I am preparing a paper for what looks like a very promising workshop to be held in May at the Konrad Lorenz Institute for Theoretical Biology near Vienna, on the topic of causes and processes in biology. The workshop is organized by Kevin Laland (St. Andrews, UK) and Tobias Uller (Lund, Sweden), and aims at initiating close interaction and exchange between philosophers of science and biologists to reflect on the nature of causation in biological evolution. The Extended Evolutionary Synthesis — a project in which I am involved — has a different perspective on causation in evolution, and ascribes evolutionary significance to a greater range of processes, than traditional perspectives. As the organizers put it, “the workshop will set out to scrutinize these claims, with both philosophers (acting as independent arbiters) and non-project members (including non-sympathizers) present to ensure good debate.”
My talk will be on “Causality and the role of philosophy of science,” and while preparing the accompanying paper I ran into a very interesting contribution to the debate on causality by Carl Craver and William Bechtel, entitled “Top-down causation without top-down causes.” I think readers of this blog will be interested, so I’m going to present a summary of the Craver and Bechtel paper, with a little commentary to draw out its more general lessons.
Biologists and other scientists often talk about “top-down” causation, apparently without concern for the fact that physicists don’t seem to recognize any such category of causal interactions, instead seeing everything from a bottom-up perspective (which, as we shall see, turns out to be equally problematic!).
The topic often comes up in discussions about free will and determinism, even though as I’ve argued elsewhere, determinism is entirely irrelevant to the issue of free will. Besides, I tend to be agnostic concerning the question of whether we live in a deterministic universe or not, since that depends on how one thinks of the implications of quantum mechanics for the question (my understanding — and I’m not a physicist — is that q.m. equations are deterministic, and yet q.m. phenomenology appears to be irreducibly stochastic). I do, however, subscribe to the existence of universal cause and effect (meaning that every phenomenon has causes), so causality is an important topic for me.
Philosophers are not necessarily wedded to one view or the other about the existence of top-down causation, but are obviously very much interested in the nature and manifestations of causality. They are also typically cautious not to unnecessarily multiply entities or levels of description, attempting to keep their ontology as sparse as it is possible given the actual structure of the world, as W.V.O. Quine maintained we should.
Craver and Bechtel provide a splendid example of rigorous philosophical analysis of the issue, arriving at a sensible position that they, somewhat paradoxically, term top-down causation without top-down causes, whence the title of their paper. These authors’ concern is that when scientists invoke top-down (or bottom-up) causation they call upon a concept that is either incoherent or implies the existence of “spooky” forces that wholes somehow exert over their components (or vice versa).
Their solution to the problem is to grant that talk of top-down or bottom-up causation is perfectly legitimate as a shortcut, as it captures a number of observable relationships between the activities of wholes and the behaviors of (some of) their parts, but they recast the explanation of what is going on in such cases as not actually consisting (entirely) of causal relations. Rather, Craver and Bechtel propose to think in terms of mechanistically mediated effects that are themselves hybrids of two components: i) intra-level causal relationships, and ii) inter-level constitutive relationships.
[Before you ask, yes, they discuss in detail what they mean by “level,” limiting themselves to levels of mechanisms acting in any particular case. They also provide a discussion of different accounts of causality to argue that only intra-level causes are not “spooky.” It will be clearer what they mean when we get through a couple of examples, but the full paper is linked to above, for the reader who wishes to dig deeper.]
Hal the tennis player and top-down causation
Let us consider just one of the several examples of top-down causation presented by Craver and Bechtel in the course of their thorough analysis of the issue. They introduce us to Hal, a tennis player, who steps on the court and begins to serve. While this is happening, at the physiological level the membranes of Hal’s cells absorb the glucose that was at that moment circulating in his blood; once transported inside the cell, the glucose is phosphorylated and bound into molecules of hexosediphosphate.
A very reasonable description of what’s going on — and one that biologists routinely use — is that the fact that Hal, the organism, began to play tennis initiated a cascade of lower level physiological and molecular effects. These processes started because Hal began to play, and so the scenario is a classical example of top-down causation: the behavior of the whole (Hal) has affected the behavior of the parts (cells and metabolites).
