undeserved

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prominent place. Gauthier appears to defends the thesis that all acts are motivated by self-interest, but he does not make this salient point explicit. TEXT 9 ETHICS: A VACUOUS THEORY OF SELF-INTEREST Source: Scott, S. Motive and justification. The Journal of Philosophy 85: 479-499, 1988. Level: elementary; theme from philosophy Criteria and guidelines: Ml 2, Ml 4, Ml 6, Ml 7 Related texts: 8, 10, 11 Conceptual analysis in philosophy that aims to solve problems concerning self-interest are often self-defeating. The philosopher Scott aims to show by conceptual analysis, that human behavior is always self-interested. I take up a distinction . . . between direct and reflexive purposes. An action is directly self-interested if its purpose is a good (as a means or as an end) for the agent. It is reflexively self-interested if his doing it is a good for him, whether its purpose is or not.. .. The point to which the distinction moves is that a selfless life is one whose direct aim is selfless. If it is also reasonable, its reflexive aim is self-interested. I am not saying that the agent's motive must entirely consist in the reflexive good, but I am saying that a selfless direct motive makes no sense by itself, (pp. 493^494) Comments Scott properly distinguishes between the intended effects of acts and the actual effects of acts. He appears to assume that acts that have no actual effects representing a good for the actor do not make sense. We are at a loss to understand this assumption, which is presented as a general, universal thesis. Would my helping a needy person be irrational if I do not benefit from it? It is implausible that this should be irrational. Perhaps Scott means that benefits for myself must always be present, as I always aim to do the things I desire to do. However, from this interpretation, the thesis "All acts should have a purpose that is a good for the actor" becomes a boring, logical statement.

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TEXT 10 A PHILOSOPHICAL LESSON FOR ETHICISTS Source: Taylor, P. W. Principles ofEthics: An Introduction. Encino, CA: Dickenson, 1975. Level: elementary; theme from philosophy Criteria and guidelines: Ml 2, M14 Related texts: 8, 9, 11 Some philosophers usefully argue that, in their discipline, much theorizing about self-interest is futile. The philosopher Taylor shows in a nice way that we must reject the thesis of pervasive psychological egoism. There is one argument given by the psychological egoist, however, which rests on a semantic confusion and not on factual claims about human motivation. Suppose an egoist is presented with a [paradigm case of "altruism"]. The egoist might then say the following about such a case: "Granted that in doing this act the person did not have what most people would call a selfish motive, or even a motive of self-interest. Still the act was a voluntary one, and all voluntary acts have some motive behind them. By doing the act the person was satisfying the motive. Hence he did gain satisfaction from doing the act. He would not have done it if no satisfaction of any of his motives would result from his doing it. Consequently the act served his self-interest after all, since it was done to satisfy whatever motive he did have in doing it." Here the egoist has made a basic change in his position. For he is now claiming that the satisfaction of any motive is to be taken as self-interest, whereas what he had been saying before was that all action is motivated by a certain kind of motive, the kind we would all classify under the general category of selfishness or self-interest, (p. 41) Comments Taylor points out that the thesis "All acts are self-interested" becomes true from a broad definition of "interest." He rightly notes that we would have to pay dearly for this inclusivenes: The thesis degenerates in this situation into a logical statement. It is a scandal of philosophy that this point

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is often put aside, even though it has been substantiated during past centuries by philosophers such as Hume (see also Text 12). Philosophers again and again get trapped into the pitfall that Taylor describes. The general thesis, "Human behavior is on all counts self-interested," is sheer nonsense. TEXT 11 ETHICS: DISCARDING A SPURIOUS PUZZLE OF SELF-INTEREST Source: Lemos, N.M. High-minded egoism and the problem of priggishness.MW93: 542-558, 1984. Level: elementary; theme from philosophy Criteria and guidelines: Ml, Ml 4, G6 Related texts: 8, 9, 10 Some philosophers use conceptual analysis to argue against pervasive self-interest. Their arguments tend to be unsuccessful. The philosopher Lemos suggests that the thesis, "Psychological egoism is pervasive," is false for conceptual reasons. If a man were motivated solely by the desire that he acts friendly, but not by a desire for the well-being of his friends, then such a person would not be friendly and we should not say that his act was motivated by friendship. If a man is motivated solely by the desire that he be virtuous, but not by any of those other characteristics of his act which would make it virtuous, then we would not properly call his act virtuous. On this view, the goodness or moral worth of an act of friendship depends, for example, on its being motivated by a desire for the well-being of one's friends. Similarly, the goodness or moral worth of an act of virtue depends on its being motivated by certain features of the act apart from its being an instance of one's acting virtuously, (p. 554) Comments Lemos suggests that the thesis, "All acts are selfish," is contradictory: It is, in our terminology, a false logical statement. In particular, my (self-interested) desire to act friendly—a form of "high-minded egoism" in Lemos' terminology—should have to be inconsistent with acting friendly in fact.

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What Lemos states is apparently simple. However, some reconstruction shows that the issue is complicated. If Lemos' point were merely that the thesis of psychological egoism is false for logical reasons, then we would be dealing with a boring issue since the thesis would then not express any facts; it would in this situation have the status of a logical statement. However, we can also see the situation in a different light. Lemos is claiming that genuine altruism exists as a matter of empirical fact—friendship being an example. He attributes conceptual tricks to others who would dismiss his claim. One trick, according to him, would be to assume that a selfish aim to act friendly is the covert motive in acts of friendship. Moves of this kind are inappropriate, according to Lemos, for conceptual reasons. We should reject Lemos' entire approach, because it resides at an inappropriately high level of generality. That level helped Lemos create a situation that is odd from a methodological point of view: He is in fact rejecting an empirical claim on the basis of conceptual analysis. Such a thing should be impossible, because arguments in which empirical claims are inferred from logical statements are invalid. TEXT 12 A LESSON FROM HISTORY: MORE ABOUT SELF-INTEREST Source: Holmes, S. The secret history of self-interest. In J.J. Mansbridge (ed). Beyond Self-interest, pp. 267-286. Chicago: The University of Chicago Press, 1990. Level: elementary; theme from psychology and philosophy Criteria and guidelines: Gl, G14 Related texts: 7, 13 Self-interest is like a Medusa-monster with many heads: You chop off one head, and a new one sprouts from a different part of the beast so that you have to begin all over again. Theories from many disciplines allot a foundational place to the thesis that egoism is natural and commendable, surreptitiously or indeed through shameless explicit pronouncements. To beat the monster, we have to know about its origin. The odd thing is, that philosophers from past centuries did recognize it for what it is. Their lessons have almost been forgotten. Let this situation be a reminder: provided that we are perceptive, history has lessons in store for us that may help us set appropriate courses toward the future. As other texts show, researchers from many disciplines do attend to history from evolutionary biology. That

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engenders restrictive views: An emphasis on evolution easily obscures valuable insights from the humanities concerning our more recent past. Holmes indicates why the thesis, "Psychological egoism is pervasive," is conceptually odd. Hume himself was echoing Shaftesbury, Hutcheson, and others when he denounced the false "love of simplicity" underlying motivational reductionism. To say that patriots and misers, cowards and heroes all aim exclusively at "their own happiness and welfare" illustrates only how little we can learn about behavior by adducing self-interest. We can always say that the altruist includes the welfare of others in his own utility function. But when the motivational reductionist traces all action to self-love or the rational pursuit of personal advantage, he "makes use of a different language from the rest of his countrymen, and calls things not by their proper names." Theorists are free to indulge in such linguistic idiosyncrasy, of course. If they make no distinctions, then, naturally enough, everything will be the same. (p. 269) Comments Holmes rightly points out that the philosopher Hume and other philosophers have long ago uncovered the conceptual pitfalls generated by overly broad psychological notions of "egoism" and "altruism." Many philosophers and many scientists still have to learn this lesson. TEXT 13 MARRIAGE, SELF-INTEREST, AND PSYCHOTHERAPY Source: Wallach, M.A., and L. Wallach. Psychology's Sanction of Selfishness: The Error of Egoism in Theory and Therapy. San Francisco: Freeman and Company, 1983. Level: elementary; theme from psychology Criteria and guidelines: M7 Related texts: 1, 2, 4, 5, 8, 12 Much psychology—and psychotherapy—has succumbed to the erroneous idea that people should cherish self-interest for their own good.

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The psychologists Wallach and Wallach oppose tendencies to promulgate self-interest. Considering marriage and other close relationships, they note: "Conditionally as the key to keeping one's relationships healthy and happy, is a theme sounded by many researchers" (Wallach and Wallach 1983: 178). Conditionally amounts to an attitude that aims to benefit others on the condition that favors are returned. Wallach and Wallach show that researchers in psychology commonly regard this form of selfishness as rational and commendable. It is promoted in many psychotherapies. Therapists who take this line foster, in fact, a form of ethical egoism that in their view should work out well. The implication is that, to make the relationship work better, each partner has to be assured of deriving sufficiently favorable net benefits from maintaining it. Neglected is the possibility that instead the very terms of the analysis—as applied both by the couple and by the psychologist—are at fault. What may be wanting is not more attention to balances of returns but an approach to relationships that views another's welfare and commitment to furthering it as primary considerations, (p. 179) Wallach and Wallach deplore this attitude. Evidence shows that conditionally is pronounced in the reciprocation of negative affect in distressed couples. Happy marriages involve more of something like commitment and trust. Comments Wallach and Wallach's examples—marriage in the passage quoted— show that we should distinguish between the intended effects and the actual effects of acts. If we benefit others whereas one of our motives is to get something back in return, then our attitude may register with others, so that we shall be in for a disappointment. Wallach and Wallach uncover an interesting theme: Paradoxically, we may benefit if our motives are not self-interested. Some acts with a selfless motivation therefore benefit everyone concerned. The important message of Wallach and Wallach is this: Nobody would quarrel with the thesis "It is proper for us to serve some of our own interests." It is tempting to infer from this the thesis "We should be motivated to serve these interests." However, that would be an invalid argument. In some situations, we serve our interests better if we do not have this motivation.

Chapter 3

Genes, Behavior, and Psychopathology

In research on mental illnesses, Western science exhibits much focus on the physical abnormalities that accompany symptoms of disease. For example, molecular biology and genetics play a dominant role in research on etiologies of serious mental illnesses such as schizophrenia. These disciplines are by many researchers conceived as the best source for explaining such illnesses—and also normal behavior—in human beings. However, there are also researchers who oppose this emphasis on biology. The texts in the present Chapter are a representative sample of existing viewpoints. They come from different disciplines that are often out of touch with each other. TEXT 14 PSYCHOPATHOLOGY: A MATTER OF GENES? Source: Mellon, CD. The Genetic Basis of Abnormal Human Behavior. Placitas, NM: Genetics Heritage Press, 1997. Level: moderately advanced Criteria and guidelines: Ml, M7, M i l , Ml 8, Ml 9, Gl, G8, G9, G10 Related texts: 15, 16, 17, 18, 41, 42 Genetics is becoming salient in the study of health and disease. Clear cases do exist of diseases that are genetically determined—in the sense that persons with particular genes always get the disease, whereas persons

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without the genes do not contract it. Most diseases do not have this strong form of genetic determination. However, many diseases are commonly conceptualized as having a genetic component. Mellon's textbook represents the common view that genes are important in serious mental illnesses such as schizophrenia. Mellon first points out that schizophrenia runs in families, but that this does not prove much. Families share environmental factors in addition to genetic factors. Therefore, if no additional evidence were available, environmental factors could well explain the commonness of the disorder in particular families (p. 106). However, additional evidence, most notably from twin studies, does exist. In over 15 [twin] studies, all but one of which confirms that genetic factors are undeniably important in schizophrenia. Even allowing for diagnostic ascertainment and statistical problems, monozygotic concordance rates are consistently 3 to 5 times higher than dizygotic concordance rates. This translates to a 40 to 60 times higher risk for a co-twin than the general population. Twin studies are a tremendous tool in psychiatric genetics, but the schizophrenia studies shown here point out their biggest limitation. Other than proving that a strong genetic component exists, they do not provide much more solid information, (p. 112) Schizophrenia is clearly caused, at least in part, by genetic factors. The classic approaches of family, twin and adoption studies have contributed greatly to our knowledge of schizophrenia, but they have not and cannot answer the more important questions that are now being asked. Only a molecular genetic approach holds the promise of localizing genes involved in its transmission, (p. 115) Comments We have already commented extensively on genetics and schizophrenia in Part II, Chapter 1, where we argued for the following standpoint: Twin studies concern the population level. They do not allow for any inference about the role of genetic factors in individuals who develop schizophrenia. Even knowledge of the localization of genes responsible for concordance patterns among identical twins (high concordance) and nonidentical twins (low concordance), would have no implications for etiology at the level of individuals.

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To know about individuals, we need information concerning the mechanism of pathogenesis and the role of the psychosocial, biological, and physical environment. Mellon overemphasizes the causal role of genes on the basis of inadequate evidence. His premises concern population data. From the premises he infers conclusions concerning etiology at the level of individuals; this is a problematic move. The arguments presented by Mellon—and by many other researchers— are for this reason invalid. The arguments have irrelevant premises without explanatory and predictive value for individuals. These methodological problems are ultimately caused by an improper use of the notion of genetic determination—a point repeatedly explained in Part I, and in Part II, Chapter 1. The tendency in current science to overemphasize roles for genes, as illustrated by Mellon's text, is associated with the idea that fundamental explanations of phenomena should ultimately focus on lower levels of organization; for example, levels covered by genetics and molecular biology. This idea must be rejected. The explanatory significance of levels of organization is context-dependent. The context determines what factors are causally salient. If you are fired for the wrong reasons, and you get depressed by this, neurotransmitters released through mechanisms involving genes should be implicated causally in the depression. However, it would be proper to regard being fired as a more salient cause in this situation. TEXT 15 TOWARD A FULL EXPLANATION OF PSYCHOPATHOLOGY BY GENETICS? Source: Cloninger, C.R., R. Adolfsson, andN.M. Svrakic. Mapping genes for human personality. Nature Genetics 12: 3-4, 1996. Level: moderately advanced Criteria and guidelines: Ml, M7, M i l , Ml 8, Ml 9, Gl, G8, G9, G10 Related texts: 14, 17, 18 Genes are commonly assumed to play important roles in personality and in psychopathology. The article by Cloninger and colleagues is a representative illustration of the assumption that genes have a crucial role in psychopathology.

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People differ greatly from one another in temperament.... Individual differences in temperament are known to be moderately heritable and stable.... Now, two groups, Ebstein et al. and Benjamin et al., have identified a specific genetic locus that contributes to variation in a human personality trait. They have detected an association in unrelated individuals and have independently confirmed this in the general population and within sib pairs, (p. 3) In contrast to the quick and clear replication of the D4DR association with Novelty Seeking by Ebstein et al. and Benjamin et al., replication of specific genetic contributions to developmentally complex disorders like schizophrenia has been elusive.... [I]t may be more fruitful to map genes contributing to temperament, which has a relatively simple genetic architecture and can be quantified easily and reliably by questionnaire. Later susceptibility to complex disorders like schizophrenia and alcoholism can be evaluated in terms of risk from heritable personality traits and possible disease-specific factors. In this way, success in mapping genes for a normal personality trait may signal a fruitful way to map genes for psychopathology as well, (p. 4) Comments We reject the view of Cloninger and colleagues for methodological reasons. The first paragraph quoted concerns the level of populations. We have already argued (Part II, Chapter 1, and Text 14) that information in behavior genetics concerning this level has no implications whatsoever for the level of individuals, not even if genes that explain part of the variation in populations have been identified. Several expressions in the second paragraph of the text ("contribute to," "susceptibility to," "risk from") are ambiguous: They may refer to either level. From the most plausible interpretation, they refer here to the level of individuals. This would result in an invalid argument with irrelevant premises and without explanatory and predictive value. A correlation between psychopathology and personality, as envisaged by the authors, would not be informative unless we knew how personality should causally affect psychopathology. Correlations may come about in many different ways. If it did make sense to postulate a causal pathway from genes—together with environmental factors—to personality, a correlation between personality and psychopathology, contrary to what the authors

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appear to suggest, would by no means imply that the identified genes are also implicated in psychopathology. The text is one among many that overemphasize causal factors at lower levels of organization. TEXT 16 BIOLOGY FOR DEVIANT FORMS OF HUMAN BEHAVIOR Source: Stoff, D.M., and R.B. Cairns (eds). Aggression and Violence: Genetic, Neurobiological and Biosocial Perspectives. Mahwah, NJ: Lawrence Erlbaum, 1996. Level: elementary Criteria and guidelines: M4, G2, G8 Related texts: 14,18, 22, 25, 41, 42, 45 Many researchers assume that psychopathology, and also aggression, are in part determined by genetic factors. In their introduction to the volume edited by them, Stoff and Cairns are at pains to dismiss myths concerning the genetic determination of deviant behavior. Here is what they say about two of the myths: Myth 1. Violence can be reduced to and explained on the basis of disordered biological processes. The relation between a biological substrate and aggressive behaviour can be understood in terms of a one-to-one coordinate model, a unidirectional causal influence of biology on behaviour. Considering this myth, the authors state: [EJcological risk factors such as poverty and exposure to violence in the home and neighbourhood will be shown to have long-standing traumatic impact on brain structure and function as well as subsequent behavioural adaptation.... Biological variables influence social behaviour and, vice versa, social behaviour influences biological variables. Myth 3. Biological factors directly cause aggression with "biology" driving aggression. The authors dismiss this myth in the following way:

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Biological factors may exert their effects on aggression via intervening processes which, in turn, influence aggression per se; these intervening processes may include proximal social mechanisms, threshold for aggression, impulsivity, cognition, learning, prosocial behaviours, or other biological events. Comments It is true that we should do away with myths as here portrayed. However, in dealing with the myths, the authors introduce another myth. They equate biological factors with internal factors—factors inside the organism—and social factors with external factors. This generates a classification that is not exhaustive; most notably, the classification has no place for external factors in the domain of biology. Due to this, some causal factors are overemphasized, whereas other factors are overlooked. The authors disregard ecology in the primary sense of the term. This is unfortunate, since many authors outside mainstream science have demonstrated that ecological factors—for example diet—have a marked influence on psychopathology and aggression. A generalist search of the literature should result in a marked change of emphasis. TEXT 17 THE GENETICS OF SEPARATION ANXIETY Source: Silove, D., V. Manicavasagar, D. O'Connell, and A. Morris-Yates. Genetic factors in early separation anxiety: Implications for the genesis of adult anxiety disorders. ActaPsychiatrica Scandinavica 92: 17-24, 1995. Level: advanced Criteria and guidelines: Ml, Ml 1, Ml 8, Ml 9, Gl, G6, G7, G8 Related texts: 5, 14, 15, 26, 27, 29 Genetic factors loom large in the study of psychopathology. Silove and colleagues focus on the genetics of anxiety disorders. The authors suggest on the basis of a twin study that the role of genes is gender-specific. They also argue that evolutionary theory can explain this. [H]ereditary factors appeared to play an important role in the genesis of early separation anxiety only in women, accounting for

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approximately 41% of the variance. In contrast, all the variance ... in males could be accounted for by environmental factors.... [T]he present findings add considerable support to past impressions that separation anxiety may be particularly dependent on genetic determinants in females.... Women consistently report higher levels of separation anxiety in early life.... From an evolutionary perspective, it is tempting to speculate whether such a gender difference in liability to separation anxiety may have conferred some survival value on the species.... In traditional societies . . . heightened separation anxiety in females may have fostered the survival of tribes and clans by promoting cohesiveness within social cultures. Women acted as agents of security by cementing together family and social relationships, thereby creating a safe and nurturing environment of child-rearing. In that environment, women who feared venturing far from the home would be more likely to attend to the needs of the young and to provide them with effective protection against the threat of predators.. .. Hinde & Stevenson-Hinde . . . have pointed out how evolutionary vestiges of behavior may conflict directly with the cultural dictates of changing societies. In the modern world, gender equality in the workplace is now established both as a right and as an expectation within society. According to Horner . .. women now face a conflict between the drive to preserve the integrity of relationships and the need to act competitively in work situations. In this connection, it is pertinent that panic disorder—agoraphobia has been conceptualized repeatedly as arising out of an "attachment—autonomy" conflict, (pp. 21-22) Comments The views of Silove and colleagues confront us with pitfalls concerning levels of organization. It is true that twin research as conducted by them explains variation at the population level as resulting from genetic and environmental sources of variation. Contrary to their suggestion, however, this implies nothing about the level of individuals (for reference, see Part II, Chapter 1 and Texts 14 and 15, comments). The authors do see implications for etiology in individuals. They rely here on an invalid argument with irrelevant premises and without explanatory and predictive value. Therefore, considering separation anxiety, we see no warrant for their view that particular factors—for example, genetic factors—should be causally salient at the level of individuals.

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We note here that few other studies concerning the genetics of separation anxiety are available. That is one reason to stipulate that highly general claims about the genesis of separation anxiety are out of the question. Furthermore, the merits of conclusions drawn by the authors are contextdependent: They apply only to the populations studied. Another population, with a dissimilar environment, may reveal different patterns of genetic and environmental variation. For example, if the norm of gender equality in the workplace were not a social force, we would presumably get different results. This implies that extrapolating done by the authors—back to situations that our ancestors faced—is incorrect. In addition to all this, we suspect that existing degrees of workplace equality are a far cry from the picture evoked by the authors: Discrimination against women, even in Western cultures, is still a common phenomenon. Discrimination exposes men and women to different social environments. Indeed, such environmental differences may well explain differences—between men and women, or between different populations—in genetic sources of variation at the population level. As already indicated, the authors extrapolate from particular populations to populations in general. A reconstruction of their argument should make explicit their presupposition that all relevant populations are subject to similar environmental forces. We conjecture from common sense and common knowledge that this presupposition is false. TEXT 18 A SIMPLISTIC VIEW OF GENES AND HUMAN BEHAVIOR Source: Wright, W. Born That Way: Genes, Behavior, Personality. New York: Routledge, 1999. Level: elementary Criteria and guidelines: Gl, G2, G8, G9, G10 Related texts: 14, 15, 42, 45 Considering the development of behavior, Wright regards genetic factors as much more important than environmental factors. The interaction between genes and environment is, we know now, essential to the developing child—and for psychologists the term "environment" means every influence on an organism that is not

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genetic. Not only in children, but in adults too, the environment can have powerful effects. But to a greater degree than ever before realized, the genetic influences on behavior, barring an extraordinary childhood (malnutrition, social deprivation, prolonged abuse), express themselves pretty much as configured before birth. Scholars have traditionally divided up the human into an array of discrete vantage points—anatomy, psychology, anthropology, sociology, economics, political science, history. We now see these disciplines converging on a component of our physical selves that mounting evidence indicates is the underlying basis of it all: the twenty-three pairs of chromosomes, containing approximately 100,000 genes, that exist in every human cell. Whatever the term— chromosomes, genes, DNA, the double helix, nucleic acids, ribosomes, alleles—all refer to our biochemical blueprints, (pp. 4-5) Comments All features of organisms—behavioral dispositions not excluded—are "determined" by genetic factors as well as environmental factors. The present climate in science fosters the idea that genes, and in the wake of this other factors at low levels of organization, are somehow more important causally than environmental factors. We have never seen an adequate argument in support of this view. Wright offers an argument that is plainly false. He suggests that organisms develop in accordance with a genetic blueprint, provided that negative, abnormal environmental influences do not interfere. This suggestion is odd: developmental pathways depend on normal varieties of environment as much as on genes. A generalist search of the literature in biology easily uncovers many examples of environments within normal ranges affecting development. Furthermore, the idea that a kind of one-way traffic exists from genotype to phenotype is false: The expression of genes is context-dependent, as phenotype features and the environment continually influence the expression of genes. Wright's view represents a tenacious myth that is at odds with a large literature in biology.

