Intelligent Design

Edge of Evolution review in Science Magazine

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Sean Carroll writes a review of Michael Behe’s new book “Edge of Evolution” for Science Magazine titled God as Genetic Engineer. Professor Behe can’t respond to this for at least a week so let’s give him a hand by fisking it. Please keep your comments topical, focused, and well supported by evidence arguing against the reviewer’s conclusions.

God as Genetic Engineer
Sean B. Carroll*

The Edge of Evolution
The Search for the Limits of Darwinism
by Michael J. Behe
Free Press, New York, 2007. 331 pp. $28, C$33.99. ISBN 9780743296205.

“The Lord hath delivered him into mine hands.”

Those are the words that Thomas Huxley, Darwin’s confidant and staunchest ally, purportedly murmured to a colleague as he rose to turn Bishop Samuel Wilberforce’s own words to his advantage and rebut the bishop’s critique of Darwin’s theory at their legendary 1860 Oxford debate. They are also the first words that popped into my head as I read Michael J. Behe’s The Edge of Evolution: The Search for the Limits of Darwinism. In it, Behe makes a new set of explicit claims about the limits of Darwinian evolution, claims that are so poorly conceived and readily dispatched that he has unwittingly done his critics a great favor in stating them. . . .

[The AAAS copyright people asked for this review to be removed from this site. –WmAD]

31 Replies to “Edge of Evolution review in Science Magazine

  1. 1
    DaveScot says:

    Here’s one glaring mistake in the author’s review (my emphasis):

    In Darwin’s Black Box, he posited that genes for modern complex biochemical systems, such as blood clotting, might have been “designed billions of years ago and have been passed down to the present but not ‘turned on'”. This is known to be genetically impossible because genes that aren’t used will degenerate, but there it was in print.

    It’s easily possible. Error checking to insure data integrity to any arbitrary reliability standard is de rigueur in computer memory systems. In my experience most things that human designers have come up with in electronic information processing has antecedents in biological information systems. I therefore anticipate things we’ve invented on our own to have parallels in organic systems and mechanisms for insuring any required level of data integrity is no exception.

    An organic mechanism for that level of data integrity has not been identified that does not rely on natural selection but it appears that the effect of such a mechanism has been discovered recently. I blogged the discovery here

    In a nutshell 1000 highly conserved sequences of non-coding DNA between mice and men (140-180my of reproductive isolation) were knocked out of the mouse genome in a block spanning some 1.5 million base pairs. The GM mice were then raised and examined for genetic abnormalities. The researchers expected to find a lot of problems and thus gain insight into the loci of genetic disorders in humans. To their great surprise the mice were quite healthy in every way. The surprise was because they’d presumed one of many evolutionary tautologies (circular reasoning) was an axiom that goes without question. The tautology:

    “If it is highly conserved it must have important biological activity. If it has important biological activity it must be highly conserved.”

    The reviewer also takes this tautology as an evolutionary axiom. This deficiency in the reviewer’s knowledge of recent findings in experimental biology should be pointed out along with why he holds to an axiom that no longer appears to be true.

  2. 2
    tragicmishap says:

    That statement in bold caught my attention as well, but for a different reason. He uses the word “degenerate” when the idea that gene duplication says that one inactive copy may evolve while the other one is open to selective pressure. Shouldn’t he have said “evolve” instead of “degenerate”?

  3. 3
    jpark320 says:

    Unfortunately, these errors are of a technical nature and will be difficult for lay readers, and even some scientists (those unfamiliar with molecular biology and evolutionary genetics), to detect. Some people will be hoodwinked

    How very convenient… I see these sorta statements all the time “We got the evidence, but you wouldn’t understand anyway”

    He assumed such forms would not or could not be found, but three transitional species were identified by paleontologists within a year of that statement.

    Are they still holding on to this stuff?

    This, of course, is the everyday stuff of evolution. Examples of cumulative selection changing multiple sites in evolving proteins include tetrodotoxin resistance in snakes (3), the tuning of color vision in animals (4), cefotaxime antibiotic resistance in bacteria (5), and pyrimethamine resistance in malarial parasites (6)–a notable omission given Behe’s extensive discussion of malarial drugresistance.

    My favorite non-sequitur…

    I haven’t read Dr. Behe’s book, but cefotaxime and pyrimethamine resistance is hardly the random tinkering we need to build different structures. Slight modifications of these proteins hardly shows speciation, but rather shows designed tools of survival. These mutations are nowhere near the level of showing added information, the correct expression of that info, and significant change in the species.

    All it does is show, small changes, can keep the same species alive, and all species seem to naturally have this ability, hmmm… shame on them for using these genetic events to show the development of macroscopic/phenotype lvl changes.

  4. 4
    DLH says:

    Carroll asserts:
    “But it is a non sequitur to leap to the conclusion, as Behe does, that such multiple-amino acid replacements therefore can’t happen.”

    1) It is Carroll who is actually leaping to conclusions asserting:
    “Multiple replacements can accumulate when each single amino acid replacement affects performance, however slightly, because selection can act on each replacement individually and the changes can be made sequentially.”
    Carroll fails to recognize that numerous population dynamics articles listed below by well known evolutionists quantify the unreasonably extreme low probability of such sequential mutations being fixed in populations. Instead, these articles demonstrate the progressive degradation of the genome. i.e., “Genetic entropy”.

    See the devastating expose and compilation by plant geneticist and “gene-gun” inventor:
    Dr. John C. Sanford, Genetic Entropy & The Mystery of the Genome. 2005 Ivan Press ISBN 1-59919-002-8.

