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Dennis Venema’s Vacuous Arguments Against ID

Those of you who follow the Biologos site may have noticed a recent series of articles by Dennis Venema. In this series of articles Dr. Venema purports to recount his journey from being an ardent ID supporter to being an ID critic. The latest installment, Part 4, can be found here.

In Part 4, Venema explains how reading Michael Behe’s second book, The Edge of Evolution, caused him to do a complete about-face. As a graduate student in biology, he had greatly admired Behe’s first book, Darwin’s Black Box, but now, as a new junior faculty member, he decided that Behe’s arguments in The Edge of Evolution were all wrong, and as a result, he decided that he must reject Behe and ID.

A number of questions are raised by Venema’s account. First of all, the argument in Behe’s first book, Darwin’s Black Box, is logically independent of the argument in the second book. Darwin’s Black Box centers on the theoretical difficulties for Darwinian mechanisms raised by irreducible complexity, whereas the second book is a wholly empirical argument about what Darwinian mechanisms have in fact accomplished in the case of microorganisms. So even if Behe’s empirical arguments in his second book could be proved completely invalid, it would not follow that his arguments in the first book were invalid. Venema does not explain why he threw out the first book on the basis of alleged flaws in the second.

A number of other questions are raised by Venema’s account of the alleged flaws in Behe’s second book. Here is his argument in full:

“To this day I wish I could have recorded myself reading those opening chapters of EoE. It was not long before the first suggestion of a frown would appear. Not many pages hence the frown would deepen into a furrow. I could hardly believe what I was reading: where was the Behe of Darwin’s Black Box that had so captivated me years ago? Though it is not polite to recount it (and I want to be clear that I hold no animosity towards Dr. Behe, but merely want to share my initial reaction) I clearly recall putting EoE down on my desk thinking, “What is this?” I was shocked: I had fully expected to once again be amazed and amused watching Behe take evolution down a peg or two. Yet here I was, knowing virtually nothing of evolution, and already I was seeing nothing but holes in Behe’s argument. Later on, when Behe began to discuss a topic I was familiar with (population genetics) I confirmed what I suspected: Behe was out of his area of specialty and out of his depth. Later work would convince me that this pattern applied to the whole of the book and the core of Behe’s arguments. My note pad was filling up, but not with what I had expected.

“Before I had finished Edge of Evolution, I was done with ID. I would lose my faith in ID not by comparing it to the science of evolution, but by reading one of its leading proponents and evaluating his work on its own merits. ID, I decided, was an argument from analogy, ignorance and incredulity. I was looking for an argument from evidence. Due to an interesting set of circumstances, I was able to read Behe both as a credulous lay reader and as a skeptical trained scientist. Behe, I realized, hadn’t changed: I had changed, and what a difference it had made.”

A number of points should be noted. First, if Venema, by his own confession, at the time knew “virtually nothing of evolution,” what made him qualified to criticize Behe’s work, to see the alleged “holes” in his argument?

Second, even Behe was “out of his area of specialty” when discussing population genetics, that by itself does not invalidate the argument he was making. A scientist from a different field might make some slips or errors in commenting on another field, but what needs to be shown is that the specific slips or errors are such as to be fatal to the argument the scientist is making. It is so typical of Biologos columnists to say things like: “On Page 259 Meyer misnames this chemical, and therefore he is scientifically incompetent, therefore ID is false.” But in fact what has to be shown is that the misnaming of the chemical, or the error in population genetics jargon, is such as to invalidate the argument of an entire book, or chapter, or paragraph. Never has any Biologos columnist ever done this, and Venema has again failed to do it here. He simply makes vague unspecified charges about Behe’s incompetence, without showing how the argument is invalidated by said incompetence. This is the lazy man’s way of arguing, not the scientist’s way of arguing, and Dr. Venema should not be proud of it.

(I might add by way of parentheses that it is very odd for Dr. Venema, a leading player on Biologos, to complain about ID people writing outside of their specialties, when on the Biologos site, many columnists — Karl Giberson, Darrel Falk, Oliver Barclay, Ard Louis, and others, frequently write columns about, or make comments about, theology and the history of ideas — fields in which they are completely incompetent — and say embarrassingly ignorant things. Perhaps Dr. Venema can take his complaint about non-specialists to the Biologos management and get something done about the theological and historical dilettantism of the scientists there. But I digress.)

Third, how does it follow that if Behe is wrong, all ID theorists are wrong? Did Venema take the time to read the careful argument in No Free Lunch by William Dembski? Did he read The Design of Life by Dembski and Wells, with its careful critique of Darwinian mechanisms? Did he read the many essays by Paul Nelson, Stephen Meyer, Richard Sternberg, David Berlinski, etc. which have either argued for ID or criticized Darwinism, and show the flaws in those? How can he know that ID is entirely wrong when he has found flaws in the argument of only one book by one ID proponent? The lack of logic in Venema’s conclusion is staggering, and makes the case that biologists need to add a good strong liberal arts component to their education, so that they can learn to reason competently.

(Of course, we know how Venema has dealt with Stephen Meyer’s book, Signature in the Cell. A few months back, he wrote a series of columns on that book which purported to be a refutation of it. Interestingly enough, almost of all of Venema’s comments in those columns concerned Darwinian evolution, which was not the topic of Meyer’s book. The topic of Meyer’s book was the origin of the first life. Venema did not provide one shred of evidence that Meyer had made any errors in his research and critique of chemical evolutionary theories of the origin of life. Nor is this surprising, as Venema knows next to nothing about origin-of-life theories; his field is fruit-fly population genetics, and he has published nothing at all in the origin-of-life field. So it’s understandable why he might stay away from criticizing Meyer in the area where Meyer did his Ph.D. work.  But the staggering thing is that Venema was not able to grasp, even when it was pointed out to him by several commenters, that his critique of Meyer was off-topic.  Again, one wonders what kind of general intellectual training a scientific education these days provides, when a Ph.D. in Biology cannot keep his focus on the argument that is on the table.)

Finally, if Behe was so wrong, why did Venema not publish, in a peer-reviewed scientific journal, or in a major newspaper or general-interest magazine, a review of The Edge of Evolution, pointing out its many faults? What was stopping him? Dawkins, Carroll, Coyne, Ruse and many others did so. Why didn’t Venema, if he was so sure that he was right? Venema makes sweeping generalities about Behe’s incompetence, but when it comes time to trot out the evidence, he is missing in action.

And that’s not the only place Dr. Venema has been missing in action. He says he was an ardent supporter of ID. Really? Then how come no one in the ID movement has any memory whatsoever of his support? What conferences did he organize to bring in pro-ID speakers? What positive book reviews of ID books did he write on Amazon, or in his local newspaper, or in any other venue? On what internet debating sites did he sign his name to defenses of ID against its critics? Where on Panda’s Thumb or Pharyngula or TalkOrigins will we find his sterling defense of ID?  On what platform did he debate Eugenie Scott or P. Z. Myers?

Overall, Dr. Venema’s series on why he abandoned ID is much like his series of articles on Signature in the Cell — an intellectual washout. It contributes nothing to the serious discussion of ID notions and ID arguments. If this is the best argument that Biologos can marshal against ID, its days are numbered.

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62 Responses to Dennis Venema’s Vacuous Arguments Against ID

  1. I really don’t believe this person. EoE is nothing like DBB. But so what.

    What, is he trying to get tenure?

  2. “Vacuous” is right. First, Venema arbitrarily “decided” that “ID was an argument from analogy, ignorance and incredulity”. Then, he goes on to state, “Due to an interesting set of circumstances, I was able to read Behe both as a credulous lay reader and as a skeptical trained scientist. ”

    Really? A skeptical trained scientist knows nothing of evolution? What type of scientist is he, anyway?

    Then, “On Page 259 Meyer misnames this chemical, and therefore he is scientifically incompetent, therefore ID is false.” True science lives or dies on the evidence, not on the personal feelings or beliefs of the scientist(s).

  3. An interesting account, but I think Eric Rothschilds crossexamination of Behe is a much better read and takes down both DBB and EOE.

  4. It- the crossexamination- is an interesting read but it exposes both Rothchilds’ agenda and ignorance.

    Is that what you were shooting for?

  5. The strange part is there isn’t any chemical named on page 259…

  6. Hey Grunty…could you perhaps give an example or two of the so called “taking down” of the DBB and EOE. Personally, I’ve never read a rebuttal to Behe’s claims that is satisfactory.

  7. I don’t think it’s fair to attack this piece, since it is a generalized recounting of Venema’s thought life regarding this topic. Venema has written more technical criticisms, for example here.

    Frankly I had already been convinced with the finding of a channel forming protein with preference for cations (VPU), new findings also suggest that there is protein-protein interaction with other ion channels.

  8. Here’s Granville Sewell’s take: “But certain carnivorous plants pose these problems in such a spectacular way that they are a focal point of the Darwinism debate, ever since Alfred Wallace warned Darwin about the problems posed by Utricularia, saying “I feel sure they will be seized on as inexplicable by Natural Selection” and implored him to address these difficulties in a future edition of his book “On the Origin of Species.””

    Granville, couldn’t you have at least Googled ‘darwin carnivorous plants’ before writing that? That would have taken you to “Carnivorous Plant” at wikipedia which mentions Darwin’s book, “Insectivorous Plants” where he answered Mr. Wallace’s questions and then some. With the name of Darwin’s book, it’s not hard to find it online at http://darwin-online.org.uk/co.....;pageseq=1 if you want to read it.

    And NEWS, what is so difficult about a pitcher plant? They have leaves which collect water, insects fall into the water and drown. They rot and the plant absorbs some nuturients from them. I don’t see where evolution is even necessary there.

  9. Well, once again my comment wound up in the wrong thread. This should be in the Carnivorous Plants thread.

  10. Starbuck; As to VPU’s: Behe responded here;

    Response to Ian Musgrave’s “Open Letter to Dr. Michael Behe,” Part 4
    Excerpt: One should, however, also make some distinctions with this example. First, although there apparently are five or so copies of Vpu in the viroporin complex, that does not mean that five binding sites developed. Only one new binding site need develop for one area of a protein which binds to a different area of the same protein, to form a homogeneous complex with, say, C5 symmetry. That is all that is required for a circularly symmetric structure to form. Second, the viroporin is not some new molecular machine. There is no evidence that it exerts its effect in, say, an ATP- or energy-dependent manner. Rather, similar to other viroporins, the protein simply forms a passive leaky pore or weak channel. (4,5) This situation is probably best viewed as a foreign protein degrading the integrity of a membrane, rather than performing some positive function.

