What Should Count as a Mental Disorder in DSM-V?
What exactly is a “mental disorder”? For that matter, what criteria should determine whether any condition is a “disease” or a “disorder”?
If sick men fared just as well eating and drinking and living exactly as healthy men do . . . there would be little need for the science [of medicine].
attributed to Hippocrates
Well, while I’m here, I’ll do the work-and what’s the work? To ease the pain of living. . . .
Allen Ginsberg
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What exactly is a “mental disorder”? For that matter, what criteria should determine whether any condition is a “disease” or a “disorder”? Is “disease” something like an oak tree-a physical object you can bump into or put your arms around? Or are terms like “disease” and “disorder” merely abstract, value-laden constructs, akin to “injustice” and “immorality”? Are categories of disease and disorder fundamentally different in psychiatry than in other medical specialties? And-by the way-how do the terms “disease,” “disorder,” “syndrome,” “malady,” “sickness,” and “illness” differ?
Anyone who believes there are easy or certain answers to these questions is either in touch with the Divine Mind, or out of touch with reality. To appreciate the complexity and ambiguity in this conceptual arena, consider this quote from the venerable Oxford Textbook of Philosophy and Psychiatry:
"The term 'mental illness' is probably best used for those disorders that are intuitively most like bodily illness (or disease) and, yet, mental rather than bodily. This of course implies everything that is built into the mind-brain problem!"1(p11)
In a single sentence, we are already grappling with the terms “illness,” “disorder,” and “disease,” not to mention Cartesian psychology! And yet-daunting though these issues are-they are central to the practical task now before the DSM-V committees: figuring out what conditions ought to be included as psychiatric disorders.
To prefigure one element of my own position, I again quote from the Oxford Textbook’s chapter 20, “Values in Psychiatric Diagnosis”:
"Our conclusion . . . [is] that the traditional medical model, and the claim to value-free diagnosis on which it rests, is unsupportable; and that, to the contrary, diagnosis, although properly grounded on facts, is also, and essentially, grounded on values. . . . [This] is consistent with late twentieth century work in the philosophy of science . . . showing the extent to which the scientific process, from observation and classification to explanation and theory construction, does not depend on merely passively recording data, but is instead actively shaped in complex judgments. . . ."1(p565)
The Oxford authors wisely observe that “adding values” does not entail “subtracting facts.” Thus, when we assert that someone with paraplegia has a pathological (from the Greek pathos, “suffering”) condition, we are making a claim grounded in a certain kind of value judgment; namely, that the inability to move one’s legs is in some sense “not a good thing.” In a society that greatly valued paralysis and devalued walking, paraplegia would not constitute “pathology.” On the other hand, we also “add facts” in reaching the conclusion that Mr Jones-who cannot move his legs-has suffered a fracture-dislocation of the lumbar vertebrae. In short, medical diagnosis is a matter of “facts plus values.”1 (Incidentally, we do not escape this evaluative dimension by appealing to some putative “evolutionary standard” based on notions of how we humans were “designed.”2 As clinicians, we must still make value judgments as to what degrees of departure from supposed evolutionarily designed responses should-or should not-count as “disease”).
Similarly, when psychiatrists adduce evidence of suffering and incapacity in diagnosing a psychiatric disorder, we implicitly invoke certain broad values; for example, that it is generally “not a good thing” when a human being is unable to eat, sleep, think, and work. At the same time, we “add facts”: we note that the patient has lost 20 lb in the last month; that she gets only 3 hours of sleep each night; that she cannot subtract serial 7s accurately; and perhaps, in some cases, that she shows marked elevation of her serum cortisol level.3 That the facts we adduce as psychiatrists often differ from the kind cited by, say, orthopedists, does not render our data less “factual”! Indeed, some of the most important facts about the suffering and incapacitated psychiatric patient are facts intrinsic to the person’s experience-the phenomenology or “life world” of the patient.4-6 Thus, when the depressed patient tells us, “I feel like I’m being suffocated by my depression” and “I feel like an empty shell about to be crushed,” we justifiably regard these as facts of the patient’s felt experience.
