Epistemic and Nonepistemic Values in Psychiatric Explanation And

pistemic and Nonepistemic Values in Psychiatric xplanation and Classification

A dissertation submitted to the

Graduate School

of the University of Cincinnati

in partial fulfillment of the

requirements for the degree of

Doctor of Philosophy

in the Department of Philosophy

of the College of Arts and Sciences

Aaron T. Kostko

M.A. University of Cincinnati June 2008

Committee Chair: Valerie Hardcastle, Ph.D. Abstract My dissertation addresses two longstanding debates in the philosophy of psychiatry: the debate between objectivists and evaluativists regarding the relative significance of factual descriptions and evaluative judgments in attributions of psychiatric disorder and the debate between reductionists and pluralists over whether explanations of psychiatric disorders should proceed at a single level or multiple levels of explanation. The standard way to distinguish philosophical accounts of psychiatric disorder is in terms of the relative significance they grant to factual descriptions of abnormal functioning and evaluative judgments of this abnormal functioning. I argue that this way of categorizing philosophical accounts is overly simplistic and that a more fruitful approach is to focus on the role of epistemic and nonepistemic evaluative judgments in the contexts of psychiatric diagnosis, classification, and research. Using debates regarding the diagnostic criteria for diagnoses of Bipolar Disorder, I highlight the interaction between epistemic and nonepistemic value judgments and argue that the latter play a legitimate role in decisions regarding the relative risks of false positive and false negative diagnoses and whether to draw an inference quickly or wait for further evidence to reduce uncertainties. I show how this approach provides for a more straightforward comparison of the various accounts of psychiatric disorder by making explicit the role and type of evaluative judgments that are either ignored or often tacitly assumed by each account. The second half of my dissertation focuses on the debate between reductionists and pluralists. I outline and evaluate five specific reductionist theses within the philosophy of psychiatry literature: 1) ontological reductionism, 2) eliminative reductionism, 3) methodological reductionism, 4) epistemological reductionism, and 5) causal reductionism. I argue that eliminative, epistemological, and causal reductionism will likely not be borne out by the empirical evidence and that only ontological reductionism, characterized as a general commitment to physicalism, and methodological reductionism are consistent with the current evidence and explanatory aims of psychiatry. I then consider why reductionism has received so much attention and criticism despite the fact that there is no author who explicitly defends the view. I attribute this focus on reductionism to recent proposals to synthesize psychiatry with neuroscience. However, I argue that these proposals advocate nothing more than a general commitment to physicalism and a localized version of methodological reductionism and, therefore, that concerns about reductionist trends in psychiatry and the alleged harms associated with such trends are unwarranted. Pragmatism and pluralism are often defended as alternatives to reductionism in psychiatry. I examine three proposals for incorporating pragmatism into psychiatry and argue that they all fail to provide specific guidance as to how pragmatic considerations should influence decisions regarding psychiatric diagnosis and classification. I then examine proposals for incorporating empirically based pluralism and explanatory pluralism into psychiatry and argue that each view fails to fully address the problem of how to determine the relative explanatory significance of various levels of explanation. I argue that one can only address these shortcomings if one acknowledges a role of nonepistemic value judgments and that the inclusion of such judgments is the inevitable consequence of recognizing the complexity of psychiatric disorders and the provisional nature of psychiatric classification and explanation.

iii Acknowledgements

I would like to thank my dissertation director, Valerie Hardcastle, for supervising my project, and the members of my dissertation committee, John Bickle, Tom Polger, and Robert Richardson, for their support and patience. I am especially grateful to my advisor, John Bickle, for his continued encouragement and guidance. Much of my success is due to his mentorship and the congenial environment that he created both within and outside the department.

I would also like to thank the faculty in the Department of Philosophy at the University of Cincinnati for their support and instruction as well as the graduate students for fostering a friendly and comfortable environment in which to exchange philosophical ideas. I have especially benefitted from conversations with Dan Hartner and Matt Van Cleave.

I would also like to thank my parents for their unconditional love and support as I finished this project and for their encouragement to pursue a career that I truly enjoyed.

Finally, I was able to pursue this project because of a Graduate Student Research Fellowship provided by the University Research Council at the University of Cincinnati and a Taft Dissertation Fellowship provided by the Charles Phelps Taft Research Center at the University of Cincinnati. I am very grateful for the generous support of these organizations.

iv Table of Contents

Abstract ii Acknowledgments iv Table of Contents v

Chapter 1: Introduction: The Philosophical Landscape of Psychiatry 1-24 Causalism vs. Descriptivism 2 Reductionism vs. Pluralism 7 Objectivism vs. valuativism 11 Internalism vs. xternalism 14 Categorical vs. Dimensional 15 ssentialism vs. Nominalism 17 Personal vs. Impersonal 18 Conservatism vs. Revisionism 19

Chapter 2: The Role of Values in Philosophical Accounts of Psychiatric Disorder 25-93 The Constructivist and Anti-Psychiatry Challenge 27 Abolitionism 37 Objectivism 43 valuativism 52 Hybrid Accounts (Weak valuativism) 58 Reconceptualizing the Philosophical Landscape: pistemic and Nonepistemic valuative Judgments 73

Chapter 3: Reductionism in Psychiatry 94-155 What is Reductionism? 96 Ontological Reductionism 100 liminative Reductionism 103 Methodological Reductionism 105 pistemological Reductionism 106 Causal Reductionism 122 Are Proposals to Synthesize Psychiatry with Neuroscience Reductionist? 141

Chapter 4: Pragmatism and Pluralism in Psychiatry 156-181 Pragmatism in Psychiatry 157 Pluralism in Psychiatry 164 mpirically Based Pluralism (Integrative Pluralism) 169 xplanatory Pluralism 175

Bibliography 183

v Chapter 1: The Philosophical Landscape of Psychiatry

Socrates: Now does not the science of medicine, which we have just mentioned, make men able to think and to speak about their patients? Gorgias: Assuredly. Socrates: Then medicine also, it seems, is concerned with words. Gorgias: Yes. Socrates: Words about diseases? Gorgias: Certainly. (Gorgias, 450a1-a9)

The concepts of “health” and “disease” have long occupied the attention of philosophers of medicine. Philosophical debate in this area centers around which words one should use to describe health and disease. Of course, the words that one chooses to describe health and disease are typically intended to be more than just talk; they are intended to track real properties of an individual and an individual’s environment that are implicated in the etiology of disease. Moreover, the concepts of “health” and “disease” function to demarcate the proper domain of clinical medicine by distinguishing those bodily states that should be “medicalized” from those that should not. This is no less the case in psychiatry, where the scientific legitimacy of the discipline has critically depended upon choosing the right words to reliably distinguish the “mentally healthy” from the “mentally unhealthy” and the “mentally disordered” from the “mentally ordered.” One of the greatest challenges facing philosophers of psychiatry, however, is navigating and integrating the numerous ways of talking that permeate the discipline.

Psychiatry, much more so than clinical medicine, is comprised of a relatively disconnected collection of theoretical perspectives, each equipped with distinct vocabularies, methodologies, explanatory targets, and philosophical commitments. This diversity of theoretical perspectives gives rise to a number of fundamental philosophical disagreements regarding the very nature of psychiatric disorders, the reliability of

1 diagnostic criteria for psychiatric disorders, the role of values in defining psychiatric disorders, and the very nature and structure of explanation and classification in psychiatry.

This chapter introduces these fundamental philosophical disagreements by categorizing them along eight dimensions: causalism vs. descriptivism, reductionism vs. pluralism, essentialism vs. nominalism, objectivism vs. evaluativism, internalism vs. externalism, personal vs. impersonal, categorical vs. dimensional, and conservatism vs. revisionism. Kendler and Zachar (2007) first proposed six of these dimensions for categorizing philosophical disagreements, but I have added the dimensions of reductionism vs. pluralism and conservatism vs. revisionism, as these represent further fundamental philosophical disagreements within the literature. Addressing each of these debates in sufficient detail is beyond the scope of this dissertation. Some of the debates are already relatively settled while others must await further empirical evidence and will likely have to be settled on a case-by-case basis. My aim in this chapter is simply to introduce the fundamental philosophical disagreements that arise in the context of philosophy of psychiatry. I will only focus exclusively on two of these debates in the dissertation: the debate between objectivism and evaluativism and the debate between reductionism and pluralism. Although nonepistemic evaluative judgments are operative in each of these debates, they are particularly relevant to the debates between objectivists and evaluativists and between reductionists and pluralists.

Causalism vs. Descriptivism

The debate between causalism and descriptivism concerns the explanatory relevance of causal explanations in psychiatry. Causalism maintain that psychiatric

2 disorders should be categorized according to their underlying causal structure whereas descriptivist approaches contend that psychiatric disorders should be categorized according to their common symptoms, typical course, and prognosis.

The tension between these two perspectives is evidenced by the shifts in the

DSM’s nosology over the last half of the century. The DSM-I (American Psychiatric

Association, 1952) relied heavily psychodynamic theories, which traced the etiology of psychopathology to reactions to developmental or recent adverse experiences. The DSM-

II (American Psychiatric Association, 1968) incorporated more psychoanalytic concepts in classifying psychopathology and eliminated reference to “reactions” in an attempt to become more neutral with respect to etiology. Both editions, however, lacked standardized diagnostic and assessment criteria and; therefore, suffered from poor inter- rater reliability (Frances, Mack, Ross, First, 2000). The publication of the DSM-III

(American Psychiatric Association, 1980) attempted to overcome these problems by incorporating empirical data from the operationalized criteria of the previous DSM’s.

More importantly, the DSM-III represented a shift away from the psychoanalytic and psychodynamic theoretical commitments of DSM-I and II to a purely descriptive, atheoretical classification that avoided any commitment to etiology (Frances & Cooper,

1981). The publication of DSM-IV (American Psychiatric Association, 1994) brought with it few changes. The number of diagnostic categories increased from 265 to over

300, but the classifications were still entirely descriptive and neutral with respect to underlying etiology.

The criticisms of the DSM-IV have been numerous and I will not review all of them here. The criticism most relevant to the present discussion concerns the etiological

3 neutrality of the DSM. The justification for this neutrality rests upon the claim that classifying psychiatric disorders according to descriptions of symptoms while remaining neutral on controversial debates regarding underlying etiology is the best way to establish diagnostic criteria that pick out genuine disorders from normal conditions. This justification holds, however, only to the extent that there is a consensus across most theoretical perspectives as to what constitutes a disorder. As numerous critics have pointed out, this is not the case, and the failure to recognize this has only exacerbated problems of diagnostic reliability and validity. For instance, strictly descriptive, symptom-based categories tend to be heterogeneous, leading to the possibility of two patients with a wide disparity in the number and nature of symptoms to be classified as having the same disorder. In addition, relying solely on descriptive, symptom-based categories tends to lead to high rates of co-morbidity: when two alleged disorders co- occur, there is no way to determine if they are really separate disorders or simply alternative manifestations of a single disorder. Presumably, taking into account etiology could help to determine if there are distinct underlying mechanisms for each disorder or if each disorder shares the same mechanisms (or perhaps are not two distinct disorders after all). Finally, the problems of reliability and validity that result from etiological neutrality creates further difficulties for the application of diagnostic categories as well as for the integration of clinical and neuroscientific research.

Few clinical psychiatrists, of course, would disavow the therapeutic relevance of causal explanations; however, the disagreement between the two approaches concerns the status of psychiatric disorders that lack a complete causal understanding and whether causal explanations are even possible for most psychiatric disorders. At one end of the

4 spectrum are etiological approaches that require causal explanations to legitimize attributions of psychiatric disorder. On this view, one must be an anti-realist about any psychiatric disorder that lacks a complete causal explanation. This extreme position, however, seems untenable in light of the rarity of complete causal explanations for behaviors that are intuitively indicative of a psychiatric disorder. At the other end of the spectrum are descriptivist approaches that argue that an emphasis on causal explanations is misguided and futile due to the variety and complexity of causal interactions at work in most psychiatric disorders. This view does not contend that causal explanations are empirically intractable in principle; rather it asserts that causal explanations are likely to have limited clinical utility and that current symptom-based categorizations of psychiatric disorders are sufficient for therapeutic purposes. This position, however, is counter to the current trend in psychiatry and seems to over-estimate the effectiveness of symptom- based classification to the exclusion of causal factors. As psychiatry has become more aligned with clinical medicine, there has been an increasing acknowledgement that causal explanations are needed to successfully diagnose and treat mental illness (Guze, 1992;

Murphy, 2005). Moreover, despite difficulties of identifying the relevant causal variables for many psychiatric disorders, general frameworks have been developed to make causal explanations more tractable in psychiatry (Woodward, 2008) and progress has been made towards identifying and isolating specific causally relevant variables for particular psychiatric disorders, e.g., schizophrenia (Pies, 2008).

Between these two extremes lie a number of hybrid positions. For instance, one could uphold the necessity of providing causal explanations for psychiatric disorders and yet settle for descriptivist approaches until the relevant causal factors are identified and

5 isolated. This is the default position within psychiatry and, in many respects, is

representative of the methodology of researchers whose aim is to elucidate the underlying

causal structure of psychiatric disorders: researchers encounter symptoms that typically

co-occur, infer a common underlying cause (or causes) to explain this co-occurrence, and

then attempt to identify this underlying cause for purposes of therapeutic intervention.

Autism provides an illustrative example of this hybrid position. Autism is currently

diagnosed on the basis of its symptoms, a triad of behavioral impairments: impaired

social interaction, impaired communication and restricted and repetitive interests and

activities. However, as researchers have attempted to identify the underlying common

cause(s) for these symptoms, they have discovered evidence suggesting that the causes

for each of these behavioral impairments are independent of each other (Happe, Ronald,

& Plomin, 2006). This has led many researchers to abandon the attempt to find a single

causal explanation for autism and instead focus on providing causal explanations for each

distinct symptom of the triad1. This example illustrates how descriptivism may be

tentatively accepted until further evidence is acquired to determine the relevant causal

factors. Moreover, it demonstrates how acquiring information about the relevant causal

factors may lead to modifications of the initial description and categorization of

symptoms.

Another possible hybrid position is to adopt a largely descriptivist approach,

acknowledging the variety and complexity of causal interactions at work in most

psychiatric disorders, and yet grant priority to a particular class of causal factors because

1 Instances in which a single kind (in this instance autism) is divided into two or more kinds (in this instance the triad of behavioral impairments) are typically referred to as “splitting.” Conversely, instances in which what were initially thought to be two different kinds are combined into one are typically referred to as “lumping.”

6 they show promise as diagnostic markers or as therapeutic interventions. A somewhat controversial example of this would be Major Depressive Disorder (MDD). Although there are many causal factors that influence the onset and maintenance of MDD, clinicians and researchers may choose to give priority to causal factors involved in neurotransmission because these factors have shown promise both as a diagnostic marker and as a therapeutic intervention. These two hybrid positions, privileging causal explanations while temporarily settling for descriptions of symptoms and prioritizing a particularly promising causal factor, are not mutually exclusive and often co-exist.

Reductionism vs. Pluralism

The debate between reductionism and pluralism typically takes place within a general commitment to causalism and concern for explaining the causes of psychiatric disorders. Once one acknowledges the priority of providing causal explanations of psychiatric disorders, one must determine whether a single level of explanation is sufficient to adequately explain the causes of a particular psychiatric disorder or whether multiple levels of explanation will be required. However, there are a variety of reductionist and pluralist theses that one could defend and a variety of contexts within psychiatry in which one could defend them.

Reductionism is rarely explicitly advocated as an explanatory framework within psychiatry2 despite the fact that it is frequently criticized as an inadequate explanatory framework for most psychiatric disorders (Kendler, 2005, 2008; Brendel, 2003; Murphy,

2005; Regenmortel, 2004; Gold, 2009). The lack of explicit advocacy of reductionism within psychiatry obscures the heterogeneity of the view and makes it an easy target for critics. On the one hand, it gives critics extensive leeway in their characterization of the

2 Kandel (1995) does explicitly defend reductionism.

7 view, which often leads to attacking an outdated, straw man version of reduction. On the other hand, it obscures the various metaphysical, epistemological, and methodological reductionist theses that one can defend and the specific contexts in which one can defend them.

There are at least five different, though closely related, reductionist theses that one could defend in the context of psychiatry. The first of these is to defend reductionism on ontological grounds, namely, that one must be a reductionist in order to be a physicalist or naturalist. Rudnick (2002) and Gold (2009) explicitly discuss this view. In the context of psychiatry, the view would entail that the symptoms of psychiatric disorders as well as the causes of these symptoms are physical in nature.

More controversially, the view would entail that psychiatric disorders just are brain disorders. One could also defend an eliminativist version of reductionism (Zachar, 2000;

Karlsson & Kamppinen, 1995). According to this view, higher-level theories, e.g., psychological and/or sociological theories, about the causes of psychiatric disorders will eventually be eliminated in favor lower-level, presumably neuroscientific or genetic, concepts and explanations. A third strategy is to defend reductionism on methodological grounds (Rudnick, 2002). This strategy is compatible with non-reductive research strategies, but prescribes developing research strategies that aim to explain the causes of psychiatric disorders in terms of lower-level causal mechanisms. A fourth strategy is to defend reductionism on epistemological grounds. This position aligns closely with classical models of inter-theoretic reductionism and is discussed by Karlsson &

Kamppinen (1995), Rudnick (2002), Brendel (2003), and Gold (2009). Although there are multiple versions of this view, the basic idea is that a higher-level theory of

8 psychiatric disorders, e.g., one couched in sociological or psychological terms, could be explained in terms of some lower-level theory, e.g., one that only makes references to concepts from neuroscience or genetics. Finally, one could defend reductionism on strictly causal grounds. Karlsson & Kamppinen (1995) explicitly discuss causal reductionism within the context of psychiatry while Woodward (2008), Murphy (2005),

Kendler (2005, 2008) and Gold (2009) implicitly discuss the view. The view is similar to epistemological (inter-theoretic) reductionism in that it contends that a higher-level theory of psychiatric disorders, e.g., one couched in sociological or psychological terms, could be explained in terms of some lower-level theory, e.g., one that only makes references to neurobiological or genetic concepts. However, it differs from epistemological reductionism in that it explicitly treats genuine causal relations as only occurring at the lowest level of a system and maintains that explaining the interactions at this lowest level is sufficient to explain the behavior of the system as a whole.

There are clear connections between many of these varieties of reductionism, but they each make distinct claims that affect their plausibility and applicability within psychiatry. Nonetheless, most reductionists will maintain that the explanation(s) and classification of psychiatric disorder should be couched in the vocabulary of some lower- level science, e.g., neuroscience, and that, at the very least, one should adopt research methods for studying disorder that aim to investigate hypothesized lower-level causal mechanisms.

Whether and to what extent the explanation(s) and classification of psychiatric disorder should be couched in the vocabulary of neuroscience as well as whether one should adopt reductionist research methods for the study of psychiatric disorder remain

9 contested issues. Pluralists will typically deny that psychiatric disorders can be explained exclusively in the vocabulary of some lower-level science; rather, they contend that complete explanations of most psychiatric disorders will involve concepts from a multitude of disciplines, including sociology, psychology, neurobiology, and genetics.

There are at least five general strategies for defending pluralism that are discussed in the literature: ontological, cognitive, methodological, epistemological, and pragmatic.

The first of these is to defend pluralism on ontological grounds, namely, that we must be pluralists with respect to explanations about nature because nature itself is inherently pluralistic. Such a view is found in Dupree’s (1995) promiscuous pluralism and

Kitcher’s (2003) pluralistic realism. One could also defend pluralism on cognitive grounds, namely, that explanatory pluralism is an inevitable consequence of the way that our cognitive architecture models the world. Such a view is advocated by Horst (2005).

A third strategy is to defend pluralism on epistemological grounds, or what might be referred to as metascientific grounds. This strategy acknowledges the existence of multiple epistemological virtues and maintains that these virtues cannot all be maximized by any one theory at a given time, resulting in a plurality of explanations that are dependent upon which epistemic virtues are privileged. Murphy (2005) adopts this strategy specifically with respect to explanations in psychiatry. A fourth strategy is to defend pluralism on methodological grounds. This view maintains that one should use the concepts and research strategies of a multitude of disciplines to study and explain psychiatric disorders. Finally, one could defend pluralism on pragmatic grounds. This strategy closely resembles the epistemological strategy and could be defended in a variety of ways, but the general idea is that our explanatory practices are intimately tied to our

10 practical interests and, therefore, that pluralism is the only reasonable stance given the

diversity of our practical interests. Brendel (2007), who emphasizes the ethical

dimensions of explanatory paradigm choice, recommends this strategy particularly with

respect to explanations in psychiatry.

Objectivism vs. Evaluativism

The nature of facts and values and the relationship between the two lies at the

heart of the theoretical divide between objectivism and evaluativism in psychiatry. The

point of contention between these two perspectives is typically construed as a

disagreement about the meaning of psychiatric disorder. Objectivists argue that

psychiatric disorder is a purely descriptive concept and maintain that attributions of

psychiatric disorder are exhausted by descriptive facts about the internal states or

processes of an individual and/or the environment. Once one has acquired the facts about

the normal psychological and physiological functioning of the individual (and perhaps

the environment in which the individual is functioning), one can “read off” whether the

individual is mentally disordered. Thus, the presence of some type of abnormal

functioning is both necessary and sufficient for the attribution of psychiatric disorder and

no evaluative assessment regarding the harmfulness of the abnormal functioning is

required. In contrast, evaluativism maintains that attributions of psychiatric disorder

necessarily embody an evaluative component as part of their meaning3. To label a

condition as indicative of a psychiatric disorder is, at minimum, to condemn that

condition as harmful. In between these two extremes lie a number of hybrid positions

3 This view is also often referred to as normativism since it maintains that normative judgments are a necessary component of attributions of psychiatric disorder. I prefer to use evaluativism to avoid any confusion about appeals to norms. Objectivists also appeal to norms, but they typically have in mind biological norms and think that these norms can be explicated without reference to evaluative judgments.

11 that maintain that attributions of mental health and psychiatric disorder embody both a descriptive and an evaluative component: they require facts about the proper psychological and physiological functioning as well as an evaluative assessment of these facts. Although the evaluative assessment will typically precede the discovery of the descriptive facts, the descriptive facts that ground the attribution of psychiatric disorder remain independent of the evaluation.

However, debate about the meaning of the concept of psychiatric disorder is only one context within psychiatry whereby the interaction between facts and values might play out. To see this, consider a simplified account of the typical psychiatric clinical encounter. The typical encounter begins with a presentation of symptoms and attempts to describe these symptoms. The psychiatrist then draws upon an existing body of research to classify the symptoms and construct a reliable diagnosis that explains the likely course and causes of these symptoms. Finally, the psychiatrist again draws upon an existing body of research as well as the patient’s preferences to develop a treatment plan with the goal of intervening into the hypothesized causes so as to alleviate the symptoms. In this brief summary of the typical clinical encounter, debate about the relationship between facts and values in the meaning of the concept of psychiatric disorder is splintered into debate about the relationship between facts in values in the description of the symptoms of psychiatric disorder, the explanation(s) of the causes of psychiatric disorder, the classification and diagnosis of psychiatric disorder, research on psychiatric disorder, and the treatment of psychiatric disorder. Thus, one could be an objectivist, evaluativist, or offer a hybrid account along any of these dimensions. Few objectivists would deny that evaluative judgments play a role in treatment decisions, e.g., certain treatment plans may

12 be more appropriate in light of patient values, or descriptions of the symptoms of psychiatric disorder, e.g., a patient complaining that his/her depressed mood is debilitating and undesirable. However, whether and to what extent evaluative judgments play a role in the explanation and classification or diagnosis of psychiatric disorder as well as in decisions about research design and data analysis is a contested issue.

This suggests at least four plausible and yet distinct varieties of objectivism, evaluativism, or hybrid accounts that one could defend depending upon the presumed relationship between facts and values in each of the aforementioned contexts: 1) a semantic thesis regarding the relationship between factual descriptions and evaluative judgments in the meaning of psychiatric disorder, 2) an explanatory or epistemological thesis regarding the relationship between factual descriptions and evaluative judgments when drawing inferences to the best explanation of a psychiatric disorder, 3) a nosological thesis regarding the relationship between factual descriptions and evaluative judgments in classificatory and diagnostic decisions, or 4) a methodological thesis regarding the relationship between factual descriptions and evaluative judgments in decisions about research design and data analysis. An objectivist, evaluativist, or hybrid theorist could argue for the inclusion or exclusion of evaluative judgments in all or some of these contexts. For instance, one could defend a semantic version of objectivism but acknowledge that evaluative judgments play a role in diagnostic or research decisions.

Conversely, one could defend a semantic version of evaluativism but maintain that diagnostic or research decisions are straightforwardly objective matters.

13 Internalism vs. Externalism

The debate between internalists and externalists concerns whether processes that are internal or external to the organisms should be constitutive of definitions of psychiatric disorder. Internalism maintains that one should define psychiatric disorders solely in terms of processes internal to the organism and that external processes should be treated as distal causes of only secondary importance. Internalists contend that psychiatric disorders are “in the head” and that one cannot be labeled as mentally disordered without a corresponding abnormal or malfunctioning internal process. The appropriate level for articulating the internal processes is an open empirical question and relates to the aforementioned debate between reductionists and pluralists. For instance, one could argue that the relevant internal processes are psychological in nature or that they are best explained at some other level of neurobiological description, e.g., brute anatomy, neural circuits, or cells and molecules, or some combination of these.

Nonetheless, internalism is the received view within psychiatry and forms the philosophical basis of classification in the DSM.

xternalism maintains that current psychiatry focuses too exclusively on internal processes and that one should define psychiatric disorders solely in terms of processes external to the organism. xternalists typically view internal processes as relatively fixed and constant and, therefore, that one cannot be labeled as mentally disordered without reference to some corresponding external process. ating disorders, post-traumatic stress disorder, and several variations of depression provide illustrative examples of the externalist position.

14 One could also defend a hybrid position, acknowledging a constitutive role for both internal and external processes in the definition of psychiatric disorder. On this view, external processes cannot be constitutive of psychiatric disorder without a corresponding abnormal or malfunctioning internal process; likewise, internal processes cannot be isolated from and defined without reference to some corresponding external process. Moreover, the relative causal significance of internal and external processes are likely to vary among disorders, thereby enabling one to adopt a localized version of any of the above positions.

Categorical vs. Dimensional

The debate between categorical and dimensional approaches in psychiatry concerns whether psychiatric disorders are discrete categories with well-defined boundaries or abnormal extremes along a continuum of normal functioning. Categorical approaches maintain that psychiatric disorders are discrete entities with non-arbitrarily defined boundaries that clearly demarcate conditions that are indicative of a disorder from those that are not. On this view, psychiatric disorders are analogous to medical conditions such as broken bones, infectious diseases, and cancer in that each condition is distinct from one another and one either has the condition or one does not. Ideally, proponents of categorical approaches aim to identify the set of necessary conditions that are jointly sufficient to bring about the presence of the disorder. For instance, the presence of abnormal cell division is a necessary and sufficient condition to warrant the attribution of cancer. Proponents of the categorical approach in psychiatry aim to identify similar conditions for psychiatric disorders.

15 Dimensional approaches contend that psychiatric disorders are not discrete categories but instead represent differences in degree along a continuum of normal functioning. On this view, the criteria that demarcate conditions indicative of a disorder from those that are not are relatively arbitrarily. Psychiatric disorders, then, are analogous to concepts such as “fat.” There may exist an objective continuum labeled

“weight” that can be objectively measured, but concepts such as “fat” and “thin” represent subjective and arbitrary selections of dimensions along the continuum. In other words, there are no necessary and sufficient conditions that demarcate individuals who are “fat” from individuals who are “thin.” Proponents of dimensional approaches often appeal to medical conditions such as hypertension or osteoporosis as more appropriate models for psychiatric disorders (Zachar & Kendler, 2007). For instance, although an individual’s arterial blood pressure may be based upon objective facts, there are no necessary and sufficient conditions that ground the attribution of hypertension.

These approaches represent a general philosophical outlook regarding the nature of psychiatric disorders. However, one could adopt either of these approaches with respect to a particular disorder or class of disorders but not others. For instance, one could defend a categorical approach with respect to schizophrenia but advocate a dimensional approach with respect to personality disorders (Widiger et al, 2007).

Moreover, one could adopt a hybrid position that incorporates a dimensional component within a categorical system (or vice versa). For instance, Krueger et al (2007) have proposed a dimensional account of personality disorders that aims to construct prototypes

16 of each personality disorder4. ach prototype represents a cluster of symptoms that

typically co-occur in patients but none of which are necessary or sufficient to warrant

attribution of the disorder. The prototypes serve to demarcate relatively discrete

categories along a continuum of normal functioning. As with categorical and

dimensional approaches in general, one could defend a prototypical account for some

disorders, e.g., personality disorders, but not for others.

Essentialism vs. Nominalism

The debate between essentialists and nominalists concerns whether psychiatric

disorders have an underlying nature by which they should be defined. ssentialists

maintain that psychiatric disorders exist independently of our classifications of them and

that the goal of psychiatric nosology is to discover their underlying natures and classify

them accordingly. The periodic table of elements is a paradigm example of the

essentialist perspective. Individual elements of the periodic table, e.g., gold, share the

same underlying causal structure and interact in a law-like fashion. ssentialists contend

that psychiatric classification should aim to categorize psychiatric disorders in terms of

their underlying causal structure in the same way as the periodic table of elements.

Moreover, essentialists typically adopt categorical approaches to defining psychiatric

disorder in that the underlying causal structure of psychiatric disorders can be articulated

in terms of necessary and sufficient conditions in the same way, for example, that having

the atomic number 79 is a necessary and sufficient condition for an element to be gold.

Nominalists deny that psychiatric disorders have an underlying causal structure by

which they can be defined. Radical versions of the view maintain that classifications of

4 Prototype approaches are also often referred to as exemplar approaches (see, e.g., Murphy, 2005). The general framework for such approaches originates in leanor Rosch’s (1978) work on the categorization of objects and was first applied to the concept of psychiatric disorder by Lillenfeld & Marino (1995).

17 psychiatric disorder are grounded in their practical utility rather than some independently existing, underlying nature. Such views are often, though not always, associated with constructivist and anti-realist critiques of psychiatry that view psychiatric categories as a means of labeling and controlling social deviance. More moderate versions of nominalism acknowledge that psychiatric disorders may exhibit some underlying causal structure, but they contend that there is not necessarily “one unique categorization that stands above the others on a priori grounds (Zachar & Kendler, 2007; p. 558).” Rather, there are multiple ways of categorizing psychiatric disorders relative to practical purposes and no single categorization will be adequate for all purposes. On this view, the concept of psychiatric disorder is analogous to the concept of “weeds”: any plant that gets labeled as a “weed” does exhibit some underlying causal structure, but which plants get labeled as “weeds” will be relative to practical interests.

ach of these positions represents a general philosophical outlook on the nature of psychiatric disorders and psychiatric classification. However, it is possible to defend localized versions of each of these positions. For instance, one may adopt an essentialist position with respect to a particular disorder or class of disorders, e.g., mood disorders, but advocate a nominalist position with respect to other disorders, e.g., personality disorders.

Impersonal vs. Personal

The debate between impersonal and personal approaches in psychiatry concerns the relationship between psychiatric disorders and the individuals to whom they are attributed. Impersonal approaches typically view psychiatric disorders as “things” that people “get.” On this view, psychiatric disorders are relatively stable, constant entities

18 that manifest themselves in patients in a uniform manner. As such, they form lawlike relationships and can be explained using traditional scientific methods. For instance, an impersonal approach to schizophrenia would treat it as a disease that afflicts an individual and that afflicts different individuals in the same manner. This stability, presumably, is what enables researchers to study and treat the disease in a patient population.

Personal approaches view psychiatric disorders as inseparable from the people to whom they are attributed. On this view, people possess dynamic intentions and purposes and the symptomatology of a psychiatric disorder cannot be isolated and fully understood independent of these changing psychological states. Therefore, each psychiatric disorder uniquely manifests itself in each individual, making it more difficult to form lawlike generalizations regarding the causes of symptoms and, therefore, creating barriers to explaining psychiatric disorders using traditional scientific methods.

ach of these positions represents a general philosophical outlook on the nature of psychiatric disorders and their relationship to the individuals to whom they are attributed.

However, as with the other dimensions discussed above, it is possible to defend localized versions of each of these positions. For instance, one may adopt an impersonal approach for some particular disorder or class of disorders, e.g., on the grounds that the symptoms associated with the disorder are not influenced by the dynamic psychological states of the individual, but defend a personal approach for other disorders.

Conservatism vs. Revisionism

The debate between conservative and revisionist approaches concerns how psychiatric classifications should be revised in light of new information about the nature and/or presence of symptoms or new information about the causal processes involved in

19 the development and/or maintenance of these symptoms. A conservative approach tends to be resistant to classificatory revision in light of new information. Typically, this approach is grounded in concerns about the harmful iatrogenic effects of psychiatric labels, particularly when there is no disciplinary consensus as to whether the evidence warrants the proposed revisions. Alternatively, a revisionist, or what is sometimes referred to as an activist or innovationist approach, tends to encourage classificatory revision in light of new information. This approach is more willing to lump previously separate diagnostic categories together or split a diagnostic label into separate categories based on preliminary information with the expectation that doing so will increase diagnostic validity and reliability.

These two approaches represent general dispositions regarding the willingness to revise existing classificatory schemes in light of new evidence. However, one could also adopt either of these approaches with respect to a particular disorder or class of disorders but not others. For instance, one could be a revisionist with respect to personality disorders on the grounds that the diagnostic categories that comprise this group were poorly defined from the outset but adopt a more conservative approach with respect to diagnostic categories that have historically been more reliable, such as schizophrenia.

Murphy (2005) draws the further distinction between conservative and revisionist approaches along closely related but somewhat different lines. His distinction focuses on the relationship between our folk concepts of mental health and mental disease and the empirical sciences that investigate these concepts. According to the conservative approach, our folk psychological concepts of mental health and mental disease are largely correct and genuinely refer to real entities. Conservative approaches are typically

20 grounded in a commitment to objectivism as discussed above and uphold the priority of folk psychological concepts over empirical findings. For instance, conservative objectivists argue that we are likely to find pathological neurological correlates for most of our common sense conceptions of mental disorder and that in cases in which we do not find such correlates it is likely due to the shortcomings of our empirical sciences rather than our folk psychological concepts. Revisionists, on the other hand, maintain that our folk psychological concepts of mental health and mental disease are largely mistaken and do not genuinely refer to real entities. According to Murphy, revisionist approaches are typically grounded in a commitment to constructivism and claim that our attributions of psychiatric disorder are attempts to medicalize socially deviant behavior. However, revisionists need not be committed to constructivism. Murphy, for instance, defends a revisionist objectivist approach in which many of our folk psychological conceptions of mental health and mental disease may be mistaken and eventually replaced by the findings of the empirical sciences that investigate these concepts. In particular, Murphy argues that the cognitive neurosciences could potentially deliver descriptive facts about proper psychological functioning that could serve as an objective basis for our attributions of mental health and mental disease.

Addressing each of these debates in further detail is beyond the scope of this dissertation. Some of the debates, for instance, the debates between causalism and descriptivism and internalism and externalism, are already relatively settled. Most accept the necessity of providing causal explanations for psychiatric disorders and yet settle for descriptivist approaches until the relevant causal factors are identified and isolated.

Similarly, most acknowledge a constitutive role for both internal and external processes

21 in the definition of psychiatric disorder, even if the relative causal contribution of internal and external processes for particular disorders is not yet determined. Most of the remaining debates must await further empirical evidence and will likely have to be settled on a case-by-case basis. For instance, whether psychiatric disorders are discrete categories with well-defined boundaries or abnormal extremes along a continuum of normal functioning (categorical vs. dimensional), whether they can be defined according to their underlying causal structure or their practical utility (essentialism vs. nominalism), whether they are inseparable from the people to whom they are attributed (personal vs. impersonal), and whether the risks of revising psychiatric classification are justified in light of new information (conservatism vs. revisionism) cannot be settled a priori and will likely vary depending on the particular condition or class of conditions that one considers.