    Carroll appears unaware that selection acts on the ENTIRE organism, NOT on “each replacement individually”.
    His assertion is particularly refuted by papers addressing near neutral selection, particularly Kimura (1968, 1983) etc.

    Sanford describes this as problem of “the Princess and the Nucleotides”. i.e., the “Princess” (natural selection) cannot select amongst very numerous “peas” (nucleotide mutations) when separated by a mountain of mattresses (the whole organism).

    2) Examine Behe’s actual usage of “multiple” and “instantaneous” for this popular audience.

    Is this any different from a precise technical statement to the effect that these sequential mutations must occur and be fixed in the population before they are degraded by other mutations or “genetic entropy”?

    Since Carroll objects to Behe’s usage of “instantaneous”, should he not equally critique the numerous assertions that “saltational evolution” or “saltational speciation” occurs? See:

    Carroll does not cite any of major papers listed below that quantitatively support Behe’s arguments and refute Carol’s assertions. Neither does Carroll address Remine’s detailed development of Haldane argument.

    See brief quotes from these authors at:

    Each of these evolutionists torpedo Carroll’s assertions.

    These extracts are extracted from more extensive quotes cited by Sanford in his Appendix.

    J.B.S. Haldane 1957. The Cost of natural selection. J. Genetics 55:511-524

    Kimura, M. 1968. Evolutionary rate at the molecular level. Nature 217:624-626.

    Kimura, M. The Neutral Theory of Molecular Evolution, 1983 Cambridge Univ. Press p 27

    Muller, H.J. 1950. Our load of mutations. Amer. J. Human Genetics 2:111-176.

    Muller, H.J. 1964. The relation of recombination to mutational advance. Mutation Research 1:2-9.

    J. V. Neel et al. 1986. The rate with which spontaneous mutation alters the electrophoretic mobility of polypeptides. PNAS 83:389-393.

    A. S. Kondrashov. 1995. Contamination of the genome by very slightly deleterious mutations: Why have we not died 100 times over? J. Theor. Biol. 175:583-594.

    S. Kondrashov. 2002. Direct estimates of human per nucleotide mutation rates at 20 loci causing Mendelian diseases. Human Mutation 21:12-27.

    M. W. Nachman & S.L. Crowell 2000. Estimate of the mutation rate per nucleotide in humans. Genetics 156:297-304.

    A. Eyre-Walker and P Keightley. 1999. High genomic deleterious mutation rates in Huminids. Nature 397:344-347.

    J. F. Crow. 1997. The high spontaneous mutation rate: is it a health risk? PNAS 94:8380-8386.

    M. Lynch, J. Conery & R. Burger, 1995. Mutation accumulation and the extinction of small populations. The American Naturalist 146:489-518.

    K. Higgins & M. Lynch. 2001. Metapopulation extinction caused by mutation accumulation. PNAS 98:2928-2933.

    Fred Hoyle. 1999. Mathematics of Evolution. Acorn Enterprises, LLC Memphis.

    Howell et al. 1996. Evolution of human mtDNA. How rapid does the human mitochondrial genome evolve? A. J. Hum. Genet. 59:501-509.

    Walter Remine 2005. Cost of Selection Theory. Technical Journal 19:113-125.

  5. 5
    Borne says:

    “The “no transitional fossils” argument…”

    The “no transitionals”, contrary to the reviewers bare assertion, is more valid than ever.

    When will Darwinists figure out that calling something a transitional because it shares morphological traits doesn’t make it such?

    This is the most concise example of the “affirming the consequent”, and the “undistributed middle” logical fallacies that Darwinism is based on. “It looks like this and precedes this, therefore it comes from this”.

    Isn’t it perfectly obvious that one must assume Darwinism to be true to even consider such a statement? Thus making it a tautology and logical fallacy.

    I still believe one of the major defects of Darwinist scientists is a lack of training in logic and information. That’s what perpetually leads them astray into nonsense.

    “and the “designed genes” model have been cut clean off”

    Really? Since when? No one has yet produced the slightest evidence for this – just so stories and conjecture do not count as proof.

    “the courts have debunked the “ID is science” claim,…”

    Ah yes, here we are again, “the courts” (majoritarily run by secular humanists – all Darwinists) “have said”, therefore that establishes it as true science!! 😮

    Laughable if it were not seriously advanced as a valid argument. This one statement shows where the reviewer is coming from.

    “The knights of ID may profess these blows are “but a scratch” or “just a flesh wound,””

    What blows? All the blows are being given to Darwinism as any one with a clear, unprejudiced mind can see.

    “but the argument for design has no scientific leg to stand on”

    Keep up the hand-waving and empty assertions Darweenies, your ship is still sinking fast.

  6. 6
    Bob O'H says:

    tragicmishap – no. Carroll’s point is that if you start with a functional but inactive gene, then over time random mutations will accumulate, which will reduce its ability to function. I think “degenerate” is a more apt description here.

    Incidentally, some may recognise this as the principle behind “genetic entropy”.

    jpark – Carroll wasn’t linking his argument to speciation, or indeed to changes in information content. He was commenting on Behe’s claims about cumulative selection.


  7. 7
    DLH says:

    Further per Bob O’H’s observation,
    Carroll criticizes Behe’s supposition regarding genes “designed billions of years ago and have been passed down to the present … but not ‘turned on’.” stating: “This is known to be genetically impossible because genes that aren’t used will degenerate, . . .”

    By this observation, Carroll destroys his own argument. His hypothetical gradual accumulation of mutations to form complex genes would be rapidly removed.

    1) Avida developers stated:”…our experiments showed that the complex feature never evolved when simpler functions were not rewarded.”
    Lenski, Ofria, Pennock & Adami, “The evolutionary origin of complex features.” Nature vol 423, 139-144 (8 May 2003)

    2)Genomic extensions always require extra energy and extra materials.

