Human evolution Intelligent Design

Why do we need to make a decision about common descent anyway?

Spread the love

To “Why, exactly, should we believe that humans are descended from simpler forms of life?”, Mark Frank responds,

This is really very simple. Either:

1. We descended from a simpler form of life.

2. We descended from an equally complicated form of life which has left no trace.

3. We didn’t descend from any form of life but somehow sprang into existence (as adults I guess as human babies can’t survive by themselves).

Be honest – which seems the most plausible?

Actually, it is even simpler than Mark Frank makes out. Nothing is at issue if I just decline to offer an opinion.

His 1. would seem plausible except for the people shouting that we are 98 percent chimpanzee. And they’re the strongest supporters of common descent. They want it rammed down everyone’s throat from kindergarten to the retirement home.

Yet not only is their claim implausible on its face (anyone can tell the difference between a human and a chimpanzee), it is unsatisfactory. It leaves unaccounted for everything of which we would like an account.

His 2. is hardly implausible. It would be a familiar situation to any adopted child who can’t trace birth parents. As an account, is it unsatisfactory principally because it amounts to saying that there is no information available? That might be true, but I don’t know that it is.

His 3. is really not much different from 2., in that no further information about origins is likely to be available.

So the actual choice, assuming Frank’s list is exhaustive, is between an account offered by people whose judgement can be seriously questioned and accounts that point to the futility of seeking further information.

It’s a good thing Thomas Huxley coined the term agnostic (“it is wrong for a man to say he is certain of the objective truth of any proposition unless he can produce evidence which logically justifies that certainty”). That just about characterizes what I consider the wisest position just now on common descent.

See also: What can we responsibly believe about human evolution?

Follow UD News at Twitter!

134 Replies to “Why do we need to make a decision about common descent anyway?

  1. 1
    awstar says:

    Why do they say we “descended” from a simpler form of life. Shouldn’t they be saying we ASCENDED from a simpler form of life? Without this conflicting terminology, the arguments become much clearer as to whether science shows we are ascending or descending as human beings.

  2. 2
    Evolve says:

    ///Why do they say we “descended” from a simpler form of life.///

    Gosh! It’s should be descent, not descend.
    There’s a difference between the two words.

  3. 3
    Evolve says:

    ^^^^

    It should be…

  4. 4
    Evolve says:

    ///They want it rammed down everyone’s throat from kindergarten to the retirement home.///

    The evidence only supports scenario 1. So yes, people have to be taught about it. If you want a science literate population, that is.

    ///That just about characterizes what I consider the wisest position just now on common descent.///

    Nobody with a proper understanding of the evidence will take an agnostic position on common descent. Only those with a certain agenda will try to shoo away the overwhelming evidence in support of it.

  5. 5
    Joe says:

    What evidence supports scenario 1?

    Loci that are obviously variable within natural populations do not seem to lie at the basis of many major adaptive changes, while those loci that seemingly do constitute the foundation of many if not most major adaptive changes are not variable.- John McDonald, “The Molecular Basis of Adaptation: A Critical Review of Relevant Ideas and Observation”, Annual Review of Ecology and Systematics: 14, 1983, p77-102

  6. 6
    fossil says:

    I agree with Joe #5. Further if we only consider the general physical strength of the Neanderthal’s then we must conclude that we have been in descent for a very long time. Besides we have the genetic load of accumulating harmful mutations that is tearing us down – not building us up which is exactly opposite to what evolution teaches.

  7. 7
    Mark Frank says:

    His 1. would seem plausible except for the people shouting that we are 98 percent chimpanzee. And they’re the strongest supporters of common descent. They want it rammed down everyone’s throat from kindergarten to the retirement home.
    Yet not only is their claim implausible on its face (anyone can tell the difference between a human and a chimpanzee), it is unsatisfactory. It leaves unaccounted for everything of which we would like an account.

    Denyse I suggest you repeat this until you have learned it by heart:  Biologists do not claim that people are descended from chimpanzees. For some reason it seems to keep slipping your mind. There may well be a reasonable dispute about how much people differ from chimpanzees. It may even be that those who claim we are similar are wrong. They may even be the same people who argue for common descent (but remember the latter group includes many ID proponents – so I think it is unlikely).  None of this weakens the overwhelming evidence that we are descended from a simpler life form which to put it simply comprises:

    * Every living thing that we know of (including every person) was descended from another living thing. We have zero examples of living things appearing do novo. We have many millions of proven cases of descent.

    * Descendants are not identical to their parents. They change.
    * Once upon a time there were only much simpler life forms on this planet.

    Notice – no mention of chimpanzees or even apes.

    His 2. is hardly implausible. It would be a familiar situation to any adopted child who can’t trace birth parents. As an account, is it unsatisfactory principally because it amounts to saying that there is no information available. That might be true, but I don’t know that it is.

    It is unsatisfactory for a deeper reason.  It raises the question  – what was the more complex life form descended from?

    His 3. is really not much different from 2., in that no further information about origins is likely to be available.

    So we are left with a hypothesis which says we arose through an extension of processes we see around us all the time or it happened as a unique event we know nothing about and nothing resembling which has ever been observed (assembling a viable population of people at one time in one place from inanimate matter). Sure you don’t have to choose.  But I have to suspect your motives.

    So the actual choice, assuming Frank’s list is exhaustive, is between an account offered by people whose judgement can be seriously questioned and accounts that point to the futility of seeking further information.

    Criticise the account, not the people who offer it.

  8. 8
    Joe says:

    Mark Frank-

    Was the alleged common ancestor of chimps and humans more like chimps and apes or more like humans? All of the examples of descent have organisms producing the exact same type of organism as the parents. Human babies are slightly different from their parents but they are still human and nothing suggests they will be anything else other than humans.

    There aren’t any known evolutionary events that can be used to extrapolate universal common descent. No known mechanism can produce the changes required. That means the extension of processes hypothesis is refuted.

  9. 9
    awstar says:

    Mark Frank at 7 said:

    So we are left with a hypothesis which says we arose through an extension of processes we see around us all the time or it happened as a unique event we know nothing about and nothing resembling which has ever been observed

    Specifically which processes would these be?

  10. 10
    Mark Frank says:

    #9 awstar

    Specifically which processes would these be?

    Biological reproduction as observed millions of times.

  11. 11
    News says:

    Mark Frank at 7: No one said anyone says humans are descended from chimpanzees.

    BUT claimed 98% similarity due to a common ancestor (a claim that hundreds of science writers regularly make, in support of common descent) *undermines anything else they have to say on the subject.*

    I do not know how to put the matter more simply than this: A person who does not see the problem is not a credible source of information.

    You write, “There may well be a reasonable dispute about how much people differ from chimpanzees. It may even be that those who claim we are similar are wrong.”

    Indeed. Recognizing such facts may even function as a sanity test.

    It is not just a “reasonable dispute.” It is a sine qua non (without which, nothing) for taking their position seriously.

    If the people who claim common ancestry DO ever want to get serious about their figures, I’m all for taking a look at their arguments.

    If not, well, they can always pull in people who can live with blatant contradiction, but not everyone is so logic-free, it seems.

  12. 12
    Mark Frank says:

    #11 News

    I remind you once again that the people who believe in Common Descent (which is a stronger claim than We Are Descended from Simpler Life Forms) include many of ID’s leading proponents including VJ Torley and Gpuccio on this forum (I can’t remember whether Barry does). I doubt they make any claim about the similarity of people and chimpanzees. So why don’t you calm down about that particular bee in your bonnet and examine the arguments.

  13. 13
    awstar says:

    Mark Frank 7 and 10

    So we are left with a hypothesis which says we arose through an extension of processes we see around us all the time

    [i.e.]

    Biological reproduction as observed millions of times.

    or

    it happened as a unique event we know nothing about and nothing resembling which has ever been observed

    So does the process of “Biological reproduction as observed millions of times.” also have a unique initial event we know nothing about? or has it always been what we observe since the beginning of time?

  14. 14
    Acartia_bogart says:

    Joe @8:

    Was the alleged common ancestor of chimps and humans more like chimps and apes or more like humans?

    Why is that important? We had a common ancestor. Nothing more, nothing less. It is not even correct to say that we are more complex than our common ancestor with the apes. All we can say is that we are different.

  15. 15
    Sirius says:

    To mark Frank and allies. We are told with dogmatic certainty that we had a common ancestor, “nothing more, nothing less.”

    Please identify the common ancestor of humans and chimps. Have you ever seen this creature? What did it look like? What is its name? We are talking science here. Why should we believe in what we cannot see?

    More generally, why are common ancestors never identified?

    If your rule is, All life from other life, how did life originate?

  16. 16
    Acartia_bogart says:

    Sirius:

    Please identify the common ancestor of humans and chimps. Have you ever seen this creature? What did it look like? What is its name? We are talking science here. Why should we believe in what we cannot see?

    Nobody is making you believe in something that you can’t see. But let me list a few other things that you can’t see:
    Air, the atom, gravity, a thought. But I am fairly certain that they all exist.

