Benjamin Smart’s short philosophical volume is a model of clarity for students, teachers, and practitioners in relevant domains, beyond philosophy, of anthropological and psychological, bio-medical and socio-cultural research. The four key chapters of Concepts and Causes in the Philosophy of Disease, although brief, are tightly integrated. Indeed, Smart wastes no time pursuing a set of salient debates about the nature of disease and its cause in the three major contexts of medical practice and enquiry: the clinical, the pathological, and the epidemiological. We shall firstly consider the wider context of this short monograph before briefly examining its key strategies. We shall then conclude by outlining a crucial implication of Smart’s approach to disease for mental disorders.

                                                            I

The Anglophone world uses a cacophony of terms to convey ailments that are or should be able to be mitigated if not fully cured medically, be it remedially or preventively, pharmaceutically or surgically. In common discourse, talk of disease readily emerges when referring to abnormality and disorder, affliction and distress, disability and degeneration, disturbance and infection, defect and illness, decay and morbidity, without including a plethora of colloquial expressions. Such a network of terms appears to traffic between bodily and mental ailments. This sheer variety of terms may, on the one hand, signal an assumption that loss of health is itself variable, which, if short of being clearly chronic or terminal, admits of gradations or degrees, or the variety may, on the other hand, testify to highly heterogenous if not conflated conceptions at play.

Presumed rather than probed by Smart, the medical curriculum over the last four or five generations, largely initiated by William Osler in North America and Archibald Garrod in Britain, has kept practitioners focused upon the nature, cause, and treatment of disease as exemplified by the former’s 1892 The Principles and Practice of Medicine. Osler’s text is divided into eleven sections devoted to corporal diseases, ranging from the infectious to the parasitic in which circulatory, digestive, and muscular, nervous, respiratory, and vascular systems receive close attention. Although the findings of his colleagues and recent predecessors are synthesized, Osler’s discussion of the “what” of disease is removed from the “when” and “where” of it. In other words, he is not particularly concerned with its historical identification and categorisation, let alone its geographic and ethnic occurrence.

What emerges from the above background sketch is the choice still confronting philosophers. To what extent should they, for example,

* analyse the actual conceptions of practitioners or patients or both or reframe these from the perspective of relevant theorists?

* examine stipulated and shifting as well as metaphorical and technological concepts and their instantiations in medical practice and theory?

* justify the theoretical and/or practical demarcations between being healthy and not being healthy or between being diseased and not being diseased?

* explicitly focus their investigation into present and/or past medical practice and theory as, say, an epistemological or ethical, a logico-linguistic or metaphysical enquiry, or as some combination of them?

Although readers of Metapsychology can readily modify the choices listed, these should enable us to clarify the tack taken by Benjamin Smart.

                                                           II

Chapter One reveals Smart’s overall strategies. It questions “what, for the clinician, is disease?”; a question “necessary to demarcate the diseased from the healthy” whether in personal or familial, economic or legal, or other related institutional contexts (6). Three recent conceptions are immediately confronted: those associated with Rachel Cooper, Peter Schwartz, and Jerome Wakefield.

Cooper upholds a threefold set of individually necessary and jointly sufficient criteria for disease. The first criterion regards disease as deleterious for the individual affected; the second, the individual is “judged by the uninformed layman” as “unlucky” in the sense of being “worse off than the majority” of individuals of “the same sex and age”; and the third, the condition must potentially be “medically treatable” (7). However, Smart rightly suggests that enough non-pathological counter-examples exist, such as a mistranscribed tattoo (8-9), to undermine Cooper’s thesis.

Schwartz re-visits the nature of mathematical or statistical measurement of physiological characteristics–organs, tissues, cells, etc.–of a large population upon which to erect a normal distribution of its probability. (Historically speaking, bio-statistics basically applies the “normal distribution” or “bell curve” associated with the 1809 Theoria Motus by Carl Friedrich Gauss and the 1814 edition of Théorie analytique des probabilités by Jean-Pierre de Laplace.) Now, where a given characteristic is measured as being beyond two standard deviations from the mean (in effect, 4.55% of the population), it is regarded as dysfunctional and thus diseased. However, a purely statistical approach “faces insurmountable objections” (11). These include, for instance, neglecting improvements in health over the centuries owing to, say, hygiene and nutrition which results in precisely the same proportion of the population remaining healthy at all times. Again, not all physiological characteristics beyond two standard deviations are diseases, such as having supernumerary fingers or toes, nor are all common diseases confined to 4.55% of the population, such as chronic periodontitis which, according to a 1990-2010 global disease study reported in The Lancet of the 15th December 2012, affects over 10% of people worldwide. Accordingly, Schwartz introduced frequency and negative consequences into statistical analysis in accordance with the pathological condition per se rather than with the clinician’s notion of disease or, for that matter, the aetiology, that is, the origin or cause, of that condition (14-15).

Without dismissing Cooper’s “personal” conception of disease nor Schwartz’s “consequential” analysis of disease, Smart turns to the aetiological underpinnings of Wakefield’s efforts to define disease as harmful dysfunctions (14ff.). The task at hand is to incorporate an aetiological conception of the natural or evolved function of physiological characteristics into an evaluation of what comprises their being or becoming diseased. Here, Smart basically adopts Mahesh Ananth’s distinction between naturalist and normative conceptions of health (detailed in the latter’s 2008 volume, In Defense of an Evolutionary Concept of Health) both of which appear in Wakefield’s March 1992 contribution to American Psychologist.There, a twofold definition of disorder is articulated (in which “mental disorder” is “a special case” (1992: 384)):

A condition is a disorder if and only if (a) the condition causes some harm or deprivation of benefit to the person as judged by the standards of the person’s culture (the value [or normative] criterion), and (b) the condition results from the inability of some internal mechanism to perform its natural function, wherein a natural function is an effect that is part of the evolutionary explanation of the existence and structure of the mechanism (the explanatory [or naturalist] criterion) (17, citing 1992: 384).

