Intelligent Design Irreducible Complexity

Asked at Evolution News: How much can evolution really accomplish?

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A Mousetrap for Darwin: Michael J. Behe Answers His Critics by [Michael J. Behe]

Eric Anderson offers response to biochemist Larry Moran, who has argued that Michael Behe has misunderstood and misinterpreted the evidence re chloroquine resistance in A Mousetrap for Darwin:

In 2007, biochemist Michael Behe had the temerity to ask a question — a question that should have been asked with repeated and urgent sincerity by all biologists since the ink from Darwin’s quill first dried on his manuscript: What can evolution actually accomplish?

The question is at once reasonable and utterly crucial to the evolutionary story. Yet, for the most part it has been ignored in the history of evolutionary thought. The deeply held assumption of nearly all evolutionists is that evolution can do everything. After all, we’re here aren’t we! So there is little point in even asking the question. To be sure, occasional lip service has been paid to this inquiry over the decades, but such efforts typically descend into a question-begging exercise that simply assumes evolution must have this great creative power. Again, we’re here, and so even if we don’t understand the precise mechanisms of evolution, even if we’re still trying to fill in the details, even if there is some as-yet-undiscovered evolutionary mechanism, evolution simply must have this great creative power.

Paleontologist Stephen Jay Gould famously used this tactic, arguing that even if we don’t understand exactly how evolution works, we must still regard evolution as a fact, because, well, things have evolved. Phillip Johnson rightly called out Gould for this self-serving circular attempt to prop up evolution, with Johnson’s careful analysis revealing that Gould’s “fact” of evolution turned out to mean nothing more than the theory.

Eric Anderson, “How Much Can Evolution Really Accomplish?” at Evolution News and Science Today (February 25, 2022)

Actually, in religious circles, if anyone treated their sect’s creed the way Darwinians have treated evolution, they would be regarded as a cult.

9 Replies to “Asked at Evolution News: How much can evolution really accomplish?

  1. 1
    bornagain77 says:

    Here are all the responses from Dr. Behe to his critics, after the 2014 Summers’ results came out. Empirical results that verified Dr. Behe’s claim that, (at least), two coordinated mutations are required to achieve the 1 in 10^20 chloroquine resistance.

    An Open Letter to Kenneth Miller and PZ Myers – Michael Behe July 21, 2014
    Dear Professors Miller and Myers,
    Talk is cheap. Let’s see your numbers.
    In your recent post on and earlier reviews of my book The Edge of Evolution you toss out a lot of words, but no calculations. You downplay FRS Nicholas White’s straightforward estimate that — considering the number of cells per malaria patient (a trillion), times the number of ill people over the years (billions), divided by the number of independent events (fewer than ten) — the development of chloroquine-resistance in malaria is an event of probability about 1 in 10^20 malaria-cell replications. Okay, if you don’t like that, what’s your estimate? Let’s see your numbers.,,,
    ,,, If you folks think that direct, parsimonious, rather obvious route to 1 in 10^20 isn’t reasonable, go ahead, calculate a different one, then tell us how much it matters, quantitatively. Posit whatever favorable or neutral mutations you want. Just make sure they’re consistent with the evidence in the literature (especially the rarity of resistance, the total number of cells available, and the demonstration by Summers et al. that a minimum of two specific mutations in PfCRT is needed for chloroquine transport). Tell us about the effects of other genes, or population structures, if you think they matter much, or let us know if you disagree for some reason with a reported literature result.
    Or, Ken, tell us how that ARMD phenotype you like to mention affects the math. Just make sure it all works out to around 1 in 10^20, or let us know why not.
    Everyone is looking forward to seeing your calculations. Please keep the rhetoric to a minimum.
    With all best wishes (especially to Professor Myers for a speedy recovery),
    Mike Behe
    http://www.evolutionnews.org/2.....88041.html

    Laurence Moran’s Sandwalk Evolves Chloroquine Resistance – Michael Behe August 13, 2014
    Excerpt: That’s the reason I issued the challenge in the first place. In my experience almost all Darwinists and fellow travelers (Professor Moran doesn’t consider himself a Darwinist) simply don’t think quantitatively about what their theory asks of nature in the way of probability. When prodded to do so, they quickly encounter numbers that are, to say the least, bleak. They then seem to lose all interest in the problem and wander away. The conclusion that an unbiased observer should draw is that Darwinian claims simply don’t stand up to even the most cursory calculations.
    http://www.evolutionnews.org/2.....88811.html

