Intelligent Design

Is this the best the Darwinist All-Stars can offer?

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Renowned Darwinist Sean Carroll is by all counts part of the Darwinist All-Stars. He made a lame attempt to refute Behe’s recent book in a review published by the prestigious journal Science.

Carroll writes:

pyrimethamine resistance in malarial parasites (6)–a notable omission given Behe’s extensive discussion of malarial drug resistance

Carroll argues Behe omitted mention of pyrimethamine resistance! But what did Mike actually write? He did not omit mention of pyrimethamine resistance:

One successor drug is called pyrimethamine. Interestingly, malaria can counter it with a single amino acid substitution. That single amino acid change makes malaria one hundred times more resistant to the drug.

Is Carroll’s fabrication the best the Darwinist All-Stars can offer? Mike Behe has written the editors of Science regarding Carroll’s mistake, along with other mistakes. I look forward to Mike answering his Critics, and this is just a taste of things to come.

Darwinists like Carroll inspired the NCSE to claim Behe is the Black Knight of Monty Python. Let me suggest, Behe in the ID debates, should rather be likened to one of the Black Knights of the USMC.

[update: per the wonderful suggestion of Bill, I changed the word varsity to All-Stars

23 Replies to “Is this the best the Darwinist All-Stars can offer?

  1. 1
    Bob O'H says:

    I don’t get your complaint – a single amino acid substitution would not be an example of cumulative selection, would it?

    Bob

  2. 2
    scordova says:

    Bob observes:

    I don’t get your complaint – a single amino acid substitution would not be an example of cumulative selection, would it?

    Carroll classifies it as cumulative:

    Examples of cumulative selection changing multiple sites in evolving proteins include ….pyrimethamine resistance in malarial parasites (6)–a notable omission given Behe’s extensive discussion of malarial drugresistance.

    If it is only a single substitution, and you don’t count it as cumulative, then all the worse for Carroll, not Behe.

  3. 3

    Should be go with a variant metaphor: “First-Team All-American” or “All-Star.” The higher they are in the Darwinian pantheon, the longer their plunge into ignominy.

  4. 4
    jpark320 says:

    Well, given Science’s amazing unbiased” view toward ID – I know I’m a subscriber

    I’m sure they’ll recant, err, take back what they said about Behe’s book swiftly..

    yea right. I totally agree w/ you sal, but as you prb agree, the chance they’ll give Behe a fair shot is just about as good as flagellum being brought about by random tinkering ie Zero

  5. 5
    Jehu says:

    Is this the best the Darwinist varsity can offer?

    Yes.

  6. 6
    Jehu says:

    It gets worse. Sean Carroll made the following claim:

    And Behe’s argument against the evolution of flagella and the immune system have been dismantled in detail (13, 14) and new evidence continues to emerge (15), yet the same old assertions for design reappear here as if they were uncontested.

    Footnotes 13 and 14 in the above quote from Carroll are screeds co-written by Matzke that are not worth discussing. But footnote 15 is *cough* actually the Liu and Ochman article that Behe has already responded to and William Dembski blogged about in April suggesting it was a Sokal-style hoax. Even Matzke distanced himself from it at Panda’s Thumb saying it was “kind of strange” and “wildly unsupportable.”

    The same could be said about Carroll’s article.

  7. 7
    mike1962 says:

    Jehu, “Footnotes 13 and 14 in the above quote from Carroll are screeds co-written by Matzke that are not worth discussing.”

    I got a jolt of excitement for a second when I read the original. I thought there might really be some obscure exposition of flagellar evolution, a full detailed including how the construction sequences evolved, etc, etc. When I got to the footnote I was deflated. At that point the guy lost credibility and I went and had some supper.

  8. 8
    DLH says:

    Carroll further asserts:
    “Furthermore, any pair of interacting proteins can readily recruit a third protein, and so forth, to form larger complexes.”
    http://www.sciencemag.org/cgi/...../5830/1427

    By this quaint anthropomorphic statement Carroll denies the very foundations of naturalistic materialism, that mutation and evolution and random and not goal oriented.