    For every hypothesized increment, Carroll must show positive selection that outweighs the negative selection from additional energy and mass for sequential mutation leading to the complex system.

    3)Carroll fails to account for the severely adverse ratio of beneficial to harmful mutations.

    Genomics is identifying a deluge of mutations. e.g. Lee et al. 2007 find: “The 589 articles that Mutation GraB was evaluated against contained 3,216 unique point mutations, resulting in an average of 5.45 point mutations per article.”

    Lee LC, Horn F, Cohen FE (2007) Automatic Extraction of Protein Point Mutations Using a Graph Bigram Association. PLoS Comput Biol 3(2): e16 doi:10.1371/journal.pcbi.0030016

    Gerrish and Lenski estimate the rate of harmful to beneficial mutations at 1 million:1
    Gerrish, P.J. & R. Lenski, 1998. The fate of competing beneficial mutations in an asexual population. Genetica 102/103: 127-144.

    With multiple mutations per generation, negative mutations outweigh positive ones. The probability of demonstrating positive selection for each mutation is remote, especially considering that selection is at the organism level and is weighted across numerous mutations combined with the highly adverse ratio of positive to negative mutations.

    Carroll has further failed to recognize that the multiplied probability of beneficial/harmful selection for the overall sequence is consequently unreasonably remote to the extreme.

    3) Carroll’s blithe assertions further fail to address Haldane’s Dilemma of the numerous generations required to fix a mutation in the population resulting in a limited number of mutations that can be fixed over the known habitable time in the universe. See above for Haldane (1957) who estimated a minimum of 300 generations/fixed mutation. Walter Remine (2005) further quantifies this.

  8. 8
    jpark320 says:

    @ Bob O’H

    Well noted.

    I hope he wasn’t using those as examples of supporting his “new motifs” that are “well within” the limits of evolution ie those changes in resistance are not impressive enough to really drive any sort of mass evolution.

  9. 9
    bornagain77 says:

    Here is a refutation I found of his assertion that cefotaxime antibiotic resistance in bacteria was proof of evolution.

    Point mutations confer cefotaxime resistance, but they compromise ampicillin resistance. Thus, selection for both drug resistances in a bacterium with two copies of beta-lactamase should favor the divergence of one copy to improve cefotaxime resistance while maintaining the other copy to preserve ampicillin resistance. This selection was performed on a bacterium with identical sequences of beta-lactamase on two separate, compatible plasmids. As expected, one plasmid evolved increased cefotaxime resistance when appropriately strong cefotaxime selection was applied. However, the cefotaxime-resistant plasmid maintained sufficient ampicillin resistance to tolerate the concentration of ampicillin used, and the other plasmid was lost. Hosts carrying both the cefotaxime-resistant and wild-type plasmids were then subjected to various higher concentrations of both drugs to find conditions that would ensure the maintenance of both plasmids. In a striking contradiction to our model, no such conditions were found. The fitness cost of carrying both plasmids increased dramatically as antibiotic levels were raised, and either the wild-type plasmid was lost or the cells did not grow. This study highlights the importance of the cost of duplicate genes and the quantitative nature of the tradeoff in the evolution of gene duplication through functional divergence.

    This is a typical bait and switch tactic of evolutionists. They try to sell you on micro-evolution then tell you bears can transform into whales and someday pigs will fly. Yet , though they pretend they have proven evolution, they still have not shown the generation of meaningful information on the molecular level that has violated the principle of genetic entropy.
    All the examples he list as proof of micro-evolution will be found to obey genetic entropy at the molecular level though they may confer some temporary benefit of resistance to the organism. Thus as DLH points out they are still far from overcoming the principle of Genetic Entropy. DLH has listed some studies that are absolutely devastating to the theory of evolution. Evolution as a possible solution is absolutely crushed because of the principle of Genetic Entropy. Evolutionists just do not have the brains to know they are finished yet.

  10. 10
    Mung says:

    In it, Behe makes a new set of explicit claims about the limits of Darwinian evolution…

    Explicitly rebuts any claim that there is nothing new in this book from Behe.

  11. 11
    Mung says:

    Carroll’s point is that if you start with a functional but inactive gene…

    Does Carroll tell us what a functional inactive gene does?

  12. 12
    kallikak says:

    Hmmmm…. well call me crazy, but Carroll states (emphasis mine)

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

    Which book did he read? Pyrimethamine resistance is discussed on page 75 and 76 of Behe’s book. Is this a glaring oversight on the reviewers part, or I am just misreading the review?

  13. 13
    Sladjo says:

    Been in US, bought the new Behe’s book… Very proud of myself! 😉

  14. 14
    bFast says:

    DaveScott: In a nutshell 1000 highly conserved sequences of non-coding DNA between mice and men …

    In addition, it is my understanding from a chat I had over at telicthoughts that there are nine specific non-coding ultraconserved DNA sequences (conserved to 99% in all vertibrates) whose purpose has not been determined by the knock-out and test method. Within the context of darwinian theory this is non-sequitor — period.

    As to the challenges of multiple parallel mutations, the HAR1F gene. It is ultra-conserved at least between mammals and birds, yet in humans it has taken on 18 mutations. This thing cannot mutate as demostrated by all bird and mammal species, yet it suddenly took on 18 mutations!? Non-sequitor within darwinism.

  15. 15
    Jason Rennie says:

    “Behe’s chief error is minimizing the power of natural selection to act cumulatively as traits or molecules evolve stepwise from one state to another via intermediates.”

    This seems like an odd claim for Dr Carroll to make. After all, isn’t Dr Behe’s claim of IC based on exactly this point and how it is problematic ? Unless, at the very least, some reasonable approximation to demonstrating all of the functional intermediates this isn’t going to work.

