Intelligent Design

Mark, This is What all the Fuss is About

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Mark Frank wants to know what all of the fuss is about regarding the recent empirical verification of Michael Behe’s prediction in Edge of Evolution.

In response to the News post Evolutionary biologist Larry Moran tries calculating with big numbers re evolution Mark asks:

I must be missing something important. As far as I can see everyone seems to agree that the mutations required for chloroquine resistance are extremely improbable and this is born out by the rarity of such resistance in the wild. So what?

Fair question, to which gpuccio aptly responds:

Mark:

The point is simple. The malaria parasite under the extremely strong selection of chloroquine is a model extremely favourable to the neo darwinian algorithm: huge populations, very high reproduction rate, very strong and precise selective pressure, and a rather simple advantageous variation thta can be attained (just two AA variation to confer resistance to a lethal drug).

We can say that this the perfect scenario for the neo darwinian model, and a good way to measure its powers.

Now, in such a favourable scenario, how does the model work? It works (in the end, chloroquine resistance arises), but it definitely requires a lot of time and huge population numbers. IOWs, it happens with some difficulty.

That’s all. That difficulty is exactly what is needed to infer how much more “difficult” (indeed, impossible) it would be for the same neo darwinian model to explain the emergence of a new complex protein when the necessary transition is, say, of 300 AAs, and the population number, reproduction rate and selective pressure are much less favourable to the model. For example, to evolve just one new useful protein in vertebrates or mammals.

That is, and always has been, Behe’s point. And the point of ID.

Can you really say “so what” to that argument?

I would add to gpuccio’ response an issue that BA77 brought up earlier in the thread:

It is interesting to note that Chloroquine Resistance, as hard as it is for Darwinian processes to account for, (whether in the 1 in 10^14 calculation or in the 1 in 10^20 observation), it is not even a gain in functional complexity for the malaria parasite in the first place but is a loss of functional complexity for the parasite. . . . Thus the resistance, as crushing as it is, number-wise, for Darwinists to explain the origin of, is doubly crushing for Darwinists, since the adaptation, as hard as it was for Darwinian processes to acquire, was still ‘downhill’ evolution anyway and adds nothing as to explaining microbes to man evolution is remotely possible in a Darwinian scenario!

Conclusion. So what Mark? The “what” is that it has been mathematically demonstrated that Darwinian processes are real and they can account for small scale changes — which everyone concedes — but the same math demonstrates convincingly that they are not up to the larger task assigned to them by the theory — i.e., large scale changes requiring dozens if not hundreds of mutations.

66 Replies to “Mark, This is What all the Fuss is About

  1. 1
    humbled says:

    “I must be missing something important.”

    Mark, if you believe Darwinian Evolution works at any level, you aren’t just missing something but rather everything!! 😉

  2. 2
    JGuy says:

    In larger animals, like humans. After 100 million years or so waiting for this mutation, I wonder in the rest of the genome what genetic degeneration had occurred. LOL. One step sorta (i.e. sorta, since it’s a degenerative benefit) forward, how many steps back?
    Must truly suck to be a Darwinian. Then again, maintaining that view amidst the math would require a certain level of dimness that further insulates one from the raw mathematical embarassments.

    Reminds me of this Sternberg talk…

    https://www.youtube.com/watch?v=KbAzZEu13_w

  3. 3
    jerry says:

    ID in the evolution debate is mainly about the origin of new alleles. Mark Frank has been here longer than I have and I that is over 8 years. If he doesn’t understand this by now, it is either pathetic or willful insertion of obstructive comments just for the hell of it.

    Gpuccio’s response is excellent.

  4. 4
    Jehu says:

    It takes a tiny bit of conceptual comprehension to “get it.” It is not as simple as a pig tail photoshopped onto a baby picture or a National Geographic artist rendering of a Neandertal.

  5. 5
    JoeCoder says:

    I’m inclined to think the one in 10^14 calculation is wrong. Take a look at the bottom of the comment:

    After 30 generations:
    Population size = 1.07 billion
    single mutants = 53.7

    If you take a doubling series: 1, 2, 4, 8, 16…, it’s sum is twice the last number minus 1. So after 30 generations the cumulative population would have been 2.14 billion cells. The mutation rate is 2.5 x 10^-9. Times 2.14 billion is 5.35, not 53.7. But somehow diogenes has malaria finding the first mutation 10 times faster than it’s possible to look for it. That can’t be right.

  6. 6
    JoeCoder says:

    It would be good if someone could check my work.

  7. 7
    TSErik says:

    willful insertion of obstructive comments just for the hell of it.

    Ding! I think you got it.

  8. 8
    wd400 says:

    JoeCoder,

    You are both wrong 🙂

    It’s not the sum of the number of cells that have existed that matter, so we don’t need to sum the series. Instead, we want to know how many cell divisions have occured.

    Diogenes has calculated the population size presuming the infection starts form two sporozites, which is indeed 2^30 or about a billion. Seems like he created a complex way of tracking the mutations, but we can’t instead use basic probability.

    We are looking for cells that have acquired exactly one mutation in 30 generations. If we call the mutation rate u the probability this happens is

    p = 30 * u *(1-u)^29

    and the expected number of these from n trials is n.p so

    E = 2^30 * (30 * (2.5e-9) * (1-2.5e-9)^29)
    ~ 80.5

    Diogenes then multiplies that by 2/3 to get ~53.7.

    But diogenes has assumed that the infection starts from two sporozites, which is not necessarily the case, and that the malaria paraise it diploid (in fact it’s haploid).

    If an infection started from 10 sporozites, factor in the haploidy and say only one of 3 possible mutations is the right one you’d end up with

    (10 * 2^30) * (30 * (2.5e-9) * (1-2.5e-9)^29) * 1/3

    ~268 single mutants.

  9. 9
    wd400 says:

    (the above should say the malaria parasite is haploid in humans, it’s diploid in other stages. THere are many other subtlties these back of the envelope calculations ignore too)

  10. 10
    Mark Frank says:

    #3 Jerry

    ID in the evolution debate is mainly about the origin of new alleles.

