Here I respond to the unfavorable review of The Edge of Evolution by Kenneth R. Miller inNature. 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 1020chances, 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 Naturereview, 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.
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.