    I interviewed Dr Carroll for the upcoming “Darwin or Design ?” audio book (yep finally I have a name and hopefully a release date at the end of this month) and he seemed pretty clued in so this seems an odd claim to make.

  16. 16
    Bob O'H says:

    One thing I’m curious about (having not read Sandford’s book), how does “genetic entropy” explain the observations DaveScot mentions?


  17. 17
    bornagain77 says:

    Genetic entropy is a primary first cause principle of science similar to the second law of thermodynamics that is becoming more obvious as the molecular black boxes of genomes are revealed by modern science. Unlike the second law which depends on a input of energy from an outside sourse in order to violate entropy, Genetic Entropy is of a different level and is proving more robust that the second law for it requires the input of “information” from an outside intelligent source in order to be violated and is not as integrally connected to energy as the second law is. All lines of evidence studied at the molecular level are confirming this Genetic Entropy Principle is indeed true. There are no known examples of adaptation in molecular biology in which this principle of Genetic Entropy has been violated.
    Evolutionists have no evidence on this primary level of proof (the generation of functional information that has not in reality degraded preexisting information) thus they allude to the suggestive evidence of similarities between genomes to try to make their case for evolution. Yet, as Dave Scot points out, even on this “similarity” level of evidence they are running into severe problems since their primary presumptions about the nature of the information in the genome are false. i.e. their presumptions of how the information originated in the genome are false.
    The fact is that information will indeed be found to be introduced at the level of parent species with each adaptation of sub-species away from parent species to be shown to degrade the information of the parent species in some way. In fact this is how the fossil record reads, As long as a species is stable it will remain in the fossil record until natural genetic entropy brings genetic meltdown (I believe this is found to be an average of 4 million years for the fossils that went extinct on their own without catastrophe). Whereas if a fossil in the fossil record is shown to start drifting (adapting) from its parent species it soon goes extinct, a lot quicker than the species that have not been forced to adapt. So in reality, Too much change brings quick extintion in the fossil record!
    As well bacteria are commonly known to quickly become less fit for survival the more they are forced to adapt away from their original state. Needless to say this mounting evidence is extremely bad news for evolutionists who are set in their materialistic ways.

  18. 18
    DaveScot says:

    Bob O’H

    Nothing known explains the mouse knockout experiment. Obviously something is working to conserve those sequences. They have no identifiable biologic activity so it isn’t natural selection preserving them. They are by virtue of their existence demonstrably immune to genetic entropy over a period approaching 100 million years. The $64,000 question raised is What the heck is conserving them and why?

    It’s estimated that 99.9% (a figure I have no good reason to dispute) of all species that ever existed have become extinct without spawning any new species – evolutinary dead ends. Genetic Entropy explains that observation. The question then becomes what factor is responsible for remaining 0.1% of cell lines’ survival for billions of years.

    Natural selection doesn’t work as a rule by rewarding beneficial mutations but rather by punishing deleterious mutations and as others have pointed out in various studies the rate of deleterious to beneficial mutations is in the neighborhood of 1 million to 1. Since selection works on the whole organism, not individual mutations, it’s hard to conceive of it doing anything but eliminating the deleterious and thus conserving the essential characters of any given cell line until such time as Genetic Entropy causes the cell line to become extinct. Mutations that are nearly neutral escape the culling effect of natural selection but, since the ratio of bad to good is so overwhelming, nearly neutral mutations are still going to be overwhelmingly a bit bad instead of a bit good. The accumulation of these is what IMO spells the eventual extinction of 99.9% of the cell lines.

    So again we come to the question of why a few rare cell lines manage to evade extinction. I think perhaps when we discover what mechanism has thwarted both Genetic Entropy and Natural Selection in the mouse knockout experiment we may have in hand the mechanism that has kept those few rare cell lines alive for billions of years.

  19. 19
    kairosfocus says:


    On that Fisking, could we not note that the very opening words are meant to put the issue in the context of the C19 Huxley-Wilberforce debate.

    Thus, there is again the ever so present improper equating of ID with Biblical Creationism.

    But equally, the review fails to address that on the merits Bishop Wilberforce evidently was not a mere simplistic creationist, nor was he scientifically or philosophically ignorant.

    Indeed, on the strict merits, Lucas notes that he may well have had the better of the case back in 1860 (and recall this is Darwin’s original theory, not NDT we are dealing with which dates from about the 1930’s to 40’s]:

    On the strength of the [Bishop’s published] review [Of Origin in the Quarterly Reivew]it would be quite impossible to make out Wilberforce as the prelatical apostle of ecclesiastical authority trying to down the honest observations of simple science. In the speech he may have been less cautious; but we can be sure he made something of the same points. At the beginning of The Athenaeum report we read `The Bishop of Oxford stated that the Darwinian theory, when tried by the principles of inductive science, broke down. The facts brought forward, did not warrant the theory.’ Wilberforce’s scientific criticisms are then reported, and finally: `Mr Darwin’s conclusions were an hypothesis, raised most unphilosophically to the dignity of a causal theory. He was glad to know that the greatest names in science were opposed to this theory, which he believed to be opposed to the interests of science and humanity.18 According to Jackson’s Oxford Journal he condemned the Darwinian theory as `unphilosophical; as founded, not on philosophical principles, but upon fancy, and he denied that one instance had been produced by Mr Darwin on the alleged change from one species to another had ever taken place [sic]. He alluded to the weight of authority that had been brought to bear against it – men of eminence, like Sir B. Brodie and Professor Owen, being opposed to it, and concluded, amid much cheering, by denouncing it as degrading to man, and as a theory founded upon fancy, instead of upon facts.’29

    Huxley — at least on the typical suspect, long after the fact media reports — took advantage of a rhetorical flourish to try to imply that Bishop Wilberforce was being disingenuous.