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TEXT 19 PSYCHOPATHOLOGY AND BIOLOGY: A REPORT FOR THOSE IN POWER Source: Office of Technology Assessment, Congress of the U.S. The Biology of Mental Disorders: New Developments in Neuroscience. Washington, DC: U.S. Government Printing Office, 1992. Level: moderately advanced Criteria and guidelines: G6, G12, G13, G14 Related texts: 23, 25, 26 A report by the Office of Technology Assessment (OTA) notes that we do not have an adequate scientific theory of panic disorder. Several theories have been postulated to explain panic disorder.... One views panic as the result of hyperactivity of the physiological mechanisms that are normally activated in stressful situations (i.e., the sympathetic nervous system). Another posits that individuals have an increased psychological sensitivity to normal fluctuations in physiological responses. This theory suggests that patients may misinterpret normal physiological changes as dangerous, inducing more anxiety and precipitating a panic attack. Another theory suggests that there is a primary defect in brain mechanisms related to the neurotransmitter norepinephrine, which is associated with the sympathetic response. . . . There is experimental evidence to support, or in some cases refute, these various theories. Thus, while there are a lot of puzzle pieces, there is currently no unified theory of panic disorder, (p. 90) Comments The authors of the OTA report do not make explicit any relations between the three theories of panic disorder mentioned by them. Arguably, the authors are not to be blamed for this. They presumably rely on sources without visible interconnections that represent different scientific approaches. Despite this, a better presentation should have been possible. Both the first theory and the third theory mentioned by the authors concern the sympathetic nervous system. The third theory could indeed be construed as a detailed version of the first theory. Something like this had

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better be made explicit. The relations between the second theory and the other theories are less obvious. We could reconstruct the text as indicating that psychological causes are implicated by the second theory, whereas the other theories postulate biological causes. From this reconstruction, the second theory emerges as inconsistent with the other theories. However, it is implausible that such an inconsistency should exist: psychological causes could not be operative without biological changes. The second theory indicates that the nervous system is involved. Conceivably, the implied idea is this: in addition to the sympathetic system, other parts of the nervous system play a role. This is an additional type of assumption that should have been made explicit. This texts illustrates that scientific texts that seem entirely clear, at times, after methodological analysis, turn out to contain much obscurity. TEXT 20 CONCENTRATION CAMPS AND PSYCHOPATHOLOGY Source: Zuckerman, M. Vulnerability to Psychopathology: A BiosocialModel. Washington, DC: American Psychological Association, 1999. Level: main message elementary, details advanced Criteria and guidelines: G1, G6, G13 Related texts: 29, 35 Zuckerman provides a comprehensive survey of psychiatric disorders. In the passage quoted here, he considers the impact of concentration camp experiences on psychopathology. One cannot imagine any more prolonged stress than confinement in a German concentration camp during World War II. Eitinger (1972) and Eitinger and Strom (1973) followed psychiatric outcomes in Norwegian and Jewish prisoners confined in concentration camps during World War II for 20 years postwar and compared the incidence of various psychological and medical disorders with controls in the Norwegian group. Whereas the figures for neurosis and substance abuse were high, that for psychosis was low, although still significantly higher than that for controls. . . . Can a severe stress of this type produce a persistent psychosis? After eliminating those cases of

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schizophrenia in which there was evidence of a hereditary background for the disorder and those who showed suspicious personality abnormalities preceding the concentration camp experience, Eitinger concluded that for slightly more than half of the cases the patients' schizophrenia developed as a function of the horrendous camp experiences. . . . [I]t is possible that some of these cases were produced by the stress of the experience alone. But one may always ask, why them and not others exposed to the same extreme conditions? (p. 11) Comments We would not criticize the substance of the passage quoted. Our comments merely uncover an interesting theme of methodology: on the face of it, the last two sentences of this passage are inconsistent. The first sentence suggests that the camp experience may in some cases have been the sole cause of psychosis. The second sentence appears to contradict this. The inconsistency disappears after a proper reconstruction: The idea that a phenomenon can have a single cause is meaningless without qualification. Phenomena always have numerous causes. A thesis with the form, "X is the cause of phenomenon Y," should therefore be reconstructed as a thesis with the form, "X is causally salient with respect to phenomenon Y in context Z." Salience is a matter of comparison. The text makes clear how we should understand the notion that the camp experience has been—in some cases— the sole cause of psychosis. The comparison is here between the psychosis of the actual persons involved, and the condition of the same persons in hypothetical, normal situations. Evidence bearing on this comparison serves as an indirect test of the theoretical hypothesis that these persons would not have suffered from psychosis in normal situations. The evidence appears to confirm this hypothesis. However, a different comparison, between afflicted persons and other persons who had the same experience without developing a psychosis, appears to imply that the camp experience was not the "sole" cause of the psychosis. This seemingly counts against the theoretical hypothesis. In fact, however, we are looking at two entirely different hypotheses. Our reconstruction articulates the inconsistency in a more explicit form. The trouble is clearly that the apparently innocuous word "cause" refers to different things in two theses—accompanied by two implicit hypotheses— that are jointly a flat contradiction if they are taken literally. The inconsistency dissolves once contexts of comparison have been made explicit.

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TEXT 21 SHOULD BIOLOGY ENGULF PSYCHIATRY? Source: Guze, S.B. Biological psychiatry: is there any other kind? Psychological Medicine 19: 315-323, 1989. Level: advanced Criteria and guidelines: M4, M8, Ml4, Ml 6, Ml 7, G8 Related texts: 30, 34, 42 Psychiatry has always been infused with elements from other areas of science. Currently, the emphasis is on biology. Guze argues that this is as it should be. Guze notes that the brain is the organ of mental functions, and that mental functions of the brain are made possible by the genotype. This has, according too him, the following implications. We need biology to understand mental functions, normal or pathological. It is true that reciprocal interactions exist between the genotype and the cultural environment, but disciplines of biology such as ethology and ecology do accommodate the environment. I have argued explicitly that the science of biology comprises a very broad view of human life, including mental experiences, within an evolutionary framework that places appropriate emphasis on the individual's social, cultural, and physical environment. It is within such a context that I have concluded that there can be no psychiatry that is not biological, (p. 319) [T]here remains only one way in which psychiatry and psychiatrists could reasonably be considered too biological. If it could be asserted that few if any of the states or conditions that constitute the focus of psychiatry are the result of differences in the development or physiology of the brain, biology would seem to be of only marginal interest. If it could be argued that all or most of our patients develop their disorders primarily, if not exclusively, through normal learning processes that are independent of brain variability, the emphasis on biology might justifiably be seen as excessive and unjustifiable, (pp. 316-317) Guze argues that the emphasis on biology in psychiatry is justified, as hypothetical situations of this kind have not been demonstrated for any psychiatric disorder.

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Guze grants that psychologically meaningful experiences are significant in the development of psychiatric disorders. However, psychological causes reflect, according to him, the usual range of human troubles, which result in illness only in particular persons. "[E]ven if ultimately it can be shown that these experiences play causal roles in illness, it is to the specific vulnerability [a matter of biology] that we must direct our attention if we are to hope for essential scientific understanding and effective therapeutic intervention" (p. 317). A strategy aiming to reduce or to eliminate the troubles is unlikely to be helpful. Clinical pharmacology, says Guze, is the core of psychiatry, but we also need psychotherapy. He offers the following, obvious rationale for alotting room to psychotherapy: Psychologically meaningful experiences affect physiology, and discussions concerning personal problems can be helpful for sick persons. This could suggest that the situation is unproblematic: We could simply accept that psychiatry contains solid biology, while admitting that biology is not enough. However, Guze does see a problem: Psychotherapy, however useful, has problematic features that prevent its attaining the rank of biology within psychiatry. That is because psychotherapy is unable to uncover causal links: "the psychotherapeutic process is inherently incapable of distinguishing between two possibilities: (1) that the mental event hypothesized or described through the insight process is the cause of the overt clinical problem .. . and (2) that these mental events . . . are the result or the manifestation of the clinical problem (pp. 320-321). Comments We agree with Guze that brain processes are always involved in mental functioning. There can be no doubt, therefore, that biological factors play a role in psychiatric disorders. Guze grants that cultural factors also play a role. In our view, he therefore should have subscribed to the default position that psychiatry must be an interdiscipline with sources from biology and from sciences concerned with human culture. Guze, however, puts biology at center stage. He maintains that ethology and ecology can account for the cultural environment. We regard this as a linguistic trick: ethology and ecology do not normally deal with human culture. Guze apparently departs from an unusually broad definition of "biology" that undervalues contributions from other disciplines (see the quotation from p. 319). His definition ensures that his claim becomes true. This amounts to circular reasoning. The general, universal claim that psychiatric disorders are entirely a matter of biology becomes in this way

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a logical statement. The claim exhibits the virtue of simplicity, but Guze pays a price for this: He is unable to justify in a sound manner a selective focus on biological causes. Apart from this, the fact that biological factors—narrowly conceived— play a role in psychiatric disorders, need not imply that they should be causally salient. If you get depressed due to enforced overloads of work that few people could endure without getting depressed, the overload is a salient cause of the depression. The overload would produce the depression via changes in brain biochemistry, but these changes should be regarded here as less salient. Our position would be that, presumably, different instances of psychiatric disorders are due to different kinds of salient causes: biological causes, or psychosocial causes, or a combination of biological causes and psychosocial causes. In the passage from pages 316-317, Guze appears to argue that the emphasis on biology in psychiatry is misplaced only if biological causes are never or almost never salient. It should be obvious, by now, that this argument is odd. The existing emphasis on biology comes down to the view that salient biological causes always exist in psychiatric disorders. We can rightly reject this extreme view, if some disorders or instances of disorders have psychosocial factors as the most salient causes. Guze provides no evidence to rule out this possibility. He simply disregards it as he is concerned with two extreme hypotheses: Psychiatric disorders always have salient biological causes, or they never have salient biological causes. He rejects the latter hypothesis and then infers that the former hypothesis must be correct. This will not do, because his classification of hypotheses is not exhaustive. Guze's view of human troubles and vulnerability is not acceptable either. Why should psychological causes always reflect the "usual" range of human troubles? Some persons do have the misfortune of being exposed to much trouble. Furthermore, biological vulnerabilities need not always be causally salient. Suppose that an employer does not treat his employees well, with the result that half of them become depressed. Conceivably, the depressed employees are more vulnerable biologically than those who do not get depressed. However, it would be odd—indeed morally irresponsible—to infer from this that we should primarily direct our attention toward biological vulnerability. In an extensive discussion of psychotherapy, quoted here in part, Guze notes that the therapeutic process can be helpful, but that it cannot help us distinguish between mental events as primary causes of a disorder and

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mental events as a secondary manifestation of biological abnormalities. This is perhaps true, but the distinction could be made in some other way. In any case, there is no warrant for Guze's claim that features of psychotherapy, as described by him, help to justify primacy for biology in psychiatry. TEXT 22 MENTAL HEALTH AND FOOD Source: Prasad, C. Food, mood and health: A neurobiologic outlook. Brazilian Journal of Medical and Biological Research 31: 1517-1527, 1998. Level: elementary, but presupposes knowledge of molecular biology Criteria and guidelines: Gl, G8 Related texts: 16, 23, 30, 34, 45 The role of diet in health and disease is undervalued in medical science. Prasad does focus on the importance of diet. Proteins, carbohydrates and fats—the major constituents of our diet— serve not only as an energy source but as precursors to a variety of neuroactive substances. The so-called minor constituents of food— minerals and vitamins—are just now being recognized for their many nontraditional functions (e.g., as antioxidants) in health maintenance and promotion. In addition, food is a rich source of many bioactive substances like amino acids, peptides, and others. While some of these bioactive substances (CHP, casomorphins, and a variety of other substances capable of interacting directly with neurotransmitter receptors) can have a direct effect on neuronal functions, others serve as precursors (tryptophan, tyrosine, etc.) or modulators (heterocyclic amines, phenylalanine, etc.) of classical neurotransmitters (DA, norepinephrine, serotonin, acetylcholine, endorphin, etc.). Furthermore, the use of neurotransmitter precursors as dietary supplements in both humans and animals has shown profound effects on neurochemistry and behavior. Food and dietary supplements, if used properly and wisely, may help us live healthier lives. Although ingestion of minute amounts of any given compound through food may not have any good or bad

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consequences, a variety of foods in combination may indeed affect mood and health (p. 1525). Comments Prasad rightly argues that the composition of our diet affects brain biochemistry. Diets, therefore, may well affect mental disorders. Research concerning the effects of diet on health call for ecological approaches that are sorely missing in some areas of medicine and psychiatry. To Prasad's valuable reminders, we would add that the social context of research promotes a causal selectivism that hampers research on diet (see Part IV). TEXT 23 PSYCHOPATHOLOGY AND NEUROTRANSMITTERS Source: Davis, K.L., R.S. Kahn, G. Ko, and M. Davidson. Dopamine in schizophrenia: A review and reconceptualization. American Journal of Psychiatry 148: 1474-1486, 1991. Level: advanced Criteria and guidelines: M6, M7, M8, M15, M20, G6, G8, G i l , G12,G14 Related texts: 19, 22, 34, 45 To test the hypothesis "Dopamine is involved in schizophrenia," Davis and colleagues review postmortem studies of dopamine receptor densities. The evidence reviewed by Davis and colleagues is conflicting. Previous authors had attributed their results concerning the hypothesis that dopamine is involved in schizophrenia to effects of medication on patients. Davis and colleagues, however, think that medication history cannot explain all the findings. They state, for example, that patients who have been drug-free for at least a year, also have abnormal receptor counts. Not mentioned by them is literature showing that neuroleptics can cause longterm effects—indeed, irreversible brain damage. The argument quoted here is meant to strengthen their case. Rodents treated with neuroleptics have 30% more D2 receptors than untreated rodents, whereas the brains of schizophrenic patients have

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50% to 60%o more D2 receptors than those of normal subjects. Neuroleptic-treated patients with Alzheimer's disease or Huntingdon's disease have 25% more striatal dopamine receptors than do comparison subjects, whereas the number for schizophrenic patients exceeds that of comparison subjects by more than 100% . . . providing suggestive evidence that neuroleptics account for only some of the excess of D2 receptors seen in schizophrenia, (p. 1476) Comments At first sight, the analysis performed by Davis and colleagues is convincing. We show, by a methodological reconstruction, that their arguments are in fact problematic. The authors rightly suggest that neuroleptics account only for some of the excess D2 receptors seen in schizophrenia. But this suggestion is unclear, because it can be interpreted in several ways. The excess is less in Alzheimer patients than in schizophrenics. From this we would infer: The excess in schizophrenia must be caused by the neuroleptics together with physiological features that are different in schizophrenics from those in Alzheimer patients. The authors come up with a different, stronger inference. We can easily imagine that schizophrenics have features such that their dopamine response to neuroleptics is more marked than the response in Alzheimer patients to these drugs. The passage quoted does not justify the assumption that schizophrenia in itself—in the absence of treatment with neuroleptics—should cause an excess of dopamine receptors. Our reconstruction shows that the argument of the authors relies on an implicit assumption: Dopamine responses to neuroleptics are similar in the two categories of patients. No evidence is offered to justify this assumption. The authors' argument is therefore invalid, and their evidence does not confirm the hypothesis. If the authors were simply assuming that the implicit assumption is true, then they would be guilty of circular reasoning. For similar reasons, the evidence concerning the rodents is problematic. The hypothetical example in the next paragraph makes this clear by a so-called reductio ad absurdum—a pattern of reasoning that unmasks an argument as having absurd implications. A researcher wants to test the hypothesis "Being female is a symptom of a disease that should be treated with free-fall therapy." In the envisaged therapy, subjects are thrown from a tower. The researcher treats ten females; seven of them die during the treatment. No mortality is observed in an untreated control group of males. The researcher assumes that being female

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caused the mortality, but he is aware that the treatment might also be responsible for the observed mortality. Fortunately, this possibility is ruled out by data in literature on birds. In an experiment with female and male birds, no mortality was observed in either sex: All the birds survived the experiment—they flew away. The researcher infers that the disease explains the mortality in human females, and that the treatment did not cause mortality as a side effect. We hope that you get our point. The authors present heterogenous sources of evidence without logically proper interconnections. They suggest that evidence confirms their hypothesis—neurotransmitters are causally salient—but this suggestion is plainly false. The explanation envisaged by the authors is inadequate for lack of a proper identification of causes. TEXT 24 HOW NOT TO THINK ABOUT EVOLUTION AND DEPRESSION Source: Corrigan, F.M. Depression: immunological resignation of the will to live? Medical Hypotheses 50: 9-18, 1998. Level: elementary, but requires some knowledge of evolutionary biology Criteria and guidelines: Ml, M2, M12, M15, G2, G4, G9, G10 Related texts: 5, 27, 28, 29 Evolutionary thinking has been introduced during the last few decades in many areas outside biology. Here is how Corrigan deals with evolutionary biology in the context of medicine. Abstract—Evolution is assumed to promote the survival of the fittest by the greater success of the reproductive potential of those with the characteristics most suited to their environment. Little thought is given to how those least adapted fail to survive to reproduce. If the species, rather than the individual, has a drive to adaptation and survival, there should be a specific mechanism for those least adapted to withdraw from life. The immunological changes accompanying depression may facilitate heart disease, infection, parasitic infestation or other ill health, so that depression is a mechanism for those least resilient, or faced with most adversity, to succumb to illness. If depression is a state facilitating withdrawal from competition for

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reproductive success, major depressive illness may be the inappropriate and spontaneous occurrence of a mental state which has advantages for the species in allowing those 'least fit' to fail to survive. This hypothesis gives an empirically testable challenge to the view that the species has no evolutionary drive to survival and increased adaptedness to the environment, as well as explaining the more and more frequent occurrence of a specific mental state and its associated changes in the immune system, (p. 9) Comments Whenever resources of a discipline are used in another discipline, we need to know about the discipline where the resources come from, and we should take heed to check sources by generalist research. Within evolutionary biology, the search for ideas such as those defended by Corrigan would not be rewarding. Evolutionary biologists have long taken pains to point out that natural selection does not produce traits for the good of the species. Corrigan therefore faces a tough burden of proof. Nowhere in the article does he describe the mechanism that should generate depression as a species adaptation. We can imagine that variation exists among human beings in the disposition to develop depression under adversity, but that would not necessarily implicate selection above the level of individuals. One would in this situation expect the result that the incidence of depression can but decrease. Instead, depression appears to have become more common recently. Evolutionary biologists may be able to explain this as the result of special mechanisms (see Text 29), for example, potential benefits in our culture linked to disadvantages of depression. Such mechanisms should, according to biologists, also operate at the level of individuals. Corrigan regards his view as a testable challenge, but he does not indicate in the article how tests could be performed. We would argue that his view is untestable, because it falls short of the requirement of clarity. Corrigan assumes that species have a drive to adaptation and survival. To us, the notion of a drive at the species level is unclear, and we would not be able to make it operational. How could we recognize such a thing? If it is to be recognized by effects at the level of individuals, the most plausible assumption would be that drives, if postulated at all, have to be located at that level.

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Note. Some biologists do recognize special forms of "group selection" and "species selection." Corrigan's views do not sit well with the views of these biologists either. TEXT 25 BIOLOGICAL ABNORMALITY AND PSYCHOPATHOLOGY Source: Bowers, L. The Social Nature of Mental Illness. London: Routledge, 1998. Level: elementary Criteria and guidelines: M20, G3 Related texts: 16, 19 Bowers defends this thesis: "It is impossible to define 'mental illness' in biological terms." For the sake of argument, let us suppose that we do find a clear physiological correlate for a mental illness (whether this be Munchausen by proxy, schizophrenia, depression or whatever). This will never be able to mean that it is an abnormal physiological process, because normality in this case is not determined by structure or process in the brain, but by function. And with the brain, function will always have entirely social and psychological criteria. We will not be able to look at a brain and say: there, that particular neuronal/biochemical system is abnormal, it's obvious, anyone can see it. It might just as well be considered normal. It is the symptoms that are the criteria for deciding normality/health, and these are always psychosocial with mental illness.. . . Difference or variation in brain activity does not by itself equal malfunction, (p. 175) Comments Suppose that we made the following discovery: Persons with a particular mental illness—even those not treated with medication—always have a high concentration of a particular chemical in their brains, whereas concentrations are low in other persons investigated by us. Suppose further, that healthy persons, upon administration of this chemical, would develop all the symptoms that characterize the illness.