    How Many Ways Are There to Win at Sandwalk? – Michael Behe – August 15, 2014
    Excerpt: ,, with chloroquine resistance in Plasmodium falciparum. The best current statistical estimate of the frequency of de novo resistance is Nicholas White’s value of 1 in 10^20 parasites. That number is now essentially fixed — no pathway to resistance will be found that is substantially more probable than that. Although with more data the value may be refined up or down by even as much as one or two orders of magnitude (to between 1 in 10^18-10^22), it’s not going very far on a log scale. Not nearly far enough to lift the shadow from Darwinism.
    What’s more, we can also conclude that the mutations that have already been found are the most effective available of any combination of mutations whose joint probability is greater than 1 in 10^20, since more effective alternatives would already have occurred and been selected if they were available.,,,
    The bottom line for all of them is that the acquisition of chloroquine resistance is an event of statistical probability 1 in 10^20.,,,
    http://www.evolutionnews.org/2.....88981.html

    Guide of the Perplexed: A Quick Reprise of The Edge of Evolution – Michael Behe – August 20, 2014
    Excerpt: *Any particular adaptive biochemical feature requiring the same mutational complexity as that needed for chloroquine resistance in malaria is forbiddingly unlikely to have arisen by Darwinian processes and fixed in the population of any class of large animals (such as, say, mammals), because of the much lower population sizes and longer generation times compared to that of malaria. (By “the same mutational complexity” I mean requiring 2-3 point mutations where at least one step consists of intermediates that are deleterious, plus a modest selection coefficient of, say, 1 in 10^3 to 1 in10^4. Those factors will get you in the neighborhood of 1 in 10^20.)
    *Any adaptive biological feature requiring a mutational pathway of twice that complexity (that is, 4-6 mutations with the intermediate steps being deleterious) is unlikely to have arisen by Darwinian processes during the history of life on Earth.,,,
    What’s more, Nicholas White’s factor of 1 in 10^20 already has built into it all the ways to evolve chloroquine resistance in P. falciparum. In the many malarial cells exposed to chloroquine there have surely occurred all possible single mutations and probably all possible double mutations — in every malarial gene — yet only a few mutational combinations in pfcrt are effective. In other words, mutation and selection have already searched all possible solutions of the entire genome whose probability is greater than 1 in 10^20, including mutations to other genes. The observational evidence demonstrates that only a handful are effective. There is no justification for arbitrarily inflating probabilistic resources by citing imaginary alternative evolutionary routes.
    http://www.evolutionnews.org/2.....89161.html

    Drawing My Discussion with Laurence Moran to a Close – Michael Behe – August 26, 2014
    Excerpt: And just as those alternative chloroquine resistance pathways are imaginary, Professor Moran’s “millions and millions of possible evolutionary outcomes” are imaginary. In the absence of actual evidence that a huge number of relevant unrealized biochemical features could have been built by Darwinian processes, it is illegitimate to arbitrarily multiply probabilistic resources.
    Moran is right that there is “no a priori requirement that Earth contain red pines and white pines.” But he doesn’t follow his own logic far enough. In fact there’s no a priori requirement that Earth contain any life at all, or that any life that does exist be able to successfully traverse a mutational pathway by Darwinian means to give rise to a form of life significantly different from itself.
    In the absence of an a priori requirement, science is obliged to investigate whether or not such pathways exist. Right now the evidence we have in hand militates strongly against it.
    https://evolutionnews.org/2014/08/drawing_my_disc/

  2. 2
    bornagain77 says:

    Kenneth Miller Resists Chloroquine Resistance – Michael Behe – January 14, 2015
    Excerpt: Kenneth R. Miller has posted a (11 page) reply to my challenge to him to give a quantitative account for the extreme rarity of the origin of chloroquine resistance in malaria.,,,
    The first two and a half pages of the PDF version of Miller’s essay consist of stage-setting and throat-clearing. The last six pages are a reprise of his review of The Edge of Evolution and a defense of the evolutionary musings of University of Chicago biologist Joseph Thornton from my skepticism. I’ll deal with those later. Miller’s only response to my take on the importance of Summers et al. is in the section “Parasites and Drugs.” Although the section is less than three pages (including several large figures), as we shall see it includes a number of serious mistakes.
    Unfortunately, Miller dodges my challenge to provide a quantitative account of the rarity of the origin of chloroquine resistance. I had asked him to “Please keep the rhetoric to a minimum.” Alas, to no avail. He cites no relevant numbers, makes no calculations — just words.,,,
    Miller’s reading of Summers et al. is seriously mistaken. Sadly, a person who can’t accurately report the results of a paper makes for an unreliable guide. I urge everyone who has sufficient background to read at least the disputed parts of Summers et al. Determine for yourself which account is correct.
    http://www.evolutionnews.org/2.....92691.html