    But, Lucas observes that the truth of the matter looks a lot different:

    It was as a good as a good Union debate. We can sympathize with Huxley’s reluctance to perform in such a setting, though not with his way of expressing himself. Two days earlier, `Prof. Huxley, having been called on by the Chairman, deprecated any discussion on the general question of the truth of Mr Darwin’s theory. He felt that a general audience, in which sentiment would unduly interfere with intellect, was not the public before which such a discussion should be carried on. Dr Daubeny had brought forth nothing new to demand or require remark.15 Huxley was being rather rude. Later accounts of the Saturday session state that the audience was initially hostile to Huxley, and suggest it was due to clerical partisanship. But some of those present may have been feeling unduly deprecated. Again, later accounts suggest that Huxley by his bearding of the bishop on the Saturday had secured at least a hearing for Darwinism.16 But this is the reverse of the truth: every one wanted to hear about Darwinism; Darwin himself could not be there on account of his health, and it was naturally to Huxley, as a leading protagonist on the Darwinian side, that people turned for a defence of Darwin’s views. Before turning to Wilberforce, the chairman had invited Huxley to speak, only to be met with a sarcastic response.17 We can sympathize with the organizers, who finding Huxley in turn coy and belligerent, may well have wanted Wilberforce, who was something of an ornithologist18 and a Vice-President of the British Association, to put across some of the main points at issue. One of the complaints against Wilberforce was that he, no scientist himself, presumed to speak of scientific matters. It should be remembered that what was required on that occasion was not so much a first- hand knowledge of scientific enquiry as an ability to communicate with an audience larger than a full House of Commons. Huxley, too, although he did not see himself as a gladiator, did gladiate. His interventions were not always courteous19 or relevant.20 And if Wilberforce was to be taken to task for being humorous, it is well to remember that Huxley, too, had tried his hand at humour.21

    Five weeks earlier Wilberforce had written22 a review of Darwin’s Origin of species, which was published in the July issue of The Quarterly Review.23 His speech was a condensed version of the review.24 Two passages of the review are of crucial importance, and show that Wilberforce, contrary to the central tenet of the legend, did not prejudge the issue. The main bulk of the review25 is given over to an entirely scientific assessment of Darwin’s Theory . . .[read on . . .]

    So, the review irresponsible, strawmannish and ad hominem coming our the starting gate. I suspect it goes downhill from there.

    GEm of TKI

  20. 20
    Jehu says:

    I was surprised to read this part,

    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.

    They way Carroll cites the footnotes you would think there has been some research that has refuted Behe. Checking the footnotes I see that the first two appear to be peer review science articles but rather commentary or perspective articles, albeit in prestigious journals. See here for the supposed immune system refutation and here for the supposed refutation of the flagellum argument. The last one, which Carroll cites as “further evidence” was just published this month and is available here and is titled “Stepwise formation of the bacterial flagellar system.” I don’t know how Behe was supposed to respond to this article since it was just now published.

  21. 21
    gpuccio says:

    I have just read the first part of the “review” (I really will need all my patience to go on…). I tried to check some of the first assertions about multiple mutations conferring evolutionary advantages. I had not luck with some sources (they were not freely accessible), but for the moment I would like to comment briefly on the case of pyrimethamine resistance in malarial parasites (reference 6). After a brief check of the literature, I found that it is the same old type of “example” of evolution that evolutionists cyte when they have nothing better to say (that is, always). Pyrimethamine is a drug which works by binding to a very important enzyme of the parasite, DHFR. As it happens in bacterial antibiotic resistance, a single mutation which changes the structure of the enzyme can confer some resistance to the drug. Obviously, if we use the drug, mutants will be selected. Nothing new here. But listen to the fundamental novelty: the selected, mutant enzyme, can undergo other single mutations, usually just another one in different sites, which can furtherly reduce the affinity to the drug and therefore confer more resistance. Obviously, if we continue to use the drug, the more resistant strain will be selected.
    Well, is that unlikely? No. Is that an example of multiple evolutionary mutation? No. Why? Because, again, like in bacterial resistance to antibiotics, here there is no new function created, no new functional information. There is only a modified structure of an enzyme, which in some way retains its original function, but loses the affinity of structure which was the target of the “weapon” against the parasite, that is the drug. In other words, in the beginning the drug “fitted” the enzyme, after one or more mutations, neutral enough not to affect seriously the enzime function, it doesn’t fit anymore. A new function? No. Just a lucky loss of a recognizable structure. It’s exactly the same thing which happens when cancer cells, through accumulating mutations, become resistant to anti-cancer drugs which have been used in the patient, when the disease progresses. Resistance through random change of the target of an administered drug is certainly not an instance of information creation.

    The fact is, the only examples of selected single or double sequential mutations provided by darwinists are always, for some strange reason, of this type: bacterial resistance to antibiotics, parasite resistance to pyrimethamine, mosquito resistance to OP, and so on. Never an example of truly random multiple sequential mutations building up a new function, through step by step increase of some important function, as the theory would require.

    By the way, I have already ordered Behe’s book, and I am looking forward to reading it!

  22. 22
    magnan says:

    Carroll: “But it is a non sequitur to leap to the conclusion, as Behe does, that such multiple-amino acid replacements therefore can’t happen. …….New motifs can arise readily at random, and any weak interaction can easily evolve, via random mutation and natural selection, to become a strong interaction……..Indeed, it has been demonstrated that new protein interactions (10) and protein networks (11) can evolve fairly rapidly and are thus well within the limits of evolution.”

