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Understanding mechanisms in the health sciences

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Abstract

This article focuses on the assessment of mechanistic relations with specific attention to medicine, where mechanistic models are widely employed. I first survey recent contributions in the philosophical literature on mechanistic causation, and then take issue with Federica Russo and Jon Williamson’s thesis that two types of evidence, probabilistic and mechanistic, are at stake in the health sciences. I argue instead that a distinction should be drawn between previously acquired knowledge of mechanisms and yet-to-be-discovered knowledge of mechanisms and that both probabilistic evidence and manipulation are essential with respect to newly discovered mechanisms.

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Notes

  1. For a general introduction to mechanistic accounts, see, for instance, Stathis Psillos [4] and S. Glennan [5].

  2. A world line is, in turn, defined as ‘the collection of points on a spacetime diagram that represents the history of an object. This means that processes are represented by elongated regions, or “worms” in spacetime’ [9, p. 90].

  3. Machamer, Darden, Craver, and Glennan have been labeled as ‘neo-mechanists’; see Faucher [14].

  4. See Campaner [15].

  5. A different view is supported by Daniel Sirtes [16], who has been developing a ‘pragmatic-ontic account of mechanistic explanation’.

  6. While criticizing the most recent revival of the mechanistic approach, and especially Machamer, Darden, and Craver’s notion of ‘activity’ as ‘far too opaque’, Schaffner admits that he has ‘frequently utilised references to “mechanisms” as another way to describe the “models” that are so widely found in biology, and which function broadly as surrogates for theories in the biomedical sciences’ [18, p. 398].

  7. For some remarks on Salmon’s view, see Galavotti [24, esp. pp. 236–237]; for some criticisms on his theory, see Hitchcock [25, 26].

  8. The role of interventions in the assessment of mechanistic relations has been discussed by Machamer, Darden, and Craver in various contributions; see, for instance, Darden and Craver [30], Machamer [31], Craver [32]. These scholars conceive of interventions mainly in a counterfactual sense. On this, see Campaner [33] and Campaner and Galavotti [34].

  9. I thank Prof. Vineis for drawing my attention to this example. Mycotoxins are a broad class of toxic fungal metabolites estimated to contaminate up to 25% of the world’s food supplies. One potent group of mycotoxins are the aflatoxins, which are secondary metabolites of Aspergillus flavus (aflatoxins B1 and B2) and Aspergillus parasiticus (aflatoxins B1, B2, G1, and G2), aflatoxin B1 (AFB1) being the most common. They are present as mixtures in food (cereals, figs, oilseeds, nuts, tobacco, etc.), which work as substrates that allow for the growth and production of aflatoxin by aflatoxigenic moulds and are especially frequent in developing countries.

  10. See, for instance, Strosnider et al. [35]; Williams et al. [36]; Wang and Tang [37]; Bennett and Klich [38]. Investigating the role that aflatoxins can play in the pathogenesis of hepatocellular carcinoma presents a number of difficulties. It is complicated to differentiate the influence of aflatoxins from that of HBV, to understand how representative the sampling of dietary components is at the population level, to estimate precisely human exposure, and, more generally, to collect data in the most affected countries (the poorest in the world). The use of animal models in studying aflatoxin carcinogenicity is controversial; see, for instance, Cardwell and Henry [39]; Montesano et al. [40]; Sylla et al. [41]; Turner et al. [42].

  11. For some critical discussion of the adoption of Hill’s criteria, see, for instance, Charlton [47], Weed [48], and Wynder [49].

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  1. Department of Philosophy, University of Bologna, Via Zamboni 38, 40126, Bologna, Italy

    Raffaella Campaner

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Campaner, R. Understanding mechanisms in the health sciences. Theor Med Bioeth 32, 5–17 (2011). https://doi.org/10.1007/s11017-010-9166-5

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