    I total agree this is true but I am afraid I don’t see the relevance of this remark. It is not a case of wilful insertion of obstructive comments so I guess it must be pathetic. So help this poor pathetic person understand the relevance of the point.

  11. 11
    JoeCoder says:

    wd4000, thank you for the friendly feedback, but I think you are wrong :). Specifically here:

    p = 30 * u *(1-u)^29

    I’m not sure where this formula comes from but I tried plugging some different numbers into it:

    2^24 * (24* (2.5e-9) * (1-2.5e-9)^23) = 1

    That would mean that a single mutant arises once once the population reaches 2^24=16.7 million in size. Times two would be a total cumulative population of 33 million.

    Those 33 million cells times u=2.5e-9 times a 23 million base genome size = 1.9 million mutations that would have occurred.

    1.9 million / 23 million is 8.2%.

    That would mean that on average they find the first single-point mutation after only exploring 8.2% of their genome. But that can’t be right because you can’t find it faster than you can look for it. So I think that must be a wrong result. Are your formulas the correct ones to use in this exercise?

    Please check my work to see if I’m wrong 🙂

  12. 12
    JoeCoder says:

    Above you can remove the steps of multiplying and then dividing by 23 million to simplify the calculation. But the result it the same.

  13. 13
    Larry Moran says:

    We all agree that some genotypes, like chloroquine resistance in Plasmodium, are extremely rare. That’s not an issue. We also agree that such combinations of mutation will be beyond the reach of some species.

    What we’re contesting is the claim that Behe’s predictions were recently confirmed. They were not. Behe predicted that only two mutations were required and that the probability of this happening is 10^-20. We said his calculation was wrong. Behe challenged us to come up with our own numbers. We did – to the best of our ability.

    Turns out that that the probability of two mutations is much higher than Behe claimed but that there’s more to the issue than just the occurrence of a mutation. Behe didn’t take fixation/detection into account. He also doesn’t admit that you probably need FOUR mutations in order to get effective chloroquine resistance.

    Some of us are still waiting to see if Michael Behe can meet his own challenge.

    The rest of Behe’s argument is as bogus as his calculation of the probability of chloroquine resistance.

  14. 14
    Andre says:

    Am i reading this right? Larry Moran says it is even more complicated than what Behe suggests so therefor he is wrong?

    LOL!!!! thank you for proving Behe’s point Larry….. This post is a keeper!

    This just shows even if the IDIOT is more right than materialists they will cook up a scheme to say….. “You’re wrong because its even worse than you claimed”

    Did a professor just say that?

    Hahahaha!!!!!

    Just admit it Larry Behe busted you lot…..

  15. 15
    JoeCoder says:

    wd400 I think I see the problem in your math now, the error (30) is in bold:

    E = 2^30 * (30 * (2.5e-9) * (1-2.5e-9)^29)

    You’re calculating the odds for 30 generations with each generation having 2^30. Not a population that’s growing up from a small number to 2^30 in size.

    So your result of 268 single mutants is after a cumulative population of 30 x 2^30 = 32 billion cells.

    Or one mutant arising every 32 billion / 80.5 = 397 million cells. Which is the inverse of the mutation rate we started with, as it should be.

  16. 16
    JoeCoder says:

    Sorry the above should say “So your result of 80.5 single mutants…”

  17. 17
    Joe says:

    Strange that Dr Behe flat out states that more than 2 mutations are required. As for fixation, well when has that ever been observed in wild populations of the malaria parasite?

    With stochastic processes, such as natural selection and drift, specific combinations of mutations are beyond the reach of all species.

  18. 18
    wd400 says:

    JoeCoder,

    Ha, seems Diogenes and I made the same mistake by different routes.

    p = 30 * u *(1-u)^29 is from the biomial distribution, which would apply if each cell went through 30 cell divisions all by itself, but doesn’t count here since all cells share some history with each other.

    You approach is right (though I’d stress the number of cell divisions, not the number of cells that have existed, ,which is slipery with daughter cells anyyway). Ignoring the starting population you end up with 2^(N+1)-2 trials so 5 single mutants after 30 gens.

  19. 19
    JoeCoder says:

    Andre I don’t think that’s what Dr. Moran is saying. It looks like it takes less than 10^20 for the mutation to appear, and probably pretty close to 10^18 — which itself is close to the inverse square of the mutation rate.

    But because it’s only very weakly beneficial, it must appear multiple times before selection will cause it to spread. And it must spread at least to a population in the millions before the third and fourth single-step mutations have a good probability of arising.

    So IMHO, while it takes less than 10^20 to appear (as Behe said), it still likely takes around 10^20 to appear and be headed toward fixation. Which at the end of the day is all that matters in studying chloroquine resistance. But if there’s a two-step mutation that is strongly beneficial, it will take less than 10^20 to fix in the population.

  20. 20
    wd400 says:

    We cross posted JoeCoder,

    So just to clarify I wan’t assuming the population didn’t grow. The 30 is the is the number of ways you can get one success and 29 failures in 30 trials (“30 choose 1”), It would work if each cell was one experiment to itself, but doesn’t here because they share some of the divisions.

  21. 21
    JoeCoder says:

    wd400 I’m sure I’ve made some mistakes in my comments here too! Thanks for all of your past contributions to UD. Even though I’m an ID person I generally look forward to seeing your comments on a thread.

  22. 22
    Joe says:

    Dr Behe got his numbers from peer-review. The numbers are not as Behe said, they are as Behe cites.

    When your numbers appear in peer-review Behe will consider them- or even if you send him an email once you hammer it all out.

  23. 23
    JoeCoder says:

    Joe @22

    I’m on Behe’s side, Edge of Evolution was actually one of my favorite books, and I think Behe was right on many his points.

    But because two mutations confer only very weak chloroquine resistance, those two mutations would have to occur hundreds of times before they spread far enough to be detected. So it’s probably closer to 10^18 than to 10^20. I think that’s close enough and if you swap that number into Edge, the rest of Behe’s arguments aren’t significantly affected. And it still means the reviewers were wrong in their bickering that a simultaneous mutation was significantly less likely than a stepwise one through neutral space, or saying that selection at each step.