    Then why hasn’t the malaria plasmodium developed any new protein-protein binding sites, especially over ten thousand years in response to the strong selective pressure of sickle cell? Carroll carefully avoids addressing this, which is one of Behe’s main points. If it has, then Carroll would certainly have used that ammunition. This is only one of Behe’s arguments from evidence that Carrol studiously ignores. Behe probably gets to the core of it when he states “It may be that there simply is no effective mutational response that is available to malaria.” (chapter 8 pg. 158). Considering the total size of the Plasmodium Falciparum genome, it is hard to believe there isn’t at least one possible even complicated change that would confer resistance to sickle cell. If there is even one, then according to neoDarwinism RM & NS should have found it by now.

    Carroll doesn’t argue with Behe regarding the actual observed data on malaria, but concentrates on the theoretical analysis of protein evolution. One of Behe’s major theses is the extrapolation of the observed data with malaria to human (and other higher animal) population genetics. Carroll carefully avoids specifically showing how this is invalid. He doesn’t even use the “pixie dust” argument (I like that term) of a time changing fitness landscape.

  23. 23
    Jehu says:

    Footnote 15 in Carroll’s review is a just publisher article by Liu and Ochman called, “Stepwise formation of the bacterial flagellar system.” In this article, Liu and Ochman claim to show that the flagellum “evolved in a stepwise fashion through a series of gene duplication, loss and transfer events.” How they do this is interesting and will probably leave much to be desired from readers of UD.

    One thing the article notes very early is that

    Most evidence, including their much broader phylogenetic distribution, supports the view that the flagellum arose much earlier that the TTSS (Type III Secretion System), which are largely limited to Proteobacteria.

    Are you reading this Ken Miller and Nick Matzke?

    Getting back to the focus of the article, what Liu and Ochman did is identify 24 genes that are essential to the construction of the flagellum. They then decided these genes were the “core” of the original flagellum and the rest of the >50 genes that generally construct a flagellum were added later. Next they compared the 24 genes with other genes in various bacteria and decided that flagellum proteins are mostly similar to flagellum proteins. The conclusion they reached from this is as follows,

    we have shown the bacterial flagellum too originated from … a single gene that under went successive duplications and subsequent diversification during the early evolution of Bacteria.

    Interestingly, the authors note as follows,

    It was originally hypothesized that biological pathways and structures might expand through the successive addition and modification of their preceding components. Although there is diminishing evidence that the recruitment of new enzymes into metabolic pathways occurs by this process, it is apparently the manner by which the bacterial flagellum arose.

    Next, to determine how the flagellum evolved, they arranged all 24 proteins into a phylogenetic tree. The order of the tree they claim gives them the order of evolution of flagellum.

    Based on their relationships and on the physical locations of proteins forming the flagellum, the rod, hook, and filament proteins originated in an order that mirrors the ‘‘inside-out’’ flagellar assembly process. The earliest proteins are proximate to the cytoplasmic membrane with later proteins situated distally, first spanning the outer membrane and then giving rise to structures (i.e., the hook, junction, filament, and capping proteins) that extend outside of the bacterial cell. Thus, the flagellum represents a case whereby its order of assembly recapitulates its evolutionary history. The structural features of the flagellum, along with the evidence of homology between FliI and ATP synthase subunits and between MotA/B and the secretion proteins TolQ-TolR, suggests that it originated as a primitive secretion system, first involving ATPase and then adding the rod, hook, and filament components by gene duplication and diversification.

    Well there you have it. Very interesting.

    One thing they don’t dwell on is the degree of homology between these flagellum genes. How many residues must a protein change to go from a ring to a hook to a rod to a cap? The article doesn’t say, what the article does mention is that protein FlgF, which forms the proximal rod, has a 31% homology to what appears to be its next closest protein, FlgG, which forms the distal rod (not a big difference in function). Out of 260 amino acids, that is approximately 180 that are not identical, which takes us back to Behe’s math.

    There is no showing in the article that there is a stepwise path with selective benefit between these proteins.

    The phylogenetic tree of the flagellum proteins itself is not well explained. (Or should I say revealed?)

    Finally, if each of the steps between the alleged secretion system and the flagellum have selective benefit, are these intermediate steps ever found in nature? I doubt it or they would have mentioned it for sure.

  24. 24
    Joseph says:

    With each critique of ID or a pro-ID book, it becomes clearer that ID needs to be introduced and discussed in schools around the world. I say that because of the total lack of ID understanding displayed by these critics.

    First to refute ID just substantiate YOUR (anti-ID) claims.

    Next know that ID is NOT anti-evolution. The structure in question could have been designed to evolve.

    And that is why the genes would not get corrupted over generations (in a front-loading scenario).

    Carroll obviously doesn’t understand that there should be about 50,000 transitional forms between the alleged land mammal ancestor and modern whales. The few alleged transitionals we have could very well be independent organisms that have nothing to do with any cetacean lineage.

  25. 25
    Jehu says:

    In regards to Liu and Ochman’s article. It occurs to me the idea that the claimed development of the flagellum by “successive addition and modification of their preceding components” is amazingly telic.

    If you think about it, what are the odds that the next step in the development of the flagellum would derive from the last step? In the scenerio that Matzke imagined, the flagellum evolved by the exaptation of various proteins already used elsewhere in the bacteria.

    It seems exceeding improbable that flagellum would evolve, in the same order that it is presently constructed, by tinkering with the previous protein one after the other. That seems far more similar to how a designer would put something together.