    And third, I explicitly pointed out in Chapter 8 of The Edge of Evolution that HIV had undergone enough mutating in past decades to form all possible viral-viral binding sites, but commented that apparently none of them had been helpful (now I know that one of them helped). This I discussed as the “principle of restricted choice”:

    A third reason for doubt is the overlooked problem of restricted choice. That is, not only do new protein interactions have to develop, there has to be some protein available that would actually do some good. Malaria makes about 5,300 kinds of proteins. Of those only a very few help in its fight against antibiotics, and just two are effective against chloroquine. If those two proteins weren’t available or weren’t helpful, then, much to the joy of humanity, the malarial parasite might have no effective evolutionary response to chloroquine. Similarly, in its frantic mutating, HIV has almost certainly altered its proteins at one point or another in the past few decades enough to cover all of shape space. So new surfaces on HIV proteins would have been made that could bind to any other viral protein in every orientation. [Emphasis added here.] Yet of all the many molecules its mutated proteins must have bound, none seem to have helped it; no new protein-protein interactions have been reported. Apparently the choice of proteins to bind is restricted only to unhelpful ones. (pp. 157-158)
    ‘So Dr. Musgrave’s “core argument” turns out to be a decidedly double-edged sword. Yes, one overlooked protein-protein interaction developed, leading to a leaky cell membrane. However, in the past fifty years many, many more potential viral protein-viral protein interactions must have also developed but not been selected because they did the virus little good. That, dear readers, is “restricted choice,” a very large contributor to the edge of evolution.’
    http://behe.uncommondescent.co.....he-part-4/

    and,,

    Response to Ian Musgrave’s “Open Letter to Dr. Michael Behe,” Part 4
    “Yes, one overlooked protein-protein interaction developed, leading to a leaky cell membrane — not something to crow about after 10^20 replications and a greatly enhanced mutation rate.” – Behe

    —————-

    further notes:

    In fact, I followed this ‘VPU’ debate very closely and it turns out the trivial gain of just one protein-protein binding site being generated for the non-living HIV virus, that the evolutionists were ‘crowing’ about, came at a staggering loss of complexity for the living host it invaded (People) with just that one trivial gain of a ‘leaky cell membrane’ in binding site complexity. Thus the ‘evolution’ of the virus clearly stayed within the principle of Genetic Entropy since far more functional complexity was lost by the living human cells it invaded than was ever gained by the non-living HIV virus. A non-living virus which depends on those human cells to replicate in the first place. Moreover, while learning HIV is a ‘mutational powerhouse’ which greatly outclasses the ‘mutational firepower’ of the entire spectrum of higher life-forms combined for millions of years, and about the devastating effect HIV has on humans with just that one trivial binding site being generated, I realized if evolution were actually the truth about how life came to be on Earth then the only ‘life’ that would be around would be extremely small organisms with the highest replication rate, and with the most mutational firepower, since only they would be the fittest to survive in the dog eat dog world where blind pitiless evolution rules and only the ‘fittest’ are allowed to survive.

    An information-gaining mutation in HIV? NO!
    http://creation.com/an-informa.....ion-in-hiv

    ————-

    As well Starbuck; as to your linked article, I noticed they mentioned Doug Axe’s quote from this video:

    Nothing In Molecular Biology Is Gradual – Doug Axe PhD.
    http://www.metacafe.com/watch/5347797/

    “Charles Darwin said (paraphrase), ‘If anyone could find anything that could not be had through a number of slight, successive, modifications, my theory would absolutely break down.’ Well that condition has been met time and time again. Basically every gene, every protein fold. There is nothing of significance that we can show that can be had in a gradualist way. It’s a mirage. None of it happens that way. – Doug Axe PhD.

    Starbuck I also noticed that they did not refute Axe by actually ‘physically demonstrating’ the origination of any new gene or protein, but merely trotted out ‘just so stories’ of how it could have happened. Does this truly constitute a rebuttal for you??? If so you have left the bounds of empirical science and have let your materialistic philosophy cloud your judgment!

    further notes:

    Estimating the prevalence of protein sequences adopting functional enzyme folds: Doug Axe:
    Excerpt: The prevalence of low-level function in four such experiments indicates that roughly one in 10^64 signature-consistent sequences forms a working domain. Combined with the estimated prevalence of plausible hydropathic patterns (for any fold) and of relevant folds for particular functions, this implies the overall prevalence of sequences performing a specific function by any domain-sized fold may be as low as 1 in 10^77, adding to the body of evidence that functional folds require highly extraordinary sequences.
    http://www.ncbi.nlm.nih.gov/pubmed/15321723

    Correcting Four Misconceptions about my 2004 Article in JMB — May 4th, 2011 by Douglas Axe
    http://biologicinstitute.org/2.....le-in-jmb/

    ID Scientist Douglas Axe Responds to His Critics – June 2011 – Audio Podcast
    http://intelligentdesign.podom.....9_43-07_00

    Stephen Meyer – Functional Proteins And Information For Body Plans – video
    http://www.metacafe.com/watch/4050681

    ==================

    etc.. etc.. etc..

  11. If it interacts with other ion channels than there are more protein interactions going on right? But at any rate, that gp120 binds CD4 is similar to the way MHCII binds to CD4, is quite impressive to me. In fact, gp120 covers much more area on CD4 than MHCII does. That is the reason gp120 can compete MHCII in binding to CD4, resulting in viral infection.

    As far as the creation.com article, I’m not completely caught up with the studies in this area, but afaik the vpu gene has been found only in HIV-1 and simian immunodeficiency viruses isolated from chimpanzees (SIVcpz), and three species of old world monkeys within the genus Cercopithecus (SIVsyk). These proteins are quite diverse in sequence and predicted secondary structure. Most of the functional characterization of Vpu, including viroporin capabilities, has been limited to a small number of subtype B and more recently subtype C Vpu proteins from HIV1. Recent genetic characterization of a new SIVsyk showed that SIVden which carries the vpu gene (bearing no resemblance to any known vpu) is phylogenetically related to other Syk members which do not encode vpu.

    As for Venema’s article, there are people that guess the WGD at the origin of vertebrates may have increased neofunctionalization, but others argue that it did not, because there is no strong evidence to prove that claim. Actually the evidence might well have been largely erased by 450 million years. However, his discussion of the one family, shows strong positive selection on sequence evolution after the genome duplications, and this provides some direct evidence for the claim.

    Not enough for you perhaps, how about all the studies that show, from a protein “foldability” and stability standpoint, you can get from here to there in a plausible step-wise manner (“here” being extant protein and “there” meaning simple peptide motif) involving gene duplication & fusion processes.

    Or the fact that the evolution of different proteins towards creation of binding ligands against a target molecule may go different ways. When you have the same target, fibrinogen, and very different libraries of the major coat protein, we received competing ligands having absolutely different binding peptides.

    Also I am a Christian and do not have a “materialist philosophy”, the equation of acceptance of evolution with materialism is a folly that you share with the new atheists.

  12. posted to quickly, these are meant to be quotes:

    vpu is found only in HIV-1 and simian immunodeficiency viruses isolated from chimpanzees (SIVcpz), and three species of old world monkeys within the genus Cercopithecus.

    has been limited to a small number of subtype B and more recently subtype C

  13. If you accept evolution via an accumulation of genetic accidents lading to the diversity of living organisms from some unknown population(s) of single-celled organisms, that is the materialistic philosphy.

    That said Intelligent Design is not anti-evolution. Rather ID claims that not all mutations are genetic accidents.

  14. Starbuck, me thinks you are much too easily impressed. Until Darwinists can actually generate novel functional genes and/or proteins by what are perceived to be purely evolutionary processes (or even significantly modify existing genes and/or proteins by what are perceived to be purely evolutionary processes), everything you claim as evidence is in fact merely speculation. Whereas to refute Doug Axe’s work experimental verification is exactly the burden that Darwinism must bear to be considered scientifically legitimate.,,, Imagination is a wonderful thing for forming a hypothesis but it has absolutely no place in the testing phase of the scientific method that determines whether that hypothesis is actually feasible or bunk!!! i.e. Darwinists have completely failed to concretely demonstrate, by empirical science, the feasibility of their claims!!!

    notes;

    Proteins Did Not Evolve Even According to the Evolutionist’s Own Calculations but so What, Evolution is a Fact – Cornelius Hunter – July 2011
    Excerpt: For instance, in one case evolutionists concluded that the number of evolutionary experiments required to evolve their protein (actually it was to evolve only part of a protein and only part of its function) is 10^70 (a one with 70 zeros following it). Yet elsewhere evolutionists computed that the maximum number of evolutionary experiments possible is only 10^43. Even here, giving the evolutionists every advantage, evolution falls short by 27 orders of magnitude.
    http://darwins-god.blogspot.co.....d-not.html

    Fancy footwork in the sequence space shuffle – 2006
    “Estimates for the density of functional proteins in sequence space range anywhere from 1 in 10^12 to 1 in 10^77. No matter how you slice it, proteins are rare. Useful ones are even more rare.”
    http://www.nature.com/nbt/jour.....6-328.html

    It is interesting to note the ‘low end’ 1 in 10^12 (trillion) estimate for functional proteins (Szostak), is still very rare and of insurmountable difficulty for a materialist to use in any evolutionary scenario,

    How Proteins Evolved – Cornelius Hunter – December 2010
    Excerpt: Comparing ATP binding with the incredible feats of hemoglobin, for example, is like comparing a tricycle with a jet airplane. And even the one in 10^12 shot, though it pales in comparison to the odds of constructing a more useful protein machine, is no small barrier. If that is what is required to even achieve simple ATP binding, then evolution would need to be incessantly running unsuccessful trials. The machinery to construct, use and benefit from a
    potential protein product would have to be in place, while failure after failure results. Evolution would make Thomas Edison appear lazy, running millions of trials after millions of trials before finding even the tiniest of function.
    http://darwins-god.blogspot.co.....olved.html

    =============

    The Case Against a Darwinian Origin of Protein Folds – Douglas Axe – 2010
    Excerpt Pg. 11: “Based on analysis of the genomes of 447 bacterial species, the projected number of different domain structures per species averages 991. Comparing this to the number of pathways by which metabolic processes are carried out, which is around 263 for E. coli, provides a rough figure of three or four new domain folds being needed, on average, for every new metabolic pathway. In order to accomplish this successfully, an evolutionary search would need to be capable of locating sequences that amount to anything from one in 10^159 to one in 10^308 possibilities, something the neo-Darwinian model falls short of by a very wide margin.”
    http://bio-complexity.org/ojs/.....O-C.2010.1

    The Case Against a Darwinian Origin of Protein Folds – Douglas Axe, Jay Richards – audio
    http://intelligentdesign.podom.....9_03-07_00

    When Theory and Experiment Collide — April 16th, 2011 by Douglas Axe
    Excerpt: Based on our experimental observations and on calculations we made using a published population model [3], we estimated that Darwin’s mechanism would need a truly staggering amount of time—a trillion trillion years or more—to accomplish the seemingly subtle change in enzyme function that we studied.
    http://biologicinstitute.org/2.....t-collide/

  15. While I agree with the broad critique of Venema’s argument, is there technically anything wrong with making an argument from analogy? Granted, that isn’t all that ID has to offer, but an analogical argument can be quite compelling, and it can conform to all available evidence. In “The Cell’s Design” Fazale Rana’s argument is pretty much unapologetically analogical. He basically attempts to resuscitate Paley’s watchmaker argument by noting that the analogy between products of human design and certain biological machines and motors is actually valid (contra Hume), given the wealth of new knowledge on their specific characteristics.

