[Same disclaimer as before: some of the following gets pretty technical, sorry guys, but we are talking professional philosophy here...]
Just two speakers for this symposium: Justin Remhof (University of Illinois-Urbana), on “Nietzsche’s reconception of science: overcoming nihilism,” and Robert Northcott (University of Missouri-St. Louis) on “Rethinking genetic drift.”
We start with Remhof. There are apparently two views of Nietzsche’s understanding of science: either in terms of scientific naturalism and its power to discover things about the world, or in terms of science as inherently nihilistic (jee, you think? Nietzsche as a nihilist?).
Remhof is going to argue that for Nietzsche science is actually life-affirming, as opposed to Christian-inspired nihilism. The basic idea is that determinate truths (coming from religion) are life-denying because they cannot be satisfied (i.e., verified). Science, on the other hand, is life-affirming because it is comfortable with the indeterminacy of our truths about the world.
I am not a Nietzsche scholar by any means, but I find it uncomfortable to put “science” in the same paragraph as words like “life-affirming reconception of ontology,” “will to power ontology,” or “extensionally individuated.” But that’s just me and my instinctive skepticism about anything that smells too much of continental philosophy...
Ok, an example straight from Remhof’s outline, seemingly quoting Nietzsche:
“If I make up the definition of a mammal, and then, after inspecting a camel, declare ‘look, a mammal,’ I have indeed brought a truth to light in this way. ... “[This] contains not a single point which would be ‘true in itself’ or really and universally valid apart from man.”
Hmm, really? It seems to me that a mammal remains a mammal whether or not there are men around to verify that fact. It is trivially true that without humans around nobody would conceptualize what a mammal is, or that the term “mammal” is linguistically arbitrary, but that’s not what Nietzsche is saying. “Mammals” are in fact an objective truth about the world, specifically they are a particular phylogenetic lineage of organisms on planet earth, with a given history and a number of non-arbitrarily distinctive features (despite the existence of Platypi).
More explicitly, again Remhof presumably quoting or paraphrasing Nietzsche:
“‘Truth’ is therefore not something there, that might be found or discovered — but something that must be created and gives name to a process ... [it is an] active determining — not a becoming conscious of something that is in itself firm and determined.”
No, no, no. Truth is something “out there,” and the only sensible discussion is about the epistemic limitations of human beings, which make it so that we can rarely be certain of the truths we think we discover. We don’t create truth, we discover it (partially, under certain conditions, using some methods, of which science is certainly a primary one).
One more perhaps obvious comment: it seems to me that “life affirming” and “life negating” are not attributes that are properly applied to science. Science’s object, unlike religion, is not to help us figure a way out of nihilism — that’s the job of philosophy!
[Incidentally, the talk referred to above is “philosophy of science” in a fairly non-standard sense of the term, from my experience.]
And now to Northcott and drift, a surprisingly controversial topic in both evolutionary genetics and philosophy of biology, about which I have written in collaboration with Jonathan Kaplan. So, generally speaking, drift is a sort of population-level “sampling error” that creates random fluctuations in gene frequencies as a result of the finiteness of the size of biological populations. (This is directly analogous to the observation that short runs of coin-flipping do not typically result in exactly 50-50 outcomes of tail and head, again because the run is short and subject to stochastic outcomes.)
According to Northcott “selection probabilities leave out many idiosyncratic [causal, as opposed to systematic] factors. The ‘sampling error’ presumed to generate drift is the result of these latter factors.”
So, we can think of drift as an outcome (instead of a process), but outcomes cannot explain themselves, so we still need a causal explanation of the outcome of drift.
Another thought is that drift is a sort of causal dustbin, something that captures the action of all factors the effects of which are not captured by selection probabilities. The problem here is that drift then becomes a placeholder for unknown causes.
A third possibility is to conceptualize drift as indiscriminate sampling (as opposed to the discriminate sampling of natural selection). This is hardly better than the dustbin scenario, since whatever factors are responsible for such indiscriminate sampling remain unknown.
Northcott puts forth the view that the real causal factor is in fact population size itself, which needs to be distinguished by other non-selective factors. He points out, though, that if in a given population we start with two alleles (A and B) at equal frequencies, and there is no selection going on, and A drifts to fixation, this is not fully explained by drift-as-finite population size because that level of population size is also compatible with B going to fixation instead.
Generally speaking, Northcott takes the currently standard view that explanations are contrastive (X rather than Y explains Z) and admits of degrees of explanation. One can in fact use probability theory to calculate an explanatory score, or degree of explanatory strength for each proposed contrast (equations provided in the paper by the author).
Applying this approach to the example of the A,B alleles above (where the explanatory contrast is between finite and infinite population size), Northcott concludes that finite population size only weakly explains why A goes to fixation rather than B, but it fully explains why either A or B will go to fixation without selection.
I actually like Robert’s approach, but some fundamental questions remain, it seems to me: in what sense, precisely, is population size a causal factor in (as opposed to just being a correlate of) changing gene frequencies? And, as the calculation above clearly shows: what other factors do explain why a particular allele rather than another goes to fixation?
