Diseases are Not Adaptations and Neither are Their Causes
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DISCUSSION
Diseases are Not Adaptations and Neither are Their Causes A Response to Ardern’s "Dysfunction, Disease, and the Limits of Selection" (Biological Theory 13:4–9, 2018) Paul E. Griffiths1 · John Matthewson2 Received: 25 February 2020 / Accepted: 3 April 2020 © Konrad Lorenz Institute for Evolution and Cognition Research 2020
Abstract In a recent article in this journal, Zachary Ardern criticizes our view that the most promising candidate for a naturalized criterion of disease is the "selected effects" account of biological function and dysfunction. Here we reply to Ardern’s criticisms and, more generally, clarify the relationship between adaptation and dysfunction in the evolution of health and disease. Keywords Disease · Dysfunction · Function · Selected effects In a recent article in this journal Zachary Ardern (2018) has questioned our view that the best prospect for introducing an objective, biological criterion into a definition of disease is to make use of a "selected effects" account of biological function and dysfunction (Griffiths and Matthewson 2018). Ardern argues that (1) small effective population sizes in hominin lineages make it unlikely that the genetic bases of disease are the result of natural selection, (2) that both the genetic basis of disease and the selective history of disease variants are likely to be “experimentally intractable” (2018, p. 4), and (3) that some diseases have been positively selected for, or at least have not been selected against. We welcome Ardern’s introduction of more biological detail into the debate over definitions of disease, something we called for in our paper. However, his criticisms reveal that he has misunderstood both our specific proposal and the relationship between adaptation and disease more generally. Diseases are not adaptations. Nor, except in some specific cases, are the causes of disease adaptations. Moreover, as we will demonstrate below, a causal factor that makes the difference between a normal, functional phenotype and its * Paul E. Griffiths [email protected] 1
Department of Philosophy and Charles Perkins Centre, The University of Sydney, Sydney, NSW, Australia
School of Humanities, Massey University Auckland, Auckland, New Zealand
2
dysfunctional alternatives need not be an adaptation for producing the normal phenotype. When these three points are clarified, it will be seen that the genomic findings Ardern introduces to the discussion are entirely consistent with our view. Beyond any specific disagreement we may have with Ardern, this is an opportunity to clarify the relationship between adaptation and disease and to highlight what appear to be common misapprehensions about that relationship. We begin by restating the central claims made (and not made) in our paper, and then turn to address Ardern’s three points.
What We Claimed About Dysfunction and Disease Griffiths and Matthewson (2018) outlined the selected effects account of function and dysfunction, and defended its use as the naturalistic component in de
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