Response to Kenneth R. Miller 10:16 PM PDT, July 11, 2007, updated at 11:26 AM PDT, July 12, 2007
Dear Readers,
Here I respond to the unfavorable review of The Edge of Evolution by Kenneth R. Miller in Nature. Like Sean Carroll, whose review in Science I discussed earlier, he employs much bluster. But Miller goes well beyond simple bluster. I overlooked Carroll’s rhetoric and dealt only with his substantial arguments. This time I’ll do things differently. Today I’ll respond to Miller’s substantive points. Tomorrow we’ll take a closer look at his style of argumentation.
After mentioning that de novo resistance to chloroquine is found roughly once in every 1020 malaria parasites, and quoting several sentences from The Edge of Evolution where I note “On average, for humans to achieve a mutation like this by chance, we would need to wait a hundred million times ten million years,” Miller writes:
Behe, incredibly, thinks he has determined the odds of a mutation “of the same complexity” occurring in the human line. He hasn’t. What he has actually done is to determine the odds of these two exact mutations occurring simultaneously at precisely the same position in exactly the same gene in a single individual. ....
Behe obtains his probabilities by considering each mutation as an independent event, ruling out any role for cumulative selection, and requiring evolution to achieve an exact, predetermined result.
Miller makes the same mistake here that I addressed earlier when replying to Jerry Coyne’s response. The number of one in 1020 is not a probability calculation. Rather, it is statistical data. It is perhaps not too surprising that both Miller and Coyne make that mistake, because in general Darwinists are not used to constraining their speculations with quantitative data. The fundamental message of The Edge of Evolution, however, is that such data are now available. Instead of imagining what the power of random mutation and selection might do, we can look at examples of what it has done. And when we do look at the best, clearest examples, the results are, to say the least, quite modest. Time and again we see that random mutations are incoherent and much more likely to degrade a genome than to add to it — and these are the positively-selected, “beneficial” random mutations.
Miller asserts that I have ruled out cumulative selection and required Plasmodium falciparum to achieve a predetermined result. I’m flattered that he thinks I have such powers. However, the malaria parasite does not take orders from me or anyone else. I had no ability to rule out or require anything. The parasite was free in the wild to come up with any solution that might help it, by any mutational pathway that was available. I simply reported the results of what the parasite achieved. In 1020 chances, it would be expected to have undergone huge numbers of all types of mutations — substitutions, deletions, insertions, gene duplications, and more. And in that astronomical number of opportunities, at best a handful of mutations were useful to it.
Miller makes two specific points:
Not only are each of these conditions unrealistic, but they do not apply even in the case of his chosen example. First, he overlooks the existence of chloroquine-resistant strains of malaria lacking one of the mutations he claims to be essential (at position 220). This matters, because it shows that there are several mutational routes to effective drug resistance.
As I wrote in response to Coyne, however, my argument does not depend on any particular amino acid position being required, and in the paper Miller was referring to (Chen et al., 2003, Antimicrob. Agents Chemother. 47:3500-3505, apparently accidentally omitted in the Nature review, according to Coyne) other mutations are found in the malarial strain in which position 220 remained unchanged. Miller says this matters because there are several routes to drug resistance. It matters much less than he implies. Certainly, there may be several routes, maybe permutations of pathways, too. But whether or not there are several routes, the bottom line is that resistance arises only once for every 1020 parasites.
Miller continues:
Second, and more importantly, Behe waves away evidence suggesting that chloroquine resistance may be the result of sequential, not simultaneous, mutations (Science 298, 74–75; 2002), boosted by the so-called ARMD (accelerated resistance to multiple drugs) phenotype, which is itself drug induced.
If you read that paper, however, you find that it presents no “evidence” whatsoever for cumulative mutations; rather, it merely speculates about them. What’s more, the paper makes no mention of the ARMD phenotype, and Miller says nothing about its relevance. Here Miller is simply throwing references and words around, but saying nothing meaningful.
Response to Kenneth R. Miller, Continued 6:28 PM PDT, July 12, 2007
Yesterday, in the first part of my response to Kenneth Miller’s review, in which I addressed his substantive points, I ended by showing that a reference he cited did not contain the evidence he claimed it did. In this final part, I more closely examine Miller’s tendentious style of argumentation.
