Re: [asa] Behe Responds To Ken Miller - Edge of Evolution

@ Some of Ken Miller's style of argumentation as
presented below, seems almost identical to that
I've seen employed by Pim van Meurs. Has anyone
ever seen the two of them together in the same place at the same time? :)

~ Janice ..... happy to quote two truths which go _precisely_ together:

"... political correctness is nothing more or
less than an intellectual burqa to cover up
various anxiety-provoking truths." http://tinyurl.com/2adnfb

"If Only Mustachiod H*mophobic Terrorists Drove
Gas-Guzzling SUVs into Buildings In San
Francisco, The Left Would See the Threat" http://tinyurl.com/youxbo

At 05:49 AM 7/13/2007, (Matthew) Yew Hock Tan wrote:

>
><http://www.amazon.com/gp/blog/post/PLNK1WNX2AI5EMGXN>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.
>
>
>
>
><http://www.amazon.com/gp/blog/post/PLNK3GNLGXQXVL2KT>Response
>to Kenneth R. Miller, Continued
>
>
>
>6:28 PM PDT, July 12, 2007
>Yesterday, in
><http://www.amazon.com/gp/redirect.html/ref=cm_plog_item_link/002-1611024-5243226?ie=UTF8&location=http%3A%2F%2Fwww.amazon.com%2Fgp%2Fblog%2Fpost%2FPLNK1WNX2AI5EMGXN&token=140366954749F2F36BBAC56DF4E2F0C31778BC1E>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 07:53:24 2007