The above point applies equally to the debates between objectivism and evaluativism and reductionism and pluralism. However, I will focus exclusively on these two debates for several reasons. First, although philosophers of psychiatry have focused on objectivism and evaluativism as semantic and nosological theses regarding the relationship between factual descriptions and evaluative judgments in the meaning of psychiatric disorder and in classificatory and diagnostic decisions respectively, relatively little attention has been paid to their relationship in psychiatric research or when drawing inferences to the best explanation for the causes of psychiatric conditions. Chapter 2 aims to address this shortcoming. I review several objectivist, evaluativist, and hybrid analyses of the concept of psychiatric disorder and consider their relative strengths and weaknesses. I defend a hybrid position and trace the role of nonepistemic value

22 judgments in drawing inferences to the best explanation of a psychiatric disorder, weighing the relative risks associated with the inclusion or exclusion of diagnostic criteria, and comparing the relative risks of drawing an inference quickly versus waiting for further evidence to reduce uncertainties. I argue that nonepistemic value judgments play a legitimate and inevitable role in each of these contexts. The second reason I focus exclusively on the objectivism vs. evaluativism and reductionism vs. pluralism debates is that the latter is particularly replete with ambiguity and in need of conceptual clarification. There is little consensus as to what constitutes reductionism or pluralism in the context of psychiatry, with many authors overlooking the various metaphysical, epistemological, and methodological reductionist and pluralist theses that one can defend and the specific contexts in which one can defend them. Chapter 3 and chapter 4 aim to address these shortcomings. Chapter 3 reviews five reductionist theses in the context of psychiatry and assesses their relative strengths and weaknesses. I examine several proposals to synthesize psychiatry with neuroscience and argue that none of the proposals are reductionist in any substantive metaphysical or epistemological sense of the term. I conclude with a brief defense of a localized version of methodological reductionism.

Chapter 4 reviews several pragmatist and pluralist theses in the context of psychiatry and assesses their relative strengths and weaknesses. I defend a version of explanatory pluralism on the grounds that no single explanation will likely be able to maximize all of the epistemic values that one would desire in an explanation and that those explanations that we accept as adequate will depend upon which epistemic values we choose to privilege in light of our pragmatic interests. I conclude by showing how this version of

23 explanatory pluralism is compatible with the localized version of methodological reductionism that I defend in Chapter 3.

24 Chapter 2: The Role of Values in Philosophical Accounts of Psychiatric Disorder

At the beginning of the previous chapter, I noted that the status of psychiatry as a legitimate scientific discipline has critically depended upon choosing the right words to reliably distinguish behaviors that are indicative of psychiatric disorder from those that are simply the result of “problems of living.” The prospect of such a project, however, has been met with much skepticism. Most notably, anti-psychiatry critiques, pioneered by the publication of Thomas Szasz’s The Myth of Mental Illness (1960), have claimed that a distinction between psychiatric disorder and “problems of living” cannot be maintained and that the concept of psychiatric disorder is a scientifically useless concept.

The major premise underlying these critiques is that the norms or values that ground attributions of psychiatric disorder are importantly different from the norms that ground attributions of physical disease. Attributions of psychiatric disorder are determined by contingent societal values whereas attributions of physical disease are determined by fixed biological facts about proper functioning. If sound, these critiques would introduce an unwelcome level of relativism into psychiatry, making psychiatric classification futile at best and harmful at worst.

Responses to the anti-psychiatry challenge have typically adopted one of the four following strategies: 1) provide an account of psychiatric disorder that rests upon a purely descriptive, value-free account of abnormal functioning, 2) acknowledge the role of evaluative judgments in attributions of psychiatric disorder but maintain that such judgments are not arbitrary, 3) acknowledge the role of evaluative judgments in attributions of psychiatric disorder but maintain that such judgments must be accompanied by a purely descriptive, value-free account of abnormal functioning, or 4)

25 argue that psychiatry does not need an account of psychiatric disorder to establish itself as a legitimate science or branch of medicine. The first strategy is associated with objectivist or descriptivist accounts of psychiatric disorder and maintains that the concept of psychiatric disorder is a purely descriptive concept that refers to facts about the abnormal functioning of internal states or processes of an individual. The second strategy is associated with evaluativist or normativist accounts of psychiatric disorder and maintains that attributions of psychiatric disorder necessarily embody an evaluative component as part of their meaning. On this view, to label a condition as indicative of a psychiatric disorder is, at minimum, to condemn that condition as harmful. The third strategy is associated with hybrid accounts of psychiatric disorder, which contend that attributions of psychiatric disorder require a factual description of abnormal functioning as well as an evaluative judgment regarding the harmfulness of this abnormal functioning. The final strategy, which I refer to as abolitionism, argues that an account of psychiatric disorder is unnecessary for psychiatry to be a legitimate science. This strategy purports to eliminate the need for a philosophical account of psychiatric disorder by showing that the current philosophical debates are misguided or that any explanatory work that such an account could provide can be accomplished by other, less controversial, concepts.

This chapter examines each of these strategies in detail and assesses their relative strengths and weaknesses in addressing the anti-psychiatry challenge. I begin by discussing the anti-psychiatry critiques in more detail and show that they rely on an unwarranted account of psychiatric disorder and lead to an unreasonable degree of relativism. I then assess the abolitionist proposals of Hesslow (1993) and Kincaid

26 (2008), the objectivist proposal of Boorse (1975, 1976, 1977, 1997), the evaluativist proposals of Nordenfelt (1995, 2007) and Fulford (1989), and the hybrid accounts of

Wakefield (1992, 2007), Cooper (2002), and reshefsky (2009). Finally, I argue that the factual-evaluative way of carving up the philosophical landscape is overly simplistic and that a more fruitful approach is to distinguish accounts of psychiatric disorder in terms of the relative significance placed on the role of epistemic and nonepistemic value judgments in the attribution of psychiatric disorder. I conclude that nonepistemic value judgments should play a legitimate role in classification and research decisions and that, once this is acknowledged, the distinctions between the aforementioned philosophical positions becomes less relevant than determining when appeals to nonepistemic value judgments are legitimate.

The Constructivist and Anti-Psychiatry Challenge

Constructivism represents a broad spectrum of theoretical positions spanning a variety of disciplines. As philosopher of mathematics Paul rnest (1995) points out,

"there are as many varieties of constructivism as there are researchers (p. 459).” One common way of distinguishing varieties of constructivism is in terms of the kinds of things that allegedly are constructed. Boghossian (2006), for instance, distinguishes metaphysical and epistemological constructivism. pistemological constructivists maintain that it is beliefs about things or facts, rather than the things or facts themselves, which are constructed. More specifically, epistemological constructivists contend that the reason(s) we hold some particular belief is primarily, or entirely, the result of the social, political, economic, or cultural value of the belief. Often it is thought that these values, rather than the evidence in favor of the belief, determine whether we hold a

27 particular belief, though this is not necessarily the case. Metaphysical constructivists

maintain that it is things or facts that are constructed and not just our beliefs about these

things or facts. Although metaphysical constructivism may be directed at different kinds

of things5, e.g., social facts, scientific facts, everyday facts, all possible facts, the general

idea is that some particular thing or fact is real but only contingently so. Boghossian’s

metaphysical constructivism parallels Hacking’s (1999) use of ‘constructivism’, which he

characterizes in the following way: “X need not have existed or need not be at all as it is.

X, or X as it is at present, is not determined by the nature of things; it is not inevitable (p.

6)6.”

In the context of psychiatry, epistemological constructivism is committed to the

claim that our beliefs about psychiatric disorder, e.g., our beliefs about how to classify

psychiatric disorder, are the result of various social, political, cultural, and ethical values.

Put another way, epistemological constructivists assert that psychiatric diagnoses

necessarily embody an evaluative component as part of their meaning. To label an

individual as mentally disordered is, at minimum, to attribute to that individual a

condition that is undesirable or harmful. pistemological constructivism as I have

defined the term here is simply a denial of objectivism, the view that psychiatric

diagnoses are value-neutral. Metaphysical constructivists take this denial of objectivism

a step further and argue that the value-ladenness of psychiatric diagnoses supports anti-

realism about psychiatric disorder, the view that psychiatric disorders do not really exist.

5 See, for instance, Kukla (2000). Kukla distinguishes four specific varieties of metaphysical constructivism, or what he refers to as constitutive constructivism: 1) reasonable social constructivism restricts the domain of constructed facts to social facts, 2) scientific social constructivism maintains that both social facts and scientific facts are socially constructed, 3) strong social constructivism applies to scientific facts as well as everyday facts, and 4) very strong social constructivism applies to all possible facts (p. 24-31). 6 Hacking’s account of constructivism includes two additional evaluative judgments, namely, that X is bad and that we would be much better off if X were done away with or at least radically transformed.

28 On this view, psychiatric diagnoses are nothing more than a convenient and arbitrary grouping of symptoms, i.e., psychiatric disorders are not real in the sense that

“symptoms” are indications of an underlying disorder or pathology. Metaphysical constructivism can be intended to apply globally, e.g., all psychiatric disorders are constructed (e.g., Szasz, 1961) or locally to a specific disorder, e.g., Major Depressive

Disorder is constructed (Horwitz & Wakefield, 2007).

pistemological and metaphysical constructivism are often defended together.

For instance, to argue that psychiatric diagnoses embody an evaluative claim as part of their meaning is often taken to imply that there are no facts about underlying pathology that ground psychiatric diagnoses. Conversely, to argue that psychiatric diagnoses are nothing more than a convenient and arbitrary grouping of symptoms is often taken to suggest that psychiatric diagnoses are constructed in light of prevailing societal values.

However, there are good reasons for keeping the two positions separate. Most importantly, each position is typically motivated by distinct concerns. pistemological constructivism is primarily motivated by a concern to illuminate the role of values in psychiatric diagnoses, a project which need not entail any commitment to anti-realism about psychiatric disorders. Hybrid accounts, for instance, acknowledge a role for values in psychiatric diagnoses and yet uphold the reality of psychiatric disorders

(Wakefield, 1992; Cooper, 2002). Metaphysical constructivism, on the other hand, is explicitly aimed at defending, either globally or locally, anti-realism about psychiatric disorders. Highlighting the role of values in psychiatric diagnoses may constitute part of the anti-realist arsenal, but it is neither necessary nor sufficient for such an argument to proceed.

29 The anti-realism of metaphysical constructivism poses the greatest threat to the philosophical and scientific foundations of psychiatry and, for this reason, is often associated with the anti-psychiatry movement. The anti-psychiatry movement developed in the 1960’s through the works of Michel Foucault (1964/1988), Thomas Szasz (1961),

R.D. Laing (1960), and David Cooper (1967) and represents an eclectic array of theoretical and practical critiques of psychiatry. A common theme of these critiques was the harmful iatrogenic effects of psychiatric diagnoses, for example, the unnecessary social stigma of labeling, the potential “looping effects” of psychiatric diagnoses, and the possibility of abolishing personal responsibility. Others focused on the negative effects of particular psychiatric treatments, e.g., electroconvulsive therapy, and the growing commercial influence of the pharmaceutical industry on psychiatry. Still others challenged the involuntary commitment of mental patients and the use of psychiatric diagnoses as a means of coercion and control7. Motivating each of these criticisms, however, was an implicit or explicit commitment to metaphysical constructivism and a denial of the reality of mental illness.

This commitment to metaphysical constructivism is evident in the works of

Michael Foucault (1964), who is often credited with originally formulating the view in

7 None of these claims, however, are essential to the metaphysical constructivist’s position in psychiatry. Metaphysical constructivists need only deny that clusters of symptoms are in any way indications of some underlying disorder or pathology. This is entirely compatible with accepting that certain clusters of symptoms are positively correlated with one another. In this sense, they can maintain that psychiatric diagnoses are not entirely arbitrary and have some level of internal consistency and inter-rater reliability. In addition, metaphysical constructivists need not deny that patients can respond to the same interventions with some homogeneity. For example, patients could experience a reduction in symptoms, e.g., fever, in response to the same intervention, e.g., aspirin, despite suffering from different conditions, e.g., influenza or pneumonia (Borsboom, 2008). Although the metaphysical constructivist will likely deny these latter claims as well, it is only the denial that clusters of symptoms are in any way indications of some underlying disorder or pathology that is essential to metaphysical constructivism.

30 the context of medicine and psychiatry. Linguist Richard Harland summarizes Foucault’s view as follows:

…psychiatric medicine works only to the extent that patients are persuaded into speaking a scientific language about themselves. Patients are 'mad' because they have evaded the primary socialization which ordinarily enters into human beings along with their society's language; but they can still be subdued and at least partially socialized by a secondary web of restraining language… [This] seemingly successful result in no way proves the validity of the psychiatrist's language. The psychiatrist has not caught the truth of madness in his language, he has merely taught it to speak the same language back to him (Harland 1987, p. 104).

Foucault’s characterization of psychiatry, like much of his other work, emphasizes the centrality of power relations: psychiatrists construct diagnoses of psychiatric disorder as a means of controlling individuals whose behaviors do not cohere with the predominant values of the society. By construing abnormal or deviant behaviors as symptomatic of an underlying disorder, psychiatric diagnoses function to legitimize the removal and

“treatment” of abnormal or deviant individuals and to reinforce the predominant values of the society. For Foucault, however, such diagnoses are nothing more than a convenient and arbitrary grouping of symptoms with no objective validity. Put another way, psychiatric diagnoses are socially constructed kinds rather than naturally existing ones.

Thomas Szasz offers a similar constructivist critique in his well-known work The

Myth of Mental Illness (1961). Szasz’s particular target is the biomedical/disease model of mental illness. He argues that a disease is an objectively verifiable lesion or abnormal pathophysiological state of the body; a definition that he takes as uncontroversial. Since alleged mental “diseases” such as schizophrenia or Major Depressive Disorder are not associated with any such objectively verifiable lesions or abnormal pathophysiological states of the body, Szasz concludes that they cannot be diseases. Szasz further argues

31 that a commitment to the disease model makes the concept of psychiatric disorder a meaningless and scientifically useless concept: “once a putative disease becomes a proven disease it ceases to be classified as a psychiatric disorder and is reclassified as a bodily disease; or, in the persistent absence of such evidence, a psychiatric disorder becomes a nondisease (p. 6).” Finally, Szasz echoes Foucault’s assertion that psychiatric diagnoses are nothing more than a convenient and arbitrary grouping of symptoms that reflect the predominant values of the society: “[Psychiatric diagnoses] are the products of the medicalization of disturbing or disturbed behaviors – that is, the observer's construction and definition of the behavior of the persons he observes as medically disabled individuals needing medical treatment (p. 3).”

It should be noted that Szasz does not identify himself as part of the anti- psychiatry movement, a term he reserves strictly to the works of Laing and Cooper, and explicitly distances himself from the movement. Nonetheless, his criticisms have influenced much of the work that is done in the name of the anti-psychiatry movement.

For instance, Lawrence Stevens, a lawyer who represents psychiatric patients and who administers the website antipsychiatry.org, reiterates Szasz’s arguments against the disease model of mental illness:

the label schizophrenia, like the labels pornography or mental illness, indicates disapproval of that to which the label is applied and nothing more. Like ‘mental illness’ or pornography, ‘schizophrenia’ does not exist in the sense that cancer and heart disease exist but exists only in the sense that good and bad exist. As with all other so-called mental illnesses, a diagnosis of ‘schizophrenia’ is a reflection of the speaker's or ‘diagnostician's’ values or ideas about how a person ‘should’ be, often coupled with the false (or at least unproven) assumption that the disapproved thinking, emotions, or behavior results from a biological abnormality. Considering the many ways it has been used, it's clear ‘schizophrenia’ has no particular meaning other than ‘we dislike it’ (Stevens, 2003).

32 Psychologist Bruce Levine (2001) and sociologist Thomas Scheff (1999) share

Stevens’ skepticism of the validity of psychiatric diagnoses also appeal to Szasz’s criticisms of the disease model. Levine, in his work entitled Commonsense Rebellion:

Debunking Psychiatry, Confronting Society, offers the following reminder: "Remember that no biochemical, neurological, or genetic markers have been found for attention deficit disorder, oppositional defiant disorder, depression, schizophrenia, anxiety, compulsive alcohol and drug abuse, overeating, gambling, or any other so-called mental illness, disease, or disorder (Levine, 2001)." The implication is that psychiatric disorders are not real because “no biochemical, neurological, or genetic markers have been found.”

Thomas Scheff (1970/1999) grounds his critique of psychiatry in labeling theory.

On his view, mental illness is what he refers to as “residual deviance”: individuals that are labeled as mentally disordered are simply people that society would like to label as deviant but have no other label, such as a criminal, pervert, or person with bad manners.

In short, psychiatric diagnoses are simply the label that we construct for behaviors that conflict with the predominant societal values and for which have no pre-existing label. In defense of this position, Scheff offers the following critique of the disease model of mental illness: “Although their hypotheses are plausible, they are still, at this writing, unproven. To date, no clearly demonstrable linkage between neurotransmission or genetics has been found for any major mental illness. The idea that the mentally ill suffer from deficient neurotransmission or genes is only a theory (p. 2).” Again, the implication is that psychiatric disorders are not real so long as there is “no clearly demonstrable linkage between neurotransmission or genetics” for any purported psychiatric disorder.

33 I do not here wish to criticize the specific claims of each of these authors as they

(particularly the work of Foucault and Szasz) have been thoroughly criticized elsewhere

(see, e.g., Murphy, 2005; Pies, 1979, 2004). Nor do I intend to provide evidence of abnormal pathophysiology for each of the purported psychiatric disorders that they challenge. Such evidence is not required to show the errors in their reasoning. All of the authors discussed above assume that realism about psychiatric disorders requires that one conceive of psychiatric disorders as diseases. However, there are good reasons for thinking that realism about psychiatric disorders requires no such commitment.

Nonetheless, even if realism did require such a commitment, there are good reasons for thinking that evidence of abnormal pathophysiology is not necessary for the attribution of disease, even physical disease. For instance, Amyotrophic Lateral Sclerosis (ALS), also known as Lou Gehrig’s Disease, has no known cause and no specific biomarker that reliably allows physicians to diagnose the condition, yet no one doubts whether ALS is a disease.

These considerations alone are sufficient to rebut the metaphysical constructivist theses discussed above. However, even if one grants that evidence of abnormal pathophysiology is a necessary condition for disease attribution and that no such evidence currently exists, Murphy (2006) provides two strong arguments against metaphysical constructivism and its anti-realist commitments. First, metaphysical constructivism conflicts with intuitive judgments about psychiatric disorder. To see this, recall again the sorts of claims that the metaphysical constructivist makes. Szasz claimed that,

“[Psychiatric diagnoses] are the products of the… observer's construction.” Stevens asserted that all psychiatric disorders are “a reflection of the speaker's or ‘diagnostician's’

34 values or ideas about how a person ‘should’ be.” Finally, Scheff argued that psychiatric disorders are instances of “residual deviance;” psychiatric diagnoses are labels for people that society would like to label as deviant but have no other label. If each of these claims is correct and attributions of psychiatric disorder are just reflections of violations of social norms, then all violations of social norms should be taken as evidence of a psychiatric disorder. Behaviors such as celibacy, vegetarianism, choosing not to get married, choosing not to have children, all of which are violations of predominant social norms, should all be considered psychiatric disorders. However, nobody seriously contends that such behaviors are indicative of a psychiatric disorder. Intuitively these behaviors are different from the delusions associated with schizophrenia or the panic attacks associated with anxiety disorder in that they are not symptomatic of some underlying disorder or pathology. However, since the metaphysical constructivism denies that any behaviors are indications of some underlying disorder or pathology, they cannot help themselves to this response. In short, certain behaviors or symptoms seem to be indications of an underlying disorder whereas others are not, but the metaphysical constructivist cannot account for these intuitions.

This is an admittedly weak argument since intuitions about which behaviors are or are not indicative of a psychiatric disorder can turn out to be wrong or revised in light of new empirical evidence. Nonetheless, these intuitions form the basis for a closely related argument against metaphysical constructivism, namely, that it cannot avoid relativism.

This may seem like an odd charge since historically much of the impetus for metaphysical constructivism has been the presumed relativity of psychiatric diagnoses.

Metaphysical constructivists cite numerous historical examples of false positive

35 diagnoses in defense of this claim. Drapetomania, a diagnosis used for runaway slaves, hysteria, a diagnosis used for highly emotional women who sought divorce from abusive husbands, masturbation, and homosexuality are just some of the commonly cited false positive diagnoses used to illustrate the value-ladenness and relativity of psychiatric classification. Such misdiagnoses are undoubtedly disturbing and have led to unfair social stigma and harmful “treatments” for “patients.” The problem, however, is that metaphysical constructivists cannot explain why these are cases of misdiagnoses. The intuitive response is that these are not psychiatric disorders because the behaviors are not symptomatic of some underlying disorder or pathology. Once again, however, metaphysical constructivists cannot help themselves to this response since they deny that any behaviors are indications of some underlying disorder or pathology.

A possible response for metaphysical constructivists would be to fully embrace the relativistic implications of their position and adopt some sort of cultural criterion for demarcating psychiatric disorders from non-disorders. For instance, they could accept that drapetomania was a real psychiatric disorder for that particular culture at that particular time, but that it is no longer a real psychiatric disorder because the cultural values have changed. Thus, a behavior could be judged as indicative of an underlying disorder or pathology so long as the judgment coheres with the predominant values of the culture, even if that same behavior would not be considered indicative of a disorder according to a different culture with different values or to the same culture that had changed its values over time. This response, of course, would require metaphysical constructivists to at least partially relinquish their anti-realist commitments. Regardless, such a response would not be very attractive.

36 Abolitionism

Most of the constructivist and anti-psychiatry critiques rest upon the unreasonable demand that psychiatric disorders be analogous to physical diseases. They mistakenly conclude that the failure to establish this parallel undermines the scientific legitimacy of psychiatry. However, one line of reasoning maintains that psychiatry does not need an account of psychiatric disorder to establish itself as a legitimate science or as a branch of medicine. This line of reasoning originates in the work of Germund Hesslow (1993) and was later applied to psychiatry by Kincaid (2008). Hesslow is primarily concerned with the utility of the concepts of “health” and “disease” for clinical medicine. He argues that

“the health/disease question is irrelevant - we never really need to know whether someone has a disease or not, and consequently, we do not need a definition of 'disease'

(2).” Hesslow considers several reasons why one might want a definition of ‘health’ and

‘disease’: 1) health and disease function to justify who receives treatment and who does not, 2) disease diagnoses are often used by third-parties in making reimbursement decisions, e.g., an insurance company may only reimburse for interventions aimed at treating disease, 3) attributions of disease often excuse one from normal moral obligations, e.g., the duty to work, and 4) attributions of disease often excuse one from moral responsibility and legal liability, e.g., an individual with schizophrenia may be found incompetent and unable to stand trial or be eligible for the death penalty.

Hesslow argues that a conceptual analysis of health and disease is unnecessary in each of these contexts. First, he points out that decisions about who does and does not receive treatment are often made independent of any disease diagnosis. For example, individuals seeking cosmetic surgery are typically not diseased, whereas individuals with

37 benign tumors or small fibromas are diseased but nonetheless do not receive treatment.

Second, Hesslow argues that decisions about whether to reimburse for medical interventions are made independent of any disease diagnosis. He cites the examples of eyeglasses and cosmetic surgery as counterexamples. yeglasses are not covered by medical insurance in most countries despite the fact that most cases of poor eyesight are the result of disease. Conversely, many countries do cover cosmetic surgery despite the fact that being unattractive is not indicative of an underlying disease. According to

Hesslow, what matters for reimbursement decisions is the difficulty of predicting and controlling the condition and whether the condition is judged to be undesirable by the members of the particular society. Those conditions that are difficult to predict and control and judged to be undesirable by most members of a particular society are deemed worthy of reimbursement. Third, Hesslow asserts that attributions of disease are irrelevant when deciding whether one should be excused from normal moral obligations.

For instance, he points out that decisions as to whether one should be excused from the obligation to work are based upon considerations of “the nature of the work in question and the nature of the discomfort (9)” rather than the presence of a disease. Finally,

Hesslow argues that attributions of disease are irrelevant when deciding whether to excuse one from moral responsibility and legal liability. Here Hesslow is directly concerned with the concepts of “mental health” and “mental disease” and their role in justifying punishment. He contends that punishment is grounded in consequentialist concerns and, therefore, that the “crucial consideration is the inability of the individual to be influenced by the consequences of her actions, not the reason for this disability (10).”

38 Hesslow is correct to point out that not all treatment and reimbursement decisions are based upon the diagnosis of disease and that decisions about whether to excuse one from normal moral obligations and responsibilities are often made for reasons other than the presence of a disease. However, the reasons that he provides do not support his pessimistic conclusions. First, Hesslow’s appeal to individuals seeking cosmetic surgery does not show that physicians treat patients without a disease diagnosis. Whether cosmetic surgery for non-therapeutic reasons should be considered a proper part of medicine is a contested issue, but few cosmetic surgeons would claim that performing such surgeries on individuals would constitute “treatment.” Furthermore, pointing out that there are individuals with disease who do not receive treatment does not establish that the concept of “disease” is irrelevant for deciding who should receive treatment. It only shows that either there are considerations other than just the presence of disease that are relevant for treatment decisions, e.g., the severity of the disease and patient values, or that the concept of “disease” embodies more than simply the presence of abnormal functioning, e.g., a judgment that the abnormal functioning is undesirable.

Second, although decisions about whether to reimburse for medical interventions are sometimes made independent of any disease diagnosis, such cases are typically the exception rather than the rule. This is evidenced by the medical insurance industry’s reliance on the DSM for providing guidance about which psychiatric conditions warrant treatment and, thus, which treatments warrant reimbursement. The case of Posttraumatic

Stress Disorder (PTSD) provides an illustrative example (McNally, 2011). Throughout the 20th century psychiatrists used a variety of diagnostic categories to describe maladaptive responses to combat, such as “shell shock,” “combat exhaustion,” and “war

39 neurosis.” However, the government and Veterans Administration did not recognize the legitimacy of these categories and maintained that the maladaptive responses were a manifestation of prior psychiatric problems rather than the result of combat experience.

According to McNally, this changed when proponents of the syndrome linked these combat responses to similar responses experienced by Holocaust survivors, rape victims, and those experiencing natural disasters. Lumping these conditions together and recognizing what they had in common led to the introduction of Posttraumatic Stress

Disorder. The disorder was included as an official diagnosis in the DSM-III and, shortly thereafter, was eligible for a wide variety of services provided by the Veterans

Administration Hospitals. Cases such as PTSD demonstrate the importance of “disease” concepts for decisions about medical reimbursement and challenge Hesslow’s pessimistic conclusions.

Finally, although attributions of disease are sometimes irrelevant when deciding whether to excuse one from moral obligations and responsibilities, they are typically relevant considerations. For instance, on May 3rd, 2013, the Minnesota Senate approved a Worker’s Compensation Bill (SF 1234) that allows for coverage of “mental only” injuries for the first time in the state. To qualify for coverage, a worker must demonstrate

“mental impairment” as a result of working conditions. The bill defines “mental impairment” as: “a diagnosis of post-traumatic stress disorder by a licensed psychiatrist or psychologist. For the purpose of this chapter, ‘post-traumatic stress disorder’ means the condition as described in the most recently published edition of the Diagnostic and

Statistical Manual of Mental Disorders by the American Psychiatric Association

(Minnesota House of Representatives, SF 1234, 2013).” This not only further

40 demonstrates the relevance of disease diagnosis for decisions about medical reimbursement, but it also shows its relevance for decisions about whether to excuse one from normal moral obligations, such as the obligation to work. Furthermore, Hesslow’s claims that that punishment is grounded solely in consequentialist concerns and that responsive to consequences is all that matters when deciding whether to punish an individual are problematic. Certainly some laws reflect consequentialist concerns, but many laws in the United States are grounded in retributivist concerns. As such, whether a convicted offender is responsive to consequences is often not a relevant consideration for justifying punishment. This, of course, must be determined on a case-by-case basis, but Hesslow clearly overstates his case by claiming that the justification for all punishment is grounded in consequentialist concerns. For these reasons, Hesslow’s pessimistic conclusions do not follow. On the contrary, there are good reasons for thinking that diagnoses of disease and psychiatric disorder are relevant to making decisions about treatment, reimbursement, and when to excuse an individual from moral obligations and responsibilities.

ven if the above considerations are correct, Hesslow is right to point out that debates about how best to define the concepts of “health” and “disease” can often obscure more important issues in philosophy of medicine and philosophy of psychiatry. Kincaid

(2008) makes a similar point, although he is concerned with the futility of attempting to define “health” and “disease” specifically in terms of a set of necessary and sufficient conditions. He argues that much of clinical medicine and psychiatry can proceed without such a definition. Kincaid draws a parallel between cancer research and research on depression. He points out that a cancerous cell is not a natural kind, by which he means

41 that there is no definition of a cancerous cell in terms of a set of necessary and sufficient conditions. Moreover, cancer is heterogeneous in that it displays a multiple of developmental trajectories and is caused by a variety of molecular pathways. Finally, there is no well-developed, parsimonious theory of cancer that articulates the normal functioning from which it is a deviation. Nonetheless, Kincaid contends that cancer research is successful and that one would be misguided to argue the contrary solely on the grounds that it lacks the features listed above. Kincaid then shows that research on depression exhibits the same features as cancer research. Depression cannot be defined in terms of a set of necessary and sufficient conditions, it displays a multiple of developmental trajectories, and it is caused by a variety of internal and external factors.

Moreover, it lacks a well-developed theory that articulates the normal functioning from which it is a deviation. However, just as in the case of cancer research, Kincaid contends research on depression can still be successful and that one would be a mistake to argue the contrary solely on the grounds that it lacks the features listed above.

Kincaid is not arguing that the concepts of “health” and “disease” (or

“mental health” and “mental disease”) are irrelevant to the practice of medicine and psychiatry. Rather, he is arguing for the more conservative claim that these disciplines do not need definitions of these concepts in terms of a set of necessary and sufficient conditions to proceed. He is explicit about this point:

My claim is not that there is no use for the concept of disease in medicine— it is rather hard to imagine medicine without it—but that there is no reason to expect it to be defined in necessary and sufficient conditions, and that no very interesting implications about the practice of medicine can be gathered from either having such a definition or from a failure to find one (370).

In this sense, Kincaid’s position is less radical than Hesslow’s. Nonetheless, if

42 Kincaid is correct, then his position offers a response to the constructivist and

anti-psychiatry critiques. Whereas their critiques rest upon the failure of

psychiatry to show that psychiatric conditions are relevantly similar to physical

diseases, Kincaid shows that the concept of “physical disease” upon which their

arguments rest is itself too demanding. If their concept were applied consistently,

then the anti-realism of the constructivist and anti-psychiatry movement would

apply equally to most conditions and areas of research in medicine as well, a

conclusion that they presumably would not be willing to defend.

Objectivism

ven before psychiatry first emerged as a distinct discipline during the 19th

century, a common criterion for warranting the status of a medical condition was that one

could identify an organic etiology for the condition of interest. The failure to do so often

served to undermine the reality of the condition as well as the legitimacy of the

discipline(s) that aimed to understand and treat it8. Thus, a more traditional response to

constructivist and anti-psychiatry critiques has been to defend the reality of psychiatric

disorders by showing them to be analogous to physical diseases. Just as attributions of

physical disease are grounded in descriptive facts about malfunctioning physical

mechanisms, attributions of psychiatric disorder are grounded in descriptive facts about

malfunctioning mental and/or physical mechanisms. To label a condition as mentally

unhealthy is, at minimum, to assert the existence of an underlying pathological state of

the body and/or mind as the cause of that condition. This position is referred to as

8 Martin (2002) highlights this point in his historical sketch of Alzheimer’s Disease and Tourette’s Syndrome. Disorders for which one could identify a clear organic basis, such as Alzheimer’s Disease, were considered real conditions and relegated to the medical field of neurology, while disorders for which one could not identify a clear organic basis, such as Tourette’s Syndrome, were often ignored and relegated to psychiatry.

43 objectivism and represents the most direct response to constructivist and anti-psychiatry critiques9.

Murphy (2006) distinguishes two types of objectivism: simple objectivism and minimal objectivism. Simple objectivism maintains that attributions of psychiatric disorder are exhausted by descriptive facts about the body and/or mind. Once one has acquired the facts about proper psychological and physiological functioning, one can

“read off” whether an individual is psychiatrically disordered. On this view, descriptions of psychological and/or physiological malfunctioning are both necessary and sufficient for the attribution of psychiatric disorder. Thus, attributions of psychiatric disorder do not require any evaluative assessment. Minimal objectivism denies this and instead adheres to what Murphy refers to as the two-stage picture of the foundations of psychiatry. According to this picture, attributions of psychiatric disorder embody both a factual and an evaluative component: they require facts about the proper psychological and physiological functioning as well as an evaluative assessment of these facts, namely, that deviations from this proper functioning are harmful. Although the evaluative assessment will typically precede the discovery of the descriptive facts, the descriptive facts that ground the attribution of psychiatric disorder remain independent of the evaluation. Murphy’s minimal objectivism is what I refer to as a hybrid account, which will be discussed in more detail below. In this section I am only concerned with simple objectivism, which I will refer to as objectivism in the rest of the section.

Christopher Boorse (1975, 1976, 1977, 1997) originally articulated the objectivist position within psychiatry10. His account was initially formulated as a general theory of

9 The view is sometimes referred to as descriptivism or naturalism as well.

44 health and disease (1975, 1977) and later applied to the concept of mental health and mental illness (1976)11. On Boorse’s account, to be healthy is to be functioning normally in an appropriate reference class. A reference class is a “natural class of organisms of uniform functional design; specifically, an age group of a sex of species (1977, p.555).”

Normal function is a purely statistical notion on Boorse’s account. He defines it as “a statistically typical contribution by [a part or process within members of the reference class] to their individual survival and reproduction (p. 555).” Although Boorse’s account of normal function makes reference to survival and reproduction, it is not intended to be an evolutionary account of function. Rather, Boorse defines “function” ahistorically in terms of the causal contribution that a part or process makes to current goals: “X is performing the function of Z in the G-ing of S at t’ means ‘At t, X is Z-ing and the Z-ing of X is making a causal contribution to the goal G of the goal-directed system S. (Boorse,

1976, p. 80).” To be healthy, then, is for an individual’s internal parts or processes to perform their normal functions on normal occasions so as to contribute to the individual’s survival and reproduction with at least statistically normal efficiency. Accordingly, a disease is any internal state that causes a part or process to perform its normal function below statistically normal efficiency.

Boorse’s account extends to the concepts of “mental health” and “mental illness” with only slight modification. To be mentally healthy is for an individual’s psychological processes to perform their normal functions on normal occasions so as to contribute to the individual’s survival and reproduction with at least statistically normal efficiency. One

10 Boorse’s account is also often referred to as the Biostatistical Theory of Health, a name coined by Lennart Nordenfelt. 11 Hesslow (1993; footnote #2), despite arguing that the concepts of “health” and “disease” are irrelevant to much of the practice of medicine, argues that this approach is the most promising.

45 can attribute a psychiatric disorder to an individual whenever that individual’s psychological processes fail to perform their normal function with at least statistically normal efficiency.

Boorse’s account is intended to be an empirical, objective, value-free analysis of the concepts of “health” and “disease” (and “mental health” and “psychiatric disorder”).

If sound, his account would undermine constructivist and anti-psychiatry critiques by providing an objective criterion for distinguishing conditions that are indicative of an underlying disorder from mere “problems of living.” However, numerous authors have rightly questioned the soundness of Boorse’s analysis as applied to psychiatric disorders

(Fulford, 2001; Cooper, 2002; Kingma, 2007)12. The majority of these criticisms have challenged the ability to provide objective, value-free analyses of the concepts of

“reference class” and “normal function.”

Kingma (2007), for instance, focuses his criticism on Boorse’s claim to have provided a value-free account of the concept of “reference class.” According to Kingma,

Boorse fails to distinguish appropriate from inappropriate reference classes in an objective, value-free way. Kingma considers three possible ways for Boorse to meet this challenge. The first is to define appropriate reference classes as those classes that are

“natural.” Kingma finds any plausible interpretation of “natural” to be unsatisfying. If

“natural” means “occurring in nature,” then it would fail to distinguish appropriate from inappropriate reference classes since both occur in nature. Interpreting “natural” to mean

“normal” would also fail to distinguish appropriate from inappropriate reference classes since some races would be appropriate reference classes despite the fact that they are

12 Numerous other authors have challenged Boorse’s general theory of health and disease. Boorse counts the number of critics to be in the hundreds (1997).

46 statistically abnormal within a population. Similarly, some references classes, e.g., near- sighted individuals, may justifiably be labeled diseased despite being statistically normal.

Finally, one could define “natural” by appeal to “natural kinds.” However, Kingma argues that this would either lead to a circular definition in which the appropriate reference classes are defined in terms of health and disease or entail that diseases are not natural kinds, a claim that Kingma finds implausible.

A second possible way to distinguish appropriate from inappropriate reference classes that Kingma considers is to appeal to uniformity. The idea is that appropriate reference classes are those that exhibit uniform characteristics that enable one to identify similarities and dissimilarities within and between reference classes. However, as

Kingma points out, inappropriate reference classes may also exhibit remarkable uniformity. Kingma cites the example of genetic syndromes, which may be easily identifiable but which would not form an appropriate reference class within a population.