    The Very Neutral Kenneth Miller – Michael Behe – January 15, 2015
    Excerpt: But is there any direct, positive, experimental evidence indicating whether a single, uncompensated K76T mutation is deleterious or neutral?
    Yes, there is. As I wrote earlier, to see if a mutation is harmful by itself, at the very least you have to test it without any other mutations present in the relevant organism. Lakshmanan et al. did this carefully in the lab in 2005:,,,
    Miller’s claim that the individual mutation is neutral is wrong.
    http://www.evolutionnews.org/2.....92721.html

    The Many Paths of Kenneth Miller – Michael Behe – January 16, 2015
    Excerpt: Suppose you were given a choice of a billion trillion roads to travel, but were told that only one of them led to safety; the others all led to certain death. You would likely feel pretty pessimistic about your chances.,,,
    The number of 1 in 10^20 against developing chloroquine resistance comes from estimating the number of malaria cells without resistance that it takes to produce and select one with resistance, no matter what genetic route is taken. So the number of routes that Miller emphasizes turns out to have no effect at all on the statistical likelihood of developing chloroquine resistance. Each route itself is actually less likely than the cumulative probability. All of the routes together add up to only 1 in 10^20.
    http://www.evolutionnews.org/2.....92761.html

    Kenneth Miller Steps on Darwin’s Achilles Heel
    Michael Behe – January 17, 2015
    Excerpt: So what should we conclude from all this? Miller grants for purposes of discussion that the likelihood of developing a new protein binding site is 1 in 10^20. Now, suppose that, in order to acquire some new, useful property, not just one but two new protein-binding sites had to develop. In that case the odds would be the multiple of the two separate events — about 1 in 10^40, which is somewhat more than the number of cells that have existed on earth in the history of life. That seems like a reasonable place to set the likely limit to Darwinism, to draw the edge of evolution.
    https://evolutionnews.org/2015/01/kenneth_miller_1/

    Moreover, to top it all off, and to add insult to injury, the I in 10^20 chloroquine resistance in the malaria parasite came at a loss of fitness for the parasite, not a gain. (Which is exactly the opposite type of experimental evidence that Darwinists need in order to give their theory even a tiny semblance of being remotely feasible, as far as experimental science itself is concerned).

    Metabolic QTL Analysis Links Chloroquine Resistance in Plasmodium falciparum to Impaired Hemoglobin Catabolism – January, 2014
    Summary: Chloroquine was formerly a front line drug in the treatment of malaria. However, drug resistant strains of the malaria parasite have made this drug ineffective in many malaria endemic regions. Surprisingly, the discontinuation of chloroquine therapy has led to the reappearance of drug-sensitive parasites. In this study, we use metabolite quantitative trait locus analysis, parasite genetics, and peptidomics to demonstrate that chloroquine resistance is inherently linked to a defect in the parasite’s ability to digest hemoglobin, which is an essential metabolic activity for malaria parasites. This metabolic impairment makes it harder for the drug-resistant parasites to reproduce than genetically-equivalent drug-sensitive parasites, and thus favors selection for drug-sensitive lines when parasites are in direct competition. Given these results, we attribute the re-emergence of chloroquine sensitive parasites in the wild to more efficient hemoglobin digestion.
    http://www.plosgenetics.org/ar.....en.1004085

    As to Eric Anderson’s astute observation that Behe’s, very basic, question of, “what can evolution really accomplish?”, is “a question that should have been asked with repeated and urgent sincerity by all biologists since the ink from Darwin’s quill first dried on his manuscript”,,,

    “In 2007, biochemist Michael Behe had the temerity to ask a question — a question that should have been asked with repeated and urgent sincerity by all biologists since the ink from Darwin’s quill first dried on his manuscript: What can evolution actually accomplish?”

    This, ahem, ’empirical oversight’ on the part of Darwinists to ask this most basic question of “what can evolution really accomplish?” is simply completely inexcusable for any theory of science that claims to be a true and testable science.

    As I’ve said years ago, “I don’t know what Darwinists are doing, but they sure in blue blazes are not doing science!”

    1 Thessalonians 5:21
    but test all things. Hold fast to what is good.

  3. 3
    bornagain77 says:

    Moreover, Dr. Behe’s 1 in 10^20 observation is not a stand alone, and/or an anomalous, observation. But Dr. Behe’s 1 in 10^20 observation is in general agreement with several other lines of empirical and mathematical evidence.