    FWIW, Venema had an extensive dialogue with Rana on this, and this may be where he’s getting the idea that ALL of ID is an argument from analogy. But what’s wrong with a strong analogical argument anyway?

  16. 17

    Grunty @3:

    You should check your chronology before making statements. The Dover Trial was in 2005; Behe’s book The Edge of Evolution came out in 2007. The lawyer could hardly have “taken down” an argument which Behe had not yet formulated. And no lawyer would capable of “taking down” Behe anyway; the legal team was simply parroting talking points fed to them by the “expert” witnesses — Miller, Pennock, etc. (And even those arguments were lousy, and have been refuted dozens of times since the trial.)

  17. 18

    Starbuck @4:

    It’s perfectly fair to attack the piece. Venema makes audacious claims in it that he does not substantiate. He says that Behe is incompetent in population genetics and evolutionary theory. He implies that this incompetence invalidates Behe’s argument. This is demeaning to Behe and his work, and is dishonorable scientific behavior unless it is accompanied by argument to establish the claims being made.

    It is no excuse to say that Venema has made technical arguments against ID elsewhere. If he made specific arguments *against Behe’s Edge of Evolution* elsewhere, and linked to them, that would be acceptable, but he did not provide any such link. In any case, much better biologists than Venema — Coyne, Carroll — have offered detailed critiques of Behe’s book, and Behe has refuted them in detail. I wouldn’t expect to hear from Venema anything but the same set of arguments repeated. But he can surprise me, and show his mettle, by making the effort of actually writing a detailed refutation of EOE and putting it out for scientific scrutiny. Until he does so, his claims are all bluster, like most of columns (and comments) published on Biologos.

    By the way, your link breaks. It takes one to Biologos but not to the Venema article you are directing people to. The note says that the article is not found there. It would help if you would give a title. I do not recall any article dedicated specifically to criticism of EOE by Venema on the Biologos site.

  18. That’s interesting.

    Can you expand on what you mean by “accidents”? (I would agree that they may not be entirely “random”.)

  19. 20

    Venema’s review of Meyer’s Signature in the Cell in PCSF contains a link to Steve Matheson’s detailed review of Behe’s mistakes in Edge of Evolution, see footnote 34:

    http://www.asa3.org/ASA/PSCF/2.....Venema.pdf

    Odds and Ends

    Although other flaws are less serious in and of
    themselves, they are still indicative of the level of
    argumentation in the book, as well as of the quality
    of its peer review. For example, it was in chapter
    three that I first arrived at what I now call a “Behe
    moment” when reading antievolutionary literature.
    In Michael Behe’s book Edge of Evolution, he makes
    a few obvious “rookie errors” when discussing how
    probabilities work in population genetics.34 This,
    for me, was the clear signal that the book was written
    by an amateur in the field and not adequately peer
    reviewed. In Signature, this moment arrived when
    Meyer calls Pnemonococci a bacterium and a virus
    in the same paragraph.35 This impression was confirmed
    anew when Meyer describes, over the course
    of several pages, his epiphany that DNA bases do
    not have bonds between them and thus cannot selforganize
    into specified sequences. This “epiphany”
    is something that biology majors learn (or at least,
    should learn) in their introductory courses. This
    theme continued apace in the figure describing translation.
    36 Signature shows tRNAs aligning to the
    mRNA in a 5′ to 5′ orientation, tRNAs with codon
    instead of anticodon sequences, and several inappropriate
    nucleotide pairings: all very basic mistakes.
    In short, Signature clearly was not written or peer
    reviewed by individuals with a working knowledge
    of molecular biology.

    Now, these issues in and of themselves would not
    be a serious problem for Signature, if not for the fact
    that the strength of Meyer’s argument rests entirely
    on his assertion that he has made a thorough search
    through all proposed mechanisms for generating
    biological information through natural means and
    found them lacking. Meyer is asking his audience to
    trust him that his analysis is thorough and sound.
    However, that Meyer’s understanding of molecular
    biology appears to be at or below a first-year college
    level should give even the most pro-ID reader pause
    here. It means that Meyer, well intentioned though
    he may be, is simply not equipped to grapple with
    these issues beyond an introductory textbook level.
    Nor has Meyer sought the advice of those who are
    able to do so. And as we have seen, Meyer has made
    neither a thorough search for the origin of biological
    information by natural mechanisms, nor a fair
    assessment of current origin-of-life research.

    [...]

    34 See http://sfmatheson.blogspot.com.....obability-
    one-more-try.html (last accessed September 28,
    2010).

    This presumably tells us the specific problems that Venema sees with Behe’s argument as well — e.g., Behe completely misunderstands basic probability, which is rather a problem, when Behe draws such grand conclusions based on probability.

    Even more problems with Behe’s argument, specifically empirical ones, are here:
    http://www.pandasthumb.org/arc.....of-th.html

    …which Behe mostly didn’t even try to address in his reply:
    http://pandasthumb.org/archive.....es-to.html

    As for Venema’s criticism of Meyer, it’s pretty tenditious to claim the following:

    (Of course, we know how Venema has dealt with Stephen Meyer’s book, Signature in the Cell. A few months back, he wrote a series of columns on that book which purported to be a refutation of it. Interestingly enough, almost of all of Venema’s comments in those columns concerned Darwinian evolution, which was not the topic of Meyer’s book.

    First, this isn’t really true — the review is about half-and-half (I’m looking at the PDF right now). Second, Meyer himself makes the core of his argument the claim that only intelligent processes can produce new information. If evolution can produce new genes with new functions, new binding sites, new specificity, etc., then Meyer’s own argument, as he himself phrased it, is shot down. If natural processes can create new information, then intelligence isn’t the only explanation of new information. Meyer’s claim that information is uniquely a product of intelligent processes, which he relies on throughout the book, is sunk.

    Third, how does it follow that if Behe is wrong, all ID theorists are wrong?

    Behe is the most famous and most credible ID proponent. If he’s badly wrong, it’s a huge problem. It’s also a problem if other ID advocates don’t notice and correct his errors — which they don’t. It indicates a lack of intellectual seriousness.

  20. 21

    I’ve read through Venema’s critique in SITC, and it becomes glaringly obvious (by his repetition that ‘Meyer’s won’t deal with RM+NS’ that the poor man just doesn’t understand the distinction between evolution and origins.

  21. 22
    material.infantacy

    “In light of this, I formulated a conservation law of my own as a working hypothesis to distill my experience and what I had discovered about origin-of-life research. Since I was not principally concerned with whether biological evolution could generate specified information, I decided to formulate a “conservative” conservation law—one that applied only to a nonbiological context (and thus not to an information-rich initial state). My statement of the law does not say anything about whether undirected natural processes could produce an increase in specified information starting from preexisting forms of life. But it does encapsulate what repeated experience had demonstrated about the flow of information starting from chemistry and physics alone.”

    “Here’s my version of the law of conservation of information: “In a nonbiological context, the amount of specified information initially present in a system, Si, will generally equal or exceed the specified information content of the final system, Sf.” This rule admits only two exceptions. First, the information content of the final state may exceed that of the initial state, Si, if intelligent agents have elected to actualize certain potential states while excluding others, thus increasing the specified information content of the system. Second, the information content of the final system may exceed that of the initial system if random processes have, by chance, increased the specified information content of the system. In this latter case, the potential increase in the information content of the system is limited by the “probabilistic resources” available to the system. As noted in Chapter 10, the probabilistic resources of the entire universe equal 10^139 trials, which, in turn, corresponds to an informational measure of less than 500 bits. This represents the maximum information increase that could be reasonably expected to occur by chance from the big-bang singularity to the present—without assistance from an intelligent agent.”

    Meyer, Stephen C. (2009-06-06). Signature in the Cell (pp. 293-294). HarperCollins e-books. Kindle Edition.

  22. The Fact-Free “Science” of Matheson, Hunt and Moran: Ridicule Instead of Reason, Authority Instead of Evidence
    Jonathan Wells June 8, 2010
    Excerpt: One might think that professors Matheson, Hunt and Moran would address the conceptual issue calmly, rationally, and collegially. But they don’t; instead, they stoop to misrepresentation and ridicule. And one might think that they would address the empirical issue by citing published scientific evidence. But they don’t; instead, they simply proclaim themselves the only authorities on the subject.

    Who you gonna believe, them or your own eyes?
    http://www.evolutionnews.org/2.....35521.html

  23. Richard Dawkins’ The Greatest Show on Earth Shies Away from Intelligent Design but Unwittingly Vindicates Michael Behe – Oct. 2009
    Excerpt: The rarity of chloroquine resistance is not in question. In fact, Behe’s statistic that it occurs only once in every 10^20 cases was derived from public health statistical data, published by an authority in the Journal of Clinical Investigation. The extreme rareness of chloroquine resistance is not a negotiable data point; it is an observed fact.
    http://www.evolutionnews.org/2.....est_s.html

  24. Nick, you know you could forever silence ID by creating life in the lab, or by passing the bacterial fitness test by 500 bits!!! This should be a piece of cake for someone as certain as you are that you are the product of purely material processes!~!!

  25. 26

    Nick Matzke @8:

    Venema does not link to Matheson’s criticism of Edge of Evolution *in the article we are discussing*. He therefore provides no documentation for his criticism of Behe *in the article we are discussing*. In any case, for him to lean on Matheson’s arguments would be spineless. A scientist should argue for himself. He indicates clearly that he had *his own* objections to Behe’s book, independent of anything that Matheson might have said. It’s his academic obligation to provide those objections, not simply to dismiss a senior scientist (Behe, who has published far more than Venema) as incompetent with a sweep of the hand, as he does in the article we are discussing. You have a lot to learn about professional ethics, Nick.