A final possible way to distinguish appropriate from inappropriate reference classes is to appeal to species design. Kingma finds any plausible interpretation of

“design” to be unsatisfying. If “design” means “innate,” in the sense that individuals in the appropriate references class possess a particular trait innately, then it would fail to distinguish appropriate from inappropriate reference classes since certain genetic diseases are innate. Moreover, other traits that are typically considered to be definitive of appropriate reference classes, e.g., age and sex, are sometimes acquired. Interpreting

“design” to mean “intended by nature” would also fail to distinguish appropriate from inappropriate reference classes. However, assuming that “intended by nature” is taken to mean “the result of evolutionary processes,” then Boorse cannot accept this interpretation

47 since he explicitly denies that evolution is relevant to his analysis of health and disease.

ven if it were relevant, it would fail to distinguish appropriate from inappropriate reference classes because evolutionary processes are involved in maintaining both classes. In summary, Kingma’s arguments show that, at the very least, Boorse has not provided an objective, value-free criterion for selecting appropriate reference classes.

Without such a criterion, Boorse cannot provide an account of normal function and, therefore, his analysis of health and disease is incomplete. More importantly, it cannot serve as an adequate response to constructivist and anti-psychiatry critiques because it still leaves open the possibility that psychiatric disorders are defined solely in terms of evaluative judgments.

The second common criticism of Boorse’s account is its inability to provide objective, value-free analyses of the concept of “normal function.” Numerous critics have raised this point about Boorse’s general theory of health and disease, but Cooper

(2002) and Fulford (2001) raise the challenge specifically with respect to its application to psychiatry. Fulford (2001) criticizes Boorse’s account of normal function on the grounds that Boorse fails to satisfy his own goal of providing an objective, value-free analysis of the concept. He points out that Boorse frequently includes evaluative terms in his description of normal function. For instance, shortly after defining disease as a deviation from functional norms, Boorse defines it as “deficiencies in functional efficiency (Boorse, 1975; p. 59; italics added).” Similarly, after acknowledging that most diseases are the result of “environmental causes,” Boorse refers to diseases as being the result of a “hostile environment (Boorse, 1975; p. 59; italics added).” Fulford cites these

48 examples to demonstrate Boorse’s inability to fully eliminate evaluative concepts from his account of health and disease.

Fulford argues that these appeals to evaluative concepts are not due simply to the inconsistency of Boorse; rather, they reflect the fact that the concepts of “health” and

“disease” must necessarily embody an evaluative component. To see this, consider again

Boorse’s definition of “normal function:” “X is performing the function of Z in the G-ing of S at t’ means ‘At t, X is Z-ing and the Z-ing of X is making a causal contribution to the goal G of the goal-directed system S. (Boorse, 1976, p. 80).” Here “normal function” is defined by reference to the goals of survival and reproduction. According to Fulford, any appeal to “goals” necessarily involves an evaluative element of meaning. He makes this point explicit:

A goal is not, merely, something which is hit or missed, as, say, a comet merely hits or misses a planet: a goal is aimed at or targeted; it may (according to the teleological resources of the organism or part-organism in question) be desired, needed, wished for, intended, etc; a goal is something which (in itself) it is good to hit and bad to miss (p. 83).”

Thus, any account of health and disease that makes reference to “goals” will necessarily embody an evaluative component. Fulford thinks that all accounts of health and disease will require such a reference, a feature that he argues makes all objectivist accounts of health and disease inadequate13. I will address Fulford’s account in more detail in the following section on evaluativist accounts of psychiatric disorder. Nonetheless, if

Fulford’s concerns are on the right track, then Boorse cannot provide an objective, value- free criterion for determining normal function. Without such a criterion, his account cannot serve as an adequate response to constructivist and anti-psychiatry critiques

13 Wakefield’s (1992) harmful dysfunction analysis relies on an evolutionary account of function. However, as will be discussed below, this account faces its own set of challenges.

49 because it still leaves open the possibility that psychiatric disorders are defined in terms of evaluative judgments. In the next section I will outline why Fulford does not think that an adequate response to constructivist and anti-psychiatry critiques requires defending such a claim.

Cooper (2002) criticizes Boorse’s analysis of the concepts of “reference class” and “normal function,” although her main target is Boorse’s account of “normal function.” A common desideratum for any account function is the need to distinguish genuine from accidental contributions to the goals of a system. Cooper uses the example of sweating to illustrate this challenge. Sweating has the function of cooling down the body; however, this goal can also be achieved by accidentally knocking a bucket of water on me when I am hot. Presumably, knocking buckets of water on oneself does not have the function of cooling down the body despite the fact that it makes a causal contribution to this goal. Boorse handles this challenge by claiming that the normal function of a part or process is whatever it typically does in members of the reference class that causally contributes to the goals of survival and reproduction (Boorse, 1977; p. 556). Thus, the normal function of sweating is to cool the body because that is what it typically does for members of the reference class. However, knocking a bucket on oneself is not a normal function because that is not what members of the reference class typically do.

The success of Boorse’s response depends upon being able to adequately distinguish appropriate from inappropriate reference classes. However, as Kingma pointed out, Boorse fails to provide such a distinction. Cooper raises similar worries.

She argues that reference classes will need to be more fine-grained than the classes of age, race, and sex that Boorse mentions. What constitutes “normal” for an individual will

50 depend not only on factors such as age, race, and sex, but also on a variety of other factors such as shared environment and learning history. To fully understand the etiology of certain psychiatric disorders, for instance, anxiety disorders, one will need to know not only the age, race, and sex of members of the reference class, but also any relevant early childhood experiences such as the presence of abuse or other traumatic events. Age, race, and sex will be insufficient to adequately distinguish appropriate reference classes so as to reliably ground attributions of psychiatric disorder. As the appropriate reference classes become smaller, as will be the case when one includes additional factors, it will be more difficult to identify the normal functions of members in the reference class because it will be more difficult to distinguish genuine from accidental contributions to the goals of the members in the reference class.

ven if Boorse could provide an objective, value-free analysis of the concepts of

“reference class” and “normal function,” it would seem to generate counter-intuitive judgments about psychiatric disorder. For instance, homosexuality would seem to count as a disease on Boorse’s analysis since it is statistically abnormal within the population and because homosexuals are not using their genitalia, at least not obviously so, to contribute to the goals of survival and reproduction. Boorse has even suggested that homosexuality might be a disease (Boorse, 1975; p. 63). Of course, the fact that common sense intuitions about psychiatric disorder conflict with scientific concepts of psychiatric disorder does not entail that the latter is mistaken. Boorse argues along these lines and claims to only be offering an account of the concepts of “health” and “disease” as they appear in medical theory. This response, however, is not very satisfying. First, it relies upon a clear distinction between folk and scientific concepts. Perhaps such a distinction

51 exists, but Boorse does not offer any justification for thinking that it does. Moreover, even if such a distinction does exist, one would need to provide an argument as to why the scientific concept of psychiatric disorder should be favored over the folk concept.

Again, perhaps such an argument can be provided, but Boorse does not offer any such argument. Nonetheless, the failure to provide objective, value-free analyses of the concepts of “reference class” and “normal function” provide sufficient reason for thinking that objectivism is an incomplete account of psychiatric disorder.

Evaluativism

Whereas objectivists accept that an adequate response to constructivist and anti- psychiatry critiques requires providing an objective, value-free account of psychiatric disorder, evaluativists maintain that attributions of psychiatric disorder necessarily embody an evaluative component as part of their meaning. To label a condition as indicative of a psychiatric disorder is, at minimum, to condemn that condition as harmful or undesirable. However, evaluativists differ from constructivists and the anti-psychiatry movement in that they deny that acknowledging a role for evaluative judgments undermines the reliability of psychiatric diagnoses or threatens the scientific legitimacy of psychiatry. There are two broad varieties of evaluativism that differ with respect the proposed relationship between facts and values or, more specifically, between factual descriptions of psychological malfunctioning and evaluative judgments about this malfunctioning. Weak evaluativists contend that attributions of psychiatric disorder embody both an evaluative and a descriptive component and that each of these components are independent of one another. I refer to weak evaluativism as hybrid accounts and will discuss several versions of the view in the next section. Strong

52 evaluativists contend that evaluative judgments are a necessary condition for the attribution of psychiatric disorder and that factual descriptions of psychological malfunctioning and evaluative judgments about this malfunctioning cannot be separated from one another. I will focus on this version of evaluativism in this section and will refer to this view simply as evaluativism.

Tauber (2005) exemplifies the evaluativist commitment to the inseparability of facts and values14. He argues that all facts must be interpreted within a context and that they only have meaning within a network of values:

…each so-called “fact” exists in a context that confers a distinctive meaning. That meaning is determined by factors usually unrecognized, and thus the grounding of the molecular fact - its valuation, so to speak - only can assume its significance in the context of the individual patient. That contextualization immediately shifts the ontological character of clinical facts from a positivist aspiration to a more complex value- dependent ontology (p. 47).

The notion that a factual description of a disease or psychiatric disorder “only can assume its significance in the context of the individual patient” is a common theme among evaluativist views. It serves as the foundation of Nordenfelt’s (1995, 2007) Holistic

Theory of Health and Fulford’s (1989) reverse theory of disease and illness, two closely related, paradigm defenses of evaluativism. On Nordenfelt’s view, health pertains to the organism as a whole and not to any particular part of the organism, e.g., an organ such as the heart. The health of the organism as a whole is tied to the well being of the organism:

“A is completely healthy if, and only if, A has the ability, given standard circumstances, to reach all his or her vital goals (2007, 7).” Nordenfelt defines one’s vital goals as “his or her most essential goals in life (2007, 7)” or as “ the set of goals which are necessary

14 However, at times Tauber does seem to suggest that the two can be separated (see, e.g., p. 51) but that we should at least make more of an effort to acknowledge their interdependence.

53 and jointly sufficient for his minimal happiness (1995, 90).’’ Nordenfelt defines

“standard circumstances” as those circumstances that are culturally normal and explicitly states that they are not to be understood as circumstances that are merely statistically normal. I will return to these notions later when assessing Nordenfelt’s holistic theory of health.

A central feature of Nordenfelt’s theory is his modified adoption of Fulford’s

(1989) reverse theory of disease and illness. On Fulford’s view, the concept of illness is an evaluative term that is temporally and logically prior to the concept of disease; thus, the concept of disease is likewise evaluative. Nordenfelt adopts Fulford’s reverse theory with a slight modification: although he agrees with Fulford that the concept of illness is temporally and logically prior to the concept of disease, he argues that the concept of health is an evaluative concept that is temporally and logically prior to both the concept of illness and the concept of disease. Nordenfelt considers an example of the typical medical encounter as evidence for this claim. The typical medical encounter begins with a patient complaint about a problem that he or she is experiencing, e.g., a numbing pain in the arm. Nordenfelt points out that although the patient may suspect that something is wrong internally, he or she “does not presuppose any internal inspection on the organ level (8).” The physician then attempts to identify the cause of the problem and to treat it accordingly, a part of the encounter that typically involves the use of standard “disease language” and relies on commonly recommended standards of care. Finally, the patient is considered healthy once the original problem no longer subsists, which may extend beyond treating the original cause of the problem, i.e., the disease. Nordenfelt takes this last point as evidence that health “is a state of affairs over and above the absence of

54 disease (9).” His definition of disease further emphasizes this point: “A has a disease if, and only if, A has at least one organ which is involved in such a state or process as tends to reduce the health of A,” where the phrase ‘tends to reduce health’ is intended to capture the possibility that one may have a disease without experiencing suffering or disability, e.g., the disease is in remission, disappears before compromising one’s vital goals, or has not yet compromised one’s vital goals (7). This definition makes clear that the concept of disease is derivative on the temporally and logically prior concept of health and, therefore, is a value-laden concept that cannot be divorced from the evaluative judgment regarding the health of the patient.

Three significant problems emerge with Nordenfelt’s holistic theory of health.

The first problem concerns Nordenfelt’s reliance on Fulford’s reverse theory of disease and illness. The other two problems, the problem of relativism and the problem of counter-intuitiveness, are similar to the problems raised for metaphysical constructivists, although they take on a somewhat different character due to the intended realism of the holistic theory of health. I will address each of these in turn.

Recall that Nordenfelt’s appeal to Fulford’s reverse theory of disease and illness was intended to show that the concept of health, an evaluative concept, is temporally and logically prior to both the concept of illness and the concept of disease. Nordenfelt defended this claim with a description of the typical medical encounter. Although the typical medical encounter that Nordenfelt discusses pertains specifically to physical disease, it can apply to the typical psychiatric encounter with a minor caveat. One difference between the two encounters is that the rationality of the patient in the psychiatric encounter may be compromised along with his/her ability to identify a

55 problem in the first place. However, under the assumption that mental health problems involve compromised rationality and that rationality is an evaluative notion, the concept of psychiatric disorder will turn out to be evaluative as well. In Nordenfelt’s terms, the concept of psychiatric disorder will be derivative on the temporally and logically prior concept of mental health/rationality and, therefore, will be a value-laden concept that cannot be divorced from the evaluative judgment regarding the mental health/rationality of the patient.

The problem with this line of reasoning, however, lies in Nordenfelt’s notion of

“logical priority.” As Schramme (2007) points out, there are good reasons for thinking that logical priority does not capture the relationship between medical concepts such as mental health and psychiatric disorder. Rather, the appropriate relationship seems to be one of epistemological priority. The typical clinical experience begins with a patient reporting about his/her problem(s), usually with the use of mental concepts. The psychiatrist is also likely to invoke mental concepts in his/her observations and descriptions of the patients’ symptoms. But the fact that we typically begin with a mental characterization of the symptoms before looking for the cause of those symptoms is an epistemological fact and has no bearing whatsoever on the logical relation between the concepts involved. Schramme illustrates this point with the example of determining the cause of death. Although we first observe that a person is dead before searching for the cause of death, nothing interesting follows concerning the logical relationship between the concept of death and the concepts that explain the cause of death. To use a more relevant medical example, consider the case of a patient with a herniated cervical disc.

Just because a physician first encounters a patient who describes his/her back pain and

56 arm numbness using mental concepts, nothing follows about the logical relationship between the concepts of pain or numbness and the physical cause of the pain and numbness. From a clinical perspective, the mental descriptions of the symptoms are simply epistemologically prior to the explanation of the causes of those symptoms.

This point challenges Nordenfelt’s claim that psychiatric disorder is an evaluative concept, at least to the extent that it depends on a commitment to his modified version of

Fulford’s reverse theory of disease and illness. However, a greater challenge arises from

Nordenfelt’s explicit aim to connect the concept of health to well-being and vital goals.

Recall Nordenfelt’s definition of health: “A is completely healthy if, and only if, A has the ability, given standard circumstances, to reach all his or her vital goals.” The concern here is that Nordenfelt fails to provide an analysis of the concept of “vital goals” that would be sufficient to alleviate constructivist and anti-psychiatry worries. Nordenfelt provides two different but closely related definitions of “vital goals.” The first definition characterizes “vital goals” as one’s “most essential goals in life (2007, 7).” It is easy to see why this definition would raise relativistic concerns about psychiatric diagnoses.

Individuals differ with respect to what they take to be their most essential goals in life and some individuals’ most essential goals may be unreasonable. For instance, one of my most essential goals in life may be to play in the NBA. I may dedicate my life to realizing this goal and yet still fall short. On Nordenfelt’s account, I would justifiably be labeled as mentally unhealthy, and thus warrant the attribution of a psychiatric disorder, since I am unable to reach all of my vital goals. This label would be justified even if I were able to reach all of my other vital goals in life and if my goal to play in the NBA is seemingly unreasonable. Moreover, Nordenfelt’s theory would imply that I could

57 become mentally healthy, and thus no longer warrant the attribution of a psychiatric disorder, simply by relinquishing my goal to play in the NBA.

Similar problems arise for Nordenfelt’s second definition of “vital goals.” On this definition, “vital goals” are “the set of goals which are necessary and jointly sufficient for his minimal happiness (1995, 90).’’ It is easy to see why this definition would raise relativistic concerns about psychiatric diagnoses as well. Individuals differ with respect to which set of goals is necessary to make them minimally happy and some individuals’ necessary goals may be unreasonable. Consider again my desire to play in the NBA.

This goal may be necessary to secure my minimal happiness. On Nordenfelt’s account, I would justifiably be labeled as mentally unhealthy, and thus warrant the attribution of a psychiatric disorder, since I am unable to reach all of my vital goals. I could also become mentally healthy, and thus no longer warrant the attribution of a psychiatric disorder, simply by relinquishing my goal to play in the NBA. The upshot of these counterintuitive implications is that Nordenfelt’s account of “vital goals” is too subjective to distinguish conditions that are indicative of an underlying disorder from those that are merely the result of “problems of living.” Similar problems plague other evaluativist proposals. Just as objectivism errors by trying to exclude any reference to evaluative judgments in their analyses of psychiatric disorder, evaluativists error by being too reliant on such judgments.

Hybrid Accounts (Weak Evaluativism)

Hybrid accounts of psychiatric disorder offer a possible compromise position between objectivism and evaluativism. These views maintain that attributions of psychiatric disorder embody both an evaluative and a descriptive component. Thus,

58 contrary to strong evaluativists, hybrid accounts maintain that there are factual descriptions that ground attributions of psychiatric disorder, i.e., psychiatric disorders are not merely harmful or disvalued conditions, and that these descriptions are independent of evaluative judgments. Contrary to objectivists, they maintain that psychiatric disorders are not merely deviations from some biological, developmental, or statistical norm of functioning; this deviation must also be harmful. However, despite agreeing that both factual and evaluative judgments are necessary to ground attributions of psychiatric disorder, there is widespread disagreement as to the specific content of these judgments.

Jerome Wakefield’s (1992, 2007) harmful dysfunction analysis (HDA) is the most developed and well-known hybrid account and it is his view on which I will primarily focus. Wakefield’s HDA is intended to capture common sense intuitions about the difference between behaviors that are indicative of psychiatric disorder and those that are simply the result of “problems of living.” The crux of these intuitions, Wakefield maintains, is that “when we attribute disorder, we attribute a harmful failure of natural function (1992; p. 259).” More specifically, psychiatric disorder involves a “harmful failure of some internal mechanism(s) to perform a naturally selected (designed) function” whereas “problems of living” do not (p. 253). The HDA is thus a hybrid account because it embodies both a factual component, i.e., the failure of an internal mechanism to perform its naturally selected function, as well as an evaluative component, i.e., the failure to perform this naturally selected function causes harm.

Wakefield’s appeal to “function” in his account of psychiatric disorder is importantly different from Boorse’s objectivist account of normal function. Although

Boorse’s account makes reference to survival and reproduction, it is not intended to be an

59 evolutionary account of function. Rather, he defines “function” ahistorically in terms of the causal contribution that a part or process makes to current goals. Wakefield, on the other hand, offers a purely historical account of function that is grounded in evolutionary theory. On his account, the function of a part or process means that the presence of the part or process is best explained by its prior performance of the particular function. For example, to claim that hearts have the function of pumping blood means that the spread of hearts in an ancestral population is best explained by their ability to pump blood, i.e., ancestors who had hearts were able to pump blood, which enabled them to survive and reproduce.

It is important to make explicit the assumptions underlying what Wakefield takes to be our “common sense” intuitions about psychiatric disorder, especially in light of his appeal to evolutionary theory. First, Wakefield assumes that all of human psychology is the product of natural selection. Second, as a corollary of this assumption, Wakefield conceives of the mind as a collection of discrete, internal mechanisms that have been selected because of their ability to perform specific adaptive functions. Thus, Wakefield is advocating a version of the modularity view of the mind in which discrete, internal mechanisms are the units of selection. It is not clear that these assumptions are actually constitutive of our common sense intuitions, but I will return to this problem later. If they are in fact constitutive of our common sense intuitions about psychiatric disorder, then the HDA is committed to two important empirical claims about psychiatric disorder.

First, it implies that every disorder originates in a mental mechanism with an

60 evolutionary function15. Second, it entails that there must be at least one malfunctioning mental mechanism for every disorder.

This second empirical commitment proves to be particularly problematic for

Wakefield’s analysis. It leads to the exclusion of conditions that in actual scientific practice are classified as psychiatric disorders. More specifically, it excludes the possibility that psychiatric disorders can result from exposure to dysfunctional inputs despite the proper functioning of one’s internal mechanisms. As Murphy & Woolfolk

(2000) point out, one can articulate this possibility in a variety of ways. First, it may be possible for disorder to result from a mismatch between the evolutionary design of one’s internal mechanisms and one’s current environment. On this articulation, an individual may possess internal mechanisms that were designed to bring about desirable behavior in earlier environments, but those behaviors are no longer desirable in the current environment. Second, on the assumption that mental mechanisms need appropriate inputs (information) in order to produce appropriate outputs (behavior), it may be possible for disorder to result from inappropriate inputs into normal learning mechanisms rather than the result of a malfunctioning mental mechanism16. Following Murphy and

Woolfork, I will refer to such disorders as “learned disorders.”

To see the problem that “learned disorders” poses for Wakefield’s analysis, consider research on anxiety and other mood disorders. Research has demonstrated that childhood emotional abuse and neglect increases one’s vulnerability to develop Major

15 I do not address this claim here as it has already been extensively criticized elsewhere (see Murphy & Woolfolk, 2000). Murphy & Woolfolk argue that this claim is inadequate because it excludes the possibility of mental disorders originating in mental mechanisms that are the by-products of evolution but have never possessed any adaptive function themselves. Nonetheless, while such “spandrel disorders” are a possibility, there is no empirical evidence to date to suggest that they do exist. 16 It may even be possible that the same harmful behavior could be the result of a malfunctioning mental mechanism in one individual at one time and a properly functioning mental mechanism that is processing inappropriate information in another individual at another time.

61 Depressive Disorder, post-traumatic stress disorder, and anxiety disorders (Shea et al.,

2004, Gunnar et al., 2007, Tarullo et al., 2006). Although a full understanding of the neurobiological mechanisms underlying this relationship is still unknown, research has shown that the hypothalamic-pituitary-adrenal (HPA) axis, which mediates responses to stress and regulates bodily processes such as mood and sexuality, becomes hyper- responsive when exposed to “social stressors”, e.g., childhood abuse and neglect (Shea et al., 2004, Gunnar et al., 2007, Tarullo et al., 2006)17. In fact, the ability to use “social stressors” to activate the HPA and induce anxious/panic behaviors is a result that has been replicable in humans (Shea et al., 2004), monkeys (Parker et al., 2004), rodents

(Weaver et al., 2004, 2005), and trout (Overli et al., 2005). Some of the strongest evidence for the mechanisms underlying this relationship comes from pre-clinical animal studies, in particular the research discussed in the next chapter by Meaney’s lab (Weaver et al., 2004, 2005) on the epigenetic affects of maternal behavior on the stress response of their offspring.

This area of research provides a counterexample to the HDA by showing how psychiatric disorder can originate from exposure to dysfunctional inputs, i.e., childhood abuse and neglect, despite the proper functioning on one’s internal mechanisms, i.e., the

HPA’s regulation of responses to stress. To avoid this problem and defend the adequacy of the HDA, Wakefield must argue either 1) that the hypothalamic-pituitary-adrenal axis is “broken” and not performing its naturally selected function or 2) that the harmful behaviors that result from childhood abuse and neglect are not indicative of psychiatric disorder. To argue for the former option, Wakefield would have to provide an account of

17 This hyper-responsiveness is typically determined by measuring cortisol, corticosterone, or adrenocorticotropin hormone levels.

62 how exposure to dysfunctional inputs such as childhood abuse and neglect causes the

HPA to “break”, i.e., to fail to perform its evolutionary function. This approach, however, does not show much promise. The function of the HPA to regulate stress responses in humans as well as other mammals and vertebrates is well established.

Moreover, the ability to use “social stressors” to activate the HPA and induce anxious/panic behaviors is a result that has been replicable in humans (Shea et al., 2004), monkeys (Parker et al., 2004), rodents (Weaver et al., 2004, 2005), and trout (Overli et al., 2005). Thus, to argue that the HPA is malfunctioning when exposed to dysfunctional input, e.g., childhood abuse or neglect, seems to either ignore the empirical facts or to beg the question as to what constitutes a malfunction of the HPA.

Wakefield’s discussion of this problem suggests that he would adopt the latter option and maintain that the harmful behaviors that result from childhood abuse and neglect are not indicative of psychiatric disorder. He draws a distinction between psychiatric disorders and learned problematic behaviors and argues, “If normal learning processes involving no dysfunctions of any kind did explain some condition now considered a disorder, we would reclassify that condition as a non-disorder (1992, p.

261).” Wakefield argues further that even if a learned problematic behavior satisfies the

DSM’s criteria for disorder, it does not ensure that the condition will be considered a disorder. As evidence for this claim, Wakefield cites the example of conduct disorder and argues that clinicians “overwhelmingly judge youths whose symptoms satisfy the

DSM’s criteria for conduct disorder to be nondisordered if the problematic behaviors are explained by learned normal reactions to environmental factors (p. 261).” According to

Wakefield, it is simply not the case that a condition that is a direct learned response to

63 continual environmental stressors but involves no consequent dysfunctions would be considered a disorder.

It is not clear, however, that Wakefield’s appeal to the reluctance of clinicians to attribute disorder to antisocial youths supports his case. The case of antisocial youths, contrary to Wakefield’s claim, is not a condition that is a direct learned response to continual environmental stressors but that involves no consequent dysfunctions. In such instances, although the dysfunction may not be a malfunctioning internal mechanism, there is clearly a behavioral dysfunction. In this respect, the case of antisocial youths parallels the research on anxiety disorder discussed previously; both are cases in which harmful behaviors result from dysfunctional inputs, despite the proper functioning of one’s internal mechanisms.

Moreover, Wakefield’s response raises a potential inconsistency within his view.

Recall that the HDA intends to capture our common sense intuitions regarding attributions of disorder. However, it is not clear whose common sense intuitions the

HDA intends to capture. For instance, Wakefield acknowledges that the case of the antisocial youths satisfies the DSM’s criteria for conduct disorder while at the same time arguing that most clinicians do not recognize it as a disorder. So whose intuitions are correct, the intuitions of the clinicians and researchers that developed the DSM criteria for disorder or the intuition of the clinicians that Wakefield cites? This tension emerges with the research on anxiety disorder as well. Researchers working in this area take their task to be explicating the etiology of anxiety or other mood disorders. As the work by

Shea et al. demonstrates, this research need not share Wakefield’s intuition that the etiology of anxiety disorders necessarily involves a malfunctioning internal mechanism.

64 The intuitions of these researchers seem to be at odds with the intuitions of the HDA, i.e., their intuitions seem to countenance the fact that mental disorder can arise from exposure to dysfunctional inputs despite the proper functioning of one’s internal mechanisms.

Rather than accept that the harmful behaviors that result from childhood abuse and neglect are not indicative of psychiatric disorder because they do not involve a failure of some internal mechanism(s) to perform a naturally selected function, Wakefield qualifies the HDA to allow for dysfunction without malfunctioning internal mechanisms.

He states, “To have a dysfunction, there has to be a failure of function for internal reasons, but that state can occur for many reasons other than a broken mechanism (p.

262).” He offers two examples to illustrate how this may occur. First, it may be possible for a mechanism to fail to perform its function because the input is outside the designed range of the mechanism. In this situation, there may be dysfunction without a malfunctioning mechanism. Wakefield points out that some experiences may be so traumatic that no mechanisms have been selected to cope with the trauma. In such instances, it is possible that the “‘inputs’ cause enduring dysfunction in mental processing

(p. 263).” According to Wakefield, such cases would still constitute a disorder. This response, however, does not show that there is a failure of function for internal reasons.

The enduring dysfunction in mental processing that ensues is not due to a dysfunctional internal reason, for all of the internal mechanisms are performing their naturally selected function. As Wakefield himself points out, the cause of the behavioral dysfunction is the input, i.e., an external reason. To locate the reason internally would amount to the trivial claim that there should be a mechanism to cope for the trauma even though there is not

65 one. Thus, when properly interpreted, this example supports the case of psychiatric disorder arising from dysfunctional inputs rather than undermine it.

The second example that Wakefield discusses is the possibility that the input and the mechanism could both be functioning within normal ranges, but their interaction might not fall within the designed range of interactive outcomes. Wakefield constructs a case in which one’s neurobiological mechanisms produce a neurotransmitter at the extreme high end of the normal range and produce the neurotransmitter’s inhibitor at the extreme low end of the normal range. ach substance is being produced within normal range when considered separately, but as a result of their interaction, there is a level of neurotransmitter that is outside the designed range and that generates harmful behaviors.

According to Wakefield, an evolutionary dysfunction exists in this case, but the dysfunction is due to a failure of function without any particular mechanism being

“broken”. Although this is more clearly a case of behavioral dysfunction for internal reasons, it is not a clear case of evolutionary dysfunction for internal reasons. Wakefield does not provide an account of the evolutionary function that is failing to be performed; he simply assumes that there is such a function. Setting aside the difficulty of how there can be an evolutionary function without a corresponding mechanism to perform that function, the problem in this example stems from Wakefield’s mistaken assumption that the evolutionary, causal-historical concept of function is the primary concept of

‘function’ in the biological sciences. Certainly having a level of neurotransmitter outside a particular range can make a causal contribution to the harmful behavior, but it does not follow that the harmful behavior is therefore due to evolutionary dysfunction for internal reasons.

66 The above considerations show that Wakefield’s analysis fails to satisfy its own criterion in that it fails to capture common sense intuitions about the difference between behaviors that are indicative of psychiatric disorder and those that are simply the result of

“problems of living.” Moreover, they demonstrate the difficulties of relying on an evolutionary account of function to ground attributions of psychiatric disorder. This latter point has led to other hybrid accounts that avoid making reference to “function.”

Cooper (2002), for instance, provides such an account. She provides three necessary conditions that are jointly sufficient to warrant the attribution of psychiatric disorder.

First, the condition must be a bad thing to have. This criterion represents the evaluative component that is constitutive of hybrid accounts of psychiatric disorder. The second criterion is that the individual afflicted with the condition must be unlucky. Cooper does not intend “unlucky” to be a robust statistical notion, as she explicitly states that she does not take it to mean “unpredictable by medical science (276).” Rather, it is intended to capture the common sense intuition that one is “worse off than the majority of humans of the same sex and age (276).” What constitutes “worse off” is, of course, a vague notion.

Cooper suggests three possible interpretations. First, a patient could be unlucky in the sense that he/she could be better off than he/she was before. Second, a patient could be unlucky in the sense that others are generally better off than him/herself. Finally, a patient could unlucky in the sense that others who are in a relevantly similar situation are generally better off than him/herself. According to Cooper, a diseased individual will typically be unlucky in all three senses of the term. The third criterion is that the condition is potentially medically treatable. According to Cooper, this requirement means that, “…there is reasonable hope that a medical treatment might become available

67 in the future (277).” This final criterion is intended to distinguish genuine psychiatric disorders from harmful or undesirables conditions such as economic problems, social problems, and bad haircuts.

Problems arise for each of Cooper’s three criterion. I will address challenges to her first criterion, that a condition must be a bad thing to have, at the end of the section, as it is a problem that all hybrid accounts face. Recall Cooper’s second criterion, that the afflicted individual must be unlucky, is not intended to reflect the unpredictability of the condition on the part of the medical community, but rather is intended to capture the common sense intuition that one is “worse off than the majority of humans of the same sex and age (276).” Given that “worse off” is clearly an evaluative notion that Cooper states should not be explicated quantitatively, it is difficult for her to avoid a relativistic interpretation of “unlucky.” Two patients in the same situation could each make different judgments with respect to whether they are better off than they were before. Moreover, a patient could mistakenly judge him/herself to be better off than he/she was before. These problems do not disappear by comparing oneself to others in general or to others who are in a relevantly similar situation. In each case, two patients in the same situation could each make different judgments with respect to whether they are better off than others in general or to others who are in a relevantly similar situation. Similarly, a patient could mistakenly judge him/herself to be better off than others in general or to others who are in a relevantly similar situation. In short, appealing to “unluckiness” as a necessary condition for attribution of psychiatric disorder, especially a non-quantitative notion of

“unluckiness,” introduces an unwelcome degree of relativism into psychiatric diagnoses.

68 Cooper’s third criterion, that the condition is potentially medically treatable, also raises concern. First, it is not entirely clear what constitutes a medical treatment as opposed to a non-medical treatment. Cooper recognizes this problem, but fails to offer a satisfying solution. She correctly acknowledges that her account would be circular if medicine was defined as the discipline that aims at treating diseases. She then considers the possibility of defining medicine sociologically as the discipline that is “practiced by doctors and other medical personnel (278).” Cooper doesn’t state whether she finds this definition plausible, but there are good reasons for rejecting this definition as a means for distinguishing between medical and non-medical treatments. First, it would entail that a condition would cease to be a psychiatric disorder simply because the psychiatric community decided that it would be unacceptable to treat the condition. Second, it would imply that the status of a condition as a psychiatric disorder would change depending on who administered the treatment. If two patients with the same condition were given the same treatment, but a doctor treated one of the patients and a layperson treated the other, then only the patient treated by the doctor would warrant the attribution of a psychiatric disorder. These considerations show that Cooper’s account fails to adequately distinguish behaviors that are indicative of psychiatric disorder from those that are simply the result of “problems of living.”

A final hybrid account worth mentioning is reshefsky’s (2009) state description account. Like Cooper, reshefsky explicitly aims to avoid references to concepts such as

“function” and “normal.” He argues that attributions of disease should embody an evaluative component, namely, that the condition is harmful or undesirable, as well as what he refers to as state descriptions. State descriptions are descriptions of

69 physiological or psychological states and are intended to replace appeals to “function” and “normal” upon which objectivist and hybrid accounts such as Wakefield’s rely.

reshefsky mentions “measurement of the amount of calcium in a patient’s tissues” and

“a patient’s red blood cells are rupturing” as examples of physiological state descriptions.

Descriptions of how a patient feels are examples of psychological state descriptions.

reshefsky argues that focusing on state descriptions better captures the interests of medical professionals and, more importantly, avoids the evaluative judgments implicit in concepts such as “function” and “normal.”

reshefsky’s recommendation to ground attributions of health and disease in state descriptions rather than function and normality is a promising approach. However, as even he acknowledges, an exclusive focus on state descriptions may still not completely eliminate references to evaluative judgments. I will consider this problem in more detail in the next section where I examine the role of nonepistemic evaluative judgments in attributions of psychiatric disorder and psychiatric research. A more significant problem facing reshefsky’s proposal is providing an account of how to determine whether a condition is harmful. This problem, however, is not unique to reshefsky. It is a problem for all evaluativist and hybrid accounts of psychiatric disorder.

Which deviations from normal functioning (or which state descriptions) one chooses to label as disordered will vary depending on one’s conception of harm. For example, if one construes harm as ‘harmful to society,’ then deviations from normal functioning that harm society will be considered a psychiatric disorder even if these deviations are not harmful to the individual. Conduct disorder provides a good example of this. Conduct disorder involves persistent behavioral problems in childhood and

70 adolescence, such as impulsive and/or antisocial behavior, drug use, and criminal activity, which is more extreme than normal adolescent rebellion (Searight et al., 2001).

Diagnoses of conduct disorder are often made on the grounds that such behaviors are harmful to society even if they are not considered harmful from the perspective of the individual. Alternatively, if one construes harm as ‘harmful to the individual,’ then deviations from normal functioning that harm the individual will be considered a psychiatric disorder even if these deviations are not considered to be harmful from the perspective of the individual. Homosexuality provides a good example of this.

Homosexuality was classified as a psychiatric disorder in the DSM-II under Sexual

Deviations. Implicit in this classification is the claim that the condition is harmful to the individual:

This category is for individuals whose sexual interests are directed primarily toward objects other than people of the opposite sex, toward sexual acts not usually associated with coitus, or toward coitus performed under bizarre circumstances as in necrophilia, pedophilia, sexual sadism, and fetishism. ven though many find their practices distasteful, they remain unable to substitute normal sexual behavior for them. This diagnosis is not appropriate for individuals who perform deviant sexual acts because normal sexual objects are not available to them (DSM-II, 1968).

However, after persistent criticisms as well as well-popularized boycotts by gay and lesbian groups at the APA conference in San Francisco in 1973, the DSM advisory committee decided to change the classification of homosexuality as a psychiatric disorder in the DSM-III (1980). Homosexuality would now only be classified as a psychiatric disorder only if it were considered harmful from the perspective of the individual rather than harmful to the individual. This shift is explicit in the wording in the DSM-III:

This category is for individuals whose sexual interests are directed primarily toward people of the same sex and who are either disturbed by,

71 in conflict with, or wish to change their sexual orientation. This diagnostic category is distinguished from homosexuality, which by itself does not constitute a psychiatric disorder. Homosexuality per se is one form of sexual behavior and, like other forms of sexual behavior which are not by themselves psychiatric disorders, is not listed in this nomenclature of psychiatric disorders (DSM-III; my italics added).

