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Two arguments for the etiological theory over the modal theory of biological function


This paper contains a positive development and a negative argument. It develops a theory of function loss and shows how this undermines an objection raised against the etiological theory of function in support of the modal theory of function. Then it raises two internal problems for the modal theory of function.

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  1. A reviewer notes that there are other theories of function that are not subject to Nanay’s criticism; some are amongst the use theories of function described in Jespersen and Carrara (2011). Cummins’ causal role theory is also, arguably, not subject to Nanay’s criticism (McLaughlin 2001). These theories also analyze the functional properties of a token trait at a time in terms of properties of that very token.

  2. This is contested, first, by Kiritani (2011) who argues that using different notions of function on the left and right hand side of the biconditional avoids the charge of vicious circularity; Nanay (2011) objects that this proposal fails to satisfy his desideratum of accounting for malfunctioning token traits. Second, Neander and Rosenberg (2012) argue that a reformulation of the etiological theory eliminates the presupposition of a criterion of trait-type individuation; Nanay (2012) disagrees.

  3. The suggestion that counterfactuals may have true antecedents seems contradictory, though the possibility is widely acknowledged in the literature on counterfactuals. We continue to use the term ‘counterfactual’ rather than the leading alternative, ‘subjunctive conditional’, for consistency with Nanay. Discussions of this terminological problem appear in Lewis (1973), Lycan (2001), Bennett (2003), and many others.

  4. This is another uncomfortable piece of terminology; since the literature does not offer a widely used alternative that is clearly superior, we stick with this option.

  5. Herein lies our simplification. We have defined \(\le \) and accessibility only relative to \(\alpha \). A fully general semantics would define an accessibility relation and a comparative similarity relation for every possible world \(w\in W\) in any model \(\fancyscript{M}\). So the presented model can be thought of as the pointed model \(\left\langle \left\langle W, \le , V\right\rangle , \alpha \right\rangle \).

  6. Not all authors of this paper are convinced that this distinction can be sensibly drawn, but all are willing to admit the possibility for the sake of argument.

  7. We assume that any world that is as similar to \(\alpha \) as \(\alpha \) itself is a relatively similar world according to any explanatory project.

  8. McGee (1985) and Lycan (2001) argue that modus ponens is invalid anyway, though perhaps weakenings of modus ponens hold, such as modus ponens restricted to conditional premises that do not nest other conditionals. Iatridou’s semantics also invalidates this weaker principle, though we will not discuss those principles here.


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We would like to thank Bence Nanay, John Troyer, members of the Lake Geneva Biological Interest Group, and two anonymous referees for their valuable assistance. B. Leahy was supported by DFG Research Group 1614 “What if: On the meaning, relevance, and epistemology of counterfactual claims and thought experiments”. M. Huber was supported by the Swiss National Science Foundation Grant 140885 “Counterfactual Reasoning in Biology”.

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Correspondence to Brian Leahy.

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Leahy, B., Huber, M. Two arguments for the etiological theory over the modal theory of biological function. Synthese 194, 1169–1187 (2017).

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  • Function
  • Function loss
  • Modal theory
  • Counterfactuals
  • Etiological theory
  • David Lewis
  • Ruth Millikan