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Contrary to Bowers' suggestion, this would surely indicate that the high concentration of the chemical represents a biological abnormality. However, it is true that the biological difference between patients and healthy persons in itself would have no evidential force. The additional discovery that the biological feature studied does affect mental symptoms, would be telling evidence. It would amount to an explanatory identification of a cause. Bowers does have an important point: This kind of evidence—or stronger evidence showing how a biological feature produces mental symptoms—is hardly available for mental illnesses. We only have controversial claims about biological differences between patients and nonpatients. Indeed, the stronger evidence, if available, would not imply that a biological abnormality is the primary cause of the illness. It is conceivable that environmental factors cause the biological abnormality and thereby the mental symptoms. Bowers is implicitly suggesting that defenders of biological psychiatry would defend the following view: Biological abnormalities should suffice in principle to characterize mental illness—without reference to mental functions. This suggestion amounts to a violation of the principle of charity. Nobody would defend such a view. TEXT 26 THE PUZZLE OF ATTENTION DEFICIT HYPERACTIVITY DISORDER Source: Baird, J., J.C. Stevenson, and D.C. Williams. The evolution of ADHD: A disorder of communication. Quarterly Review of Biology 75:17-33,2000. Level: advanced Criteria and guidelines: Ml, M8, M13, M15, M18, M19, M20, G6, G8,G9,G10 Related texts: 5, 17, 19, 24, 27, 28, 29 Attention Deficit Hyperactivity Disorder (ADHD) in children is seemingly an elusive disorder. However, to some extent the elusiveness may be a social fabrication. Baird and colleagues present an extensive review of ADHD—the psychiatric condition most frequently identified in children in some countries, most notably the United States. ADHD behavior, which has such manifestations as excessive impulsivity and physical activity, problems with persevering at boring tasks, impaired performance in social skills, self-control,

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and time management. It occurs in 3 percent to 9 percent of the population, especially in children, and it has a high heritability. Several authors have concluded from this that the disorder must have been selectively advantageous in ancestral environments. Baird and colleagues oppose this view. A reduced ability to inhibit responses appears to be a core feature of ADHD. Baird and colleagues assume that the ensuing behavior can hardly be adaptive in any environment. All authors who place ADHD behaviors in a positive framework imply that there may be many settings where these behaviours were selectively advantageous. Hartmann (1993) captures the essence of the various theories when he argues that ADHD is not a malfunction but a harmonious and functional response to different contexts. The issue under consideration is: how can it be advantageous in any setting to be unable to inhibit a response? Hyperactive children may make choices faster, but they also make more mistakes.... Would they make the right choice if stalked by a saber-toothed tiger? (p. 22) This is a nice rethorical question: the choice would be entirely wrong. This example, and similar ones, certainly do not uncover advantages of ADHD. The authors subsequently review research that indicates that brain biochemistry in ADHD children is different from that in normal children. This invites biological models of ADHD. According to one model, for example, ADHD would arise not from a lack of stimulation from the LC (locus coeruleus), with its attendant focus and attentiveness, but rather from the kind of attentiveness and focus in which the LC mandates do not allow the addressing of non-threatening tasks such as reading, writing, painting, and casual conversation. Forced by a kind of scanning focus that monitors potential threats from the environment, the LC prevents assessment of the relative value of different tasks, or follow-through in a lengthy, perhaps unrewarding, task. Much of ADHD can be explained by the view that it represents the behavior of an individual who is "stuck" in a scanning focus, (p. 26) Baird and colleagues subsequently argue that language is important in ADHD. They suggest that language processes compete with other cognitive processes, since both kinds of processes require the attentional system. Interdependencies must therefore exist, according to them, between the evolution of language and the evolution of the attentional system. This

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causes problems for human beings in our culture as social interactions have become complex. Selection has probably favored those individuals better able to filter the significant from the insignificant and to suppress automatic language responses in order to generate ways of expressing new ideas. Individuals with ADHD have trouble "keeping up," but do their differences in neuroanatomy and biochemistry (and resulting behaviors) reflect normal functioning for what the system was adapted to do, or do they suggest dysfunction? (pp. 29-30) Considering etiology, they suggest that ADHD is a biochemical dysfunction that—via development and neuroanatomy—ultimately causes social dysfunction. Comments The thesis "ADHD has been adaptive in the past" might explain the high incidence of ADHD. Baird and colleagues reject this thesis. They should therefore explain how ADHD can be common, even though natural selection should work against it. No explanation is offered in the article; the passage from page 29 to page 30 is mere speculation. We regard the rejection of the thesis by the authors as problematic. Notice that their line of reasoning presupposes that ADHD children would perform their problem behaviors also in different environments. The presupposition is not made explicit, and the article does not contain materials confirming it. A reconstruction of the main argument should therefore show that it is invalid. We would hypothesize that many children exhibit ADHD, since they are exposed to highly unnatural environments. This hypothesis—unlike the hypothesis of the authors—has the virtue of simplicity. The children are forced to stay in schools, hour upon hour, day after day, during many years. It should not come as a surprise that many children would prefer to be in a different situation. Abnormal environments invite abnormal behaviors. Why should the behaviors also occur in more natural environments? Barring exceptions, we regard this as implausible in the extreme. To avoid misunderstandings: We are not rejecting the possibility that some sort of disorder resembling ADHD as described in psychiatry texts, could be present in our culture to some degree. However, we are dealing

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here with the thesis that ADHD occurs on a massive scale. That is the thesis which invites our criticism. Let us continue the criticism: Once abnormal behaviors are in place, we can but expect correlative changes in biochemistry: All mental phenomena and all behaviors should be accompanied by such changes. However, the authors do not come up with criteria to demonstrate that these changes should represent biological abnormalities. Therefore, the biological data presented by them fail to substantiate the view that ADHD behaviors are pathological in a biological sense. The dominant focus of the authors on biological causes at low levels of organization is not justified by them in any way. "Abnormal" behaviors serve here as a criterion of biological abnormality, and the biological abnormality putatively explains the "abnormal" behaviors. This amounts to circular reasoning that generates an unconfirmed theory without explanatory and predictive value. The identification of biological abnormality as the cause of "abnormal" behavior is spurious. The article is symptomatic: it exemplifies widespread trends of medicalization in our society. At first reading, it is seemingly convincing. Once an important implicit assumption is made explicit by reconstruction, their entire theory collapses. TEXT 27 EVOLUTIONARY BIOLOGY DISTORTED Source: Wilson, D.R. Evolutionary epidemiology: Darwinian theory in the service of medicine and psychiatry. Acta Biotheoretica 41:205-218, 1993. Level: advanced Criteria and guidelines: G2, G4 Related texts: 5, 17, 24, 28, 29 Wilson argues that we should explain the persistence of psychiatric disorders by the assumption that they are linked to advantages in some way. Indeed, evolutionary epidemiology may require a refinement in the notion of disease itself, at least as such a label might be attached to several of the most common and genetical syndromes in medicine and especially psychiatry. Several important psychiatric conditions (manic-depression, sociopathy, obsessive compulsity, anxiety and even drug abuse and some disorders of personality) are so common

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and so strongly epigenetic that their epidemiological frequencies surpass even quite conservative thresholds of evolutionary selection. The deduction follows that such frequency thresholds were surpassed due to the Darwinian selection of genes advantageous over the course of evolution. They most certainly served, and perhaps still serve, useful functions in human society, (p. 209) Comments Wilson aims to explain the commonness of some psychiatric conditions. He opts for the view that the genes implicated must carry advantages with them, because, otherwise, they should have lower frequencies from natural selection. This view is a specimen of "adaptationism"—the idea that all common features of organisms are in some way adaptive. Adaptationism in this strong sense represents poor evolutionary thinking. Many different mechanisms may result in the persistence of maladaptive features (see Text 29). Wilson's view is one example among many of evolutionary theory distorted in other disciplines. This can be checked only by generalist research that attends to sources in the parent discipline. TEXT 28 EVOLUTION AND PSYCHOPATHOLOGY: A METHODOLOGICAL RIDDLE Source: Crow, T.J. A Darwinian approach to the origins of psychosis. British Journal of Psychiatry 167: 12-25, 1995. Level: moderately advanced Criteria and guidelines: M2, M7, M9, G2, G4, G6, G8 Related texts: 5, 17, 24, 27, 29 In the last few decades, evolutionary thinking has become common in many disciplines. Tentative beginnings of this are now visible in medicine and psychiatry. Crow's article is an example. The illnesses that (following Kraepelin, 1919) are classified as manicdepressive disorder and schizophrenia (the 'recurrent and chronic psychoses') form the core of serious psychiatric morbidity. Yet their boundaries are ill-defined and their origins obscure. A genetic predis-

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position is generally accepted but few regard the contribution of genes as overwhelming, and much epidemiological research is directed at identifying environmental causes. Multifactorial theories proliferate but their number and diversity reveal a frailty of empirical foundation. There is little challenge to the generalisation that these disorders are present in all human societies. For schizophrenia, restrictively defined, a rather stronger conclusion was drawn from the World Health Organization Ten-Country Study (Jablensky et al., 1992): schizophrenic illnesses are ubiquitous, appear with similar incidence in different cultures and have clinical features that are more remarkable by their similarity than by their difference. The core dysfunction is thus invariant with respect to substantial variations in climatic, social and industrial environment; the fact that it now occurs at approximately the same incidence in populations that have been separated for thousands of years suggests that there are unlikely to have been sustained and divergent secular trends. These illnesses (perhaps in contrast to any physical disorder) are in some way characteristic of the human condition. But if the psychoses are primarily genetic, the uniformity of incidence across populations and the apparent lack of variation over time are singular features, the more so when one considers that lifetime prevalence (between 1 and 3 %, depending on the definition of psychosis adopted) (Hare, 1987; Eaton, 1985) is high, and there is an associated fecundity disadvantage (MacSorley, 1964; Haverkamp et al., 1982). The problem is an evolutionary one—why have the manifest disadvantages associated with the psychosis genes not ensured their elimination from the human population? (p. 12) Comments We can safely assume that Crow knows the literature concerning genetic factors in schizophrenia. Twin research, for example, is generally assumed to indicate that genetic factors are implicated in the etiology of schizophrenia, since the concordance in monozygotic twins is 50 percent, much higher than in dizygotic twins, where it is lower than 10 percent (for comments, see Part II, Chapter 1, Texts 14 and 15). Indeed, such data unambiguously show that the environment should play a prominent role in schizophrenia. It is odd, therefore, that Crow maintains:

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"The psychoses are primarily genetic." His text suggests that he infers this from similar incidences of schizophrenia in cultures with very different environments. Implicit in his line of reasoning is the following argument: Premise 1: if the environment played an important role in etiology, then incidences in cultures with different environments should be different. Premise 2: we do not find different incidences. Conclusion: the environment cannot be important etiologically. From this reconstruction, we get a valid argument with the modus tollens format. However, the first premise is false, so that the argument is not acceptable. It is possible that different environmental adversities are etiologically implicated in different cultures. The argument is also flawed for another reason: The conclusion is at odds with a large literature; the premises therefore cannot be true. If they were true, the conclusion should also be true, as the argument is valid. Crow selectively focuses on genetic factors, which is improper in view of the evidence. He downplays the role of the environment, which is at variance with the literature—as a check of sources in behavior genetics would immediately reveal. Sources from other disciplines confirm all this. Schizophrenia is studied in many disciplines, so that a generalist approach of the literature is indicated. TEXT 29 EVOLUTIONARY BIOLOGY AS A PROFITABLE SOURCE FOR MEDICINE Source: Nesse, R.M., and G.C. Williams. Evolution and the origins of disease. Scientific American 279: 58-65, 1998. Level: elementary, but presupposes some knowledge of evolutionary biology Criteria and guidelines: M4, M5, M9, M20, G7 Related texts: 5, 17, 20, 24, 27, 28, 30 Nesse and Williams present the most exhaustive survey of evolutionary mechanisms that may explain the persistence of diseases. The evolutionary explanations for the body's flaws fall into surprisingly few categories. First, some discomforting conditions, such as

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pain, fever, cough, vomiting and anxiety, are actually neither disease nor design defects but rather are evolved defenses. Second, conflicts with other organisms—Escherichia coli or crocodiles, for instance— are a fact of life. Third, some circumstances, such as the ready availability of dietary fats, are so recent that natural selection has not yet had a chance to deal with them. Fourth, the body may fall victim to trade-offs between a trait's benefits and its costs; a textbook example is the sickle cell gene, which also protects against malaria. Finally the process of natural selection is constrained in ways that leave us with suboptimal design features, as in the case of the mammalian eye. (p. 60) Another common condition, anxiety, obviously originated as a defence in dangerous situations by promoting escape and avoidance. [Nesse and Williams refer here to a study by Dugatkin, done in 1992, concerning benefit of fear in guppies, a species of fish. Dugatkin grouped them as timid, ordinary or bold, according to their reaction to the presence of smallmouth bass, afishthat eats guppies.] The timid hid, the ordinary simply swam away, and the bold maintained their ground and eyed the bass. Each guppy group was then left alone in a tank with a bass. After 60 hours, 40 percent of the timid guppies had survived, as had only 15 percent of the ordinary fish. The entire complement of bold guppies, on the other hand, wound up aiding the transmission of bass genes rather than their own. Selection for genes promoting anxious behaviors implies that there should be people who experience too much anxiety, and indeed there are. There should also be hypophobic individuals who have insufficient anxiety, either because of genetic tendencies or anti-anxiety drugs. The exact nature and frequency of such a syndrome is an open question, as few people come to psychiatrists complaining of insufficient apprehension. But if sought, the pathologically nonanxious may be found in emergency rooms, jails and unemployment lines, (pp. 60^61) Comments Nesse and Williams' survey of evolutionary medicine is the best one known to us. We do hope that it will affect medicine and psychiatry in positive ways. We focus here on one possible, intriguing shortcoming that may have substantial implications. The shortcoming is this: Their classification of evolutionary mechanisms is not entirely exhaustive.

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Variation in some features of an organism—a population, or a species— may be explained in some situations by the assumption that different variants of the organism are adapted to different environments. Nesse and Williams do not mention this possibility, which might go some way toward explaining differences in anxiety. Nesse and Williams' own explanation sounds unconvincing. If selection would favor particular dispositions facilitating anxiety, then the variation in dispositions is hard to understand without additional assumptions. For that matter, we wonder about the guppies. Would the result have been the same in natural environments? All in all, the evolutionary causes of anxiety postulated by Nesse and Williams remain to be confirmed. Nesse and Williams avoid the trap of overgeneral theories. They rightly stress that evolutionary mechanisms explaining disease come in different kinds. We would also note that one of Nesse and Williams' categories is somewhat misleading: "some circumstances . . . are so recent that natural selection has not yet had a chance to deal with them." What about the atomic bomb? No amount of selection would ever suffice for organisms to adapt to an atomic blast. The same is true for many other situations created by human beings. We have created many unnatural environmental events and unnatural standing environments. That may promote all sorts of diseases. Such things should not be put into a single evolutionary category. To the extent that unnatural environments created by us are unhealthy, we should aim to improve them. The idea that we still have to adapt to these environments may detract from this, and limitless adaptation is, in any case, not feasible. The heterogeneity of one of Nesse and Williams' categories suggests that it would not be easy to formulate consistent criteria of classification for the categories. Nesse and Williams certainly would not defend the oddities we signalized. So we may seem to have been splitting straws. However, our comments do reveal pitfalls that are often overlooked.

Chapter 4

Medication

From a naive view of medical research, established treatments for patients represent the best options we have: they are based on well-confirmed theses and theories of science. The actual situation is more complicated: Scientific work is done in an influental social setting. Considering medicine, you should know that the pharmaceutical industry—which has a vested interest in particular treatments—exerts a strong influence on research. We should not cast representatives of the industry in the role of villains, but we also should not overlook that the influence of the industry may not always be beneficial. The texts in this chapter—and also Part IV—provide an inventory of problems with medications, some of which implicate the industry. TEXT 30 OSTEOPOROSIS, MENOPAUSE, AND THE PHARMACEUTICAL INDUSTRY Source: Bian, T.R. The Drug Lords: America's Pharmaceutical Cartel. Kalamazoo, MI: No Barriers Publishing, 1997. Level: elementary Criteria and guidelines: Ml, M10, Gl, G2, G3, G4, G5, G6, G8, G10,G13 Related texts: 21, 22, 29, 44

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Relations between medicine and the pharmaceutical industry have recently been scrutinized by representatives of many disciplines, and by informed laypersons. Overall, well-founded comments invite the view that the industry does not always enhance a proper functioning of medical theory and medical practice. The book by Bian is one among many provocative sources that help us understand social contexts. The passage quoted here claims to show how the industry may foster medicalization. Menopause has become feared because of the taboos society has placed on aging. The news media acts as the orchestra—playing out a stereotyping of women who happen to be making the transition from child-bearing to non-child bearing years. The media has played its part, but the menopause performance itself has been directed by another interest—the estrogen manufacturer as the orchestra's conductor. Unfortunately, this performance is rife with the discords of the unknown. According to the Health Research Group (HRG), the Ralph Nader consumer advocacy branch of Public Citizen, the medical industry has re-worked menopause, has taken a normal body process and turned it into a disease. Medicine has convinced women that menopause is something that needs to be "taken care of," an illness that needs to be "cured." Medicine calls menopause a deficiency disease, namely, of the estrogen hormone, (p. 110) Comments We share Bian's view that the pharmaceutical industry has a vested interest in maximizing the use of estrogen, and that it has stimulated the conceptualization of menopause as a kind of deficiency disease that calls for estrogen-replacement therapy. The therapy has been promoted on the ground that it should help prevent osteoporosis—brittle bones. Bian does not address the issue of osteoporosis; she appears here to violate the principle of charity. If other arguments in favor of the therapy were as improper as Bian suggests, the therapy could all the same be appropriate. To understand this, one should pause to contemplate what the word "normal" in her text might mean. Evolutionary biologists would point out that natural selection fails to foster health during postreproductive periods (see Text 29). Therefore, the

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view that menopause represents "normal" body processes might be entirely consistent with the following thesis: Estrogen production wanes after reproduction ceases; this enhances the risk for osteoporosis, and estrogen suppletion may lower this risk. "Normality" is a slippery concept to rely on. It is "normal" for animal populations to be infested with all sorts of parasites. It would be odd if human beings were told by the medical profession that they should simply accept such a "natural" phenomenon as their fate. Instead of this, we aim to get rid of parasites—not least by the use of proper medication. In brief, the argument presented by Bian, however persuasive from casual reading, is invalid. The concept of biological normality is in some respects irrelevant for the postreproductive period in a medical context. The concept easily generates theorizing that is medically irresponsible. Let us reconstruct Bian's line of reasoning in a more formal way. She criticizes the industry and the medical community on the ground that they medicalize normal body processes into disease symptoms that call for a therapy with estrogen. She stipulates that the need for therapy is inferred here from false premises. To the extent that the therapy is indeed promoted in this way, Bian is rightly militating against an invalid mode of reasoning. However, this does not imply that the conclusion concerning the need for therapy is false. Bian rejects this conclusion on the basis of two premises: normal processes do not call for medical intervention, and a decreased estrogen production during menopause is a normal process. The first premise is a general, universal statement that is clearly false. We reject Bian's argument without implying that we take estrogen replacement therapy for granted. Considering the therapy, we have to take possible side effects into account: For example, does the therapy increase the risk of cancer? Furthermore, we would not assume that research about estrogen against osteoporosis—funded to a large extent by the industry—is entirely unbiased. Even a superficial inspection of the literature about the prevention and the treatment of osteoporosis shows that the emphasis on estrogen is overwhelming. That does count as an example of causal selectivism fostered by the industry. We can safely assume that bone metabolism is influenced by many different physiological variables. Therefore, the common assumption that estrogen therapy should be the best treatment against osteoporosis is a priori implausible. Here is an example of an alternative. R. Martin and J. Gerstung (1997) militate against common estrogen wisdom. On the basis of extensive published evidence, they opt for progesterone—another hormone involved

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in reproduction. This hormone may work well in our culture since diets in the West are unnatural in many respects. More natural diets would contain plant substances from which human beings are able to synthesize progesterone. Our comments indicate how we would write about estrogen and osteoporosis. Bian's argument is a good starter, but there is a hole in it; it needs to be formulated with more caution. Once it is recognized as invalid, we see the need for additional information to shed light on the relation between estrogen and osteoporosis. Biased emphasis on estrogen replacement therapy should make us suspect that relations between the industry and medical research may not be pervasively beneficial. A context of industry for research can but generate some forms of bias. For that reason alone, a thorough evaluation of the methodology used in this research is imperative. Indeed, set ups commonly used in trials for drug testing are problematic (see Text 32 and the Part IV). Apart from this, a thorough search in the literature for other therapies may be rewarding. If we wish to opt for the best therapies, we need generalist backing. In a brief search of our own, we happened to come across one alternative therapy: the botanical progesteron option. Our hunch is that more possibilities can be uncovered, but we have not done an in-depth study of the literature. We are afraid that researchers paid by the industry run the risk of getting dirty hands if they disregard possible treatments outside the industry's domain of interest. Reference Martin, R., and J. Gerstung. The Estrogen Alternative: Natural Hormone Therapy with Botanical Progesteron. Rochester: Healing Arts Press, 1997.

TEXT 31 MEDICAL JOURNALS AND THE PHARMACEUTICAL INDUSTRY Source: Stelfox, H.T., et al. Conflict of interest in the debate over calcium-channel antagonists. The New England Journal of Medicine 338: 101-106,1998. Level: elementary Criteria and guidelines: M6, Ml 5, G2, G4, G5, G6 Related texts: 32, 38, 40, 44

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The theme of bias in medical research resulting from relationships with the pharmaceutical industry is seldom addressed in medical journals. Therefore, we should welcome the article by Stelfox and colleagues, which explicitly deals with the issue. The article was published in a high-ranking medical journal. Stelfox and colleagues did uncover potential conclicts of interest between the industry and medical research. Our study was designed to examine financial conflicts of interest in the debate over calcium-channel antagonists. The results demonstrate a strong association between authors' opinions about the safety of calcium-channel antagonists and their financial relationships with pharmaceutical manufacturers. Supportive authors were much more likely than critical authors to have financial associations with manufacturers of calcium-channel antagonists, as well as with manufacturers of other products. Conversely, critical authors were much less likely to be financially associated with manufacturers of competing products, (pp. 103-104) The authors grant that their study has limitations due to the survey instrument. They further state that temporal relations between financial support and publication are unknown. "Hence, we cannot conclude that the industry influenced the researchers. It is also possible that financial support was incited by positive opinions about the drugs published by the researchers" (p. 104). After noting that the industry does benefit academic medicine, the authors argue that it would be wrong to restrict publication of results that favor products of the industry that funded the research. We . . . believe that medical journals risk severely limiting the pool of experts available to debate medical issues if they restrict the publication of articles by clinicians and researchers with conflicts of interest. Physicians and researchers simply need to disclose their financial relationships with pharmaceutical manufacturers appropriately. Medical professionals should be able to evaluate the merit of individual articles in the light of the authors' disclosure of conflicts of interest. The extent to which the pharmaceutical industry influences clinicians' and researchers' opinions cannot be determined by the results of our study. We believe that the authors we surveyed expressed their

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own opinions and were not influenced by financial relationships with pharmaceutical manufacturers, (p. 105) Comments We welcome that Stelfox and colleagues have introduced in an important medical journal the theme of links between the industry and medical research. However, we regard their views as overly optimistic. Considering the last statement in the passage quoted, we note that it merely expresses a belief. Other sources (see Part IV and the Appendix) indicate that the industry does on occasion foster biased views, for example, in the form of selective reporting. Furthermore, we wonder if it is true that "medical professionals should be able to evaluate the merit of individual articles in the light of the authors' disclosure of conflicts of interest" (p. 105). Mere analysis of articles would not suffice for the detection of selective reporting; we can but take for granted that data as reported have not been fabricated through significant deletions. However, indirect methods of detection are possible. If temporal relations between financial support and publication (p. 104) were known, we would be able to infer whether financial support by the industry does promote biased reporting or even fraud. It is conceivable that some of the researchers surveyed by the authors had dirty hands. We feel that this possibility calls for further research. Furthermore, a generalist check of sources in the literature is desirable to test the possibility that we are dealing with bias that may harm patients (see Part IV, Appendix). The authors believe that restriction of publication where conflicts of interest exist would entail "that medical journals risk severely limiting the pool of experts available to debate medical issues" (p. 105). Up to a point, this is true. The pool of experts would be limited from one interrelation of this passage: The quantity of experts would decrease in the situation envisaged. However, this interpretation assigns a particular meaning to the expression "limiting the pool of experts available." The expression falls short of clarity. It can also be reconstructed in a different way: we should consider the possibility that a pool of experts is limited in the sense that qualitatively different sorts of expertise are not represented in a balanced way. Funding by the industry does tend to limit expertise in this way: The industry funds research on drug therapy, whereas it has less interest, for example, in diet therapy.