However, this shift from construing harm as ‘harmful to the individual’ to ‘harmful from the perspective of the individual’ has its own counterintuitive implications. Most notably, it introduces an element of relativity into classifications of psychiatric disorder. For instance, if this conception of harm is correct, then two individuals that are equally deviant from some measure of normal functioning will not both be considered mentally disordered so long as one of the individuals does not find this deviation harmful. This is quite possible in cases of addiction where the addict’s judgment is so impaired that he/she is not capable of competently evaluating harms. Defenders of this conception of harm can point out that this element of relativity is counterbalanced by the benefits of including patient perspectives into psychiatric nosology or that such relativity is unavoidable and is present in the other conceptions of harm as well18. These points have their merit; however, it is not clear that relativizing considerations of harm to the perspective of the individual is the most desirable way of including patient perspectives into psychiatric nosology. In addition, even if other conceptions of harm suffer from some degree of relativism, relativizing harm to the perspective of the individual would seem to undermine any attempt to construct generalizations that would apply across individuals, a problem that would not arise as dramatically for the other conceptions of harm.

18 Cooper seems to adopt this latter perspective when she makes the following claim: “It should be noted that the question of what is good for an individual is not only a problem for me but is a problem that arises in many other areas of philosophy (Cooper, 2002; p. 272-273).”

72 The failure of hybrid positions to provide an adequate account of what constitutes the harmfulness of a condition limits their ability to serve as a response to constructivist and anti-psychiatry critiques. Without such an account, it’s not clear how hybrid accounts can distinguish between those conditions that are indicative of an underlying disorder from those that are merely the result of “problems of living.” In the end, hybrid positions run the risk of inheriting the problems of both objectivism and evaluativism.

To the extent that they appeal to concepts such as “function” and “normality,” they inherit the objectivists’ difficulties of providing value-free analyses of these concepts. To the extent that they appeal to evaluative judgments regarding the harmfulness of a condition, they inherit evaluativists’ difficulties of avoiding relativism.

Reconceptualizing the Philosophical Landscape: Epistemic and Nonepistemic

Evaluative Judgments

Given the problems facing objectivist, evaluativist, and hybrid accounts, abandoning the project of providing an account of psychiatric disorder may seem to be the more promising route to take. However, whatever the merits the abolitionist proposals of Hesslow and Kincaid may have, such a position would be premature. The difficulty of providing an account of psychiatric disorder does not lie primarily with the futility of identifying a set of necessary and sufficient conditions for the attribution of psychiatric disorder. Rather, the primary problem lies with the fact-value dichotomy that has dominated philosophical discussions of psychiatric disorder. The factual-evaluative approach for carving up philosophical accounts of psychiatric disorder is overly simplistic and ignores the variety of evaluative judgments that are operative in psychiatry. In this section, I distinguish epistemic and nonepistemic evaluative

73 judgments and suggest that a more fruitful alternative is to focus on the relative significance placed on the role of epistemic and nonepistemic evaluative judgments in psychiatric classification and research. I begin with a brief history of the conceptual distinction between facts and values and its influence in upholding the value-free ideal of science. I then appeal to the argument from inductive risk to challenge this ideal and argue that nonepistemic evaluative judgments can play a legitimate role alongside epistemic evaluative judgments in psychiatric classification and research. I show how these arguments, when applied to the context of psychiatric classification and research, shift the attention away from a narrow focus on facts and values and towards the complex interplay of epistemic and nonepistemic evaluative judgments. I argue that this proposal has the advantage of making explicit the role and type of evaluative judgments that are often tacitly assumed by various accounts of psychiatric disorder. Moreover, it enables a more straightforward comparison of accounts of psychiatric disorder in terms of the particular evaluative judgments that are prioritized by each account.

The conceptual dichotomy of facts and values has a longstanding tradition throughout the history of philosophy. According to this tradition, facts describe the way the world is and values describe the way the world ought to be. The ancestry of the dichotomy traces back to the work of David Hume (2003), who famously declared that an

“ought” could not be derived from an “is.” Hume’s aim was not to denigrate values, but rather to show that reason was an insufficient source of moral motivation. At the turn of the twentieth century, the dichotomy was again lamented by G.. Moore (1993), whose open question argument asserted that evaluative terms, for instance, “good”, could not be defined in terms of descriptive/naturalistic terms.

74 The conceptual separation of facts from values has typically coincided with another longstanding dichotomy throughout the history of philosophy, the metaphysical distinction between the objective and the subjective. According to this distinction, an entity is objective if its existence is not dependent upon human interests and is subjective if its existence is wholly or partially dependent upon human interests. Facts, so the story goes, are objective in that they describe the way the world is independent of human interests and values are subjective in that they describe the way the world ought to be in light of particular human interests.

Conceptualizing facts and values in this way has typically not boded well for values. This has been the case particularly in the philosophy of science, where values have struggled to reside comfortably within the naturalistic and mechanistic worldview of contemporary science. The reason for this struggle stems from a particular conception of science, one in which the aim of science is to produce a body of objective facts which are immune from the influence of human values, moral, political, social or otherwise.

Historically, the value-free ideal of science was most notably and forcibly defended by the logical positivists, who argued for a noncognitivist interpretation of values.

According to this interpretation, values are mere expressions of attitudes or emotions and devoid of any factual content. Their presence in scientific discourse would compromise the objectivity of science and, therefore, should be avoided at all costs.

Despite the widespread influence of the logical positivist account of science and evaluative statements, critics have pointed to the pervasiveness and indispensability of values within actual scientific practice. At minimum, considerations of value could potentially influence the following aspects of scientific practice:

75 x Which aspects of nature scientists choose to investigate x How the fruits of scientific research are to be distributed x Who can “do” science x Who receives recognition for scientific discoveries x How is the meaning of theoretical entities determined x How to choose a scientific theory/hypothesis from a set of alternative theories/hypotheses

It is generally accepted that values at least partially determine which aspects of nature scientists decide to investigate. The concern for the prevention and eradication of disease as well as the United States’ militaristic culture of post-World War II serve as illustrative examples of how values shape our scientific inquiries. In addition to influencing what scientists choose to study, values influence how the fruits of scientific research are to be distributed amongst the population. This is evidenced by current debates about health care reform, where there is disagreement as to the most fair and equal means for allocating medical resources and technologies amongst urban and rural areas. Values have also played a role, at least historically, in determining who can participate in scientific research and who receives recognition for scientific discoveries19.

Logical positivists and defenders of the value-neutrality of science often acknowledge that values influence these more peripheral, external aspects of science but maintain that the epistemologically relevant, internal aspects of science, e.g., scientific methodology, the meaning of theoretical entities, the evaluation and selection of scientific theories, are value-free. However, even the value-neutrality of these more epistemologically relevant aspects of science has been called into question, most famously in the work of Thomas Kuhn (1970, 1977). Kuhn argued that theory selection was underdetermined by considerations of empirical data alone and that “extra-scientific”

19 The most notable example of this is Rosalind Franklin, whose work in x-ray crystallography was overlooked despite its contribution to the discovery of DNA.

76 values played an ineliminable role in theory selection. He cited accuracy, consistency, generality, simplicity, and fruitfulness as examples of these “extra-scientific” values and pointed out that the relative significance of each these values to the evaluation and selection of competing theories could not be determined by any objective decision procedure. Rather, subjective factors such as the experience and personality of the scientists involved as well as the social and political context of the time influenced which

“extra-scientific” values were privileged.

The value-free ideal of science has been further challenged by a closely related argument, the argument from inductive risk (Douglas 2000, 2009; Steel 2010). This argument maintains that nonepistemic values should influence the standards of evidence required for accepting or rejecting hypotheses when there are significant risks to human health or the environment associated with errors. The argument from inductive risk originated in the work of Rudner (1953), but has resurfaced primarily in the context of risk assessments regarding exposure to toxic chemicals (Cranor 1993, 2006; Douglas

2000).

Central to the argument is a distinction between epistemic and nonepistemic evaluative judgments. Daniel Steel (2010) provides a useful framework for thinking about the distinction between epistemic and nonepistemic values. On his account, epistemic values are those values that promote the attainment of truth. pistemic values can promote the attainment of truth either intrinsically or extrinsically. Intrinsic epistemic values are those values that are necessary for and directly promote the attainment of truth, e.g., empirical adequacy, predictive accuracy, and internal and external consistency. The idea is that a theory that is not empirically adequate, fails to

77 make accurate predictions, contradicts itself, or conflicts with accepted background theories is unlikely to be true. xtrinsic epistemic values are those values that indirectly promote the attainment of truth by supporting or enabling the realization of intrinsic epistemic values. xamples of extrinsic epistemic values include testability, simplicity, generality, and fundability. xplanations which fail embody at least some of these values fail to realize intrinsic epistemic values and, therefore, fail to promote the attainment of truth. Nonepistemic values are those values that aim at the attainment of some particular practical, moral, or social good. Common examples of nonepistemic values include the minimization of harms, justice and equity, social utility, controllability, and respect for autonomy.

According to the value-free ideal of science, the acceptance or rejection of hypotheses is to be decided solely in terms of epistemic values. Nonepistemic values bear no logical relation to decisions about which hypotheses to accept or reject.

However, the argument from inductive risk denies this and maintains that decisions about whether to accept or reject a hypothesis should depend in part on nonepistemic value judgments. In particular, there are two contexts in which nonepistemic value judgments should legitimately influence decisions about whether to accept or reject a hypothesis.

First, nonepistemic value judgments should play a role whenever one must balance the relative risks of false positive and false negative diagnoses. Second, they should play a role whenever one must compare the relative risks of drawing an inference quickly and waiting for further evidence to reduce uncertainties. If either of these contexts obtain, then nonepistemic values should influence decisions about whether to accept or reject a hypothesis.

78 Given the practical nature of psychiatry and its general commitment to promoting mental health and eradicating psychiatric disorder, these contexts will inevitably and frequently arise in decisions about classifying and researching psychiatric disorders. To see this, consider the first situation in which one must balance the relative risks of false positives and false negatives. This issue pervades psychiatry, from decisions about proper research design to decisions about which criteria to include or exclude in psychiatric diagnoses. This latter concern undoubtedly receives the most attention, from both psychiatrists and the media. Psychiatrists must balance the risks of over-diagnosing a particular disorder and failing to diagnose a disorder when it is in fact present. The iatrogenic effects of over-diagnosis represents one the primary motivations of constructivist and anti-psychiatry critiques. “Medicalizing” normal problems of living not only can lead to the treatment of individuals with potentially harmful and expensive therapies, but it also runs the risk of stigmatizing individuals who are not actually suffering from a disorder. The risks associated with over-diagnosis extend beyond potential harms to the individual and include potential harms to society in terms of increased health care costs. On the other hand, failing to diagnose a disorder when it is present runs the risk of not treating an individual who needs and could benefit from treatment. As with over-diagnosis, the risks associated with under-diagnosis extend beyond potential harms to the individual. Diminished work productivity and, depending on the nature of the disorder, threats to public safety represent just some of the potential harms to society.

The relative risks associated with the inclusion or exclusion of certain criteria for psychiatric diagnoses is evidenced by the numerous disputes surrounding the release of

79 the DSM-V. The relative risks associated with the inclusion or exclusion of certain criteria for Body Dysmorphic Disorder (Phillips et al, 2010), the Paraphilias (First &

Frances, 2008), especially the proposal of Paraphilic Coercive Disorder as a new diagnostic category (Frances et al, 2008), Bipolar Disorder (Zimmerman, 2011; Phelps &

Ghaemi, 2012; Ghaemi, 2010; Ghaemi, 2010b; Phillips, 2010; Frances, 2010a; Frances,

2010b), Post-Traumatic Stress Disorder (Forbes et al, 2011), Major Depressive Disorder

(Frances, 2010), and Autism Spectrum Disorder (Frances, 2010), among numerous others, have generated contested debates. For instance, the DSM-IV only required an active avoidance of emotional distress or an emotional numbing for a diagnosis of Post-

Traumatic Stress Disorder (PTSD). However, the DSM-V (2013) requires both symptoms to be present for a diagnosis to be made. Forbes et al. (2011) argue that this runs the risk of increasing false positive diagnoses of PTSD, as individuals experiencing emotional numbing due to depression will get misdiagnosed as having PTSD. First &

Frances (2008) raise similar concerns for diagnoses of paraphilia. The DSM-IV (1994) added the requirement that an individual must experience intense sexually arousing fantasies, urges, or behaviors involving sexual activity with a pre-pubescent child for a diagnosis of paraphilia to be made. First & Frances (2008) advise removing the clause

“or behaviors” from the DSM-V because they worry that it will increase false positive diagnoses of paraphilia by allowing sexual offenders to qualify as having a psychiatric disorder based solely on having committed sexual offenses.

The most notable of these debates regarded the inclusion or exclusion criteria for

Bipolar Disorder (Ghaemi, 2010; Ghaemi, 2010b; Phillips, 2010; Frances, 2010a;

Frances, 2010b). Bipolar disorder is a mood disorder in which a patient experiences

80 shifts between episodes of depression and mania. mil Kraepelin extensively studied the natural course of the disorder, which he referred to as “manic-depressive illness,” in the beginning of the twentieth century and distinguished it from “dementia praecox,” which later came to be labeled as “schizophrenia.” Bipolar disorder became an official diagnostic category in the DSM-III (1980), replacing the diagnosis of “manic-depressive disorder.” The disorder was split into Bipolar-I and Bipolar-II in the DSM-IV (1994).

The rationale for the division was to more reliably distinguish genuine differences in patients based upon the severity of manic episodes that they experience. To be diagnosed with Bipolar I, an individual must have at least one manic episode and one depressive episode; to be diagnosed with Bipolar II, an individual must have at least one hypomanic episode and one depressive episode. The manic episode accompanying Bipolar I is marked by abnormally elevated mood and often the presence of hallucinations and/or delusions. These symptoms cause significant impairment in daily functioning and typically require hospitalization. The hypomanic episode accompanying Bipolar II is less severe than manic episodes and is marked by noticeably elevated mood and typically do not include the presence of hallucinations and/or delusions. Although these symptoms may interfere with daily functioning, the individuals experiencing hypomanic episodes do not typically require hospitalization (American Psychiatric Association, 1994).

The split between Bipolar I and Bipolar II, although intended to more reliably distinguish genuine differences in patients, also ran the risk of blurring the lines between

Bipolar II and unipolar depression (Frances, 2010a). Several revisions to the diagnostic criteria for Bipolar I and Bipolar II in the DSM-V are intended to address this problem.

One of the revisions requires the presence of elevated levels of energy and activity in

81 addition to elevated mood for both manic and hypomanic episodes. This requirement is clearly intended to tighten the criteria for both Bipolar I and Bipolar II with the expectation of minimizing the risks of over-diagnosis and more clearly demarcating

Bipolar Disorder from unipolar depression.

A second revision allows for the diagnosis of Bipolar I and/or Bipolar II if the manic and/or hypomanic episodes are induced by the use of antidepressants. This revision has been met with skepticism. Since the creation of Bipolar II as a diagnostic category, many clinical psychiatrists and researchers have raised concerns that the milder hypomanic episodes accompanying Bipolar II could not be reliably distinguished from the periodic elevated moods of patients diagnosed with unipolar depression (Frances,

2010a). The problem is further exacerbated by the fact that antidepressants often induce periodic elevated moods in depressed patients. Ghaemi (2010a), however, argues that the best available evidence suggests that the presence of antidepressant-induced hypomanic episodes is a reliable diagnostic marker for Bipolar II. He cites the meta-analysis of

Tondo et al (2010) as support for this claim. Their review examined the results of 109 studies that included 114,521 patients and found that antidepressant-induced mania was

2.6 times higher in individuals diagnosed with Bipolar Disorder than in individuals diagnosed with Major Depressive Disorder. Although the use of antidepressants increased the risk of manic episodes in all participants, the greater prevalence of such episodes in individuals with Bipolar Disorder led Ghaemi, as well as the DSM-V Task

Force, to conclude that a diagnosis of Bipolar Disorder can be justified on the basis of antidepressant-induced manic and/or hypomanic episodes. Although this requirement expands the criteria for both Bipolar I and Bipolar II, they contend that it enables

82 clinicians to more reliably distinguish individuals with Bipolar Disorder from those with

Major Depressive Disorder.

Frances (2010a), however, remains unconvinced and is concerned that the revision will lead to individuals with unipolar depression to be treated with antipsychotics and mood stabilizers. Moreover, Frances is generally skeptical of the research on which the revision was based and the ability of clinicians to clearly distinguish between antidepressant-induced hypomanic episodes and the return of normal mood in patients with unipolar depression. Although he doesn’t specifically challenge the Tondo et al review, he points out that most of the data upon which the diagnostic revisions are based

“has been mostly derived in specialized research settings with highly trained clinicians and highly selected patients. These are very different than the settings where most bipolar diagnosis is made (2010b).” Frances also questions the ability of researchers to be impartial in their recommendations to the DSM Task Force. He makes this point in light of his prior experience on the Task Force: “xperts are also all biased in the same direction - they always worry themselves greatly about false negatives and are relatively indifferent to false positives. In my work on three DSM's over twenty years, never once did an expert make a suggestion that would reduce the boundary of his pet disorder

(2010b).”

This dispute serves as an example of a legitimate role for nonepistemic evaluative judgments when assessing the relative risks associated with the inclusion or exclusion of certain criteria for psychiatric diagnoses. Ideally, such decisions would be based solely by appeal to epistemic evaluative judgments such as the empirical adequacy, predictive accuracy, and internal and external consistency of the proposed revisions. Ghaemi seems

83 to think that this is the case and that the best available evidence does establish a clear boundary between antidepressant-induced hypomanic episodes and the return of normal mood in patients with unipolar depression; however, he also acknowledges that the line is tentative and can be redrawn in light of further evidence (Ghaemi, 2010a). Although epistemic evaluative judgments are clearly operative in this dispute, each side is also appealing to nonepistemic evaluative judgments in defense of their position. Frances is clearly concerned with the prevalence of false positive diagnoses and the risks of treating patients suffering from unipolar depression with potentially harmful antipsychotics and mood stabilizers. Ghaemi is concerned with the possibility of under-diagnosing or misdiagnosing individuals with Bipolar Disorder and the potential harms associated with not receiving appropriate treatment. Moreover, both Frances and Ghaemi are justifiably concerned about decisions regarding proposed revisions being made solely on the basis of nonepistemic evaluative judgments. Frances is concerned about the partiality of clinical researchers and Ghaemi expresses a general worry about the decline of psychiatric classification were such a situation to arise. However, both are equally concerned about minimizing harm to patients suffering from psychiatric disorders. Whether the proposed revision to allow for the diagnosis of Bipolar I and/or Bipolar II on the basis of antidepressant-induced manic or hypomanic episodes causes more harm remains to be determined. However, one point remains clear: the determination will depend on both epistemic and nonepistemic evaluative judgments.

A final illustration of the role of nonepistemic evaluative judgments in psychiatric classification and research was the proposed revision to reduce the current required duration of a hypomanic episode for Bipolar II from four days to two days. Although this

84 proposal ultimately was not included in the DSM-V, it generated heated debate among clinical psychiatrists and researchers. The rationale for the proposed change was to more reliably distinguish individuals with Bipolar II from those with Major Depressive

Disorder. Ghaemi (2010a; 2010b), for instance, argued in favor of the revision on the grounds that the best available evidence supports a shorter duration period. He argued that a longer duration period would lead to misdiagnosing individuals with Bipolar II as having Major Depressive Disorder. As evidence for this claim, he cited research by

Benazzi and Akiskal (2006) in which differences between 246 individuals diagnosed with

Bipolar II and 178 individuals diagnosed with Major Depressive Disorder were assessed based upon the four day duration period for hypomanic episodes and a two to three day duration period. Benazzi and Akiskal found no statistically significant difference in diagnostic validators, such as early age at onset, depressive recurrence, atypical feature specifier, depressive mixed state, and bipolar family history, for the two duration periods.

Moreover, 72% of the hypomanic episodes lasted longer than four weeks, further evidence that the longer duration period is unwarranted. Ghaemi pointed out that similar results have been found in other studies as well (Wicki & Angst, 1991; Angst et al,

2003), leading him to conclude that the longer duration period is arbitrary and that the shorter duration period is a more reliable criterion for distinguishing individuals with

Bipolar II from those with Major Depressive Disorder.

Frances (2010a, 2010b), however, raised similar worries as he did with the previous revision. He expressed concerns that the shorter duration period would lead to more individuals with unipolar depression to be diagnosed with and treated for Bipolar II.

Frances cautioned against this misdiagnosis given the risks of weight gain and diabetes

85 associated with the use of antipsychotics and mood stabilizers (2010b). More generally, he highlighted the arbitrariness of any diagnostic threshold: “Choosing a duration or severity cutoff is always a somewhat arbitrary exercise in interpretation balancing sensitivity (the desire not to miss cases) with specificity (the desire not to overdiagnose and mislabel someone who does not have the disorder) (2010b).”

This dispute serves as a further example of a legitimate role for nonepistemic evaluative judgments when assessing the relative risks associated with the inclusion or exclusion of certain criteria for psychiatric diagnoses. Although epistemic considerations are clearly operative in this dispute, they alone are insufficient to determine the appropriate duration period of hypomanic episodes. Such decisions must appeal to nonepistemic considerations in weighing the relative risks of over-diagnosing Bipolar II, e.g., the potentially harmful effects of antipsychotics and mood stabilizers, against the risks of under-diagnosing or misdiagnosing the disorder, e.g., the potential harms associated with not receiving appropriate treatment. Whether the proposed revision of a shorter duration period for hypomanic episodes would have minimized harm remains to be determined. However, as with the previous revision, this determination will depend on both epistemic and nonepistemic evaluative judgments.

I mentioned earlier two contexts in which nonepistemic evaluative judgments should play a role in psychiatric classification and research. I used the case of weighing the relative risks associated with the inclusion or exclusion of certain criteria for Bipolar

Disorder to illustrate the first context. The second context involves comparing the relative risks of drawing an inference quickly versus waiting for further evidence to reduce uncertainties. As with the first context, this issue pervades psychiatric

86 classification and research. The prevalence of this issue is due to the evolving and tentative nature of psychiatric classification and research and the reciprocal relationship between the two. For better or worse, one of the many functions of the DSM is to establish a common language so as to improve and facilitate communication between different groups, which in turn helps to integrate and promote future research. The resulting research is then used to construct better diagnostic classifications and to make better predictions about the course of a disorder and treatment efficacy.

During the course of this process, researchers and clinicians must weigh the relative risks of drawing an inference quickly versus waiting for further evidence to reduce uncertainties. In a clinical context, this decision arises whenever a psychiatrist must apply diagnostic criteria to an individual patient to determine whether a disorder is present. Rarely will a patient display all of the diagnostic criteria listed in the DSM for a particular disorder. Rather, the typical patient will exhibit some of the diagnostic criteria in varying degrees, and different patients will rarely exhibit the same diagnostic criteria to the same degree. In such a situation, the psychiatrist must decide whether to diagnose the patient or wait for further evidence to ensure a more reliable diagnosis. ach option has its associated risks. Deciding to diagnose the patient on incomplete evidence runs the risk of misdiagnosis and administering unnecessary and/or potentially harmful and expensive therapies, which in turn can also lead to increased health care costs. On the other hand, deciding to wait for further evidence runs the risk of prolonging the patient’s suffering as he/she awaits treatment, which in turn can lead to diminished work productivity and, depending on the nature of the disorder, threats to public safety.

Sometimes the decision of whether to wait for further evidence or to diagnose is fairly

87 straightforward and is dictated primarily by epistemic considerations along with a general commitment to minimizing harm to the patient. However, in situations in which this is not the case, the psychiatrist must appeal primarily to nonepistemic considerations when deciding whether to wait or diagnose.

The problem of how to balance the risks of drawing an inference quickly versus waiting for further evidence persists even after a psychiatrist has made a diagnosis, at which point the psychiatrist must make a decision regarding the most appropriate treatment for the patient. Although there is often a clear standard of care given the particular diagnosis, this may not always be the case. Depending on the particular diagnosis, there may be multiple possible treatment options or the efficacy of existing treatments may not be well established. Moreover, the likely efficacy of each option may depend on the unique clinical presentation of the patient’s symptoms as well as the patient’s preferences, in the sense that the patient may be more or less willing to follow a certain treatment regimen. Thus, which treatment is most appropriate for a particular patient is not always a straightforward decision. A psychiatrist will have to weigh the risks selecting a treatment based upon incomplete evidence and waiting for further evidence to reduce uncertainties. Choosing a treatment based upon incomplete evidence runs the risk of exposing the patient to the potential side effects of an unnecessary treatment as well burdening the patient with increased health care costs. On the other hand, deciding to wait for further evidence runs the risk of prolonging the patient’s suffering as he/she awaits treatment. This balancing act is common throughout clinical medicine and is not unique to psychiatry. Nonetheless, in either case, the psychiatrist

88 will have to appeal primarily to nonepistemic considerations, for instance, deciding which option will minimize harm to the patient, when making a decision.

The decision of whether to draw an inference quickly or wait for further evidence to reduce uncertainties also arises in research contexts. The issue of clinical equipoise represents the most notable instance of this. Clinical equipoise is typically considered to be an ethically necessary condition for the proper conductance of any research involving human subjects. It refers to a state of genuine uncertainty on the part of the individual clinical investigator or the medical community regarding the therapeutic merits of each arm in a clinical trial. quipoise is present when there exists an honest, professional disagreement among expert clinicians about the preferred treatment for a particular disorder and when each side recognizes that the opposing side has evidence to support its position. In such cases, a clinical trial is instituted with the aim of resolving the dispute.

However, as data accumulate during the course of the clinical trial, it may become apparent that one arm of the clinical trial is either benefiting or being harmed by the target intervention. At this point, equipoise no longer obtains and it would presumably be unethical to continue the trial because one group of participants would knowingly either be harmed or denied access to beneficial treatment by the continuation of the trial. Of course, determining the point at which equipoise no longer obtains is rarely a straightforward matter20. A clinical researcher may suspect that one arm of the clinical trial is either benefiting or being harmed by the target intervention, but he/she may not have sufficient evidence to justify this suspicion until the trial is completed. This issue is further complicated by the fact that many clinical trials are multi-site studies and no

20 The case of Nancy Olivieri, a hematologist evaluating the use of deferiprone in the treatment of iron overload in patients with thalassemia major, provides an excellent example of this. See Schafer (2003) for a discussion of this case.

89 individual clinical researcher has access to the data regarding adverse events from all of the sites. In situations such as this, the researcher must decide whether to infer that the target intervention is harming or benefiting the participants, and thus terminate the trial, or to wait for further evidence and continue the trial. In either case, although epistemic considerations clearly play a role, such decisions will rely on nonepistemic evaluative judgments.

I have discussed how the issue of balancing the risks of drawing an inference quickly versus waiting for further evidence arises independently in clinical and research contexts. However, the issue also arises in the interaction between the two contexts.

This issue underlies the debate between conservative and revisionist approaches that was briefly discussed in the introductory chapter. The debate between the two approaches concerns how psychiatric classifications should be revised in light of new information about the nature and/or presence of symptoms or new information about the causal processes involved in the development and/or maintenance of these symptoms. A conservative approach tends to be resistant to classificatory revision in light of new information and recommends waiting for further evidence to reduce uncertainties.

Typically, this approach is grounded in concerns about the harmful iatrogenic effects of psychiatric labels, particularly when there is no disciplinary consensus as to whether the evidence warrants the proposed revisions. Alternatively, a revisionist approach tends to encourage classificatory revision in light of new information and recommends drawing inferences more quickly. This approach is more willing to lump previously separate diagnostic categories together or split a diagnostic label into separate categories based on preliminary information with the expectation that doing so will increase diagnostic

90 validity and reliability. The debate between conservative and revisionist approaches applies equally to the case discussed above regarding the relative risks associated with the inclusion or exclusion of certain criteria for Bipolar Disorder, where much of the dispute concerned how to revise the criteria for Bipolar Disorder in light of new research.

However, one point remains clear: whether weighing the risks of including or excluding diagnostic criteria or deciding whether to draw conclusions rather than waiting for further evidence, the decision will depend in part on nonepistemic evaluative judgments.

The role of nonepistemic evaluative judgments in each of these contexts has important implications for the philosophical accounts of psychiatric disorder outlined earlier. First, it implies that objectivists, strong evaluativists, and hybrid accounts (weak evaluativists) all fail to acknowledge the complex interplay of both epistemic and nonepistemic values in psychiatric classification and research. Strong evaluativists such as Nordenfelt and Fulford fail to fully countenance the role of epistemic values in attributions of psychiatric disorder and focus too exclusively on nonepistemic value judgments. Moreover, their focus on nonepistemic value judgments is confined to the attribution of psychiatric disorder in a clinical context. Although such judgments are certainly operative in this context, they overlook their role in research contexts and the broader influence that this has on psychiatric classification and the attribution of psychiatric disorder.

Objectivists such as Boorse, on the other hand, fail to acknowledge the role of nonepistemic value judgments altogether, both in research and clinical contexts. This is evident in their attempts to provide value-free analyses of the concepts of “function” and

“normality.” However, in addition to the aforementioned problems with such attempts,

91 the role of nonepistemic value judgments in the dispute over the diagnostic criteria for

Bipolar Disorder further demonstrates the difficulties of providing such analyses.

Moreover, even if objectivists could provide value-free analyses of the concepts of

“function” and “normality,” they fail to recognize the inherent negotiation between various epistemic values in these analyses. This is a point emphasized by Kuhn with respect to theory selection in general and by Murphy (2006) with respect to reductive explanations in particular. For instance, one’s description of a malfunctioning mechanism may have certain built in idealizations and assumptions that minimize its empirical adequacy but maximize its predictive accuracy. A lower-level description, on the other hand, may minimize predictive accuracy but maximize empirical adequacy. If

Kuhn and Murphy are correct, then there is unlikely to be one correct description of what constitutes “function” and/or “normality.” However, objectivists fail to countenance this complexity inherent in attributions of function and normality.

Hybrid accounts tend to inherit the shortcomings of both strong evaluativism and objectivism. As with strong evaluativist accounts, their focus on nonepistemic value judgments tends to be confined to the attribution of psychiatric disorder in a clinical context, causing them to overlook their role in research contexts and the broader influence that this has on psychiatric classification and the attribution of psychiatric disorder. Moreover, to the extent that hybrid accounts rely on value-free analyses of the concepts of “function” and/or “normality,” as does Wakefield’s HDA, they face the same problems as objectivist accounts. They fail to acknowledge the potential role of nonepistemic value judgments in their analyses of the concepts of “function” and

92 “normality.” In addition, they fail to recognize the inherent negotiation between various epistemic values in these analyses.

These shortcomings suggest that the traditional factual-evaluative approach for carving up philosophical accounts of psychiatric disorder is overly simplistic and ignores the variety of evaluative judgments that are operative in psychiatry. A more fruitful alternative is to focus on the relative significance placed on the role of epistemic and nonepistemic evaluative judgments in psychiatric classification and research. Such a proposal enables a more straightforward comparison of the various accounts of psychiatric disorder in terms of the particular evaluative judgments that are prioritized by each account. More importantly, it has the advantage of making explicit the role and type of evaluative judgments that are often tacitly assumed by the various accounts of psychiatric disorder.

93 Chapter 3: Reductionism in Psychiatry

The previous chapter outlined problems with objectivist, abolitionist, evaluativist, and hybrid accounts of psychiatric disorder. Despite the differences between these accounts, they all share the aim of undermining constructivist and anti-psychiatry critiques and upholding the scientific legitimacy of psychiatry. A common strategy for succeeding in this task relies on interpreting psychiatry as a branch of medicine. Since medicine is a science (or at least scientific), so the argument goes, psychiatry could establish itself as a legitimate scientific discipline by successfully aligning itself with medicine. However, each of the above accounts of psychiatric disorder may differ with respect to what it means for psychiatry to be a branch of medicine or scientific as well as which sciences are most relevant for explaining psychiatric disorder. Put another way, although each of the above accounts may generally subscribe to a medical model of psychiatric disorder, they may disagree about the precise meaning and utility of this model. Objectivists and some hybrid accounts, for instance, may interpret the medical model as embodying a commitment to treating psychiatric disorders as “brain disorders” or “brain diseases” (Boorse, 1977; Guze, 1989; Martin, 2002; Insel & Quirion, 2005;

Graham, 2013). If this is the case, then neuroscience and perhaps genetics and evolutionary biology and psychology will likely occupy central roles in explaining psychiatric disorder. valuativists and some abolitionists, on the other hand, would likely deny that the medical model requires any such commitment. valuativists, in particular, would likely make such a denial and countenance disciplines that are more likely to acknowledge a role for evaluative judgments and that directly study their role in attributions of psychiatric disorder, such as psychology and sociology.

94 The crux of the issue, therefore, is whether the medical model should be interpreted as reductionistic or pluralistic in nature. More specifically, although all of the accounts of psychiatric disorder are likely to acknowledge some role for neuroscientific explanations of psychiatric disorders, the issue is whether these explanations are (or at least will be) sufficient to explain psychiatric disorders or if other disciplines will be required as well. If psychiatric disorders are just “brain disorders” or “brain diseases,” then psychiatrists should have to look no further than neuroscience to find explanations for psychiatric disorder. Psychiatry, it would seem, is simply nothing other than clinical or applied neuroscience. If, on the other hand, neuroscientific explanations are not sufficient to explain psychiatric disorders, a sentiment echoed in ngel’s (1977) biopsychosocial model, then explanations in psychiatry will turn out to be pluralistic in nature.

This disagreements open up the possibility for a wide variety of views regarding the exact role that neuroscience should play within psychiatry and it’s prospective relationship with other higher-level psychiatric disciplines, e.g., psychology and sociology. At one extreme, one could argue for the complete autonomy of higher-level psychiatric sciences and maintain that neuroscience is entirely irrelevant to explaining the causes of psychiatric disorder. Given the potential dualistic implications of such a view and the fact that there is at least preliminary evidence to suggest a role for neuroscience in the explanation of psychiatric disorder (Caspi et al., 2003; Koponen et al., 2002; Leroi et al., 2002), such a view is neither common nor promising. At the other extreme, one could argue for the complete elimination of higher-level psychiatric sciences on the grounds that they are explanatorily inadequate and that a future completed neuroscientific

95 will fully explain psychiatric disorder. Such a view, however, is highly speculative and overly optimistic given that folk psychological concepts such as belief, desire, and judgment seem to be important, perhaps indispensable, concepts for describing the symptoms and causes of psychiatric disorders. Between these two extremes lie a number of possible reductionist and pluralist positions. In this chapter, I focus exclusively on the variety of reductionist theses that one could hold within psychiatry, the motivations for defending some of these theses, and several shortcomings that each thesis faces in the context of psychiatry. In particular, I examine five different reductionist theses that are discussed in the literature: 1) ontological reductionism, 2) eliminative reductionism, 3) methodological reductionism, 4) epistemological (inter-theoretic) reductionism, and 5) causal reductionism. Later in the chapter I examine several proposals to synthesize psychiatry with neuroscience and consider if and to what extent they embody a commitment to any of the reductionist theses discussed above. I conclude the chapter by briefly arguing for a local version of methodological reductionism within psychiatry. In the next chapter, I will consider the variety of pluralist theses that one could hold within psychiatry.

What is Reductionism?

A brief perusal of the literature in philosophy of psychiatry can leave one with the impression that biological psychiatry, and particularly its commitment to reductionism, is responsible for all of the ills currently plaguing the discipline (Kendler, 2005, 2008;

Brendel, 2003; Regenmortel, 2004; Gold, 2009). Reductionism, even if not always explicitly blamed, is alleged to be responsible, either wholly or partially, for everything from the prevalence of false positive diagnoses, i.e., the over-medicalization of normal

96 “problems of living” and all of its associated iatrogenic harms, the occurrence of false negative diagnoses, the absolving of personal responsibility and, worse yet, persons altogether, the neglect or outright rejection of social and environmental causes and treatments of psychiatric disorders, and the rise of the biopharmaceutical complex and the conflicts of interest with which it creates (Andreason, 1998; Yudofsky & Robert, 2002).

There are no doubt instances of grandiose predictions about the explanatory and therapeutic prospects of biological psychiatry as well as the occasional overstatement of

“alleged findings.” 21 However, the above allegations typically rely on vague references to general reductionist trends in psychiatry or to pop culture coverage of neurobiological and genetic research on psychiatric disorders, e.g., headlines espousing the discovery of

“a gene for X.” This reliance owes largely to the fact that reductionism is rarely explicitly advocated as an explanatory framework within psychiatry. The lack of explicit advocacy of reductionism within psychiatry obscures the heterogeneity of the view and makes it an easy target for critics. On the one hand, it gives critics extensive leeway in their characterization of the view, which often leads to attacking an outdated, straw man version of reduction. On the other hand, it obscures the various metaphysical, epistemological, and methodological reductionist theses that one can defend and the specific contexts in which one can defend them. To see this, consider the variety of reductionisms discussed within the philosophy of psychiatry literature: 1) Ontological reductionism (Rudnick, 2002; Gold, 2009), 2) pistemological reductionism (Rudnick,

2002), 3) Methodological reductionism (Rudnick, 2002), 4) Inter-theoretic reductionism

(Karlsson & Kamppinen, 1995; Brendel, 2003; Gold, 2009), 5) Causal reductionism

21 See Leo & Jacasse (2007) for an interesting discussion of the misrepresentation of the chemical imbalance theory of depression by the psychiatric profession and the media.

