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The Concept of Causation in Biology

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Abstract

This paper sets out to analyze how causation works by focusing on biology, as represented by epidemiology and by scientific information on how the body works (“physiology”). It starts by exploring the specificity of evolved physiological systems, in which evolutionary, developmental and proximal causes all fit together, and the concept of function is meaningful; in contrast, this structure does not apply in epidemiology (or outside biology). Using these two contrasting branches of biology, I examine the role both of mechanism and of difference making in causation. I find that causation necessarily involves both mechanism and difference making, and that they play complementary roles. Both are seen as ontologically necessary, even if the evidence is not always available for both. Influential monist accounts that focus on one of these, at the expense of ignoring the other, are found to be inadequate on these and on other grounds. Recent attempts to combine them are reviewed, notably that of Russo and Williamson (Int Stud Philos Sci 21:157–170, 2007), and it is argued that their epistemic view requires there to be a source of the different types of evidence that a rational agent would consider, and that this source must be ontic. I then analyze how causal relationships work in evolved physiological systems and in those studied by epidemiology, with a particular focus on how mechanism interacts with input. Finally, I consider this concept of causation from the perspective of everyday language, and of its possible generalisability outside biology.

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Notes

  1. A similar point has been made by Strevens (2007). In addition, doubts have been raised concerning the ability of the manipulationist view to apply to observational statistical studies in social science (Russo 2012), an argument that would also apply in the case of epidemiology.

  2. Most obviously, if the component parts of a system link together neatly, an additional causal account of this neatness is required. Evolution or design could achieve that, but his account would then be limited to physiology and to technology in the broadest sense—a limitation that surely needs to be highlighted. He has more recently recognised “ephemeral mechanisms”, e.g. in a chain of historical events (Glennan 2010a), but does not explicitly acknowledge the impact of this realisation on his fundamental conception.

  3. See also Illari and Williamson (2012).

  4. Bechtel also draws on Palmer and Kimchi, who take a more “complex systems” view, which involves decomposition into ever-smaller parts, ending with the simplest components that have a physical embodiment (structure) and a function; they identify the difference making with the transformation of input information to output information at system level. This is similar to my conception of causal systems, that takes the individual causal link as the primary focus, with a bottom-up view of system behaviour as composed of these links.

  5. Time order is thus assumed in this account, rather than explained.

  6. A similar characteristic is found in purposive creations, notably technology—as in the examples of a clock or a lock and key commonly found in the philosophical literature on mechanisms. “Ephemeral mechanisms” (Glennan 2010a) do not have this characteristic. The evolved or designed nature is what has given rise to the idea that mechanisms must be complex, but it is not even true of all technology: the mechanism by which a piano produces its sound is indeed complicated, but the mechanism of a clavichord key depends just on a simple pivot.

  7. It does form part of a system in the sense of a chain of causal links, and a control mechanism, in the apparatus for its synthesis and release. But this is not part of its mechanism of action.

  8. For example, animal experiments have shown that anti-androgens that interfere with testosterone synthesis can impair male development in utero (Fisher et al. 2003). This has been suggested as having caused the large rise in testicular cancer in some populations during the twentieth century. However, the health effects in the animals are small unless exposures are used that are far higher than real human exposures; furthermore, exposures to these substances began too late to explain the start of the rise in cancer (Joffe 2010). The mechanism is plausible but the difference-making evidence shows that something else must be causing (most of) the observed trend.

  9. “… not in the logical relationship between … descriptions but in the causal relationship between the parts of the mechanism …” (Glennan 2002).

  10. The distinction between responsive and continuous mechanisms is also made by Glennan (2002) who refers to “input–output mechanisms”, and by Bechtel (2008), who makes continuous mechanisms—in the mental-mechanism context, “acting”—central to his argument.

  11. In physics, the phenomenal success of mathematics has arguably led to the neglect of causation and especially of mechanism: sometimes it is too obvious to mention, as when one object collides with and moves another. In other cases it is totally obscure, the prime example being Newton’s law of gravitation, which established the difference-making relationship but postulated instantaneous action at a distance, an idea as fanciful as any in quantum theory. In terms of mechanism, then, this theory was deficient until Einstein completed it—not overturned it, as is sometimes thought. Thus, the view arose that the idea of causation adds nothing to the equations and therefore is superfluous (Russell 1913; Norton 2009). This makes it a bad model for other sciences.

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    Michael Joffe

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Joffe, M. The Concept of Causation in Biology. Erkenn 78 (Suppl 2), 179–197 (2013). https://doi.org/10.1007/s10670-013-9508-6

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