  17. 17
    Joe says:

    Acartia_bogart- what the alleged common ancestor (between humans and chimps) was is important for the reason Mark Frank provided- Biologists do not claim that people are descended from chimpanzees. It could very well be that the alleged common ancestor was a chimpanzee- Mark doesn’t know and neither do any biologists.

  18. 18
    Joe says:

    Mark Frank:

    Biological reproduction as observed millions of times.

    Humans reproducing humans doesn’t help you, Mark. All observed instances of reproduction support baraminology, not universal common descent.

  19. 19
    Mung says:

    4. Humans are a simplification of a more complex entity.

  20. 20
    Mung says:

    Notice – no mention of chimpanzees or even apes.

    Notice – the conclusion which does not follow from the premises.

    We have zero examples of living things appearing do novo.

    Every human birth is a de novo appearance. We have numerous examples.

  21. 21
    Gordon Davisson says:

    Let me ask a counter-question for those on the ID side here: do you want ID to be taken seriously as science? The reason this is relevant is because the scientific evidence for common ancestry is overwhelmingly strong, and all of the counterarguments I’ve ever seen from the antievolution side are overwhelmingly weak (and generally based on ignorance of either the evidence or how science evaluates evidence or both). Basically, if you can’t figure out common ancestry, you’ve immediately marked yourself as clueless on the subject, and even if you have good points on other aspects of the origins question, nobody in the scientific community is going to bother listening to them.

    In other words, I’m agreeing with Denyse here:

    BUT claimed 98% similarity due to a common ancestor (a claim that hundreds of science writers regularly make, in support of common descent) *undermines anything else they have to say on the subject.*

    I do not know how to put the matter more simply than this: A person who does not see the problem is not a credible source of information.

    …just disagreeing about which side is not credible. Take the 98% similarity figure as an example: one of the basic principles of science is that you must follow the evidence. If the evidence supports the 98% figure, and that conflicts with your intuition, then you either have to throw that intuition into the trash bin, or stop claiming to be doing science.

    Mind you, it’s entirely reasonable to dispute measurements, theories, etc. But if you want your disputes to be taken seriously, they must be based on understanding the subject. If your response to the 98% figure is just “I don’t understand that, it doesn’t make sense to me, it must be wrong”, you just proved you’re really not even trying to do science.

    Now, let me take a look at the primary counterargument I’ve seen against the 98% figure: many variants of “here’s another measurement, and it got a completely different figure”. Which would be reasonable if they were measuring the same thing, but I haven’t seen any that were. Let me give you an analogy:

    Suppose you hear that the liner Queen Mary 2 is more than twice the size of her predecessor, the Queen Elizabeth 2. This seems rather extreme, so you look around and find another figure that says the QM2 is only about 1.5x the size of the QE2. Then you find another that says it’s only 1.2x, and another that says 1.3x, and even one that says 1.4x. Should you conclude that the claim that she’s more than twice the size of the QEM is bogus?

    Of course not; all of the figures I just gave are correct (although rounded), but there’s more than one way to measure size, and hence more than one way to measure difference in size (hint: tonnage, displacement, length, beam, and height).

    Suppose someone claimed, based on those figures, that the QM2 was clearly not twice the size of the QE2, or that we didn’t know how to measure ships’ sizes, or that we really needed more data to make a judgement, or… You’d probably dismiss them as clueless, wouldn’t you? I certainly would.

    Essentially the same thing is going on with all the different figures you’ll see for Human-chimp similarity: different ways of defining and measuring similarity will give different results, and this is completely normal and expected. There is no single “right” figure. (Mind you, some ways of comparing may be more useful for some specific purpose, but this’ll depend on the purpose you have in mind.)

    Let me make a closer analogy: how similar are the two sentences:

    “It was a blue-grey camper van.”

    “It was a gray-blue van.”

    Answer 1: 71%, because 5 of the 7 words are identical between them.

    Answer 2: 85%, because 6 of the 7 words are essentially the same (“grey”=”gray”).

    Answer 3: 39%, because 9 of the 23 letters match up between them.

    Answer 4: 69%, because 16 of the 23 letters match up between them (ignoring rearrangements).

    Answer 5: 82%, because there are only 3 changes (swap the order of “blue” and “grey”, change “e” to “a”, delete “camper”) between them out of 17 characters (in the smaller one).

    The truly correct answer, of course, is answer 6: all of the above (and more), and which one(s) will be most useful depend on what you’re trying to learn. #5 is probably closest to the way the standard 98% figure is calculated (although it was originally done in a very indirect form, by measuring annealing temperature).

    #5 is also the most relevant for supporting common ancestry, not because it’s so high — that doesn’t actually matter than much — but because it’s the best measure of the number of genetic changes (base substitutions, sequence reordering, insertions and deletions), and therefore the best measure of evolutionary distance (note that it doesn’t take any more generations for a 500-base section of DNA to be deleted than a 5-base section).

    Or all of these measures might all be pretty irrelevant, if (for instance) you’re trying to figure out how similar the meanings of the two sentences are. That’s more-or-less the problem you’re running into when you compare the phenotype of Humans and chimps and think that must correspond to more than 2% of difference. To the extent we’ve examined the specific genetic differences between Humans and chimps, it’s clear that the vast majority of the changes make little or no difference in the resulting phenotype, while a tiny minority cause huge differences in the phenotype.

    In my sentence above, you could change “was” to “wasn’t”, and completely reverse the meaning with only a very small change in letter sequence. Expecting the difference in meaning to correspond to the difference in letter sequence is completely unreasonable, and essentially the same is true of differences in genotype vs. differences in phenotype.

  22. 22
    Box says:

    Gordon Davidson #21,

    ID is a theory about the cause of complex biological information. Common descent (CD) is a theory about the modalities of implementation of that information. They are two separate theories about two different aspects of the problem, totally independent and totally compatible. In other words, one can affirm CD and ID, CD and Darwinian Evolution, or ID and not CD. However, if one believes in Darwinian Evolution, CD is a necessary implication. [source: section f.a.q. #10]

  23. 23
    Gordon Davisson says:

    I should probably expand on my comment that “#5 is also the most relevant for supporting common ancestry, not because it’s so high — that doesn’t actually matter than much…”. The 98% figure gets waved around a lot because it looks simple and easy to understand. It’s the sort of argument that can fit on a bumper sticker. But it’s also too oversimplified and glib to really mean much (“any argument that fits on a bumper sticker belongs there”).

    The real important evidence isn’t any specific bit of similarity between any two organisms, it’s the pattern of similarities and differences across all organisms. It’s not that we’re some specific genetic distance from chimps, it’s that we’re just a hair closer to chimps than gorillas, and a little further from orangs and siamangs, and a little further from baboons and macaques and vervets, and …

    It’s the nested hierarchy of similarity, and its congruence with the fossil record, that really matters. But that’s a huge pattern involving a huge amount of data, and knowing enough about the subject (and understanding the theory well enough to evaluate the match between it and the data) is well beyond the effort most people are willing to invest. But if you haven’t put in the time & effort to get to that point, you cannot expect your opinion on the subject to be given any real weight.

    The 98% figure is the tip of a very very very large iceberg. If you don’t deal with the iceberg, mocking the tip will only get you into trouble.

  24. 24
    Gordon Davisson says:

    Box: I agree completely; my objection isn’t that common ancestry refutes ID (it clearly doesn’t), it’s that the ID movement’s unwilling to look at the evidence for common ancestry clearly indicates that science, and following the evidence, simply is not a priority for the ID movement.

  25. 25
    Mung says:

    As for me, I am still waiting on Nick Matzke’s book on Macroevoluton. I’m sure he’s working on it.

  26. 26
    Box says:

    Gordon Davisson #24, exactly which evidence for common ancestry is the ID movement unwilling to look at?
    BTW you may be interested in this article by Denyse O’Leary.

  27. 27
    Gordon Davisson says:

    Box: the nested hierarchy of similarity, and its agreement with the fossil record (and biogeography and…). And I wound’t say they’re unwilling to look at it, just unwilling to seriously look at its implications

    Cornelius Hunter has probably done the best job I’ve seen in trying to refute the evidence from a nested hierarchy, and while he’s the best I’ve seen … he’s not made much of a case IMO. In fact, he’s the one I had in mind when I mentioned ignorance of how science evaluates evidence. His objections generally consist of noting various anomalies, pointing out that they don’t fit in a nice clean nested hierarchy, and claiming this refutes the argument for common ancestry.

    This is a lot like pointing out that some objects fall slower than others (feathers vs. rocks), some don’t fall at all (helium balloons), and claiming that since the theory of gravity implies everything should fall at the same speed, gravity is clearly wrong. The basic problem with this argument is that gravity isn’t the only force acting on these objects, and if you take into account all of the forces (including gravity), their behavior fits the theory.

    In the case of common ancestry, if it were the only thing influencing the similarities of different organisms, we’d get a nice clean anomaly-free nested hierarchy of similarities. The fact that we don’t get a nice clean hierarchy just shows that CA isn’t the only thing going on. Since CA isn’t the only thing influencing similarities, we expect the real picture to be much messier.