    Compare Miller and Levine’s statement of evolutionary dogma:

    (4)“[E]volution works without either plan or purpose … Evolution is random and undirected.”
    (Biology, by Kenneth R. Miller & Joseph S. Levine, pg. 658 (4th edition, Prentice Hall, 1998); emphasis in original)
    http://www.evolutionnews.org/2.....direc.html

  9. 9
    Bob O'H says:

    If it is only a single substitution, and you don’t count it as cumulative, then all the worse for Carroll, not Behe.

    Why? Here’s the abstract to the paper Carroll cites:

    Single and multiple mutations at residues 16, 51, 59, 108, and 164 of Plasmodium falciparum dihydrofolate reductase (pfDHFR) have been linked to antifolate resistance in malaria. We prepared and characterized all seven of the pfDHFR mutants found in nature, as well as six mutants not observed in nature. Mutations involving residues 51, 59, 108, or 164 conferred cross resistance to both the antifolates pyrimethamine and cycloguanil, whereas mutation of residue 16 specifically conferred resistance to cycloguanil. The antifolate resistance of enzyme mutants found in nature correlated with in vivo antifolate resistance; however, mutants not found in nature were either poorly resistant or had insufficient catalytic activity to support DNA synthesis. Thus, specific combinations of multiple mutations at target residues were selected in nature to optimize resistance. Further, the resistance of multiple mutants was more than the sum of the component single mutations, indicating that residues were selected for their synergistic as well as intrinsic effects on resistance. Pathways inferred for the evolution of pyrimethamine-resistant mutants suggested that all multiple mutants emerged from stepwise selection of the single mutant, S108N. Thus, we propose that drugs targeted to both the wild-type pfDHFR and S108N mutant would have a low propensity for developing resistance, and hence could provide effective antimalarial agents.

    The bolding is mine: I hope it’s evident that the authors are talking about cumulative selection. Yes, one mutation can cause resistance, but having further mutations increases the amount of resistance. Look at Table 3 of the paper, if you can access it. This looks like a very clear example of cumulative selection to me.

    Bob

  10. 10
    IDist says:

    it appears to me that the darwinian reaction to Behe’s book is essentialy this:

    1- Darwin is right
    2- Therefore, Behe must be wrong

  11. 11
    Jehu says:

    Bob O’H,

    You have completely missed it. Carroll has accused Behe of ignoring pyrimethamine resistance in Malaria as an example of cumulative selection. In fact, Behe doesn’t deny the existance of cumulative selection, nor does he omit a mention of pyrimethamine as an example. Behe actually spends more than a full page discussing pyrimethamine resistance. Here is small portion of what Behe wrote about it in The Edge of Evolution.

    Although the first mutation (at position 108 of the protein, as it happens) grants some resistance to the drug, the malaria is still vulnerable to larger doses. Adding more mutations (at positions 51, 59, and a few others) can increase the level of resistance.

    It is not clear whether Carroll has actually even read the book.

  12. 12
    DaveScot says:

    Carroll just got the labels mixed up. The Black Knight is the NeoDarwinian hypothesis and King Arthur is experimental science. It’s not us that’s hacking apart Darwinism. It’s the evidence from experimental sciences doing the hacking.

  13. 13
    scordova says:

    Bill suggested:

    Should be go with a variant metaphor: “First-Team All-American” or “All-Star.” The higher they are in the Darwinian pantheon, the longer their plunge into ignominy.

    Thanks for the suggestion. I amended the wording from varsity to All-Stars. I couldn’t quite bring myself to use the phrase “All-American” to describe certain Darwinists.

    Sal

  14. 14
    scordova says:

    I don’t get your complaint – a single amino acid substitution would not be an example of cumulative selection, would it?

    Bob

    It seems you answered your own question.