Speaking of throwing around irrelevant references, Miller writes:
Telling his readers that the production of so much as a single new protein-to-protein binding site is “beyond the edge of evolution”, [Behe] proclaims darwinian evolution to be a hopeless failure. Apparently he has not followed recent studies exploring the evolution of hormone-receptor complexes by sequential mutations (Science 312, 97-101; 2006), the ‘evolvability’ of new functions in existing proteins — studies on serum paraxonase (PON1) traced the evolution of several new catalytic functions (Nature Genet. 37, 73-76; 2005) — or the modular evolution of cellular signalling circuitry (Annu. Rev. Biochem. 75, 655-680; 2006).
Now, dear reader, when Miller writes of “protein-to-protein” binding sites in one sentence, wouldn’t you expect the papers he cites in the next sentence would be about protein-to-protein binding sites? Well — although the casual reader wouldn’t be able to tell — they aren’t. None of the papers Miller cites involves protein-protein binding sites. The Science paper concerns protein-steroid-hormone binding; the Nature Genetics paper deals with the enzyme activity of single proteins; and the Annual Reviews paper discusses rearrangement of pre-existing protein binding domains. What’s more, none of the papers deals with evolution in nature. They all concern laboratory studies where very intelligent investigators purposely re-arrange, manipulate, and engineer isolated genes (not whole cells or organisms) to achieve their own goals. Although such studies can be very valuable, they tell us little about how a putatively blind, random evolutionary process might proceed in unaided
nature.
Miller’s snide comment, that apparently I haven’t followed these developments, seems pretty silly, since it’s so easy to find out that I followed them closely. You’d think he should have noticed that I cited the Annual Reviews article in The Edge of Evolution in Appendix D, which deals in detail with Wendell Lim’s interesting work on domain swapping. You’d think he easily might have checked and seen that I was quoted in the New York Times commenting on Joseph Thornton’s Science paper when it first came out a year ago. You’d also think he’d then have to tell readers of the review why I thought the papers weren’t pertinent. You’d be thinking wrong.
Much worse, Miller is as subtly misleading when writing about the substantive points of The Edge of Evolution as he is when making supercilious offhand comments. Miller writes: “Telling his readers that the production of so much as a single new protein-to-protein binding site is ‘beyond the edge of evolution’, [Behe] proclaims darwinian evolution to be a hopeless failure.” But the book says plainly that it is two, not one, binding sites that marks the edge of evolution. That was not an obscure point. Chapter 7 is entitled “The Two-Binding-Sites Rule”; Figure 7.4 has a line at two binding sites, with a big arrow pointing to it labeled “Tentative molecular edge of evolution.” What’s more, the book goes out of its way to say that Darwinism is certainly not a “hopeless failure”, that there are important biological features it clearly can explain. That’s why one chapter is called “What Darwinism Can Do”.
Regrettably, that’s Miller’s own special style. He doesn’t just sneer and thump his chest, as some other Darwinists do. He uses less savory tactics, too. His tactics include ignoring distinctions the author draws (cellular protein-protein binding sites vs. other kinds of binding sites), mischaracterizing an argument by skewing or exaggerating its claims (“so much as a single ...”), and employing inflammatory, absolutist language (“[Behe] proclaims darwinian evolution to be a hopeless failure”). He turns the principle of charitable reading on its head. Instead of giving a text its best interpretation, he gives it the worst he can.
Call it the principle of malignant reading. He’s been doing it for years with the arguments of Darwin’s Black Box, and he continues it in this review. For example, despite being repeatedly told by me and others that by an “irreducibly complex” system I mean one in which removal of a part destroys the function of the system itself, Miller says, no, to him the phrase will mean that none of the remaining parts can be used for anything else — a straw man which can easily be knocked down. Unconscionably, he passes off his own tendentious view to the public as mine. People who look to Miller for a fair engagement of the arguments of intelligent design are very poorly served.
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Received on Fri Jul 13 05:50:21 2007
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