    This sort of thing is entirely normal in science. Experiemtal data is never nice and simple and clean and only influenced by the effect you’re trying to measure (and if it is nice and clean, that probably means something’s wrong). You pretty much always have to deal with confounding effects, even in an experiment you designed to minimize those. Without controlled conditions, it’s generally even messier. That doesn’t mean you throw up your hands and conclude that there’s no way to tell what’s going on; it means that you dig in and try to figure out as much as you can. You squeeze the data any way you can think of to wring as much useful information as you can out of it.

    In the case of the similarity hierarchy, it actually isn’t very hard to get the basic picture out. The basic overview of the nested hierarchy of similarity is pretty obvious once it’s pointed out. (Picking out fine details is harder, and subject to constant adjustment based on new information/better analysis.)

    Anomalies? You bet! But we’re now able to look at thousands of traits across millions of species, so even if we find millions of anomalies that’s a very small fraction of the overall data. You really need to look at the weight of the evidence, and that’s not where Cornelius looks; he only ever looks at the anomalies, and acts like that’s all that exists. He’s wrong.

    …And it’t actually even worse than that for the anti-CA side, because most of the anomalies that appear are the sorts of anomalies that are explicable under CA and/or evolution. Horizontal transfer comes to mind as an example. If you use a more complex & complete model of evolution (rather than plain branching ancestry), you get a better fit to the data. What that means is that any competing theory that might hope to replace CA as the explanation of the nested hierarchy has to explain not only the hierarchy but also the anomalies at least as well as CA+evolution. VJTorley, for example, has proposed an alternate explanation for the hierarchy of similarity (I can’t seem to find the articles right now, sorry) but I don’t think his explanation had any way of explaining the anomalies.

    So, I’ll throw it open for anyone in the anti-CA crowd: do you have a better explanation for the nested hierarchy of similarity? Does it explain the consistency with the fossil record? Does it explain the anomalies from both of the above at least as well as CA+evolution? Is your explanation at anywhere close to as well worked-out and studied as CA+evolution?

    If not… don’t expect your objections to CA to be taken seriously in scientific circles.

  28. 28
    Gordon Davisson says:

    “And I wound’t say they’re unwilling to look at it…” -> “And I shouldn’t say they’re unwilling to look at it…”

    Sorry, my proofreading sucks.

  29. 29
    Acartia_bogart says:

    GD: “Box: I agree completely; my objection isn’t that common ancestry refutes ID (it clearly doesn’t), it’s that the ID movement’s unwilling to look at the evidence for common ancestry clearly indicates that science, and following the evidence, simply is not a priority for the ID movement.”</I

    Gord, I am afraid that the name of this website (Uncommon Descent) displays the bias inherent in the conversation.

  30. 30
    bornagain77 says:

    A then there is that whole monkey wrench of the Cambrian explosion, as was illustrated in Meyer’s ‘Darwin’s Doubt’, that was thrown into the whole theory of common descent.

    A Graduate Student (Nick Matzke) Writes – David Berlinski July 9, 2013
    Excerpt: Representatives of twenty-three of the roughly twenty-seven fossilized animal phyla, and the roughly thirty-six animal phyla overall, are present in the Cambrian fossil record. Twenty of these twenty-three major groups make their appearance with no discernible ancestral forms in either earlier Cambrian or Precambrian strata. Representatives of the remaining three or so animal phyla originate in the late Precambrian, but they do so as abruptly as the animals that appeared first in Cambrian. Moreover, these late Precambrian animals lack clear affinities with the representatives of the twenty or so phyla that first appear in the Cambrian.
    http://www.evolutionnews.org/2.....74221.html

    But not to worry, Matzke was there to save the day for the Darwinian faithful, give are take a few setbacks from Berlinski 🙂

    A One-Man Clade – David Berlinski – July 18, 2013
    http://www.evolutionnews.org/2.....74601.html

    Hopeless Matzke -David Berlinski & Tyler Hampton August 18, 2013
    http://www.evolutionnews.org/2.....75631.html

  31. 31
    Querius says:

    But bornagain77,

    Don’t you want to be taken seriously? Just because there’s a few tiny questions and trivial inconsistencies left open by the Cambrian explosion doesn’t mean that there isn’t an Enormous Mountain of Evidence just waiting to be discovered!

    LOL

    -Q

  32. 32
    bornagain77 says:

    But alas Querius, I have the fatal flaw of preferring honest inquiry to bluff and bluster, thus I’m forever condemned to be not taken seriously by the likes of Coyne, Dawkins, Myers, Moran, Davisson, etc… and for that ‘I am a man of constant sorrows’ 🙂

    But then again, perhaps I’m blessed and favored to earn their scorn ,,

    Music

    Phillips, Craig and Dean – Man Who’s Blessed and Favored – live
    https://www.youtube.com/watch?v=KKaBM7BAxKE

  33. 33
    Acartia_bogart says:

    “A then there is that whole monkey wrench of the Cambrian explosion, as was illustrated in Meyer’s ‘Darwin’s Doubt’, that was thrown into the whole theory of common descent.”

    Meyer’s ‘Darwin’s Doubt’ has been refuted by “real biologists” so many times that the book ranks up there with “Chariots of the God” as good science.

    He completely ignores the reams of evidence of life before the “Cambrian explosion”. But who am I (a biologist) to question Meyers (a non-biologist)?

  34. 34
    jerry says:

    Meyer’s ‘Darwin’s Doubt’ has been refuted by “real biologists” so many times that the book ranks up there with “Chariots of the God” as good science.

    He completely ignores the reams of evidence of life before the “Cambrian explosion”. But who am I (a biologist) to question Meyers (a non-biologist)?

    Of course this is nonsense.

  35. 35
    Querius says:

    A-B sourly noted,

    He completely ignores the reams of evidence of life before the “Cambrian explosion”. But who am I (a biologist) to question Meyers (a non-biologist)?

    No, it’s not “reams or evidence,” it’s Mountains of Evidence ™ that’s waiting to be discovered.

    As to the question of credibility, you’re right. It’s far more important whether a person has a degree, in what, and where it’s from than the silly things that come out of their mouth. It’s sort of like playing cards. My 4 of spades trumps your jack of clubs, but her 9 of spades beats both of our cards. Think of how much time we would save in peer reviews if we just rank the universities, the degrees, how many papers published and where, and finally the date of the degree as a tie-breaker.

    -Q

  36. 36
    bornagain77 says:

    AB, not missing a beat, bluffs and blusters this statement:

    Meyer’s ‘Darwin’s Doubt’ has been refuted by “real biologists” so many times that the book ranks up there with “Chariots of the God” as good science.

    Hmmm, interesting claim. Perhaps you can point me to the critical review that adequately addressed the information problem instead of dodged it?

    Stephen Meyer – The Biggest Failure of Critics (In Addressing Darwin’s Doubt) – video
    https://www.youtube.com/watch?v=Ljy1yfGdC5Y

    “Conversations with Stephen Meyer,” short videos in which Dr. Meyer reflects on the past year’s controversy over his book, what the criticisms of Darwin’s Doubt reveal about the weakness of his critics and what that suggests about the future of the discussion as a whole.
    https://www.youtube.com/playlist?list=PL7Wwl5TzliiESzJlMgqCo6ogMIZWL7gmj

    Here is a more detailed look at the major flaws in all the critical reviews of ‘Darwin’s Doubt’:

    Darwin’s Doubt – Reviews – Part 1 – by Paul Giem – video
    https://www.youtube.com/watch?v=YW8SLKoSZqM
    Darwin’s Doubt – Reviews – Part 2 – by Paul Giem – video
    https://www.youtube.com/watch?v=nPqN0-YiJgg
    Darwin’s Doubt – Reviews – Part 3 – by Paul Giem – video
    https://www.youtube.com/watch?v=5Mj1thPrSgc
    Darwin’s Doubt – Reviews – Part 4 – by Paul Giem – video
    http://www.youtube.com/watch?v=IfEfa6KaEXU

    And AB, since you fancy yourself an expert on ‘good science’, perhaps you could tell us the demarcation criteria that separates Darwinian evolution from pseudoscience? i.e. Exactly what is the mathematical basis of Darwin?

  37. 37
    bornagain77 says:

    Dr. Giem has a new lecture up:

    “The Edge of Evolution” Strikes Again 8-2-2014 by Paul Giem – video
    https://www.youtube.com/watch?v=HnO-xa3nBE4&list=UUaBAwmf0uZeTYejbXpXV7VQ

  38. 38
    Joe says:

    Acartia_bogart- What happens in your dreams and/ or imagination- someone refuting Meyer- does not count in the real world. 😉

    Saying that the Cambrian explosion wasn’t an explosion does not help natural selection. Saying that there were many pre-Cambrian organisms doesn’t help natural selection. The only thing natural selection has going for it is the story evolutionary biologists have spun.