    Behe has discussed probability theory in relation to biology with Bill Dembski, who has two Ph.D.s in the subject and knows more about it than you and Steve Matheson and Dennis Venema combined. So it is unlikely that your charge against Behe has any substance, but if it does, you should publish it in a peer-reviewed journal, showing exactly what he gets wrong about probability theory. (It would be amusing to see a biologist try to do some math; when I was in natural science, biology was the haven of all the science undergrads who were afraid of math. The good math students all went into physics, chemistry and engineering.)

    As for Matheson, his point that someone made the trivial slip of calling something a virus in one place and a bacterium in another is worthless *unless he can show that that slip results in an invalid conclusion to an argument.* Errors of that trivial kind occur in scientific books all the time, and Darwinists *never* point them them out when they are in pro-evolution books, only when they are in ID books. The double standard is painfully obvious.

    Your defense of Venema’s articles on Signature in the Cell is the same as Venema’s, and equally inadequate. Even if you are right that only *half* of Venema’s review of Signature in the Cell is about Darwinian evolution, that still means that half of it is off-topic. That’s still a pretty solid indictment of Venema’s inability to stay focused. The point is that the core argument of Meyer’s book is about the origin of life, not about Darwinian evolution. Venema seizes upon some remarks about Darwinian evolution which are in the *Appendix* of the book, not part of its main argument, and spends an inordinate amount of time arguing about those. Venema says *nothing at all* which would explain how life could have arisen by chemical evolutionary means and he has no refutation at all of Meyer’s detailed criticism of the various chemical origin-of-life scenarios. Which is not surprising, as Venema is a fruit fly geneticist, not an origin of life researcher. (Nor, by the way, does Matheson have any special competence to discuss origin of life issues; his field of publication is developmental biology. Maybe if he wouldn’t spend hundreds of hours blogging against ID people, he could pick up another scientific specialty, like origin of life. Until then, since Meyer did his Ph.D. in the subject of origin-of-life theories, and his book is chock-full of references to recent technical literature on the subject, I’ll take Meyer’s word over Matheson’s any day.)

    By the way, I notice that you vanished on my previous thread, after I showed in excruciating detail the dishonesty of your treatment of Behe and other ID proponents. Are you incapable, Nick, of ever admitting error or exaggeration of any kind? It is precisely that dogmatic, intransigent aspect of your personality that marks you off as a culture warrior rather than a genuine seeker after truth. Why don’t you just admit that in the past you have willfully distorted and misrepresented the position of Behe and other ID proponents, and say that it was unprofessional and academically dishonest to do so, and that you are sorry, and that in the future you will never do so again? Then I might have an ounce of respect for you.

  26. Nick,

    It is obvious that you do not understand the information argument. It is also obvious that you do not undertsand that ID is not anti-evolution.

    Also the way to refute Behe and Meyer are with actual evidence, which is something you still sorely lack.

  27. The figure- 5.7 on page 128 shows 5′ – 3′ not 5′ – 5′ as DV states.

  28. 29

    …other than that, pull up your pants. and don’t wear those shoes with that shirt.

  29. 30

    J/k

  30. 31

    And as for TC, thanks for a nice thread. I’m glad you contribute here.

  31. 32

    Starbuck:

    Thanks for fixing the URL. It is now plain that this technical criticism was aimed at Meyer, not Behe. So my criticism still remains valid: in the article in question, Venema declares that Behe is incompetent and his conclusions invalid, without indicating any of the reasons for that judgment. I find this to be the unprofessional treatment of one scientist by another, especially given that we are talking about a junior scientist speaking to a senior one.

  32. Elizabeth re genetic accidents-

    What Causes Mutations?:

    Mutations in DNA sequences generally occur through one of two processes:
    1. DNA damage from environmental agents such as ultraviolet light (sunshine), nuclear radiation or certain chemicals

    2. Mistakes that occur when a cell copies its DNA in preparation for cell division.

    Causes of Mutations:

    1. DNA fails to copy accurately
    Most of the mutations that we think matter to evolution are “naturally-occurring.” For example, when a cell divides, it makes a copy of its DNA — and sometimes the copy is not quite perfect. That small difference from the original DNA sequence is a mutation.

    2. External influences can create mutations
    Mutations can also be caused by exposure to specific chemicals or radiation. These agents cause the DNA to break down. This is not necessarily unnatural — even in the most isolated and pristine environments, DNA breaks down. Nevertheless, when the cell repairs the DNA, it might not do a perfect job of the repair. So the cell would end up with DNA slightly different than the original DNA and hence, a mutation.

    DNA Replication and Causes of Mutation:

    DNA replication is a truly amazing biological phenomenon. Consider the countless number of times that your cells divide to make you who you are—not just during development, but even now, as a fully mature adult. Then consider that every time a human cell divides and its DNA replicates, it has to copy and transmit the exact same sequence of 3 billion nucleotides to its daughter cells. Finally, consider the fact that in life (literally), nothing is perfect. While most DNA replicates with fairly high fidelity, mistakes do happen, with polymerase enzymes sometimes inserting the wrong nucleotide or too many or too few nucleotides into a sequence. Fortunately, most of these mistakes are fixed through various DNA repair processes. Repair enzymes recognize structural imperfections between improperly paired nucleotides, cutting out the wrong ones and putting the right ones in their place. But some replication errors make it past these mechanisms, thus becoming permanent mutations. These altered nucleotide sequences can then be passed down from one cellular generation to the next, and if they occur in cells that give rise to gametes, they can even be transmitted to subsequent organismal generations. Moreover, when the genes for the DNA repair enzymes themselves become mutated, mistakes begin accumulating at a much higher rate. In eukaryotes, such mutations can lead to cancer. (bold added)

    A majority of biologists subscribe in one form or another to the main tenets of the theory, first proposed by Charles Darwin, that biological evolution is the outcome of accidentally arising genetic variations passively screened by natural selection according to the ability of the variants to survive and reproduce progeny under prevailing environmental conditions.- Christian de Duve in Mysteries of Life: Is there “Something Else”?

    I was taught over and over again that the accumulation of random mutations led to evolutionary change — led to new species.-Dr Lynn Margulis

    And if you read “What Evolution Is” by Ernst Mayr variation arises by chance- ie accidents/ mistakes/ errors

  33. I fixed the url in my next comment. Look, I completely understand you’ze guyz responses, but I implore you, for at least a second, put away your emotions and see the 500 pound gorilla before your eyes. The evidence just doesn’t support creationism. That’s not the end of teleology though.

  34. This may be of interest to Dr. Behe’s 1 in 10^20 rarity of protein-protein binding site number:

    Dr. Behe, in an important Table 7.1 on page 143 of Edge Of Evolution, finds that a typical cell might have some 10,000 protein-binding sites. Whereas a conservative estimate for a multicellular creature is,,,

    Largest-Ever Map of Plant Protein Interactions – July 2011
    Excerpt: The new map of 6,205 protein partnerings represents only about two percent of the full protein- protein “interactome” for Arabidopsis, since the screening test covered only a third of all Arabidopsis proteins, and wasn’t sensitive enough to detect many weaker protein interactions. “There will be larger maps after this one,” says Ecker.
    http://www.sciencedaily.com/re.....144936.htm

    So taking into account that they only covered 2%, of the full protein-protein “interactome”, then that gives us a number, for different protein-protein interactions, of 310,000. Thus, from my very rough ‘back of the envelope’ calculations, we find that this is at least 30 times higher than Dr. Behe’s estimate of 10,000 different protein-protein binding sites for a typical single cell (Page 143; Edge of Evolution; Behe). Therefore, at least at first glance from my rough calculations, it certainly seems to be a gargantuan step that evolution must somehow make, by purely unguided processes, to go from a single cell to a multi-cellular creature.,,, And Darwinian atheists say they don’t believe in miracles?!?

  35. 36

    Starbuck:

    When have I ever, in any of my columns here over the past few years, argued for “creationism”? Read them all; you won’t find any such argument. In almost every one of my columns, from the very first, I have stressed that ID is perfectly compatible with evolution, where evolution is broadly defined.

    As for teleology, that is precisely the problem with neo-Darwinism; it doesn’t have any. And in principle can’t have any, without being untrue to itself. And people like Dennis Venema are trying to make a round square by supporting a biology (neo-Darwinian) that’s inherently anti-teleological while upholding a doctrine of creation that’s inherently teleological.

    Here at UD, we can’t stand such fuzzy-mindedness. We find Dawkins and Coyne much intellectually clearer and more consistent. Dawkins and Coyne know what Darwin’s project implied; for Venema, Falk, etc., the penny hasn’t dropped yet. When it does, they will say, “Oh, so THAT’S what the ID people have been saying all along! Why didn’t I see it before?” (And of the course the answer will be that they didn’t see it before because they hardened their wills so as not to see it.)

  36. 37

    But, Meyer makes an argument against origins, the central premise of which is that natural processes can’t produce new information — but that premise absolutely involves the efficacy of RM&NS to produce new genes, which Meyer doesn’t seriously address.

  37. 38

    The 1 in 10^20 statistic comes from an offhand remark in a paper, not a serious analysis. As I pointed out in a review, it records the number of times CQR spread to a high level in a malarial population and then got noticed by humans. This is much different than the number of times CQR has originated. And there is evidence that CQR originates gradually anyway, from places where it is evolving and all sorts of intermediate alleles are found.

  38. 39

    LOL, I linked to my published review of Behe in Trends in Ecology and Evolution, and you didn’t even notice when you claimed I should publish my criticisms in a journal.

    Then, you say Venema shouldn’t rely on Matheson, but you feel fine with Behe relying on Dembski for probability. Dembski is currently employed as a theologian at a Bible college, he’s an apologist not an actual mathematician. Google Jeff Shallit’s expert report in Kitzmiller. If you’re going to say that arguments from authority are valid, ID loses on all counts.

    Re: creationism — we’ve been through all that, rebut my published work and the evidence therein on those topics if you want to cast stones about academic respectability. You yourself admitted the extensive creationist history of ID, connections which the ID movement denies but which exist nonetheless. Once those points are admitted — and, independently, it is shown that the scientific arguments don’t work, which they don’t and which I have written and published on more than most — then it’s pretty much game over for ID.