    For instance, Doug Axe and Ann Gauger found that, “The waiting time required to achieve four mutations is 10^15 years. That’s longer than the age of the universe.”

    New Paper from Biologic Institute, “Shared Evolutionary History or Shared Design?”
    Ann Gauger – January 1, 2015
    We went on to test for cooption the two most likely enzymes by generating two-base combinations of mutations. After testing 70 percent of all possible two-base mutations for each enzyme, or about 40 million cells each, that also failed.
    What does this mean? In an evolutionary scenario, to get an enzyme to switch functions the first step is to make a spare copy that can be mutated without destroying a function the cell needs. Second, the cell has to overproduce the mutating enzyme, because any newly emerging enzyme will be very bad at the job at first. To compensate there will need to be lots of enzyme around. Third, there is the problem of finding the right combination of mutations by random search.
    Taken together, since we found no enzyme that was within one mutation of cooption, the total number of mutations needed is at least four: one for duplication, one for over-production, and two or more single base changes. The waiting time required to achieve four mutations is 10^15 years. That’s longer than the age of the universe. The real waiting time is likely to be much greater, since the two most likely candidate enzymes failed to be coopted by double mutations.
    https://evolutionnews.org/2015/01/happy_new_year/

    And in the following 2015 paper entitled, “Quantum criticality in a wide range of important biomolecules” it was found that “Most of the molecules taking part actively in biochemical processes are tuned exactly to the transition point and are critical conductors,” and the researchers further commented that “finding even one (biomolecule) that is in the quantum critical state by accident is mind-bogglingly small and, to all intents and purposes, impossible.,, of the order of 10^-50 of possible small biomolecules and even less for proteins,”,,,

    Quantum criticality in a wide range of important biomolecules – Mar. 6, 2015
    Excerpt: “Most of the molecules taking part actively in biochemical processes are tuned exactly to the transition point and are critical conductors,” they say.
    That’s a discovery that is as important as it is unexpected. “These findings suggest an entirely new and universal mechanism of conductance in biology very different from the one used in electrical circuits.”
    The permutations of possible energy levels of biomolecules is huge so the possibility of finding even one (biomolecule) that is in the quantum critical state by accident is mind-bogglingly small and, to all intents and purposes, impossible.,, of the order of 10^-50 of possible small biomolecules and even less for proteins,”,,,
    “what exactly is the advantage that criticality confers?”
    https://medium.com/the-physics-arxiv-blog/the-origin-of-life-and-the-hidden-role-of-quantum-criticality-ca4707924552

    Moreover, to drive this point even further home, this follow up 2018 article stated that “There is no obvious evolutionary reason why a protein should evolve toward a quantum-critical state, and there is no chance at all that the state could occur randomly.,,,”

    Quantum Critical Proteins – Stuart Lindsay – Professor of Physics and Chemistry at Arizona State University – 2018
    Excerpt: The difficulty with this proposal lies in its improbability. Only an infinitesimal density of random states exists near the critical point.,,
    Gábor Vattay et al. recently examined a number of proteins and conducting and insulating polymers.14 The distribution for the insulators and conductors were as expected, but the functional proteins all fell on the quantum-critical distribution. Such a result cannot be a consequence of chance.,,,
    WHAT OF quantum criticality? Vattay et al. carried out electronic structure calculations for the very large protein used in our work. They found that the distribution of energy-level spacings fell on exactly the quantum-critical distribution, implying that this protein is also quantum critical. There is no obvious evolutionary reason why a protein should evolve toward a quantum-critical state, and there is no chance at all that the state could occur randomly.,,,
    http://inference-review.com/ar.....l-proteins
    Gábor Vattay et al., “Quantum Criticality at the Origin of Life,” Journal of Physics: Conference Series 626 (2015);
    Gábor Vattay, Stuart Kauffman, and Samuli Niiranen, “Quantum Biology on the Edge of Quantum Chaos,” PLOS One 9, no. 3 (2014)

    etc.. etc..

    And Behe’s 1 in 10^20 observation is also in general agreement with the mathematics of population genetics.

    As Ann Gauger observed, “You don’t have to take my word for it. In 2007, Durrett and Schmidt estimated in the journal Genetics that for a single mutation to occur in a nucleotide-binding site and be fixed in a primate lineage would require a waiting time of six million years. The same authors later estimated it would take 216 million years for the binding site to acquire two mutations, if the first mutation was neutral in its effect.”

