The capabilities approach to health and social justice: moving from the individual/bio-medical or natural scientific level of causation to supra-individual/social or social scientific causal pathways

In a previous post, I promised we would examine Sridhar Venkatapuram’s “impressive and urgent book,” Health Justice: An Argument from the Capabilities Approach (Polity Press, 2011). I’m not prepared to do that quite yet, but I do want to share with you something from his book on the limitations of the “bio-medical” model of health and the corresponding need to change the prevailing epidemiological paradigm in modern medicine, which is “substantively linked to the notion of disease.” The “bio-statistical theory of health” ensconced in this epidemiology “is the informational engine of medical care and public health.” Venkatapuram’s “capability approach” to health and health justice (which entails a ‘conception of health as a meta-capability to achieve a cluster of basic capabilities and functionings’) endeavors to transcend (thus not eliminate) the “dominant biomedical and risk factor model of disease causation and distribution” in its role as the overarching theory that, in turn, governs this epidemiology. In his words,

“…as it currently stands, the dominant explanatory model in epidemiology is significantly constrained even in explaining diseases. It is not able to explain fully the causation and distribution of diseases most prevalent in developed economies, namely chronic and degenerative conditions. The current paradigm is not providing satisfactory explanation for all the observable facts of disease and its social distribution patterns. [….]

Three specific limitations of the prevailing model of disease aetiology are often at the centre of debates about the ‘paradigm crisis’ in epidemiology. These include its level of analysis, its inability to recognize distribution patterns, and its partially informed recommendations for policy. The current model, which evolved from the late-nineteenth-century germ theory of disease, recognizes three categories of causal factors. These factors include biological endowments, behaviours and external exposures to harmful substances or ‘agents.’ The resulting limitation of this model is that it operates only a single level, at the individual level, and expresses a form of explanatory individualism. Short causal pathways confined to the human body are studied, while the model precludes recognizing and supra-individual level factors or social processes as part of the longer causal chain in the production of disease. As a result, the model studies individuals in a vacuum and disconnected from other individuals; it is only focused on what happens on and within the skin of individuals.”

The significance of the “level” of causal analysis, in this case, as “supra-individual level factors or social processes,” was in fact appreciated in some quarters in the early nineteenth century. In doing research for my latest bibliography on “philosophy, psychology and methodology for the social sciences,” I came across the following passage from Richard W. Miller’s unduly neglected or under-appreciated work (inferred from the comparatively few references found in the literature), Fact and Method: Explanation, Confirmation and Reality in the Natural and Social Sciences (Princeton University Press, 1987):

“In the organized pursuit of explanation, practical concerns may…dictate choice of a standard causal pattern. In the early nineteenth century, many investigators had come to explain the prevalence of certain diseases in certain places as due to filth and overcrowding. For example, the prevalence of tuberculosis in urban slums was understood this way. In these explanations, the microbial agent was not, of course, described. But the causal factors mentioned were actual causes of the prevalence of some of those diseases. If Manchester had not been filthy and overcrowded, tuberculosis would not have been prevalent. On the purely scientific dimension, acceptance of accurate environmental explanations probably did not encourage as many causal ascriptions as would a standard requiring explanation of why some victims of filth and overcrowding became tubercular, some not. Those who pressed the latter question were to lead the great advances of the germ theory. But in a practical way, the environmental explanations did a superior job, encouraging more important causal accounts. Guided by those accounts, sanitary measures produced dramatic reductions in tuberculosis and other diseases, more dramatic, in fact, than the germ theory has yielded. A perspicacious investigator might have argued, ‘We know that some specific and varied accompaniment of filth and overcrowding is crucial, since not every child in the Manchester slums is tubercular. But we should accept explanations of the prevalence of disease which appeal to living conditions. For they accurately, if vaguely, describe relevant causal factors, and give us the means to control the prevalence of disease.” [emphasis added]

Incidentally, Paul Thagard’s fairly sophisticated model of “disease explanation” as “causal network instantiation,” elaborated in his book How Scientists Explain Disease (Princeton University Press, 1999), includes a possible causal role for environmental factors, but the concept and meaning of health as such is not addressed, the implication being that disease is simply the converse of health (along with illness or, socially speaking, sickness), namely, “ill-health” (understood as an instance of a clinically identifiable biological pathology). As we will see at a later date, Venkatapuram’s capabilities approach to health spells out a normatively robust conception of health and well-being that is far more than the mere converse of “ill-health,” however important that life condition remains indicative of a significant social achievement.