  39. Nick, Speculation about ‘bridge burning’ mutations that did not spread throughout the population, much less those that did spread throughout the population, is all fine and well, save for the fact that it does not provide the actual empirical, and thus scientific, support you need to support your materialistic fantasies that purely blind, material, processes can actually build the unmatched, staggering, levels of complexity found within the cell. Unmatched levels of complexity that truly boggles the human mind (references upon request);

    Antimalarial drug resistance – Nicholas J. White 1,2
    Excerpt: Resistance to chloroquine in P. falciparum has arisen spontaneously less than ten times in the past fifty years (14). This suggests that the per-parasite probability of developing resistance de novo is on the order of 1 in 10^20 parasite multiplications. The single point mutations in the gene encoding cytochrome b (cytB), which confer atovaquone resistance, or in the gene encoding dihydrofolate reductase (dhfr), which confer pyrimethamine resistance, have a per-parasite probability of arising de novo of approximately 1 in 10^12 parasite multiplications (5). To put this in context, an adult with approximately 2% parasitemia has 10^12 parasites in his or her body. But in the laboratory, much higher mutation rates thane 1 in every 10^12 are recorded (12).
    http://www.jci.org/articles/view/21682

    Complex polymorphisms in an approximately 330 kDa protein are linked to chloroquine-resistant P. falciparum in Southeast Asia and Africa.
    http://www.ncbi.nlm.nih.gov/pubmed/9393853

    =====================

    Further notes that will be ignored, or severely misrepresented, by Nick

    Is Antibiotic Resistance evidence for evolution? – ‘The Fitness Test’ – video
    http://www.metacafe.com/watch/3995248

    “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain – Michael Behe – December 2010
    Excerpt: In its most recent issue The Quarterly Review of Biology has published a review by myself of laboratory evolution experiments of microbes going back four decades.,,, The gist of the paper is that so far the overwhelming number of adaptive (that is, helpful) mutations seen in laboratory evolution experiments are either loss or modification of function. Of course we had already known that the great majority of mutations that have a visible effect on an organism are deleterious. Now, surprisingly, it seems that even the great majority of helpful mutations degrade the genome to a greater or lesser extent.,,, I dub it “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain.(that is a net ‘fitness gain’ within a ‘stressed’ environment i.e. remove the stress from the environment and the parent strain is always more ‘fit’)
    http://behe.uncommondescent.co.....evolution/

    The Law of Physicodynamic Insufficiency – Dr David L. Abel – November 2010
    Excerpt: “If decision-node programming selections are made randomly or by law rather than with purposeful intent, no non-trivial (sophisticated) function will spontaneously arise.”,,, After ten years of continual republication of the null hypothesis with appeals for falsification, no falsification has been provided. The time has come to extend this null hypothesis into a formal scientific prediction: “No non trivial algorithmic/computational utility will ever arise from chance and/or necessity alone.”
    http://www.scitopics.com/The_L.....iency.html

    The GS (genetic selection) Principle – David L. Abel – 2009
    Excerpt: Stunningly, information has been shown not to increase in the coding regions of DNA with evolution. Mutations do not produce increased information. Mira et al (65) showed that the amount of coding in DNA actually decreases with evolution of bacterial genomes, not increases. This paper parallels Petrov’s papers starting with (66) showing a net DNA loss with Drosophila evolution (67). Konopka (68) found strong evidence against the contention of Subba Rao et al (69, 70) that information increases with mutations. The information content of the coding regions in DNA does not tend to increase with evolution as hypothesized. Konopka also found Shannon complexity not to be a suitable indicator of evolutionary progress over a wide range of evolving genes. Konopka’s work applies Shannon theory to known functional text. Kok et al. (71) also found that information does not increase in DNA with evolution. As with Konopka, this finding is in the context of the change in mere Shannon uncertainty. The latter is a far more forgiving definition of information than that required for prescriptive information (PI) (21, 22, 33, 72). It is all the more significant that mutations do not program increased PI. Prescriptive information either instructs or directly produces formal function. No increase in Shannon or Prescriptive information occurs in duplication. What the above papers show is that not even variation of the duplication produces new information, not even Shannon “information.”
    http://www.bioscience.org/2009.....6/3426.pdf
    http://www.us.net/life/index.htm

    Three subsets of sequence complexity and their relevance to biopolymeric information – Abel, Trevors
    Excerpt: Shannon information theory measures the relative degrees of RSC and OSC. Shannon information theory cannot measure FSC. FSC is invariably associated with all forms of complex biofunction, including biochemical pathways, cycles, positive and negative feedback regulation, and homeostatic metabolism. The algorithmic programming of FSC, not merely its aperiodicity, accounts for biological organization. No empirical evidence exists of either RSC of OSC ever having produced a single instance of sophisticated biological organization. Organization invariably manifests FSC rather than successive random events (RSC) or low-informational self-ordering phenomena (OSC).,,,

    Testable hypotheses about FSC

    What testable empirical hypotheses can we make about FSC that might allow us to identify when FSC exists? In any of the following null hypotheses [137], demonstrating a single exception would allow falsification. We invite assistance in the falsification of any of the following null hypotheses:

    Null hypothesis #1
    Stochastic ensembles of physical units cannot program algorithmic/cybernetic function.

    Null hypothesis #2
    Dynamically-ordered sequences of individual physical units (physicality patterned by natural law causation) cannot program algorithmic/cybernetic function.

    Null hypothesis #3
    Statistically weighted means (e.g., increased availability of certain units in the polymerization environment) giving rise to patterned (compressible) sequences of units cannot program algorithmic/cybernetic function.

    Null hypothesis #4
    Computationally successful configurable switches cannot be set by chance, necessity, or any combination of the two, even over large periods of time.

    We repeat that a single incident of nontrivial algorithmic programming success achieved without selection for fitness at the decision-node programming level would falsify any of these null hypotheses. This renders each of these hypotheses scientifically testable. We offer the prediction that none of these four hypotheses will be falsified.
    http://www.tbiomed.com/content/2/1/29

  40. 41

    Nick:

    On what pages of your Trends in Ecology and Evolution review did you show that Behe gets probability wrong, as you claim above?

    I trust you are aware that Behe issued a decisive rebuttal to your criticism in that review; it was published in his Amazon blog and is now found here at UD. Behe also noticed the unprofessional tone of your review. Apparently you are of the “Abbie Smith” school of science debate, whereby sneering at the opposition counts as argument.

    The fact that Dembski is currently teaching theology, not probability theory, does not mean that he has forgotten his probability theory. But even if he has forgotten half of what he once know, that still means he knows more about the subject than you, Venema and Matheson all put together. And do you think that Behe wouldn’t run his basic numbers by Dembski before publishing?

    Re creationism: Yes, we’ve been through all that, and I showed decisively that you were wrong. You could not find a single text to prove that Behe, Sternberg or Denton were creationists, despite my repeated requests for such. You could not find a single text which showed that ID *as such* implied creationism. Yet, in the complete absence of texts, you stood your ground. To believe something without evidence is completely irrational. But then, you are a culture warrior, not a seeker after truth, so irrationality is just what we have all come to expect from you.

    Regarding Shallit, his field is not probability theory, as he himself admits. And Shallit knows absolutely zero about biology, far less than Dembski. Plus, he has a chip on his shoulder the size of the rock of Gibraltar. He’s intellectually insignificant in origins debates, having contributed nothing to them but spleen and atheist rage. And he’s also, like you, incapable of admitting error in debate, and therefore can’t be taken seriously as a conversation partner.

    Give it up, Nick. No one is going to take you seriously except for those who are already firmly in your camp. You can’t even pretend to be a fair-minded scientist with a neutral perspective. You’re a committed warrior; you know it, we know it, and the world knows it.

  41. 42

    Rather than getting mad, address my criticisms of Behe, because Behe didn’t. As I posted before:

    TREE review:
    http://www.pandasthumb.org/arc.....of-th.html

    Response to Behe’s non-reply:
    http://pandasthumb.org/archive.....es-to.html

  42. Nick, I know you are a busy, busy man arguing utterly trivial points that don’t even matter to addressing the elephant in the living room complexity that Darwinism must face square on, but perhaps, after you have satisfied (deluded) yourself enough to truly believe that you are the, +90% junk, vestigial or whatever, product of blind, pitiless, material processes, (hey its a free country), you can address this falsification of neo-Darwinism, I really would like to see what tripe a neo-Darwinists would answer in response to the falsification instead of just being ignored!:

    Neo-Darwinian evolution purports to explain all the wondrously amazing complexity of life on earth by reference solely to chance and necessity processes acting on energy and matter (i.e. purely material processes). In fact neo-Darwinian evolution makes the grand materialistic claim that the staggering levels of unmatched complex functional information we find in life, and even the ‘essence of life’ itself, simply ‘emerged’ from purely material processes. And even though this basic scientific point, of the ability of purely material processes to generate even trivial levels of complex functional information, has spectacularly failed to be established, we now have a much greater proof, than this stunning failure for validation, that ‘put the lie’ to the grand claims of neo-Darwinian evolution. This proof comes from the fact that it is now shown from quantum mechanics that ‘information’ is its own unique ‘physical’ entity. A physical
    entity that is shown to be completely independent of any energy-matter space-time constraints, i.e. it does not ‘emerge’ from a material basis. Moreover this ‘transcendent information’ is shown to be dominant of energy-matter in that this ‘information’ is shown to be the entity that is in fact constraining the energy-matter processes of the cell to be so far out of thermodynamic equilibrium.

    notes:

    Falsification of neo-Darwinism;

    First, Here is the falsification of local realism (reductive materialism).

    Here is a clip of a talk in which Alain Aspect talks about the failure of ‘local realism’, or the failure of reductive materialism, to explain reality:

    The Failure Of Local Realism – Reductive Materialism – Alain Aspect – video
    http://www.metacafe.com/w/4744145

    The falsification for local realism (reductive materialism) was recently greatly strengthened:

    Physicists close two loopholes while violating local realism – November 2010
    Excerpt: The latest test in quantum mechanics provides even stronger support than before for the view that nature violates local realism and is thus in contradiction with a classical worldview.
    http://www.physorg.com/news/20.....alism.html

    Quantum Measurements: Common Sense Is Not Enough, Physicists Show – July 2009
    Excerpt: scientists have now proven comprehensively in an experiment for the first time that the experimentally observed phenomena cannot be described by non-contextual models with hidden variables.
    http://www.sciencedaily.com/re.....142824.htm

    (of note: hidden variables were postulated to remove the need for ‘spooky’ forces, as Einstein termed them — forces that act instantaneously at great distances, thereby breaking the most cherished rule of relativity theory, that nothing can travel faster than the speed of light.)