  26. 26
    bornagain77 says:

    Lui and Ochman also forget or ignore that proteins have been experimentally proven to quickly lose their function in the cell with random point mutations. What are the odds of a functional protein mutating into any other folded protein, of very questionable function, by pure chance?

    “From actual experimental results it can easily be calculated that the odds of finding a folded protein are about 1 in 10 to the 65 power (Sauer). To put this fantastic number in perspective imagine that someone hid a grain of sand, marked with a tiny ‘X’, somewhere in the Sahara Desert. After wandering blindfolded for several years in the desert you reach down, pick up a grain of sand, take off your blindfold, and find it has a tiny ‘X’. Suspicious, you give the grain of sand to someone to hide again, again you wander blindfolded into the desert, bend down, and the grain you pick up again has an ‘X’. A third time you repeat this action and a third time you find the marked grain. The odds of finding that marked grain of sand in the Sahara Desert three times in a row are about the same as finding one new functional protein structure (from chance transmutation of an existing functional protein structure). Rather than accept the result as a lucky coincidence, most people would be certain that the game had been fixed.” Michael J. Behe, The Weekly Standard, June 7, 1999 (Professor Department of Biological Science Lehigh University)

    “Mutations are rare phenomena, and a simultaneous change of even two amino acid residues in one protein is totally unlikely. One could think, for instance, that by constantly changing amino acids one by one, it will eventually be possible to change the entire sequence substantially… These minor changes, however, are bound to eventually result in a situation in which the enzyme has ceased to perform its previous function but has not yet begun its ‘new duties’. It is at this point it will be destroyed – along with the organism carrying it.” Maxim D. Frank-Kamenetski, Unraveling DNA, 1997, p. 72. (Professor at Brown U. Center for Advanced Biotechnology and Biomedical Engineering)

    Lui and Ochman postulate that it happens by blind chance yet the hard evidence says it can’t be done. Until they say exactly how it is done they are no better than the writers of children’s books.

  27. 27
    gpuccio says:

    The “review” by Sean Carroll is ever more demonstrating that it is only a libel made up with lies and more lies, hoping to confound the readers who have not the time, patience or motivation to check what is said and the references given.

    I cite here a sentence from the review:

    “Indeed, it has been demonstrated that new protein interactions (10) and protein networks (11) can evolve fairly rapidly and are thus well within the limits of evolution”

    Well, for now I took the time to check reference number 10, which is an article freely accessible at this link:

    As you probably can imagine, the above article has practically nothing to do with demonstrating “that new protein interactions… can evolve fairly rapidly and are thus well within the limits of evolution.” Indeed, I cannot understand why Carroll has reached such a strange conclusion (or can I?). The article is about the successful application of the usual methods of analysis of conserved sites in yeast genomes to find out possible target proteins for a specific enzyme, PKA (a protein kinase acting on a vast number of substrates). I may be stupid, but it seems to me that the only conclusion of the article is that, if you seek in a single genome or in different genomes for protein coding genes containing a fairly recognizable site on which the PKA enzyme can work, surprise, surprise, those proteins are usually targets for the PKA enzyme!

    I give no further comments. While everybody here tries to rebuild his own life and dignity after such a revelation, I will try to find the time to check other references. It’s hard work, but it’s worthwhile…

  28. 28
    Mung says:

    The problem is what Behe asserts Darwinian evolution can’t do: produce more “complex” changes than those that have enabled humans to battle malaria or allowed malarial parasites to evade the drugs we throw at them. Behe’s main argument rests on the assertion that two or more simultaneous mutations are required for increases in biochemical complexity and that such changes are, except in rare circumstances, beyond the limit of evolution. He concludes that “most mutations that built the great structures of life must have been nonrandom.”

    Contrary to the above claim, the problem is not “what Behe asserts Darwinian evolution can’t do.” The problem is that Behe asserts that there are things that Darwinian evolution cannot do. That it is not the all-powerful all-capable God-like theory that it is claimed to be. The “problem” is with anyone saying that there is anything that Darwinian evolution cannot do. The “what” matters little.

    And note the subtle misrepresentation as well. Behe concludes that “most mutations that built the great structures of life must have been nonrandom.” So Behe is not claiming that these complex structures are beyond the limits of evolution.

    Here is what should have been written:

    Behe’s main argument rests on the assertion that two or more simultaneous mutations are required for increases in biochemical complexity and that such changes are, except in rare circumstances, beyond the limit of Darwinian evolution.

    And it’s not just that simultaneous mutations are required, it’s that beneficial mutations are required. Which themselves are extremely rare. So how rare are two beneficial mutations? And how even more improbable are two simultaneous beneficial mutations that affect the same selectable trait?

    Evolution is so improbable, that it is for all practical purposes, indistinguishable from a miracle.

    Yet for some reason the simple assertion that these miraculous changes are not miraculous at all because they are not attributed to God, but rather to some other “force” and therefore this is sufficient to qualify Darwinism as “science.” HAW!

  29. 29
    Jehu says:


    I agree. Carroll’s use of footnote 10 must be an example of the venerable Darwinian tradition of making grandiose claims from piddling results. Except in this case the results are so piddling I can’t even see the connection to the claim being made. From the paper,

    In summary, this report describes a systematic, sequence based approach that uses a basic tenet of the theory of natural selection to identify the functionally relevant occurrences of a given sequence element in a eukayotic proteome. The success we had identifying potential substrates of the S. cerevisiae PKA illustrates the potential inherent in this general strategy. In addition to identifying autophagy as an important target of the RasPKA pathway, the other substrates identified here are likely to provide fundament al insights into the manner in which this signaling pathway controls the growth of these budding yeasts. Finally, further comparisons between the consensus sites that are phosphorylated by PKA and those that are not could identify additional sequence elements that are important for PKA substrate recognition.