    The issue, as Jehu pointed out, is that Carroll misrepsresented Behe by insinuating Behe ignored the evidence of cumulative selection and pyrimethamine. Behe did no such thing.

    Behe accepts that cumulative selection happens. At issue is the sufficency and ubiquity of the mechanism. Behe make a good case that what is claimed as innovation is more akin to destruction.

    It is like one army blowing up it’s own bridges in an attempt to slow and invasion. The affects of blowing up multiple bridges are cumulative, but not innovative.

  15. 15
    Bob O'H says:

    It is not clear whether Carroll has actually even read the book

    It’s good to see someone has, if neither Carroll or Sal had seen that quote!

    Bob
    P.S. I’m perfectly willing to admit that I haven’t read it either. 🙂

  16. 16
    Jehu says:

    I haven’t finished reading the book but so far pyrimethamine resistance is not the only example of cumulative selection Behe discusses in detail.

  17. 17
    Charlie says:

    When Behe discusses pyrimethamine he is not only acknowledging the effects of cumulative mutations, but also highlighting with the specific case that even these beneficial mutations can have a net negative effect on the organism. In order to achieve the added resistance of the new mutations protein function is lost.
    In order to make the new mutations selectable the virus must simultaneously acquire an independent mutation to compensate for this loss.
    Behe acknowledges the existence of the cumulative effect, investigates the actual empirical evidence, compares this to the huge population of mutating malaria, and draws his conclusions based upon the relevant data.
    He also discusses in the same chapter the very Darwinian hypothesis for the existence of anti-freeze in the blood of the Notothenioids. Gene duplication, cumulative beneficial mutations, and even a serendipitous deletion.
    “Instead of pointing to greater things, as Darwinists hoped, the antifreeze protein likely marks the far border of what we can expect of random mutation in vertebrates.” page 82
    This is what his book is about – what Darwinian evolution can do, and what it cannot.
    “…random variation doesn’t explain the most basic features of biology. It doesn’t explain the elegant, sophisticated molecular machinery that undergirds life. To account for that – and to account for the root and thick branches of the tree of common descent – multiple coherent mutations are needed.

    Most mutations that built the great structures of life must have been non-random.”
    page 83

  18. 18
    Bob O'H says:

    The issue, as Jehu pointed out, is that Carroll misrepsresented Behe by insinuating Behe ignored the evidence of cumulative selection and pyrimethamine.

    Indeed. Which is why your quoting of Behe talking about a single substitution is irrelevant to Carroll’s point.

    Bob

  19. 19
    scordova says:

    Which is why your quoting of Behe talking about a single substitution is irrelevant to Carroll’s point.

    Fine. I’ll quote the rest.

    Although the first mutation (at position 108 of the protein, as it happens) grants some resistance to the drug, the malaria is still vulnerable to larger doses. Adding more mutations (at positions 51, 59, and a few others) can increase the level of resistance.

    Are you satisfied now that there’s enough evidence that Carroll completely botched his review in the Journal Science?

  20. 20
    jerry says:

    I am about half way through Behe’s book and he discusses cumulative selection in detail in places. Mostly, in terms of probability. It is certainly not a main focus but it is discussed and he talks about the C-Harlem variant of sickle cell as a two step selection process.

    It seems that the normal mode for main stream science is to attack Behe based on any way you can and who cares if it has any relationship to truth or what is in the book. It doesn’t even require reading the book. The best review so far that reflects what is happening is by Galapagos Finch.

  21. 21
    scordova says:

    Behe, in front of the C-Span cameras this past Wednesday, pointed out the very things I’m discussing here. Behe, furthermore said in front of the cameras that he has written the editors of Science pointing out Carroll’s outright fabrication.

    The Journal Science is now in a precarious position:

    1. print Behe’s response

    2. Allow an obvious fabrication to go unconfessed, for all the world to see.

    It is a curious question as to how such a dumb mistake could have entered Carroll’s review. I have a theory.