    And yet, quantum entanglement, which rigorously falsified local realism (reductive materialism) as the complete description of reality, is now found in molecular biology on a massive scale!

    Quantum Information/Entanglement In DNA & Protein Folding – short video
    http://www.metacafe.com/watch/5936605/

    Quantum entanglement holds together life’s blueprint – 2010
    Excerpt: When the researchers analysed the DNA without its helical structure, they found that the electron clouds were not entangled. But when they incorporated DNA’s helical structure into the model, they saw that the electron clouds of each base pair became entangled with those of its neighbours (arxiv.org/abs/1006.4053v1). “If you didn’t have entanglement, then DNA would have a simple flat structure, and you would never get the twist that seems to be important to the functioning of DNA,” says team member Vlatko Vedral of the University of Oxford.
    http://neshealthblog.wordpress.....blueprint/

    The relevance of continuous variable entanglement in DNA – July 2010
    Excerpt: We consider a chain of harmonic oscillators with dipole-dipole interaction between nearest neighbours resulting in a van der Waals type bonding. The binding energies between entangled and classically correlated states are compared. We apply our model to DNA. By comparing our model with numerical simulations we conclude that entanglement may play a crucial role in explaining the stability of the DNA double helix.
    http://arxiv.org/abs/1006.4053v1

    Quantum Information confirmed in DNA by direct empirical research;

    DNA Can Discern Between Two Quantum States, Research Shows – June 2011
    Excerpt: — DNA — can discern between quantum states known as spin. – The researchers fabricated self-assembling, single layers of DNA attached to a gold substrate. They then exposed the DNA to mixed groups of electrons with both directions of spin. Indeed, the team’s results surpassed expectations: The biological molecules reacted strongly with the electrons carrying one of those spins, and hardly at all with the others. The longer the molecule, the more efficient it was at choosing electrons with the desired spin, while single strands and damaged bits of DNA did not exhibit this property.
    http://www.sciencedaily.com/re.....104014.htm

    Information and entropy – top-down or bottom-up development in living systems? A.C. McINTOSH
    Excerpt: This paper highlights the distinctive and non-material nature of information and its relationship with matter, energy and natural forces. It is proposed in conclusion that it is the non-material information (transcendent to the matter and energy) that is actually itself constraining the local thermodynamics to be in ordered disequilibrium and with specified raised free energy levels necessary for the molecular and cellular machinery to operate.
    http://journals.witpress.com/paperinfo.asp?pid=420

    i.e. It is very interesting to note that quantum entanglement, which conclusively demonstrates that ‘information’ in its pure ‘quantum form’ is completely transcendent of any time and space constraints, should be found in molecular biology on such a massive scale, for how can the quantum entanglement ‘effect’ in biology possibly be explained by a material (matter/energy space/time) ’cause’ when the quantum entanglement ‘effect’ falsified material particles as its own ‘causation’ in the first place? (A. Aspect) Appealing to the probability of various configurations of material particles, as neo-Darwinism does, simply will not help since a timeless/spaceless cause must be supplied which is beyond the capacity of the energy/matter particles themselves to supply! To give a coherent explanation for an effect that is shown to be completely independent of any time and space constraints one is forced to appeal to a cause that is itself
    not limited to time and space! i.e. Put more simply, you cannot explain a effect by a cause that has been falsified by the very same effect you are seeking to explain! Improbability arguments of various ‘specified’ configurations of material particles, which have been a staple of the arguments against neo-Darwinism, simply do not apply since the cause is not within the material particles in the first place!
    ,,,To refute this falsification of neo-Darwinism, one must falsify Alain Aspect, and company’s, falsification of local realism (reductive materialism)!

    ,,, As well, appealing to ‘non-reductive’ materialism (multiverse or many-worlds) to try to explain quantum non-locality in molecular biology ends up destroying the very possibility of doing science rationally;

    BRUCE GORDON: Hawking’s irrational arguments – October 2010
    Excerpt: For instance, we find multiverse cosmologists debating the “Boltzmann Brain” problem: In the most “reasonable” models for a multiverse, it is immeasurably more likely that our consciousness is associated with a brain that has spontaneously fluctuated into existence in the quantum vacuum than it is that we have parents and exist in an orderly universe with a 13.7 billion-year history. This is absurd. The multiverse hypothesis is therefore falsified because it renders false what we know to be true about ourselves. Clearly, embracing the multiverse idea entails a nihilistic irrationality that destroys the very possibility of science.
    http://www.washingtontimes.com.....arguments/

    ,,,Michael Behe has a profound answer to the infinite multiverse (non-reductive materialism) argument in “Edge of Evolution”. If there are infinite universes, then we couldn’t trust our senses, because it would be just as likely that our universe might only consist of a human brain that pops into existence which has the neurons configured just right to only give the appearance of past memories. It would also be just as likely that we are floating brains in a lab, with some scientist feeding us fake experiences. Those scenarios would be just as likely as the one we appear to be in now (one universe with all of our experiences being “real”). Bottom line is, if there really are an infinite number of universes out there, then we can’t trust anything we perceive to be true, which means there is no point in seeking any truth whatsoever.

    “The multiverse idea rests on assumptions that would be laughed out of town if they came from a religious text.” Gregg Easterbrook

    =================

    Alain Aspect and Anton Zeilinger by Richard Conn Henry – Physics Professor – John Hopkins University
    Excerpt: Why do people cling with such ferocity to belief in a mind-independent reality? It is surely because if there is no such reality, then ultimately (as far as we can know) mind alone exists. And if mind is not a product of real matter, but rather is the creator of the “illusion” of material reality (which has, in fact, despite the materialists, been known to be the case, since the discovery of quantum mechanics in 1925), then a theistic view of our existence becomes the only rational alternative to solipsism (solipsism is the philosophical idea that only one’s own mind is sure to exist). (Dr. Henry’s referenced experiment and paper – “An experimental test of non-local realism” by S. Gröblacher et. al., Nature 446, 871, April 2007 – “To be or not to be local” by Alain Aspect, Nature 446, 866, April 2007

    =========================

  43. To dovetail into Dembski and Marks’s work on Conservation of Information;,,,

    LIFE’S CONSERVATION LAW: Why Darwinian Evolution Cannot Create Biological Information
    William A. Dembski and Robert J. Marks II
    http://evoinfo.org/publication.....ation-law/

    ,,,Encoded classical information, such as what we find in computer programs, and yes as we find encoded in DNA, is found to be a subset of ‘transcendent’ quantum information by the following method:,,,

    This following research provides solid falsification for Rolf Landauer’s contention that information encoded in a computer is merely physical (merely ‘emergent’ from a material basis) since he believed it always required energy to erase it;

    Quantum knowledge cools computers: New understanding of entropy – June 2011
    Excerpt: No heat, even a cooling effect;
    In the case of perfect classical knowledge of a computer memory (zero entropy), deletion of the data requires in theory no energy at all. The researchers prove that “more than complete knowledge” from quantum entanglement with the memory (negative entropy) leads to deletion of the data being accompanied by removal of heat from the computer and its release as usable energy. This is the physical meaning of negative entropy.
    Renner emphasizes, however, “This doesn’t mean that we can develop a perpetual motion machine.” The data can only be deleted once, so there is no possibility to continue to generate energy. The process also destroys the entanglement, and it would take an input of energy to reset the system to its starting state. The equations are consistent with what’s known as the second law of thermodynamics: the idea that the entropy of the universe can never decrease. Vedral says “We’re working on the edge of the second law. If you go any further, you will break it.”
    http://www.sciencedaily.com/re.....134300.htm

    ,,,And here is the empirical confirmation that quantum information is ‘conserved’;,,,

    Quantum no-hiding theorem experimentally confirmed for first time
    Excerpt: In the classical world, information can be copied and deleted at will. In the quantum world, however, the conservation of quantum information means that information cannot be created nor destroyed. This concept stems from two fundamental theorems of quantum mechanics: the no-cloning theorem and the no-deleting theorem. A third and related theorem, called the no-hiding theorem, addresses information loss in the quantum world. According to the no-hiding theorem, if information is missing from one system (which may happen when the system interacts with the environment), then the information is simply residing somewhere else in the Universe; in other words, the missing information cannot be hidden in the correlations between a system and its environment.
    http://www.physorg.com/news/20.....tally.html

  44. 45

    For those who wish to read Michael Behe’s 3-part reply to Nick’s “tediously disdainful” review, the columns can be found here:

    http://behe.uncommondescent.co…..nd-part-i/

    http://behe.uncommondescent.co…..d-part-ii/

    http://behe.uncommondescent.co…..-part-iii/

    By the way, Nick, where has Behe ever argued that the mutations must be simultaneous (or “evolve at once” to use your term)? Nowhere, to my knowledge. As far as I can tell, you either just made this up, or are inferring it from the fact that Behe squares the probability. But squaring the probability has nothing to do with simultaneity of events, as you should know if you know as much about probability as you imply that you do.

  45. Nick sez:

    He is obsessed with “randomness,” which he incorrigibly associates with “Darwinism” and cosmic purposelessness. This is one of many incorrect but blindly-held assumptions common with creationists. But randomness in evolution is no more metaphysically significant than randomness in weather systems. If creationists realized this, we might finally see the edge of creationism, if not the end of it. But if Behe is any indication, that won’t be any time soon.

    “Randomness” in the theory of evolution refers to pure chance and your attempt to link evolution with weather is dishonest at best. IOW Nick, according to the ToE all genetic changes are accidents/ errors/ mistakes. Deal with it.

    IOW Nick you don’t have any propoer criticisms of either Behe nor ID.

  46. Matzke:

    8. Criticism: Behe is driven not by science but by his mistaken but obsessive-held view that evolution is “random” in a metaphysical sense meaning “purposeless.” Behe’s reply: “Wasn’t it Darwin himself, we are constantly assured, who based his theory on ‘random’ variation?” Surreply: The word “random” does not appear in the Origin of Species. Search for yourself. Darwin based his theory on natural selection, which is nonrandom. The source of variation was unknown. But thanks to Behe for proving my point – for him, evolution = randomness = purposelessness = no God or meaning of life, this is precisely why he keeps playing the same old game: set up an all-at-once chance event as if it were a good model for a gradual evolutionary process operating under the guidance of natural selection, then declare the all-at-once chance event wildly improbable, then infer ID and thereby rescue the world from the purposelessness which is somehow produced by mere description of a physical process.

    Please provide the valid scientific reference that demonstrates natural selection is non-random. Natural selection = non-random exists only in the minds of you and your ilk, Nick.

    Also Darwin used the word “chance” quite a bit in his book.