    All they did was find a sequence that relates to a protein being a PKA target. How that uses a “basic tenet of the theory of natural selection” is not obvious. And how it demonstrates that “new protein interactions … can evolve fairly rapidly,” as Carroll claims, is a mystery.

  30. 30
    kairosfocus says:


    Seems there is a collective decision to address the two reviews together. Okay, reasonable.

    And, as the points are addressed one by one, we see that an elephant was being hurled, and that there was the usual literature bluffing. That is, issues that are subject to serious technical debate were presented by smooth words as an alleged “consensus” and the articles being cited to “prove” points do no such thing.

    I observe on the Chu-Carroll citation on the flagellum, a point or two that deserve a bit of a further comment:

    1] IT is a real issue:

    Elucidating the origins of complex biological structures has been one of the major challenges of evolutionary studies. The bacterial flagellum is a primary example of a complex apparatus whose origins and evolutionary history have proven difficult to reconstruct . . . . The bacterial flagellum has received attention as an exemplum of biological complexity; however, how this complexity and diversification have been achieved remains rather poorly understood. Although several scenarios have been posited to explain how this organelle might have been originated (13), the actual series of evolutionary events that have given rise to the flagellum, as might be inferred from the relationships of all genes thatcontribute to the formation and expression of this organelle across taxa, has never been accomplished.

    In other words, they have not succeeded in cogently addressing the issues Behe raised in 1996, after eleven years of intense trying.

    Given the PC, censorship-riddled climate out there in the world of journaldom, due to the self-selecting nobility that constitutes today’s Academe [witness the unjust crucifixion of a certain Mr Gonzalez, and that of a certain Mr Sternberg], this is about as far as one can expect that such an admission will go.

    So, Behe has won the day so far — but they are not about to give up the battle. [Nor are they going to give him any explicit acknowledgement or credit if they can help it.]

    2] 24-gene core

    occurrence and histories of each of these proteins, we could distinguish an ancient core set of 24 structural genes that were present in the common ancestor to all Bacteria. Within a genome, many of these core genes show sequence similarity only to other

    Now, first, how many base-pairs constitute a typical gene? Let’s be generous, and say, 10 – 20. That makes up a string of 240- 480 base pairs, or some 480 – 960 bits of information [crudely speaking]. 4^240 ~ 3.12*10^144. In short, we are credibly well within the Dembski-type range for a unique functionally specified code.

    Next, observe that the 24 genes are strongly preserved across the many groups of bacteria that have flagella. In short, we have reason to believe that it is close to unique as a basis for functionality — the island of functionality exists, and it is small and preserved over whatever span of time was required to originate all these bacteria and is sustained ever since to today — and bacterial breeding times are very short indeed — so it can be observed.

    So we have more or less isolated complex integrated functionality that is preserved by virtue of what happens when change occurs of any serious consequence: loss of core functionality.

    Sure sounds a lot like what Behe, Dembski and Lonnig have been saying to me — not to mention Meyer et al.

    3] Conclusion-jumping . . .

    Within a genome, many of these core genes show sequence similarity only to other flagellar core genes, indicating that they were derived from one another, and the relationships among these genes suggest the probable order in which the structural components of the bacterial flagellum arose. These results show that core components of the bacterial flagellum originated through the successive duplication and modification of a few, or perhaps even a single, precursor gene.

    Now, lets observe: because the core genes share sequence similarity, they were derived from one another back to just one gene. But, does such actually entail that, apart from assuming what was to be proved?

    [Different car engines have very similar materials and structures of many types, but does that show common origin through a random process or design based on common principles, similar operating environment and underlying laws of physics?]

    Also, how did that initial gene originate and function [with the relevant probabilities and/or empirics shown under RM + NS],and how did each incremental gene stage emerge and function, and how did the clusters of genes function and how did the final product emerge by co-opting and/or innovating etc?

    Silence. (Apart from guesswork.)

    In short, Behe’s challenge to show detailed darwinian pathways – not just-so stories, and circular argument based reconstructions buttressed by assuming what they were meant to prove — still stands unmet; Liu and Ochman notwithstanding.

    Surprise — not!

    Therefore, even moreso, the Chu-Carroll review fails on the merits yet again. Worse, it shows an unjustified contempt towards Mr Behe, who has raised an important issue on the merits, and after eleven years, that challenge has yet to be cogently addressed. Liu and Ochman admit that, and then make their own try — which fails.

    So, Mr Chu-Carroll shows himself in a very poor light indeed, if he on the evidence cannot read the direct implications [much less, what is between the lines] of what he cites to see what is really going on there.

    GEM of TKI

  31. 31
    tragicmishap says:

    Hey I’ve been arguing the points Behe makes in his book with a theistic Darwinist on a message board, and I noticed what might be a slight weakness in the book, not really the argument itself. Unlike in Darwin’s Black Box, Behe does not give numbers and timespans of journal articles written on the topics of malaria, HIV, E coli and such. A key contention of this guy I’m arguing with is that we simply haven’t observed enough of the organisms to be so sure that novel functions or binding sites haven’t evolved. Behe sort of glosses over how much of the genome of malaria and HIV was actually observed during the time he says that the full range of probabilistic variances in the genome would have occurred. I know the references are in the back and I intend to look at them, but it would be nice to have a summary of how much data was collected from these populations over time. I say this because it’s a possible argument he’ll get from opponents and he might want to prepare a response.

    Of course, if any mutations had arisen that were relevant to drug resistance or the effects of the disease, it’s likely we would have known about it because it would’ve shown up in the human population. But it would be nice to see a more extensive treatment of the raw data. Don’t break your back though, Mike. Anybody can do this.

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