  39. 39
    Joe says:

    Gordon Davisson- You are sadly mistaken if you think that the “evidence” for universal common descent is strong, never mind “overwhelmingly strong”. We don’t even know what makes an organism what it is and all evidence for this alleged common ancestry can easily support a common design.

    As for nested hierarchies- LoL! Common ancestry would predict many transitional forms. That means we should, at best, be able to create an overlapping Venn diagram, not a nested hierarchy. Denton goes over this in “Evolution: A Theory in Crisis”.

    Linnean taxonomy, ie the observed nested hierarchy, was based on a common design and has nothing to do with common ancestry. The US Army, another observed nested hierarchy, has nothing to do with common ancestry.

    Nested hierarchies are purely a man-made construct and have nothing to do with natural processes, let alone natural selection.

    That said, the genes responsible for micro-evolution will never produce the type of change common ancestry requires. And the genes that may be able to make those changes cannot be changed. Don’t you think that is a problem?

    So what mechanism brought about all of this change and how can we test it? You do want common ancestry to be scientific, right? How can we measure it- how many mutations to go from fish to amphibian?

  40. 40
    jerry says:

    Did we know that Acartia_bogart was a biologist?

  41. 41
    Upright BiPed says:

    Gordon Davisson,

    my objection isn’t that common ancestry refutes ID (it clearly doesn’t), it’s that the ID movement’s unwilling to look at the evidence for common ancestry clearly indicates that science, and following the evidence, simply is not a priority for the ID movement.

    I have no position to defend on common ancestry, but I certainly understand your sentiment. I feel exactly the same way about ID critics who throw their arms in the air and refuse to engage the physical conditions required for the translation of an informational medium into a functional physical effect – i.e. the very thing that organizes the living cell as know it.

    For instance, on this website right now we have an ID critic, who like a child with an untied shoe, does not seem to be able to take another step without knowing the ID antecedent to the modern human form. But in reality, he is not actually interested in rational antecedents. If he was interested in such things, he would take his appeal to “the best explanation” and apply it to what we already know to be a fundamental observed truth about life on earth – that is, that living systems are locally organized by the translation of recorded information.

    The simple fact of the matter is that the physical conditions required of translation are anathema to his ideology, and he simply wants to know nothing about it.

    So, like you, I see a wall erected between the explanations and the physical evidence. The distinction between us is that common descent, as you’ve already pointed out, is not even a problem for ID, whereas, the physical requirements of organizing the living cell (via translated information) is a virtually intractable deal-stopper for the unguided organization of life on earth.

    Certainly, if one does actually address and acknowledge in earnest the physical conditions required to organize the living cell, then the oft-made claim of ID critics that “no evidence of design exist” is nothing less than a bold-faced lie told by intellectuals for public consumption. As you suggest, such a statement “clearly indicates that science, and following the evidence, simply is not a priority” to those who make such statements.

  42. 42
    Moose Dr says:

    This is a funny debate. For the most part its the neo-Darwinists screaming that common descent has an evidentiary base. The IDers mostly are saying that common descent doesn’t have a great evidentiary base.

    As an IDer, I say, what if common descent is correct? Does it weaken our position one iota? There is something fundamentally superior about humanity. How a process that has no direction could produce such strategic superiority is puzzling to me. If we were designed by someone twiddling with the DNA of existing creatures, then mating them to produce something superior, or if we are designed by someone running a master DNA compiler and producing a new organism makes very little difference to the ID case.

    ID is not in any way diminished by common descent. Descent with intelligent modification remains to be intelligently designed.

  43. 43
    Acartia_bogart says:

    Jerry, actually A_B is a biologist and a statistician, but what are a couple credentials between friends?

    BA77, unfortunately, I don’t perceive YouTube videos as qualified rebuttal. Call me old fashioned.

    BA77: “Exactly what is the mathematical basis of Darwin?”

    Darwin never proposed a mathematical basis for his theory. But you know this. In fact, you will be hard pressed to find any evolutionary biologist who would call themselves a Darwinist, so I don’t understand why you and the other creationists insist on labelling all evolutionary biologists as such (actually, we all understand the strategy. Childish as it is).

    But, if you want to talk about modern evolutionary biology, there is a very good mathematical basis to it (if, by mathematical, you mean probabilistic, which is not the same, but you know this as well). The difference between the statistics behind evolutionary theory, and Behe’s voodoo magic pseudostatistics is that one is defensible and testable. And the other one is creationism.

  44. 44
    Acartia_bogart says:

    Moose Dr. Finally an intelligent comment from an IDist, even though I disagree with it. You are absolutely correct. But only if your fundamental assumption, that humans are superior, is correct. I agree that we are dominant. But that does not mean superior. For most of earth’s history, anaerobes were dominant. Based on that record, maybe they should be superior. Bacteria still make up the vast majority of living organisms on earth. By most accounts, that would make them superior.

    Insects are far more resilient to environmental changes than humans.

    In short, I don’t see how you can consider that we are the superior life form on the planet. But what do I know?

  45. 45
    Moose Dr says:

    Acartia_Bogart, “But only if your fundamental assumption, that humans are superior, is correct.” Evolutionarily correct answer. The fact that we are by a long way the most knowledgeable species be damned.

    Acartia_Bogart, “(actually, we all understand the strategy. Childish as it is).” No, “IDiot” is Childish. (I know, you haven’t used the term, but you are familiar with it, are you not.) The Darwinist thing is there to separate the term “evolution” (change over time) with the philosophical commitment to naturalism held by those whose views incorporate Darwinism.

    The current dominant view of evolutionary biology has put a lot of meat on the bones of Darwin’s theory. However, they only extend the theory, they do not replace it.

    What should one call an evolutionary biologist that holds to common descent, but does not buy into the naturalistic interpretation?

  46. 46
    Acartia_bogart says:

    Moose Dd. “What should one call an evolutionary biologist that holds to common descent, but does not buy into the naturalistic interpretation?”

    Delusional.

  47. 47
    Querius says:

    A-B@43 claimed,

    But, if you want to talk about modern evolutionary biology, there is a very good mathematical basis to it (if, by mathematical, you mean probabilistic, which is not the same, but you know this as well). The difference between the statistics behind evolutionary theory, and Behe’s voodoo magic pseudostatistics is that one is defensible and testable. And the other one is creationism.

    OK, so, what precisely are you talking about when you refer to Dr. Behe’s “voodoo magic pseudostatistics”? His calculations made some pretty good predictions regarding malaria. Please tell us in precise terms what was incorrect about his calculations from which you make your defamatory statement.

    -Q

  48. 48
    kairosfocus says:

    A_b:

    Paul Giem, FYI, is a medical doctor with a long term interest in these subjects who undertook a long term video review of DD and issues surrounding it.

    Your dismissal of “YouTube” — a publishing technology — and blanket endorsement of the dominant schools in Biology [which BTW are ideologically driven by a priori evolutionary materialism brought in the back door of a seemingly innocuous methodological premise . . . ] constitutes a case of fallacious appeal to modesty in the face of a reigning orthodoxy’s authority.

    UB has put his finger on the real issue . . . the info, communication and control systems and content of life forms in the deep past of origins must be adequately explained on vera causa plausible cause. Blind chance and/or mechanical necessity do not fill that bill once, say one ponders the implications of the configuration space of 500 – 1,000 bits vs the atomic search resources of our observed cosmos.

    And BTW, I will never forget my first exposure to keys based taxonomy as taught to biology students: paper clips and similar fasteners laid out in a resultant nested hierarchy — hierarchy and design with adaptation to particular tasks is 100% compatible with design. So nested hierarchy is not decisive between common descent and common design.

    Likewise, Berra’s blunder on the Corvette family of cars shows how design with modification can easily account for what he intended to illustrate: “family resemblance” explained on incremental, blind chance and mechanical necessity driven common descent with modification.

    Where also, until it was pointed out to you, you did not seem to be aware of the UD Weak Argument Corrective remarks on common descent vs common design. Namely, that CD, even UCD — as is adhered to by Michael Behe, BTW — is fully compatible with common design. I should add, that common design of living forms on earth — the cell based life we observe — is likewise 100% compatible with a molecular nanotech lab at work, i.e. strictly, inference to design of life on earth is not equal to inference to extracosmic designer. (It is Sir Fred Hoyle and others who have drawn out a “mountain” of evidence on cosmological fine tuning that sets up the sort of cosmos in which C-chemistry, aqueous medium, gated, encapsulated, metabolising, von Neumann self replicating cell based life is facilitated, from basic physics up, which points to extracosmic designer capable of building a cosmos fitted for such life. And, the two together point to a significant profile of the best candidate for designer of cosmos and cell based life alike.)

    I suggest a shift from strawmannising and dismissive talking points to a pondering of pivotal evidence. Which, BTW STILL needs to account for the origin of dozens of major — phylum and sub-phylum level — body plans in a reasonably narrow window on the conventional geological timescale, perhaps 10 MY, at c 540 MYA.