    More from Ann Gauger on why humans didn’t happen the way Darwin said – July 2012
    Excerpt: Each of these new features probably required multiple mutations. Getting a feature that requires six neutral mutations is the limit of what bacteria can produce. For primates (e.g., monkeys, apes and humans) the limit is much more severe. Because of much smaller effective population sizes (an estimated ten thousand for humans instead of a billion for bacteria) and longer generation times (fifteen to twenty years per generation for humans vs. a thousand generations per year for bacteria), it would take a very long time for even a single beneficial mutation to appear and become fixed in a human population.
    You don’t have to take my word for it. In 2007, Durrett and Schmidt estimated in the journal Genetics that for a single mutation to occur in a nucleotide-binding site and be fixed in a primate lineage would require a waiting time of six million years. The same authors later estimated it would take 216 million years for the binding site to acquire two mutations, if the first mutation was neutral in its effect.
    Facing Facts
    But six million years is the entire time allotted for the transition from our last common ancestor with chimps to us according to the standard evolutionary timescale. Two hundred and sixteen million years takes us back to the Triassic, when the very first mammals appeared. One or two mutations simply aren’t sufficient to produce the necessary changes,, in the time available. At most, a new binding site might affect the regulation of one or two genes.
    http://www.uncommondescent.com.....rwin-said/

    And Dr. John Sanford, (who’s credentials in genetics are impeccable, i.e. he invented the ‘gene gun’ and taught at Cornell for 20 years), found, via the mathematics of population genetics, (and computer simulation), that, “the waiting time for the fixation of a “string-of-one” is by itself problematic (Table 2). Waiting a minimum of 1.5 million years (realistically, much longer),, the fixation of two co-dependent mutations is extremely problematic – requiring at least 84 million years,,, Certainly the creation and fixation of a string of three (requiring at least 380 million years) would be extremely untimely (and trivial in effect),,, When we increase the hominin population from 10,000 to 1 million (our current upper limit for these types of experiments), the waiting time for creating a string of five is only reduced from two billion to 482 million years.”

    The waiting time problem in a model hominin population – 2015 Sep 17
    John Sanford, Wesley Brewer, Franzine Smith, and John Baumgardner
    Excerpt: The program Mendel’s Accountant realistically simulates the mutation/selection process,,,
    Given optimal settings, what is the longest nucleotide string that can arise within a reasonable waiting time within a hominin population of 10,000? Arguably, the waiting time for the fixation of a “string-of-one” is by itself problematic (Table 2). Waiting a minimum of 1.5 million years (realistically, much longer), for a single point mutation is not timely adaptation in the face of any type of pressing evolutionary challenge. This is especially problematic when we consider that it is estimated that it only took six million years for the chimp and human genomes to diverge by over 5 % [1]. This represents at least 75 million nucleotide changes in the human lineage, many of which must encode new information.
    While fixing one point mutation is problematic, our simulations show that the fixation of two co-dependent mutations is extremely problematic – requiring at least 84 million years (Table 2). This is ten-fold longer than the estimated time required for ape-to-man evolution. In this light, we suggest that a string of two specific mutations is a reasonable upper limit, in terms of the longest string length that is likely to evolve within a hominin population (at least in a way that is either timely or meaningful). Certainly the creation and fixation of a string of three (requiring at least 380 million years) would be extremely untimely (and trivial in effect), in terms of the evolution of modern man.
    It is widely thought that a larger population size can eliminate the waiting time problem. If that were true, then the waiting time problem would only be meaningful within small populations. While our simulations show that larger populations do help reduce waiting time, we see that the benefit of larger population size produces rapidly diminishing returns (Table 4 and Fig. 4). When we increase the hominin population from 10,000 to 1 million (our current upper limit for these types of experiments), the waiting time for creating a string of five is only reduced from two billion to 482 million years.
    http://www.ncbi.nlm.nih.gov/pm.....MC4573302/

    Thus, it is not as if Dr. Behe is harping on some anomalous piece of evidence with his 1 in 10^20 observation, just so to try to unfairly criticize Darwinian evolution, but Dr. Behe is, in fact, in general argreement with several other lines of mathematical and empirical evidence that also find Darwin’s theory to be severely wanting.

    All in all, Dr. Behe is practicing good, old fashioned, empirical science. Whereas, on the other hand, his Darwinian critics are found to be providing, basically, ‘my dog ate my homework’ lame excuses for why Darwinian processes are found to be grossly inadequate in explaining the, (fairly astonishing), integrated molecular complexity of life found at the protein level.