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The authors fail to note that undesirable forms of bias would be possible even if the industry did not influence the outcomes in studies concerning effects of drugs. These forms of bias are presumably common. It is to be hoped that persons and organizations without conflicts of interest will manage to reduce this bias by proper research policies and editorial policies. TEXT 32 DRUGS AND PLACEBOS: METHODOLOGICAL BIAS IN RESEARCH Source: Fisher, S., and R.P. Greenberg. What are we to conclude about psychoactive drugs? Scanning the major findings. In S. Fisher, and R.P. Greenberg (eds). From Placebo to Panacea: Putting Psychiatric Drugs to the Test, pp. 3-56. New York: John Wiley & Sons, 1997. Level: advanced Criteria and guidelines: Ml 5 Related texts: 31,33,34 Methodological problems may cause a biased view of drug effects amounting to overestimated positive effects and underestimated long-term side effects. Fisher and Greenberg survey in an excellent text some methodological problems. We quote Fisher and Greenberg without comments. A number of variables need to be considered when trying to decide whether a drug is the treatment of choice for psychological discomfort. Besides such factors as the availability of other treatment options, serious attention must be directed to the so-called side effects each drug will induce. The euphemistically labeled side effects can have such serious consequences as delirium, neurological damage, sexual dysfunction, memory loss, Parkinsonism, orthostatic hypotension, addiction, and even death (Dewan & Koss, 1989). Customarily, most side effects are dismissed as transient and unimportant. However, it is documented that they can cause real suffering, and little is factually known about their potential long-term consequences. We were unable to find any studies that actually measured, over extended follow-up periods, the probabilities that drug side effects like sexual dysfunction will largely dissipate. Obviously, an informed decision whether to take

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psychotropic drugs calls for fairly detailed and accurate knowledge concerning their impact on multiple body systems. Troubling doubts have been repeatedly raised about the cogency of the typical double-blind design for evaluating the efficacies of psychoactive medications. Studies have shown that the double-blind is usually vulnerable to bias; that the often used initial washout to control placebo response is useless; and that the patients who participate are simply unrepresentative of the modal clinical population. What can be done to devise a more sensible design? First of all, inert placebos can no longer be justified and should be replaced by placebo substances that arouse body sensations mimicking the active drug being tested. This would close a big hole in the objectivity of the double-blind as it is now practiced. Another technique for attaining greater objectivity would be to introduce periodic inquiries of both patients and research staff concerning whether they have a greater-than-chance accurate awareness of who is receiving active drug versus placebos, (pp. 372-373) TEXT 33 PLACEBOS, ANIMALS, AND MAN Source: Ader, R. The role of conditioning in pharmacotherapy. In A. Harrington (ed). The Placebo Effect: An Interdisciplinary Exploration, pp. 138-165. Cambridge: Harvard University Press, 1997. Level: advanced Criteria and guidelines: Ml 5 Related texts: 33 Placebo effects are sometimes looked upon in a desultory way: They may be thought merely to represent a nuisance phenomenon due to suggestion. This idea is false. Ader has shown that placebo effects may involve conditioning, and that they occur in some animals as well as in human beings. This may have substantial implications for the practice of medicine: Medications that are pharmacologically beneficial while having negative side effects may have to be replaced in some situations by placebos that constitute a superior genuine treatment. We quote from Ader's book without comments.

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In a separate experiment (Ader 1985), lupus-prone mice that had been treated with saccharin and CY [cyclophosphamide] for two and a half months were divided into three subgroups: one subgroup continued to receive CS-UCS [conditioned stimulus-unconditioned stimulus] pairings; another continued to receive weekly exposures to the CS followed by an injection of saline rather than CY; and a third subgroup received neither saccharin nor CY. Pharmacologically, the latter two subgroups were the same; neither received any active drug therapy. Mice that continued to be reexposed to the CS survived significantly longer than the conditioned group that experienced neither the drug nor the CS. In fact, animal that continued to be exposed to the CS did not differ from animals that continued to receive active drug. Reexposure to saccharin had no effect on nonconditioned animals; these mice did not differ from those for whom both the CS and UCS were discontinued. Such findings suggested that there might be considerable heuristic value in viewing a pharmacotherapeutic regimen as a series of conditioning trials and in adopting a conditioning model for manipulating, controlling, and predicting placebo effects in pharmacotherapeutic situations, (pp. 144-145) TEXT 34 SHOULD WE DO AWAY WITH BIOLOGICAL PSYCHIATRY? Source: Breggin, P. Brain Disabling Treatments in Psychiatry: Drugs, Electroshock, and the Role of the FDA. New York: Springer, 1997. Level: elementary Criteria and guidelines: Ml 5, G8 Related texts: 21, 22, 23, 32 Breggin, a psychiatrist, is presumably the most staunch critic of drugs in psychiatry. He is somewhat one-sided, but he does provide much published evidence in support of theses defended in his book. Because evidence in favor of Breggin's views is often disregarded in mainstream psychiatry, we present here Breggin's theses, without comments. He does provide much evidence, but an adequate analysis thereof would here take up too much space.

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Modern psychiatric drug treatments gains its credibility from a number of assumptions that professionals and laypersons alike too often accept as scientifically proven. These underlying assumptions qualify as myths: fictions that support a belief system and a set of practices. [Breggin states that he improves on the myths by identifying principles of psychopharmacology based on scientific evidence and common sense.] Together these [the principles] form the brain-disabling principles of psychiatric treatment. While the book in its entirety provides the evidence for these principles, this chapter will summarize them (pp. 3-10): I. All biopsychiatric treatments share a common mode of action the disruption of normal brain function.... II. All biopsychiatric interventions cause generalized brain dysfunction. .. . III. Biopsychiatric treatments have their "therapeutic" effect by impairing higher human functions, including emotional responsiveness, social sensitivity, self-awareness or self-insight, autonomy, and self-determination. More drastic effects include apathy, euphoria, and lobotomy-like indifference.... IV Each biopsychiatric treatment produces its essential or primary brain-disabling effect on all people, including normal volunteers and patients with varied psychiatric diagnoses. . . . V Patients respond to brain-disabling treatments with their own psychological reactions, such as apathy, euphoria, compliance, or resentment. . . . VI. The mental and emotional suffering routinely treated with biopsychiatric interventions have no known genetic and biological cause... . VII. To the extent that a disorder of the brain or mind already afflicts the individual, currently available biopsychiatric interventions will worsen or add to the disorder. . . . VIII. Individual biopsychiatric treatments are not specific for particular mental disorders.... IX. The brain attempts to compensate physically for the disabling effects of biopsychiatric interventions, frequently causing additional adverse reactions and withdrawal problems.... X. Patients subjected to biopsychiatric interventions often display poor judgment about the positive and negative effects of the treatment on their functioning. . . .

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XI. Physicians who prescribe biopsychiatric interventions often have an unrealistic appraisal of their risks and benefits, (pp. 3-10)

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Chapter 5

Stress

Stress represents one of the most difficult subjects of research. Researchers from many areas investigate stress. The areas range from sophisticated subdisciplines of the life sciences such as molecular biology—via a great variety of interdisciplines such as psychoneuroimmunology and psychosomatic medicine—to subdisciplines of psychology. The texts and comments in this chapter are a sample that highlight some methodological problems in research on stress. TEXT 35 LIFE EVENTS: STRESS FOR MEDICINE FROM PSYCHOLOGY Source: Martin, P. The Healing Mind: The Vital Links between Brain and Behavior, Immunity and Disease. New York: St. Martin's Press, 1997, Level: moderately advanced, source from psychoneuroimmunology Criteria and guidelines: MA, Ml 8, Gl, G2, G7 Related texts: 20, 36, 37 The study of stress in human beings calls for inputs from biology, psychology and medicine. Stress in a psychological sense may cause disease. In the last few decades, researchers have come to recognize, that the immune system plays a vital role in this process.

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Many interdisciplines in which stress is a salient theme have recently emerged. We would regard one particular interdiscipline as the most promising offspring of the parent disciplines: psychoneuroimmunology. Many approaches within this interdiscipline have a salient focus on molecular biology, whereas other approaches take heed, for example, to make life event research a prominent topic. We take from the book by Martin a few passages that indicate how life events may mediate between stress and disease (pp. 35-36). A life event is defined as any significant change in a person's circumstances which requires them to make psychological and practical readjustments. The disruptive event can be either desirable or undesirable; the prime criterion is that it causes a degree of upheaval. Examples of life events include the death of a partner or family member, divorce, marriage, starting a new job, moving house or financial problems. At the other end of the scale, minor upheavals such as family holidays and Christmas are also classified as life events.... The basic hypothesis underlying this work is that any disruptive changes, whether desirable or undesirable, are potentially stressful and can increase our chances of falling ill. Life events come in many different kinds. A unifying framework has been developed to study them in a general way: most researchers assess life-event stress by the so-called Social Readjustment Rating Scale (SRRS). In its simplest form this involves asking each individual to record which of forty-three types of life event they have experienced over a specified period, usually between six months and two years. . . . If it is true that life events act as risk factors for illness then people who register high life-event scores should, on average, have more illnesses than those whose lives have been undisturbed by change. By and large, this is what the research has found. Comments Nothing is wrong with the life event approach in itself, but it has obvious limitations. Exhaustive specialist studies of particular types of life events would be unacceptably time-consuming. Moreover, such studies would have a limited scope, and they would yield therory at a very low level of generality.

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Research that uses an overall rating scale to cover all sorts of life events is more promising, but it has limitations of its own. This research does attain generality. However, the generality is bought at a price: The overarching notion of life event associated with rating scales is somewhat elusive, as life events are a mixed lot. For this reason alone, general hypotheses departing from this notion, do not allow inferences concerning individuals. In the last paragraph of the passage quoted, Martin considers with approval such a general hypothesis. In our view, the hypothesis does not have much value for theory and practice concerning individual patients, even though it usefully makes us aware that life events may have been salient causes of illness in particular persons. We see additional methodological problems. For one thing, the hypothesis envisages one-way causation from life events to disease, whereas causation could also go the other way around: Illness, or latent illness, could well result in particular life events. Furthermore, we should be aware that life events affect illness in indirect ways, via other etiological factors. These things are obvious. Beyond the obvious, a generalist approach should uncover a more fundamental problem with life event research: Its research agenda is overly one-sided, since ecological factors from biology are disregarded as a possible source of illness. Life event research shares this problem with much medicine. In medicine, etiological factors are often put into two overarching categories, biological factors—equated to internal factors—and psychosocial factors—equated to external factors. Ecology, the discipline concerned with external biological factors, thus falls by the wayside. The classification is not exhaustive, so that we get causal selectivism. For example, influences of diet are disregarded in many mainstream areas of medicine, even though research outside these areas has demonstrated that the food we eat may be etiologically significant. This should have had implications for life event research. It is conceivable, for example, that life events induce bad eating habits and thereby illness. Considering food as an ecological factor, we note that modern food processing alters fatty acid profiles in harmful ways. That should be important here since fatty acids are known to affect the immune system. Food processing may indeed be a potent source of illness. Conceivably, persons whose immune system is weakened by inappropriate food may more easily succumb to illness in situations of psychosocial stress. The hypothesis "Life events cause illness" may therefore have force only in particular contexts; for example, a culture where particular food preparation

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techniques and eating habits are common. We need a generalist search of the literature to check this. TEXT 36 A CONCEPTUAL PITFALL Source: Biondi, M. and L.-G. Zannino. Psychological stress, neuroimmunomodulation, and susceptibility to infectious diseases in animals and man: A review. Psychotherapy and Psychosomatics 66: 3-26, 1997. Level: elementary Criteria and guidelines: Ml 6, Ml 7, Gl, G7 Related texts: 35,37,43 Conceptual pitfalls are common in stress research.Bondi and Zannino uncover some conceptual pitfalls. We quote them with approval. Many studies have demonstrated that the exposure of an animal to a stressor is associated with alterations of its susceptibility to pathogenic bacteria. These have been estimated mainly through the measure of mortality or, more rarely, through an evaluation of the incidence of the disease, the intensity or duration of the symptoms, and the extent or severity of tissue lesions. Susceptibility usually increases in stress conditions. . . . In a more limited number of experiments, stress appears not to alter, or even to reduce, the susceptibility of animals to bacterial pathologies. . . . A moderate number of studies has shown that certain characteristics of the host, bacterium and stressor condition the type, entity and direction of the effects of stress on resistance to pathogenic bacteria, (p. 5) Comment Biondi and Zannino correctly point out that universal, general claims concerning stressors and stress responses are hard to come by. Researchers do aim at general theories in science, but biological variability limits possibilities for such theories in the life sciences. Variability causes stressors to have different effects in different organisms. More accurately, particular environmental conditions represent a stressor for some organisms, whereas

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other organisms are not harmed by them. Biondi and Zannino's article is a useful reminder that we must not overlook these methodological issues. TEXT 37 THE FATE OF PIGS IN HUSBANDRY Source: Spencer, G.S.G. Hormone and metabolite changes with stress in stress-susceptible Pietrain pigs. Endocrine Regulations 28: 73-78, 1994. Level: advanced Criteria and guidelines: Ml, M9, Ml 5, G6, Gl 1 Related texts: 35, 36 Some general theories of stress are a conceptual nightmare. Much stress research departs from the assumption that stressors cause stress responses, but this assumption is problematic: it is difficult to define the notion of stressor without reference to stress responses. Difficulties are compounded in research on animals, because the experience of stress has to do with emotions, and knowledge of animal emotions is hard to come by. To know about emotions in animals, we have to rely on sophisticated analogical reasoning. Spencer is in search of useful indicators of stress responses in pigs. His stated motive is a concern to improve animal welfare, and thereby postmortem meat quality. We quote here the abstract of the article. Pigs of the stress-susceptible Pietrain breed . . . were fitted with indwelling jugular vein catheters . . . to allow stress-free blood sampling. After surgery, the animals were placed in metabolism crates and allowed at least seven days to recover and to become accustomed to handling, and to their environment, before experimentation. On the day of study, the pigs were subjected to a stimulated loading stress. [That is, loading onto a lorry was simulated by removing the pigs from their crates, shepherding them around a pen and then reloading them back into their crates.] Blood samples were taken both before, and a number of times after, the simulated loading procedure. Plasma levels of glucose, insuline, lactate, and thyroxin rose rapidly to peak levels at 10 min after simulated loading. [The responses did not occur in controls not subjected to simulated loading.] Cortisol and triodothyronine rose to peak levels 15-20 min after the stressor was applied, while free fatty acid levels were initially depressed, but later showed a rise at 120 min. From these results it seems that plasma cortisol,

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thyroid hormones and lactate concentrations may prove to be useful indicators of stress, either individually or in combination. In the discussion of the article, Spencer notes that the interpretation of some physiological data is difficult. In line with a large literature, he regards cortisol as a reliable indicator of stress. "Adrenal corticoid secretion, and the changes in plasma cortisol concentrations in the present study are consistent... with those previously reported.... Plasma cortisol has been widely advocated (and used) as a practical indicator of stress and is the benchmark with which to compare the other indices measured in this study" (p. 47). As Spencer explains in the discussion, other data are more problematic. For example, the effect of stress on thyroid function varies with the stressor applied and the species studied. Other authors had found that thyroxine levels decrease upon application of halothene anesthesia as a stressor, whereas Spencer observes an increase in these levels. This discrepancy may be explained, according to Spencer, by the assumption that halothene induces malignant hyperthermia; this should imply that the thyroxine decrease may not be generally representative for stress responses. Spencer also notes the following problem: some physiological changes, for example those in plasma lactate, may have been caused in part by physical exercise. 'The contribution due to the physical exercise . . . and the contribution due to emotional effects, can not be determined in the present studies, but a similar elevation in plasma lactate during prolonged transport . .. without a large exercise component suggests that the increased plasma lactate is not solely due to muscle exertion" (p. 48). We note here that this passage represents the only reference to emotions in the article. Comments Spencer suggests on the basis of his results that cortisol, thyroid hormone, and lactate may be useful indicators of stress. But considering thyroid hormone and lactate, he admits that the evidence is weak. It is true that Spencer is able to offer an ad hoc explanation of the thyroid discrepancy. However, we would like to see more evidence in favor of his assumption that other stressors should also increase thyroid levels. Spencer's reasoning concerning lactate is suspect for the following reason: He assumes that both prolonged transport and simulated loading represented unpleasant situations for the animals. We should pause here to consider why prolonged transport should be unpleasant. We would assume

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that it interferes with normal behavior, since—during transport—the animals had been trapped in a small enclosures. In this respect, prolonged transport resembles being trapped in a crate! Indeed, the simulated loading may well have represented the termination rather than the beginning of unpleasantness. The cortisol data are possibly less problematic: They confirm the existing view that stressors cause cortisol elevation. We may therefore choose to reconstruct the article as a test of this view. We get in this way the following logic of Spencer's experiment: Hypothesis (accepted by Spencer as already well-confirmed): Stressors cause cortisol elevation. Additional premise: Simulated loading is a stressor for the pigs. Test implication (inferred by deduction): Simulated loading causes cortisol elevation in the pigs. The test implication is true. It therefore represents a further confirmation of the hypothesis—by way of induction, not deduction. We omit a full analysis of Spencer's argument as reconstructed. Instead we focus on the weakest link: Nowhere in the article does Spencer provide arguments for the additional premise that we should regard simulated loading as a stressor. In assessing the article, we therefore should not focus on the evidence presented. Salient should be instead what is left unsaid. Spencer apparently takes for granted: Simulated loading is stressful, whereas nothing is wrong with staying in a crate. That fits in with common practice in intensive husbandry. Animals are often kept in enclosures wherein they can hardly move. Those in favor of this practice would not feel comfortable with the view that animal welfare is severely impaired in this situation.

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Chapter 6

Genetic Engineering

Genetic engineering is transforming our society in drastic ways. Some applaud this, whereas others are critical. The texts in this chapter represent different standpoints. TEXT 38 AGAINST GENETIC ENGINEERING Source: Ho, M.-W. Genetic Engineering: Dream or Nightmare. Dublin: Gateway, Gill & Macmillan, 1998. Level: main message elementary, some details advanced Criteria and guidelines: Ml, M9, Ml 1, Ml 5, Ml 9, G4, G6, G8 Related texts: 31, 39,40 Modern biotechnology is increasingly a matter of genetic engineering. Salient are applications in agriculture, where genetically modified crops are cultured on a massive scale. Genetic engineering is highly controversial. Most molecular biologists are enthusiastic about the new techniques, whereas many ecologists regard them as dangerous. The book by Ho is an excellent source of evidence pointing to unacceptable risks. We endorse her views to a large extent. We summarize them succinctly through paraphrases and quotations, without comments. From a naive interpretation of the science underlying genetic modification—a common interpretation in industries concerned with genetic engi-

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neering— genes code for particular proteins, and the proteins are responsible for the expression of particular phenotype features. Ho aptly summarizes the naive interpretation as applied to agriculture: If, for example, a particular crop suffers from insect pests, you have to search for a species that produces a natural pesticide against the insects, find the gene responsible for pesticide production, excise it, and insert it in the genome of your crop. The crop will then manufacture the pesticide also, and you will have solved your pest problem. Through a similar technique, you may introduce herbicide resistance, so that you can eliminate weeds without impairing your crop. Ho surveys an impressive quantity of scientific evidence, accumulated during the last two decades, that shows that this interpretation is entirely false. No causal one-way traffic from genes to phenotypes exist. Many feedback relations are involved instead, and genes interact in countless ways. Furthermore, the genomes of organisms are anything but static. Organisms are stable despite the fluidity of the genome, and mechanisms exist that prevent the assimilation of foreign genetic material. "Horizontal gene transfer" among unrelated species does occur to a limited extent, but the transfer effectuated by genetic engineering should here be regarded as unnatural, qualitatively and quantitatively. Genetic engineers use artificial vectors made from viruses and other infectious agents that help to transfer genes. These vectors are designed to overcome species barriers that often exist between non-interbreeding species. By such techniques, transgenes from engineered crops are easily transmitted to other organisms, for example soil bacteria and fungi (p. 159). It is impossible to predict how the artificial insertion of genes in crops will work out, because the effects depend strongly on the genetic context. Ho reviews many examples of unforeseen effects. For example: a transgenic yeast was engineered for an increased rate of fermentation with multiple copies of one of its own genes, which resulted in the accumulation of the metabolite methylglyoxal at toxic, mutagenic levels. This should serve as a warning against the "familiarity principle" or "substantial equivalence" in risk assessment, (pp. 148-149) [These notions refer to a simplistic assumption: A genetically modified organism is considered as harmless on the ground that a nonmodified relative is harmless.]

