If there is any value in the idea that disease is something other than the mere absence of health then that value must lie in the way that diseases are defined. Once we move from the knowledge that someone lacks health in respect of their fever and diarrhoea to the knowledge that they have cholera, we are able to make a number of inferences about the likely progression of the disease, the effectiveness of various possible treatments, and the relevance or otherwise of various circumstances (e.g. age, sex) to both these. These inferences depend on the way the disease “cholera” has been defined. They hold across most cases of cholera, but they are not reliable for diarrhoea or fever more generally. And they hold across most cases of cholera because cholera has been defined in terms of a cause that is, by definition, shared by every case of cholera, and is such that, by definition, no case of diarrhoea and fever can be a case of cholera without the cause, however symptomatically similar.

That cause is the presence of vibrio cholerae in the small intestine. K Codell Carter has done an excellent job of bringing out the extent to which the definition of diseases in terms of infectious agents really was an act of definition – a conceptual feat, not something to be settled by empirical evidence (Carter 2003). But this conceptual exercise has fallen out of fashion. The diseases of primary interest to modern medical science are “multifactorial”, meaning that, for whatever reason, they have not been classified according to particular causes. I have argued that multifactorial thinking has been endorsed too enthusiastically, and that there are merits to the old “monocausal” way of thinking about disease – even if the obsession with identifying just one explanatory cause is wrong. My “contrastive” model of disease is intended to retain the benefits of the monocausal model without the implausible commitment to classification in terms of just one cause (Broadbent 2009; a better-expressed version is forthcoming in Broadbent 2013, Ch 10).

An obvious difficulty for my account is that some kinds of ill health, such as instances of particular cancers, seem to be fruitfully treated as belonging together. Yet on my account they cannot be called instances of a disease unless a classificatory constellation of causes is known or at least suspected. (Of course one might prefer to mark the distinction with a word other than “disease”; but my hope is to get at an important distinction without getting tangled in semantic disputes.) This raises an objection of irrelevance: the objection would be that my account lays down distinctions that are irrelevant both to clinical practice and to scientific understanding.

A particular instance of this difficulty arises in the case of cancers that are caused by viruses. For example, cervical cancer seems to be caused by the human papillomavirus in over 90% of cases (Kumar et al. 2007) – but not 100%. According to the logic of my contrastive model of disease, we ought to say that those cases of cervical cancer caused by the virus form a disease – let’s call it “HPV-cancer” – while the small remainder do not. But is this really a good idea, either from a clinical perspective, or from the perspective of advancing our conceptual grasp on the health-condition(s) in question? Conversely, the circumstances in which the virus is sufficient to produce the cancer are not known: HPV infection does not always result in cervical cancer, and it is not known why. According to my contrastive model this means that the notional disease “HPV-cancer” is not well-defined, and that to call it a disease is to express the hope or conviction that some further causes can be found which are jointly sufficient for the development of cervical cancer. This raises questions, again, as to whether such a hope or conviction is very helpful from either a clinical or a scientific perspective; or whether, rather, we are better off thinking of cervical cancer as a multifactorial disease arising from various constellations of causes, and sometimes failing to arise from the very same constellations of causes.

In short, the question is whether a contrastive approach to disease classification really would help either scientific understanding or medical effectiveness, as I have claimed that it would. Cancers caused by viruses present a good case for studying this question because if the recommendations of the contrastive model can be followed for any multifactorial diseases, these are among the most viable candidates.

I’m starting work on a paper in which I attempt to get to grips with some of these questions and to answer this irrelevance objection to the contrastive model of disease. My gut feeling remains that there is an important distinction to be drawn between disease and mere lack of health (thus my starting point is the opposite of that of Boorse 1975). Yet I am not satisfied that I have made clear exactly what this importance is; nor have I given enough thought to exactly what one is supposed to do with cases that do not fit the model. And for the distinction to be important, as I claim, there must always be cases that do not fit the model – that is, there must be cases of ill health that are not disease, otherwise the distinction between them cannot be important. I hope to get further into these issues and I would welcome any thoughts.

Boorse, Christopher. 1975. “On the Distinction Between Disease and Illness.” Philosophy of Public Affairs 5: 49–68.

Broadbent, Alex. 2009. “Causation and Models of Disease in Epidemiology.” Studies in History and Philosophy of Biological and Biomedical Sciences 40: 302–311.

———. 2013. Philosophy of Epidemiology. New Directions in the Philosophy of Science. London and New York: Palgrave Macmillan.

Carter, K. Codell. 2003. The Rise of Causal Concepts of Disease. Aldershot: Ashgate.

Kumar, Vinay, Abul K. Abbas, Nelson Fausto, and Richard Mitchell. 2007. Robbins Basic Pathology. 8th ed. Philadelphia: Saunders Elsevier.