  24. 24
    Joe says:

    I thought his point about mutations was to show how difficult they were to get specific combinations of, let alone be able to get beyond the Edge of two new protein-protein binding sites.

  25. 25
    Mung says:

    Joe:

    As for fixation, well when has that ever been observed in wild populations of the malaria parasite?

    All the time Joe, all the time.

    But it’s the allele that does not confer chloroquine resistance that gets fixed!

    🙂

  26. 26
    Joe says:

    True and humans have a fixation with the malaria parasite in the wild. So that’s something. 😉

  27. 27
    Andre says:

    JoeCoder

    It is true that Larry Moran’s calculations take him to 10^18 and I guess in a mathematical sense he could say “the probability is much higher” but that is not what I’m alluding to…….

    Larry said;

    He also doesn’t admit that you probably need FOUR mutations in order to get effective chloroquine resistance.

    Larry makes Behe’s point here about the difficulty and then tells us that he’s wrong!!!!!

    Dies 4 instead of 2 not lower the odds considerably? Want to some math around that?

  28. 28
    JoeCoder says:

    Does 4 instead of 2 not lower the odds considerably? Want to some math around that?

    The odds of the first two mutations are about one in 10^18, since you need both before selection can start to act on them. Mutations 3 and 4 have odds of about one in 10^9 because selection can act at each step.

  29. 29
    jerry says:

    So help this poor pathetic person understand the relevance of the point.

    In order for naturalistic evolution to take place, new alleles have to arise naturally. These calculations show that just simple modifications of current alleles to reach a new function seem out of reach of naturalistic processes. Let alone of de novo functional alleles. Thus, it is impossible for naturalistic evolution to take place and one must look for an alternative explanation.

    If you do not understand this then you should go to lurker status till you understand the basic issue. But, you have been here longer than I have and I first came here over 8 years ago. How could you not understand what it is all about. Thus, my two alternatives. You do not have to agree but you have to know. If you know, willful obstruction is the diagnosis. If you do not know this, then the word “pathetic” is appropriate.

  30. 30
    Larry Moran says:

    In order for naturalistic evolution to take place, new alleles have to arise naturally. These calculations show that just simple modifications of current alleles to reach a new function seem out of reach of naturalistic processes. Let alone of de novo functional alleles. Thus, it is impossible for naturalistic evolution to take place and one must look for an alternative explanation.

    If you do not understand this then you should go to lurker status till you understand the basic issue.

    Isn’t it amazing that thousands of evolutionary biologists over the past one hundred years don’t understand this simple explanation? We must be really, really, stupid.

    Or is there another possibility?

  31. 31
    bornagain77 says:

    We must be really, really, stupid.

    LOL, surely you don’t think you are going to get disagreement on UD do you?

  32. 32
    bornagain77 says:

    But don’t feel too bad Moran, we are ALL really, really, stupid when it comes to trying to understand the unfathomed complexity of even the simplest of cells!

    “Although the tiniest living things known to science, bacterial cells, are incredibly small (10^-12 grams), each is a veritable micro-miniaturized factory containing thousands of elegantly designed pieces of intricate molecular machinery, made up altogether of one hundred thousand million atoms, far more complicated than any machine built by man and absolutely without parallel in the non-living world”. Michael Denton, “Evolution: A Theory in Crisis,” 1986, p. 250.

    The Cell as a Collection of Protein Machines
    “We have always underestimated cells. Undoubtedly we still do today,,, Indeed, the entire cell can be viewed as a factory that contains an elaborate network of interlocking assembly lines, each which is composed of a set of large protein machines.”
    Bruce Alberts: Former President, National Academy of Sciences;

    “To grasp the reality of life as it has been revealed by molecular biology, we must first magnify a cell a thousand million times until it is 20 kilometers in diameter and resembles a giant airship large enough to cover a great city like London or New York. What we would see then would be an object of unparalleled complexity,…we would find ourselves in a world of supreme technology and bewildering complexity.”
    Michael Denton PhD., Evolution: A Theory In Crisis, pg.328

    “Each cell with genetic information, from bacteria to man, consists of artificial languages and their decoding systems, memory banks for information storage and retrieval, elegant control systems regulating the automated assembly of parts and components, error fail-safe and proof-reading devices utilized for quality control, assembly processes involving the principle of prefabrication and modular construction and a capacity not equaled in any of our most advanced machines, for it would be capable of replicating its entire structure within a matter of a few hours”
    Michael Denton PhD. Evolution: A Theory In Crisis pg. 329

    “a one-celled bacterium, e. coli, is estimated to contain the equivalent of 100 million pages of Encyclopedia Britannica. Expressed in information in science jargon, this would be the same as 10^12 bits of information. In comparison, the total writings from classical Greek Civilization is only 10^9 bits, and the largest libraries in the world – The British Museum, Oxford Bodleian Library, New York Public Library, Harvard Widenier Library, and the Moscow Lenin Library – have about 10 million volumes or 10^12 bits.” – R. C. Wysong

    ‘The information content of a simple cell has been estimated as around 10^12 bits, comparable to about a hundred million pages of the Encyclopedia Britannica.”
    Carl Sagan, “Life” in Encyclopedia Britannica: Macropaedia (1974 ed.), pp. 893-894

    HISTORY OF EVOLUTIONARY THEORY – WISTAR DESTROYS EVOLUTION
    Excerpt: A number of mathematicians, familiar with the biological problems, spoke at that 1966 Wistar Institute,, For example, Murray Eden showed that it would be impossible for even a single ordered pair of genes to be produced by DNA mutations in the bacteria, E. coli,—with 5 billion years in which to produce it! His estimate was based on 5 trillion tons of the bacteria covering the planet to a depth of nearly an inch during that 5 billion years. He then explained that,, E. coli contain(s) over a trillion (10^12) bits of data. That is the number 10 followed by 12 zeros. *Eden then showed the mathematical impossibility of protein forming by chance.