    Where, on just genome observations and an easy to do back of envelope calc, we are looking at 10 – 100+ mn bits of info, perhaps 3 dozen times over; where there is strong evidence of the deep isolation of protein folds in AA sequence space. The 10^80 atoms of our observed cosmos, searching for 10^17s, at a shuffling rate of one search every 10^-14 s [generous for org chem based processes], each examining a tray of 1,000 H/T coins, would be utterly swamped out by the 1.07*10^301 possibilities. Each additional bit DOUBLES the config space.

    As well, pondering a chimp-like common ancestor at 6 – 10 MYA, reasonable generation times for primates and population numbers, plus reasonable mutation rates, we see another decisive body plan origin challenge. For 2% of 3*10^9 = 6*10^7, 60 mn bases, or 120 mn bits more or less.

    That is, we again need to account for spanning a vast config space, in a tight window of time with utterly inadequate search resources.

    In short, the information accounts do not add up under any reasonable blind chance and mechanical necessity based search strategy on the gamut of the earth or the solar system or the observed cosmos. The incrementalist algorithm is fatally inadequate to tackle an exponential field of possibilities.

    That leaves one serious candidate on the table, common design. Where, we routinely produce successful information based entities of relevant scope.

    KF

  49. 49
    kairosfocus says:

    PS: A-b, Behe used standard epidemiological facts about malaria, and reasonable calculations. You seem, again, to be resorting to ad hominem laced strawman rhetoric, rather than a sober assessment of the material issue.

  50. 50
    jerry says:

    Ad hominems are an admission that my opponent is right and I am wrong especially when it is not in response to a personal attack. Why don’t we just accept the admission when it is offered? We all have trouble doing this.

  51. 51
    jerry says:

    Here is a post I made over 6 years ago about why things look alike but are different. The discussion of common descent reminded me of it and it really gets at this issue. My comment is pure speculation but hopefully offers food for thought on just what evolution is and why common descent seems so obvious to many.

    Denyse,

    I will comment here rather than at Design of Life. Earlier this week I had planned on writing a detailed description of what I believe the evidence points to. Your post at Design of Life just reinforces my point of view.

    Namely, everyone who believes in ID should embrace the modern theory of evolution (MET) but in a limited way. It is good design and thus should be part of the ID scenario. To many here this is heretical but if we are truly endorsing science here then it makes good sense. I just rejected the naturalistic approach to evolution on another thread because there is no forensic evidence. But here I am going to endorse significant parts of the modern evolutionary theory because 1) I believe the forensic evidence is there and 2) it is great design.

    The modern theory of evolution explains downward evolution but not upward evolution. We first saw this in the Cambrian Explosion. In fact there may not be anything as upward evolution but that is still to be proven. There is definitely downward evolution and the mechanism for it MET.

    The gene pools contain a lot of possibilities that are not expressed and over time different morphologies will appear because of the three main elements that reshuffle the genes in members of a gene pool. They are natural selection, genetic drift and gene flow. Your hybrid examples are the result of gene flow. In all of this is the interaction of the environment.

    Over time the gene pool is able to create the families and genera and from these flow new species. The traditional Darwinian explanation is that the gene pool is constantly being expanded by mutations and over time these mutations create complexity and novelty in an upward fashion. There is absolutely zero evidence of any upward evolution as Behe’s Edge of Evolution indicates. But there is loads of downward evolution.

    But what is completely reasonable and seems to be in sync with the data is that population gene pools may contract because of geographical separation and environmental conditions. There may be many other ecological changes that may also affect the gene pool of a population. Essentially reducing the gene pool with the occasional mutation adding to it in some trivial way.

    And when this happens we get the richness of life we see in the world but not by any upward creation of new species but a downward creation. We see different types of iguana, fruit flies, birds, fish, cattle, canines etc that are the result of geographic dispersion and environmental conditions. And the mechanism is natural selection, genetic drift and gene flow along with an occasional mutation that modifies but does not create any complexity or novelty. This is exactly what Darwin saw on the Beagle but he extrapolated the wrong way and that is why we are in the mess we are in today.

    As I said this process increases the richness of life which we see about us. Your hybrid examples just add to the evidence supporting this position It is folly to think that each species was created separately but that does not mean that everything has a purely naturalistic mechanism for its origin. The real debate is where did the gene pools come from because Darwinian processes are constantly winnowing them down.

    This system which enables populations to adapt is fantastic design and any designer would be proud of it. It allows for organisms to morph into slightly different variations over time to adapt to different environmental conditions and thus to prosper and avoid extinction. I would bet the actual design of the DNA and its reproductive mechanisms are what lets this happen but only to a limited degree (I understand transcription and translation and error checking but the system is designed to allow some modification but not a lot.). And the whole is an amazingly interrelated system that lets this limited adaptation take place but does not let it get out of hand.

    This has been a little bit rambling and when I have time will try to put it in a more organized fashion. But if anyone has any suggestions for improvements, criticisms etc. I would appreciate it.

    No one at the time commented on it including Denyse to whom it was directed. Here is the link

    http://www.uncommondescent.com.....w-species/

  52. 52
    peter_G says:

    To BA in 36,37:

    Can you post the individual video links instead a link to a video list? because it is the only way i can download them.(you know somewhere in the world we don’t have access to YouTube.)

    like here what you did is fine for me:

    Darwin’s Doubt – Reviews – Part 1 – by Paul Giem – video
    https://www.youtube.com/watch?v=YW8SLKoSZqM
    Darwin’s Doubt – Reviews – Part 2 – by Paul Giem – video
    https://www.youtube.com/watch?v=nPqN0-YiJgg
    Darwin’s Doubt – Reviews – Part 3 – by Paul Giem – video
    https://www.youtube.com/watch?v=5Mj1thPrSgc
    Darwin’s Doubt – Reviews – Part 4 – by Paul Giem – video
    http://www.youtube.com/watch?v=IfEfa6KaEXU

  53. 53
  54. 54
    bornagain77 says:

    Here you go Peter:

    Conversations with Stephen Meyer – videos
    Responding to Critics
    https://www.youtube.com/watch?v=Bw71sAizuCQ
    The Most Frivolous Criticism
    https://www.youtube.com/watch?v=Ljy1yfGdC5Y
    Surprised By Praise
    https://www.youtube.com/watch?v=Xe6AYlELsXQ
    Response to Critics – Prothero – Part 1
    https://www.youtube.com/watch?v=sI4USR9BWT8
    Response to Critics – Prothero – Part 2
    https://www.youtube.com/watch?v=yEWQYqtnaIM
    Response to Critics – Marshall – Part 1
    https://www.youtube.com/watch?v=zqYUoRVswRY
    Response to Critics – Marshall – Part 2
    https://www.youtube.com/watch?v=Cg8Mhn2EKvQ
    Response to Critics – Marshall – Part 3
    https://www.youtube.com/watch?v=fR_Agl41TbE

    “The Edge of Evolution” Strikes Again 8-2-2014 by Paul Giem
    https://www.youtube.com/watch?v=HnO-xa3nBE4

  55. 55
    bornagain77 says:

    OOOPS, missed the most important one from Meyer’s list:

    The Biggest Failure of Critics
    https://www.youtube.com/watch?v=Ljy1yfGdC5Y

  56. 56
    Acartia_bogart says:

    K

    PS: A-b, Behe used standard epidemiological facts about malaria, and reasonable calculations. You seem, again, to be resorting to ad hominem laced strawman rhetoric, rather than a sober assessment of the material issue.

    I have read a bit about this but he was talking about the high improbability of chloroquine resistance developing because it requires two, more or less, simultaneous mutations. But he missed one simple point. These mutations do not have to be simultaneous. In fact, it has been demonstrated that they are not.

  57. 57
    Querius says:

    A-B

    But he missed one simple point. These mutations do not have to be simultaneous.

    Yeah, some Desperate Darwinists ™ are using that straw–man argument. Behe never claimed that the mutations must *occur* simultaneously, merely that they both need to be *present* together in order to be effective.

    So, Behe used the binomial theorum to predict how long it would take for micro-evolution to produce chloroquine resistance. It now turns out his prediction was actually correct.

    Since the binomial theorum doesn’t include anything that distinguishes simultaneous from sequential events, he was justified in using it.

    So, as a biologist and statistician, tell us what evolutionary factor *could* have falsified Behe’s prediction? And why didn’t it? (This would be a good quiz question).

    -Q

  58. 58
    Acartia_bogart says:

    Querius, his probability estimates are based on the assumption that the two mutations necessary are simultaneous (stats 101). If step wise accumulation of mutations is an option, which has demonstrated to be the case, then the numbers are vastly different. But, by all means. Don’t allow basic statistics get in the way of Behe’s preposterous claims.

  59. 59
    Box says:

    AB #58, you are ill informed.