97 (Karlsson & Kamppinen, 1995; Murphy, 2005; Woodward, 2008), 6) liminative

Reductionism (Zachar, 2000; Karlsson & Kamppinen, 1995), 7) hard reductionism

(Kendler, 2005, 2008). There are clear connections between many of these varieties of reductionism, but they each make distinct claims that affect their plausibility and applicability within psychiatry.

Before discussing these views, however, it is important to consider the variety of contexts within psychiatry in which one could defend reductionist theses. To see this, consider a simplified account of the typical psychiatric clinical encounter. The typical encounter begins with a presentation of symptoms and attempts to describe these symptoms. Here both the patient and the psychiatrist attempt to understand the phenomenology of and the meaning attached to the symptoms. The psychiatrist then draws upon clinical experience and an existing body of research to classify the symptoms, to construct a reliable diagnosis, and to explain the likely course and causes of these symptoms. Finally, the psychiatrist again draws upon an existing body of research, clinical experience, and the patient’s preferences to develop a treatment plan with the goal of intervening into the hypothesized causes so as to alleviate the symptoms. In this brief summary of the typical clinical encounter, several contexts arise in which one could defend a reductionist thesis: 1) the description of the symptoms of psychiatric disorder, 2) the classification and diagnosis of psychiatric disorder, 3) the explanation(s) of the causes of psychiatric disorder, 4) the appropriate research methods by which to study psychiatric disorder, and 5) the treatment of psychiatric disorder. One could defend a reductionist position with respect to some or all of these five contexts. A reductionist, for instance, could argue that the description of symptoms, the diagnosis of disorder, and the

98 explanation of the causes of the symptoms should be (or at least should aim towards being) couched in the vocabulary of cellular and molecular neuroscience (or some other lower-level science) and that the research methods for studying disorder and the treatment of disorder should aim to investigate and intervene into hypothesized cellular and molecular mechanisms.

Few reductionists would likely defend their position with respect to the description of symptoms since, at least given the current state of neuroscience, the use of folk psychological concepts seems to be indispensable for understanding the phenomenology of and the meaning that patients attach to their symptoms. Similarly, few reductionists would likely defend their position with respect to the treatment of psychiatric disorder, although they would likely prioritize neurobiological interventions to the extent that they are available and maintain that cognitive and environmental interventions are efficacious to the extent that they exert their influence via underlying neurobiological mechanisms. In the discussion of the various reductionist theses that follows, I take the explanation and classification of psychiatric disorder as well as the proper methodology for studying psychiatric disorders to be the contexts that are of primary interest to reductionists. However, even within this narrowed context, there are a wide variety of reductionist theses that one could defend. For the sake of simplicity, I will treat inter-theoretic reductionism as a version of epistemological reductionism and

Kendler’s hard reductionism as a version of causal reductionism. I will focus primarily on epistemological and causal reductionism as these, or variations of them, are the most commonly discussed versions of reductionism in the literature.

99 (1) Ontological Reductionism: Rudnick (2002), drawing upon the work of Ayala

(1974) and Vicedo (1998), suggests distinguishing ontological, epistemological, and methodological varieties of reductionism in the context of psychiatry. Ontological reductionism, according to Rudnick, is the position that all living systems are composed of nothing but physical/chemical processes. On this account, ontological reductionism is simply a commitment to some form of naturalism or physicalism. In the context of psychiatry, the view would entail that the symptoms of psychiatric disorders as well as the causes of these symptoms are physical in nature. Such a view, Rudnick suggests, is widely accepted on the grounds that “there does not seem to be much point nowadays in postulating non-physical entities” and that “such attempts have not advanced science to date (290).”22 This interpretation of ontological reductionism is simply a logical consequence of the denial of Cartesian Dualism and an acceptance of a reductionistic interpretation of the medical model. After all, if psychiatric disorders are brain disorders, then it seems that the causes of psychiatric disorders should be reducible to brain processes.

Despite just representing a commitment to some form of naturalism or physicalism, Rudnick’s characterization of ontological reductionism does suffer from several ambiguities. First, Rudnick construes ontological reductionism strictly as a negative thesis without providing a positive account of what makes a property physical or natural. Thus, his account is unclear as to which explanatory constructs in psychiatry an ontological reductionist should consider legitimate. For instance, it is not clear on this construal whether beliefs, desires, and judgments, mental states that are often alleged to

22 See Jeffrey Schwartz’s (2002) The Mind and The Brain: Neuroplasticity and the Power of Mental Force as an alternative dualist framework in psychiatry.

100 be constitutive of the symptomatology and/or etiology of numerous psychiatric disorders, count as physical or natural properties and, if they are, in what sense they are physical or natural properties. Perhaps such an account can be provided, but Rudnick does not offer one.

A second closely related concern is that Rudnick fails to distinguish between local and global varieties of ontological reductionism. Rudnick construes ontological reductionism strictly as a global thesis pertaining to all higher-level entities or properties found within psychiatry. However, this ignores the possibility of defending a local ontological reductionism and makes the reductionist committed to more grandiose claims than he/she needs to be. For instance, to accept ontological reductionism as a global thesis would commit one to the claim that all types of higher-level entities and processes implicated in the symptomatology and etiology of psychiatric disorders are reducible to abnormal neurobiological mechanisms. Thus, a global ontological reductionist would have to accept that a type of symptom is caused by the same type of malfunctioning neurobiological mechanisms in all individuals in which the symptom appears and that this would be the case for all types of symptoms that arise for all types of psychiatric disorders in all individuals diagnosed with the disorder. This is a tall order to fill and

Rudnick provides no evidence for thinking that it has been or can be filled. A local ontological reductionist, on the other hand, could argue for the more modest claim that only some particular higher-level entities and processes implicated in the symptomatology and etiology of psychiatric disorders are reducible to some particular abnormal neurobiological mechanism. Thus, ontological reductionism as a local thesis pertains only to the ontological status of the specific symptoms and causes of particular

101 psychiatric disorders causing distress for particular individuals, and not to the symptoms, causes, or individuals as general types of things. Moreover, local ontological reductionism is compatible with the possibility that the symptoms and causes of a psychiatric disorder are multiply realizable by a number of different abnormal neurobiological mechanisms.

The example of delusions can help to illustrate the difference between these two views. Delusions, a symptom present in a variety of patients and psychiatric disorders, form a general class of symptom that, on the global ontological reductionist view, would be reducible to general types of malfunctioning neurobiological processes that are common in all individuals. However, on the local ontological reductionist view, even if delusions form a general class of symptom, the neurobiological processes to which they reduce in one individual may be different from the neurobiological processes to which they reduce in another individual. Moreover, the local ontological reductionist need only accept that such an account can be given for some symptoms of psychiatric disorders; they need not accept that this would be the case for all types of symptoms that arise for all types of psychiatric disorders. In this sense, local ontological reductionism is an empirical claim to be settled on a case-by-case basis.

Ontological reductionism might seem to be a relatively uncontroversial thesis in psychiatry to the extent that it is simply a commitment to some form of physical or naturalism; however, the view still requires justification. I do not intend to defend the merits of physicalism or naturalism here. The important point is that the merits of ontological reductionism, particularly as a local thesis, must be settled on a case-by-case basis and, at this point, has not been empirically validated. This is not to say that such

102 validation will not occur, but doing so will require explaining the symptomatology of specific psychiatric disorders in terms of underlying neurobiological or genetic mechanisms and showing that, in some sense, psychiatric disorder are just brain disorders. In this sense, ontological reductionism is best interpreted as a methodological and metascientifically driven hypothesis about where explanations for the symptomatology of psychiatric disorders will be found and the kinds of entities that will ultimately figure in these explanations.

(2) Eliminative Reductionism: Karlsson & Kamppinen (1995) and Zachar (2000) critically discuss eliminative reductionism in the context of psychiatry23. liminative reductionism, a view derived primarily from the work of Churchland (1981) in philosophy of mind, maintains that folk psychological concepts, such as belief, desire, and judgment, are explanatorily inadequate to explain human behavior and will eventually be replaced by concepts from a completed neuroscience. Churchland points out that folk psychology has not advanced over the past 2,000 years and, more importantly, it makes no attempt to explain features of the mind that it should be able to explain, such as sleep, learning, memory, perception, imagination, and psychiatric disorder. Furthermore, Churchland offers a pessimistic inductive argument for the likely failure of folk psychological explanations. Given the past failures of other folk theories, such as folk theories of motion, celestial bodies, fire, life, and mental illness, it would be highly improbable if folk psychology turned out to be true. Churchland doesn’t explicitly apply his view to psychiatry, but it implies that the psychological and/or sociological concepts used to describe the symptoms of psychiatric disorders and the psychological

23 Zachar (2000) also traces the view to the radical behaviorism of B.F. Skinner.

103 and/or sociological theories used to explain their causes are so vague and imprecise that they will eventually be replaced by neuroscientific concepts and explanations.

liminative reductionism is a version of Rudnick’s ontological reductionism in that it typically embodies a commitment to some form of naturalism or physicalism.

However, as with Rudnick’s discussion of ontological reductionism, the authors that discuss the view (Karlsson & Kamppinen,1995; Zachar, 2000) fail to distinguish between global and local versions of the position. liminative reductionism as a global thesis would entail that all psychological and/or sociological concepts used to describe the symptoms of psychiatric disorders and all psychological and/or sociological theories used to explain their causes will eventually be eliminated in favor of neuroscientific concepts and explanations. Such a view is highly speculative view and, as with global ontological reductionism discussed above, simply seems to represent a commitment to some form of physical or naturalism. As such, it is best interpreted as a methodological and metascientifically driven hypothesis about where explanations for the symptomatology of psychiatric disorders will be found and the kinds of entities that will ultimately figure in these explanations. Local eliminative reductionism, on the other hand, asserts that only some psychological and/or sociological concepts used to describe the symptoms of psychiatric disorders and some psychological and/or sociological theories used to explain their causes will eventually be eliminated in favor of neuroscientific concepts and explanations. Which psychological or sociological concepts and explanations will be eliminated and for which disorders will need to be determined on a case-by-case basis.

Nonetheless, defending the view will require explaining the symptomatology of specific psychiatric disorders in terms of underlying neurobiological mechanisms and showing

104 that other purported higher-level explanations fail to explain these symptoms in some important respect(s). However, as it stands, higher-level folk psychological concepts such as belief, desire, and judgment seem to be important, perhaps indispensable, concepts for describing the symptoms and explaining the causes of most psychiatric disorders.

(3) Methodological reductionism: Methodological reductionism is only explicitly discussed by Rudnick (2002), although the view serves as a general regulative ideal for most other versions of reductionism. The view maintains that the most promising approach in science is to search for the most basic constituents of a process and its explanation in terms of these basic constituents. In the context of psychiatry, methodological reductionism prescribes developing research strategies that aim to explain the symptoms and causes of psychiatric disorders in terms of entities and activities at the neurobiological level of organization. Although methodological reductionism is often guided by ontological and epistemological concerns, it is not necessarily committed to either ontological or epistemological reductionism. It closely resembles epistemological reductionism in that it encourages searching for lower-level explanations, but it differs, at least in the sense that Rudnick uses the term, in that it is not committed to the claim that explanations are only found at lower-levels. Moreover, the view is compatible with the co-existence of non-reductive research strategies, particularly in the early stages of research.

Although Rudnick fails to make this distinction, methodological reductionism can be cast as a global or local thesis in the same way as ontological reductionism. As a global thesis, methodological reductionism would entail that researchers should develop

105 strategies that aim to explain the symptoms and causes of all psychiatric disorders in terms of entities and activities at the cellular and molecular level of organization. Thus, a global methodological reductionist would maintain that one should always attempt to explain the symptoms and causes of all psychiatric disorders in terms of the lowest possible level. Of course, such a view is compatible with acknowledging that one will not find adequate explanations at the lowest possible level, but it at least advises that one should attempt to search for lower-level explanations. A local methodological reductionist, on the other hand, need only contend that one should develop research strategies that aim to explain the symptoms and causes of some psychiatric disorders in terms of entities and activities at the cellular and molecular level of organization. For instance, a local methodological reductionist may advise searching for lower-level explanations for the presence of delusions while at the same time recommending searching for higher-level explanations for the presence of delusions in a different disorder or for the presence of different symptoms altogether.

(4) Epistemological reductionism: pistemological reductionism is the most commonly discussed view of reductionism in the philosophy of psychiatry literature.

Rudnick (2002) characterizes it as committed to the claim that the laws, theories, or explanatory generalizations of one science can be derived from the laws, theories, or explanatory generalizations from a lower-level, more fundamental science. Cast in this way, epistemological reductionism is tantamount to a version of inter-theoretic reductionism, a view most famously articulated by Nagel (1961). Karlsson &

Kamppinen (1995), Rudnick (2002), Brendel (2003), and Gold (2009) specifically have inter-theoretic reduction in mind when they discuss reductionism in the context of

106 psychiatry24. The basic idea is that a higher-level theory of a psychiatric disorder, e.g., one couched in sociological or psychological terms, could be explainable in terms of some lower-level theory, e.g., one that only makes references to concepts from neuroscience. Classical models of inter-theoretic reduction were typically committed to the epistemological priority or explanatory fundamentalism of lower-level sciences25.

However, epistemological reductionism need not require any commitment to such a view.

pistemological reductionism is only committed to the view that the laws, theories, or explanatory generalizations of one science can be better accounted for by some singular science, but this science need not be a lower-level science or require any commitment to general claims about explanatory fundamentalism. For instance, a Freudian psychoanalyst could be considered an epistemological reductionist because he/she contends that the symptoms of psychiatric disorders are best accounted for exclusively by the concepts of psychoanalytic theory (Brendel, 2003).

Gold (2009) is the only author who attempts to explicitly connect his discussion of reductionism in psychiatry up with most of the features typically associated with classical models of inter-theoretic reduction. Two common features of classical models are that reduction is to be a relation between theories, where theories were understood to be a small set of generalizations that were able to explain a broad range of phenomena, and that the concepts of the reduced and reducing theory are to be connected via bi- conditional bridge laws so as to establish contingent identities between each domain.

Thus, inter-theoretic reduction in psychiatry would proceed as follows. First, there would

24 Brendel (2003) doesn’t explicitly refer to the view as inter-theoretic reduction, but he does mention .O. Wilson’s notion of “consilience” as representative of the view and situates it within the context of the “unity of sciences” debate. 25 I use the term causal reductionism, a view that I will discuss below, to refer to the version of reductionism that is committed to the explanatory and causal fundamentalism of lower-level sciences.

107 need to be higher-level theories consisting of laws or generalizations relating the presence of a particular type of symptom with some type of psychological or sociological property, for instance, delusions with a type of personality trait or depressed mood with a type of traumatic experience. Bridge laws would then be required to establish identities between the type of symptom and some neurobiological mechanism as well as between the type of psychological or sociological property and some other neurobiological mechanism. For instance, if there were a law-like generalization that held between depressed mood and traumatic life experience, then one would need a bridge law to identify depressed mood with some particular type of neurobiological mechanism and then a bridge law to identify traumatic life experience with some other type of neurobiological mechanism, and do so in a way that resulted in a law-like generalization between the respective types of neurobiological mechanisms.

The motivations for defending such a view are numerous. First, one may think that inter-theoretic reduction is a means for achieving ontological simplicity by showing that the higher-level psychological or sociological properties are nothing but lower-level properties. Second, one may be think that a lower-level explanation of psychiatric disorders will be more unified than the muddled collection of higher-level explanations.

Third, inter-theoretic reduction could lead to greater explanatory adequacy and predictive success, virtues that could generate a more accurate and systematic classification of psychiatric disorders as well as novel treatments via more efficacious neurobiological interventions. Finally, and closely related to the previous motivation, one might think that a successful inter-theoretic reduction can serve a corrective function by accounting for any exceptions that the higher-level explanation fails to explain.

108 Although these are worthwhile goals, successful inter-theoretic reductions in psychiatry are a tall order to fill and face familiar problems. First, it’s simply not clear that there are any higher-level, law-like generalizations in psychiatry that are suitable candidates for reduction. This, of course, must be determined on a case-by-case basis and may change as higher-level theories become more refined in light of further evidence, but such law-like generalizations do not seem to be forthcoming at present.

Second, even if there were such generalizations, they would likely be extremely complex and include many variables. Most psychiatric disorders are unlikely to be caused by one single factor; rather, they are likely the result of multiple causal factors that exert a synergistic affect on the development and maintenance of the disorder. If this is correct, then the higher-level generalizations will require relating the presence of a particular type of symptom with multiple types of psychological or sociological properties. For instance, depressed mood would have to be related to traumatic life experience as well as perhaps other variables such as personality traits and early childhood experiences. Whether one could formulate such law-like generalizations for psychiatric disorders is an open empirical question, but it is not difficult to see why a successful inter-theoretic reduction for a particular psychiatric disorder would quickly become intractable. One would not only need to formulate bridge laws to establish identities between the type of symptom and some neurobiological mechanism, but one would also need bridge laws between each of the types of psychological or sociological properties and distinct neurobiological mechanisms, and do so in a way that resulted in a law-like generalization between the respective types of neurobiological mechanisms. Again, a successful inter-theoretic

109 reduction of this sort is not impossible in principle, but, even if it were possible, there would be reasonable concerns about its empirical tractability and clinical utility.

The most commonly cited concern facing inter-theoretic reduction is the problem of multiple realizability (Fodor, 1974). To see the force of the problem, consider the simple higher-level generalization that relates the presence of depressed mood with a type of traumatic experience. As mentioned above, a successful inter-theoretic reduction would require a bridge law to identify depressed mood with some particular type of neurobiological mechanism and then a bridge law to identify traumatic life experience with some other type of neurobiological mechanism, and do so in a way that resulted in a law-like generalization between the respective types of neurobiological mechanisms.

The challenge that multiple realizability presents for this picture is that it undermines the likelihood of a one-to-one mapping between depressed mood or traumatic life experience and some distinct type of neurobiological mechanism. Depressed mood may be realized by a distinct type of neurobiological mechanism in one individual and yet realized by a similar but different type of neurobiological mechanism in another. It may even be realized by a distinct type of neurobiological mechanism in one individual at one time and a different distinct type of neurobiological mechanism in the same individual at a different time. The same could be the case with respect to the neurobiological mechanisms that realize traumatic life experience. If this is the case, then it would be unlikely to ever establish identities between the properties in each domain and; therefore, the possibility of formulating a lower-level, law-like generalization between the respective types of neurobiological mechanisms would be unlikely. This conclusion is not intended to imply that depressed mood and traumatic life experiences do not in some

110 sense depend upon lower-level cellular and molecular mechanisms. Rather, it is intended to establish the autonomy of higher-level psychiatric sciences from lower-level neuroscience.

The general motivation for defending the multiple realizability thesis is that higher-level psychiatric sciences seem to be provide an ineliminable component of explanations for the etiology of at least some psychiatric disorders. Gold (2009), Graham

(2013), and Wakefield (2006) all offer arguments along these lines, although in varying degrees of detail. Gold (2009) acknowledges that explanations in cognitive neuroscience are an important component for describing the structural and functional properties of neurons and that these details will constitute part of an explanation for the etiology of psychiatric disorders. However, Gold contends that a complete explanation for the etiology of psychiatric disorders will also require an account of how the structural and functional properties of neurons contribute to the global functioning of the organism, and such an account cannot be provided by neuroscience alone. Gold makes this point clear:

An adequate theory of an organ or biological system requires an answer to the global functional question of what the organ or system does as a whole… how does the amygdala and other structures produce emotional states? How do the language centres develop to allow a person to master their language? How does the hippocampus contribute to long-term memory? Currently, the concepts required to answer these questions belong exclusively to psychology. Indeed, the questions themselves are psychological questions. If, as reduction requires, we were to restrict psychiatric theory to neuroscience and genetics, then a great deal of our understanding of mental illness would be lost in the process. Indeed, it is not clear whether much of anything would remain because the neurobiological knowledge concerning mental illness would be very hard to articulate (510-511).

Gold envisions psychology as autonomous from lower-level neuroscience in that it, and it alone, provides the concepts necessary to explain the global functioning, and

111 malfunctioning, of an organism. Gold does not fully articulate what these concepts are; he only offers a brief discussion of depression in which he asserts that a complete explanation of depression will require “a psychological theory of mood, including deviations from normal (511).” Gold’s idea seems to be that attributions of psychiatric disorder involve deviations from some standard of normality and that these standards cannot be derived solely from the causal-mechanistic explanations that cognitive neuroscience provides. However, why psychology is the only discipline equipped to provide this standard of normality is left unclear.

Graham (2013) and Wakefield (2006) offer more detailed proposals for the autonomy of higher-level psychiatric sciences than Gold. Graham’s argument against reducing psychiatry to cognitive neuroscience rests upon his commitment to realism about psychiatric disorders. According to Graham, such a commitment entails that an explanation of psychiatric disorder must refer to “feelings, beliefs, memories, or other mental states or attitudes as causes or sources (41)” and that this precludes “thinking about psychiatric disorder in exclusively and exhaustively neuroscientific terms (24).”

Part of Graham’s argument for this claim is the alleged circularity of attempts to define psychiatric disorders in terms of brain disorders:

…it is contrary to its scientific aspiration to propose that ‘brain disorder’ should be defined first in terms of the conceptually prior notion of a psychiatric disorder and then and then only recommend that the notion of a psychiatric disorder should be re-described as that of a brain malfunction or disorder, all the while continuing to use the criterion of a psychiatric disorder as the criterion of a brain disorder (25; my italics added).

Graham asserts that such attempts would be “viciously circular” and “would make the notion of a brain disorder depend on the notion of a psychiatric disorder rather than the other way around (25).” The force of his argument rests upon the purported connection

112 between rationality and the intentionality of mental states (p. 117-127): since mental states are intentional states that exhibit rational connections, and the brute causal connections that cognitive neuroscientists investigate cannot fully explain these rational connections, Graham concludes that psychiatry cannot be reduced to cognitive neuroscience.

Graham’s appeal to the rational connections between mental states is more developed than Gold’s vague appeal to standards of normality in that it articulates the standards in terms of rational norms. However, as with Gold, Graham seems to think that the relevant norms are constitutive of folk psychological concepts but does not provide a detailed account of from where these norms are derived. Moreover, Graham’s argument for the alleged circularity of attempts to define psychiatric disorders in terms of brain disorders rests upon the ambiguous notion of “conceptual priority.” If what Graham means by “conceptual priority” is “logical priority”, as seems to be the case, then beginning with a mental conceptualization of a disorder would indeed restrict the extension of that concept to the concepts of some lower-level science. However, as pointed out in Chapter 2 for Nordenfelt’s evaluativist account, there are good reasons for thinking that logical priority does not capture the relationship between medical concepts of this sort, particularly the concept of psychiatric disorder. Rather, the appropriate relationship seems to be one of temporal or epistemological priority (Schramme, 2007).

The fact that we typically begin with a mental characterization of the symptoms before looking for the cause of those symptoms is an epistemological fact and has no bearing whatsoever on the logical relation between the concepts involved. From the fact that a psychiatrist first encounters a patient who describes his/her mood using mental concepts,

113 nothing follows about the logical relationship between the concepts of distress or helpless and the physical causes of the distress and helplessness. From a clinical perspective, the mental descriptions of the symptoms are simply epistemologically prior to the explanation of the causes of those symptoms.

Graham offers an additional argument against construing psychiatry as a branch of cognitive neuroscience that rests upon a distinction between a disorder being of the brain and a disorder being in the brain. To claim that psychiatric disorder is a disorder of the brain, what he refers to as “the broken brain view,” is to claim “that various neurologically specifiable breakdowns occur in the brain…and that such breakdowns constitute or compose the conditions referred to as psychiatric disorders (25).” However,

Graham argues that a disorder could be in the brain without being of the brain. He uses the example of somatic illness to illustrate this. Fever, diarrhea, cough, vomiting, nausea, or fatigue may indicate that something is wrong in the body without themselves being an illness of the body. These symptoms may actually indicate that the body is functioning well. Graham concludes: “A fever or a case of diarrhea may be a disturbance in the body without being an illness of the body. Analogously, a psychiatric disorder may be a disorder ‘in’ the brain without being a disorder ‘of’ the brain (25).”

Graham’s distinction seems intuitive enough to ground his argument against “the broken brain view.” However, it suffers from a potential serious flaw. Bodily reactions such as fever or diarrhea are typically thought to be performing an invaluable survival function. Graham explicitly acknowledges this when he cites the work of Nesse and

Williams (1996): “Fever and diarrhea, for instance, may, on occasion, be a body’s evolutionary selected defenses against disease, danger, or bodily damage (25).” If we

114 take Graham’s analogy with psychiatric disorders at face value, this would suggest that psychiatric disorders also perform an invaluable survival function. Although this may be the case, it certainly goes against the mainstream view of characterizing psychiatric disorder as a dysfunction (Murphy, 2006; Wakefield, 2006). Graham could argue that fever and diarrhea are dysfunctions as well, though this would not be a successful line of argument as even Graham admits that they serve useful functions. More plausibly, he could argue against characterizing psychiatric disorder as mental dysfunction or that the symptoms of psychiatric disorders are caused by traits that perform an invaluable survival function. However, Graham doesn’t offer any such argument for either of these claims and; therefore, it is difficult to make sense of his distinction between a disorder being in the brain as opposed to of the brain.

Graham offers a final, more traditional line of reasoning for thinking that psychiatry is autonomous from cognitive neuroscience: the computer analogy. Graham points out that much of the reasoning behind the “broken brain view” rests upon the claim that the mental is somehow nothing other than the physical and, therefore, that if a condition is a psychiatric disorder it must be a physical disorder of the brain.

Analogously, one would be forced to accept that a malfunction in the software of one’s computer must be a malfunction in the hardware of the computer since the software is somehow nothing other than the hardware. However, computer software is obviously not identical to the hardware of the computer, as it can be realized by multiple different hardware systems. Thus, just as there can be software malfunctions without a corresponding hardware malfunction, there can be mental malfunctions without a

115 corresponding brain malfunction. Graham takes this argument to establish the irreducibility of higher-level psychiatric sciences.

Wakefield (2006) offers a similar line of reasoning. As mentioned in Chapter 2,

Wakefield defends the harmful dysfunction view of psychiatric disorder, which states that a psychiatric disorder is a harmful dysfunction of an internal mechanism to perform its naturally selected function. Like Graham, Wakefield intends to show that one can have a mental dysfunction without a corresponding physical dysfunction. Wakefield offers two primary arguments for this claim, both of which rest upon the distinction between token physicalism, the view that each mental state token is identical to a brain state token, and type physicalism, the view that each mental state type is identical to a brain state type.

The first argument is simply a restatement of the multiple realizability thesis: a particular mental dysfunction may be token identical to a particular brain dysfunction without being type identical. Wakefield states: “if token–token identity but not type–type identity exists between mental states and physical states in a domain, then a type-describable mental dysfunction in that domain need not correspond to a type-describable physical dysfunction, and there may be no basis for anything other than an attribution of psychiatric disorder (129).” Consider again the case of depression. Wakefield’s argument entails that any particular token of distressed mood may be identical to a particular brain state, but that distressed mood as a type of mental dysfunction may not be identical to a type of brain dysfunction. Wakefield does not develop this line of reasoning any further other than to say that he thinks that type identities between mental dysfunctions and brain dysfunctions will not be as rare as many think: “…the rarity of type–type identities is likely incorrect …many major psychiatric disorders probably do

116 correspond to neurologic dysfunctions (129).” I will have more to say about this argument below since I think that Wakefield’s second argument, although purported to be a distinct argument, is really just a more detailed version of his first argument.

Despite Wakefield’s insistence on the likelihood of type identities between mental dysfunctions and brain dysfunctions, he develops a second argument that accepts type identity but yet maintains the possibility of mental dysfunction without brain dysfunction.

He states: “…even if every mental feature is type identical to some physical feature, that does not imply that every mental dysfunction is type identical to a physical brain dysfunction. A mental dysfunction type might be type identical to a physical type that is not a physical dysfunction (129).” Similar to Graham, Wakefield invokes the computer analogy to defend this claim. He argues that the software “is always at any given moment identical to some hardware state, but the software can nevertheless malfunction even though there is no malfunction whatever in the hardware (129; my italics added).” It is difficult to make sense of Wakefield’s argument here, as he seems to either confuse type identity with token identity or to improperly describe the computer analogy. The computer analogy is typically invoked to undermine type identity: since multiple different types of hardware can realize the same type of software program, software types cannot be identified with hardware types. However, Wakefield uses it to show how one can accept type identity without thinking that all mental dysfunctions are brain dysfunctions. Perhaps this is Wakefield’s intent, but his characterization of the computer analogy relies on describing software as being token identical to the hardware, e.g., the software “is always at any given moment identical to some hardware state,” not type identical. Thus, his appeal to the computer analogy does not support his conclusion that a

117 type of mental dysfunction can be identical to a physical type that is not a physical dysfunction. Rather, it seems to support his previous argument, namely, that a mental dysfunction can be token identical to a brain dysfunction without thereby being type identical, an argument which he doesn’t seem to think is particularly promising given the likelihood of finding type identities between mental dysfunctions and brain dysfunctions.

Confusions between token and type identity aside, the force of Wakefield’s argument lies in the examples he provides to support his claim that one can have a mental dysfunction without brain dysfunction. Wakefield considers the case of fear conditioning. He argues that it is possible that a harmless yet unusual stimulus could elicit danger signals and cause a “glitch that biases processing to the point of there being a mental dysfunction” without there being a corresponding brain dysfunction, or at least a dysfunction that is describable in purely physical terms (129). What makes the dysfunction mental, according to Wakefield, is the nature of the meaning that the danger signals have for the individual, and this meaningful content cannot be described in purely physical terms. In other words, any explication of the dysfunction must make reference to “danger” contents and how these contents relate to standard “danger” contents.

Wakefield cites the DSM-IV criteria for anxiety disorder as further support of this claim.

According to the DSM-IV, a necessary criterion for the diagnosis of anxiety disorder is that the anxiety must be “unreasonable” in response to the stimulus (129). Wakefield argues that since “it is hard to imagine that there is any way to assess reasonableness for a given individual without referring to mental states and the individual’s meaning system,” it follows that one could have a mental dysfunction, in this case anxiety disorder, without a corresponding brain dysfunction (129).

118 Wakefield is drawing upon the supposed rational connections among mental states to make his case. The idea is that mental states such as beliefs and desires have rational connections among them that account for their reasonableness, and these rational connections are not explained by elucidating the causal connections within the brain.

This is a point also made explicit by Graham: “…the norms or standards for healthy and proper brain function are not the same as those for satisfying or prudent personal activity or rational or reason-responsive behavior (54).” Consider again Wakefield’s example of fear conditioning. The reasonableness of one’s belief that danger is present depends upon how it relates to standard beliefs about the presence of danger. Wakefield does not state from where he thinks these standards are derived, a problem which arose for the views of

Gold and Graham as well, but I will assume that he means something like the following: if one forms the ‘danger’ belief in the presence of stimuli that people typically consider dangerous, then the belief is reasonable; conversely, if one forms the ‘danger’ belief in the presence of stimuli that people typically do not consider dangerous, then the belief is unreasonable. However, Wakefield does not think that merely forming a ‘danger’ belief in situations where most people would not is sufficient to ground the attribution of a psychiatric disorder. Recall his description from above, where he states that the harmless stimuli must cause a “glitch that biases processing to the point of there being a mental dysfunction” (without there being a corresponding brain dysfunction). This additional requirement stems from Wakefield’s harmful dysfunction analysis, which requires an internal mechanism that is failing to perform its naturally selected function as well as a negative evaluation of this dysfunction. In this case, the “glitch that biases processing” constitutes the dysfunction and serves to ground the attribution of psychiatric disorder.

119 Two problems emerge with Wakefield’s example. First, positing a “glitch that biases processing to the point of there being a mental dysfunction” does not address the problem of from where our standards of rationality are derived; it merely shifts the problem from standards of reasonable beliefs to standards of unbiased processing.

Second, and most importantly, Wakefield’s position either begs the question or is internally inconsistent. Recall that Wakefield’s argument begins with assumption that type identity holds between the mental and the physical: “…even if every mental feature is type identical to some physical feature, …a mental dysfunction type might be type identical to a physical type that is not a physical dysfunction.” He then proceeds to defend this claim with the examples of fear conditioning and anxiety disorder, arguing that they essentially involve unreasonable types of beliefs. If this is the case, then the types of unreasonable beliefs must be identical to types of brain states; otherwise one is not taking seriously the notion of type identity. One cannot claim that mental state types have the property of “being unreasonable” that brain state types do not have without giving up on the claim of type identity. In asserting that, “a mental dysfunction type might be type identical to a physical type that is not a physical dysfunction,” Wakefield simply seems to contradict his own position by denying type identity. Thus, Wakefield faces a dilemma: he can either uphold his commitment to type identity by giving up his insistence that the rational connections between mental states cannot be explained in physical terms, or he can uphold the irreducibility of rationality by giving up his commitment to type identity. Given that Wakefield finds it “hard to imagine that there is any way to assess reasonableness for a given individual without referring to mental states and the individual’s meaning system (129),” it seems that he would choose the latter

120 option and forego his commitment to type identity. However, if this is his position, then he owes a stronger argument for thinking that the rational connections between mental states cannot be explained by the causal connections in the brain. Wakefield’s inability to imagine how this could be possible is not evidence against its possibility or in favor of the view that psychology can provide such an account.

At this point I am not taking a stand on the irreducibility of rationality other than to point out that Graham and Wakefield have not provided sufficient arguments to warrant the conclusion. However, at the very least, the arguments of Wakefield and

Graham highlight the importance of accounting for the rational connections among mental states as a desideratum for any theory of psychiatric disorder. If normative features are constitutive of psychiatric diagnoses or play a central role in any theory of psychiatric disorder, then reductionists and anti-reductionists alike will need to provide an account of from where these norms are derived. If psychiatry is to be reduced to cognitive neuroscience, then reductionists will need to explain how the concepts of cognitive neuroscience can be used to derive these norms. Perhaps reductionists can provide such an explanation, but, as of now, no such explanation is forthcoming. Anti- reductionists, on the other hand, will need to provide an account of why psychology, and only psychology, is capable of explaining the rational norms involved in the attribution of psychiatric disorder. Graham and Wakefield both appeal to the computer analogy to motivate this view. However, the success of this analogy hinges largely upon whether mental states are individuated in the same way as software, i.e., in terms of their abstract causal roles. If not, then anti-reductionists will need further arguments to establish the irreducibility of rationality and the autonomy of higher-level psychiatric sciences. If so,

121 then the analogy provides at least some support for the irreducibility of rationality and the autonomy of higher-level psychiatric sciences. The final version of reductionism, causal reductionism, challenges the computer analogy and the irreducibility of rationality on the grounds that abstract, higher-level properties such as mental states or software cannot be causally efficacious.

(5) Causal reductionism: Karlsson & Kamppinen (1995) explicitly discusses causal reductionism within the context of psychiatry while Woodward (2008), Murphy

(2006), Kendler (2005, 2008) and Gold (2009) implicitly discuss the view. Causal reductionism is similar to epistemological (inter-theoretic) reductionism in that it contends that a higher-level theory of psychiatric disorders, e.g., one couched in sociological or psychological terms, could be explainable in terms of some lower-level theory, e.g., one that only makes references to neurobiological or genetic concepts.

However, the view differs from epistemological reductionism in two important respects.

First, the view explicitly treats explanation as a matter of citing the causes for why an event or property occurs. This may be implied by the versions of epistemological reductionism discussed above, but it is not specifically stated by any of the authors.

Second, and most importantly, the view explicitly treats genuine causal relations as only occurring at the lowest level of a system and maintains that explaining the interactions at this lowest level is sufficient to explain the behavior of the system as a whole. For instance, Karlsson & Kamppinen characterize the view as entailing that causation only works “in a “bottom-up” direction, from neurobiological events to psychological phenomena (434).” Kenneth Kendler (2008) illustrates the position, which he refers to as

“hard reductionism,” with the example of a home heating system: “The hard reductionist

122 identifies the thermostat and furnace as the fundamental features of the system – those that drive the basic processes. He takes them apart and explains their key working parts through well-understood engineering principles. That, he argues, ‘is all there is to it

(696)26.’” Ian Gold (2009) makes a similar point, but adds an additional component: “A belief in reduction in psychiatry is the view (roughly) that neuroscience—primarily cellular neurobiology—and molecular biology will, on their own, eventually provide an exhaustive explanation of mental illness and form the basis for treating it successfully

(506; my italics added).” Here, reductionism is not only committed to certain claims about the fundamental status of lower-level neurobiological causes of psychiatric disorders, but also to certain claims about the most causally efficacious way to treat them, namely, via cellular and molecular interventions27.