    “It has become clear in the past ten years that the concept of design is not merely an add-on meta-description of biological systems, of no scientific consequence, but is in fact a driver of science. A whole cohort of young scientists is being trained to “think like engineers” when looking at biological systems, using terms explicitly related to engineering design concepts: design, purpose, optimal tradeoffs for multiple goals, information, control, decision making, etc. This approach is widely seen as a successful, predictive, quantitative theory of biology.”
    David Snoke*, Systems Biology as a Research Program for Intelligent Design
    OT: podcast: “David Snoke: Systems Biology and Intelligent Design, pt. 1”
    http://intelligentdesign.podom.....9_09-07_00
    podcast: David Snoke: Systems Biology and Intelligent Design, pt. 2
    http://intelligentdesign.podom.....0_01-07_00

  33. 33
    anthropic says:

    Larry Moran 30

    Stupid, not in the least.

    Blinkered by a priori materialist assumptions, yes. Just as many brilliant minds believed in the Ptolemaic system of epicycles because of an a priori commitment to circular orbits.

  34. 34
    littlejohn says:

    Yes, there is another possibility- some hybrid of naturalistic evolution, ID, and creation is true.

    Let us take advantage of every opportunity to advance knowledge and understanding, with sincere and honest dialogue, and brotherly love.

    Amen?

  35. 35
    Mark Frank says:

    #29 Jerry
     
    I think there is a misunderstanding between us.  Of course I know that new alleles have to arise naturally. I also understand that in this particular case it took a lot of generations to get to a fairly simple change. But it doesn’t follow that a more complex change such as new allele should take proportionally more generations.  There are so many other factors to take into account. That is why I wrote:

    As far as I can see everyone seems to agree that the mutations required for chloroquine resistance are extremely improbable and this is born out by the rarity of such resistance in the wild. So what?

    On the original thread I had a brief but interesting discussion with the polite and intelligent Gpuccio about the factors that might make a difference (of course he did not agree with me but I don’t think he found my position either wilfully obstructive or pathetic). I expect you were not aware of that – (which is quite understandable – no one can read everything that is posted) – and that may account for the misunderstanding.

  36. 36
    Dionisio says:

    BA77

    But don’t feel too bad Moran, we are ALL really, really, stupid when it comes to trying to understand the unfathomed complexity of even the simplest of cells!

    The more I try to understand the mechanisms behind the cell fate determination, intrinsic asymmetric mitosis, timely centrosome segregation, precise spindle checkpoints, cell polarization, extrinsic or intrinsic factors, signaling pathways, the whole nine yards, mind-boggling, overwhelming, I feel more and more stupid, completely ignorant. In my many years working on engineering design software development I never ever felt this way. Looking back at those years, now it seems like my work was so easy and simple. Now for every outstanding question that gets answered, new questions are raised. Unending revelation of the ultimate reality.
    Then when I talk to friends biologists and ask them to help me with understanding all that, everyone and their cousins look at me with wide open eyes and confess they don’t understand that either.
    We are approaching a major ‘told you so’ moment in science. Someone said, long ago, that He will make us feel this way, realizing our limitations to comprehend everything, and swallowing our ridiculous pride.
    It’s not too late to humbly admit we are studying and trying to understand an amazing creation.
    But we are free to continue in our foolishness going back to our vomit too.
    It’s up to each of us to decide.

  37. 37
    Jehu says:

    Larry Moran,

    What we’re contesting is the claim that Behe’s predictions were recently confirmed. They were not. Behe predicted that only two mutations were required and that the probability of this happening is 10^-20.

    It is an empirical observation by Nicholas White that chloroquine resistance arises in 1 in 10^20 parasites. As to the question of how many mutations this takes, you are prevaricating. From the abstract of the Summers paper:

    A minimum of two mutations sufficed for (low) CQ transport activity, and as few as four conferred full activity.

  38. 38
    Jehu says:

    It is amazing that Miller, Coyne, Dawkins, Matzke, and Carroll all went on record stating that each mutation could provide cumulative resistance. Behe said no, a minimum of two is required. Now here comes Moran ex post facto saying, “No it’s not one, it’s not two, it’s four!”

    Moving. Goalposts.

  39. 39
    Jehu says:

    Larry Moran

    Isn’t it amazing that thousands of evolutionary biologists over the past one hundred years don’t understand this simple explanation? We must be really, really, stupid.

    Or is there another possibility?

    For one thing, nobody new about DNA 100 years ago. And it is only relatively recently that DNA could be sequenced and empirical observations made about the fidelity of the sequence information and how many/few changes were required to make a selective difference.

  40. 40
    Jehu says:

    Larry Moran

    [Behe] also doesn’t admit that you probably need FOUR mutations in order to get effective chloroquine resistance.

    Really? I am not sure what you mean by “effective chloroquine resistance” from an evolutionary perspective. But are you willing to bet against the fact that two mutations sufficient for a selective advantage? From the Summer’s paper:

    Given that all known PfCRT haplotypes contain either N75E/D or N326D, these results indicate that PfCRT acquires the ability to transport CQ via one of two main mutational routes, both of which entail the introduction of K76T plus the replacement of an asparagine (N75 or N326) with an acidic residue.

    Funny that before the Summer’s paper the Darwinists argued in favor of cumulative selection. Now after the Summer’s paper Moran goes the other way and tries to argue against cumulative selection. Moving. Goalposts.

  41. 41
    Jehu says:

    I went back and looked at Moran’s comments about Behe’s Edge prior to the Summer paper, and he didn’t throw in with the rest of the crowd and argue for cumulative resistance at each mutation. So I can’t claim that Moran has moved goal posts.

  42. 42
    Jehu says:

    Larry Moran,

    Here is what you said in 2010:

    There may be millions of possible mutations that would lead to the same result.

    No. No there are not. From the Summer’s paper:

    Given that all known PfCRT haplotypes contain either N75E/D or N326D, these results indicate that PfCRT acquires the ability to transport CQ via one of two main mutational routes, both of which entail the introduction of K76T plus the replacement of an asparagine (N75 or N326) with an acidic residue.

  43. 43
    bornagain77 says:

    It is funny that Darwinists would be so up in arms about the math whilst Behe’s focus is on the 1 in 10^20 empirical observation.

