I gave a talk last week at the New College of the Humanities in London. I was aiming for a general introduction to the work of the EBM+ project for a non-specialist audience. This is always an interesting challenge. So much of what philosophers of science do is based on very fine distinctions and disagreements, which makes it a real challenge to give general overviews of the literature (like, here, the difference between mechanisms and evidence of mechanisms). I think that it went really well – lots of interest from the audience, and some intriguing questions. You can read the abstract below.
The aim of this paper is present the core motivation for attempting to characterise quality of evidence of mechanism linking C and E, when attempting to establish whether C causes E in the health sciences. I will also begin to identify a useful approach to such a characterisation.
The first part of the paper will explain why one might – epistemically – value evidence of mechanism linking C and E, as complementary to evidence of correlations between C and E in populations, such as is gained from Randomised Controlled Trials or observational studies. Based on the work of Clarke, Illari, Gillies, Russo and Williamson (2014), the crucial idea is that evidence of mechanism helps address the major weakness of evidence of correlation, i.e. the problem of confounding, or the possibility that C and E are in fact common effects of a third variable, D. In reverse, if you are unsure whether the effect of the mechanism you have identified might be ‘masked’ by the effects of unidentified mechanisms also linking C and E – the major weakness of evidence of mechanism – seeking evidence of a correlation in a population. This means evidence of both correlation and of linking mechanism is complementary in an important way.
The second part of the paper will then focus on two sources of scepticism about evidence of mechanism. The overriding aim is to identify important insights to inform a positive characterisation of evidence of mechanism. The first source is the startling absence of evidence of mechanism from most current medical evidence ‘hierarchies’, with particular reference to the GRADE (2009) system of the National Institute for Care and Health Excellence in the UK. I will examine a mixture of political, historical, and methodological concerns, to disentangle two important lessons: evidence of mechanism should not mean either a mere story about mechanism, which is merely a hypothesis, or knowledge of a complete mechanism, which we almost never have. The second source is various pluralist philosophers, of which I focus on Dupre (2012, 2013). Again, I disentangle two insights: that a characterisation of evidence of mechanism must not be vacuous, nor rigid in ways inappropriate to the life sciences.
In the final part of the paper, I use the four insights to criticise Craver’s (2007) mutual manipulability account of constitutive relevance, interpreted as a story about mechanism discovery. I argue instead that a heuristic approach, deriving from Bechtel and Richardson (1993) is valuable, and indeed offers a reinterpretation of other work by Craver (2006), and by Darden (2006).