Murphy (2006) and Woodward (2008) focus specifically on the causal reductionist’s commitment to the existence of fundamental causal explanations.

Murphy explicates the notion of a fundamental explanation in terms of the epistemic virtues of robustness and multidimensionality. A robust explanation of a psychiatric disorder is “one that continues to apply when one moves from an idealization to the real world, and is thus largely unaffected by variation in context (109).” In other words,

26 Kendler’s hard reductionism, as well as several of the other versions of causal reductionism, also incorporate aspects of ontological and eliminative reductionism in that they suggest that the entities referred to in any higher-level theories do not really exist and that only lower-level entities are real. 27 Gold argues that it is “…a near universal belief among psychiatrists that the future of psychiatric theory and treatment lies in a reductionist research program (506).” Gold does not cite any evidence for this latter claim and, apart from an opening quotation of Guze’s often-cited claim that “There is no such thing as a psychiatry that is too biological (1989),” Gold doesn’t cite any explicit defender of this version of reductionism. Whether a causal reductionist must be committed to Gold’s claim that cellular neurobiology will “form the basis” of successful treatment for psychiatric disorder is not entirely clear. If by “form the basis” of successful treatment Gold means that only cellular and molecular interventions in psychiatry are admissible, then this claim seems overly restrictive. However, if one interprets Gold’s claim to mean that successful treatments in psychiatry, whether they be cognitive, environmental, or molecular interventions, ultimately exert their causal influence by bringing about changes in cellular and molecular mechanisms, then this claim may be more acceptable. However, all of the above authors take issue with this latter interpretation as well.

123 robust explanations account for the presence or absence of a psychiatric disorder across a variety of individual and environmental contexts28. A multidimensional explanation of a psychiatric disorder is one that “explains many (at the limit, all) of the symptoms of a disorder (110)29.” According to Murphy, explanations of this sort will cite the distal, i.e., environmental, causes of the symptoms as well as the proximal, neurobiological causes that mediate the effects of the distal causes.

On Murphy’s account, a fundamental explanation of a psychiatric disorder will be one that maximally realizes robustness and multidimensionality. Murphy cites the explanation of Huntington’s disease as an example of such an explanation. Huntington's disease is explained in terms of the presence of the huntingtin gene. The presence of the gene explains the multidimensional nature of Huntington’s disease not because the explanation involves genes, but because the presence of the gene is sufficient to explain the symptoms associated with each occurrence of the disease. Furthermore, it is robust in that the presence of the gene explains the symptoms of Huntington’s disease irrespective of individual and environmental variation.

Murphy contends that fundamental explanations of this sort are unlikely to be found in psychiatry. To see this, compare the case of Huntington’s disease with Major

Depressive Disorder. Whether someone develops Major Depressive Disorder is determined by a multitude of factors that span a variety of levels, such as the individual’s genetic predisposition for the disorder as well as environmental triggers, e.g., traumatic life events. According to Murphy, this heterogeneity of causal factors makes it unlikely

28 Murphy’s notion of robustness is analogous to what many philosophers of science refer to as accuracy or empirical adequacy. 29 Murphy’s notion of multidimensionality is analogous to what many philosophers of science refer to explanatory power.

124 that one will be able to provide a fundamental explanation for Major Depressive Disorder because it entails that robustness and multidimensionality cannot be maximally realized at a single level of explanation. For instance, there is no gene or set of genes, no individual psychological attributes, or distinct social factors that have been discovered that can account for all, or even most, of the symptoms of Major Depressive Disorder across individual and environmental contexts.

Murphy thinks that most psychiatric disorders will turn out to be more like Major

Depressive Disorder than Huntington's in that they will involve a variety of causal processes interacting at multiple levels of organization. However, this is not to suggest that one will be unable to provide robust and multidimensional explanations of Major

Depressive Disorder. Although Murphy acknowledges that lower-level explanations will typically be more robust and multidimensional, he argues that robust, multidimensional explanations in psychiatry will typically span levels of organization and involve multiple levels of explanation: “…psychiatric explanations will range over multiple causal processes, and each of these may cross levels, rather than track phenomena at only one level (141).” Thus, Murphy is clearly denying the causal reductionist’s claim that genuine causal relations only occur at the lowest level of a system and that explaining the interactions at this lowest level is sufficient to explain the behavior of the system as a whole. The causal processes at the cellular and molecular level will be necessary but insufficient components of a robust and multidimensional explanation.

Murphy’s claim that psychiatric explanations will range over multiple causal processes has been a common assertion of anti-reductionists in psychiatry ever since

ngel’s (1977) introduction of the biopsychosocial model. However, to fully rebut the

125 causal reductionist’s commitment to causal fundamentalism, anti-reductionists owe an account of exactly how the causal processes at multiple levels can interact so as to generate the symptomatology of psychiatric disorders. Kim’s (1989) causal exclusion argument provides a challenge for meeting this demand. The problem of causal exclusion arises for any anti-reductionist model in psychiatry that accepts physicalism and that takes higher-level psychological and sociological variables to be irreducible, causally efficacious properties. To see the force of the argument, consider the case of a psychological explanation for depression: the psychological property of negative self- evaluation (M1) causes the psychological property of distressed mood (M2). If one accepts some form of physicalism, then each psychological property will be realized by a distinct neurobiological property, e.g., negative self-evaluation (M1) will be realized by neurobiological property (P1) and distressed mood (M2) will be realized by neurobiological property (P2). If this is the case, so the argument goes, then the only way for negative self-evaluation (M1) to cause distressed mood (M2) is for it to cause its realizer, neurobiological property (P2). However, since negative self-evaluation (M1) only has causal powers in virtue of its physical realizer, neurobiological property (P1), then, as a matter of law, neurobiological property (P1) must be sufficient to bring about the physical realizer of distressed mood (M2), neurobiological property (P2), as well.

However, if neurobiological property (P1) is sufficient to bring about both negative self- evaluation (M1) and neurobiological property (P2), then it seems that negative self- evaluation (M1) is epiphenomenal with respect to distressed mood (M2) and should just be eliminated altogether. If Kim’s argument is sound, then it would imply that higher-

126 level psychological and sociological causes of psychiatric disorders should be eliminated in favor of lower-level causal processes.

Woodward (2008), however, resists this conclusion and the commitment to fundamental causal explanations that it entails. Woodward explicates this commitment as follows: “we somehow know a priori, as a matter of principle, that variables like H

[where H is a higher-level property] are always causally epiphenomenal, with all of the

‘real causal action’ going on at some lower, more fundamental level that needs to be specified in a much more fine grained way (146).” Woodward attempts to argue against this view by showing how his interventionist account of causation and causal explanation can countenance the causal efficacy of higher-level properties while avoiding the problem of causal exclusion. The interventionist account rests upon the basic premise that two variables are causally related when one variable makes a difference to the other variable. More specifically, two variables are causally related when an intervention that changes the value of one variable changes the value of the other variable in some regular, stable way in a range of background conditions. Consider again the psychological explanation for depression from above. On the interventionist account, one can claim that negative self-evaluation (M1) causes distressed mood (M2) to the extent that one can intervene to change an individual’s self-evaluation from positive (or some other value) to negative in such a way so as to reliably change the individual’s mood from content (or some other value) to distressed. So long as the relationship between the two variables remains invariant in a range of background conditions, then the interventionist account provides a way for anti-reductionists to salvage higher-level causes. Moreover, a proclaimed benefit of Woodward’s account is that it enables one to accommodate inter-

127 level causal relations as well. For instance, one can claim that negative self-evaluation

(M1) causes the physical realizer of distressed mood (M2), neurobiological property (P2), so long as one can intervene to change an individual’s self-evaluation from positive (or some other value) to negative in such a way so as to reliably change the value of neurobiological property (P2). If Woodward’s account is sound, then it provides a possible response to the problem of causal exclusion as well as general framework for thinking about inter-level causal processes in psychiatry.

The success of the interventionist account hinges upon two distinct features. First, the variables that figure into the invariant generalization must be well-defined variables.

Woodward (2008) characterizes such a variable as follows: “it must be the sort of thing that it makes sense to think of as a target for an intervention and there must be a well- defined, unambiguous answer to the question of what will happen to other variables of interest under this intervention (142).” For instance, for negative self-evaluation to count as a well-defined variable it must be clear what would constitute an intervention on negative self-evaluation and the results of such interventions must be relatively invariant.

The failure to satisfy either of these conditions provides reason for thinking that negative self-evaluation is not actually the variable upon which one is intervening and/or that one needs to split the variable into more fine-grained variables. Second, the invariant generalization relating the two variables must exhibit what Woodward refers to as a contrastive focus. He articulates this notion as follows: “it is the contrast between X’s taking some value x and taking some different value x’ that causes the contrast between

Y’s taking value y and taking some different value y’ (143).” This feature highlights the significance of discovering causal thresholds and the possibility of systems to

128 differentially respond to a particular range of inputs but not others, both of which are important for disentangling the complex causal processes involved in most psychiatric disorders. For instance, to determine the causal relevance of negative self-evaluation to distressed mood, it will be necessary to establish a certain threshold of self-evaluation that, if exceeded, will bring about a change in mood. It will also be necessary to establish the range of negative self-evaluation to which a particular individual (or class of individuals) will respond. Failure to establish these features can lead to misleading causal claims and skepticism about the causal relevance of the variable in question.

However, to the extent that one can intervene into a well-defined variable so as to reliably bring about a threshold effect or range of effects with respect to another well-defined variable, it makes no difference if the variables are more coarse-grained, higher-level variables. In this respect, the interventionist account provides anti-reductionists with a way to countenance the autonomy of higher-level psychiatric sciences while avoiding the problem of causal exclusion and the causal reductionist’s commitment to causal fundamentalism.

Although the interventionist account removes any a priori obstacles to establishing the autonomy of higher-level sciences, whether there are any higher-level generalizations and generalizations relating higher-level and lower-level variables that exhibit the degree of stability required for genuine causal explanations in psychiatry is still an open empirical question. Karlsson & Kamppinen (1995) cite several examples that suggest such explanations do in fact exist. They cite the work of Spiegel et al (1989) and Fawzy et al (1993) as examples of psychosocial interventions that have increased survival rates in patients with metastatic breast cancer and malignant melanoma

129 respectively. They also cite the work of Mohl (1987), who suggests that psychotherapy should be considered a type of biological intervention given its established effect on underlying biological mechanisms. More recently, Dichter et al (2009) have argued that psychotherapy can lead to improved functioning of neural structures involved in reward anticipation, such as the dorsal striatum, in patients diagnosed with Major Depressive

Disorder. Similar studies on the biological effects of psychotherapy have been conducted for other disorders as well, such as PTSD (Lindauer, 2005), schizophrenia (Dickerson,

2000), and bipolar disorder (Miklowitz, 2008). Karlsson & Kamppinen take studies such as these as reason to conclude “that the search for explanation needs to reach out to other levels besides the biological: the psychological and the social (435).”

It is not clear, however, what it means to “reach out” to the psychological and social levels. Causal reductionists will not deny a need to “reach out” to higher-level sciences such as psychology and sociology in the search for causal explanations in psychiatry; they simply contend that these explanations will ultimately be found only at lower-levels of organization and that higher-level sciences will be nothing more than useful aids in the search for discovering such explanations. “Reaching out” in this non- causal sense is certainly compatible with the main tenets of causal reductionism.

Moreover, it is not clear that the results from the studies cited in the previous paragraph exhibit the degree of stability that Woodward has in mind for genuine causal explanations.

Although the studies are suggestive of potentially stable relationships involving higher- level variables, they do not establish a clear threshold effect for the causal efficacy of psychotherapy and would require much more evidence to do so.

These concerns may seem to support the causal reductionist’s position and provide

130 reason for thinking that generalizations involving higher-level variables, despite being possible, are unlikely to be borne out by the empirical data. However, recent research in social neuroscience and environmental epigenetics, disciplines that prototypically rely on reductionist strategies, suggests otherwise. Two particularly relevant examples are the models of cocaine addiction and anxiety disorder used by Michael Nader’s lab (Nader,

2005; Morgan et al, 2002; Czoty et al, 2004) and Michael Meaney’s lab (Weaver et al,

2002 & 2004) respectively. ach of these models attempts to track the affects of environmental variables on underlying neurobiological and epigenetic mechanisms. I will discuss each of these models in turn and explain why they pose a challenge to the causal reductionist’s commitment to causal fundamentalism.

The research by Michael Nader’s lab investigates the affects of social rank in macaque troop dominance hierarchies on the number and availability of dopamine D2 receptors in the brain, and subsequently individual monkeys’ susceptibility to self- administer cocaine. Previous rodent studies had shown that disruptions to dopaminergic systems alter responses to reward and the reinforcing effects of cocaine. Nader’s lab extends this research to nonhuman primates, measuring the impact of individual versus social housing on number and availability of dopamine D2 receptors and cocaine self- administration. In the Morgan et al. (2002) study, twenty macaque monkeys were individually housed for 1.5 years. PT scans were administered to determine the relative distribution of D2 dopamine receptors, a class that has been implicated in cocaine reinforcement and addiction. All individually housed monkeys, regardless of their future role in dominance hierarchies following social housing, had statistically similar D2 receptor distribution volume ratios in the basal ganglia. However, once the transition

131 from individual to social housing occurred and a stable dominance hierarchy had established, there was a statistically significant increase in D2 receptor distribution ratios in the monkeys that achieved dominant status (mean percent change of 22.0 ± 8.8%), with no increase (compared to their individual housing ratios) in monkeys that obtained subordinate positions. This increase produces a decreased amount of synaptic dopamine

(since more receptors are available for ligand binding). Higher levels of synaptic dopamine, referred to as “dopaminergic hyperactivity,” have been associated with an increased vulnerability to drug abuse. Not surprisingly, the socially housed dominant monkeys of Nader’s lab self-administered cocaine less frequently than the subordinate monkeys, both in terms of the number of intravenous injections self-administered per session and the total amount of cocaine injected (mgs per kg body weight per session).

At optimal doses, total intake per session by subordinate monkeys more than doubled that of dominants.

While monkeys’ social rank had a significant influence on D2 receptor distribution and cocaine reinforcement during initial exposure to the drug, follow up studies with the same monkeys have shown that continued, long-term cocaine exposure can attenuate this influence. Czoty et al. (2004) found no significant differences in D2 receptor distribution volume ratios in basal ganglia or cocaine self-administration in all socially housed monkeys who had self-administered cocaine several times a week for 2-5 years.

Continued exposure to cocaine led to increased self-administration by dominant monkeys, suggesting that the drug eventually served as a reinforcer in all monkeys regardless of social rank. The authors hypothesize that this attenuated effect of social rank indicates a progression of cocaine use “phases.” The Morgan et al. (2002) study represents the

132 effects of initial exposure, referred to as the “acquisition” phase. The Czoty et al. (2004) study, on the other hand, tracks the impact of continuous exposure, referred to as the

“maintenance” phase. Nader and his colleagues contend that one should not expect that environmental variables influencing cocaine’s initial reinforcing effects (acquisition), namely, social rank, are the same ones influencing the drug’s later reinforcing strength

(maintenance).

Although further research is required to determine the neurobiological states associated with the progression of drug abuse, the authors suggest that one implication of their results is clear. Since the changes in D2 receptor number and distribution in basal ganglia and susceptibility to self-administer cocaine initially could not be predicted prior to the emergence of a monkey’s status in a dominance hierarchy, vulnerability to drug abuse is more a consequence of social/environmental factors than of genetic predisposition. Regardless of the relative causal significance of environmental and biological factors, the research clearly establishes the causal relevance of environmental variables. The authors make this explicit: “An organism’s environment can produce profound biological changes that have important behavioral associations (Morgan, 2002; p. 169).” Although neurobiology is necessary to understand changes in D2 receptor distributions, these results seemingly cannot be interpreted correctly without acknowledging the causal relevance of the social influences, particularly the monkeys’ positions within dominance hierarchies.

The causal reductionist is likely to resist this interpretation and maintain that the relationship between social rank and D2 receptor number and distribution is not a genuine causal relationship. To be a genuine causal relationship, the causal reductionist would

133 demand a specification of the neuronal mechanisms whereby social rank exerts its influence on behavior, and this would mean that it must ultimately connect with the molecular mechanisms driving gene expression and protein synthesis in particular neurons. More generally, according to the causal reductionist, before one can refer to the environment, or any property postulated by higher-level psychiatric sciences as a cause of measured neurobiological or behavioral effects, one must be able to explain how they are transduced down to neuronal and molecular mechanisms. For it is only the latter that drive neurotransmitter release into neuromuscular junctions to elicit muscle contractions

(i.e., behavior), and gene expression and protein synthesis that changes receptor distribution.

This line of reasoning, however, is exactly what Woodward’s interventionist account is intended to undermine. ven if there were relevant causal details regarding gene expression and protein synthesis, these details would only add to an already existing causal explanation rather than replace it. The relationship that holds between social rank and D2 receptor number and distribution would still hold even with the addition of further causal details. On the interventionist account, so long as social rank is a well-defined variable and that interventions that change the value of social rank bring about changes in

D2 receptor number and distribution in a regular, stable way, then the generalization relating social rank and D2 receptor number and distribution should be treated as a genuine causal explanation.

If the generalization relating social rank and D2 receptor number and distribution admits of numerous exceptions, then it would likely be too unstable to constitute a genuine causal explanation and the causal reductionist would have good reason to

134 recommend looking to lower levels to find a more stable generalization. ven if such a generalization was relatively stable, the causal reductionist may try to appeal to Kim’s causal exclusion argument and contend that its stability is better explained by the stability of the underlying molecular mechanisms driving gene expression and protein synthesis.

Such a response, if successful, would indeed support the causal reductionist’s position.

However, consider what the causal reductionist would have to do to actually make good on this claim. The causal reductionist would have to establish type identities between social rank and the relevant molecular mechanisms that drive gene expression and protein synthesis. These identities would have to be such that one could determine a monkey’s position in a dominance hierarchy simply by examining the relevant molecular mechanisms as well as be able to intervene in these mechanisms so as to change D2 receptor number and distribution in a reliable, stable way. In short, for all hypothesized environmental causes of behavior, the causal reductionist would require an explanation of how they are transduced down to neuronal and molecular mechanisms before attributing to them any causal status. Perhaps satisfying this requirement is both possible and desirable, but it would seem to be overly demanding and, in many cases, empirically intractable. As stated above, so long as there is a relatively stable generalization relating social rank to D2 receptor number and distribution, then such a generalization would still hold even with the addition of further causal details about gene expression and protein synthesis. Moreover, even in the particular study cited above, the relevant molecular mechanisms for gene expression and protein synthesis underlying position in a dominance hierarchy are likely to be multiply realizable in that they are likely to vary between different monkeys holding the same relative position in different dominance

135 hierarchies as well as within the same monkey holding the same relative position at different times in the same dominance hierarchy. Although abstracting away from the molecular mechanisms for gene expression and protein synthesis underlying social rank and focusing exclusively on the latter may compromise explanatory power, it will also provide a greater degree of generality. To the extent that Nader’s research ultimately aims at clinical applicability, this increase in generality may actually provide greater therapeutic utility by suggesting variables that are more tractable and amenable to manipulation. In this sense, nonepistemic considerations can place constraints on decisions involving trade-offs between explanatory power and generality. Whether increased generality leads to enhanced therapeutic utility, of course, is an open empirical question that will require further evidence to substantiate. If molecular mechanisms are discovered that enable researchers to more systematically identify a monkey’s position in a dominance hierarchy and to more reliably intervene so as to change D2 receptor number and distribution and susceptibility to self-administer cocaine, then, at least in this case, the causal reductionist position would be vindicated. However, the burden of proof lies with the causal reductionist. Until he/she can provide sufficient evidence to show that a lower-level generalization is more stable and offers greater therapeutic applicability than one involving higher-level variables, then the generalization involving higher-level variables, to the extent that it is relatively stable, should be treated as a genuine causal explanation.

Research from Michael Meaney’s (2002, 2004) lab on the epigenetic affects of maternal behavior provides a further illustration of these points. Their model begins with observations about the affects of variations in maternal behavior on the behavior of their

136 offspring. They found that rat mothers who frequently licked and groomed (LG) their offspring and used an arched-back style of nursing (ABN) had offspring who were less fearful and showed a more modest stress response compared to the offspring of mothers who did not frequently lick and groom their offspring and did not use an arched-back style of nursing. This response was measured by corticosterone levels and the amount of time the offspring spent immobile during a forced swim task. Furthermore, cross- fostering studies showed that these behavioral effects were reversible. When the offspring from low LG-ABN mothers were reared by high LG-ABN mothers, they became less fearful and showed a more modest stress response. Similar results were found for the offspring that were initially raised by high LG-ABN mothers. These findings suggest that variations in maternal behavior serve as a mechanism for the non- genomic transmission of individual differences in stress reactivity across generations.

The goal of Meaney’s research, however, was to determine the mechanisms whereby these maternal effects exert their influence so as to bring about these behavioral changes over the lifespan. By looking at hippocampal tissue assays, they found that the offspring that were reared by low LG-ABN mothers had significantly higher levels of methylation of the glucocorticoid receptor gene in the hippocampus compared to offspring reared by high LG-ABN mothers. Moreover, they found significantly higher levels of methylation of the glucocorticoid receptor gene in the hippocampus of both the offspring that were born to and reared by low-LG-ABN mothers as well as those that were born to high-LG-ABN mothers but reared by low-LG-ABN mothers compared to the offspring that were born to and reared by high-LG-ABN mothers and those that were born to low-LG-ABN but reared by high-LG-ABN mothers.

137 Leaving aside many of the mechanistic details, the idea is that the increased methylation of the glucocorticoid receptor gene blocks transcription factors from gaining access to the gene, causing a decreased expression of hippocampal glucocorticoid receptors and resulting in decreased glucocorticoid negative feedback sensitivity.

Normally, this negative feedback causes the synthesis of the stress hormone corticotropin-releasing hormone to be inhibited. Thus, in the absence of such feedback, there are higher levels of hypothalamic corticotropin-releasing factor (CRF), leading to less modest responses to stress. Meaney acknowledges that further research needs to be done to fully determine how maternal behavior causally interacts with the exon region of the glucocorticoid receptor gene, but he argues that their results provide compelling preliminary evidence of what he refers to as “environmental programming” of adaptive stress responses across generations (2004, p. 852).

Meaney’s research differs from Nader’s research on the effects of social rank and

D2 receptor number and distribution in that it provides more of the mechanistic details whereby the hypothesized environmental cause, in this case maternal behavior, exerts its influence on behavior. Thus, if the causal reductionist were to resist interpreting the higher-level generalization relating maternal behavior to increased methylation of the glucocorticoid receptor gene as genuinely causal, he/she would likely have to do so for reasons other than the demand for more mechanistic details. As with Nader’s research, even if there were further relevant causal details regarding gene expression and protein synthesis, these details would only add to an already existing causal explanation rather than replace it. The relationship that holds between maternal behavior and increased methylation of the glucocorticoid receptor gene would still hold even with the addition of

138 these further causal details. Again, on the interventionist account, so long as maternal behavior is a well-defined variable and that interventions that change the value of maternal behavior bring about changes in methylation of the glucocorticoid receptor gene in a regular, stable way, then the generalization relating maternal behavior and methylation of the glucocorticoid receptor gene should be treated as a genuine causal explanation.

Similar problems as discussed above with Nader’s research would also arise if the causal reductionist were to appeal to Kim’s causal exclusion argument and contend that the generalization relating maternal behavior and methylation of the glucocorticoid receptor gene will eventually be replaced by a more stabile generalization that referred exclusively to lower-level variables. Such a response, if successful, would indeed support the causal reductionist’s position. But again, consider what the causal reductionist would have to do to actually make good on this claim. The causal reductionist would have to establish type identities between maternal behavior and the relevant molecular mechanisms that drive gene expression and protein synthesis. These identities would have to be such that one could determine the type of maternal behavior, e.g., high-LG-ABN vs. low-LG-ABN, simply by examining the relevant molecular mechanisms as well as be able to intervene in these mechanisms so as to change the methylation patterns of the glucocorticoid receptor gene in a reliable, stable way. This may indeed by possible, but there are good reasons to skeptical of its empirical tractability. The relevant molecular mechanisms for gene expression and protein synthesis underlying the effects of maternal behavior are likely to be multiply realizable in that they are likely to vary between different offspring, e.g., between different

139 offspring raised by the same high-LG-ABN mother as well as those born to low-LG-

ABN mothers but reared by high-LG-ABN mothers, as well as within the same offspring at different times. Thus, although abstracting away from the molecular mechanisms for gene expression and protein synthesis underlying maternal behavior and focusing exclusively on the latter may compromise explanatory power, it will also likely provide a greater degree of generality. To the extent that Meaney’s research ultimately aims at clinical applicability, this increase in generality may actually provide greater therapeutic utility by suggesting variables that are more tractable and amenable to manipulation. As with the Nader research, this is an open empirical question that will require further evidence to substantiate. If molecular mechanisms are discovered that enable researchers to more systematically identify the type of maternal behavior and to more reliably intervene so as to change methylation patterns of the glucocorticoid receptor gene and the subsequent stress response of the offspring, then, at least in this case, the causal reductionist position would be vindicated. However, the burden of proof lies with the causal reductionist. Until he/she can provide sufficient evidence to show that a lower- level generalization is more stable and offers greater therapeutic applicability than one involving higher-level variables, then the generalization involving higher-level variables, to the extent that it is relatively stable, should be treated as a genuine causal explanation.

Woodward’s interventionist account of causation and the above case studies don't show that causal reductionism is necessarily false. However, they do show that there are no a priori reasons for ruling out generalizations involving higher-level variables as genuine causal explanations and that there are solid empirical reasons for thinking that such explanations exist and can be useful in psychiatry. The fate of causal reductionism

140 will ultimately be borne out by the empirical data, but given the currently available data, its fate does not look promising.

Are Proposals to Synthesize Psychiatry with Neuroscience Reductionist?

At the beginning of the chapter I considered several allegations lodged against reductionism in psychiatry, ranging from perpetuating the over-medicalization of normal

“problems of living” to the neglect or outright rejection of social and environmental causes and treatments of psychiatric disorders. Nonetheless, none of these allegations cite a specific author who defends reductionism nor do they distinguish between the types of reductionist theses that one could defend. The previous section addressed the latter concern by distinguishing and assessing five different reductionist theses. In this section,

I focus on the former concern and consider why reductionism has received so much attention despite the fact that critics fail to cite any authors who explicitly defend the view. What is all the fuss about and on what basis are the alleged harms of reductionism founded if nobody is actually defending the view? As mentioned at the beginning of the chapter, the occasional overstatement of “alleged findings” and grandiose predictions about the explanatory and therapeutic prospects of biological psychiatry partially explain the motivation for critics’ attacks on reductionism. However, I suspect that the primary motivation is due to concerns over recent proposals to synthesize psychiatry with neuroscience as a strategy for responding to constructivist and anti-psychiatry critiques.

In the remainder of the chapter I outline several such proposals and show that none of the proposals, despite appearing to implicitly advocate reductionism, actually defend any substantive metaphysical or epistemological reductionist theses. I argue that each of the proposals can, at most, be interpreted as advocating a general commitment to some form

141 of methodological reductionism and/or global ontological reductionism. I argue that these relatively uncontroversial commitments should be welcomed in psychiatry and that their presence does not justify the alleged harms that critics associate with reductionism.

The notion that psychiatry should be synthesized with cognitive neuroscience is motivated by the presumed need to respond to the anti-psychiatry challenge of demarcating genuine psychiatric disorders from “problems of living.” If psychiatry is able to identify the organic basis of psychiatric disorders, i.e., if one can treat psychiatric disorders as “brain disorders” or “brain diseases,” so the argument goes, then one can ground attributions of psychiatric disorder in facts about malfunctioning neurobiological processes. If this is correct, then psychiatry will become more aligned with clinical medicine and psychiatrists should have to look no further than neuroscience, and perhaps genetics, to find explanations for psychiatric disorder. This line of reasoning is most clearly exemplified by Insel and Quirion’s (2005) proposal to align psychiatry with clinical neuroscience. They point out: “By re-defining the foundation of psychiatry as clinical neuroscience, we also accelerate the integration of psychiatry with the rest of medicine (2213).” Insel & Quirion advocate synthesizing psychiatry with clinical neuroscience in a way that will transform the current training of psychiatrists and the tools/practices used. To facilitate this synthesis, they contend that psychiatry “will require that psychiatric disorders be understood and treated as brain disorders (2221).”

They emphasize this point further: “The recognition that psychiatric disorders are brain disorders suggests that the psychiatrist of the future will need to be a brain scientist

(2213).”

142 Insel and Quirion’s claim that psychiatry “will require that psychiatric disorders be understood and treated as brain disorders” certainly sounds like an endorsement of global ontological reductionism within psychiatry. It is difficult to make sense of why psychiatric disorders would need to be understood and treated as brain disorders without such a commitment. Moreover, their proposal represents an endorsement of methodological reductionism as well. Their claim that the “psychiatrist of the future will need to be a brain scientist” suggests that psychiatrists should at least aim to explain the symptoms and causes of psychiatric disorders in terms of entities and activities at the lowest possible level of explanation. They also envision a future in which psychiatrists will be able to utilize an individual’s unique neurobiology and genetic make-up to better diagnose the presence of a psychiatric disorder and to individualize treatment:

For a person with schizophrenia or bipolar illness, one can imagine that a future psychiatrist would use a cognitive task accompanied by functional and structural neuroimaging to diagnose and select a specific treatment, just as a contemporary cardiologist uses a nuclear stress test and echocardiogram to diagnose ischemic heart disease and select the appropriate intervention (2213).

Indeed, such research is already underway to determine individual differences in neural circuitry underlying depression (Smith et al., 2011) as well as individual differences to treatment response in depressed patients based upon the presence of particular genes

(Hall-Flavin et al, 2012). Insel and Quirion’s vision for the future of psychiatry provide good reasons for interpreting their proposal as an endorsement of methodological reductionism.

It is less clear, however, whether their proposal can be interpreted as endorsing eliminative, epistemological, or causal reductionism. Despite claiming that psychiatric disorders should be treated as brain disorders, they also clearly acknowledge that

143 psychosocial interventions should be an essential component to treatment: “…ideally the psychiatrist will increasingly be part of a team that provides culturally-valid, psychosocial rehabilitation along with medications to help those with psychiatric disorders recover and return to a productive and satisfying life (2213).” Perhaps Insel and Quirion consider this “culturally-valid, psychosocial rehabilitation” to be a form of neurobiological intervention, but given that it is a form of treatment that they claim would be used in addition medication, this does not seem to be the case. To the extent that “culturally-valid, psychosocial rehabilitation” relies on concepts not derived from lower-level sciences, as is presumably the case, and that these concepts are indispensable to treatment of psychiatric disorders, it is difficult to interpret Insel and Quirion as endorsing eliminative reductionism. This point also makes it difficult to interpret their proposal as supporting epistemological reductionism. Although they do clearly state that psychiatric disorders will be explained at the neurobiological level, particularly the level of discrete neural circuits, it is unclear how the concepts that are constitutive of

“culturally-valid, psychosocial rehabilitation” could relate to neural circuits such that one could explain the former in terms of the latter. One cannot fault Insel and Quirion for failing to provide such an account, but it is difficult to interpret their proposal as endorsing epistemological reductionism without one. The recognition of “culturally- valid, psychosocial rehabilitation” as an efficacious form of treatment also makes interpreting their proposal as an endorsement of causal reductionism problematic. To the extent that the success of psychosocial rehabilitation is due to the efficacy of psychological and/or social properties, their proposal conflicts with the causal reductionist’s claim that genuine causal relations only occur at the lowest level of a

144 system and that explaining the interactions at this lowest level is sufficient to explain the behavior of the system as a whole. This point also applies to Insel and Quirion’s claim that neurobiological explanations for psychiatric disorder may not be at the level of neurotransmitters or proteins, but rather the higher level of discrete neural circuits. If their view were in fact a version of causal reductionism, then they would presumably consider the level of neurotransmitters or proteins rather than the level of discrete neural circuits to be the most appropriate level at which to explain psychiatric disorders. In the end, Insel and Quirion’s proposal can at best be interpreted as endorsing global ontological reductionism and methodological reductionism.

Martin (2002) proposes a vision of psychiatry that is similar to that of Insel and

Quirion. His account is grounded in the historical origins of psychiatry and neurology and what he contends is the arbitrary divide between them. He illustrates this arbitrariness with a sketch of the historical development of Alzheimer’s disease, which was addressed primarily by neurology, and Tourette’s Syndrome, which became the province of psychiatry. Martin argues that these two disorders “illustrate the contradictions and difficulties of attempting to label diseases as organic versus functional or as pathologically or genetically based versus sporadic or experience-based phenomena

(700).” He continues: “The separation of the two categories is arbitrary, often influenced by beliefs rather than proven scientific observations. And the fact that the brain and mind are one makes the separation artificial anyway (700).” Martin argues that disorders such as Alzheimer’s that could more easily be labeled as organic due to the identification of specific malfunctioning biological mechanisms became the proper domain of neurology.

Disorders for which the identification of malfunctioning biological mechanisms were

145 more elusive, such as Tourette’s, schizophrenia, and bipolar disorder, became the proper domain of psychiatry. However, Martin argues that this elusiveness obscures that fact that such disorders “are also brain diseases, with accompanying changes in brain structure and function (700).”

In the same manner as Insel and Quirion, Martin seems to be endorsing global ontological reductionism. It is difficult to make sense of the claim that psychiatric disorders such as Tourette’s, schizophrenia, and bipolar disorder are brain diseases without such an endorsement. However, his view suffers from a similar ambiguous appeal to brain diseases as does Insel and Quirion’s view. For instance, Martin does not think that characterizing psychiatric disorders as brain diseases requires eschewing psychosocial interventions altogether. He asserts: “…we also recognize that the best therapeutic responses seem to come from combining treatment modalities—both administering medication and talking to the patient (701).” Martin does not state whether he thinks that talking to patients is only effective to the extent that it modifies neurobiological mechanisms or that such therapies should be considered to be a form of neurobiological intervention. Moreover, his proposed synthesis of psychiatry and neurology does not entail the exclusion of higher-level sciences, e.g., psychology and sociology, especially in the context of formulating research agendas and training future neuropsychiatrists. His proposal, in fact, calls for greater collaboration and integration between disciplines. Despite this call as well as his acknowledgement that not all explanations or treatments in psychiatry may be found at the lowest possible level of explanation, Martin clearly thinks that neurobiological levels of explanation will figure prominently in psychiatry and that psychiatrists should at least aim to explain the

146 symptoms and causes of psychiatric disorders in terms of entities and activities at the lowest possible level of explanations. Thus, like Insel and Quirion, his proposal to characterize psychiatric disorders as brain diseases is best interpreted as an endorsement of some version of methodological reductionism and global ontological reductionism.

Yudofsky & Robert (2002), like Martin, argue for the “conceptual disintegration of separating brain-based disorders into neurological or psychiatric conditions (1261).”

They cite studies by Koponen et al. (2002) and Leroi et al. (2002) in defense of this claim.

The Koponen et al. (2002) study investigated over a 30-year span the prevalence of psychiatric disorders in 60 individuals who had suffered a traumatic brain injury. The study found that 48.3% of the individuals had developed an axis I disorder following the brain injury, including major depression (26.7%), alcohol abuse or dependence (11.7%), panic disorder (8.3%), specific phobia (8.3%), and psychotic disorder (6.7%). Moreover,

23.3% of the individuals developed at least one axis II personality disorder following the brain injury, the most common of which were avoidant (15.0%), paranoid (8.3%), and schizoid (6.7%). The Leroi et al (2002) study compared the incidence of cognitive, personality, and mood disorders in individuals with degenerative cerebellar disorders and

Huntington’s Disease to normal controls. They found that 77% of individuals with degenerative cerebellar disorders and 81% of individuals with Huntington’s Disease developed psychiatric disorders compared to only 41% of the normal controls.

Despite their clear appeal to reductionist research strategies to argue against separating psychiatric from neurological conditions and in defense of what they refer to as neuropsychiatry, Yudofsky & Robert do not take this as evidence in favor of reductionism. Rather, they conceive of neuropsychiatry as the “indelible inseparability of

147 brain and thought, of mind and body, and of mental and physical (1262-3)” and as “an integrative and collaborative field that eschews specialty-derived, reductionistic categorizations that recognize and address only circumscribed features of a specific brain-based illness (1263).” Moreover, like Insel & Quirion and Martin, they argue that neuropsychiatrists ought to “recognize, utilize, and prioritize psychosocial factors— including experiential, psychodynamic, interpersonal, societal, and spiritual—in the understanding and care of all patients (1263).” Given their explicit disavowal of reductionism, it may seem obvious that Yudofsky & Robert are not defending any of the reductionist theses discussed above. While this is clearly the case more so than it was for

Insel & Quirion and Martin, given their clear appeal to reductionist research strategies to argue against separating psychiatric from neurological conditions and in defense of what they refer to as neuropsychiatry, Yudofsky & Robert are best interpreted as being committed to some version of methodological reductionism.

