Repository URL:
http://philsci-archive.pitt.edu/id/eprint/11444
Author(s):
Benjamin T H Smart
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artifact description
In this paper I untangle a recent debate in the philosophy of epidemiology, focusing in particular on the Potential Outcomes Approach (POA) to causation. As the POA strategy includes the quantification of ‘contrary-to-fact’ outcomes, it is unsurprising that it has been likened to the counterfactual analysis of causation briefly proposed by David Hume, and later developed by David Lewis. However, I contend that this has led to much confusion. Miguel Hernan and Sarah Taubman have recently argued (on the grounds that well-defined interventions are a necessary condition of measuring causal effects) that meaningful causal inferences cannot be drawn from obesity. This paper (and a number of others) prompted Alex Broadbent to criticise the POA conception of causation, accusing two of the four theses its proponents are (supposedly) committed to, of circularity and falsity. Here I scrutinise Broadbent’s claims, and suggest that a Popperian approach to causal inference in epidemiology diffuses both of his objections. However, I move on to argue that the POA’s commitment to granting only manipulable conditions causal-status, renders the position implausible as a conceptual analysis of causation (even when considered from just the epidemiologist’s perspective). That said, I conclude that the strategy the POA employs is an effective tool for effect-measurement in intervention-cases; if it is a conceptual analysis of causation at all, it must be restricted to the causal analysis of manipulable conditions. The POA’s failure to successfully demarcate causal from non-causal conditions simpliciter should therefore not be viewed as a serious threat.

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