What Craver and Bechtel argue, however, is that a more reasonable account of what is going on can rely on a combination of intra-level causation and constitutive effects, doing away with top-down causality altogether. Here is their reconstruction of Hal’s case:
“When Hal started to play tennis, the nerve signals to the muscles caused them to metabolize the available ATP to ADP to provide the energy to contract the muscle cells. The increase in ADP made it available as a receptor for phosphates in high-energy bonds in 1,3-diphosphoglycerate produced at the end of the glycolytic process. This allowed a cascade of reactions earlier in the pathway to proceed, eventually allowing a glucose molecule to take up a phosphate molecule. In this and many similar cases, a change in the activity of the mechanism as a whole just is a change in one or more components of the mechanism which then, through ordinary intra-level causation, causes changes in other components of the mechanism. Hal’s playing tennis is in part constituted by activities at neuromuscular junctions, and activities at those junctions cause, in a perfectly straightforward etiological sense, changes in the organization and behavior of cellular mechanisms. … Once we have described the mechanism mediating the effect, the drive to speak of this as a case of top-down causation vanishes, although such language might be useful as shorthand.”
The heart attack killed the general: bottom-up causation
What about bottom-up causation, so dear to reductionist physicists? Well, that one too is in trouble, for the same reason, i.e., the postulation of inter-level “spooky” causality. Here is one of the examples analyzed by Craver and Bechtel.
Consider a general who is killed by a massive heart attack. Thinking of the general not as someone performing a particular social role in the military, but as a biological being, then it is obvious that the heart is one component, among many, of one of his bodily mechanisms, the circulatory system. A natural way to talk is in terms of bottom-up causation: the failure of the heart causes the failure of the circulatory mechanism, which in turn causes the death of the general. Craver and Bechtel explain:
“By combining an intra-level conception of cause and a constitutive relation between levels, we can provide an unproblematic account of what transpired: we trace the effects of the infarction through the mechanism. When the heart stops beating, it stops transporting oxygen and nutrients to the other tissues of the body, and they cease to function. We thus explain how a variety of physiological mechanisms cease to function. And insofar as that non-functioning constitutes the general’s death, we explain his death. Notice that when we reach the state of the mechanism that constitutes the state of death, we do not say, with Betty Crocker, that it causes death. It just is death. An assassin who charges extra for the general’s death — after charging for the cessation of physiological function — is pulling a fast one. Our hybrid explication thus avoids the temptation to attribute causation between a constituent and the mechanism of which it is part.”
The broader point
Craver and Bechtel discuss several other examples like the ones above, all leading to the same conclusion: any alleged case of top-down or bottom-up causation always resolves into the sum total of two components, intra-level causation plus constitutive effects.
In my mind, Craver and Bechtel’s analysis represents a very good example of one of a series of modes in which philosophy of science aids science (most of it doesn’t, focusing on its broader business of understanding how science works or fails to do so).
In another case I discuss in my contribution to the KLI workshop, concerning the issue of proximate vs ultimate causes in biology (I wrote about that on the blog, here), there was a genuine scientific debate, involving different theoretical positions staked by scientists themselves. Some biologists think that only ultimate causes (natural selection) are necessary to understand evolution, while proximate causes (developmental ones) do not play an evolutionary role. Others argue instead that developmental causes are evolutionarily important and have been neglected so far.
The philosophical analysis carried out by my colleague Raphael Scholl and myself in that case splits the difference, helping to resolve that internal debate among scientists by invoking the concept of explanatory relevance (the idea that of the entire web of causality only certain portions are pertinent to explain any given phenomenon). This allows us to distinguish cases where developmental causes are required in order to understand the evolution of a structure from those cases in which developmental explanations can be backgrounded without loss of explanatory power. Some times it is the one, at other times the other.
In the case of Craver and Bechtel’s paper, instead, there really isn’t much of a discussion or disagreement among scientists who use the concepts of top-down or bottom-up causation, insofar as I’m aware. And yet, there should be! The philosophical analysis here strongly argues for the conclusion that scientists are being sloppy when they engage in either top-down or bottom-up causal talk, since all non-spooky causation can be argued to be intra-, not inter-level. Whether the scientists in question will take heed of the philosophers’ advice is, of course, an entirely different matter, which has to do much more with the sociology of interdisciplinarity than with the merits of the proposal itself.