JAM
Posts: 517
Joined: July 2007
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| Quote (Hermagoras @ July 14 2007,19:30) | | I actually agree with Patrick, because I think this all needs to be explained to someone with a lay understanding of the issues. However, my way of doing this would differ from what he hopes for. Clearly, nobody at UD got the picture. In particular, I don't think anybody over at UD got how Behe's confusion was related to the differences between molecular biology and population genetics. I get that (and I also think, IIRC, that such confusions are present among mainstream molecular biologists, as well) but I don't have the tools to walk someone through it. (If someone more expert wrote it up -- along the lines of "why don't IDers understand the flaws in Behe's math?" -- I'd be willing to help with the translation.) |
What do you want to know? To boil it down to simple terms:
1) Behe was cherry-picking; he intended to deceive his audience. He needed a really small mutation frequency (= mutation rate) to argue that mutation frequencies are too small to drive evolution (one can't say this at UD). There's no real flaw in his math, the sophistry here is that the number isn't a quantitation of what he says it is.
2) The best way to measure mutation frequency is to measure the rate at a position that changes fitness from 1 to 0, or blue bacterial colonies to white, or vice versa. The key is absolute selection.
3) The mutation frequency has been measured in this way for P. falciparum. It is ~2.5 x 10E-9/nucleotide/cell division, right there with just about everyone else.
4) The idea that anyone would need to extrapolate from P. falciparum to humans is preposterous, because mutation rates in humans have been measured in a similar way--in the form of rates of sporadic (not inherited from parents) cases of dominant inherited diseases. You get a similar rate as in #3.
5) Behe found a number 100 billion-fold lower in a review of the chloroquine resistance (CQR) literature for the frequency with which CQR arises in populations in the real world. The author of the review gave many reasons why this is the case, but the most obvious IMO is the fact that the fitness of the CQR mutants is higher than wild-type in a human treated with CQ, but lower in a human not treated with CQ, of which there are many. Some other, less intuitive reasons are sexual reproduction (occurs in the mosquito without CQ) and immune surveillance.
6) The essence is that Behe is arguing that mutation fails to deliver sufficient variation to natural selection, but the reality in this case is that Behe is cherry-picking a case in which selection is flipping back and forth.
7) The cherry on top of Behe's cherry-picking is that once--just once--his expert, White, mislabeled this frequency as a “per-parasite resistance mutation frequency.” In every other case, he labeled it correctly as the product of complex selection.
I tried several ways to attack this, including avoiding the technical discussion and pointing out that Behe was quoting a review instead of citing the primary literature, and offering a completely dishonest argument from the animal-rights movement that used parallel deceptions. I thought that the latter strategy worked better.
Finally, I'd note that I agree that we're never going to change the minds of UD commenters. It's about the lurkers.
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