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By Benjamin Smart (auth.)

This booklet examines a few vital debates within the philosophy of drugs, together with 'what is disease?', and the jobs and viability of ideas of causation, in scientific medication and epidemiology.

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Universal exposure to a dangerous pathogen) – but this inference is incompatible with the statistical theory, since the level of functional efficiency required to be healthy would drop such that precisely the same proportion of the population were diseased.  Kingma has argued that Schwartz may have failed in this respect (2014, 596).  See Ananth (2008, 181) for further discussion.  Whether or not the appendix is vestigial is, in fact, questionable. Matsushita, Uchida, and Okazaki (2007), for example, conducted a study suggesting that it plays a significant role in the pathogenesis of ulcerative colitis.

The notion of ‘what causation is’ is context dependent, insofar as the pathologist, the clinician, and the epidemiologist must (and do) adopt different conceptions of causation. A complete discussion of the virtues and vices of the conceptual analyses dealt with in this chapter is a book in itself, so I do not set out to convince the reader to adopt any one of the views explicated. I do, however, try to present the most common objections, focusing in particular on those raised by Kerry et al in the context of EBP; where possible, I respond accordingly.

Below is the ‘etiological theory of pathological condition’ (. Note first that the effect for which a physiological subsystem was chosen differs between reference classes – natural selection chose that healthy prepubescent boys cannot reproduce, and natural selection chose that adult men can. Clause 2 refers to the ‘reference class relative effect for which that trait was selected’. This covers the need for the natural function(s) of some traits to differ between reference classes.  The reference class is a natural class of organisms of uniform functional design, specifically, an age group or sex of a species.

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