    Then we have Will Provine and a host of others saying evolution is purposeless = no God or meaning of life.

    Geez Nick you don’t even appear to understand the theory of evolution.

  47. Why does squaring the probability have nothing to do with simultaneity, Thomas? It seems to me that it does.

    Can you explain?

  48. Joseph:

    Please provide the valid scientific reference that demonstrates natural selection is non-random. Natural selection = non-random exists only in the minds of you and your ilk, Nick.

    Joseph, I’m not sure how you are defining “random” here, but the entire concept of “natural selection” is that it is the systematic increase in prevalence, in a population, of genotypes that tend to confer greater reproductive success, as opposed to “drift” which is the non-systematic increase in prevalance of genotypes are orthogonal to reproductive success.

    Also Darwin used the word “chance” quite a bit in his book.

    Sure, but mostly in the sense of “probability”, and when used in the sense of “random events” it’s to rebut it, as far as I can see:

    When we look at the plants and bushes clothing an entangled bank, we are tempted to attribute their proportional numbers and kinds to what we call chance. But how false a
    view is this!

    Mere chance, as we may call it, might cause one variety to differ in some character from its parents, and the offspring of this variety again to differ from its parent in the very same character and in a greater degree; but this alone would never account for so habitual and large an amount of difference as that between varieties of the same species and species of the same genus.

    So here is Darwin saying that “mere chance” may be responsible for new variants but that “this alone” cannot account for species.

    Then we have Will Provine and a host of others saying evolution is purposeless = no God or meaning of life.

    Geez Nick you don’t even appear to understand the theory of evolution.

    Oh, I think he does :)

  49. 50
    material.infantacy
  50. 51

    Easily answered, Elizabeth.

    Scenario 1: I throw two pairs of dice simultaneously, one with my left hand, one with my right hand. What is the probability that both pairs will turn up as twelves, and how did you calculate it?

    Scenario 2: I announce to you that I am going to throw a pair of dice in 30 seconds, and that I am going to throw that the same pair of dice again an hour from now. What is the probability that both pairs with turn up as twelves, and how did you calculate it?

    Scenario 3: I announce to you that I am going to throw a pair of dice in 30 seconds, then step into a suspended animation chamber, from which I will emerge a million years hence, whereupon I will pick up that same pair of dice and throw then again. What is the probability that both pairs will turn up as twelves, and how did you calculate it?

  51. Easily answered, Elizabeth.

    Scenario 1: I throw two pairs of dice simultaneously, one with my left hand, one with my right hand. What is the probability that both pairs will turn up as twelves, and how did you calculate it?

    Scenario 2: I announce to you that I am going to throw a pair of dice in 30 seconds, and that I am going to throw that the same pair of dice again an hour from now. What is the probability that both pairs with turn up as twelves, and how did you calculate it?

    Scenario 3: I announce to you that I am going to throw a pair of dice in 30 seconds, then step into a suspended animation chamber, from which I will emerge a million years hence, whereupon I will pick up that same pair of dice and throw then again. What is the probability that both pairs will turn up as twelves, and how did you calculate it?

    Ah, I wondered if you’d done that. You’ve forgotten about drift :)

  52. 53

    Elizabeth:

    You have not answered my question. You have not convinced me that you understand how to calculate the relevant probabilities in the examples given.

    Drift has nothing to do with the point I was making. The point I was making is that Nick has confused “independent events” with “simultaneous events”. This is an error in very basic probability theory. If Behe or Dembski or Meyer made any similar error in population genetics or virology, as you can see from the comments of Venema, Matzke, Matheson, etc. above, they would be lambasted for “writing out of their field” or as being “incompetent” or as “getting the math all wrong”. Yet when Nick makes a similar blunder, that’s just peachy-keen, and none of his friends — Shallit, Moran, Myers, etc. — says a thing about it. The double standard is plain. When you are criticizing ID proponents, absolutely no intellectual consistency is required.

    Best wishes, Elizabeth.

  53. Elizabeth Liddle:

    Joseph, I’m not sure how you are defining “random” here, but the entire concept of “natural selection” is that it is the systematic increase in prevalence, in a population, of genotypes that tend to confer greater reproductive success, as opposed to “drift” which is the non-systematic increase in prevalance of genotypes are orthogonal to reproductive success.

    Yes, but 1) those genotypes can be just about anything- ie that works good enough and 2) where are the papers I asked for? There must be volumes demonstrating natural selection is non-random. But hey, look at it this way-> natural selection is the result (ie output) of three processes (ie inputs), each is either random or has a random component. Outputs follow inputs.

    As for Nock Matzke understanding the ToE I find that very doubtful- but then again I am just going by what he posts.

  54. I think you may be confusing the generation of variance, which may or may not be “random”, with natural selection, which is by definition not “random” – that’s why it’s called “selection”.

  55. You have not answered my question. You have not convinced me that you understand how to calculate the relevant probabilities in the examples given.

    Oh, right.

    OK.

    Assuming six-sided dice, the probability of a twelve from any throw of a pair is 1/36. So the probability of two simultaneous or consecutive twelves (regardless of the time interval i.e. disregarding the decaying probability of your survival between throw 1 and throw 2) = (1/36)^2, i.e. 1/1296

    Drift has nothing to do with the point I was making.

    But it should have done, which is Nick’s point. The probabilities are not independent, as they would be if they had to be simultaneous, which they don’t.

    You have to factor in the probability that the first mutation will be replicated, which, if it is neutral, will be quite high. Then, given a first replication, the probability that it will be replicated again, is even higher, and as the number of copies in the population grow, the greater the probability that the second mutation will occur in a bearer of the first. In a sexually reproducing population this is even more likely than in a cloning population, of course, because each mutation can drift independently, and with multiple copies of each mutation drifting round the population the chances of them meeting up becomes quite probable.

    Of course this depends on drift getting started, but calculating the probability of that is a lot more complicated than the probabilities in your dice example, and the values considerably higher.

    The point I was making is that Nick has confused “independent events” with “simultaneous events”. This is an error in very basic probability theory.

    No, he hasn’t made that error. In the context of a mutation in a replicating population, squaring the probabilities of each mutation occurring ab initio is simply wrong. It ignores the fact that the first mutation, once it has occurred, has a high chance of being replicated,and re-replicated, and each replication is an opportunity for the second mutation to join it. And neutral mutations have quite a high probability of drifting through a population – even slightly deleterious ones do, and, if this happens, the chances of it being in a genotype that experiences the second mutation are hugely increased.

    If Behe or Dembski or Meyer made any similar error in population genetics or virology, as you can see from the comments of Venema, Matzke, Matheson, etc. above, they would be lambasted for “writing out of their field” or as being “incompetent” or as “getting the math all wrong”.

    Well, sure, if they made an error. But it was not an error.

    Yet when Nick makes a similar blunder, that’s just peachy-keen, and none of his friends — Shallit, Moran, Myers, etc. — says a thing about it. The double standard is plain. When you are criticizing ID proponents, absolutely no intellectual consistency is required.

    It isn’t a double standard. The mistake is Behe’s, and now yours. Nick is correct.

    Best wishes, Elizabeth.

    And to you :)

  56. Elizabeth,

    There isn’t any part of the definition of natural selection that sez it is non-random. Also it is an oxymoron as nature doesn’t select.

    Natural selection, by definition is differential reproduction due to heritable (random) variation- random as in entirely left to chance- as in errors/ mistakes/ accidents. It is a result- an output.

    “Natural selection is the result of differences in survival and reproduction among individuals of a population that vary in one or more heritable traits.” Page 11 “Biology: Concepts and Applications” Starr fifth edition

    “Natural selection is the simple result of variation, differential reproduction, and heredity—it is mindless and mechanistic.” UBerkley

    “Natural selection is the blind watchmaker, blind because it does not see ahead, does not plan consequences, has no purpose in view.” Dawkins in “The Blind Watchmaker”?

    As for the generation of variance, according to the current theory of evolution, it is entirely via genetic errors/ mistakes/ accidents. Whatever happens, happens. And whatever survives to reproduce survives to reproduce.

    You do understand that with sexual reproduction even the most beneficial mutation (that one parent has) is not guaranteed to make it to the next generation. That is part of the issue- tracking natural selection. To me and most people it is just a sound bite and has never lived up to its billing.

  57. 58

    Elizabeth (18.1.1.2):

    I’ll respond to the substance of your post later, after I have consulted my expert sources. In the meantime, I wish to make a simple point. You, not Nick, are the one who is justifying Nick’s procedure in terms of “drift”. The word “drift” is not mentioned in either of Nick’s articles against Behe cited above. So you are doing a mind-reading act by assuming that “drift” was in Nick’s mind when he made his argument.

    Maybe Nick had drift in mind and maybe he didn’t; but it formed no part of his exposition. We are all from different fields here: philosophers, theologians, biologists, physicists, engineers, biochemists, lawyers, computer programmers, etc. All of us have different levels of familiarity with jargon and concepts, and shorthand that assumes certain things about the reader will be completely lost on many. If Nick wanted to argue from drift, he should have made the argument explicit, as you have done. The place to argue in shorthand, skipping all kinds of steps, crucial definitions, and exposition of concepts, is in professional technical journals, where certain things can be assumed in the readership, not on an internet conversation site, where they cannot.

  58. as to the materialistic conjecture of ‘drift’;

    The consequences of genetic drift for bacterial genome complexity – Howard Ochman – 2009
    Excerpt: The increased availability of sequenced bacterial genomes allows application of an alternative estimator of drift, the genome-wide ratio of replacement to silent substitutions in protein-coding sequences. This ratio, which reflects the action of purifying selection across the entire genome, shows a strong inverse relationship with genome size, indicating that drift promotes genome reduction in bacteria.
    http://genome.cshlp.org/conten.....091785.109

    Thus once again the Darwinists has no real evidence but merely ‘shabby excuses’ to cover up gaping holes in their bankrupt hypothesis;

    =======================

    further notes:

    Though it is impossible to reconstruct the DNA of the earliest bacteria fossils, scientists find in the fossil record, and compare them to their descendants of today, there are many ancient bacteria spores recovered and ‘revived’ from salt crystals and amber crystals which have been compared to their living descendants of today. Some bacterium spores, in salt crystals, dating back as far as 250 million years have been revived, had their DNA sequenced, and compared to their offspring of today (Vreeland RH, 2000 Nature). To the disbelieving shock of many scientists, both ancient and modern bacteria were found to have the almost same exact DNA sequence.