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Many more examples of unanticipated negative effects are known. Also, on many occasions, anticipated positive effects have not materialized. Ho argues that traditional agriculture compares favorably with modern technology-based agriculture: Throughout the tropics, traditional agroforestry systems commonly contain well over a hundred annual and perennial plant species per field. A profusion of varieties and land-races (local varieties) are cultivated, which are adapted to different local environmental conditions and possess a range of natural resistances to diseases and pests. Spatial diversity through mixed cropping is augmented by temporal diversity in crop rotation, ensuring the recycling of nutrients that maintain soil fertility. These practices have prevented serious outbreaks of diseases and pests and have buffered food production from environmental exigencies. The diversity of agricultural produce is also the basis of a balanced nutrition.... A major cause of malnutrition throughout the world is the replacement of the traditionally varied diet provided by sustainable agriculture with one based on monoculture crops, (p. 140) Transgenic crops are created from the same high-input monoculture varieties as the 'Green Revolution' [which was a dismal failure], and are even more genetically uniform, because each transgenic line originates ultimately from a single cell. Two main traits account for almost 100 per cent of the transgenic crops planted in the world today; 70 per cent are herbicide-tolerant, with companies engineering tolerance to their own particular herbicide in order to increase the sales of herbicides, while the rest are insect-resistant. Each of these traits is associated with its own problems. Herbicide-tolerant crops make it possible to apply powerful broadspectrum herbicides, which kill many species indiscriminately [with negative effects on soil fertility and human health], (pp. 142-143) Ho notes that crops engineered to be resistant against particular insects have succumbed to new insect pests that soon had to be fought by increased spraying with insecticides. Furthermore, existing effects of insecticides readily disappear, since insects have vastly underestimated mechanisms— unkown in many areas if science—for a rapid development of resistance.

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TEXT 39 GMOs IN THE FIELD: A MISLEADING CALL FOR MODERATION Source: Beringer, J.E. Releasing genetically modified organisms: Will any harm outweigh any advantage? Journal of Applied Ecology 37: 207-214, 2000. Level: advanced Criteria and guidelines: M6, M7, M9, Ml 1, M12, M13, M16, M17, G1,G6,G7,G8,G11 Related texts: 38,40 In the controversy over genetically modified organisms (GMOs), Beringer apparently steers a middle course, but he does regard much criticism of those who oppose genetic engineering as overblown. Our limited understanding of the factors driving environmental change, and a wide-spread lack of knowledge of the environmental risks associated with traditional plant breeding, bedevil the present genetically modified (GM) debate. We see possibilities for environmental harm because we are looking at new types of organisms without making the appropriate comparisons, (p. 208) [As far as Beringer knows, no example exists of a GM crop causing more environmental harm than equivalent traditionally bred crops.] (p. 208) Genes do not belong to an organism, they are at best part of a family of genes that may be very wide-spread. Genes coding for hemoglobin synthesis provide a good example. They are found in plants and animals, and are extremely similar. In general, moving genes between species, and even families, is not perceived by many molecular geneticists to be contravening any 'natural laws' or 'divine plan.' Here we have a fundamental problem of comprehension and opinion that has not been properly debated.... For many scientists the concept that genes have unique identities derived from the organisms from which they have been isolated makes little sense. But it is quite clear that for many people a component of their sense of being human is the uniqueness of their make-up and that of other organisms, (p. 208) Subsequent to this, Beringer considers a particular risk postulated by some researchers: GM crops could give rise to gene combinations that enhance fitness, and progeny derived from crosses between the crops and wild relatives could then develop into nasty weeds. Beringer dismisses this

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possibility on the ground that traditional breeding has not resulted in problems. "We thus have a history of production of novel combinations of genes, and might assume that if novel combinations are likely to pose serious problems for the environment we would have seen them" (p. 209). This is a general, universal claim with the merit of simplicity. However, it is suspect because it is overly general. Another issue considered by Beringer is this: The possible transfer of genes from GMOs to other species is hotly debated. Considering crops, he maintains that barriers to cross-pollination ensure that intergeneric gene transfer is very rare, whereas interspecific transfer yields very few vigorous hybrids. "WTien we consider that crop breeding has for years concentrated on disease resistance, seed yield, seed size and general fitness, it is surprising that the flow of these 'fitness' genes to related species has not led to enhanced weediness" (p. 210). The complexity of genetic make-ups apparently prevents this. The same is presumably true, according to Beringer, for GMOs. Beringer also argues that lateral gene transfer ensuring heritability is limited among bacteria. We fail to understand his arguments for this, because he notes at the same time that lateral transfer of antibiotic resistance occurs on a grand scale. Comments The first passage from page 208 appears to have a convincing ring. We would note here that examples of environmental harm not known to Beringer, are known to Ho (see Text 38). We reconstruct the no-harm thesis in some detail. Precisely what should the expression "equivalent traditionally bred crops " be taken to mean? We assume that the implicit comparison is between GM crops—always cultivated in monoculture—and traditionally bred crops belonging to the same species cultivated in monocultures. We would note here that traditional agriculture, broadly conceived, comprises mixed-crop farming in addition to monoculture farming. Evidence exists that monocultures—within the category of traditional cultivation practices—cause more environmental harm than mixed-crop systems (examples of harm: decreased species diversity, soil infertility, chemical detoriation of the environment; see Text 38). Hence, we may argue that GM crops represent a continuation of relatively harmful traditional methods. Beringer incorrectly disregards this issue, which should have been salient. His argument is misleading.

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The second passage from page 208 is also misleading. Crucial is the intended meaning of "contravening natural laws." The expression may be taken to refer to processes that would not take place without the nonnatural techniques of genetic engineering, with the implication—attributed by Beringer to opponents—that the techniques must be regarded as inappropriate. We reconstruct Beringer's line of reasoning as follows: Argument I Premise 1. Many genes—for example, genes coding for hemoglobin—have by natural processes become established in dissimilar, unrelated organisms. Conclusion. If a gene occurs in dissimilar, unrelated organisms, then this represents a natural situation. Argument II Premise 1. If a gene occurs in dissimilar, unrelated organisms, then this represents a natural situation. Premise 2. Some genes occur in dissimilar, unrelated organisms as a result of genetic engineering. Conclusion. Genes that occur in dissimilar, unrelated organisms as a result of genetic engineering, represent a natural situation. Argument II is a valid deductive argument. Its first premise derives from Argument I. But Argument I is clearly invalid. It amplifies the premise by an unjustified form of inductive generalization. We recognize this as inadequate, once Beringer's line of reasoning is made fully explicit. The passage from page 209 concerning the comparison of GM crops and traditional crops also amounts to an inductive generalization. In traditional crops, novel gene combinations have not posed serious problems. Beringer infers from this that novel gene combinations—including those of GM crops—do not pose serious problems. The assumption is here that the gene combinations produced through the new techniques are as unproblematic as the old gene combinations. Beringer takes here for granted a standpoint that calls for arguments. Considering the transfer of genes from crop GMOs to other species, Beringer only discusses transfer through interbreeding. However, as others have argued (see Text 38), the issue should rather be that vectors used in

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genetic engineering promote lateral gene transfer in the absence of interbreeding. TEXT 40 GMOs IN THE FIELD: A STAUNCH DEFENSE Source: Miller, H.I. UN-based biotechnology regulation: scientific and economic havoc for the 21st century. Trends in Biotechnology 17: 185-190,1999. Level: biology elementary, methodology advanced Criteria and guidelines: Ml, M9, Ml 9, Gl, G6 Related texts: 31,38, 39 Miller is, presumably, the most staunch opponent of special regulation for genetically modified organisms (GMOs). His main point is that we should evaluate products of technological processes rather than these processes as such. [A] risk-based approach would be more defensible scientifically than the process- or technique-based approach of the European Union (EU), the UNIDO code of conduct or the biotechnology regulations at the US Environmental Protection Agency and Department of Agriculture. However,... the scope of what is to be subject to case-bycase review has been narrowed in a way that encompasses only organisms modified with the newer, molecular techniques and is wholly unrelated to the likelihood of risk that might be posed by their testing or use. This violates the fundamental principle of regulation: that the degree of oversight should be commensurate with risk. (p. 186) Miller refers to a 1993 document by UNEP (UN Environmental Program), which states that GMOs require special regulation, because there is "generally less familiarity with the behaviour of organisms whose genetic make-up is unlikely to develop naturally, such as organisms produced by modern genetic modification techniques, than with the behaviour of organisms developed traditionally" (p. 187). Miller's comments are scathing:

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These are precisely the rationales that the scientific community has repudiated consistently and categorically over the past 15 years. The UNEP document confuses various concepts, including novelty, familiarity and risk. The introduction of a new gene . . . does not necessarily affect an organism's risk. For example, a microorganism or plant may have been modified to carry a biochemical or visual marker (such as firefly luciferase, the protein that makes the insects glow in the dark) introduced by recombinant DNA techniques. If the host organism is known to pose negligible risk and the introduced gene does not make the new construct somehow 'unfamiliar' with respect to risk, then the modified organism should be treated no differently then the host organism or organisms with similar traits modified by traditional techniques. Comments Miller appears to presuppose that we are able, in principle, to predict environmental harms and other risks of GMOs in the environment. Let us inspect his luciferase example. His hypothetical GMO contains the genes of the host organism and, added to this, genes responsible for the synthesis of luciferase. Miller apparently reasons here as follows: The host organism poses negligible risk. This is also true for organisms with the luciferase gene or genes. Therefore, the host genes together with the luciferase gene(s) add up to pose negligible risk. Opponents of this view, including us, would point out that genes interact in numerous ways, and that the expression of a gene depends on the genetic context (see Text 38). We therefore cannot simply add up risks observed in different contexts, and we cannot in this way predict risks of genetic engineering. No good arguments exist to explain why products of genetic engineering techniques and products of traditional breeding techniques would pose similar risks. For all we know, the breakdown of species barriers in genetic engineering may yield products that are much more hazardous than products from traditional techniques. Miller rightly states that we should focus on risks of products, and that processes leading to the products should not be our primary concern. However, he presupposes without arguments that we already know that traditional techniques and modern techniques are similar with respect to risks of products. We would reconstruct his argument as follows.

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Premise 1. Products in category X obtained by traditional methods pose no risks. Premise 2. Products in category 7 obtained by genetic engineering are similar to products in category Xin all features affecting risk. Conclusion. Products in category Fpose no risks. This is a valid deductive argument. A long experience with traditional breeding might enable us to confirm Premise 1. However, we do not at present have the means to assess the truth or falsity of Premise 2. The premises therefore fail to support the conclusion. Our comments appear to justify the rejection of Miller's claim that no need exists for special regulation of genetically engineered organisms in the environment.

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Chapter 7

Miscellaneous Subjects

TEXT 41 GENETICS AS OUR FUTURE SAVIOR? Source: Schwartz, W.B. Life Without Disease: The Pursuit of Medical Utopia. Berkeley: University of California Press, 1998. Level: elementary Criteria and guidelines: G5, G8 Related texts: 14, 15 Schwartz thinks that modem genetics holds the pivotal cues for future treatments of diseases. The decade or two ahead of us will be a transitional period in which many of the engineering techniques of the past two decades are perfected and new ones, targeted at cellular and subcellular processes, make their debut. In particular, molecular medicine will begin to exploit the critical role genes play in human health and disease.... Molecular medicine in these decades will only begin to fulfill its revolutionary potential, and will do so predominantly in the areas of diagnosis and genetic screening. It will almost certainly take longer for a full range of useful therapeutic interventions to develop;... In the near term, the fruits of both bioengineering and molecular medicine will offer interim solutions to clinical problems: sophisticated and effective tools for mitigating the effects of disease and repairing

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its destructive consequences, but not yet the means of derailing disease at its genetic origins, (p. 65) Comments Optimism, among researchers subscribing to views like those of Schwartz, is generating massive funding for projects such as the human genome project, which selectively emphasize causal roles of genes. Considering Schwartz's stance, we ask: What about environmental pollution, work overloads due to our overcompetitive society, viruses such as the HIV, and so forth? The environment is entirely disregarded in Schwartz's book. Nowhere does he provide a substantive argument why genes should be more salient causally than the environment. We should suspect that researchers aiming to get funds on the basis of one-sided views as presented by Schwartz run the risk of getting dirty hands. TEXT 42 MAKE ROOM FOR MOLECULAR CELL BIOLOGY Source: Lodish, H., et al. Molecular Cell Biology. 4th ed. New York: Freeman and Company, 2000. Level: elementary, but requires some knowledge of molecular biology Criteria and guidelines: G8, G9, G10 Related texts: 14, 15, 18, 21 Many researchers currently appear to think that life must ultimately be explained by principles of molecular biology. The book by Lodish and colleagues—just as most textbooks in molecular biology—accords well with this view. Paralleling the work on genomic analysis, biochemists and structural biologists are collaborating to determine through structural studies all the possible folds that protein domains assume in order to expand our knowledge of the interactions between the cell's principal macromolecules, namely, protein-protein, protein-RNA, and protein-DNA interactions. The fundamental principles of interaction and a catalogue of typical macromolecular interactions will be in the hands of scientists early in the twenty-first century.

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Much of current biological research, and that in the next few years, is focused on discovering how these molecular interactions endow cells with decision-making capacity and their special properties. For this reason several of the following chapters describe current knowledge about how such interactions regulate RNA and DNA synthesis and how such regulation endows cells with the capacity to become specialized and grow into complicated organs, (p. 134) Comments We regard this passage as an example of causal selectivism for the following reason: The entire process of ontogenesis is influenced by molecular processes—and other processes—inside the organism, environmental factors in the domain of ecology, and interactions between these processes. To understand the developing organism, we therefore need ecology in addition to physiology and biochemistry. Lodish and colleagues implicitly assume, without arguments, that ecology is less important than molecular biology.

TEXT 43 STRESS IN PLANTS Source: Taiz, L. and E. Zeiger. Plant Physiology. 2nd ed. Sunderland, MA: Sinauer Associates, 1998. Level: elementary Criteria and guidelines: G7 Related text: 36 Note. Our book has a separate chapter on stress. That chapter concerns interrelated areas of science with approaches that deviate considerably from approaches of stress in plant physiology—and in ecology. That is why Text 43 has been kept outside the chapter on stress. Organisms are found in almost all environments on the Earth, but harsh environments are tolerated by less species than mild environments. Harsh environments are said to represent stress. The passage below from a chapter summary in the book by Taiz and Zeiger represents a common view of stress in plant physiology—and in ecology.

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Stress is usually defined as an external factor that exerts a disadvantageous influence on the plant. Under both natural and agricultural conditions, plants are exposed to unfavorable environments that result in some degree of stress. Water deficit, chilling and freezing, heat stress and heat shock, salinity, oxygen deficiency, and air pollution are major stress factors restricting plant growth so that biomass or agronomic yields at the end of the season express only a fraction of the plant's genetic potential. The capacity of plants to cope with unfavorable environments is known as stress resistance. Plant adaptations that confer stress resistance, such as CAM metabolism, are genetically determined. Acclimation improves resistance as a result of prior exposure of a plant to stress. (Pp. 754-755) The authors subsequently survey mechanisms whereby some species are able to tolerate particular forms of stress: drought, low or high temperatures, high salinity, low oxygen levels, and so forth. Comments Stress—as here defined—is a relation between environments and organisms. An environment may exert a disadvantageous influence on a species, whereas it does not harm a different species. In this situation, a particular factor may represent stress for one species, but not for another species. Therefore, the general notion of stress resistance is in fact a misnomer. However, we need such misnomers in science. If all connotations of general terms were spelled out in detail, we would end up with a mess of unmanageable technical details. No reason exists to oppose the conceptualizations of Taiz and Zeiger. We should be aware, however, that any casual reading of science texts may mislead us, as limitations of language alone force scientists to leave implicit many assumptions. It is obviously futile to search for general laws of stress or for a general theory of stress. Researchers have to be content with low-level theories: Particular extreme conditions are not tolerated by many species, whereas other species are adapted to these conditions in diverse ways. Taiz and Zeiger are well aware of this, but the uninitiated reader may easily overlook it.

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TEXT 44 POPULATION BOMB OR PERNICIOUS POLITICS? Source: Vandermeer, J. Reconstructing Biology: Genetics and Ecology in the New World Order. New York: Wiley, 1996. Level: elementary Criteria and guidelines: Gl, G2, G4, G5, G7, G8, G10, G13 Related texts: 30, 31 The "population problem" is salient in global politics. However, we should not always take for granted sayings of politicians and scientists addressing the problem. The recent history of Guatemala should serve here as a shocking reminder. Guatemala is a poor country. Many peasants there are trying in vain to lay their hands on a tiny plot of land. Those who have some land, barely manage to make a living. This situation naturally invites deforestation, which is indeed in progress. In this country, farmers without land migrate to the cities, where they live in shacks while fending off starvation with meager help from the social service. Situations as exist in Guatemala are often attributed to adversity caused by uncontrolled population growth. Ecologists know about this: A population crash may occasionally set in, when the density of a population exceeds the carrying capacity of the area where the population lives. Considering our own species, we can see the threat of such crashes as inviting the nightmare of doomsday scenarios. These scenarios are known as "the population problem." From a common perspective, excessive population density is indeed the salient cause of adversity in Guatemala—and, more generally, developing countries in the world. This appears to call for the normative stance: Population densities in poor countries should not increase; they had better decrease. That is how the story goes for Guatemala. There is truth in it, but a reconstruction of history yields a different story. Here is how Vandermeer (pp. 381-385) reconstmcts the history of Guatemala; we provide a brief summary. The end of the nineteenth century witnessed a boom of banana culture. Merchants from the United States developed great companies in Guatemala, most notably the United Fruit Company, which acquired vast stretches of land. The company was enormously successful, but the farmers were chased to marginal, infertile land. Poverty set in, and protest movements germi-

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nated. The situation became explosive. But in 1950 a candidate for the presidency, Jacobo Arbenz, promised that he would redistribute the land by reforms. He was elected, and he initiated the promised reforms. One hundred thousand peasants received a plot of land. An urgent population problem could have been resolved in the wake of this, almost in one stroke. The situation was not to remain this way. The United Fruit Company was adequately compensated financially for the land it lost—land that it did not use. However, politicians and merchants in the United States did not appreciate the course that developments were taking. They were afraid: Other countries could follow Guatemala's example, and valuable opportunities for investment might then be lost. Furthermore, they thought that they were looking at communism in progress. "Fortunately," some powerful persons saw opportunities for a "remedy" of the situation. The minister of the exterior, John Foster Dulles, had an important function in the law firm of the United Fruit Company, and his brother happened to be head of the CIA. They convinced President Eisenhower and Vice-President Nixon that action should be taken. In 1954, the CIA decided that an unimportant colonel in the army of Guatemala, Castillo Armas, should lead a revolution against the parliament. The CIA managed to convince Arbenz that Armas had a huge army at his disposal—a lie—and that the U.S. army was willing to support him immediately—an empty threat not known as such to Arbenz. To prevent a major bloodshed, Arbenz gave way to the revolutionaries. That was the beginnig of an era of dictatorship and poverty in Guatemala. This is by no means the only example of the United States causing a population problem elsewhere. In the 1980s, for example, similar events took place in Nicaragua. Considering these historical events, we should not regard increasing population densities as the salient cause of adversities in these countries. Comments We applaud the daring, accessible analysis by Vandermeer. Its implications are profound. It is true that increasing population densities are locally a salient cause of environmental problems and poverty. But we should not generalize. General biological theories about the growth of populations and carrying capacities do tell us much about dangers facing man. But their relevance is context-dependent.

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If we regard population growth as a salient cause of adversity throughout the developing world, then we are making a grave mistake of causal selectivism. Such a mistake may have serious consequences. It is politically convenient but highly misleading to describe the situation in Guatemala as an example of "the population problem." Such a description would lack generalist backing, and it would foster unacceptable forms of theorizing, and unpalatable politics. The description is discredited immediately once appropriate sources are checked. Considering Guatemala, we would conjecture that those who promulgate the population myth have dirty hands. The idea that population densities are now a salient cause of poverty is inconsistent with documented effects of dictatorship. TEXT 45 SHORTCOMINGS OF BIOMEDICINE: THE CHRONIC FATIGUE SYNDROME Source: Van der Steen, W. J. Chronic fatigue syndrome: A matter of enzyme deficiencies? Medical Hypotheses 54: 853-854, 2000. Level: elementary Criteria and guidelines: Gl, G2, G4, G8, G10 Related texts: 16, 18, 22, 23 The incidence of chronic fatigue—an elusive syndrome—is increasing at alarming rates. Putative causes of the syndrome are controversial; in fact we are facing ignorance. The ignorance is partly caused by one-sidedness in biomedicine. I (WJS) include here elements from an article of mine that illustrates some of the guidelines formulated in Part II. A couple of years ago, I became interested in chronic fatigue syndrome (CFS), since some persons I know suffer from it. The incidence of this syndrome—which is incapacitating—is high, and it is still increasing. One often hears that the etiology of CFS is a mystery. In the past, patients suffering from the syndrome have generally been approached with the suggestion that they fabricate a pseudo-disease. Fortunately, this suggestion is now less common. The main problem is now, rather, that existing views vaccillate between a biomedical approach and approaches focusing on psychology and psychiatry. In my country, the Netherlands—and also in Belgium and in the UK—the swing of the pendulum is, at present, toward psychology and psychiatry, with the main focus on cognitive behavior

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therapy. Competition among groups of scientists aiming at funding at times enhances this tendency in a biased way. I deplore this development: My article warrants the thesis that the potential for biomedicine to explain aspects of CFS is underestimated. The idea that the etiology of CFS is a mystery is indeed common. I saw its being voiced, for example, during television interviews in the Netherlands. Indeed, a well-known medical professional pronounced that much. I then decided to test putative common knowledge by a search of the literature. The test confirmed common wisdom for articles that explicitly deal with CFS: These articles do not have much to offer in the way of etiology and treatment. At best, they formulate tentative hypotheses that remain to be tested. I enlarged the scope of my research to encompass muscle fatigue in general. Here is what I uncovered. Muscle fatigue is a symptom in many diseases and syndromes besides CFS. It is a characteristic feature in patients suffering from enzyme deficiencies, in particular acyl CoA dehydrogenase deficiency, myoadenylate deaminase deficiency, and many types of glycogenoses. Handbooks about such deficiencies report that patients suffering from them are plagued by nasty symptoms—in addition to muscle fatigue and other symptoms that are also common in CFS patients. However, a thorough search of the literature showed that, for almost all the deficiencies, patients are known who do not have the nasty symtoms that are missing in CFS. If their deficiency had not been known, these patients would probably have received the diagnosis of CFS. I have talked about this with several medical professionals. They voiced the opinion that specialists of CFS will know about my point, and that they would take care to look for enzyme deficiencies in medical practice. However, further inquiries among specialists and patients showed that few of them know about it. This is deplorable, not least, because some so-called CFS-patients could benefit from a known treatment: Some of the patients who have an acyl coA dehydrogenase deficiency, could benefit from a simple treatment with vitamin B2. Later on, I discussed the matter with a medical professional working for an organization of patients with muscular diseases. She read my article, and commented that my point was in the process of getting the attention of some specialists. We failed to recognize this earlier, she said, because symptoms of enzyme deficiencies mostly develop at a young age, whereas CFS mostly develops later. (But, I could have commented, exceptions concerning age have been described in the literature over several years.)