    As the following article found, “Untangling the protein web,, is like comparing different degrees of infinity,,, The simple pathway models, (of Darwinists), are a gross oversimplification of what is actually happening.”

    Systems biology: Untangling the protein web – July 2009
    Excerpt: Vidal thinks that technological improvements — especially in nanotechnology, to generate more data, and microscopy, to explore interaction inside cells, along with increased computer power — are required to push systems biology forward. “Combine all this and you can start to think that maybe some of the information flow can be captured,” he says. But when it comes to figuring out the best way to explore information flow in cells, Tyers jokes that it is like comparing different degrees of infinity. “The interesting point coming out of all these studies is how complex these systems are — the different feedback loops and how they cross-regulate each other and adapt to perturbations are only just becoming apparent,” he says. “The simple pathway models are a gross oversimplification of what is actually happening.”
    http://www.nature.com/nature/j.....0415a.html

    So again, and in conclusion, “I don’t know what Darwinists are doing, but they sure in blue blazes are not doing science!”

    1 Thessalonians 5:21
    but test all things. Hold fast to what is good.

  4. 4
    Lieutenant Commander Data says:

    Bornagain77
    “So again, and in conclusion, “I don’t know what Darwinists are doing, but they sure in blue blazes are not doing science!”

    It’s enough to say that all books of Dawkins are cancelled by new discoveries in epigenetics. Now imagine the state of mind of Dawkins and his followers. First stage is to accept you were WRONG , not a little wrong but dead wrong. It’s not easy to admit you were stupid so you double triple down .
    It’s not about science it’s about fallen human nature that scientists think they are exempted. Little dictators that don’t accept anymore new evidences because they know the truth 😆

  5. 5
    polistra says:

    Resistance to a chemical is a form of immunity. Immunity is variable among individuals, and natural selection DOES cull out the more susceptible individuals in each situation and each threat.

    But natural selection couldn’t have created immunity itself. A complex system of sensors sending out warrior cells or warrior chemicals would have been a total drain on the cell’s resources unless and until it worked (almost) perfectly, complete with variation to fit different situations. Each sensor would be useless on its own, and each warrior cell would be useless without the sensors and the systematic intelligence that sends it to the appropriate location.

  6. 6
    bornagain77 says:

    Recently a Darwinist claimed that Dr. Behe was not using probability properly in his calculations.

    But then, after thinking about it for a while, I realized that Darwinists are the ones who are flagrantly misusing probability.

    Specifically, when Darwinists say something happened randomly, or that it happened by chance, they are not referring to some realistically defined mathematical probability of something happening in the universe, but are instead claiming that random chance is a cause unto itself.

    This is ‘very irrational’.

    As Wolfgang (not even wrong) Pauli himself noted, “While they (Darwinists) pretend to stay in this way completely ‘scientific’ and ‘rational,’ they become actually very irrational, particularly because they use the word ‘chance’, not any longer combined with estimations of a mathematically defined probability, in its application to very rare single events more or less synonymous with the old word ‘miracle.’”

    Pauli’s ideas on mind and matter in the context of contemporary science – Harald Atmanspacher
    Excerpt: “In discussions with biologists I met large difficulties when they apply the concept of ‘natural selection’ in a rather wide field, without being able to estimate the probability of the occurrence in a empirically given time of just those events, which have been important for the biological evolution. Treating the empirical time scale of the evolution theoretically as infinity they have then an easy game, apparently to avoid the concept of purposesiveness. While they pretend to stay in this way completely ‘scientific’ and ‘rational,’ they become actually very irrational, particularly because they use the word ‘chance’, not any longer combined with estimations of a mathematically defined probability, in its application to very rare single events more or less synonymous with the old word ‘miracle.’”
    Wolfgang Pauli (pp. 27-28)
    https://pdfs.semanticscholar.org/234f/4989e039089fed5ac47c7d1a19b656c602e2.pdf

    Moreover Charles Darwin himself honestly admitted that this is a wholly inadequate way to treat ‘chance’.

    Specifically, Darwin stated, “”I have hitherto sometimes spoken as if the variations—so common and multiform in organic beings under domestication, and in a lesser degree in those in a state of nature—had been due to chance. This, of course, is a wholly incorrect expression, but it serves to acknowledge plainly our ignorance of the cause of each particular variation.”