    Behe: The number I cite, one parasite in every 1020 for de novo chloroquine resistance, is not a probability calculation. Rather, it is a statistic, a result, a data point. (Furthermore, it is not my number, but that of the eminent malariologist Nicholas White.) I do not assume that “adaptation cannot occur one mutation at a time”; I assume nothing at all. I am simply looking at the results. The malaria parasite was free to do whatever it could in nature; to evolve resistance, or outcompete its fellow parasites, by whatever evolutionary pathway was available in the wild. Neither I nor anyone else were manipulating the results. What we see when we look at chloroquine-resistant malaria is pristine data — it is the best that random mutation plus selection was able to accomplish in the wild in 1020 tries.

  60. 60
    Box says:

    [correction post #59: it should have said “10^20” instead of “1020”]

  61. 61
    Querius says:

    LOL, A-B.

    What’s the probability of rolling a total of 7 on two normal six-sided dice simultaneously?

    Now, what’s the probability when they are instead rolled one at a time (serially)?

    -Q

  62. 62
    Querius says:

    A-B,

    Oh, and you forgot about the question:

    So, as a biologist and statistician, tell us what evolutionary factor *could* have falsified Behe’s prediction? And why didn’t it? (This would be a good quiz question).

    -Q

  63. 63
    Moose Dr says:

    Acartia_bogart, “If step wise accumulation of mutations is an option, which has demonstrated to be the case, then the numbers are vastly different. But, by all means. Don’t allow basic statistics get in the way of Behe’s preposterous claims.”

    Stepwise accumulation of mutations is only an option where at least one of the mutations is not deleterious. I suspect that in Behe’s example, each individual mutation was demonstrably deleterious.

  64. 64
    anthropic says:

    Hey, AB 58. Re the simultaneous mutations, an excerpt from my previous post to you…

    “AB, Behe’s analysis of the constraints on what can be expected from random mutation to produce drug-resistant malaria parasites was recently vindicated. Another researcher found that, as Behe correctly stated in The Edge of Evolution, anything beyond two simultaneous mutations for resistance was too much to expect, even when the population numbers a trillion and replicates rapidly.

    http://intelligentdesign.podom…..1_38-07_00

    By the way, “simultaneous” here doesn’t mean at the same replication cycle in the same cell. It just means the odds that a group of cells with one non-advantageous mutation will keep it until they get the second mutation that offers a benefit. The process is known as stochastic tunneling and is discussed in the second podcast.”

    Of course, we know Behe got the numbers basically right not because of some theoretical argument, but due to observation of how actual malarial parasite populations develop resistance.

  65. 65
    Querius says:

    anthropic,

    Bingo!

    Kinda too bad though because I was hoping that Acartia_bogart would try to defend in mathematical terms exactly what A-B meant by writing

    The difference between the statistics behind evolutionary theory, and Behe’s voodoo magic pseudostatistics is that one is defensible and testable. And the other one is creationism.

    especially in light of the experimental agreement with Andrea Summer’s results.

    I also wanted to see whether A-B could demonstrate any knowledge or proficiency in “statistics,” but apparently this is not the case, and we’re simply left with the foul odor of a flatulent assault against Dr. Behe’s competence.

    -Q

  66. 66
    Acartia_bogart says:

    Stepwise accumulation of mutations is only an option where at least one of the mutations is not deleterious. I suspect that in Behe’s example, each individual mutation was demonstrably deleterious.

    No, that was a prediction, which has since been proven to be wrong. It has now been shown that chloroquine resistance is the result of the accumulation of mutations, not the simultaneous appearance of two mutations.
    http://www.pnas.org/content/111/17/E1759

    When this was demonstrated, Behe simply redefined “simultaneous”. This sounds like ENCODE’s redefinition of “functional” to arrive at the 80% number.

    Personally, I think that Behe’s original back of the napkin calculation made logical sense, and he should definitely be commended for it. But he should also be big enough to admit that his prediction was not vindicated, as some have suggested.

  67. 67
    Querius says:

    Notice that A-B has not answered any of my questions, but simply repeated the fallacious narrative against Behe along with some added vituperation.

    Here are the questions repeated:

    What’s the probability of rolling a total of 7 on two normal six-sided dice simultaneously?

    Now, what’s the probability when they are instead rolled one at a time (serially)?

    Any bets as to whether A-B will answer these questions?
    One would think that after A-B accused Behe

    The difference between the statistics behind evolutionary theory, and Behe’s voodoo magic pseudostatistics is that one is defensible and testable. And the other one is creationism.

    So, naturally one wants to know why they’re “voodoo magic pseudostatistics” but there is no mathematical or statical reasoning forthcoming in support of these deprecatory accusations. One begins to wonder . . . 😉

    -Q

  68. 68
    Acartia_bogart says:

    Querius, the reason that I haven’t answered your question is because it is not relevant. But since you insist. 1/6 and 1/7, respectively. But that is not what we are talking about. When you roll a single die, any outcome can still result in a seven. But for chloroquine resistance, that is not the case.

    A better analogy would be what are the odds of rolling a two on the first die and a five on the second? Simultaneously? The probability is much lower than 1/6 (or 1/7). That is what Behe was arguing; you need two very specific mutations to occur simultaneously. But it turns out that they don’t need to be simultaneous. But he didn’t let that deter him. He just redefined what ‘simultaneous’ means.

  69. 69
    bornagain77 says:

    “The real question here is not whether the arguments ID makes are correct or whether they’re supported by the science when you look at it objectively. This resistance to ID is solely a sociological phenomenon. That the folks in science — at least the ones who have the microphones — don’t like it, don’t like it one bit. And they will do whatever they can, fair or foul, to suppress it.”
    -Michael Behe, Vindication for ‘The Edge of Evolution,’ Pt. 2 @ ~12.20
    intelligentdesign.podomatic.com/entry/2014-08-06T15_26_19-07_00

  70. 70
    bornagain77 says:

    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

    “The Edge of Evolution” Strikes Again 8-2-2014 by Paul Giem – video
    https://www.youtube.com/watch?v=HnO-xa3nBE4

    i.e. where’s the empirical evidence for Darwinian evolution?

    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

  71. 71
    Acartia_bogart says:

    ““The real question here is not whether the arguments ID makes are correct or whether they’re supported by the science when you look at it objectively.

    What the F$&@? Of course that is the question. That is the only question.

  72. 72
    wd400 says:

    I’m not sure where 1/7th came from AB? Perhaps you are taking “sequential” to mean something different than I would?

    In any case, the question has no relevance to biology. How could mutations be “sequential” in the sense of one after the other? One cell division then the next one? Ignoring the fact there are now two cells, what’s special about the next cell division compared with one 2 20 or 200 generations away?

  73. 73
    bornagain77 says:

    No AB, the question is why do Darwinists, despite Darwinism being a pseudo-science and despite not having one iota of evidence that Darwinian processes can generate just one sentence of the two hundred telephone directories worth of functional information in the Human Genome, so angrily, by any means possible, fair or foul, defend Darwinism as if their life depended on it?

    Is There Evidence of Something Beyond Nature? – John Lennox – video
    https://www.youtube.com/watch?v=F6rd4HEdffw

  74. 74
    Querius says:

    wd400 wondered,

    I’m not sure where 1/7th came from AB? Perhaps you are taking “sequential” to mean something different than I would?

    I thought I’d never say this, wd400, but thank you. The answer to both questions is of course 1/6. There’s no time component in the binomial theorum. The dice can be rolled together or separately.

    As a self-proclaimed “statistician,” A-B could test whether there’s a statistically significant difference empirically.

    We wait with baited breath! 😉

    -Q

  75. 75
    Acartia_bogart says:

    Sorry WD200. Big thumb, small buttons. It should have been 1/6. After all, there are only six faces on a die.

    My point was simply that the mutations don’t need to occur simultaneously, which is the basis of Behe’s weak argument. They can be the result of accumulated mutations, fixed in the population by drift. Behe either doesn’t understand this proven concept or choses to misrepresent it. I vote for intentional misrepresentation of the facts.

  76. 76
    Mung says:

    When you roll a single die, any outcome can still result in a seven

    Given it’s a seven-sided die and each face is equally probable, I suppose that’s correct.

    So given two seven sided die, where each face is equally likely …

    Does it matter whether you toss them simultaneously?

  77. 77
    Acartia_bogart says:

    Mung, no. When you roll two dice sequentially, the probability of them summing 7 is based on the second die alone. And the probability is always 1/6.

  78. 78
    Querius says:

    Let me understand this. What you’re saying is that when you wrote

    But since you insist. 1/6 and 1/7, respectively.

    you really didn’t make a mistake, but that the 7 was a typo and that you really truly meant to write the following:

    But since you insist. 1/6 and 1/6, respectively.

    Respectively? Methinks you’re a weasel.

    But now that we’ve settled that with the binomial theorem, it doesn’t matter whether events are simultaneous or sequential, let’s look at Behe’s math.

    We know that for malaria to develop chloroquine resistance, two specific mutations are required. The mutations can occur simultaneously or sequentially, it doesn’t matter, but both mutations must be in the malaria organism at the same time (i.e. simultaneously present).