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The lacuna I uncovered should have been spotted years ago. I presume that several factors have combined to leave it undetected. First, medical practitioners seldom have the time for thorough searches of the literature. Second, medicine increasingly suffers from superspecalization, so that relevant sources outside the context of a specialist domain are often disregarded within the domain. Third, medical professionals may not be sufficiently aware of biological variability; this invites causal selectivism. In any case, once the CFS label is attached to patients, they are viewed by professionals from a restrictive domain of theorizing. My enzyme hypothesis may be false, or it may apply only to few CFS patients. Just now, we do not know, because the hypothesis is outside ongoing research. I conjecture that a generalist search of the literature, aided by common sense, should uncover additional potential explanations of CFS, and that the CFS situation is by no means an anomaly in medicine.

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PART IV A Tale of Nonsteroid Anti-Inflammatory Drugs

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Chapter 1

Introduction

Many themes have been clustered in ever-changing combinations in the foregoing parts of the book, since we aimed at targets ranging from elementary academic teaching to advanced interdisciplinary research. We are aware that our goals have been ambitious. The reader will have to judge in what respects we have been successful. We would be content already if a few readers had assimilated materials from the text to ameliorate some project of theirs—scientifically, morally, or otherwise. The combined mixtures of themes presented so far, would fall short of optimal cohesiveness; therefore we have decided to supplement them with a case study that is more cohesive and extensive than those in Part III. The case study concerns nonsteroid anti-inflammatory drugs (NSAIDs for short). A text on NSAIDs prepared by one of us (WJS) is reproduced here together with invited responses. Before presenting it, we briefly indicate how it implicates the guidelines presented in Part II. Research on NSAIDs mostly belongs to the context of studies funded by the pharmaceutical industry. Research in this context illustrates intrinsic links between ethics and the methodology of science (Gl), as it fosters particular methodologies. The assessment of this research calls for a generalist approach of the literature, since articles in the mainstream disregard particular etiological factors and allied therapies. Also, many mainstream articles disregard some methodological problems with controlled trials that have been uncovered elsewhere (G2, G4). This need not imply that mainstream research is

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inadequate in itself (G3). The issue here is rather that we should not rely overmuch on specialist research done in one particular context. Sources mentioned in the text indicate that some professionals concerned with NSAIDs have dirty hands (G5). A reconstruction of the methodology underlying much research on NSAIDs—and research elsewhere in medicine—reveals sources of bias (G6). For example, classifications of etiological factors often amalgamate two dichotomies, biological versus psychosocial factors and internal versus external factors. This has the result that ecological factors such as diet do not get the attention they deserve. Few researchers working on NSAIDs consider diet therapies. This may add to bias due to funding by the industry. Controlled trials dealing with NSAIDs easily foster general claims implying that they have positive effects (G7). We should take care not to act on overly general claims, because side effects may be relatively common, and dangerous for elderly persons. Research on NSAIDs as a treatment for rheumatoid arthritis often focuses on molecular biology at the cost of promising ecological approaches (G9). We do not know much about the mechanism of action of NSAIDs. Virtually nothing was known about it as the drugs appeared on the market for the first time. The label "anti-inflammatory" may indeed be a misnomer. Nowadays the drugs are also used to alleviate pain with unknown etiology. It the drugs had been introduced originally with this use in mind, the name NSAIDs might not have been chosen. Such seemingly trivial matters of terminology may have implications for scientific theory and for applied science (G10). A generalist approach of research on NSAIDs uncovers salient points that are sorely missing in many articles (Gil). Researchers may mention funding by the industry in the acknowledgments. In the main text, they will not be explicit about relations between funding and the subjects and approaches taken. Such relations should be an important theme in the assessment of research (G12). A generalist overview of the literature reveals a major tension on the verge of inconsistency (G13): NSAIDs are prescribed on a massive scale, even though dangerous side effects are common. Many articles on NSAIDs contain brief passages in which an anti-inflammatory mechanisms of action, putative effects of the drugs on symptoms, and domains of application are mentioned in one stroke, admittedly together with references. These things are seldom worked out, since editors want articles to be succinct. A responsible elaboration of texts would show in

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many cases, that our putative knowledge is not as reliable as many authors would have it (G14). Lastly, we would applaud the use of much common sense as a supplement to technical articles concerning NSAIDs (G15). Three responses follow the text by WJS. Response 1 by Harry Cook does not concern NSAIDs. However, we felt that it should be included here, as it illustrates our themes from a different, important angle: Interactions between medicine and the industry may take nasty forms that threaten individual researchers who do not wish to comply with biased research. Response 2, by Dorine Bax, supplements my themes in a different way: She points out that relationships between conventional medicine and alternative medicine take on a new character in view of bias existing in conventional approaches. Response 1 and Response 2 accord well with our view, but Response 3, by Arjen Groen, is critical. Arjen Groen, a general practitioner, presents research concerning NSAIDs in medical practice in the Netherlands, and its implications. I (WJS) have a brief reply. First, I plead guilty. I have not been sufficiently aware of our own guideline concerning contextdependence! AG shows that the use of NSAIDs is not as irresponsible as we suggest in the context of medicine done by general practitioners (not specialist practice) in the Netherlands. Second, huge differences among countries exist in medical theory, medical practice, and the social setting of both. For example, it is normal for patients in the United States to visit specialists of their own choosing for primary consultation, while patients in the Netherlands are mostly referred to specialists via a general practitioner. So, Groen's points need not invalidate my text, but it does indicate that much more context should have been made explicit.

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Chapter 2

Biased Promotion of Drugs: The Case of NSAIDs Wim J. van der Steen Cultural factors affect science. Few researchers would deny this. Sociologists of science considering medicine are explicit about the influence of cultural factors on science, but few of them would take their cues from primary sources in medical research. Conversely, medical researchers in their writings seldom consider how culture affects their work. I aim to demonstrate that this discrepancy is unfortunate, by a case study that reveals profound negative effects of cultural factors in medical research and medical practice. My subject is a class of drugs—nonsteroid anti-inflammatory dmgs, or NSAIDs—that are used on a massive scale, although they have serious side effects. Overuse of these dmgs is caused by several forms of bias that are seldom investigated in medicine. Regulation has been biased in favor of the pharmaceutical industry to the detriment of patients. Furthermore, researchers funded by a pharmaceutical industry manufacturing a dmg tend to produce biased reports in favor of the drug. Medical research is also biased by its focus on drug therapies. Diet therapies may be equally effective and without serious side effects. Furthermore, inappropriate prescriptions are common. Some forms of bias are unavoidable. For example, the methodology chosen for controlled studies depends on ethical decisions. All the forms of bias deserve more scrutiny. It is in any case desirable that we reduce the use of NSAIDs.

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EFFECTS OF NSAIDs Many studies indicate that NSAIDs may palliate symptoms in inflammatory diseases such as rheumatoid arthritis. But the dmgs have dangerous side effects also. A recent study notes that 10^40 percent of elderly people in the populations studied use NSAIDs, even though the dmgs frequently have gastrointestinal side effects. NSAIDs increase the risk of peptic ulcer complications by three- to five-fold; estimates for several different populations indicate that 15-35 percent of all peptic ulcer complications are due to NSAIDs. In the United States alone, there are an estimated 41,000 hospitalizations and 3,300 deaths each year among the elderly that are associated with NSAIDs (Griffin, 1998). Another study concerning the United States, even presents an estimate as high as 20,000 deaths yearly (Wolfe, 1996). Any cursory inspection of the literature will uncover many articles with a similar message. Doubts about he alleged benefits of NSAIDs do exist. One source describes recent data regarding the prognosis of rheumatoid arthritis with the use of the current drug treatments as "gloomy" (Odeh, 1997), and according to another source, most standard medical approaches to treatment have had little or no impact on the course of rheumatoid disease (Schiff, 1997). Furthermore, we should not simply take positive data in the literature for granted. Controlled trials concerning drugs in rheumatoid arthritis are often problematic due to pitfalls concerning outcome measures, patient populations, characteristics of the study design, and economic evaluation (Ortiz et al., 1997). Impressions concerning the long-term natural history and results of therapy are strongly influenced by the types of measures and study designs used to assess patient status and outcomes (Pincus, 1995). Randomized controlled trials are often a poor measure of long-term outcomes (Pincus and Stein, 1997; Simon, 1995). A BROAD PERSPECTIVE How should we explain the massive use of NSAIDs? The most obvious answer would be that NSAIDs, according to controlled trials, alleviate symptoms of inflammation, and that the overall balance of evidence warrants continued usage, even though dangerous side effects exist. This answer is unsatisfactory. It presupposes that the research is unbiased, and that it affects practice in an unbiased way. I would assume that the widespread use of NSAIDs does not sit well with the observed side effects, and that it points to undesirable forms of bias. Let me review some potential sources of bias.

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Abraham offers a detailed survey spanning decades of NSAID regulation in the United States and in the United Kingdom (Abraham, 1995). The survey demonstrates that research by the pharmaceutical industry on benefits and side effects of NSAIDs has been biased in favor of its own products. That should not surprise us. Surprising is incontrovertible evidence that authorities responsible for regulation have, on a grand scale, acted in violation of their own guidelines. This attitude has favored the industry to the detriment of patients. Many dangerous NSAIDs now on the market should never have been approved for sale. Bias in favor of the industry may also exist in medical research itself. The chances that researchers observe positive effects of NSAIDs are way above average if they are paid by the industry manufacturing the drugs (Goetsche, 1989). Medical practice also appears to be biased in favor of NSAIDs, since unnecessary prescriptions are very common (Coste et al., 1995; Tamblyn et al., 1997). Furthermore, despite the side effects noted, the use of NSAIDs is fostered by their being available as over-the-counter dmgs. These kinds of bias could be avoided in principle, but other forms of bias are unavoidable. Consider the problem of false positives (statistical type I errors) and false negatives (statistical type II errors). Of course, we should aim at tests ensuring that the probabilities of errors of either kind are low. However, we cannot have it both ways, as a decrease in one type of error logically entails an increase in the other type of error (with a given sample size and effect size). Thus, the methodological set up of our research depends on ethical considerations concerning the acceptability of particular errors (Cranor, 1992). This justifies the more general claim that ideal experiments cannot satisfy all methodological requirements at the same time. We have to prioritize requirements, and that cannot be done without ethical considerations (Van der Steen, 1995). As I noted, some medical researchers have argued that the methodological set up of experiments affects conclusions about the value of NSAIDs. We should add to this that the choice of a methodology is determined, in part, by ethical issues that are seldom made explicit in medical research. They should be brought out into the open. We are not dealing here with bias in a pejorative sense, because we have to opt for some methodology, but we should be aware of normative presuppositions. Error types in drug tests affect patients and the industry in different way. In the interest of patients, we would like to minimize type I errors of falsely attributing positive effects to drugs. However, the industry would rather benefit from low levels of type II errors of falsely attributing no effects to

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dmgs. In most research, significance testing is done without power analysis. This allows for type I errors at the standard 5 percent level, while type II errors remain unknown. If tests of a dmg are repeated over and over again, a common practice nowadays, we will sooner or later get a significant result due to a type I error. To the extent that drugs are marketed on the basis of this, the type I error level is inflated while the type II error level is decreased, and we get a bias in favor of the industry, to the detriment of patients. Patients and the industry also have different interests in the study of adverse side effects. The trouble is here that methodologically proper tests are hardly feasible since the set of potential side effects is open-ended, and guidelines for the time scale of experiments are arbitrary. In the interest of patients, we should aim at comprehensive short-term and long-term studies, but this would not be acceptable for the industry. In practice, comprehensive long-term studies are rare, which again favors the industry. Next, controlled experiments are problematic if drugs are compared with a placebo without side effects. The chances are that this will generate false positives when patients conclude from experienced side effects that they are receiving the drug rather than the placebo. This kind of phenomenon has, on a grand scale, resulted in inappropriate dmg treatments in psychiatry (Jacobs, 1995). Medical research may also be biased in that the choice of subjects to be investigated is one-sided. Concerning therapies for rheumatoid arthritis, research reveals a pronounced bias in favor of drugs. When I wrote an earlier version of this text in August 1999, Medline listed as many as 11,017 articles on dmg therapy, but only 126 articles on diet therapy. This fits in with the pervasive negligence of ecology in medical research and in medical practice described by several authors (Chivian et al., 1993; Garrett, 1994; Van der Steen, 1998a). The negligence of ecology is inappropriate and unfortunate, because diet therapy does seem to have positive effects. Particular diets, or components of diet, most notably particular unsaturated fatty acids, reduce disease activity in rheumatoid arthritis (Ariza-Ariza et al., 1998; DeLuca et al., 1995; James and Cleland, 1997; Rothman et al., 1995). The therapeutic effect of these diets may indeed indicate that food plays a role in etiology. It is conceivable that poor diet is among the factors which predispose toward the disease (Kowsari et al., 1983; Morgan et al., 1993). Poor diet in our culture may be due in part by inappropriate food processing: Modem techniques of food processing cause the destruction of natural components of diets, not least unsaturated fatty acids including essential ones. This

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contributes to the etiology of degenerative and systemic diseases (Erasmus, 1995); rheumatoid arthritis may be a case in point. The emphasis in medical research on pathology is now overwhelmingly on genetics and molecular biology. In part, this may be explained by history: medicine developed biological approaches prior to the emergence of ecology. Furthermore, this emphasis fits in with current reductionistic paradigms: These paradigms foster a self-perpetuating bias. Considering genetics, I have elsewhere explained how this works, by an analysis of research on schizophrenia (Van der Steen, 1998b). Twin studies have shown that concordance for schizophrenia is much higher in identical twins than in nonidentical twins. Researchers have concluded from this that genes are implicated in etiology. The following counterexample shows how problematic this is. Suppose, a number of twin pairs are on a trip in a coastal plain. A flood wrecks the trip. Tall individuals survive, but short individuals drown since they cannot keep their heads above the water. Identical twins will show a higher concordance than nonidentical twins. If we followed the logic of schizophrenia research, we should conclude that genetic factors rather than the flood have been causally responsible for the drowning. Something is obviously wrong with the logic of common research. Researchers in psychiatry and in many areas of medicine do admit that the environment modifies the effects of genetic factors. However, they commonly conceptualize the environment as the psychosocial environment. Ecological factors are simply disregarded. CONCLUSIONS NSAIDs are reported to alleviate symptoms in inflammatory diseases. This may be tme, but we should beware of exaggerating positive effects, and we should realize that short-term benefits may not be extrapolatable. The pervasive use of these drugs is indeed problematic in view of serious side effects. If we wish to assess NSAIDs, we should not be content with an appraisal of existing controlled trials, because it is impossible to detect all sources of bias in this way. Research mostly conducted outside medicine itself has revealed many sources of cultural bias. Drug regulation is biased in favor of the pharmaceutical industry. The same is true for medical research funded by the industry. Furthermore, the emphasis in research is overmuch on dmg therapy, even though less dangerous treatments such as diet therapy may be equally effective.

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It is desirable that medical journals pay more attention to these forms of bias. More research is needed on alternative treatments, particularly diet therapy. The highest priority should go to trials that aim to compare dmg therapies with diet therapies. We might save thousands of lives if we replace dmg therapies with diet therapies.

REFERENCES Abraham, J. 1995. Science, Politics and the Pharmaceutical Industry: Controversy and Bias in Drug Regulation. London: UCL Press. Ariza-Ariza, R., Mestanza-Peralta, M., and Cardiel, M.H. 1998. Omega-3 fatty acids in rheumatoid arthritis: An overview. Seminars in Arthritis and Rheumatism 27: 366-370. Chivian, E., McCally, M., Hu, H., and Haines, A. 1993. Critical Condition: Human Health and the Environment. Cambridge, MA: MIT Press. Coste, J., Hanotin, C , and Leutenegger, E. 1995. [Prescription of non-steroidal anti-inflammatory agents and risk of iatrogenic adverse effects: a survey of 1072 French general practitioners] [French]. Therapie 50: 265-270. Cranor, C.F. 1992. Regulating Toxic Substances: A Philosophy of Science and the Law. New York: Oxford University Press. DeLuca, P., Rothman, D., Zurier, R.B. 1995. Marine and botanical lipids as immunomodulatory and therapeutic agents in the treatment of rheumatoid arthritis. Rheumatic Diseases in the Clinics ojNorth America 21: 759-777. Erasmus, U. 1995. Fats That Heal, Fats That Kill 3rd ed. Burnaby: Alive Books. Garrett, L. 1994. The Coming Plague: Newly Emerging Diseases in a World Out of Balance. New York: Farrar, Straus, and Giroux. Goetsche, P.C. 1989. Methodology and overt and hidden bias in reports in 196 double-blind trials of nonsteroid anti-inflammatory drugs in rheumatoid arthritis. Controlled Clinical Trials 10: 31-56. Griffin, M.R. 1998. Epidemiology of nonsteroidal anti-inflammatory drug-associated gastrointestinal injury. American Journal of Medicine 104: 23S-29S, 41S-^2S. Jacobs, D.H. 1995. Psychiatric drugging: Forty years of pseudo-science, self-interest, and indifference to harm. Journal of Mind and Behavior 16: 421^70. James, MJ. and Cleland, L.G. 1997. Dietary n-3 fatty acids and therapy for rheumatoid arthritis. Seminars in Arthritis and Rheumatism 27:85-97. Kowsari, B., Finnie, S.K., Carter, R.L., et al. Assessment of the diet of patients with rheumatoid arthritis and osteoarthritis. Journal of the American Dietetic Association 82: 657-659. Morgan, S.L., Hine, R.J., Vaughn, W.H., Brown, A. 1993. Dietary intake and circulating vitamin levels of rheumatoid arthritis patients treated with methotrexate. Arthritis Care Research 6: 4-10.

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Odeh, M. 1997. New insights into the pathogenesis and treatment of rheumatoid arthritis. Immunopathology 83: 103-116. Ortiz, Z., Tugwell, P., and Yocum, D. 1997. The design of clinical trials aimed at assessing the DC-ART properties of new molecules in rheumatoid arthritis. Clinical and Experimental Rheumatology. 15: S39-S44. Pincus T. 1995. Assessment of long-term outcomes of rheumatoid arthritis. How choices of measures and study designs may lead to apparently different conclusions. Rheumatic Diseases in the Clinics of North America 21: 619654. Pincus, T, and Stein, CM. 1997. Why randomized controlled clinical trials do not depict accurately long-term outcomes in rheumatoid arthritis: Some explanations and suggestions for future studies. Clinical and Experimental Rheumatology. 15: S27-38. Rothman, D., DeLuca, P. and Zurier, R.B. 1995. Botanical lipids: Effects on inflammation, immune responses, and rheumatoid arthritis. Seminars in Arthritis and Rheumatism 25: 87-96. Schiff, M. 1997. Emerging treatments for rheumatoid arthritis. American Journal ofMedicine 102: 11S-15S. Simon, L.S. 1995. Actions and toxicity of nonsteroidal anti-inflammatory drugs. Current Opinion in Rheumatology 7:159-166. Tamblyn, R., Berkson L., Dauphinee, W.D. et al. 1997. Unnecessary prescribing of NSAIDs and the management of NSAID-related gastropathy in medical practice. Annals of Internal Medicine 127: 429-438. Van der Steen, WJ. 1995. Facts, Values, and Methodology: A New Approach to Ethics. Amsterdam: Rodopi. Van der Steen, WJ. 1998a. Forging links between philosophy, ethics, and the life sciences: A tale of disciplines and trenches. History and Philosophy of the Life Sciences 20: 233-248. Van der Steen, WJ. 1998b. Bias in behavior genetics: An ecological perspective. Acta Biotheoretica 46: 369-377. Wolfe, M.M. 1996. NSAIDs and the gastrointestinal mucosa. Hospital Practice 31: 37-44, 47-48.

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Chapter 3

Responses

RESPONSE 1 Harry Cook, a Professor of Biology, emeritus, at King's University College in Edmonton, Canada, carries out research on the history and theory of biology. He provides examples showing that the influences of the pharmaceutical industry on medical professionals may take nasty forms. He proposes measures to improve on the existing situation. He does not consider NSAIDs, but his points are well worth taking note of, and they tally with Van der Steen's text. Private D r u g R e s e a r c h Harry Cook E m e r i t u s Professor of Biology, Canada When scientists at public institutions are funded by private, profit-seeking companies, conflict of interests can arise. Specifically, the testing of pharmaceuticals for drug companies on patients at public hospitals can lead to such conflicts. In North America, the operation of hospitals and medical care plans are topics of controversy and debate. And, as I hope to show in this article, when it comes to the clinical testing of pharmaceuticals, the ethics that should guide us are not clear. While medical research laboratories in universities and university hospitals can play an important role in the development of pharmaceuticals, more and more of this development is taking place under the aegis of private firms.