The notion that only conditions associated with anatomical lesions or abnormal physiology count as “real” diseases-the “lumps and labs” model of disease7-denigrates the phenomenological realm. Sadly, such misplaced positivism-based on a crude understanding of pathologist Rudolph Virchow’s views-has been used to whack psychiatry over the head for nearly 50 years.8,9 That said, in the model I shall develop, the search for abnormal neuroanatomy, physiology, and biomarkers does play an important role in the later stages of disease classification.
Mental disorders: essential definitions
Deciding what should “count” as a mental disorder is not the same as offering an essential definition of “mental disorder.” An essential definition is one that specifies necessary and sufficient conditions; for example, “a closed figure consisting of 3 line segments linked end-to-end” constitutes the necessary and sufficient conditions for ascribing the term “triangle.”
The philosopher Ludwig Wittgenstein (1889-1951) taught us that-with the possible exception of mathematical terms-commonly used words do not have essential definitions.10,11 For example, it is almost impossible to specify the necessary and sufficient conditions that define the term “game.” On the other hand, Wittgenstein argued, we can identify certain “resemblances” among members of a particular “family.” These family resemblances-blond hair, blue eyes, for example-help us to recognize the family, even though no single feature is present in every family member.
Wittgenstein likens a family resemblance to the long, overlapping fibers of a rope: no single fiber runs throughout the entire length of the rope, but the rope is still held together by these fibers.
Following the lead of the late Dr Robert E. Kendell,12 I believe that suffering and incapacity are the main “fibers” making up the disease concept. When prolonged and severe suffering and incapacity are present in the affective, cognitive, or interpersonal-behavioral realms, we are then entitled to speak generically of “psychiatric disease.” (For many reasons, I believe this term is preferable to “mental disorder” or “mental illness,” but I will retain the term “mental disorder” because it is used in the DSMs).
The failure to recognize the distinction between disease in its primordial, conceptual sense (in German, die Krankheit) and specific diseases (die Krankheiten) has led to much confusion, in my view.8,9 What we humans ordinarily “count” as disease (die Krankheit) represents a pragmatic existential decision. It is not a determination akin to observing a bacterium under a microscope. Indeed, the concept of disease (etymologically, dis-ease) does not originate in the realm of “expert” determination; rather, ordinary human beings decide that someone is “dis-eased” based on everyday observations and reports of suffering and incapacity. It does not take a microbiologist or pathologist, for example, to know that someone “has disease” or “is diseased”-even though both specialists may ultimately contribute to determining the particular type of disease.
In the words of Maurice Natanson,13 a philosopher who helped introduce the work of Jean-Paul Sartre and Edmund Husserl in the United States, “Disease [is originally recognized] not by experts, but by ordinary men.” Similarly, with respect to cognitive and emotional derangement, we do not require biological validators to identify the presence of psychiatric disease per se. Thus, my teacher, Dr Robert W. Daly,14 has written:
"To affirm that someone is mad is to make a practical judgment based on immediate and reflective knowledge of the activities, experiences, and circumstances of the person in question . . . as a particular human agent. "
The evolution of a specific mental disorder
So how do we develop a practical model for determining whether a condition represents, in the first place, dis-ease and, secondarily, whether it constitutes a specific disease, on a par with, say, bipolar I disorder? For example, how do we decide whether to consider “pathological bigotry” and “internet addiction” as specific mental disorders?
I have developed a pyramidal model (Figure) that illustrates the evolution of a condition from primordial dis-ease to a fully realized disease entity. At the base of the pyramid (stage 1) is the everyday recognition of substantial and prolonged suffering and incapacity. In my view, at least some of the “suffering” must be an intrinsic element of having the condition-not simply a consequence of society’s punitive responses to the person’s behaviors (eg, putting someone in jail because of certain sexual behaviors). We can specify “suffering and incapacity” in terms of social and vocational impairment, impaired vital functions, and distortions in the phenomenological realm (feeling “totally worthless,” “like I’m nothing.”