    Darwinists learn not to gamble with Dr. Behe:
    How Many Ways Are There to Win at Sandwalk? – Michael Behe – August 15, 2014
    Excerpt: So, too, 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. That’s a point of great public health consequence.
    Before investigating what it takes at the molecular level to confer chloroquine resistance, we might have conjectured that there was one exceedingly rare, necessary mutation, or a combination of several mutations, or a dozen different paths each with several required mutations. We would nonetheless expect that when we did uncover the pathway, we would be able to reconcile the likelihood of each of its steps with the statistical evidence. Although it was pretty easy to predict from the sequence evidence even as early as ten years ago, that is what Summers et al.’s recent work allows us to do now with great confidence. The fact that several point mutations are required before low chloroquine-pumping activity is observed for PfCRT, coupled with the known mutation rate, easily gets us very close on a log scale to Nicholas White’s statistic, 1 in 10^20. There is no particular reason to grasp for other explanations.
    Nor would it do any good. There is a lot of chatter at Sandwalk deriding the idea of “simultaneous” mutations (which was not intended in my book The Edge of Evolution in the sense it is being taken there, and which at this point I would gladly replace with other words simply to avoid the distraction). Yet it matters not a whit for the prospects of Darwinian theory whether the pathway consists of two required mutations that are individually lethal to a cell and must occur strictly simultaneously (that is, in the exact same replication cycle), or whether it consists of several mutations each with moderately negative selection coefficients, or consists of, say, five required mutations that are individually neutral and segregating at some appreciable frequency in the population, or some other scenario or combination thereof. 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

    No amount of mathematical theorizing by Darwinists is going to get them past that empirical observation of 1 in 10^20 ! Because in science, (at least in how science is practiced apart from Darwinism), empirical observation trumps theory all the time,,,

    The Scientific Method – Richard Feynman – video
    Quote: ‘If it disagrees with experiment, it’s wrong. In that simple statement is the key to science. It doesn’t make any difference how beautiful your guess is, it doesn’t matter how smart you are who made the guess, or what his name is… If it disagrees with experiment, it’s wrong. That’s all there is to it.”
    https://www.youtube.com/watch?v=OL6-x0modwY

    Moreover, If Darwinists were genuinely concerned with the math of Darwinian evolution, instead of trying to make ‘mathematical excuses’, they should focus all their attention on figuring out why Darwinism has no rigid mathematical basis in the first place as other overarching theories of science do:

    “On the other hand, I disagree that Darwin’s theory is as `solid as any explanation in science.; Disagree? I regard the claim as preposterous. Quantum electrodynamics is accurate to thirteen or so decimal places; so, too, general relativity. A leaf trembling in the wrong way would suffice to shatter either theory. What can Darwinian theory offer in comparison?”
    (Berlinski, D., “A Scientific Scandal?: David Berlinski & Critics,” Commentary, July 8, 2003)
    http://www.uncommondescent.com.....the-day-8/

    Berlinski is not whistling Dixie.

    WHAT SCIENTIFIC IDEA IS READY FOR RETIREMENT? Evolution is True – Roger Highfield – January 2014
    Excerpt:,,, Whatever the case, those universal truths—’laws’—that physicists and chemists all rely upon appear relatively absent from biology.
    Little seems to have changed from a decade ago when the late and great John Maynard Smith wrote a chapter on evolutionary game theory for a book on the most powerful equations of science: his contribution did not include a single equation.
    http://www.edge.org/response-detail/25468

    No less than Gregory Chaitin thinks it is a ‘scandal’ that evolution has no mathematical proof that it works:

    Active Information in Metabiology – Winston Ewert, William A. Dembski, Robert J. Marks II – 2013
    Except page 9: Chaitin states [3], “For many years I have thought that it is a mathematical scandal that we do not have proof that Darwinian evolution works.” In fact, mathematics has consistently demonstrated that undirected Darwinian evolution does not work.
    http://bio-complexity.org/ojs/.....O-C.2013.4

    Wolfgang Pauli, certainly no slouch in math himself, finds Darwinian biologist to be ‘irrational’ because of their treatment of math:

    Nobel Prize-Winning Physicist Wolfgang Pauli on the Empirical Problems with Neo-Darwinism – Casey Luskin – February 27, 2012
    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) –
    http://www.evolutionnews.org/2.....56771.html

    MIT’s Murray Eden echos Pauli’s concern:

    “It is our contention that if ‘random’ is given a serious and crucial interpretation from a probabilistic point of view, the randomness postulate is highly implausible and that an adequate scientific theory of evolution must await the discovery and elucidation of new natural laws—physical, physico-chemical, and biological.”
    Murray Eden, “Inadequacies of Neo-Darwinian Evolution as a Scientific Theory,” Mathematical Challenges to the Neo-Darwinian Interpretation of Evolution, editors Paul S. Moorhead and Martin M. Kaplan, June 1967, p. 109.

    Of supplemental note: It is interesting to point out, in all the trouble Darwinists have in defining their mathematical basis, that, whilst Darwinists in general adamantly deny the existence of the soul, man’s ability to do mathematics in the first place is solid evidence that man has a mind/soul. No less than the co-discoverer of Natural Selection, Alfred Wallace, held as such:

    New Thoughts on Evolution (1910)
    Views of Professor Alfred Russel Wallace, O.M., F.R.S.
    “Nothing in evolution can account for the soul of man. The difference between man and the other animals is unbridgeable. Mathematics is alone sufficient to prove in man the possession of a faculty unexistent in other creatures. Then you have music and the artistic faculty. No, the soul was a separate creation.”
    Alfred Russel Wallace – An interview by Harold Begbie printed on page four of The Daily Chronicle (London) issues of 3 November and 4 November 1910.
    http://people.wku.edu/charles......e/S746.htm

    Or if you think Alfred Wallace not qualified to make the judgment as to whether man has a soul because of his ability to do mathematics, then how about Gödel’s, who proved the ‘incompleteness’ of mathematics, opinion on the matter:

    “Either mathematics is too big for the human mind or the human mind is more than a machine”
    – Kurt Godel

    Kurt Godel and Alan Turing – Incompleteness Theorem and Human Intuition – video
    https://vimeo.com/92387854