    Carroll basically copied verbatim someone else’s writings (much like Judge Jones did in Dover). He did so with the author’s full consent, nay, full encouragement. In fact, the ghost author himself copied it from someone else, and so on and so on…..

    Ah, but what was the root source of this hoax. Let me suggest: Are there any anti-ID writings that the Panda’s Thumb won’t endorse?

    I herewith offer a prize, worth up to $200, to anyone who can pull this off and afterward reveal that it was all a hoax (the precise amount to be determined by how cleverly it is pulled off).

    Bill Dembski

    Hey, Bill, can I get my $200 now? 🙂

  22. 22
    jerry says:

    I just listened to Michael Behe on Michael Medved’s show and am about half way through the book.

    A key thing with Behe’s approach in the Edge of Evolution is that the number of malaria organisms born every year is much larger (hundreds or thousands) than the entire population of mammals ever born.

    So this parasite which is under attack by drugs etc and has had an unbelievable number of opportunities to evolve and all it has done is trivial and negative. Now it did change to avoid a couple of the drugs and this makes it even more dangerous but in all those opportunities there was no improvement in the parasite, only loss of function. It is the loss of function that enabled it to evade the drugs which were meant to fight malaria. So this is a Darwinian success story but not one on which to base the theory of everything as they do.

    So in terms of number of opportunities, here is an organism that has changed only minimally and all negatively.

  23. 23
    gpuccio says:

    About cumulative mutations…

    It seems clear from he above discussions that mutations, either single or “cumulative”, can theoretically worl in two different ways:

    a) Causing the loss, more or less partial, of a preexistent pattern of information, with consequences which can be neutral (function is not affected), are often negative (loss of function), and sometimes, very rarely, can have a positive side effect (loss of the target for some external “weapon”, with relative persistence of the real function).

    b) Building “from scratch” a new function.

    Everybody can verufy that each instance of documented random mutations bearing some selective advantage in the existing scientific literature, and cited by darwinists as evidence of natural selection, is part of group a. Most of them are single random mutations, very few are double or triple sequential mutations. In this group belong resistance to antibiotics, to pyrimetamine, to OP insecticides, and even the eventual “selection” of eterozygotes for some diseases, like sicle cell disease.

    On the contrary, no documented evidence exists, as far as I know, of truly random mutations, single or sequential, building up from scratch a new function, in particular some new protein which can present CSI according to Dembski’s criteria (but even much less…).

    This simple fact, that all the (few) documented cases of selection are of the “a” type, and that no true “b” type is known, should be enough to encourage a serious reflection.

    But there is more. Indeed, the reason why “a” vases are observed (even if not often), and “b” cases are not, should be theoretically obvious.

    In “a” cases, the result to be obtained is simply the loss, even partial, of some pre-existing, complex structure, of some complex information which is “linguistically”, and therefore funcionally, linked to the mechanism of attack, be it the structure targeted by the antibiotic, or the hemoglobin necessary for the growth of the parasite. It should be obvious that, to accomplish that task, many kinds of single random mutations (even if not all) are enough. If I want to make a castle of cards collapse by removing a single card, I have a vast choice of cards which could accomplish the task. So, the result is probabilistically very easy to attain. That explains also the existence of limited sequential random mutations “copperationg” in increasing the loss of function: if a first random mutatipns modifies critically the existing structure, I still have a lot of possible other random mutations which can increase the damage.

    But in the “b” scenario, everything is different. If I need a new enzyme which can do something which has never been done before, I have to “guess” one of the very very few structures which can accomplish that task, in the huge space of all possible configurations. In that case, the probabilities are really virtually impossible, and Dembski’s limits fully apply, even for relatively short sequences. Besides, in this case the necessary mutations, if we start from a completely different molecule which does something else, must be attained simultaneously, at least the minimal core of them which can identify one of the few structure which have the new function, otherwise no positive selection is possible. So, in that sense, any new protein with a really new function is irreducibly complex. The result is, no “b” case has ever been truly observed and proved.

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