    “I have hitherto sometimes spoken as if the variations—so common and multiform in organic beings under domestication, and in a lesser degree in those in a state of nature—had been due to chance. This, of course, is a wholly incorrect expression, but it serves to acknowledge plainly our ignorance of the cause of each particular variation.”
    Charles Darwin – Origin – Chapter V
    http://darwin-online.org.uk/Va.....-1859.html

    Yet this “wholly incorrect expression” of “chance”, which “serves to acknowledge plainly our ignorance of the cause of each particular variation”, has, in the minds of Darwinists, become a cause unto itself. As Nobel laureate Jacques Monod himself stated, “It necessarily follows that chance alone is at the source of every innovation, and of all creation in the biosphere. Pure chance, absolutely free but blind, at the very root of the stupendous edifice of evolution”,,,

    “It necessarily follows that chance alone is at the source of every innovation, and of all creation in the biosphere. Pure chance, absolutely free but blind, at the very root of the stupendous edifice of evolution: this central concept of modern biology is no longer one among many other possible or even conceivable hypotheses. It is today the sole conceivable hypothesis, the only one that squares with observed and tested fact. And nothing warrants the supposition – or the hope – that on this score our position is ever likely to be revised. There is no scientific concept, in any of the sciences, more destructive of anthropocentrism than this one.”
    – Jacques Monod, Chance and Necessity: An Essay on the Natural Philosophy of Modern Biology

    Yet, as biophysicist Donald M. MacKay pointed out, to speak of chance as a cause unto itself, without it being anchored to any realistically defined mathematical probability, “is to make an illegitimate switch from a scientific to a quasi-religious mythological concept.”

    What Is Chance? – Nicholas Nurston
    Excerpt: “The vague word ‘chance’ is used as a substitute for a more precise word such as ’cause’. “To personify ‘chance’ as if we were talking about a causal agent,” notes biophysicist Donald M. MacKay, “is to make an illegitimate switch from a scientific to a quasi-religious mythological concept.”
    Similarly, Robert C. Sproul points out: “By calling the unknown cause ‘chance’ for so long, people begin to forget that a substitution was made. . . . The assumption that ‘chance equals an unknown cause’ has come to mean for many that ‘chance equals cause.’” Others who reasoned in this fashion, Nobel laureate Jacques Monod, for one, used this chance equals cause line of reasoning. “Pure chance, absolutely free but blind, (is) at the root of the stupendous edifice of evolution,”…
    https://books.google.com/books?id=bQ5OAAAAQBAJ&pg=PT25&lpg=PT25

    In short, and as Wolfgang Pauli observed, speaking of “chance” as a cause unto itself, without any anchor to any realistically defined mathematical probability, is make chance, for all intents and purposes, synonymous with the word “miracle”.

    I think Stephen Talbott’s following illustration, which plays off the old joke “and then a miracle occurs’, gets this “chance is synonymous with the word miracle” point across very clearly.

    Evolution and the Illusion of Randomness – Talbott – Fall 2011
    Excerpt: The situation calls to mind a widely circulated cartoon by Sidney Harris, which shows two scientists in front of a blackboard on which a body of theory has been traced out with the usual tangle of symbols, arrows, equations, and so on. But there’s a gap in the reasoning at one point, filled by the words, “Then a miracle occurs.” And the one scientist is saying to the other, “I think you should be more explicit here in step two.”
    In the case of evolution, I picture Dennett and Dawkins filling the blackboard with their vivid descriptions of living, highly regulated, coordinated, integrated, and intensely meaningful biological processes, and then inserting a small, mysterious gap in the middle, along with the words, “Here something random occurs.”
    This “something random” looks every bit as wishful as the appeal to a miracle. It is the central miracle in a gospel of meaninglessness, a “Randomness of the gaps,” demanding an extraordinarily blind faith. At the very least, we have a right to ask, “Can you be a little more explicit here?”
    http://www.thenewatlantis.com/.....randomness

    Moreover, As Dr. Egnor pointed out, there simply can be no realistic mathematical definition for ‘chance’ unless it is defined against a backdrop of purposeful, i.e. teleogical, events. As Egnor succinctly put it, “Chance presupposes design.”, (at least if ‘chance’ is to be anchored to a realistically defined mathematical probability in order to make it scientifically useful).