    Verse and Music:

    Romans 1:21-23
    For even though they knew God, they did not honor Him as God or give thanks, but they became futile in their speculations, and their foolish heart was darkened. Professing to be wise, they became fools, and exchanged the glory of the incorruptible God for an image in the form of corruptible man and of birds and four-footed animals and crawling creatures.…

    All You’ve Ever Wanted – Casting Crowns
    http://myktis.com/songs/all-youve-ever-wanted/

  44. 44
    Dionisio says:

    Follow-up to # 36

    What amazes me is not so much the still unknown, but that what has been discovered already, which is so elaborate and finely orchestrated. There are many missing pieces in the puzzle, hence I look forward with much anticipation to read newer reports about discoveries that could fill the remaining gaps, because I believe the new information will shed more light on the complex mechanisms, thus allowing us to enjoy their awesomeness. As professor Lennox said, our God is not a god of the gaps, but the God of the whole show. True wisdom only comes from Him. The wisdom of this world is ridiculously inadequate. If we delight in the Lord, He will provide the good desires of our hearts. Some of those desires could be to pursue scientific research studies and enjoy what He will reveal to us about His amazing creation.

  45. 45
    gpuccio says:

    Larry Moran:

    Have you ever heard of cognitive bias?

    Consensus is no guarantee of truth.

  46. 46
    DavidD says:

    gpuccio
    “Larry Moran:

    Have you ever heard of cognitive bias?

    Consensus is no guarantee of truth.”

    Below here is an etched in stone proof example of how successful consensus has been in history. In other words, if you have consensus on your side, you win:

    http://i.imgur.com/VQDwlC8.jpg

    Problem is, people like Larry will invoke Godwin’s Law as their lame default answer and in their minds all is still well in EvoLand

  47. 47
    DavidD says:

    Jehu:
    “Moving. Goalposts.”

    Larry has no problem with moving any goalposts which favor evolution. After all, evolution is a fact, Goalpost movement is merely an evolutionary adaptation for proving that evolution is true despite the reality of how the natural world actually works. Besides, if evolution is true, there exist no moral authority which emphatically states that lying is wrong.

  48. 48
    Dionisio says:

    gpuccio

    Have you ever heard of cognitive bias?
    Consensus is no guarantee of truth.

    Excellent point. History shows examples of that.

  49. 49
    bornagain77 says:

    OT: Dionisio, I think you will be both pleased and frustrated by the following paper:

    It’s Optimal. It Must Have Evolved! – August 16, 2014
    Excerpt: “Cell-surface signaling receptors are organized into different architectures that have been arrived at multiple times in diverse contexts. To understand the trade-offs that lead to these architectures, we pose the generic information-processing problem of identifying the optimal strategy for distributed mobile noisy sensors to faithfully “read” an incoming signal that varies in space-time. This involves balancing two opposing requirements: clustering noisy sensors to reduce statistical error and spreading sensors to enhance spatial coverage, resulting in a phase transition that explains the frequent reemergence of a set of architectures. Our results extend to a variety of engineering and communication applications that involve mobile and distributed sensing, and suggest that biology might offer solutions to hard optimization problems that arise in these applications.”
    These solutions “have been arrived at” — by design? No; read the last sentence in the paper: “It is appealing that one might look to biology for insights into solutions of hard optimization problems, arrived at as a result of evolution within an information niche.” Evolution did it. Give evolution the engineering design award.
    http://www.evolutionnews.org/2.....89031.html

  50. 50
    Dionisio says:

    DavidD

    A picture is worth a thousand words. Sadly in that gathering were probably many people who claimed to be followers of ‘VIA VERITAS VITA’ but disobeyed an important commandment ‘VIA VERITAS VITA’ Himself told us to observe: to love our neighbors as ourselves. By ignoring that important commandment, one automatically ignores the main one: to love our Creator with all our strengths. There were some exceptions, whose vision were not blurred by the loud screaming around them, stood firm by their beliefs and did not submit to the consensus. One of them was Wilhelm Busch, who resisted enormous pressures to join the consensus. Few years later pastor Wilhelm’s firm resistance was proven right. Eventually history was on his side. The consensus crowd was proven wrong. Maybe there are few things we could learn from these stories and apply them to our current situation?

  51. 51
    jerry says:

    Isn’t it amazing that thousands of evolutionary biologists over the past one hundred years don’t understand this simple explanation? We must be really, really, stupid.

    Or is there another possibility?

    In the first part above it seems Larry Moran is agreeing with my comment and with ID’s assessment of the situation. In the second part of the comment he says there is another possibility. Has he elaborated on what this possibility is?

    Allen MacNeill has appeared her occasionally saying that there is a process that explains the origin of new alleles. It his 47+ engines of variation. According to Allen, these variation processes will produce the alleles that then can be chosen by environmental pressures and reproductive success to account for the changes in life forms over the eons.

    However, anyone espousing this has to be able to show the progress in genomes that actually happened that led to novel complex capabilities. In many cases this evidence should be present in current genomes. With current technology this thesis should be able to be supported or falsified. My guess is that it will be mainly falsified. There will be a couple successes but that is all.

  52. 52
    Dionisio says:

    BA77
    OT
    Thank you for the interesting link and for the warning about it.
    Perhaps unexpectedly, after being exposed to the ‘misconception’ and the ‘deceiving’ viruses for so long, apparently my ‘reading’ immune system has been substantially strengthened out and now I skip over all that ‘hogwash’ embedded in the text of some articles I read, and I can focus in on the real stuff, which by itself is quite difficult for me to understand. Perhaps other folks in this blog have gone through a similar experience? It’s a blessing after all, isn’t it? 🙂
    Again, thank you for bringing this article up to my attention now. I have used some of the links you provide in your comments in other threads within this site. 🙂

  53. 53
    jerry says:

    On the original thread I had a brief but interesting discussion with the polite and intelligent Gpuccio about the factors that might make a difference

    It has been shown that for this particular change, it will take an extremely large number of generations or reproductive events to get to a simple change. You seem to agree on that but suggest that in different circumstances this might not be true.