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When researchers at universities make a medical discovery, the testing and marketing related to products that result from this discovery are often carried out by a private firm. Testing of drugs can bring considerable financial benefits to a university, hospital, or a medical investigator. It would be difficult for the university to develop, market, and test drugs without the collaboration of a pharmaceutical company. And, conversely, it is almost impossible for drug companies to test new products without the cooperation of hospitals. The development of patented drugs makes large profits possible for pharmaceutical companies, and this development carries with it the need to carry out extensive trials to determine the safety and efficacy of these drugs. In this brief article I will examine whether the testing of pharmaceuticals in hospitals operated by governments or private organizations will benefit those people on whom they are tested, those who are most in need of them, or whether this testing is largely for the benefit of the companies that are developing the new drugs. An example from a hospital in Toronto, Canada, will illustrate the difficulties that can arise in the development and testing of pharmaceuticals. Dr. Nancy Olivieri, a blood specialist who carries out research at Toronto's Hospital for Sick Children has experienced these problematics first-hand. When treating patients with thalassemia, blood transfusions are often necessary. This causes another problem: Accumulations of iron in the body that threaten the well being of the patient. A drug that can prevent these accumulations, deferiprone, which is used routinely in some British hospitals, caused some very undesirable side effects in her patients, Olivieri suggests. Olivieri had signed an agreement with the pharmaceutical company that was marketing and testing the drug: In return for receiving financing to study the drug, she promised to keep the results of the study confidential and to turn over these results to the drug company. Because of the undesirable side effects, Olivieri felt duty-bound to make the results of the tests public. Publication of the results led to her dismissal from the hospital. Subsequent events read like a melodrama, and I will not describe them in this article. Jane O'Hara, in an article in Maclean's, a Canadian weekly news magazine, published a cover story on the Olivieri case on November 16, 1998. The article focuses on an aspect of the story that some others have ignored: whether it is desirable to have large portions of the budgets of public hospitals funded by the testing of drugs that are being marketed by private companies. O'Hara adds:

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Still, the furor has the research community hotly debating the potential for corporate interests to manipulate scientific results. With hospitals and universities around the world becoming increasingly dependent on money from the pharmaceutical industry, the Olivieri case has shone a spotlight on the conflicting pressures facing medical researchers trained to pursue the truth. The Hospital for Sick Children's Chief Executive Officer rejects the idea that hospital has sold out to the drug company that markets deferiprone. However, Dr. Robert Rango, a clinical pharmacologist in Vancouver, suggests that there can be all kinds of coercion to obtain positive evaluations of drugs, and to facilitate the approval process. Dr. R. A. Deyo and co-workers, in an article in The New England Journal of Medicine (April 17, 1997, pp. 1176-1180) state that the "huge financial implications of many research studies invite vigorous attack." They suggest that the research and testing of drugs should be shielded from external pressures and interference, and that there should be a screening process for allegations of misconduct. Research universities should play an important role in the development and testing of pharmaceuticals, these writers advise. As we consider the implications of the commercialization of the development and testing of drugs, and related problems for medical researchers, for hospitals and universities, that these processes can lead to, it is important that the medical community address the following five issues: 1. Testing of drugs should be free from interference by the company that is developing these drugs. 2. An agreement, between a hospital and a pharmaceutical company, to test a particular drug should not preclude other treatment regimes, if it is in the interest of the patient, or if the patient indicates a preference for the other regimes. 3. A drug testing agreement at a treatment facility should not compromise the freedom of patients to receive the treatment that is best for their particular condition. 4. The various interests, of hospital, researcher, and pharmaceutical company should be transparent, and be known by the patient. 5. Funding for hospitals should be adequate, so that testing of drugs is not a financial necessity, and the interests of patient and doctor are protected.

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As our use of pharmaceutical substances continues to increase, it is of vital interest to patient, doctor, and hospital that the rules under which drugs are administered and tested be regulated carefully so that the interests of none of these parties are compromised.

RESPONSE 2 Dorine Bax argues that modern media such as the Internet may help patients get balanced information. She also suggests that the medical profession should take seriously some treatments that are common in alternative medicine.

Diet Therapy as a Viable Alternative for NSAIDs Dorine Bax Student of Biomedical Science, the Netherlands In his review of NSAIDs, Wim van der Steen comments on links between medical research and the pharmaceutical industry. He suggests that the industry hampers the development of alternative therapies, such as diet therapy, since funding privileges research aiming at new drugs. Rheumatoid arthritis, for example, is mostly treated with dangerous drugs that may be effective only in the short term, even though diet therapy may constitute a safe alternative treatment. I focus here on this example. Why do people suffering from rheumatic arthritis keep using NSAIDs, despite the problems with these drugs? I conjecture that most of them do not know about the problems. The alleged benefits of NSAIDs are widely advertised by the industry, which at best provides information to the extent that the law requires it, and thereby creates bias. This bias does carry over to the popular media, and experiences of patients using the drugs may help to perpetuate the bias due to placebo effects. In principle, general practitioners and specialists who treat patients with rheumatoid arthritis should be the prime source of unbiased information, but in practice we are in for disappointment. Practicing medical professionals focus on conventional medical treatments, and we cannot reasonably ask them to cover the relevant primary literature entirely. Hence it is natural that biased research leads to biased practice. I use the expression "conventional treatment" for treatments to which positive effects are attributed by scientific research, preferably in clinical trials. Literature cited by Wim van der Steen indicates that such treatments need not always be beneficial.

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Diet therapies, which are possibly more beneficial than treatments with NSAIDs, are to some extent conventional in the defined sense. Positive effects have been observed in clinical trials, but these trials took place outside mainstream research. Much more prominent is the place of diet therapies in alternative medicine, where proper tests are often lacking. It is to be hoped that alternative practice will yield to scientific scrutiny, and that diet therapies will be conventionalized by this. In the medical world, conventional treatments are seen as more reliable, and therefore better, than alternative treatments. Conventional treatments, on one hand, are developed in accordance with the rules of science, through many cycles of trials, before they are accepted. Alternative treatments, on the other hand, are often based on positive experiences reported by patients rather then by trials. Are conventional treatments as scientific as we want them to be? I think that this is not so in the case of NSAIDs. The industry appears to be involved in the development of treatments, and trials associated with this are shaped, in part, by influences from the pharmaceutical companies. This represents a major violation of the rules of science. Indeed, if science does not adequately comply with the demand for new treatments for rheumatoid arthritis, we should not simply dismiss alternative treatments on the ground that violate the rules of science. You do not have to be a scientist to think that healthy food will benefit a patient more than junk food does. The avoidance of excessively fatty food will prevent obesity. Obesity is indeed a problem in rheumatoid arthritis, because it raises the pressure on inflamed joints. Furthermore, some kinds of food can cause hyperallergic reactions, and avoiding them may decrease rheumatic reactions, which may represent hyperallergic reactions also. Exciting is the discovery that certain fatty acids from fish-oil, omega-3 essential fatty acids, can benefit patients with rheumatic arthritis, by a mechanism still unknown. This amounts to a scientific backing of diet therapies. Other oils under investigation may have similar effects. As I indicated, it is unlikely that practicing medical professionals will come to regard diet therapies as a serious option. Most of them, noticing that these therapies have their primary locus in alternative medicine, will reject them because of being not yet "scientifically proven." Thus they will stay with the NSAIDs. This tends to generate a vicious circle. But there are manners to break through this circle. The days that patients blindly obeyed the doctor are gone. Thanks to new media, such as the Internet, the patient is able to collect information in addition to that provided by the doctor. This is the way to find information about diet therapy. There

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is a lot about it on the World Wide Web. Arthritis-foundations mention it on their homepages, and popular health information sites also have much information about this therapy. Furthermore, many popular books about the subject are on the market. It is important that all the information about diet therapy is available for the public at large, not only for scientists. The Internet is now a good source. Popular science journals and science sections of the big newspapers should also feature the subject. As this information proliferates, science may come to feel the pressure to focus more on this therapy as a viable alternative for NSAIDs. RESPONSE 3 Arjen Groen has done extensive research in the Netherlands on NSAIDs used in general practice. His results indicate that—in this setting—NSAIDs represent a responsible form of medication. This is a reason for him to criticize van der Steen's text. The pharmaceutical industry, in his view, has a positive role. He also provides arguments that major hazards for health care exist elsewhere. Not least dangerous is the increased use of over-thecounter drugs, including NSAIDs. NSAIDs in The Netherlands: The View of a General Practitioner Arjen Groen General Practitioner, The N e t h e r l a n d s Introduction The use of nonsteroid anti-inflammatory drugs (NSAIDs) is common in medical practice. As the label "NSAID" indicates, prescriptions may aim to treat inflammation. The primary target, however, is pain relief. Extensive research in the Netherlands has provided much information on the drugs in general practice. The general practice there is different than in some other countries, for example, the United States. General practitioners (GPs) in The Netherlands are the first source of help for patients, and referral to specialists is mostly done via a GP. Nowadays, GPs often work together in a single unit for a particular patient population, but many GPs still have a one-person unit.

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NSAIDs in General Practice: Data I report here on recent research, done with a colleague, on NSAIDs in general practice. The results are in, but they have not yet been published. They fit in with published information from other projects in our country. I use the results to comment on van der Steen's view. We solicited and obtained extensive information on prescription behavior—and the medical context associated with it—from six GP-units covering 19,753 patients (Okkes et al, 1998:17-23; Veetman, 1995:33-75). The data, which cover a period of five years (less in some cases), comprise 318,421 prescriptions—including repetitions—of NSAIDs. Prescriptions concern backache (17.5 percent), rheumatoid arthritis and related illnesses (5.7 percent), and some forms of non-inflammatory joint degeneration (9.7 percent). The remaining category mainly concerns pain in various illnesses, broadly defined: Temporary muscle ache would be an example. All in all, NSAIDs predominantly function as analgesics for the relief of pain. They are often prescribed if other, over-the-counter drugs (OCDs) fail to help. We also obtained extensive information on short-term versus long-term use of NSAIDs for various illnesses. The data combine to show that short-term use is the rule. We also checked for some disorders, to what extent the use of NSAIDs is associated with gastrointestinal side effects (ulceration). Such effects appeared to be rare. They were detected with 14 out of 14,130 prescriptions. So much for our data concerning general practice. Applied specialist medicine is a different matter altogether. It uses more potent drugs with dangerous side effects. I will not venture to say more about this, because it is beyond the scope of our study. Responsible Use of NSAIDs Our results concerning general practice indicate that existing criticism of NSAID use is overblown. I would suggest that existing patterns of use are responsible. General practice does not confirm the bias as portrayed by van der Steen. The drugs are often prescribed as analgesics in recognition of the patient's views, the purpose being alleviation of symptoms rather than improvement concerning disease. Hence the prevalence of short-term use. I have one caveat. Our results concern prescriptions. We do not know about the impact of over-the-counter NSAIDs. Van der Steen states that research concerning drug therapy is biased due to funding by the pharmaceutical industry. The bias does exist. It should indeed not come as a surprise, since the law requires it for drug registration.

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In The Netherlands—and Western societies in general—drug development is done primarily by the pharmaceutical industry. The government has the role of guarding indications and safety. This is the choice we have made. I applaud it, because the pharmaceutical industry generates innovative research. In our society, the gain for this industry is high, as they invest in innovative research. Let it be this way. Perhaps more research on nondrug treatments is needed. Considering this, I note that such treatments do receive attention. Organizations exist that assess merits of nontraditional treatments, by comparative studies with a sound methodology. In the wake of that, we need more research funded by independent organizations. The greatest problem in health care is probably the growing tendency toward self-medication (Vuckovic and Nichter, 1997) that—albeit in new garbs— comes close to medicalization. A decrease of medicalization has long been an important ideal. The growth of self-medication with OCDs, fostered by the myth that discomforts, impairments, and disabilities are pervasively curable, does not serve this ideal. Indeed, it may represent the greatest danger to national health, as these drugs are often taken on the advice of nonexperts. Conclusion The safety of medication in our society needs improvement, not least because overuse of drugs is common. Considering general practice, I am optimistic. Our research on NSAIDs indicates that GPs prescribe these drugs in a responsible way. They can avoid the use of potent NSAIDs with lots of side-effects. Specialist medicine is a different matter, but our research does not allow robust conclusions about this. NSAIDs should not be available as OCDs. It is indeed plausible that the increasing use of OCDs is a major hazard in health care. References Okkes, I.M, Oskam, S.K, and Lamberts, H. 1998. Van Klackt naan Diagnose. Bussum, The Netherlands: Meditekst. Veetman, M.T.M. 1995. Huisartsgenreskundige. Zorgepisoden: Analyse van een Zevenjaars Bestand (PRD thesis). Lelystad, The Netherlands: Meditekst. Vuckovic, N, and Nichter, M. 1997. Changing patterns of pharmaceutical practice in the United States. Social Science and Medicine 44: 1285-1302, 1997.

Appendix to Part IV: Improving Style

Our book deals with writing in addition to the assessment of literature. However, our methodological criteria and guidelines differ markedly from criteria in other guides for writing, and we have entirely disregarded style. If we had also implemented criteria for style, the result would have been unworkably complicated. However, style is important, and it interacts with criteria and guidelines as presented by us. Hence this Appendix. We introduce here matters of style through an artificially detonated version of the text about NSAIDs by WJS in Part III. Superscript numbers refer to notes on style at the end of this version. In going through the text, you will get acquainted with increasingly subtle issues of style (notes 1-28: elementary level; remaining notes: advanced level, but also some new elementary material). This facilitates the use of the text both in elementary and in more advanced education. THE INFLUENCE OF BIASED PROMOTION OF DRUGS: RELATIONSHIPS BETWEEN THE PHARMACEUTICAL INDUSTRY AND MEDICAL RESEARCH 1 As many authors have argued, science and culture exhibit all sorts of relationships.2 Medical science is no exception.3 Using4 reviews as a starting point,5 the influence of culture on medicine can be shown6 to be very7 large. There are8 not9 many researchers who would deny that this is indeed the case.10 The point has been made in a general way by sociologists

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of science. Primary sources of medical research, however,11 are mostly not a source from which sociologists get their materials when this point is considered12 by them.13 Conversely, medical researchers in their writings seldom consider how culture affects their work. Using14 a case study, in which it is shown15 how profoundly medical science and medical practice are influenced16 by culture,17 the gap in research is going to be closed.18 The subject that I am going to discuss19 is a class of drugs that are known as nonsteroid anti-inflammatory drugs,20 abbreviated NSAIDs, that are used on a massive scale, which is unfortunate because they have very serious side effects.21 The fact that these drugs are used much more than they should be is caused by bias, which takes several forms that are not often investigated in medicine.22 The way in which the drugs are regulated has been biased so that that the pharmaceutical industry is favored, which is a detriment for patients.23 Furthermore, researchers who receive funds from a pharmaceutical industry that manufactures a drug have a tendency to produce reports that are biased in favor of the drug.24 Medical research is also biased by its focus on drug therapies. It is possible25 that diet therapies are equally effective and without serious side effects. Furthermore, inappropriate prescriptions are common. Some forms of bias are unavoidable. For example, the methodology chosen for controlled studies depends on ethical decisions. All the forms of bias deserve more scrutiny. It is in any case desirable that we reduce the use of NSAIDs. EFFECTS OF NSAIDs Many studies indicate that NSAIDs may palliate symptoms in inflammatory diseases such as rheumatoid arthritis.26 The drugs have dangerous side effects. In a recent study it is noted that 10^40 percent of elderly people in the populations studied make use of27 NSAIDs, while28 the drugs frequently have gastrointestinal side-effects (14). NSAIDs increase the risk of peptic ulcer complications by three- to five-fold, and in several different populations it has been estimated29 that 15-35 percent of all peptic ulcer complications are due to NSAIDs. In the United States alone, there are an estimated 41,000 hospitalizations and 3,300 deaths each year among the elderly that are associated with NSAIDs. In another study the drugs are even estimated to cause 20,000 deaths in the United States each year.30 Any cursory inspection of the literature will uncover many articles with a similar message. It is important to note that31 the alleged benefits of NSAIDs are not unchallenged.32 One source describes recent data regarding the prognosis

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of rheumatoid arthritis with the use of the current drug treatments as "gloomy," and, according to another source, most standard medical treatment33 approaches have had little or no impact on the course of rheumatoid disease. Controlled trials aiming to investigate effects of34 drugs in rheumatoid arthritis are often problematic due to pitfalls to do35 with outcome measures, patient populations, characteristics of the study design, and economic evaluation. Impressions concerning the long-term natural history and results of therapy are strongly influenced by the types of measures and study designs used to assess patient status and outcomes. Many randomized controlled36 trials do not provide37 adequate information about long-term outcomes in patients using the drug which is investigated in the trials.38 Furthermore, we should not simply take positive data in the literature for granted.39 A BROAD PERSPECTIVE How should we explain the massive use of NSAIDs? The most obvious answer would be that controlled trials indicate that NSAIDs40 alleviate symptoms of inflammation, at least in the short term, that they admittedly have dangerous side effects, but that the overall balance of evidence warrants continued usage.41 This answer is unsatisfactory. It relies on the presupposition that the research is without bias and that it has effects on practice in an unbiased way.42 I would assume that the widespread use of NSAIDs does not sit well with the observed side effects, and that it points to undesirable forms of bias. Let me review some potential sources of bias. Abraham offers a detailed survey spanning decades of NSAID regulation in the United States43 and in the United Kingdom, which demonstrates that research by the pharmaceutical industry on benefits and side effects of NSAIDs44 has been biased in favor of its own products.45 That should not surprise us. Surprising is incontrovertible evidence that authorities responsible for regulation have on a grand scale acted in violation of their own guidelines, so as to favor the industry, to the detriment of patients.46 Many dangerous NSAIDs now on the market should never have been approved for sale. Bias in favor of the industry may also exist in medical research itself47 The chances that researchers observe positive effects of NSAIDs are way above average if they are paid by the industry manufacturing the drugs. Medical practice also appears to be biased in favor of NSAIDs, since unnecessary prescriptions are very common. Furthermore, despite the side

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effects noticed,48 the use of NSAIDs is fostered by their being available as over-the-counter drugs. These kinds of bias could be avoided in principle, but other forms of bias cannot be avoided.49 Consider the problem of false positives (statistical type I errors) and false negatives (statistical type II errors). Of course50 we should aim at tests ensuring that the probabilities of errors of either kind are low.51 The trouble is that a decrease in one type of error logically entails an increase in the other type of error (with a given sample size and effect size). Thus, the methodological set up of our research depends on ethical considerations concerning the acceptability of particular errors that52 are part of our culture. This can be generalized.53 Ideal experiments cannot satisfy all methodological requirements at the same time. We have to prioritize requirements, and that cannot be done without ethical considerations. As I noted, some medical researchers have argued that the methodological set up of experiments affects conclusions about the value of NSAIDs. We should add to this that the choice of a methodology is determined in part by ethical issues that are seldom made explicit in medical research, and which should be brought out into the open.54 We are not dealing here with bias in a pejorative sense, because we have to opt for some methodology, but we should be aware of normative presuppositions. Considering tests of drug effects, patients and the industry have different interests with respect to different types of error.55 In the interest of patients, we would like to minimize type I errors of falsely attributing positive effects to drugs. But56 the industry would rather benefit from low levels of type II errors of falsely attributing no effects to drugs. In most research, significance testing is done without power analysis. This allows for type I errors at the standard 5 percent level, while type II errors remain unknown. Repeating57 tests of drugs over and over again, a common practice nowadays, results will sooner or later become significant due to a type I error. To the extent that drugs are marketed on the basis of this, the type I error level shows an increase while the type II error level shows a decrease, and we get a bias in favor of the industry, to the detriment of patients.58 Patients and the industry also have different interests in the study of adverse side effects. The trouble is here that methodologically proper tests are hardly feasible since the set of potential side effects is open-ended, and guidelines for the time scale of experiments are arbitrary. In the interest of patients, we should aim at comprehensive short-term and long-term studies, but this would not be palatable59 for the industry. In practice, comprehensive long-term studies are rare, which again favors the industry. Controlled experiments are problematic if drugs are compared

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with a placebo without side effects.6 The chances are that this will generate false positives when patients conclude from experienced side effects that they are receiving the drug rather than the placebo. This kind of phenomenon has on a grand scale resulted in inappropriate drug treatments in psychiatry. Medical research may also be biased in that the choice of subjects to be investigated is one-sided. Concerning therapies for rheumatoid arthritis, research reveals a pronounced bias in favor of drugs. As I am writing61 this (August 1999) Medline lists62 11,017 articles on drug therapy,63 126 articles on diet therapy. This fits in with a pervasive negligence of ecology in medical research and64 medical practice.65 Diet therapy, for that matter,66 does seem to have positive effects. Particular diets, or components of diet, most notably particular unsaturated fatty acids, reduce disease activity in rheumatoid arthritis.67 It is indeed conceivable that poor diet is among the factors which predispose toward the disease. We should add to 68 this that modern techniques of food processing cause the destruction of natural components of diets, not least unsaturated fatty acids including essential ones. This fosters degenerative and systemic diseases, and it may well contribute to etiology in rheumatoid arthritis.69 The emphasis in medical research on pathology is now overwhelmingly on genetics and molecular biology. Medicine developed biological approaches prior to the emergence of ecology. Current paradigms in medicine are reductionistic paradigms.70 These paradigms foster a self-perpetuating bias. Considering genetics, I have elsewhere explained how this works, by an analysis of research on schizophrenia. Twin studies have shown that concordance for schizophrenia is much higher in identical71 than in nonidentical twins. It has been concluded72 from this that genes are implicated in etiology. The following counterexample shows how problematic this is. Suppose73 a number of twin pairs are on a trip in a coastal plain. A flood wrecks the trip. Tall individuals survive, and74 short individuals drown since they cannot keep their heads above the water. Identical twins will obviously75 show a higher concordance than nonidentical twins. If we follow76 the logic of schizophrenia research, we should conclude that genetic factors rather than the flood were77 causally responsible for the drowning. Something is obviously wrong with the logic of common research. Researchers78 do admit that the environment modifies the effects of genetic factors. But79 they commonly conceptualize the environment as the psychosocial environment. Ecological factors are simply disregarded. This happens in psychiatry and in many areas of medicine.