    The Paradox of the “Ancient” (250 Million Year Old) Bacterium Which Contains “Modern” Protein-Coding Genes:
    “Almost without exception, bacteria isolated from ancient material have proven to closely resemble modern bacteria at both morphological and molecular levels.” Heather Maughan*, C. William Birky Jr., Wayne L. Nicholson, William D. Rosenzweig§ and Russell H. Vreeland ;
    http://mbe.oxfordjournals.org/...../19/9/1637

    These following studies, by Dr. Cano on ancient bacteria, preceded Dr. Vreeland’s work:

    “Raul J. Cano and Monica K. Borucki discovered the bacteria preserved within the abdomens of insects encased in pieces of amber. In the last 4 years, they have revived more than 1,000 types of bacteria and microorganisms — some dating back as far as 135 million years ago, during the age of the dinosaurs.,,, In October 2000, another research group used many of the techniques developed by Cano’s lab to revive 250-million-year-old bacteria from spores trapped in salt crystals. With this additional evidence, it now seems that the “impossible” is true.”
    http://www.physicsforums.com/s.....p?t=281961

    Revival and identification of bacterial spores in 25- to 40-million-year-old Dominican amber
    Dr. Cano and his former graduate student Dr. Monica K. Borucki said that they had found slight but significant differences between the DNA of the ancient, 25-40 million year old amber-sealed Bacillus sphaericus and that of its modern counterpart,(thus ruling out that it is a modern contaminant, yet at the same time confounding materialists, since the change is not nearly as great as evolution’s ‘genetic drift’ theory requires.)
    http://www.sciencemag.org/cgi/...../5213/1060

    Dr. Cano’s work on ancient bacteria came in for intense scrutiny since it did not conform to Darwinian predictions, and since people found it hard to believe you could revive something that was millions of years old. Yet Dr. Cano has been vindicated:

    “After the onslaught of publicity and worldwide attention (and scrutiny) after the publication of our discovery in Science, there have been, as expected, a considerable number of challenges to our claims, but in this case, the scientific method has smiled on us. There have been at least three independent verifications of the isolation of a living microorganism from amber.”
    http://www.uncommondescent.com.....ent-357693

    In reply to a personal e-mail from myself, Dr. Cano commented on the ‘Fitness Test’ I had asked him about:
    Dr. Cano stated: “We performed such a test, a long time ago, using a panel of substrates (the old gram positive biolog panel) on B. sphaericus. From the results we surmised that the putative “ancient” B. sphaericus isolate was capable of utilizing a broader scope of substrates. Additionally, we looked at the fatty acid profile and here, again, the profiles were similar but more diverse in the amber isolate.”:
    Fitness test which compared ancient bacteria to its modern day descendants, RJ Cano and MK Borucki

    Thus, the most solid evidence available for the most ancient DNA scientists are able to find does not support evolution happening on the molecular level of bacteria. In fact, according to the fitness test of Dr. Cano, the change witnessed in bacteria conforms to the exact opposite, Genetic Entropy; a loss of functional information/complexity, since fewer substrates and fatty acids are utilized by the modern strains. Considering the intricate level of protein machinery it takes to utilize individual molecules within a substrate, we are talking an impressive loss of protein complexity, and thus loss of functional information, from the ancient amber sealed bacteria. Here is a revisit to the video of the ‘Fitness Test’ that evolutionary processes have NEVER passed as for a demonstration of the generation of functional complexity/information above what was already present in a parent species bacteria:

    Is Antibiotic Resistance evidence for evolution? – ‘Fitness Test’ – video
    http://www.metacafe.com/watch/3995248

    According to prevailing evolutionary dogma, there ‘HAS’ to be ‘major genetic drift’ to the DNA of modern bacteria from 250 million years ago, even though the morphology (shape) of the bacteria can be expected to remain exactly the same. In spite of their preconceived materialistic bias, scientists find there is no significant genetic drift from the ancient DNA.

    ======================

    Solid Rock – the 5th service band Featuring TRU-SERVA
    http://www.youtube.com/watch?v=G4jD70Y-mQ0

  59. 60
    material.infantacy

    From what I’m gathering, the objection is to Behe’s observation (and the probability squared) relates to the fact that his 10^20 number is empirical, so no manner of theoretical influencing factors are relevant.

    If drift was a factor, then it’s already accounted for in Behe’s 10^20. The observation that CQR requires 10^20 generations is just that, an observation — and not a calculation.

    Apparently Behe suggested that a “double” CQR function, that is, a hypothetical “CQR2” requiring double the mutations to achieve, would need a population of 10^40. This seems entirely reasonable.

    He’s not talking about a mutation occurring in a single organism, he’s talking about a mutation occurring and becoming fixed in an entire population. For that reason, the CQR2 event can be viewed as being equivalent with two independent, simultaneous CQR-type events.

    That being the case, P(CQR2) = P(CQR) * P(CQR), or 10^-20 * 10^-20 = 10^-40.

    Since 10^20 is the number of trials for a population, and not for an individual, it represents an empirical number with concrete evolutionary factors already present.

    Again, Behe doesn’t seem to be speaking about the probability of an individual acquiring the hypothetical function, he’s referring to a function becoming established in a population, over 10^40 trials, based on the very concrete, 10^20 trials.

    If I’m correct, then objections that Behe hasn’t considered various evolutionary factors, or repeated trials in a probability experiment are just not relevant, as it’s all entirely implicit within the 10^20 number.

  60. 61

    Elizabeth (re 18.1.1.1.2):

    I think we are arguing about two different things, and they are getting conflated, and that this is confusing us both. At least, it is confusing me. I want to try out a scenario on you to see if it will help us understand each other better.

    Suppose that to achieve a certain effect, say, to give a certain monkey webbed fingers, one needed two mutations, one to one sector of the genome, and another to a far-removed sector of the genome. Let’s call these changes Mutation A and Mutation B.

    Let’s suppose that the probability of either mutation’s *occurring* (not of being found in conjunction with the other, but simply of occurring) is approximately the same, and let’s say, for the sake of argument, that it is one in 10 million in each case.

    Now, if I understand you correctly, you are arguing that, *given that Mutation A has occurred*, it will have spread through the population over time and will now be found in a reasonably high percentage of individual organisms (20%, or 30%, or 50%, or whatever). This means that, *if Mutation B comes along*, there is a reasonably high probability that B will find A already there in the organism, and therefore a reasonably high probability that the desired result (webbed fingers, or whatever) will occur.

    So if you are calculating the probabiity of Mutation B finding Mutation A in a particular organism when we know Mutation A is already there in a certain proportion of the population, then of course you are not going to simply square the probabilities of abstract occurrence of the two mutations. You have to factor in not what the abstract probability of Mutation A was, before it occurred (which would produce a very low probability), but what percentage of the population Mutation A is now found in, which could produce a much higher probability.

    If this is what you are saying, I understand you and I do not contest it.

    But I am asking a different question. (I suspect Behe is asking the same question that I am, but I don’t want to speak for him on this particular point, so here I will speak only for myself.) I am asking: *In advance of the first occurrence of either A or B*, if you wanted to calculate the probability *simply that A and B will appear* (not necessarily appear in the same organism, just appear anywhere at all in the population) once each over X generations, how would you do it?

    Would you not (a) assume that the occurrence or non-occurrence of Mutation A has no influence whatsoever over the occurrence or non-occurrence of Mutation B, and vice versa? That is, would you not treat the occurrence of both mutations as the occurrence of two independent events? And would you not (b) compute the “probablistic resources” (size of litters, how many litters a female will bear in her lifetime, etc.) to figure out how many opportunities are available during X generations for both A and B to occur once somewhere in the population?

    If I may use a card analogy: Your question seems to be, “What are the odds of getting a Royal Flush given that I already have three of the five necessary cards in my hand and still have three more two-card draws?” And my question is: “Knowing nothing in advance about any cards a given person will be dealt, what are the odds that the given person will get a Royal Flush within 50 years if he plays a certain form of poker 8 hours a day, five days a week, at the rate of 4 hands per hour?” These two outcomes would be calculated in quite different ways, would they not? And my contention is that *both* of these situations are relevant to calculating probabilities of evolutionary change, but that they calculate different things. And it seems to me that part of the communications barrier between the standard neo-Darwinian population geneticists and the ID people is that, when they argue about probabilities, they do not always seem to realize that they are calculating different things.

    Does this make sense to you? If not, please provide an alternate analysis of my scenario.

  61. I think you are absolutely right that people are asking different questions and thus calculating different things!

    And yes, you have what I am saying absolutely right.

    Then you say:

    But I am asking a different question. (I suspect Behe is asking the same question that I am, but I don’t want to speak for him on this particular point, so here I will speak only for myself.) I am asking: *In advance of the first occurrence of either A or B*, if you wanted to calculate the probability *simply that A and B will appear* (not necessarily appear in the same organism, just appear anywhere at all in the population) once each over X generations, how would you do it?

    Now, you say that the probability of each mutation occurring is 1/1 million, and I assume you mean that every offspring born has a 1/1million of having that mutation de novo.

    And let us denote the size of the population as N and assume for ease of calculation that it is stable.

    The trick is to work with the probabilities of the mutation not occurring. So the probability of an offspring not having mutation A de novo is 1-(1/1million), and to get the probability of no offspring in its entire generation not having it, we raise that to the power N: [1-(1/1million)]^N. Then, to get the probability of no offspring having mutation A de novo in X generations we raise all that to the power X: {[1-(1/1million)]^N}^X. Finally, of course, the to get the probability that A willoccur, you subtract that from 1:

    1-{[1-(1/1million)]^N}^X.

    Which will steadily approach 1 with each passing generation. For example, for a population of 100,000, over 100 generations, the probability of A occurring will be .99995, and the same for B. Each new birth increases the probability that A will be present in the population.

    And to get the probability of B occurring in an organisms that already bears A, then you need to consider the drift issue – the probability of a neutral mutation being found in a given proportion of the population. Which is a bit trickier :) But we already agree on that.

    However, that isn’t the whole story of course, because the relevant calculation is not the probability of a specific feature, but the probability of a feature with a comparable function to the one we observe, otherwise we are drawing the target round the arrow, and indeed even if we specify a comparable feature, we are still drawing the target round the arrow to some extent, because we simply don’t know how many “solutions” to survival problem there are for a given population. We don’t know the size of the “search space”.

    But even sticking with a specific function, there may be a number of neutral mutations, which, when found in combination with mutation B could produce the beneficial feature, indeed there could be a number of pairs of neutral mutations which, when found together, produce that feature.

    Still, that’s getting into new territory. I hope what I have written above addresses your question.

    Cheers

    Lizzie

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