    There are literally thousands of incredibly complicated changes that have taken place in organisms over the past 500 million years. Showing genetically how some of these may have taken place would be a start to supporting your alternative thesis. Till that time, one has to acknowledge that it may be an essentially impossible process. One can not just say it may have happened. One has to provide examples and reasonable pathways that new alleles have arisen.

    ID has shown the near impossibility of such a process happening naturally just once and by extrapolation this implies it could not happen the tens of thousands of times naturally it apparently happened. To counter ID’s conclusion, it is indicative on evolutionary biologist to provide a mechanism where new alleles are not only possible but likely.

  54. 54
    Dionisio says:

    bornagain77 @ 49

    OT: I return you the favor

    Here’s another example of bad design in nature 😉

    Bats Bolster Brain Hypothesis, Maybe Technology, Too

    http://www.biosciencetechnolog.....cation=top

  55. 55
    Mung says:

    Hi Larry,

    Can you recommend a good book on macroevolution?

  56. 56
    Querius says:

    I’m not sure what Larry will come up with, perhaps Evolution is a Fact and a Theory, but why not go to the source:

    The Origin of Species by Means of Natural Selection or the Preservation of Favoured Races in the Struggle for Life by Charles Darwin, M.A., F.R.S., &c., First Edition 1859

    -Q

  57. 57
    Querius says:

    DavidD@46 observed

    Below here is an etched in stone proof example of how successful consensus has been in history. In other words, if you have consensus on your side, you win:

    http://i.imgur.com/VQDwlC8.jpg

    Excellent example!

    Just look at all those scientists lining up behind the recognition that since we have the ability to control our evolution, we also have the moral obligation to do so.

    -Q

  58. 58
    Querius says:

    I posted this elsewhere regarding the evolution of chloroquine resistance in malaria. Are any of you familiar with this 2010 paper?

    http://www.malariajournal.com/content/9/1/217

    Here’s an excerpt:

    In both panels, the red lines are centered on a mutation rate of 10^-17.2 (i.e., two independent mutations at the rate for mutations that confer SP resistance), parasite densities of 10 10, and 1 billion treatment courses per decade. The lines span parasite densities from 10^9 to 10^11 and global demand from 100 million to 5 billion.

    -Q

  59. 59
    Larry Moran says:

    Can you recommend a good book on macroevolution?

    My favorites are:

    Genetics, Paleontology, and Macroevolution 2nd ed. (2001) by Jeffrey S. Levinton, Cambridge University Press

    Macroevolution: Diversity, Disparity, Contingency (2005) Essays in honor of Stephen Jay Gould, E.S. Vrba and N. Eldredge eds., The Paleontological Society

    I’ve written a little essay on Macroevolution to help you understand the concept.

  60. 60
    bornagain77 says:

    Dr. Moran, in the recent vindication of Dr. Behe, this following quote is even more relevant now than when it was first written decades ago:

    “The central question of the Chicago conference was whether the mechanisms underlying microevolution can be extrapolated to explain the phenomena of macroevolution. At the risk of doing violence to the position of some people at the meeting, the answer can be given as a clear, No.”
    Roger Lewin – Historic Chicago ‘Macroevolution’ conference of 1980
    “Evolutionary Theory Under Fire”
    Science, vol. 210, 21 November, p. 883
    http://www.pathlights.com/ce_e.....hist12.htm

  61. 61
    Larry Moran says:

    I posted this elsewhere regarding the evolution of chloroquine resistance in malaria. Are any of you familiar with this 2010 paper?

    That’s a good paper. It illustrates the point that many biologists are trying to make—a point that Michael Behe always ignores.

    The point is that there’s a big difference between the mutation rate to a chloroquine resistant strain and the successful appearance of such a strain in a particular locality. The right combination of mutations is going to arise much more often than our ability to detect it so it’s quite wrong to equate mutation rate and appearance.

    Think of it this way. What if there was only one in a million chance of a chloroquine resistant strain becoming well-enough established to be detectable in a local population? That would mean that the mutations arise once in every 10^14 parasites and the combined probability of detecting it is one in 10^20.

    Other combinations of mutations might arise at the same frequency but 100% of them could spread in the population. That would mean that a CCC only applies to chloroquine resistance but not to, say, protein-protein interactions.

    Behe’s failure to take this into account is a major weakness in his book. However, his error is compounded by a flawed calculation of the probability of mutation and the two errors pretty much cancel out. They are still errors. His reasoning is still wrong even though he accidentally stumbled on an answer that makes a bit of sense.

  62. 62
    bornagain77 says:

    10^14 parasites???

    wow, no big deal huh Larry???

    So we only have to wait for 100 trillion (1 in 10^14) tries in humans to get a similar trait in humans???

    A degenerative trait that is not even a demonstration of ‘uphill’ evolution???

    It is interesting to note that Chloroquine Resistance, as hard as it is for darwinian processes to account for, is not even a gain in functional complexity for the malaria parasite in the first place but is a loss of functional complexity for the parasite.

    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

  63. 63
    littlejohn says:

    Obviously probabilistic barriers are not a problem for evolution, otherwise, life would not have continued to thrive for the past 4-Billion years. Why?

    A-Life evolved to evolve?
    B-Life was designed to evolve?
    C-Both of the above
    D-None of the above

  64. 64
    bornagain77 says:

    Dr. Moran, if I skimmed your macro-evolution article correctly, it seems that you believe that macro-evolution can be accounted for by mutations to DNA. i.e. through the neo-Darwinian mechanisms of Random Mutation/Variation and Natural Selection? Please correct me if you do not believe in Neo-Darwinism.

    (and Dr. Moran if you believe in Neo-Darwinism),,, There are two HUGE problems, among many problems, with your belief in neo-Darwinism. One HUGE problem is that body plan information is NOT reducible to the information on DNA.