The next level of the pyramid (stage 2) consists of the general syndromal description of the condition; for example, people with (hypothetical) Syndrome X typically experience olfactory hallucinations, memory loss, impaired calculation, and loss of taste. At the syndromal level, we usually have evidence that these signs and symptoms reliably “hang together” over long periods and in geographically distant populations.
The next level (stage 3) consists of what I call the proto-disease. By now, we have characterized the syndrome in terms of usual course, outcome, comorbidity, familial pattern, and response to treatment. We may also have preliminary data on pathophysiology and biomarkers, and a more specific understanding of the afflicted person’s phenomenology.
By stage 4, the condition has moved from proto-disease to specific disease, for which there is a known pathophysiology, cause, specific set of biomarkers, and (in some cases) inheritance pattern. Phenomenology is well characterized at this stage.
Finally, in stage 5 (“fully realized disease entity”), we are able to specify the precise chromosomal and biomolecular etiology, and the phenomenology, for all disease subtypes. (The term “biomolecular etiology” should not be construed as precluding a role for social and psychological factors, however). Clearly, stage 5 is theoretically possible but rarely achieved, even in most areas of general medicine. A syndrome (at stage 2) may ultimately yield 2 or more specific disease entities at stages 4 and 5; for example, “anemia” ultimately resolves into B12 deficiency anemia and iron deficiency anemia.
Also note that “phenomenology”-the patient’s felt experience-enters into all stages of the evolution of the disease entity (hardly a feature of the present DSM framework). There is no contradiction between biological and phenomenological data in this pluralistic model. Rather, these are complementary modes of analysis and observation, each enhancing our understanding of a disease entity. Indeed, in principle, nothing in this model would preclude a purely phenomenological set of criteria for a given disease; however, I believe the pluralistic approach taken here strengthens the evidentiary foundations of our nosology. (I am grateful to Dr Nassir Ghaemi for pointing out affinities between my approach and the “biological existentialist” approach of Karl Jaspers).
Validating our disease categories
While the designation “disease” may involve both subjectivity and “values,” there are, nevertheless, empirically based parameters that help us gauge the soundness of our judgment. As pathologist L. S. King15 observed over 50 years ago:
"A [disease] pattern has reasonable stability only when its criteria are sharp, its elements cohere, and its utility in clarifying experience remains high."
The key here is the phrase “clarifying experience.” King is pointing to the instrumental function of disease classification-what the pragmatist philosopher and psychologist William James would have termed the “cash value” of the concept. If, in the long run, a particular disease category fails in its instrumental function, then it ceases to be a useful category-even if it is grounded in molecular biology of the most sophisticated sort. And what instrumental functions should a disease category serve? First, the criteria for “Disease X” must be “sharp” enough to distinguish its sufferers from those with Disease Y or Z. Its “elements” must cohere, in the way we would expect the pieces of a jigsaw puzzle to fit together. For example, if Disease X is defined by the presence of auditory hallucinations, dry skin, elevated blood pressure, and tremor, one would expect high degrees of concordance and overlap among these features. One would also expect a good correlation between this symptom picture and the course, outcome, and response to treatment of Disease X. Finally, the overall construct of Disease X should allow us to understand the life experience of those who suffer with it: not only what these patients suffer, but how and why.
Readers may protest that very few current psychiatric disorders meet these idealized tests of utility-and I would agree! Taylor and Fink3 have argued that their construct of melancholia amounts to a “definable syndrome,” but their data on pathophysiology suggest that melancholia may already be at the level of a “proto-disease” (stage 3). This is roughly where I would place schizophrenia and bipolar disorder, although some would argue that they are still at the syndromal level.16
That few current DSM diagnoses would qualify for stage 4 (much less stage 5) of my schema does not render them “myths.” Rather, it means that we have our work cut out for us as we try to “elevate” each diagnostic category toward the top of the evidentiary pyramid. Based on this pyramidal model, I have argued that 2 diagnoses proposed for DSM-V-namely “Pathological Bigotry”17 and “Internet Addiction”18-fall well short of the threshold for specific disease or disorder in our present state of knowledge.