Whereas the normative criterion accommodates the clinician’s practical understanding that “two people with the same physiological condition can differ with respect to disease status” (17), Wakefield’s naturalist criterion according to Smart fails to accommodate acquired or non-inherited disorders nor can it identify the boundary or boundaries between health and dysfunction.

          Smart concludes Chapter One by rectifying Wakefield’s need to supply “an account of dysfunction” within his naturalist criterion (19). This is succinctly done by substituting “dysfunction” with physiological characteristics–measures of blood pressure, insulin, etc.–and the “degree of harm/benefit”–negative or positive consequences in Schwartz’s epidemiological account above–associated with them (19). In other words, instead of talking in terms of “the inability of some internal mechanism to perform its natural function” in the second criterion for disease, Smart would have us talk of “an internal mechanism performing its natural function,” but “at a harm-causing level of efficiency” which is “bad for the individual” (19).

So, what is the concept of disease from the clinician’s perspective? No more and no less than the presence of a harmful function, a conception that is explicitly normative or “inherently value-laden” (23). At this juncture of his account, what Smart seems to omit from his synthesis of Wakefield and Schwartz is the distinction between disease and risk (cf. 64 & 77). Schwartz in his 2008 paper “Risk and Disease” questions whether physiological characteristics such as hypertension and hypercholesterolemia, obesity and osteoporosis are simply pathological diseases as such or risk factors for contracting a pathological condition.

III

Having seen how Smart initially orients his readers, let us briefly summarise the purpose of his three remaining chapters before concluding with its implications for non-physiological disorders. Chapter Two switches to examining what disease is from the pathologist’s perspective. Once again, we find Smart synthesizing epidemiological analyses respectively proposed by Christopher Boorse (24ff.) and Karen Neander (38-39; cf. 14ff.) during the ‘nineties. Disease is no longer identified with harmful natural functions affecting the individual. Rather, it is calibrated aetiologically with reference to the impairment of the natural functions of organisms contributing to individual survival or genetic reproduction of the age and sexual groups of a species deemed by pathologists to have sufficient negative consequences. To that extent, Smart preserves both naturalist and normative facets of disease. The chapter ends with a dual conclusion:

For the pathologist…if a condition is a disease for one, it is a disease for all. The concept of disease, then, is context dependent (40).

Chapter Three turns to the applicability to medical practice and research of three competing philosophical conceptions of causation culled from the Anglo-American analytical tradition. After carefully assessing the more influential lines of analytical argument about causality, Smart contends that the counterfactual approach to causation (“if…then…”) meshes with the demands upon pathologists (45ff.); the dispositional approach (“tendencies”) with clinical practice (56ff.); and the regularity or sufficiency approach not only with epidemiologists but also with the methods of classifying diseases (59ff.). In brief, each major medical domain–the clinical, the pathological, and the epidemiological–operates with a distinctive notion of cause.

Finally, Chapter Four pursues the nature and role of general or multi-factorial causal inferences and measurement of effects within epidemiology with particular emphasis upon modes of “eliminative induction” (73) and falsifiable hypotheses and predictions (81ff.). Whilst so doing, Smart attempts to demonstrate the causal worth of experimental studies as distinct from observational ones. When tracing general causal factors relevant to epidemiological practices, he also upholds the value of supplementing analyses focused upon identifying potential causes and effects with the sufficiency or componential model, especially that of Kenneth Rothman (85ff.) (in his December 1976 commentary in American Journal of Epidemiology (reprinted in its 15th January 1995 issue)). This addition, argues Smart, allows epidemiologists to accommodate differing contexts, be they cultural or socio-economic, as pointedly illustrated by the respective success and failure of the same nutritional programme late last century for mothers and children in Tamil Nadu and Bangladesh (84-86).

          Smart’s construal of disease as a contextually dependent interplay of naturalist and normative considerations leaves open the question of its applicability to what we might view as mental disease or disorder. His one passing remark about the difference between the medical and the mental asserts that, whereas a medical disease is “an empirical matter of fact,” in the case of mental disorders “one need only look at The Diagnostic and Statistical Manual of Mental Disorders (DSM-5)” (31; italics inserted). Leaving aside the furore surrounding the revised categories of the recent 2013 edition of the Manual, the implication seems to be that mental disorders are consensually constructed by representatives of the psychiatric profession at a particular time and place. More generously interpreted, Smart’s philosophical interrogation of the medical domain has also presented us with a potent challenge. Is it possible that his arguments about the nature and cause of physical disease might help us make sense of other, broader dimensions of health and disease, be they spiritual or environmental, emotional or mental?

 

Note:

The copy to hand omits Dominic Murphy (2015) and Daniel Nolan (2005) from the bibliography and has two misprints: “Mackie’s 1973” (63) and “the risk of morbidity…” formula (77) is incorrectly worded in its footnoted version (89, n. 9).

 

© 2018 R.A. Goodrich

 

R.A. Goodrich is affiliated with the A.R.C. Centre for the History of Emotions (University of Melbourne) and the A.D.I. European Philosophy & History of Ideas (Deakin University), co-edits the online refereed arts journal Double Dialogues, and co-ordinates with Maryrose Hall a longitudinal project investigating linguistic, cognitive, and behavioural development of higher-functioning children within the autistic spectrum and related disorders.