Sachdev’s (2005) proposed synthesis focuses on the prospects of uniting psychiatry and neurology into the single discipline of neuropsychiatry. Although

Sachdev is clearly in support of attempting such a unification, he remains skeptical about whether neuroscience is up to the task: “…neuroscientific progress is unlikely to unite the two disciplines into one super discipline of neuropsychiatry (140).” Sachdev argues that psychiatry and neurology are distinct disciplines that require separate and unique areas of expertise:

The strengths of psychiatry lie in the rich description of mental phenomena, well-developed interviewing skills, understanding of multiple causation of behavioral disturbance, appreciation of individual variation, ability to deal with ambiguity, interpersonal context, and the combination of biological with psychological and behavioral therapies. qually,

148 neurology prides itself in its rigorous clinical examination skills, its empiricism, and its objectivity (140).

Rather than neuropsychiatry representing a complete synthesis of psychiatry and neurology, Sachdev envisions a partial overlap of the two disciplines, which would be the proper domain of neuropsychiatry, with each discipline remaining otherwise relatively autonomous.

It is not entirely clear, however, on what basis the proper “territory,” to use

Sachdev’s terminology, of each discipline is grounded. Sachdev explicitly states that the territory of each discipline is not determined on the presence of a biological basis for a disorder. Unlike Martin who argued that disorders such as schizophrenia and bipolar disorder are brain diseases despite the fact that their biological bases have not yet been discovered, Sachdev suggests that such a discovery would still not establish them as brain diseases: “the mere fact of a ‘biological’ etiology does not place a disorder outside the domain of psychiatry [and into neuropsychiatry] (142).” ven if a biological basis for disorders such as schizophrenia and bipolar disorder were found, Sachdev asserts:

“psychiatric skills would still be necessary to manage the patients in the context of their family and social environment (141).” Moreover, psychiatry is not distinguished from neuropsychiatry according to the types of therapies used. Although Sachdev argues that neuropsychiatrists will make use of treatments such as pharmacotherapy, transcranial magnetic stimulation, vagus nerve stimulation, deep-brain stimulation, gene therapy, stem cell therapy, and brain implants, he doesn’t think that neuropsychiatrists will use only these therapies. He explicitly claims that both psychiatry and neuropsychiatry will need to make use of what he refers to as “cognitive rehabilitation and nonbiological treatment modalities (142).” Sachdev’s proposal seems to amount to the idea that the

149 proper territory of neuropsychiatry will be determined by the specialized training that neuropsychiatric professionals will be expected to undergo and the research agenda that they subsequently develop. He foresees neuropsychiatric professions as acquiring expertise in both neurology and psychiatry and as making use of diagnostic tools such as

MRI, fMRI, PT, diffusion-weighted imaging, magnetic resonance spectroscopy, single- cell recording, and numerous neurophysiological techniques. Moreover, Sachdev envisions neuropsychiatry as spanning multiple disciplines and including multiple subspecialties and cites the need for neuropsychiatrists to establish collaborations with other disciplines such as neuropsychology, genetics, psychopharmacology, diagnostic radiology, immunology, neurophysiology, and rehabilitation. This may make the proper territory of neuropsychiatry a bit more precise, but it does little to clarify the proper territory of psychiatry or its relationship to neuropsychiatry.

Despite this lack of clarity, Sachdev’s vision of psychiatry and neuropsychiatry is clearly not reductionist in any substantive metaphysical or epistemological sense. Given his insistence that the strengths of psychiatry lie in its “understanding of multiple causation of behavioral disturbance” and “combination of biological with psychological and behavioral therapies (140),” Sachdev does not seem to be endorsing any version of causal or epistemological reductionism. A similar point holds for his characterization of neuropsychiatry as well, since he envisions the discipline as spanning multiple disciplines and including “cognitive rehabilitation and nonbiological treatment modalities (142).” It is also not entirely clear that Sachdev can be interpreted as advocating any form of ontological reductionism either. Although such an interpretation for Sachdev’s characterization of neuropsychiatry might seem plausible given his description of the

150 disciplines, research methods, and treatments involved in the field, it is less clear whether one could interpret his characterization of psychiatry in such a way. One can more straightforwardly interpret Sachdev as endorsing some version of methodological reductionism with respect to both psychiatry and neuropsychiatry. This endorsement is clear in the case of neuropsychiatry, where he explicitly states that neuropsychiatrists should make use of diagnostic tools and therapies that identify and target lower-level mechanisms. Although Sachdev’s commitment to methodological reductionism for psychiatry is less straightforward, he seems to be endorsing the view given that he thinks that psychiatry should at least aim to become unified with neurology.

Murphy (2006) advocates synthesizing psychiatry with cognitive neuroscience, creating a new discipline that he refers to as clinical cognitive neuroscience. Murphy takes his proposal to be clearly anti-reductionist in the sense discussed above in the section on causal reductionism: robust, multidimensional explanations in psychiatry will typically span levels of organization and involve multiple levels of explanation. Murphy is clearly denying the causal reductionist’s claim that genuine causal relations only occur at the lowest level of a system and that explaining the interactions at this lowest level is sufficient to explain the behavior of the system as a whole. However, Murphy does acknowledge that lower-level explanations in psychiatry, when possible, will typically be more robust and multidimensional than higher-level explanations. Moreover, he argues that neurobiological levels of organization, because they are the most proximal causes to behavior, offer “greater potential for developing controlled experiments that permit explanation and intervention (128).” For these reasons, Murphy is best interpreted as advocating a general commitment to ontological and methodological reductionism.

151 The five proposals discussed above all advocate, to differing degrees and for slightly different reasons, synthesizing psychiatry with neuroscience. However, all five proposals are, either implicitly or explicitly, anti-reductionist with regards to any substantive metaphysical and epistemological claims and offer nothing more than a general commitment to some form of methodological reductionism and/or global ontological reductionism. Of course, the lack of explicit advocacy of any substantive reductionist theses may be more a reflection of the perceived unimportance of philosophical debates regarding reductionism or simply a lack of awareness of these debates and the need to even provide a defense of one’s reductionist commitments. If this were the case, then perhaps the concern over reductionist trends in psychiatry would still be justified. While some of the proposals are certainly in need of further clarification, particularly the proposals of Insel & Quirion and Martin to characterize psychiatric disorders as brain disorders, there are good reasons to think that the proposed syntheses are not intended to be defending any substantive reductionist theses. First, all of the proposals acknowledge a role for higher-level sciences and call for greater collaboration and integration between higher and lower-level sciences. Second, all of the proposals countenance a role for psychosocial training of psychiatrists, research strategies, and treatment options. It is possible that the proposals only intend higher-level sciences to serve a heuristic function and recommend psychosocial research strategies and treatment options as options only until the lower-level sciences fill in the relevant details, but these considerations at least provide prima facie support for thinking that the proposed syntheses are not intending to offer anything more than a general commitment to some form of methodological reductionism and/or global ontological reductionism.

152 Such commitments may appear relatively uncontroversial and even warranted given some of the promising lines of research utilizing reductionist strategies and the prospect of more controlled experiments and interventions. However, some authors caution against adopting even such a mild form of reductionism and challenge the very project of synthesizing psychiatry with neuroscience. Paris (2009), for instance, expresses this worry explicitly: “defining our specialty as clinical neuroscience would destroy psychiatry in order to save it (517).” Paris is clearly concerned that psychiatry is becoming overly reductionist and cautions that attempting to reduce psychiatry to clinical neuroscience “… tends to support an almost exclusive dependence on drugs in practice

(516).” At points, Paris seems to be supportive of methodological reductionism, acknowledging the possibility that the need to use psychosocial therapies is simply the result of our limited understanding of the brain and that such therapies will become obsolete if the science advances. However, at other points, he seems to think that searching for lower-level explanations for psychiatric disorders will be futile. He states:

“a discrepancy between neuroscience and clinical phenomena is bound to persist because it is rooted in a conceptual gap between the mind and the brain…even if the mind cannot exist without neural activity, this does not mean that thought or complex behaviour can be predicted at the neuronal level (515).” Paris doesn’t articulate why this “conceptual gap” persists, but it informs his skepticism of finding lower-level explanations:

“Biological research has not identified any specific mechanisms behind psychoses or mood disorders…while neurotransmitters are well known to mediate synaptic pathways,

153 research has not identified specific relations between any of these molecules and psychiatric disorders (514).”

Paris raises even more worries for attempts to find a genetic basis for psychiatric disorders. He points out that molecular genetics has thus far failed to discover any specific pathways involved in the etiology of psychiatric disorders. This lack of evidence is due largely to the fact that genetic pathways involve multiple alleles. Thus, despite the fact that most psychiatric disorders likely have a heritability component, Paris thinks that any psychiatric disorder will involve complex, multiple interactive pathways that cannot be understood without considering psychosocial risk factors. Furthermore, Paris points out that the lack of specific phenotypes or endophenotypes for psychiatric disorders makes it unlikely that researchers will discover any associations between psychiatric disorders and specific biomarkers. The heterogeneity associated with psychiatric disorders simply makes it unlikely that one could provide an explanation for any psychiatric disorder in purely neurobiological or genetic terms. These concerns highlight

Paris’ skepticism about searching for lower-level explanations for psychiatric disorders.

Thus, while Paris may be interpreted as a methodological reductionist for the simple reason that he acknowledges the possibility that neuroscience may eventually explain psychiatric disorders, his skepticism of discovering lower-level explanations and clear opposition to reducing psychiatry to clinical neuroscience certainly makes it a tepid endorsement.

Paris’ points about the heterogeneity associated with psychiatric disorders and the necessary inclusion of psychosocial risk factors are valid concerns and may turn out to pose insurmountable obstacles to synthesizing psychiatry with clinical neuroscience and,

154 more generally, to defending any substantive metaphysical or epistemological reductionist theses in psychiatry. Whatever the prospects of these projects may be, one moral seems clear: reductionism as a methodological thesis will need to be a central component of any successful future psychiatry. Psychiatrists will need to develop research strategies that aim to explain the symptoms of psychiatric disorders in terms of lower-level causal mechanisms and to incorporate this information into a clinical context when making decisions about diagnosis and treatment. The extent of the relevance of lower-level causal mechanisms, of course, remains an open empirical question and will need to be determined for each psychiatric disorder individually. Nonetheless, as

Murphy points out, lower-level causal mechanisms are the most proximal causes to behavior and, therefore, offer “greater potential for developing controlled experiments that permit explanation and intervention (128).” Thus, even if more substantive reductionist theses such as causal or epistemological reductionism fail, the incorporation of relevant lower-level causal details will be a necessary component of any complete explanation of a psychiatric disorder. Moreover, acknowledging the importance of this milder form of reductionism in psychiatry should assuage concerns about reductionist trends in psychiatry and any potential harm associated with such trends. In the next chapter I will examine pragmatist and pluralist proposals within psychiatry and consider how they can accommodate the methodological reductionist commitments discussed above.

155 Chapter 4: Pragmatism and Pluralism in Psychiatry

Pluralism and pragmatism have become popular positions in the philosophy of psychiatry literature over the past decade (Frances, 2010 & 2013; Brendel, 2003 & 2004;

Kendler, 2005, 2011, & 2012; Graham, 2010; Murphy, 2006 & 2010; Ghaemi, 2007 &

2009, Pies, 2010 & 2011; Zachar, 2000 & 2002). veryone seems to agree that psychiatry must adopt a “pluralistic approach” and that explanations in psychiatry will inevitably involve “pragmatic considerations” despite the fact that what makes an approach “pluralistic” or a consideration “pragmatic” is often left unstated. Like political proclamations about supporting troops, one smiles and nods in agreement without knowing to what one is actually nodding in agreement. Pragmatic considerations are often conflated with personal idiosyncrasies, suggesting that one is free to form opinions at the expense of well-regarded epistemic values. Similarly, pluralism is sometimes interpreted as endorsing the view that every discipline or theoretical perspective is of equal explanatory relevance. It is not difficult to see why mixing one’s pragmatism with one’s pluralism could generate relativistic concerns: if all theoretical perspectives are of equal explanatory relevance, then pragmatic considerations could easily lead a clinician or researcher to conclude that his or her own theoretical perspective is on solid epistemological ground without the need of further empirical validation. Thus, for psychiatry to sidestep the pitfalls of relativism and to avoid becoming a conceptually muddled collection of disunified theoretical perspectives, one needs to be clear about the commitments of pragmatism and pluralism in the context of psychiatry. This chapter addresses each of these concerns respectively. I examine the commitments of adopting pragmatic and pluralist approaches in psychiatry and how such approaches might

156 function in distinct contexts within psychiatry. The chapter begins with a brief historical sketch of pragmatism and its application to psychiatry. Two common and closely related misconceptions of pragmatic thought are then considered, namely, that pragmatism prioritizes personal and political values over evidential standards and that pragmatic values are to be contrasted with scientific values. Understanding where these two misconceptions go wrong suggests an interpretation of pragmatism as requiring a balance between epistemic and nonepistemic values. The details of this interpretation are outlined and applied to three distinct contexts of psychiatry: 1) psychiatric classification,

2) psychiatric diagnosis, and 3) psychiatric research.

Pragmatism in Psychiatry

C. S. Peirce famously provided a succinct summary of pragmatism as a philosophical movement and as a methodology: “Consider what effects, which might conceivably have practical bearings, we conceive the object of our conception to have.

Then, our conception of those effects is the whole of our conception of the object (Peirce,

1905; p. 481).” The meaning of a concept consists in its practical consequences and is to be determined through empirical observation. This general characterization of pragmatism serves as the foundation for its application to psychiatry. Brendel (2003 &

2004), Zachar (2000 & 2002), and Frances (2010 & 2013) have all explicitly advocated adopting pragmatic approaches in psychiatry, although they each apply the view to different contexts in psychiatry. Brendel defends pragmatism as a general explanatory model in psychiatry, although his primary focus is on the clinical application of the view:

“psychiatrists’ most abiding commitment ought to be to clinical pragmatism and to the individualized and specific needs of the patients they are treating (570).” There are three

157 main features of Brendel’s clinical pragmatism. First, clinical pragmatism entails a commitment to what Brendel refers to as methodological pluralism, the idea that one should utilize all explanatory concepts and models when diagnosing and treating patients.

Brendel argues that psychiatry’s primary commitment is to clinical treatment and to addressing the specific needs of individual patients, not to resolving metaphysical disputes between competing explanatory models. He contends that methodological pluralism provides a compromise position between an overly exclusive reductionism and an overly inclusive eclecticism. Reductionism, in claiming that there is only one best explanation for the etiology of psychiatric disorders, limits the diagnostic and therapeutic choices available to clinicians and patients. As pointed out in the previous chapter, reductionism need not be committed to any claims regarding the diagnosis and/or treatment. Nonetheless, Brendel claims that the narrow focus of reductionism makes it more difficult to accommodate individual variation in symptomatology and treatment response. clecticism, in drawing upon all theoretical perspectives, may more easily be able to countenance individual variation. However, Brendel contends that it often lacks the scientific rigor necessary to provide sufficient guidance in a clinical context.

According to Brendel, methodological pluralism enables a clinician to maximize respect for individual variation in diagnosis and treatment while simultaneously respecting empirical evidence.

A second feature of Brendel’s clinical pragmatism is the necessity of patient involvement in the diagnostic and treatment process. This feature highlights the practical and social dimensions of knowledge acquisition that is constitutive of pragmatism. As

Brendel points out, “’truth’ is the outcome of a deliberative, social process aimed at

158 identifying what works in a given situation (571).” More specifically, he asserts,

“psychiatric explanations are ‘true’ only insofar as they promote beneficial real-world results for individuals with mental illnesses (569).” Incorporating the patient and significant others in decision-making facilitates this end by insuring that the diagnostic and treatment process will be as comprehensive as possible and maximize the patient’s well-being. Moreover, it illustrates the dynamic and evolving nature of the clinical encounter and the patient-psychiatrist relationship.

Finally, clinical pragmatism entails that psychiatric explanations are provisional in nature. According to Brendel, this means “psychiatrists must formulate cases in a rigorous and evidence-based fashion, but avoid taking the tempting leap of faith to presuming that current concepts are adequate and final (572).” At minimum, this means that diagnostic tools and treatment plans are always subject to revision and that psychiatrists ought to remain open to the possibility of causal risk factors that have not yet been unidentified.

This latter point serves as the foundation of the pragmatism of Zachar (2000 &

2002), and Frances (2010 & 2013). Zachar’s (2000 & 2002) practical kinds model of psychiatric disorders is intended to represent a compromise position between essentialist and social constructivist accounts of psychiatric disorder. ssentialist accounts are realist in that they contend that psychiatric disorders exist independently of our classifications of them and that the goal of psychiatric nosology is to discover their underlying causal structures and classify them accordingly. Social constructivist accounts are typically anti-realist in that they contend that psychiatric disorders do not have any underlying causal structure by which they can be defined and that psychiatric nosology is a reflection

159 of prevailing societal norms that is practically useful for labeling and controlling social deviance. Zachar’s account embodies the intuitions of each of these views. It embodies the social constructivist intuition that psychiatric nosology is grounded in its practical utility. However, rather than functioning as a means of labeling and control, psychiatric classification aims to identify categories that are most effective in meeting certain pragmatic and scientific goals, such as promoting patient welfare through the formulation of reliable diagnoses, prognoses, and treatment plans. Zachar contends that the relative weight attached to each of these goals often shifts and that what constitutes an adequate classification may shift as well. However, Zachar’s account embodies the intuitions of essentialism in that once these goals are fixed, the underlying causal structure of the world determines whether and how these goals are achieved.

The concept of “weeds” provides a good illustration of Zachar’s practical kinds model. A weed is an undesirable or unattractive plant that is growing where one does not want it to grow, e.g., in a garden. In this sense, what constitutes a weed is at least partially determined by one’s practical interests. However, once one has decided what constitutes a weed and has adopted the goal of removing the plant, there exists an underlying causal structure that one can manipulate to achieve the desired goal, e.g., using herbicides that mimic auxin to disrupt the natural hormone balance in the plant.

Applied to psychiatric disorders, Zachar’s practical kinds model implies that psychiatric classification is, first and foremost, grounded in its practical utility. Some conditions are considered to be undesirable and the goal is to alter the condition. Once there is agreement on which conditions are undesirable and on the goal to alter the condition, whether and how the goal is achieved is determined by the underlying causal structure of

160 the condition. In this way, the practical kinds model incorporates the realist commitments of essentialist without being committed to the existence of essences for psychiatric disorders. Moreover, it captures the pragmatic and provisional nature of psychiatric classification.

Frances’ pragmatism also emphasizes the provisional and pluralistic nature of psychiatric classification. The basis for his pragmatism was mentioned in Chapter 2 regarding the role of nonepistemic value judgments in psychiatric classification and research. Recall that in that context the issue concerned which inclusion and exclusion criteria should be required for a diagnosis of Bipolar Disorder. Frances argued against allowing antidepressant-induced hypomanic episodes to serve as a basis for diagnosing

Bipolar Disorder and reducing the current required duration of a hypomanic episode for

Bipolar II from four days to two days. In both cases, he was concerned with the prevalence of false positive diagnoses and the risks of treating patients who are suffering from unipolar depression with potentially harmful antipsychotics and mood stabilizers.

Frances points out that such pragmatic concerns are unavoidable in psychiatric classification: “Because it has such a powerful influence on real life (and occasionally even life or death) decisions, DSM can't ignore its practical consequences-intended or unintended (Frances, 2010).” The need to incorporate these “practical consequences” in diagnostic decisions is further supported by the provisional nature of psychiatric explanation and classification. Frances, echoing the theme of Zachar’s practical kinds model, argues that there “is no scientifically proven, just one right way to diagnose any mental disorder (Frances, 2010).” If this is correct, then psychiatric classification cannot be based solely on epistemic considerations and must appeal to nonepistemic, pragmatic

161 considerations as well. Frances suggests that these considerations enter into psychiatric classification in the form of clinical judgment, which he claims is “required in diagnosing any individual patient and Do No Harm common sense is always necessary in establishing any of the DSM thresholds (Frances, 2010).”

The difficulty facing Frances’ pragmatism is that his appeals to “common sense” or “pragmatic concerns” are vague and fail to provide any specific guidance in diagnostic and treatment decisions. This problem, however, accompanies all attempts to apply pragmatism to issues in psychiatric explanation and classification. Take for instance

Brendel’s claim that “psychiatric explanations are ‘true’ only insofar as they promote beneficial real-world results for individuals with mental illnesses (569).” Brendel does not specify what it means to “promote beneficial real-world results,” offering no more guidance than Frances’ appeal to “Do No Harm common sense.” As Ghaemi (2010) points out, this brand of pragmatism simply sneaks in personal opinion and political or professional values into psychiatric classification under the guise of “pragmatic concerns.” Ghaemi refers to this sort of pragmatism as “couch pragmatism” and claims that it is characterized by “a disregard for what is true, even when the research evidence provides reasonable evidence for what is true, at the expense of what we happen to think is useful (Ghaemi, 2010).” He continues, however, by pointing out that such a preoccupation with utility is really nothing more than utilitarianism, not pragmatism.

Moreover, using a clinician’s common sense perception of harm to inform classification decisions, a practice that Ghaemi alleges of Frances, leads to an inconsistent and relativistic classification. Ghaemi uses his dispute with Frances over the inclusion and exclusion criteria for Bipolar Disorder to illustrate this. Recall that Frances’ primary

162 concern was the overdiagnosis of Bipolar Disorder and the risks of treating patients suffering from unipolar depression with potentially harmful antipsychotics and mood stabilizers. However, as Ghaemi points out, one should also worry about the overdiagnosis of Major Depressive Disorder and the risks of treating patients suffering from Bipolar Disorder, or no disorder at all, with potentially harmful antidepressants. In focusing only on the former, Frances is assuming that antipsychotics and mood stabilizers do more harm than antidepressants without providing any evidence for this claim.

Ghaemi argues that this demonstrates the inconsistent application of “pragmatic concerns” and how such concerns are nothing more than a guise for injecting one’s personal opinions into decisions about psychiatric classification.

Similar worries arise for Zachar’s practical kinds model of psychiatric disorder.

Recall that a central claim of Zachar’s model is that classification should aim to identify categories that are most effective in meeting certain pragmatic and scientific goals and that the relative weight attached to each of these goals as well as what constitutes an adequate classification may shift over time. As such, Zachar’s model offers no guidance as to how to construct a classification or which classifications are likely to be useful. In the absence of such guidance, one is left with nothing more than the same vague appeals to “common sense” or “pragmatic concerns” that plague the pragmatist proposals of

Brendel and Frances.

Zachar acknowledges these limitations; however, he asserts that they are the inevitable consequence of denying an essentialist account of psychiatric disorder and “a refusal to accept models that oversimplify the world and therefore hide the complexity that is there (2002, p. 225).” This much seems correct. If applying pragmatism to

163 psychiatry entails accepting the provisional nature of psychiatric explanation and classification, then perhaps the best one can do is to try to make explicit the goals of classification, strive to reach a consensus on these goals, and let the best evidence and common sense perceptions of harm and utility guide decisions about when and how to revise these goals. Such a process is compatible with the hybrid account defended in chapter 2 and the role of nonepistemic judgments in psychiatric diagnosis and treatment that are constitutive of that view.

Pluralism in Psychiatry

A feature of pragmatism that was only briefly mentioned in the previous section is its commitment to pluralism. Brendel makes this commitment explicit in his discussion of methodological pluralism and Zachar alludes to the close connection between the two views (Zachar, 2002; p. 225). Given the difficulties outlined in the previous chapter of adopting reductionism as an explanatory framework for psychiatry, pleas for adopting a pluralistic perspective regarding explanations in psychiatry have become more commonplace (e.g., Brendel, 2003 & 2004; Kendler, 2005, 2011, & 2012; Graham, 2010;

Murphy, 2006 & 2010; Ghaemi, 2007 & 2009, and Pies, 2010 & 2011). However, there exists a plurality of “pluralisms” with little consensus as to what the view actually entails.

ach version has different implications for psychiatric classification and explanation and varying degrees of compatibility with pragmatism and reductionism. Moreover, each version varies with respect to its ability to respond to the constructivist and anti- psychiatry critiques. This section categorizes several pluralist proposals and evaluates them along the dimensions mentioned above.

164 To see the variety of pluralisms that one could defend within psychiatry, consider the following versions of the view that have been either explicitly or implicitly referenced within the philosophy of psychiatry literature: 1) promiscuous pluralism (Dupree, 1993),

2) pluralistic realism (Kitcher, 2003), 3) methodological (also referred to as pragmatic) pluralism (Brendel, 2003), 4) cognitive pluralism (Horst, 2007), 5) explanatory pluralism

(Murphy, 2006 & 2010), 6) compatible pluralism (Kendler, 2005), and 7) integrative pluralism (Kendler, 2005). This is not an exhaustive list, as there are numerous other nuanced versions of pluralism that one could defend in the context of psychiatry. Before discussing specific pluralist proposals, however, it is useful to distinguish between plurality in the sciences and pluralism about the sciences, a distinction originally articulated by Kellert, Longino, and Waters (2006). Plurality in the sciences refers to the plurality of approaches, representational, conceptual and/or classificatory schemes, methodologies, explanatory strategies, and models or theories that are constitutive of the current state of many areas of scientific research. This type of plurality represents a descriptive claim about the current state of science (or particular sciences) and is fully compatible with any of the reductionist theses discussed in the previous chapter.

Pluralism about the sciences, on the other hand, refers to a normative claim about why this plurality exists, namely, that it represents an

“ineliminable character of scientific inquiry and knowledge (about at least some phenomena), that it represents a deficiency in knowledge only from a certain point of view, and that analysis of metascientific concepts (like theory, explanation, evidence) should reflect the possibility that the explanatory and investigative aims of science can be best achieved by sciences that are pluralistic, even in the long run (Longino, ix-x).”

This sort of pluralism about the sciences is incompatible with most versions of reductionism in that it denies that a phenomenon can be fully explained at a single level

165 of explanation, e.g., neuroscience. However, as stated, the view is vague and doesn’t fully capture the specific theses to which most versions of pluralism are committed.

Steel (2004) provides an excellent summary of three common core commitments of pluralism, some of which were discussed above in the section on pragmatism and others that formed the basis of the anti-reductionist critiques outlined in the previous chapter. These three commitments are: 1) the Principle of Multiple Perspectives, 2) Non-

Completeness, and 3) the Autonomy of Levels. I will address each of these commitments in turn and outline how each commitment arises in the pluralist proposals of Kendler

(2005 & 2012) and Murphy (2006 & 2010).

The first commitment is what Steel refers to as the Principle of Multiple

Perspectives. This principle captures the idea that there are multiple legitimate strategies for representing, classifying, explaining, or describing nature. The Principle of Multiple

Perspectives is typically defended on ontological grounds. Some phenomena, for instance, may be so complicated or indeterminate that one is required to utilize multiple strategies to fully explain everything worth knowing about the phenomena30. In the context of psychiatry, this principle captures to intuition that multiple strategies will be required to fully explain psychiatric disorders due to the fact that they are the result of multiple, interacting causal factors, e.g., genetic, neurobiological, psychological, and sociological factors. Adherence to this principle is compatible with the versions of ontological and methodological reductionism outlined in the previous chapter, but is incompatible with eliminative, epistemological, and causal reductionism in that it acknowledges a clear explanatory and causal role for higher-level properties.

30 The idea underlies Dupre’s (1993) promiscuous realism and Kitcher’s (2003) pluralistic realism.

166 The second commitment that Steel discusses is Non-Completeness. This commitment entails that there is no single representation, classification, explanation, or description that is sufficient for all explanatory purposes. This position parallels the main theme of pragmatism, in particular Zachar’s practical kinds model of psychiatric disorder, discussed above. The Principle of Multiple Perspectives may seem to entail Non-

Completeness, but one can defend the latter without defending the former. For instance, one could accept that the ontological structure of the world is simple and determinate but that, due to epistemological limitations, no single representation, classification, explanation, or description that is sufficient to fully explain this structure31. As with the

Principle of Multiple Perspectives, this commitment is compatible with ontological and methodological reductionism, but is incompatible with global eliminative, epistemological, and causal versions of reductionism.

The final commitment is what Steel refers to as the Autonomy of Levels. This commitment embodies the notion that distinct levels of explanation are autonomous and may constitute adequate explanations in their own right. This view can be defended on several grounds, e.g., by appeals to multiple realizability, and underlies the anti- reductionist critiques of Graham (2010), Wakefield (2007), and Woodward (2010) outlined in the previous chapter. As with Non-Completeness, this commitment is compatible with ontological and methodological reductionism, but is incompatible with global eliminative, epistemological, and causal versions of reductionism.

These commitments are often justified by appeal to the notion of “levels.”

Although many have questioned the utility of the levels metaphor because the term has so

31 Horst (2007) gives an interesting account along these lines. He defends a view that he refers to as cognitive pluralism and argues that the need to appeal to multiple strategies to represent, classify, explain, or describe the world is the inevitable result of the way that our cognitive architecture models the world.

167 many different meanings and is used in so many different contexts32, the general idea is that a particular phenomenon is constituted by multiple levels of organized parts and activities and that fully explaining how the parts at a given level of organization behave and interact with the parts of other levels of organization requires multiple strategies. For instance, fully explaining the etiology of Bipolar Disorder will require citing the relevant causal details at each of the levels of organization that constitute an individual, e.g., genetic, cellular and molecular, psychological, and sociological levels of explanation, as well as how these levels of organization interact causally with one another so as to generate the specific symptoms associated with Bipolar Disorder. A complete explanation may require citing relevant developmental and evolutionary details as well.

In addition to explaining relations between various levels of organization, pluralists typically argue that multiple strategies are required, or at least allowable, to fully explain relations within a particular level of organization. For instance, a sociological level of explanation for Bipolar Disorder may require citing relevant details about the individual’s relationship(s) with his/her immediate family, his/her peers and other proximate social groups, as well as more distal social groups and larger social institutions. Multiple strategies may also be necessary to fully explain relations within a particular level of organization when feedback loops exist between the parts at that given level. Beck &

Alford (2009), for instance, argue that this may be the case with respect to psychological explanations for depression, where depressed mood can impact certain cognitive biases,

32 On my count, there are at least a dozen uses of “level” within the psychiatric and neuroscientific literature. These include: levels of explanation (Murphy, 2006), levels of description (Cacioppo, 2003), levels of analysis (Cacioppo, 2003; Kandel, 1998), levels of the mind (Kandel, 1998), levels of mechanisms (Asherson, 2005; Craver, 2007), levels of brain (Gorman, 2000), levels of categories/terms/statements (Thornton, 2003), levels of theories (Craver, 2007), levels of control (Craver, 2007), levels of entities (Craver, 2007), levels of aggregativity (Craver, 2007), and levels of science (Craver, 2007).

168 creating self-fulfilling negative expectations, which in turn further exacerbate the depressed mood.

Empirically Based Pluralism (Integrative Pluralism)

The core commitments that Steel outlines form the basis of Kendler’s (2005 &

2012) empirically based pluralism and Murphy’s (2006 & 2010) explanatory pluralism, both of which are developed specifically within the context of psychiatry. The rest of the chapter will focus on each of their accounts respectively. Kendler (2005), borrowing from the work of Mitchel et al (1997), distinguishes compatible and integrative pluralism.

Both versions of pluralism accept that there are multiple legitimate levels for explaining psychiatric disorders (Steel’s Principle of Multiple Perspectives); however, integrative pluralism actively aims to incorporate these various levels into a common framework to provide a more complete explanation whereas compatible pluralism does not. Kendler specifically advocates the need for psychiatry to adopt integrative pluralism and cites

Gutman’s (2003) research on the effects of adverse childhood experiences on the neurobiology of depression and Caspi’s (2002 & 2003) research on the interaction between functional polymorphisms and childhood maltreatment in depression and antisocial behavior as paradigm examples of this approach. The research by Nader and

Meaney discussed in the previous chapter also provide illustrative examples of integrative pluralism.

For this type of integrative pluralism and the Principle of Multiple Perspectives on which it is based to succeed, however, it must provide a plausible account of the difference between legitimate and illegitimate strategies. More specifically, it must offer some grounds for determining the relative explanatory significance of various levels of

169 explanation. Without such an account, psychiatry runs the risk of becoming a conceptually muddled collection of disunified, and perhaps contradictory, theoretical perspectives, further reinforcing constructivist and anti-psychiatry critiques. Kendler

(2012) attempts to address this challenge by proposing what he refers to as empirically based pluralism.

Central to Kendler’s account are the concepts of difference-makers and causal signatures. Kendler explicates difference-makers in terms of Woodward’s account of causation discussed in the previous chapter: a variable is said to make a difference to another variable when an intervention that changes the value of that variable changes the value of the other variable in some regular, stable way in a range of background conditions. Kendler uses the example of striking a match to light a candle to illustrate this concept. The lighting of a candle requires numerous background conditions to obtain, such as a sufficient amount of oxygen in the atmosphere, a dry match that strikes, and a candle that lights, among other conditions. The striking of the match is a difference-maker to the lighting of the candle in that, despite all of the relevant background conditions obtaining, the candle would not have lit if not for the striking of the match. The striking of the match acts as a “switch point” for the lighting of the candle. In this sense, a difference-maker is what most clinical researchers refer to as a causal risk factor: a particular symptom or disorder would not be present if not for the presence of the specific risk factor.

Kendler acknowledges, of course, that identifying difference-makers for psychiatric disorders is not as straightforward as striking a match to light a candle. He points out that there is “a long list of difference-makers that alter risk for psychiatric and substance use

170 disorders by impacting on the HMBS largely through psychological and social processes

(p. 379).” Kendler cites poor parenting, childhood sexual abuse, stressful life events, severe trauma exposure, coping strategies, social support, exposure to deviant peers, and various genetic and neurobiological variables as examples of the sorts of risk factors involved in the etiology of most psychiatric disorders. Kendler’s notion of causal signatures is intended to provide a “bird’s eye view of the distribution of known difference-makers” for particular psychiatric disorders (p. 379). He focuses specifically on schizophrenia, major depression, and alcohol dependence. stablishing causal signatures depends on what Kendler refers to as a “heuristic structure of levels (p. 379).”

He divides this structure into three broad categories of difference-makers, biological, psychological, and “higher-order,” each of which is divided into further sub-categories in terms of increasing complexity. Biological difference-makers are divided into: 1) molecular genetic, 2) molecular/neurochemical neuroscience, 3) systems neuroscience

(including both anatomy and function), 4) aggregate genetic effects (those effects not yet specified at the molecular level) and 5) miscellaneous biological influences.

Psychological difference-makers are divided into: 1) neuropsychology, 2) personality and cognitive/attitudinal patterns, and 3) trauma exposure. “Higher-level” difference makers are divided into: 1) social, 2) political, and 3) cultural (p. 379).

Utilizing evidence from review articles and meta-analyses when available, Kendler then calculated a score as a percentage out of 100 representing the risk variance that each of the 11 difference-makers contributes to the disorder. He found that each disorder involved difference-makers from all three broad categories. Moreover, aggregate genetic effects made the largest causal contribution for all three disorders, an effect that Kendler

171 attributes to the fact that these influences are the most well studied of all of the risk factors. Finally, each disorder developed a distinct causal signature: schizophrenia had more biological difference-makers, major depression had more psychological difference- makers, and alcohol dependence had more “higher-level” difference-makers.

Kendler interprets these results as clear evidence that “difference-makers are distributed across the biological, psychological and social–cultural domains, and these levels are actively inter-twined with each other in etiologic pathways (p. 383).” More generally, he argues that it establishes the need for psychiatry to adopt a more pluralistic explanatory framework. Kendler’s pluralism clearly embodies the Principle of Multiple

Perspectives, as evidenced by his proclamation that “…psychiatric disturbances, all of which arise in the HMBS [Human-Mind-Brain-System], reflect a multi-layered ‘dappled’ world on which many causal processes impact and intertwine in their influences (378).”

Moreover, Kendler endorses Non-Completeness with his contention that no single level of explanation will be sufficient to fully explain psychiatric disorders. These points clearly distinguish his empirically based pluralism from the ontological, epistemological eliminativist, and causal reductionist theses outlined in the previous chapter. However,

Kendler’s pluralism is compatible with the localized version of methodological reductionism defended in the last chapter. He clearly advocates the importance of incorporating lower-level explanations into an integrated framework, as these levels made the largest causal contribution for all three of the disorders that he examined.