We shall see how the framers of DSM-V judge these matters. My hope is that the model described here will at least serve as a rough guide to what should and should not “count” as specific psychiatric disease entities.
Acknowledgments: The author would like to thank Robert Daly, MD, Nassir Ghaemi, MD, and Derek Bolton, PhD, for their helpful comments.
References:
1. Fulford KWM, Thornton T, Graham G, eds. Oxford Textbook of Philosophy and Psychiatry. New York: Oxford University Press; 2006.
2. Horwitz AV, Wakefield JC. The Loss of Sadness: How Psychiatry Transformed Normal Sorrow Into Depressive Disorder. Oxford, UK: Oxford University Press; 2007.
3. Taylor MA, Fink M. Melancholia: The Diagnosis, Pathophysiology and Treatment of Depressive Illness. Cambridge, UK: Cambridge University Press; 2006.
4. Gallagher S, Zahavi D. The Phenomenological Mind: An Introduction to Philosophy of Mind and Cognitive Science. London: Routledge; 2008.
5. Schwartz MA, Wiggins O. Science, humanism, and the nature of medical practice: a phenomenological view. Perspect Biol Med. 1985;28:331-366.
6. Ghaemi SN. Feeling and time: the phenomenology of mood disorders, depressive realism, and existential psychotherapy. Schizophr Bull. 2007;33:122-130.
7. Szasz TS. The Myth of Mental Illness: Foundations of a Theory of Personal Conduct. New York: Hoeber-Harper; 1974.
8. Pies R. On myths and countermyths: more on Szaszian fallacies. Arch Gen Psychiatry. 1979;36:139-144.
9. Pies R. Moving beyond the “myth” of mental illness. In Schaler JA, ed. Szasz Under Fire. Chicago: Open Court; 2004:327-353.
10. Schulte J. Wittgenstein: An Introduction. Brenner WH, Holley JF, trans. Albany, NY: State University of New York Press; 1992.
11. Wittgenstein L. The Blue and Brown Books. New York: Harper & Row; 1958.
12. Kendell RE. The concept of disease and its implications for psychiatry. Br J Psychiatry. 1975;127:305-315.
13. Natanson M, Strauss EW, Ey H. Philosophy and psychiatry. In: Natanson M, ed. Psychiatry and Philosophy. New York: Springer-Verlag; 1969:85-100.
14. Daly RW. A theory of madness. Psychiatry. 1991; 54:368-385.
15. King LS. What is disease? Philos Sci. 1954;21:193-203.
16. McHugh PR, Slavney PR. The Perspectives of Psychiatry. Baltimore: Johns Hopkins University Press; 1983.
17. Pies R. Is bigotry a mental illness? Psychiatric Times. 2007;24(6). http://www.psychiatrictimes.com/ display/article/10168/55226. Accessed March 2, 2009.
18. Pies R. Should DSM-V designate “Internet Addiction” a mental disorder? Psychiatry (Edgemont). 2009;6:31-37.
For further reading:
Ghaemi SN. The Concepts of Psychiatry: A Pluralistic Approach to the Mind and Mental Illness. Baltimore: Johns Hopkins University Press; 2003. [See especially Dr Ghaemi’s discussion of “The Essentialist Fallacy” and the work of psychologist Peter Zachar and philosopher Daniel Dennett.] Ghaemi SN.
On the nature of mental disease: the psychiatric humanism of Karl Jaspers. Existenz. 2008; 3:1-9. Lloyd GE. Hippocratic Writings. New York: Penguin Books; 1978:71.
