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Sean Carroll Fails to Scale The Edge of Evolution (Part II): Carroll’s Citations Actually Confirm Michael Behe’s Arguments

Casey Luskin

[Editor’s Note: This is Part 2 of a 4-part response. The full response can be read here.]

edgeofev.jpgIn my previous post, I explained how Sean Carroll’s review of Michael Behe’s book The Edge of Evolution badly misrepresented Behe’s arguments. Behe has responded to many of Carroll’s arguments here, but unfortunately for Carroll, it gets much worse. One paper Carroll cites in an attempt to refute Behe actually explicitly confirms Behe’s position that there are limits to the creative power of Darwinian processes. Carroll argues that Behe claims that “multiple-amino acid replacements therefore can’t happen.” In contrast to Carroll’s misrepresentation, Behe’s actual position contends evolution can proceed forward where there is a stepwise advantage gained with each mutation, but Behe also contends that evolution gets stuck when intermediate states becomes harmful or do not increase fitness: “If two mutations have to occur before there is a net beneficial effect–if an intermediate state is harmful, or less fit than the starting state–then there is already a big evolutionary problem.” (Behe, The Edge of Evolution, pg. 106) Carroll cites examples of “cumulative selection changing multiple sites in evolving proteins,” but one of Carroll’s examples confirms Behe’s actual position.

One of the papers cited by Carroll demonstrates that 5 amino acid sites can change during the evolution of bacterial resistance to the antibiotic drug penicillin. Yet this paper actually confirms Behe’s view, as it reports that 102 of the 120 possible mutational combinations don’t occur naturally for precisely the reason Behe says they won’t work: they don’t give stepwise mutational advantages. Consider how similar this finding is to Behe’s argument above:

However, we demonstrate that 102 trajectories are inaccessible to Darwinian selection and that many of the remaining trajectories have negligible probabilities of realization, because four of these five mutations fail to increase drug resistance in some combinations.

(Daniel M. Weinreich, Nigel F. Delaney, Mark A. DePristo, Daniel L. Hartl, “Darwinian Evolution Can Follow Only Very Few Mutational Paths to Fitter Proteins,” Science, Vol. 312:111-114 (April 7, 2006), emphasis added.)

In other words, the evolution stopped when the evolutionary pathway encountered a point where any further mutations cause bacterial resistance to the anti-biotic drug to drop, or did not increase it. This implies that when random mutation and natural selection is asked to either do a random walk or traverse a drop in fitness, it gets stuck. Carroll’s example of bacteria evolving resistance does not address Behe’s arguments. In fact, it confirms precisely why Behe argues there is an edge to evolution.