    Response to John Wise – October 2010
    Excerpt: A technique called “saturation mutagenesis”1,2 has been used to produce every possible developmental mutation in fruit flies (Drosophila melanogaster),3,4,5 roundworms (Caenorhabditis elegans),6,7 and zebrafish (Danio rerio),8,9,10 and the same technique is now being applied to mice (Mus musculus).11,12 None of the evidence from these and numerous other studies of developmental mutations supports the neo-Darwinian dogma that DNA mutations can lead to new organs or body plans–because none of the observed developmental mutations benefit the organism.
    http://www.evolutionnews.org/2.....38811.html

    Body Plans Are Not Mapped-Out by the DNA – Jonathan Wells – video
    http://www.youtube.com/watch?v=meR8Hk5q_EM

    Stephen Meyer – Functional Proteins And Information For Body Plans – video
    https://vimeo.com/91322260

    Dr. Stephen Meyer comments at the end of the preceding video,,,
    ‘Now one more problem as far as the generation of information. It turns out that you don’t only need information to build genes and proteins, it turns out to build Body-Plans you need higher levels of information; Higher order assembly instructions. DNA codes for the building of proteins, but proteins must be arranged into distinctive circuitry to form distinctive cell types. Cell types have to be arranged into tissues. Tissues have to be arranged into organs. Organs and tissues must be specifically arranged to generate whole new Body-Plans, distinctive arrangements of those body parts. We now know that DNA alone is not responsible for those higher orders of organization. DNA codes for proteins, but by itself it does not insure that proteins, cell types, tissues, organs, will all be arranged in the body. And what that means is that the Body-Plan morphogenesis, as it is called, depends upon information that is not encoded on DNA. Which means you can mutate DNA indefinitely. 80 million years, 100 million years, til the cows come home. It doesn’t matter, because in the best case you are just going to find a new protein some place out there in that vast combinatorial sequence space. You are not, by mutating DNA alone, going to generate higher order structures that are necessary to building a body plan. So what we can conclude from that is that the neo-Darwinian mechanism is grossly inadequate to explain the origin of information necessary to build new genes and proteins, and it is also grossly inadequate to explain the origination of novel biological form.’
    Stephen Meyer – (excerpt taken from Meyer/Sternberg vs. Shermer/Prothero debate – 2009)

    This is not a minor problem for neo-Darwinism Dr. Moran!

    Another HUGE problem with Neo-Darwinism Dr. Moran, that compounds the previous problem exponentially, is what is termed ‘ontogenetic depth’

    Darwin or Design? – Paul Nelson at Saddleback Church – Nov. 2012 – ontogenetic depth (excellent update) – video
    Text from one of the Saddleback slides:
    1. Animal body plans are built in each generation by a stepwise process, from the fertilized egg to the many cells of the adult. The earliest stages in this process determine what follows.
    2. Thus, to change — that is, to evolve — any body plan, mutations expressed early in development must occur, be viable, and be stably transmitted to offspring.
    3. But such early-acting mutations of global effect are those least likely to be tolerated by the embryo.
    Losses of structures are the only exception to this otherwise universal generalization about animal development and evolution. Many species will tolerate phenotypic losses if their local (environmental) circumstances are favorable. Hence island or cave fauna often lose (for instance) wings or eyes.
    http://www.saddleback.com/mc/m/7ece8/

    A Listener’s Guide to the Meyer-Marshall Debate: Focus on the Origin of Information Question -Casey Luskin – December 4, 2013
    Excerpt: “There is always an observable consequence if a dGRN (developmental gene regulatory network) subcircuit is interrupted. Since these consequences are always catastrophically bad, flexibility is minimal, and since the subcircuits are all interconnected, the whole network partakes of the quality that there is only one way for things to work. And indeed the embryos of each species develop in only one way.” –
    Eric Davidson
    http://www.evolutionnews.org/2.....79811.html

    Membrane Patterns Carry Ontogenetic Information That Is Specified Independently of DNA – Jonathan Wells – 2014
    Excerpt: Embryo development (ontogeny) depends on developmental gene regulatory networks (dGRNs), but dGRNs depend on pre-existing spatial anisotropies that are defined by early embryonic axes, and those axes are established long before the embryo’s dGRNs are put in place.,,,
    DNA sequences do not specify the final functional forms of most membrane components. Still less does DNA specify the spatial arrangements of those components. Yet their spatial arrangements carry essential ontogenetic information. The fact that membrane patterns carry ontogenetic information that is not specified by DNA poses a problem for any theory of evolution (such as Neo-Darwinism) that attributes the origin of evolutionary novelties to changes in a genetic program—-whether at the level of DNA sequences or dGRNs.
    http://bio-complexity.org/ojs/.....O-C.2014.2

    Moreover, these regulatory regions are found to be ‘orders of magnitude’ different even between chimps and humans:

    “Where (chimps and humans) really differ, and they differ by orders of magnitude, is in the genomic architecture outside the protein coding regions. They are vastly, vastly, different.,, The structural, the organization, the regulatory sequences, the hierarchy for how things are organized and used are vastly different between a chimpanzee and a human being in their genomes.”
    Raymond Bohlin (per Richard Sternberg) – 9:29 minute mark of video
    http://www.metacafe.com/watch/8593991/

    Thus where Darwinian theory most needs plasticity in order to be viable as a hypothesis, i.e. in developmental gene regulatory networks, is the place where it is found to be least flexible. Yet, it is in these developmental gene regulatory networks where the greatest differences are found!

    ,,, If neo-Darwinism were a normal science, instead of being primarily a cornerstone of the atheistic religion that is basically impervious to empirical falsification, this finding, along with many other lines of evidence (J. Shapiro etc,,) would be enough to overturn neo-Darwinism as a hypothesis of serious consideration in science.

  65. 65
    Mung says:

    Thanks Larry,

    I have the Vrba book, not really what I was looking for, though it does contain some interesting papers and worthwhile reading.

    I’ll check out the Levinton text and your essay.

  66. 66
    jerry says:

    The Vrba book is sometimes hard to digest. The first article is the essence of macro evolution thinking. It is by Jurgen Brosius and is the crucial thinking supporting naturalistic evolution.

    Allen MacNeill first brought it up about six years ago. I have mentioned it several times but no one here pays attention to it. Brosius acts like macro evolution is a done deal. He is a very prolific author on this topic.

    My guess is that this too will pass here. If one has access to a college library over the internet, all the articles were published in a journal and are available as PDFs.

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