Moreover, the significance of each level of explanation or difference-maker is to be determined on a case-by-case basis, a claim that is consistent with local methodological reductionism.

172 Kendler’s empirically based pluralism certainly is on the right track towards meeting the challenge raised above regarding the need to determine the relative explanatory significance of various levels of explanation. His appeal to Woodward’s interventionist account of causation provides some means for evaluating the relative causal contribution of specific causal variables and his notion of causal signatures enables a fairly straightforward and evidence-based comparison of the relative causal contribution of general levels of explanation. However, Kendler’s account still embodies a potentially ineliminable component of subjectivity in much the same way as highlighted above with pragmatism. For instance, the categories (and sub-categories) that one decides to include in the heuristic structure of levels required for identifying causal signatures is somewhat arbitrary. Kendler cited three broad categories and 11 sub-categories, but there is no principle by which to distinguish broad categories from sub-categories. For instance,

Kendler considers the “social” to be a sub-category as opposed to a broad category, but one could argue that the “social” should constitute a broad category with its own set of sub-categories. How one carves up the categories could reflect prior assumptions about the nature of psychiatric risk factors, e.g., that they tend to be internal rather than external processes, which in turn could potentially influence the resulting calculations of risk variance. Moreover, the list of relevant categories and sub-categories could vary for each particular disorder or class of disorders or be further divided in light of new research. For instance, perhaps personality and cognitive/attitudinal patterns could be further divided into more fine-grained sub-categories and that only some of these sub-categories would have any relevance to a particular disorder or class of disorders.

An additional potentially ineliminable component of subjectivity in Kendler’s

173 evidence based pluralism is his calculation of risk variance for each difference-maker.

This calculation will not only change in light of the number of sub-categories that one includes, but it will also necessarily involve subjective assessments of relative risk.

Kendler explicitly acknowledges this latter point, although he claims to only be providing a sketch as to how his empirically based pluralism could be implemented in practice.

However, he later suggests that these concerns will be minimized since his version of pluralism only “…requires only the acceptance of a common metric— the quality of research evidence (p. 384).”

Appealing to the quality of research evidence is certainly a step in the right direction and is necessary to determine the relative explanatory significance of various levels of explanation and to fully defend pluralism against constructivist and anti- psychiatry critiques. However, given that assessments of research quality will necessarily involve nonepistemic value judgments, his account is unlikely to fully alleviate these concerns. Moreover, as pointed out in Chapter 2, nonepistemic value judgments, primarily in the form of considerations of harm to patients, influence decisions about how to interpret the results from clinical research, how one should revise psychiatric classifications in light of clinical research, and how quickly one should make revisions as a result of clinical research. Such decisions will ultimately depend on both epistemic and nonepistemic evaluative judgments, but the mere inclusion of the latter type of judgments further limits Kendler’s empirically based pluralism to determine the relative explanatory significance of various levels of explanation or to fully alleviate constructivist and anti-psychiatry worries. Nonetheless, as Zachar alluded to above in his defense of the practical model of psychiatric disorder, these may be the inevitable

174 consequences of denying an essentialist account of psychiatric disorder and letting empirical research dictate as much as possible diagnostic and treatment decisions. If applying empirically based pluralism to psychiatry entails, like pragmatism, accepting the provisional nature of psychiatric explanation and classification, then perhaps the best one can do is to try to make explicit one’s nonepistemic value judgments, strive to keep such judgments to a minimum, and let the best evidence and common sense perceptions of harm and utility guide diagnostic and treatment decisions. Such a process is compatible with the hybrid account defended in chapter 2 and the role of nonepistemic judgments in psychiatric diagnosis and treatment that are constitutive of that view.

Explanatory Pluralism

Murphy (2006 & 2010) develops a version of pluralism that is similar to Kendler’s although less empirically driven. His explanatory pluralism is grounded in the existence of multiple epistemic virtues and the idea that these virtues cannot all be maximized by any one explanation at a given time, resulting in a plurality of explanations that are dependent upon which epistemic virtues are privileged. I briefly introduced some of these virtues in Chapter 2 when drawing the distinction between epistemic and nonepistemic value judgments. I will explain each of these virtues, along with others, in more detail here.

The most commonly cited epistemic virtues within the philosophy of science literature are empirical adequacy, parsimony, simplicity, generality, falsifiability, unification, and utility. mpirical adequacy, or what is sometimes more generally referred to as accuracy, refers to the extent to which a particular model fits with the collected data. Parsimony refers to the extent to which a model is consistent with other

175 well-established or well-accepted models within the same domain and/or within a broader theoretical perspective. Simplicity, typically associated with Ockham’s razor, suggests that of two equally empirically adequate models, the better model is the one that posits fewer entities or makes fewer assumptions to account for the data. xplanatory power, or what is sometimes more commonly referred to as generality, refers to the scope or amount of data that is covered by the model. Falsifiability is derived from Popper’s idea that a good model is one that takes risks, that is, one that makes testable predictions that can potentially be refuted. Unification concerns a model’s ability to unify disparate domains of inquiry or collections of data under a more encompassing model. Finally, utility refers to a model’s ease of application for explanatory interests.

This is not an exhaustive list of epistemic virtues nor is it intended to suggest that there is complete agreement as to the precise meaning of each of these virtues. What constitutes empirical adequacy in one discipline, for instance, may not pass as empirically adequate in another. However, these epistemic virtues are the most commonly cited and are sufficient to demonstrate how they may be utilized to defend explanatory pluralism.

The general thrust of this strategy first depends on accepting a pragmatic view of explanation. According to this view, which features constitute a good explanation often vary in relation to the explanatory context, that is, they are often dependent upon what one is trying to explain and the intended use of the explanation. This is similar to Steel’s

Principle of Multiple Perspectives in that it entails acknowledging that each of the epistemic virtues is equally valid and that no single virtue retains a privileged status across all explanatory contexts. The strategy then proceeds by maintaining that each of these virtues cannot all be maximally realized at any given time by a single model or

176 explanation, a claim which embodies Steel’s commitment to Non-Completeness. Rather, which model or explanation that is chosen will depend upon which epistemic virtues are privileged within a particular explanatory context. For instance, a model or explanation may be empirically adequate at the cost of not generalizing to a larger domain of collected data. Conversely, a model or explanation may be generalizable, but only because it incorporates several assumptions or idealizations that sacrifice its empirical adequacy. An instance of this latter situation is often found in population genetics, where models of allele frequency within a population often depend upon certain assumptions and idealizations regarding environmental influences that may not be entirely accurate but that maximize the explanatory power of the model. The upshot is that in light of the epistemic virtues that are privileged, it is not only possible, but also likely, that there will be a plurality of explanations that are equally compatible within a given explanatory context.

The crux of this strategy for defending explanatory pluralism hinges upon adequately characterizing the features of an explanatory context. For genuine explanatory pluralism to be upheld, the explanatory context must not shift relative to the application of a particular model. More specifically, the plurality of explanations must be explanations about the same phenomena or process; otherwise explanatory pluralism does not represent a genuine alternative to reductionism. For if what were initially thought to be explanations of the same phenomena turned out upon closer scrutiny to be explanations of different phenomena, then it would remain a possibility that a reductive explanation could be provided for each of the different phenomena.

177 Another way that the problem of explanatory context can be formulated is in terms of “levels.” On this formulation, the best explanation of a phenomenon is construed as finding the most appropriate level for explaining that phenomenon. If reductionism is correct, then the most appropriate level for explaining a particular phenomenon will be the lowest-level explanation. xplanatory pluralists must deny this claim. Murphy’s explanatory pluralism, although acknowledging a role for lower-level explanations, maintains that explanations in psychiatry succeed not by proceeding at a particular level, but by maximizing the epistemic virtues of robustness and multidimensionality. As discussed in the previous chapter, a robust explanation of a psychiatric disorder is “one that continues to apply when one moves from an idealization to the real world, and is thus largely unaffected by variation in context (p. 109).” It accounts for the presence or absence of a psychiatric disorder across a variety of individual and environmental contexts. A multidimensional explanation of a psychiatric disorder is one that “explains many (at the limit, all) of the symptoms of a disorder (p.

110).” xplanations of this sort will cite the distal, i.e., environmental, causes of the symptoms as well as the proximal, cellular and molecular, causes that mediate the effects of the distal causes.

According to Murphy, explanations in psychiatry aim to maximize robustness and multidimensionality. Murphy labels explanations that successfully maximize these virtues as fundamental explanation and cites the explanation of Huntington’s disease as an example. The presence of the huntingtin gene is sufficient to explain the symptoms associated with each occurrence of Huntington’s disease and it explains the symptoms of the disease irrespective of individual and environmental variation. If explanations in

178 psychiatry were of this sort, then there would be no need for psychiatry to adopt a pluralist explanatory framework. However, as Murphy points, most psychiatric disorders, e.g., Major Depressive Disorder, are the result of a multitude of factors that span a variety of levels of organization. However, Murphy does not think that the unlikelihood of fundamental explanations in psychiatry entails that one will be unable to provide robust and multidimensional explanations for psychiatric disorders. Rather, an explanation of Major Depressive Disorder, for instance, will likely involve trade-offs between these two epistemic virtues. To the extent that an explanation for the disorder is multidimensional and attempts to incorporate all of the symptoms associated with the disorder, it will likely be less robust in that it will be less likely to hold across a variety of individual and environmental contexts. To the extent that an explanation for the disorder is robust and attempts to apply across a variety of individual and environmental contexts, it will likely fail to be multidimensional because it will not account for all of the symptoms associated with the disorder. In such a situation, there may be multiple explanations for the disorder, each with varying degrees of robustness and multidimensionality and each constituting a legitimate explanation in its own right.

These points clearly distinguish Murphy’s explanatory pluralism from the epistemological, eliminativist, and causal reductionist theses outlined in the previous chapter as it clearly acknowledges at least a potential explanatory and causal role for higher-level properties. However, his pluralism is compatible with the localized version of methodological reductionism defended in the last chapter. He clearly advocates the importance of incorporating lower-level explanations into an integrated framework.

Moreover, he contends that the trade-off between robustness and multidimensionality and

179 the significance of each level of explanation is to be determined on a case-by-case basis, a claim that is consistent with local methodological reductionism.

The main difficulty facing Murphy’s pluralism is deciding if and when to sacrifice robustness for multidimensionality (or vice versa), a difficulty that arises at each level of explanation for a particular disorder. However, the situation becomes even more complicated when one tries to incorporate multiple levels of explanation into a single explanatory framework, where decisions about if and when to sacrifice robustness for multidimensionality occur both within and between levels. In light of this problem, implementing Murphy's explanatory pluralism is likely to be extremely complicated, especially if the explanations drawn from different levels involve conflicting etiologies.

Murphy provides no clear guidance for deciding how to handle this complexity and balance the robustness of an explanation with its multidimensionality. Without such an account, Murphy’s pluralism cannot fully address the problem mentioned earlier of how to determine the relative explanatory significance of various levels of explanation. Like

Kendler, Murphy appeals to Woodward’s interventionist account of causation to provide some means for evaluating the relative causal contribution of specific causal variables.

While this may help to provide some order to Murphy’s pluralism, it does not fully alleviate the problem. Woodward’s account faces the difficulty of deciding when to utilize coarse-grained variables as opposed to fine-grained variables in one’s explanation.

Woodward suggests that this decision will depend on the degree of invariance or stability of the resulting generalization between the two variables. However, Woodward’s account of invariance is analogous to Murphy’s account of robustness in that both are intended to capture the idea that an explanation should hold across a variety of

180 explanatory contexts, so his account cannot offer any guidance for deciding how to balance the robustness of an explanation with its multidimensionality.

One possible solution would be to supplement Murphy’s explanatory pluralism with Kendler’s empirically based pluralism, particularly his notion of causal signatures.

However, the resulting account would simply inherit the difficulties of deciding which categories and sub-categories to include in the heuristic structure of levels required for identifying causal signatures and calculating the risk variance for each difference-maker.

Recall the concern in that context was that such decisions embodied an ineliminable component of subjectivity and, therefore, reinforced constructivist and anti-psychiatry critiques that allowing any subjective components into psychiatric diagnosis and research would undermine the scientific legitimacy of psychiatry.

While there are good reasons to be cautious of allowing subjective components into psychiatric diagnosis and research, e.g., the possibility of bias and conflicts of interest, the constructivist and anti-psychiatry concerns that follow from the presence of these components are unwarranted. As the above discussions of pragmatism and Kendler’s empirically based pluralism demonstrate, the inclusion of nonepistemic value judgments is the inevitable consequence of denying essentialism and accepting the complexity of psychiatric disorders. Moreover, as discussed to in Chapter 2, the inclusion of nonepistemic value judgments will be inevitable in any context in which one is required to make diagnostic and research decisions that involve weighing the relative risks of false positives and false negatives or drawing an inference quickly as opposed to waiting for further evidence to reduce uncertainties. Such contexts include deciding how to determine the relative explanatory significance of various levels of explanation, when to

181 utilize coarse-grained variables as opposed to fine-grained variables in one’s explanation, or which categories and sub-categories to include in the heuristic structure of levels required for identifying causal signatures and calculating the risk variance for each difference-maker. Rather than undermining the scientific legitimacy of psychiatry, the inclusion of nonepistemic value judgments simply reflects the provisional nature of psychiatric explanation and classification that follows from adopting a pluralistic and/or pragmatic approach to psychiatry. The best one can do, therefore, is to try to make explicit one’s nonepistemic value judgments, strive to keep such judgments to a minimum, and let the best evidence and common sense perceptions of harm and utility guide diagnostic and treatment decisions. Accepting these features as constitutive of psychiatry is completely compatible with accepting methodological reductionism, the reality of psychiatric disorders, and the scientific legitimacy of psychiatry.

182 Bibliography

American Psychiatric Association. Task Force on DSM-II. Diagnostic and statistical manual of mental disorders: DSM-II. Amer Psychiatric Pub Inc, 1968.

American Psychiatric Association. Task Force on DSM-III. Diagnostic and statistical manual of mental disorders: DSM-III. Amer Psychiatric Pub Inc, 1980.

American Psychiatric Association. Task Force on DSM-IV. Diagnostic and statistical manual of mental disorders: DSM-IV. Amer Psychiatric Pub Inc, 1994.

American Psychiatric Association. Task Force on DSM-V. Diagnostic and statistical manual of mental disorders: DSM-V. Amer Psychiatric Pub Inc, 2013.

Angst, Jules, et al. "Toward a re-definition of subthreshold bipolarity: epidemiology and proposed criteria for bipolar-II, minor bipolar disorders and hypomania." Journal of affective disorders 73.1 (2003): 133-146.

Ayala, Francisco José, and Theodosius Grigorievich Dobzhansky, eds. Studies in the philosophy of biology: Reduction and related problems. Univ of California Press, 1974.

Beck, Aaron T., and Brad A. Alford. Depression: Causes and treatments. University of Pennsylvania Press, 2009.

Benazzi, Franco, and Hagop Akiskal. "The duration of hypomania in bipolar-II disorder in private practice: methodology and validation." Journal of affective disorders 96.3 (2006): 189-196.

Boghossian, Paul. "Fear of knowledge: Against relativism and constructivism." New York (2006).

Boorse, Christopher. "On the distinction between disease and illness." Philosophy & public affairs 5.1 (1975): 49-68.

Boorse, Christopher. "What a theory of mental health should be." Journal for the Theory of Social Behaviour 6.1 (1976): 61-84.

Boorse, Christopher. "Health as a theoretical concept." Philosophy of science (1977): 542-573.

Boorse, Christopher. "A rebuttal on health." What is disease?. Humana Press, 1997. 1- 134.

Borsboom, Denny. "Psychometric perspectives on diagnostic systems." Journal of clinical psychology 64.9 (2008): 1089-1108.

183 Brendel, David H. "Reductionism, eclecticism, and pragmatism in psychiatry: The dialectic of clinical explanation." The Journal of medicine and philosophy 28.5-6 (2003): 563-580.

Brendel, David H. "Healing psychiatry: A pragmatic approach to bridging the science/humanism divide." Harvard review of psychiatry 12.3 (2004): 150-157.

Caspi, Avshalom, et al. "Role of genotype in the cycle of violence in maltreated children." Science 297.5582 (2002): 851-854.

Caspi, Avshalom, et al. "Influence of life stress on depression: moderation by a polymorphism in the 5-HTT gene." Science Signaling 301.5631 (2003): 386.

Cooper, David Graham. Psychiatry and anti-psychiatry. London: Tavistock Publications, 1967.

Cooper, Rachel. "Disease." Studies in History and Philosophy of Science Part C: Studies in History and Philosophy of Biological and Biomedical Sciences 33.2 (2002): 263-282.

Cranor, Carl F. Regulating toxic substances: a philosophy of science and the law. Oxford University Press on Demand, 1993.

Cranor, Carl F. Toxic torts: Science, law and the possibility of justice. Cambridge University Press, 2006.

Craver, Carl F. Explaining the brain. Oxford: Oxford University Press, 2007.

Czoty, Paul W., et al. "Characterization of dopamine D1 and D2 receptor function in socially housed cynomolgus monkeys self-administering cocaine." Psychopharmacology 174.3 (2004): 381-388.

Dichter, Gabriel S., et al. "The effects of psychotherapy on neural responses to rewards in major depression." Biological psychiatry 66.9 (2009): 886-897.

Dickerson, Faith B. "Cognitive behavioral psychotherapy for schizophrenia: a review of recent empirical studies." Schizophrenia research 43.2 (2000): 71-90.

Douglas, Heather. "Inductive risk and values in science." Philosophy of Science (2000): 559-579.

Douglas, Heather . Science, policy, and the value-free ideal. University of Pittsburgh Pre, 2009.

Dupré, John. The disorder of things: Metaphysical foundations of the disunity of science. Harvard University Press, 1995.

184 ngel, George L. "The need for a new medical model: a challenge for biomedicine." Science 196.4286 (1977): 129-136.

reshefsky, Marc. "Defining ‘health’ and ‘disease’." Studies in History and Philosophy of Science Part C: Studies in History and Philosophy of Biological and Biomedical Sciences 40.3 (2009): 221-227.

rnest, Paul. "The one and the many." Constructivism in education (1995): 459-486.

Fawzy, Fawzy I., et al. "Malignant melanoma: effects of an early structured psychiatric intervention, coping, and affective state on recurrence and survival 6 years later." Archives of General Psychiatry 50.9 (1993): 681.

First, Michael, and Allen Frances. "Issues for DSM-V: Unintended consequences of small changes: The case of paraphilias." American Journal of Psychiatry 165.10 (2008): 1240-1241.

Fodor, Jerry A. "Special sciences (or: the disunity of science as a working hypothesis)." Synthese 28.2 (1974): 97-115.

Forbes, David, et al. "Requiring both avoidance and emotional numbing in DSM-V PTSD: Will it help?." Journal of affective disorders 130.3 (2011): 483-486.

Frances, Allen, and Arnold M. Cooper. "Descriptive and dynamic psychiatry: A perspective on DSM-III.." The American journal of psychiatry (1981).

Frances, Allen, Shoba Sreenivasan, and Linda . Weinberger. "Defining mental disorder when it really counts: DSM-IV-TR and SVP/SDP statutes." Journal of the American Academy of Psychiatry and the Law Online 36.3 (2008): 375-384.

Frances, A. “DSM5 Should Not xpand Bipolar II Disorder.” Psychology Today. Published online on April 23rd, 2010. http://www.psychologytoday.com/blog/dsm5-in- distress/201004/dsm5-should-not-expand-bipolar-ii-disorder. Accessed: 7/13/2013.

Frances, A. “Bipolar II Revisited-Always Take The xperts With A Grain Of Salt.” Psychology Today. Published online on April 26th, 2010. http://www.psychologytoday.com/blog/dsm5-in-distress/201004/bipolar-ii-revisited- always-take-the-experts-grain-salt. Accessed: 7/13/2013.

Frances, A. "Opening pandora's box: The 19 worst suggestions for DSM-5." Psychiatric Times 27.9 (2010).

Frances, A. Should Practical Consequences Influence DSM5 Decisions? Psychology Today. Published online on April 27th, 2010. http://www.psychologytoday.com/blog/dsm5-in-distress/201004/should-practical- consequences-influence-dsm5-decisions

185 Frances, A. “Pragmatism in Psychiatric Diagnosis.” Psychology Today. Published online on January 11th, 2013. http://www.psychologytoday.com/blog/dsm5-in- distress/201301/pragmatism-in-psychiatric-diagnosis

Fulford, Kenneth William Musgrave. Moral theory and medical practice. Cambridge: Cambridge University Press, 1989.

Fulford, K. W. M. "‘What is (mental) disease?’: an open letter to Christopher Boorse." Journal of Medical Ethics 27.2 (2001): 80-85.

Foucault, Michel. Madness and civilization: A history of insanity in the age of reason. Random House Digital, Inc., 1988.

Ghaemi, S. Nassir. "Pluralism in psychiatry: Karl Jaspers on science." Philosophy, Psychiatry, & Psychology 14.1 (2007): 57-66.

Ghaemi, S. Nassir. "The rise and fall of the biopsychosocial model." The British Journal of Psychiatry 195.1 (2009): 3-4.

Ghaemi. S. Nassir. "Couch-pragmatism." Psychiatr Times 27.10 (2010): 16-21.

Ghaemi. S. Nassir. “DSM-5 and Bipolar Disorder: Science versus Politics.” Psychology Today. Published online April, 24th, 2010. http://www.psychologytoday.com/blog/mood-swings/201004/dsm-5-and-bipolar- disorder-science-versus-politics

Gold, Ian. "Reduction in psychiatry." Canadian journal of psychiatry. Revue canadienne de psychiatrie 54.8 (2009): 506-512.

Graham, George. The disordered mind: An introduction to philosophy of mind and mental illness. Routledge, 2013.

Grof, Paul. "Psychiatry and neuroscience: reduction or pluralism." Canadian journal of psychiatry. Revue canadienne de psychiatrie 54.8 (2009): 503-505.

Gunnar, Megan R. et al. (2007). “arly care experiences and HPA axis regulation in children: a mechanism for later trauma vulnerability.” Progress in Brain Research, 167, 137-149.

Gutman, David A., and Charles B. Nemeroff. "Persistent central nervous system effects of an adverse early environment: clinical and preclinical studies." Physiology & behavior 79.3 (2003): 471-478.

Guze, Samuel B. "Biological psychiatry: is there any other kind." Psychological medicine 19.2 (1989): 315-323.

186 Hacking, Ian. The social construction of what?. Harvard University Press, 1999.

Hall-Flavin, D. K., et al. "Using a pharmacogenomic algorithm to guide the treatment of depression." Translational psychiatry 2.10 (2012): e172.

Happé, Francesca, Angelica Ronald, and Robert Plomin. "Time to give up on a single explanation for autism." Nature neuroscience 9.10 (2006): 1218-1220.

Harland, Richard. Superstructuralism: The philosophy of structuralism and post- structuralism. London: Methuen, 1987.

Hesslow, Germund. "Do we need a concept of disease?." Theoretical medicine 14.1 (1993): 1-14.

Horst, Steven. "Beyond Reduction: What Can Philosophy of Mind Learn from Post- Reductionist Philosophy of Science?." Boston Colloquium in the Philosophy of Science. 2005.

Horwitz, Allan V., and Jerome C. Wakefield. The loss of sadness. New York: Oxford University Press, 2007.

Hume, David. A treatise of human nature. Courier Dover Publications, 2003.

Insel, Thomas R., and Remi Quirion. "Psychiatry as a clinical neuroscience discipline." JAMA: the journal of the American Medical Association 294.17 (2005): 2221-2224.

Kandel, ric R. "A new intellectual framework for psychiatry." American journal of psychiatry 155.4 (1998): 457-469.

Karlsson, Hasse and Kamppinen, Matti. "Biological psychiatry and reductionism. mpirical findings and philosophy." The British Journal of Psychiatry 167.4 (1995): 434- 438.

Kellert, Stephen H., Helen . Longino, and C. Kenneth Waters. "Introduction: the pluralist stance." Scientific pluralism (2006): vii-xxix.

Kendler, Kenneth S. "Toward a philosophical structure for psychiatry." American Journal of Psychiatry 162.3 (2005): 433-440.

Kendler, Kenneth S. "xplanatory models for psychiatric illness." The American journal of psychiatry 165.6 (2008): 695.

Kendler, K. S. "The dappled nature of causes of psychiatric illness: replacing the organic–functional/hardware–software dichotomy with empirically based pluralism." Molecular psychiatry 17.4 (2012): 377-388.

187 Kim, Jaegwon. "The myth of nonreductive materialism." Proceedings and Addresses of the American Philosophical Association. Vol. 63. No. 3. American Philosophical Association, 1989.

Kincaid, Harold. "Do We Need Theory to Study Disease?: lessons from cancer research and their implications for mental illness." Perspectives in biology and medicine 51.3 (2008): 367-378.

Kingma, lselijn. "What is it to be healthy?." Analysis 67.2 (2007): 128-133.

Kitcher, Philip. Science, truth, and democracy. Oxford University Press, 2003.

Koponen, Salla, et al. "Axis I and II psychiatric disorders after traumatic brain injury: a 30-year follow-up study." American Journal of Psychiatry 159.8 (2002): 1315-1321.

Krueger, Robert F., et al. "Synthesizing dimensional and categorical approaches to personality disorders: refining the research agenda for DSM V Axis II." International Journal of Methods in Psychiatric Research 16.S1 (2007): S65-S73.

Kuhn, Thomas S. "The structure of scienti¿c revolutions." Chicago/London (1970).

Kuhn, Thomas S. "Objectivity, value judgment, and theory choice." (1977): 320-339.

Kukla, André. Social constructivism and the philosophy of science. Psychology Press, 2000.

Laing, R. D. The Divided Self: an existentialist study in sanity and madness. Penguin, 1960.

Leo, Jonathan, and Jeffrey R. Lacasse. "The media and the chemical imbalance theory of depression." Society 45.1 (2008): 35-45.

Leroi, Iracema, et al. "Psychopathology in patients with degenerative cerebellar diseases: a comparison to Huntington’s disease." American Journal of Psychiatry 159.8 (2002): 1306-1314.

Levine, Bruce . "Commonsense Rebellion: Debunking psychiatry, confronting society: An A to Z guide to rehumanizing our lives." (2001).

Lilienfeld, Scott O., and Lori Marino. "Psychiatric disorder as a Roschian concept: a critique of Wakefield's" harmful dysfunction" analysis." (1995): 411.

Lindauer, Ramon JL, et al. "ffects of psychotherapy on hippocampal volume in out- patients with post-traumatic stress disorder: a MRI investigation." Psychological medicine 35.10 (2005): 1421-1432.

188 Martin, Joseph B. "The integration of neurology, psychiatry, and neuroscience in the 21st century." American Journal of Psychiatry 159.5 (2002): 695-704.

McNally, Richard J. What is mental illness?. Harvard University Press, 2011. Miklowitz, David J. "Adjunctive psychotherapy for bipolar disorder: state of the evidence." The American journal of psychiatry 165.11 (2008): 1408.

Minnesota House of Representatives. 88th Legislature 2013-2014. Bill SF 1234 Minnesota Workers’ Compensation Act. Available at: https://www.revisor.mn.gov/ bills/text.php?number=SF1234&version=latest&session=ls88&session_number=0. Accessed: 7/13/2013.

Mitchell, Sandra D., et al. "The whys and hows of interdisciplinarity." Human by Nature: Between Biology and the Social Sciences. Edited by Weingart P, Richerson P, Mitchell S, Maasen S. Mahwah, NJ, Lawrence Erlbaum Associates (1997): 103-150.

Mohl, Paul C. "Should psychotherapy be considered a biological treatment?." Psychosomatics 28.6 (1987): 320-326.

Moore, George dward. Principia ethica. Cambridge University Press, 1993.

Morgan, Drake, et al. "Social dominance in monkeys: dopamine D2 receptors and cocaine self-administration." Nature neuroscience 5.2 (2002): 169-174.

Murphy, Dominic. Psychiatry in the scientific image. Cambridge: MIT Press, 2006.

Murphy, Dominic, and Robert L. Woolfolk. "Conceptual analysis versus scientific understanding: An assessment of Wakefield's folk psychiatry." Philosophy, Psychiatry, & Psychology 7.4 (2000): 271-293.

Nader, Michael A., and Paul W. Czoty. "PT imaging of dopamine D2 receptors in monkey models of cocaine abuse: genetic predisposition versus environmental modulation." American Journal of Psychiatry 162.8 (2005): 1473-1482.

Nagel, rnest. "The structure of science." American Journal of Physics 29 (1961): 716- 716.

Nordenfelt, L. Y. On the nature of health: An action-theoretic approach. Vol. 26. Springer, 1995.

Nordenfelt, Lennart. "The concepts of health and illness revisited." Medicine, Health Care and Philosophy 10.1 (2007): 5-10.

Overli, Oyvind, et al. (2005). “Behavioral and Neuroendocrine Correlates of Selection for Stress Responsiveness in Rainbow Trout - a Review.” Integrative and Comparative Biology 45, 463-474.

189 Paris, J. “Psychiatry and Neuroscience.” Canadian journal of psychiatry. Revue canadienne de psychiatrie 54.8 (2009): 513-517.

Parker, Karen J., et al. (2004). “Prospective Investigation of Stress Inoculation in Young Monkeys.” Archives of General Psychiatry 61, 933-941.

Phelps, J., and S. N. Ghaemi. "The mistaken claim of bipolar ‘overdiagnosis’: solving the false positives problem for DSM 5/ICD 11." Acta Psychiatrica Scandinavica 126.6 (2012): 395-401.

Phelps, J. “DSM-5 Won’t Solve the Overdiagnosis Problem – but Clinicians Can.” Psychology Today. Published online on May 9th, 2013. http://www.psychiatrictimes.com/bipolar-disorder/dsm-5-won’t-solve-overdiagnosis- problem—-clinicians-can

Phillips, J. "Science versus pragmatism in the DSM: Finding a middle ground." Psychiatric Times (2010).

Phillips, Katharine A., et al. "Body dysmorphic disorder: some key issues for DSM V." Depression and Anxiety 27.6 (2010): 573-591.

Peirce, Charles S. "The issues of pragmaticism." The Monist 15.4 (1905): 481-499.

Pies, Ronald. "On myths and countermyths: more on Szaszian fallacies." Archives of General Psychiatry 36.2 (1979): 139.

Pies, Ronald. "Moving beyond the “myth” of mental illness." Szasz Under Fire. Chicago, IL: Open Court (2004): 327-53.

Pies, Ronald. "Beyond reliability: biomarkers and validity in psychiatry." Psychiatry (Edgmont) 5.1 (2008): 48.

Pies, Ronald. "The ideal and the real: how does psychiatry escape the DSM-5 ‘Fly- bottle?’” Bull Assoc Adv Philos Psychiatry 17.2 (2010): 18-22.

Pies, Ronald W. "Can Psychiatry be Both A Medical Science and A Healing Art? The Case for Polythetic Pluralism." Psychiatric Times 28.12 (2011).

Rosch, . “Principles of Categorization.” In . Rosch and B. Lloyd (eds), Cognition and categorization (pp. 27-48). Hillsdale, NJ: Lawrence rlbaum. 1978.

Rudner, Richard. "The scientist qua scientist makes value judgments." Philosophy of Science 20.1 (1953): 1-6.

Rudnick, Abraham. "The molecular turn in psychiatry: A philosophical analysis." The Journal of medicine and philosophy 27.3 (2002): 287-296.

190 Sachdev, Perminder S. "Whither neuropsychiatry?" The Journal of neuropsychiatry and clinical neurosciences 17.2 (2005): 140-141.

Schafer, Arthur. "Biomedical conflicts of interest: a defence of the sequestration thesis— learning from the cases of Nancy Olivieri and David Healy." Journal of Medical Ethics 30.1 (2004): 8-24.

Scheff, Thomas J. Being mentally ill: A sociological theory. Transaction Books, 1970. Shea, Allison et al. (2005). “Child maltreatment and HPA axis dysregulation: relationship to Major Depressive Disorder and post traumatic stress disorder in females.” Psychoneuroendocrinology 30, 2: 162-178.

Schramme, Thomas. "A qualified defence of a naturalist theory of health." Medicine, Health Care and Philosophy 10.1 (2007): 11-17.

Schwartz, Jeffrey, and Sharon Begley. The Mind and the Brain: Neuroplasticity and the Power of Mental Force. New York: Regan Books/HarperCollins Publ, 2002.

Searight, H. Russell, Rottnek, F., and Abby, S. "Conduct disorder: diagnosis and treatment in primary care." American Family Physician 63.8 (2001): 1579.

Smith, Ryan, et al. "Localizing sadness activation within the subgenual cingulate in individuals: a novel functional MRI paradigm for detecting individual differences in the neural circuitry underlying depression." Brain imaging and behavior 5.3 (2011): 229-239.

Spiegel, David, et al. "ffect of psychosocial treatment on survival of patients with metastatic breast cancer." The Lancet 334.8668 (1989): 888-891.

Steel, Daniel. "Can a reductionist be a pluralist?" Biology and Philosophy 19.1 (2004): 55-73.

Steel, Daniel. "pistemic Values and the Argument from Inductive Risk." Philosophy of science 77.1 (2010): 14-34.

Stevens, L. “Schizophrenia: A Nonexistent Disease.” http://www.antipsychiatry.org/schizoph.htm

Szasz, Thomas S. "The myth of mental illness." American Psychologist 15.2 (1960): 113.

Tarullo, Amanda R. et al. (2006). “Child maltreatment and the developing HPA axis.” Hormones and Behavior, 50, 4: 632-639.

Tauber, Alfred I. "Medicine and the call for a moral epistemology." Perspectives in biology and medicine 48.1 (2005): 42-53.

191 Tondo, L., G. Vázquez, and R. J. Baldessarini. "Mania associated with antidepressant treatment: comprehensive meta analytic review." Acta Psychiatrica Scandinavica 121.6 (2010): 404-414.

Van Regenmortel, Marc HV. "Reductionism and complexity in molecular biology." EMBO reports 5.11 (2004): 1016.

Vicedo, M. “The human genome project: Towards an analysis of the empirical, ethical, and conceptual issues involved.” In: D.L. Hull & M. Ruse (ds.), The philosophy of biology (pp. 494-521). Oxford: Oxford University Press. 1998.

Wakefield, Jerome C. "The concept of psychiatric disorder: on the boundary between biological facts and social values." American Psychologist 47.3 (1992): 373.

Wakefield, Jerome C. "What makes a psychiatric disorder mental?" Philosophy, Psychiatry, & Psychology 13.2 (2006): 123-131.

Wakefield, Jerome C. "The concept of psychiatric disorder: diagnostic implications of the harmful dysfunction analysis." World Psychiatry 6.3 (2007): 149.

Weaver, Ian CG, Moshe Szyf, and Michael J. Meaney. "From maternal care to gene expression: DNA methylation and the maternal programming of stress responses." Endocrine research 28.4 (2002): 699-699.

Weaver, Ian C.G. et al. (2004). “pigenetic programming by maternal behavior.” Nature Neuroscience 7, 8: 847-854.

Weaver, Ian C.G. et al. (2005). “Reversal of Maternal Programming of Stress Responses in Adult Offspring through Methyl Supplementation: Altering pigenetic Marking Later in Life.” The Journal of Neuroscience 25, 47: 11045-11054.

Wicki, W., and Jules Angst. "The Zurich study." European archives of psychiatry and clinical neuroscience 240.6 (1991): 339-348.

Windier, Thomas A., et al., eds. Dimensional models of personality disorders: Refining the research agenda for DSM-V. American Psychiatric Pub, 2007.

Woodward, James. “Cause and xplanation in Psychiatry: An Interventionist Perspective.” In: K. Kendler and J. Parnas, (eds.), Philosophical Issues in Psychiatry: Explanation, Phenomenology and Nosology (pp. 136-184). Johns Hopkins University Press. 2008.

Yudofsky, Stuart C., and Robert . Hales. "Neuropsychiatry and the future of psychiatry and neurology." American Journal of Psychiatry 159.8 (2002): 1261-1264.

192 Zachar, Peter. Psychological concepts and biological psychiatry: A philosophical analysis. Vol. 28. John Benjamins Publishing Company, 2000.

Zachar, Peter. "Psychiatric disorders are not natural kinds." Philosophy, Psychiatry, & Psychology 7.3 (2000): 167-182.

Zachar, Peter. "The practical kinds model as a pragmatist theory of classification." Philosophy, Psychiatry, & Psychology 9.3 (2002): 219-227.

Zachar, Peter, and Kenneth Kendler. "Psychiatric disorders: a conceptual taxonomy." American Journal of Psychiatry 164.4 (2007): 557-565.

Zimmerman, Mark. "Broadening the concept of bipolar disorder: what should be done in the face of uncertainty?" World Psychiatry 10.3 (2011): 188-189.

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