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CONCLUSIONS NSAIDs are reported to alleviate symptoms in inflammatory diseases. This may be true, but we should beware of thinking that these positive effects are very large,80 and we should realize that short-term benefits may not be extrapolatable. The pervasive use of these drugs is indeed problematic in view of serious side effects. If we wish to assess NSAIDs, we should not be content with an appraisal of existing controlled trials. Such an appraisal81 would not uncover all sources of bias. Research mostly conducted outside medicine itself has revealed many sources of cultural bias. Drug regulation is biased in favor of the pharmaceutical industry. Likewise for82 medical research funded by the industry. Furthermore, the emphasis in research is overmuch on drug therapy, while83 less dangerous treatments such as diet therapy may be equally effective. It is desirable that medical journals pay more attention to these forms of bias. More research is needed on alternative treatments, particularly diet therapy. The highest priority should go to trials that aim to compare drug therapies with diet therapies. We might save thousands of lives if we replace drug therapies by diet therapies. NOTES ON ERRORS OF STYLE OR ON TEXT WITH POTENTIALS FOR IMPROVEMENT Some notes are best understood by comparison with the original text (OT), as indicated by see (OT). Comparion of the detonated text with the original is in any case advisable. The abbreviation (AR) means "as a rule," or "in most contexts"—the context depending on type of journal, or journal versus book, or discipline, or country (particularly United States versus United Kingdom), or personal preferences. The spelling here is american. In going through the text, you will get acquainted with increasingly subtle issues of style. Notes 1-28: elementary level. Notes 29-83: advanced level, but also some new elementary material. Note 70 reveals links with the rest of the book. 1. Title unappealing and too long. 2. Bad start. Uninformative. Begin an article with a salient, substantive point. Avoid long qualifying clauses at the beginning of sentences. Aim at short sentences. 3. Avoid redundant text. This sentence becomes redundant after proper reconstruction of context. See (OT) 4. Do not use nattached participles ("dangler" = participles) without a proper subject. "Using" is a dangler. In technical writings, this is a common error of style. 5. Do not begin a sentence with a long qualifying clause. (AR) 6. Avoid the passive voice. (AR)

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7. Omit qualifying words if they do not add to information provided; "very" is redundant. 8. Avoid "there are," "there is," if you can do without these expressions. 9. Avoid negative locutions: "few" is better than "not many." 10. Avoid redundancy. "Indeed" is redundant. Replace the redundant phrase ' t h a t . . . case" by "this." 11. Use "however" only if a strong contrast exists. 12. Avoid the passive voice. 13. Avoid sentences with a complicated structure. Apply this rule here by the deletion of redundant expressions. See (OT). 14. Unattached participle. 15. Avoid the passive voice. 16. Idem. 17. Avoid subordinate clauses if you can do without them. See (OT). 18. Awkward formulation. See (OT). 19. Idem. 20. See 17. 21. This sentence contains many of the errors already mentioned. See (OT) 22. Idem. 23. Idem. 24. Avoid long expressions if shorter ones are available. See (OT). 25. Avoid expressions such as "it is possible," "it is probable." (AR) 26. Use connecting words to make relations between successive sentences visible. See (OT) 27. See 24. 28. Inappropriate preposition. 29. Avoid formulations that are at variance with intended meaning. The research has been about populations; from a literal interpretation, the text conveys that the investigators have been located in populations. Also, avoid passive voice. 30. Implement continuity of subjects by continuity of formulations. The last sentence is out of touch with the two sentences preceding it. See (OT). 31. Avoid expressions such as "it is important to note that," "it is interesting to note that." 32. Use positive formulations. Avoid the passive voice. Notice the use of "do " for emphasis: it helps the reader assimilate a contrast between text units. Take care, to an adequate extent, to have important words or expressions at the beginning of sentences and paragraphs. See (OT). Note. Do not confuse the last point with the following rule: the readability of a text is served well by relatively important theses either at the beginning or at the end of a paragraph (see 39). 33. Avoid stacked qualifying words or expressions. See (OT) 34. Do not make the obvious explicit. Controlled trials always aim to investigate effects. Replace "aiming to investigate effects" by a simple word; for example, "concerning."

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35. Popular style. (AR) 36. Avoid stacked qualifying words and expressions. See (OT) 37. Avoid negative locutions. 3 8. Do not make the obvious explicit. Avoid negative locutions. Avoid the passive voice. 39. Put the most salient point of a text unit at the beginning or at the end. (AR) The last paragraph has a salient point both at the beginning and at the end. 40. Avoid repetitive forms of expression. The repetitive use of "that" should here be avoided by a different formulation. 41. Formulation verbose and too complicated. See (OT) 42. Replace noun phrases by verbs if this yields a simpler formulation. 43. Use similar formulations throughout texts. 44. The use of comma's is an interesting subject. Grammatically, no comma is needed here, but a comma enhances readability. (AR) 45. Avoid sentences that are long and/or complex without necessity. 46. Idem. 47. Put the subject of sentences at the beginning, with occasional exceptions to avoid a dull style. (AR) 48. Take care to distinguish between the meanings of "note" and "notice." "Note" is better in this situation: the author presumably has the intention of referring to the description of a phenomenon; "notice" would refer to the phenomenon itself. 49. Barring that clarity should decrease, use different expressions for an item to avoid a dull style. Compare "cannot be avoided," "are unavoidable." (AR) 50. According to a common, traditional convention, a qualifying word or clause at the beginning of a sentence needs a comma after it. (AR) 51. Make implicit links between successive sentences explicit. 52. Avoid the ambiguous use of referential words. "Which" could here refer to "considerations," or, alternatively, to "errors." Delete the redundant clause "which are part of our culture." 53. Be aware of possible tensions among requirements of style. The intended link of subjects in successive sentences in the text has been left implicit—a potentially undesirable feature. We could take this for granted here as the link may be clear from the context. However, excessive implicitness unavoidably entails other undesirable features of style. (AR) 54. Avoid long sentences. 55. Avoid long expressions. Also avoid "considering" as used here: The participle has no subject in this sentence. "Considering this situation, we think . . . "would be an example of a proper formulation. 56. Avoid "but" if the contrast is strong; "however" is better in this case. 57. Unattached participle. 58. Replace noun phrases by verbs if this yields a simpler formulation. 59. Popular wording. (AR)

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60. Use connecting words to make relations between successive sentences visible. The formulation fails to indicate that the last sentence introduces a new theme. 61. Ensure compatibility of formulations and content. The present participle for continuing action is here incompatible with "lists": the date is in the wrong place, which changes meaning. 62. Take care to make intended contrasts explicit. Insert "as many as." 63. Insert "but only" to make the contrast explicit. 64. Some would repeat "in." (AR) 65. Avoid ambiguity. The references could refer here to the entire sentence or, alternatively, to the last part of it. 66. Avoid vagueness. See (OT). 61. Avoid unexpressed links between successive sentences. See (OT). 68. Idem. 69. Use appropriate formulations to express relations of subordination among subjects. See 70 for a more general variant of this rule. See (OT). 70. Use appropriate formulations to express relattions among subjects. The last three sentences violate this rule. See (OT). Note. The imlicit logic of texts is necessarily complicated in comparison with formulations used. This entails intimate associations among grammar, style, and methodology. The associations explain why reconstruction is a salient theme in our book. 71. Some would add "twin." (AR) 72. Awkward formulation, unfortunately common in science. 73. Some would here insert "that," and then delete the comma. (AR) 74. Replace by "but," which better evokes the intended meaning. 75. Redundant repeated word. The repeat is bad style because "obviously" is a strong word. 76. Slightly inappropriate tense. See (OT) 11. Wrong tense. See (OT) 78. Avoid vaguesness masking as generality. The word "researchers" is unacceptably general in the context. Replace it through specification, and delete the last sentence of the paragraph. 79. Replace "but" by "however." This is an example of strong contrast. 80. Avoid verbose formulations. 81. Awkward repeat. 82. Not wrong, but idiosyncratic. (AR) 83. Avoid inappropriate prepositions; replace "while" by "even though."

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Postlude

We do not know how you have wandered through our book, because you are different readers. We assume that, after getting acquainted with our approach, you have focused on particular themes, and that you have gone back to them afterward. If so, then we hope that your second thoughts deviated considerably—in a positive way—from your initial impressions. If this coming full circle happened to some readers, we would be satisfied that we did something useful.

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Bibliography: A Note Concerning Sources

We omit a bibliography with a standard format for the following reasons: The texts in Part III are represented together with the source; they already constitute a bibliography. This bibliography does have limitations as comments on the texts at times derive from many sources. Hence a full bibliography would have been out of proportion with the main text of the book. Mere inspection of sources at the end of the text by WJS in Part IV illustrates what such a biobliography would have to look like. Additional sources are to be found in the following books by WJS: Musschenga, A.W., and Van der Steen, W.J. (eds). 1999. Reasoning in Ethics and the Law: Theory, Principle, and Judgment. Aldershot: Ashgate. Van der Steen, W.J., and Thung, P.J. 1988. Faces of Medicine: A Philosophical Study. Dordrecht: Kluwer. Van der Steen, W.J. (1993). A Practical Philosophy for the Life Sciences. Albany: SUNY Press. Van der Steen, W.J. 1995. Facts, Values, and Methodology: A New Approach to Ethics. Amsterdam: Rodopi. Van der Steen, W.J. 2000. Evolution as Natural History: A Philosophical Analysis. Westport, CT: Praeger.

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Index

Accompanying features, 15 ADHD, 122-25 Ad hoc assumptions, 40-41 Affirming the consequent, 28-29 Aggression, 105-6 Agoraphobia, 107 Agriculture, 151-53, 155 AIDS, 25, 44 Air pollution, 42-43, 44 Altruism, 16-17, 32,42, 75-100; ambiguity in notion of, 23-24, 37-38,75, 78-79, 84, 85, 92, 94; evolutionary altruism, 17, 37, 78-79, 81-85, 8688, 92; psychological altruism, 7879, 81-85, 86-88, 92; reciprocal altruism, 76-81, 85, 86-88 Ambiguity, 14, 17, 21, 32, 70, 104; in notion of altruism, 23-24,37-38,75, 78-79, 84, 85, 92, 94 Anxiety disorders, 106-8, 110-11, 129-30 Arguments, 13-14, 25-33 Assumptions, 39-41, 164 Attention Deficit Hyperactivity Disorder (ADHD), 122-25

Biological factors, 38, 64-66, 105-6, 113-16,122-25,145,174 Biomedicine, 3, 46, 60, 121-22. See also Medicine By-product mutualism, 80 Causes, identification of. See Identification of causes Ceteris paribus, 33 Charity guideline, 53, 58-59, 122, 132, 174 Cheating, 77-78, 79-81, 83, 86 Chronic fatigue syndrome, 167-69 Circular reasoning. See Noncircularity Clarity, in arguments, 10, 30 Classification, 15-16. See also Consistency in classification; Exclusiveness in classification; Exhaustiveness in classification Cognitive statements, 20 Confirmability: of hypotheses, 36, 3840,41-42,59-60; of premises, 9,30; of theories, 41-42 Consistency in classification, 10, 16

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Index

Consistency guideline, 53, 60, 66-68, 174 Context-dependence, 3, 53, 55-57, 61, 84, 173, 175 Cooperation, 78, 79-81, 86-88, 93 Cortisol, 147-49 Deductive arguments: and explanations, 42, 43; hypothetical syllogism, 28; modus ponens, 26-27, 32; modus tollens, 27, 31-32, 39, 128; validity of, 10, 26-29, 30,43, 58, 61, 80-81, 98 Definitions, 15, 16-17, 23, 25, 31, 62, 93,114-15 Depression, 63, 115, 119-21, 126-27 Deyo,R.A., 187 Dichotomies, 16, 19 Diet, 56-57,62,106,116-17,134,137, 145-46, 177, 198; and rheumatoid arthritis, 174, 180-82, 188-90, 194, 197 Dirty hands. See No dirty hands guideline Disconfirmability. See Confirmability Disease, 32-33, 43, 45-46, 125-26, 131-34 Dopamine, 117-19 Double-blind experiments, 33, 138 Drugs, 31, 32-33, 43, 56-57, 60, 62, 117-19, 131-41; nonsteroid anti-inflammatory drugs (NSAIDs), 3, 173-75, 177-82, 188-92, 193-98 Ecological factors, 19, 52, 56-58, 63, 114, 163; diet, 56-57, 62, 106, 11617,134,137,145-46,174,177,18081, 188-90, 194, 197, 198 Egoism, 16-17,23-24,42,75-100. See also Altruism Eliminativist strategies, 82-83 Empirical content: of hypotheses, 11; of premises, 10, 30, 31

Empirical statements, 20,21,23-24,25, 36,37,40-41,98 Environmental determination, 122, 124-25,146^17,163-64; vs. genetic determination, 1-2, 18-19, 51-52, 102, 103, 104, 107, 108-9, 113-16, 126-28, 127-28, 162, 181, 197 Estrogen, 131-34 Ethics. See Morality and ethics Etiological factors. See Biological factors; Ecological factors; Psychosocial factors Evidence, 9, 10, 38^11 Evolutionary biology, 32, 46, 75, 93, 98-99,119-30 Evolutionary epidemiology, 125-26 Evolutionary psychology, 88-90 Evolution, theory of, 61 Exclusiveness in classification, 10, 16; case studies relevant to, 76-85 Exhaustiveness in classification, 10,16, 19; case studies relevant to, 76-85, 92-95, 105-6, 113-16, 128-30, 143-46 Existential statements, 22, 24 Explanations, 9, 35, 42-44, 148; and deductive arguments, 42, 43; identification of causes in, 11. See also Explanatory power; Hypotheses; Theories Explanatory power, 11, 36, 37, 47, 52; case studies relevant to, 76-79, 8890, 101-5, 106-8, 122-25, 143-46. See also Explanations Explicit relations guideline, 53, 60, 65, 68, 174; case studies relevant to, 110-11,117-19 Facts, 9, 20-21, 24,45-47 Fallacies, 28-29,46, 58-59, 65 False positives and false negatives, 17980, 196 Falsity, 20, 21, 38-39, 80-81, 83, 133

Index Functions, 24-25 Gender differences, 64-66, 106-8 Generalist backing, 3, 53, 57-58, 59, 173-74; case studies relevant to, 105-6, 108-9, 119-21, 125-28, 131-37, 143-46, 165-69 Generality in hypotheses, 3, 11, 36, 37, 41-42; case studies relevant to, 7679, 81-88, 95, 113-16, 146-47, 154-57 Generality, relative, 22-23 Genetic determination, 32,101—9,151— 53,161-62; vs. environmental determination, 1-2, 18-19, 51-52, 102, 103, 104, 107, 108-9, 113-16, 12628, 127-28, 162, 181, 197. See also Biological factors Genetic engineering, 151-59 Gross National Product (GNP), 15 Guatemala, 165-67 Guidelines, 2-3, 4-5, 52-53, 55, 193. See also under individual guidelines Health, 17,40,46, 116-17 Health Research Group (HRG), 132 Heterogeneity. See No heterogeneity guideline HIV, 25, 44 Homosexuality, 32 Hormones, 64-66, 131-34, 147-49 Hospital for Sick Children (Toronto), 186-87 Human Immunodeficiency Virus. See HIV Hume, David, 97, 99 Hypothetical syllogism, 28 Identification of causes, 11, 21, 42-44, 47, 51-52; case studies relevant to, 111-16, 117-19, 121-25, 128-30. See also No causal selectivism guideline

209

Immune system, 44, 143, 145-46 Implications of descriptions guideline, 53, 63, 174; case studies relevant to, 88-90, 101-5, 108-9, 119-21, 12225, 131-34, 162-63, 165-69 Inductive arguments, 26,29,30,43. See also Validity or inductive support Infanticide, 89-90 Insurance industry, 45-46 Kinship, 76, 79, 85 Lactate, 147-49 Land snails, 41 Level of populations vs. level of individuals, 51-52, 58-59, 102-3, 104, 107 Lichens, 4 2 ^ 3 , 44 Logical form, 20, 21-22 Logical statements, 23-24, 25, 31, 3738, 40-41, 83, 95, 96-98, 114-15; existential statements, 22, 24; and logical form, 20, 21-22; probabilistic statements, 22, 24; singular statements, 22, 24; universal statements, 22-23, 24, 39 Lung cancer, 39, 44 Marriages, 99-100 Medical research, 131-39, 173-75, 177-82, 185-92, 193-98. See also Pharmaceutical industry; Twin research Medications. See Drugs Medicine, 125-26, 128-30; biomedicine, 3,46,60,121-22; conventional vs. alternative, 174, 188-90 Menopause, 131-34 Mental illness, 1-2, 3, 62, 101-8, 11022, 126-30; anxiety disorders, 1068, 110-11, 129-30; depression, 63, 115, 119-21, 126-27; etiology of, 38, 51-52, 58-59, 106-7, 124, 127-

210

Index

28; schizophrenia, 51-52, 58-59, No heterogeneity guideline, 53, 68-69, 101-3, 104, 111-12, 126-28, 181, 175; case studies relevant to, 76-81, 197. See also Diseases 98-99, 110-11, 117-19 Method of agreement, 29 Noncircularity, 10, 30-31, 38, 65, 125; Method of concomitant variation, 29 case studies relevant to, 81-85, 113Method of difference, 29 16, 117-19,147-49. See also CircuMethodological criteria, 2-3, 4-5, 193; lar reasoning for arguments, 10, 29-33; for con- Noncognitive statements, 20 cepts, 10, 14-15; as conflicting, 5 1 - Nonsteroid anti-inflammatory drugs 52; for explanations, 11; for (NSAIDs), 3,173-75, 177-82,188hypotheses, 11, 36-41, 42; for prin92, 193-98 ciples of classification, 10, 16; rela- Normative statements, 20 tions between, 55; and social context, 56; and values, 56-57. See O'Hara, Jane, 186-87 also under individual criteria Olivieri, Nancy, 186-87 Operationality of concepts, 10,23; case Mind-body problem, 70 studies relevant to, 119-21, 126-28; Modus ponens, 26-27, 32 definition, 14, 15 Modus tollens, 27, 31-32, 39, 128 Molecular biology, 116-17, 143, 144, Ordinary language guideline, 53, 6 9 151-53, 162-63, 174, 181, 197 70, 175; case studies relevant to, 76Morality and ethics, 3, 17, 75-76, 93; 88 case studies from theoretical ethics, Osteoporosis, 131-34 81-85,93-98; values in science, 4 5 47,52,56-57,64-65,173,179,185- Panic disorders, 110-11 88, 194, 195. See also Altruism; No Parasitism, social, 76, 77 Pharmaceutical industry, 46, 56-57,60, dirty hands guideline 62, 131-37, 173-75, 177-82, 185Naturalistic fallacy, 46, 65 92, 193-98 Necessary conditions, 43-44 Pharmacotherapy, 137-41 Netherlands, 175, 190-92 Philosophy, 20, 70, 75-76, 91; case Neuroleptics, 117-19 studies from, 81-85, 93-99 Neuropsychology, 70 Placebos, 33, 137-39, 180, 197 Neurotransmitters, 62, 63, 116, 117- Population density, 165-67 19 Predictive power, 11,36,37,61; studies No dirty hands guideline, 53, 60, 174; relevant to, 76-79, 101-5, 106-8, case studies relevant to, 131-37, 122-25, 151-53, 157-59 161-62, 165-67. See also Morality Principles of classification, 15-16. See and ethics also Consistency in classification; Exclusiveness in classification; ExNo excessive generality guideline, 53, haustiveness in classification 61-62, 174; case studies relevant to, 81-88, 90-92, 98-99, 106-8, 128- Probabilistic statements, 22, 24 Progesterone, 133-34 30, 143-47, 154-57, 163-67

Index Proper levels of organization guideline, 53, 59, 60, 62, 63, 64, 174; case studies relevant to, 102-9, 119-21, 122-25, 162-63 Psychiatry, 113-16, 125-26, 137-41, 167-68, 197. See also Psychology Psychological egoism, 96-98 Psychological hedonism, 83 Psychology, 4,46,78-79, 143,167-68; case studies from, 88-93, 98-100; evolutionary psychology, 88-90; neuropsychology, 70; psychological egoism, 96-98; psychological hedonism, 83; social psychology, 9093. See also Psychiatry Psychoneuroimmunology, 143-46 Psychopathology. See Mental illness Psychopharmacology, 137-41 Psychosocial factors, 19, 52, 103, 11316, 145-46, 174, 181, 197 Rango, Robert, 187 Reciprocity, 76-81, 85, 86-88. See also Altruism Reconciliationist strategies, 82, 83 Reconstruction, 14, 53, 60-61, 61, 65, 66, 69, 174; case studies relevant to, 79-81,97-98, 106-8, 110-12, 11719, 122-25, 126-28, 131-37, 14649, 151-59 Reductio ad absurdum, 31-32, 118 Reductionism, 63, 99, 181, 197 Relevance of premises, 10, 30, 31; case studies relevant to, 76-79, 101-5, 106-8, 151-57 Repetition, 68-69 Rheumatoid arthritis, 174,178,180-82, 188-90, 194-95, 197 Safe concentration, 42 Salient factors, 51-52, 63, 101-2, 103, 107,112,115,162,166-67; and con-

211

text-dependence, 44, 47, 52, 62, 64, 166-67 Salient points guideline, 53, 59, 60, 62, 63,64-65,68,174; case studies relevant to, 90-92,93-95,117-19,14749, 154-57 Schizophrenia, 51-52, 58-59, 101-3, 104, 111-12, 126-28,181, 197 Self-interest, 91-92,93-95,96-97,98100. See also Altruism Separation anxiety, 106-8 Simplicity of hypotheses, 11, 36, 37; case studies relevant to, 113-16, 122-25, 154-57 Singular statements, 22, 24 Skepticism, 67-68 Smoking, 39, 44 Social factors, 105-6, 113-16, 127, 131, 132 Social psychology, 90-93 Social Readjustment Rating Scale (SRRS), 144 Source check guideline, 53, 59-60, 173-74; case studies relevant to, 119-21, 125-28, 131-37, 151-53, 165-69 Specificity, relative, 22-23 Statements, 13-14, 19-25, 29, 62; cognitive statements, 20; empirical statements, 20,21,23-24,25,36,37, 40-41, 98; logical statements, 20, 21-22, 23-24, 25, 31, 37-38, 39, 40-41, 83, 95, 96-97, 97-98, 11415; noncognitive statements, 20; normative statements, 20; relative generality/specificity of, 22-23 Stress, 23, 143^9; and diseases, 14347; in plants, 163-64; stressors, 1718, 24, 37, 42, 62, 146-49; stress responses, 24, 42, 62, 146-49 Style, 4, 193-201 Sufficient conditions, 43-44

212

Index

Symptoms, 21, 25, 51-52, 56, 101-3, 146, 167-69, 178 Testability/survival of tests, 11, 23, 35, 36, 37, 38-41; case studies relevant to, 79-85, 117-21, 122-25, 134-41, 147-49, 151-53 Testosterone, 64-66 Theories, 41-44, 52, 61, 69-70. See also Explanations; Hypotheses Thyroid hormones, 147-49 Toxic chemicals, 42 Truth or confirmation of premises, 10, 20, 21, 26, 30, 36, 38; case studies relevant to, 79-85, 126-30, 147-49, 151-59 Twin research, 20, 51-52, 58-59, 1023, 106-8, 127-28, 181, 197 UN Environmental Program (UNEP), 157-59

United Kingdom, 179, 195, 198 United States, 166, 175, 178, 190, 194, 198 Universality in hypotheses, 11, 36, 37; case studies relevant to, 81-85, 95, 113-16, 146-47,154-57 Universal statements, 22-23, 24, 39 U.S. Department of Agriculture, 157 U.S. Environmental Protection Agency, 157 Vagueness. See Ambiguity Validity or inductive support, 10,26-29, 30, 43, 58, 61, 80-81, 98; case studies relevant to, 79-81, 99-100, 1015, 106-8, 117-19, 122-25, 126-28, 131-34,147-49, 151-59 Values. See Morality and ethics; No dirty hands guideline Verifiability, 38 Viruses, 14,21,25,31,44

About the Authors WIM J. VAN DER STEEN is Professor of Philosophy of Biology at Vrije University, Amsterdam. He has published extensively, including five earlier books, among them Evolution as Natural History: A Philosophical Analysis (Praeger, 2000). VINCENT K. Y. HO is with the Faculty of Biology, Vrije University.