    Evolution Presupposes Intelligent Design: Case of the Coronavirus – Michael Egnor – April 7, 2020
    Excerpt: Aristotle saw this in his definition of chance in nature — chance is the accidental conjunction of purposeful events. Without purpose there can be no chance. His example is instructive: he considered a farmer who ploughs his field and by chance discovers a treasure buried by someone else. The treasure is discovered by chance, but everything else — the farmer’s ownership of the field, his decision to plough it, the accumulation and burial of the treasure by the other man — is purposeful, and in fact the only reason the accident of discovery happened is because it is embedded in a world of purpose. Chance can’t happen — the word has no meaning — in an entirely accidental world. Chance presupposes design.
    https://evolutionnews.org/2020/04/evolution-presupposes-design-the-case-of-covid-19/

    Thus in conclusion, although the Darwinists who criticize Dr. Behe often try to claim that he is not using mathematical probability properly, it turns out that Darwinists themselves, when you look at the foundation of their theory, are the ones who are flagrantly, and blatantly, ignoring the proper use of mathematical probability, i.e. ‘chance’, in science, and who are ‘very irrationally’, (as Pauli pout it), using the word “chance” in such a way as to make virtually synonymous with the word “miracle”.

    Moreover, since ‘chance’ does not even exist as a known cause for anything, but ‘chance’ is actually ‘our ignorance’, (C. Darwin), of a known cause, then Darwinist Atheists actually believe in magic minus any magician to perform their magic.

    A magic show without any magician to actually perform the magic? Now that is certainly one hell of a magic show for Darwinists to believe in.

    Verse:

    Psalm 77:14:
    You are the God who works wonders; you have made known your might among the peoples.

  7. 7
    jerry says:

    There are two things The author gets wrong and and |they give the game away when they do.

    First, failure to emphasize the fallacy by name that pro natural mechanism advocates constantly use. Namely, begging the question. He does use this term but in passing. By emphasizing the fallacy the advocates will be forced to admit they are using fallacious reasoning. It will be impossible to deny it.

    Second, using the term “evolution” to describe their mechanism when they mean Darwinian processes. Now Darwin’s process is indeed extremely good science, but it has nothing to do with Evolution.

    Darwin’s processes are part of genetics and indeed some significant changes are possible within genetics but these significant changes have nothing to do with Evolution debate.

    Richard Dawkins admitted the best explanation for life as we see it is an intelligence. It was acceptable as an explanation as long as the intelligence was not God. Again the begging the question fallacy.

    This article is almost there.

  8. 8
    Lieutenant Commander Data says:

    As Egnor succinctly put it, “Chance presupposes design.

    🙂 Egnor is a genius.

    ‘chance’ does not even exist as a known cause for anything, but ‘chance’ is actually ‘our ignorance’, (C. Darwin), of a known cause, then Darwinist Atheists actually believe in magic minus any magician to perform their magic.

    🙂 Atheists don’t need a magician to tell them what to do so they cut the magician from the scheme. It’s like a cartoon where somebody sitting on a branch and cutting it from the tree will make the tree falling down while the branch (they sit on) stays frozen in the air 😆 This is the atheism.

  9. 9
    bornagain77 says:

    Real-World Data and the Lesson of Chloroquine Resistance
    Eric H. Anderson – February 28, 2022
    Excerpt: “Behe’s argument was simply to observe, on the basis of White’s public health data, that chloroquine resistance arises in 1 in 10^20 cells. That’s a data point. He then asked a hypothetical question: If one CCC requires 10^20 replications, what would happen if there were a trait that was as complex as a “double-CCC”? Such a trait, Behe argued, would require 10^40 cells to arise, which is more cells than have lived over the course of the history of the Earth. This, he concluded, would pose a problem for Darwinism…” (C. Luskin)
    We can argue about whether “effective” chloroquine resistance should be defined as requiring exactly four mutations. We can quibble about whether the mutations are beneficial or neutral. We can debate the math and even be off by an order of magnitude or more. Yet none of this alleviates the significant challenge the real-world data poses to the evolutionary story.,,,
    Listen to the Parasites
    Behe is quite right to argue that if we need something like 10^20 cells to confer a relatively simple trait like resistance to chloroquine (however arrived at), then the evolutionary story is in dire straits. To his credit, Moran correctly acknowledges that developing chloroquine resistance “is an event that is close to the edge of evolution.” Now he just needs to pause and appreciate the implications for the evolutionary story.
    Are there functions in biology that are as complex or as difficult to achieve as chloroquine resistance? Of course there are. A brief look around the biosphere confirms that it would be irrational to think otherwise. Behe’s critics seem easily impressed by Plasmodium’s development of resistance to chloroquine as a shining example of the power of evolution. Yet remember, we’re not talking about forming a new organ or a new body plan, or constructing a new molecular machine, or building a new regulatory network, or even a single new gene. As Behe dryly observes, we’re only talking about “a few crummy point mutations in a pre-existing protein.”
    Yet evidently this is about all we can expect from evolution.
    https://evolutionnews.org/2022/02/real-world-data-and-the-lesson-of-chloroquine-resistance/

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