Another review of Behe’s book, The Edge of Evolution, has been published, this time in Nature and by Ken Miller. This one focuses on Behe’s central claim, that he has identified a probabilistic limit to what evolution can do that means no differences above roughly the genus level (and in many cases, the species level) can be generated by natural mechanisms. This is his CCC metric, or the probability of evolving something equivalent to the “chloroquine complexity cluster”, which he claims is the odds of evolving two specific amino acid changes in a protein. It’s a number he pegs at 1 in 1020, right at the edge of what a large population of protists can do, but beyond the reach of what a smaller population of slowly reproducing metazoans, like hominids, could hope to accomplish even with geological time limits. It’s the same problem I addressed in my earlier criticism, although Miller manages to slap it down with much greater brevity.
Behe cites the malaria literature to note that two amino-acid changes in the digestive-vacuole membrane protein PfCRT (at positions 76 and 220) of Plasmodium are required to confer chloroquine resistance. From a report that spontaneous resistance to the drug can be found in roughly 1 parasite in 1020, he asserts that these are the odds of both mutations arising in a single organism, and uses them to make this sweeping assertion:
“On average, for humans to achieve a mutation like this by chance, we would need to wait a hundred million times ten million years. Since that is many times the age of the universe, it’s reasonable to conclude the following: No mutation that is of the same complexity as chloroquine resistance in malaria arose by Darwinian evolution in the line leading to humans in the past ten million years.”
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. He then leads his unsuspecting readers to believe that this spurious calculation is a hard and fast statistical barrier to the accumulation of enough variation to drive darwinian evolution.
It’s a painfully basic error — Behe is counting on his readership being unaware of basic principles in probability and on having no knowledge of the actual, relevant research on this problem. It’s a safe bet for him, from what I’ve seen of the fans of ID. Unfortunately, when real scientists take a look at what he’s saying, they can see everywhere that he went wrong.
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. 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. 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.
A mistake of this magnitude anywhere in a book on science is bad enough, but Behe has built his entire thesis on this error. Telling his readers that the production of so much as a single new protein-to-protein binding site is “beyond the edge of evolution”, he 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). Instead, he tells his readers that there is just one explanation that “encompasses the cellular foundation of life as a whole”. That explanation, of course, is intelligent design.
This is a trend for Behe. Both of his popular books that have fed the Intelligent Design movement have relied on gross ignorance and misrepresentation at their core. One has to cringe a little bit to see it: Behe really seems to believe that he has had a deep insight into a real problem with evolution, and it’s really nothing but a deep mistake on his part…and he keeps digging his hole deeper.
Miller KR (2007) Falling over the edge. Nature 447:1055-1056.