    What Behe did was multiply the probability of mutation #1 times the probability of mutation #2. It turns out that this is an extremely small probability. But knowing the following information

    – The reproduction rate of malaria
    – The number of malaria organisms in each infected person who is being treated with chloroquine.
    – The number of people being treated with chloroquine.
    – The length of time of treatment

    He estimated how many years it would take before resistant malaria would appear. Turns out his estimate was reasonably accurate. Oh horrors.

    But you haven’t explained your statistical reasons behind your reference to “Behe’s voodoo magic pseudostatistics.” It would seem to me that these statements are simply groundless ad hominem attacks on your part. Right? Or will you explain mathematically or statistically what was wrong with Dr. Behe’s math.

    -Q

  79. 79
    wd400 says:

    I thought I’d never say this, wd400, but thank you

    Well, I wouldn’t get too carried away Querius, because everything else you said is…. confused at best.

    You’re not really taking about the binomial thereom, which is how you you expand equations of the form (x + a)^n. That thereom is the basis of the binomial distribution, but you are wrong to say sequential and silmntaneaous don’t matter in this case. In your example you calculate the probability from two back-to-back rolls. What relevance do you think this has the accumulation of mutations? What are the equivalent of the back-to-back rolls? The only comparison I can think of are back-to-back cell divisions, but that doesn’t work because there is nothing special about the order of cell divisions. Getting the second mutation 100 divisions after the first is still getting both mutation, moreover, there may be many more copies of the first mutation in the population by that time. So you are wrong to say the binomial [probability density] doesn’t rely on time, even a single lineage the probability get’s higher as more cell divisions occur.

    Finally, you are very confused about what Behe actually claimed. In the above you seem to be saying he guessed how long it would take for P. falciparum to aquire drug resistance, but that was known well before he wrote his book. Indeed — the 10^20 guestimate he pulled from a paper is based on this rate.

  80. 80
    Upright BiPed says:

    Oh, the irony.

  81. 81
    kairosfocus says:

    A_b:

    When you roll two dice sequentially, the probability of them summing 7 is based on the second die alone. And the probability is always 1/6.

    Pardon a note, the event is COMPOSITE:

    START –> {roll a, roll b} –> Read sum = a + b –> END

    The relevant probability is that at the point, start, not that at the point roll a done now for b. The odds of any given value of b will be 1 in 6 indeed, but the event is to have a and b to sum. It so happens that there are six of 36 ways to sum a 7 with the usual dice, but the result is composite.

    Now, Mung actually envisions seven-sided dice . . . most easily done with spindle-shaped dice. If the pips run 1 to 7, there are 49 possibilities and still only six ways to sum to 7, as the case where one die already is 7 forces a sum in excess of 7. Tossing a single seven sided die gives odds of 1 in 7.

    And notice, principle of indifference underlying the matter.

    Now, Q at 78:

    We know that for malaria to develop chloroquine resistance, two specific mutations are required. The mutations can occur simultaneously or sequentially, it doesn’t matter, but both mutations must be in the malaria organism at the same time (i.e. simultaneously present).

    What Behe did was multiply the probability of mutation #1 times the probability of mutation #2. It turns out that this is an extremely small probability. But knowing the following information

    – The reproduction rate of malaria
    – The number of malaria organisms in each infected person who is being treated with chloroquine.
    – The number of people being treated with chloroquine.
    – The length of time of treatment

    He estimated how many years it would take before resistant malaria would appear. Turns out his estimate was reasonably accurate. Oh horrors.

    Obviously, the issue is for malaria parasites to meed Chloroquine and resist the drug. Presumably the muts can be simultaneous or sequential. If the latter, having the first should not be too deleterious or it will be eliminated, and it cannot be too advantageous as the new variety would have rapidly dominated.

    That is, the mut must be quasi-neutral, for positions A and B, so they are effectively only significant if we have A and B and the drug providing selection pressure.

    KF

  82. 82
    kairosfocus says:

    PS: Let’s note Behe’s letter, courtesy BA77 in 70:

    >> 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 >>

  83. 83
    kairosfocus says:

    PPS: I probably should leave it at 1st mut not excessively deleterious. KF

  84. 84
    wd400 says:

    KF,

    AB is right to say the probability of getting a ‘7’ can be explained by only the outcome of the second roll. No matter what the first roll might be there is always precisely one way to get to 7 from that value, so the probability is 1/6th.

    The rest of your post just seems to agree that ‘sequential’ need not mean ‘consecutive’ so Querius was wrong to use the example?

  85. 85
    Acartia_bogart says:

    Another example. Martians syndrome is a connective tissue disorder that affects one in 5000 people. It’s symptoms can include myopia, scoliosis, mitral valve problems, aortic aneurism, spontaneous pneumothorax, among other manifestation. Now, with no background information, what is my probability of having this syndrome? One in 5000? That would be a reasonable prediction.

    And that is as far as Behe went. He completely ignored the fact that the mutations could accumulate over time.

    Now, what if I said that my father had Marfans? What are my probabilities now? One in two? That is a far cry from one in 5000. Now, what if I told you that I am myopic, have scoliosis and have had a pneumothorax. Without even having a confirmatory test I can reasonably predict that my probability of having Marfans is close to one.

    So, by taking history into account the probability has changed from one in 5000 to close to one.

    So, please explain to me again why it doesn’t make a difference whether two occurrences are simultaneous or cumulative.

  86. 86
    Querius says:

    Kairosfocus@81,

    Exactly.

    This is about as basic probability as you can get, but there are complicating factors depending on the amount of time it takes for the second mutation to appear as you pointed out. However, given the extremely large numbers of malaria organisms and the amount of time, one can calculate the time it would take to finally get a resistant individual. These calculations are already being done with antibiotics.

    Mathematical modeling suggests that heterogeneous antibiotic use may limit the emergence of resistance.

    For context, see http://aac.asm.org/content/48/8/2861.full

    For WD400 and AB, all I can say is talk to someone in your math department and try to explain to them your theory about the binomial theorum regarding “simultaneous” versus sequential events. Your ignorance on the subject is profound. Ask yourselves this, how much time can pass between two events for them to still be considered “simultaneous.” If your answer is zero, then there are no simultaneous events in nature (unless you want to argue Planck time). And AB, as a “statistician,” you should know about anecdotal evidence in statistics.

    -Q (shaking head)

  87. 87
    wd400 says:

    Querius,

    Read again. The problem is that you are conflating consecutive with sequential. It’s not the time between trials that matter, but the number of trials. To use your dice example:

    what’s the probability of getting two 5s in two throws

    That’s (1/6)^2 =1/36 yes?)

    Now, what’s the probability of getting two (or more) 5s in
    10 throws?

    It should be obvious that it’s greater than 1/36th, and indeed if you the calculation you’ll see it’s something a little more than 1/5.

    Since there is requirement that mutations giving the phenotype occur back-to-back (just that they eventually accrue in one daughter cell of the first mutant) you were wrong in #56, and subsequently, to claim there is no difference probability for the simultaneaous and sequential cases as they apply to the accumulation of mutations.

  88. 88
    Mung says:

    Upright BiPed:

    Oh, the irony.

    Being he connoisseur of irony that I am, it’s one of the things that keeps me coming back to UD. 🙂

  89. 89
    Mung says:

    -Q (shaking head)

    That rattling noise isn’t two six-sided die is it?

    It seems to me that the probability of the sum of two die faces totaling seven is 1/6. There are 6 ways in which two die faces could sum to SEVEN and 30 ways in which the two faces could sum to NOT SEVEN.

    So why does the house only pay 4 to 1 for any seven?

    Now this [probability] is the case regardless of whether both die land face up simultaneously or one comes to rest face up before the other.

    Now given that one die has come up a six, this does not impact the overall probability. The probability of a sum of SEVEN isn’t changed just because the roll of the second die has not yet been revealed.

    Isn’t this what they mean by independent events?

    But this should not be confused with conditional probability. (Aren’t all probabilities conditional?) When calculating the probability of a sum of SEVEN, it’s conditioned upon two die being thrown and the die being fair.

    So what, precisely, is the objection to Behe?

    Is it that the two events to confer chloroquine resistance are not independent? Is there equivocation over what it means for two events to be independent from a probability standpoint?

    What does whether the events are simultaneous or not have to do with anything? Pr(Newbies) want to know.

  90. 90
    Mung says:

    Nevertheless, probability is the mathematical foundation upon which statistics depends, and understanding basic probability principles helps you understand what an analysis really means—and, sometimes even more important, what it does not mean.

    oops.

    Trying to understand probability? Be sure to use fair dice. The fuzzy ones won’t work so well!

    You don’t say.

    Arcatia_bograt:

    So, please explain to me again why it doesn’t make a difference whether two occurrences are simultaneous or cumulative.

    What does it even mean to say that two events are cumulative?

    Cumulative probability measures the odds of two, three, or more events happening. There’s just one catch involved: each event needs to be independent of the others—you can’t have two events that occur at the same time, or have the outcome of a first event influence the probability of the next

    What’s the Difference Between Probability and Cumulative Probability?

    P(understanding | Arcatia_bogart)

  91. 91
    Mung says:

    wd400:

    AB is right to say the probability of getting a ’7? can be explained by only the outcome of the second roll.

    Don’t be silly.

    By the same logic, AB could also say that the probability of getting a ‘7’ can be explained by only the outcome of the first roll. And you would be obliged to declare AB is equally right to say so.

    Are you really willing to go there?

    I acknowledge that people here may find many of my posts short and cryptic. So I’ll expand (slightly):

    The difference lies in the following distinction:

    The probability of getting a ’7? can be explained by only the outcome of the second roll AND the probability of getting a ’7? can be explained by only the outcome of the first roll.

    The probability of getting a ’7? can be explained by only the outcome of the second roll OR the probability of getting a ’7? can be explained by only the outcome of the first roll.

    But now, dear reader, you’re on your own.

  92. 92
    kairosfocus says:

    WD400: You are again switching contexts, exactly as I warned against. The relevant context is quite plainly before the two die rolls. And, in the case of Chloroquine resistance, you have no right to assume an in-hand first mutation. You have to account for the double. KF

  93. 93
    wd400 says:

    Ok Mung — I meant only that AB was explaining one way you could determine the probability (“explained by only”, not “only explained by”). As you say, the order doesn’t matter.

  94. 94
    wd400 says:

    kairosfocus,

    What? I’m not “swtiching contexts”, just pointing out AB’s comment is a prefectly reasonable way of seeing why the probability is 1/6.

    In the second I’m not assuming anything. I’m saying the probability of some cell ending up with two specificed mutations isn’t the per-generation mutation rate squared. I didn’t think that would be controversial…

  95. 95
    kairosfocus says:

    F/N: It’s probably worth the while to clip Behe’s full letter:

    ___________

    >> 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 1020 malaria-cell replications. Okay, if you don’t like that, what’s your estimate? Let’s see your numbers.

    The malaria literature shows strong population genetics evidence for fewer than ten independent origins of resistance. The riddle is, why so few? Show us all your calculation for that. Here’s a number to keep in mind — 1012. That’s roughly the number of malarial cells in one sick person. Here’s another — 10-8. That’s a generous rounding-up of the mutation rate for malaria. (Multicellular eukaryotes are an order of magnitude less.) That means on average ten thousand copies of each and every point mutation of the malarial genome will be present in every person being treated with chloroquine.

    Here’s another — 3. That’s the number of patients it takes for spontaneous resistance to atovaquone to appear. That makes a lot of sense since resistance to atovaquone needs only one point mutation. If atovaquone were used as widely as chloroquine, we’d expect about a billion or more origins of resistance to it by now, not a measly handful. So how do you quantitatively account for that difference — give or take an order of magnitude?

    Your chief complaint against my ideas seems to be this:

    That the malaria parasite needs two mutations was never a point of contention, nor was it particularly worrisome. What was wrong with Behe’s work is that he naïvely claimed that the two mutations had to occur simultaneously in the same individual organism, so that the probability that could happen was the product of multiplying the two individual probabilities. That’s ridiculous.

    What’s puzzling to me is your thinking the exact route to resistance matters much when the bottom line is that it’s an event of probability 1 in 1020. From the sequence and laboratory evidence it’s utterly parsimonious and consistent with all the data — especially including the extreme rarity of the origin of chloroquine resistance — to think that a first, required mutation to PfCRT is strongly deleterious while the second may partially rescue the normal, required function of the protein, plus confer low chloroquine transport activity. Those two required mutations — including an individually deleterious one which would not be expected to segregate in the population at a significant frequency — by themselves go a long way (on a log scale, of course) to accounting for the figure of 1 in 1020, perhaps 1 in 1015 to 1016 of it (roughly from the square of the point mutation rate up to an order of magnitude more than it). So how do your calculations account for it?

    It’s also entirely reasonable shorthand to characterize such a situation as needing “simultaneous” or “concurrent” mutations, as has been done by others in the malaria literature, even if the second mutation actually occurs separately in the recent progeny of some sickly, rare cell that had already suffered the first, harmful mutation. Guys, please don’t hide behind some dictionary or Einsteinian definition of “simultaneous.” It matters not a whit to the practical bottom line. If you think it does, don’t just wave your hands, show us your calculations.

    From the recent work of Summers et al. 2014 it’s possible that a third mutation in PfCRT may also be needed (perhaps already segregating in the population as a nearly neutral or marginally deleterious mutation) to allow the parasite to survive at therapeutic levels of chloroquine. That may contribute another factor of 1 in 103 to 104 or so to the probability, to reach an aggregate factor of approximately 1 in 1020. After that minimally functioning foundation is established, further mutations could rapidly be added individually and cumulatively — the way Darwinists like — to help balance the complex demands on PfCRT for its native activity plus chloroquine transporting, as Summers et al. discuss.

    If you folks think that direct, parsimonious, rather obvious route to 1 in 1020 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 1020, 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 >>
    ___________

    A reasonable enough challenge.

    KF

    PS: Mung’s seven sided dice (think, spindle dice) bring the point about the double out neatly, as there is a condition that if one die is 7 the total cannot be 7. That case may help clarify the point that nope it’s not just P(sum = 7|a = x) = 1/6, as with 6-sided dice. The two tosses are independent but there is a lock-out condition.

  96. 96
    kairosfocus says:

    Wd400, of course you did put up a strawman, or rather back a strawman play. The issue is NOT getting to 7 given die a already tossed, but tossing two dice whether simultaneously or in succession. And with the underlying malaria case, it’s either a double mut in a single cell, or a first mut sufficiently viable to be around for the 2nd mut to hit it, and not sufficiently superior to dominate the pop or sufficiently bad to be eliminated. But, if you struggle to see that tossing two dice is not the same as tossing a second die on condition of the value of a first, the problem is at basic level. P(A AND B) is not the same as P(B | A), as say the good Rev Bayes knew quite well. KF

  97. 97
    wd400 says:

    KF, as ever I’m left with no idea what point you think you are making.

    I said AB post showed one way that you can understand why the probability was 1/6th in the particular case. That’s all.

    The rest of your comment again shows why quierius was wrong to say simultaneous and sequential are equivalent in this case:

    either a double mut in a single cell, or a first mut sufficiently viable to be around for the 2nd mut to hit it, and not sufficiently superior to dominate the pop or sufficiently bad to be eliminated

  98. 98
    Acartia_bogart says:

    Mung: “What does it even mean to say that two events are cumulative?

    Sorry, but some people were obviously having a problem with the word sequential.

  99. 99
    Mung says:

    wd400:

    I said AB post showed one way that you can understand why the probability was 1/6th in the particular case. That’s all.

    You did say this, but that doesn’t mean it’s true.

    A die with six faces where each face contains a symbol representing the integers 1 through 6, and when the die is tossed each face is equally likely to appear (or not), no matter how many times it is tossed, no matter what probability is assigned to each face, cannot produce a SEVEN.

    The idea that there is a 1/6 chance of producing a SEVEN is simply ludicrous.

  100. 100
    Mung says:

    Mung:

    What does it even mean to say that two events are cumulative?

    Acartia_bogart:

    Sorry, but some people were obviously having a problem with the word sequential.

    You thought that by introducing more ambiguity you could produce clarity?

  101. 101
    kairosfocus says:

    WD400:

    Please note my reference to the Rev Bayes, which was a clue pointing to context of reasoning.

    The famous Bayes Theorem pivots on precisely how probability of A AND B as events composing a joint event is different from the probability of B given A is already existing. However, there is a conflation of the two in A-B’s remarks, which you have backed. Remarks that seem to be the basis for his contemptuous — and fallacious — dismissal of Behe’s reasoning, with the loaded term, voodoo. (And BTW, A_B, that has a racial context of implicit contempt to esp. Haitian Blacks that you should be aware of and avoid.)

    Bayes’ theorem pivots on the relationship:

    P(A|B) * P(B) = P(A AND B) . . . 1

    Which then leads to the similar expression

    P(B | A) * P(A) = P( B AND A) . . . 2

    From which, by commutation, we may deduce the Bayes theorem expression, in the form, which instantly translates into more familiar ones:

    P(A|B) * P(B) = P(B | A) * P(A)

    A necessary entailment of this, is that P (A|B) and P(A AND B) are quite definitively distinct.

    A-B’s attempts to conflate the two are patently fallacious.

    Two dice tossed whether one go or in rapid succession have 6/36 chances of summing to seven. Though numerically the same as odds for one face of a single die, 1/6, the meaning is different. That’s why Mung’s seven sided (spindle) dice help. There are 49 possibilities now, and the first die can lock out a sum to 7 by coming up at 7, forcing the second die toss to go beyond 7. This underscores that we are dealing with a joint situation. Meaning is important, not just numerical value.

    In the context of drug resistance, two muts are req’d, and in light of the situation, we deal with a population of 10^12 parasites in a victim with a mut rate that suggests 10^4 copies of possible single muts. So, just three patients are enough (cf the Behe letter) for resistance to pop up to a drug that can be worked around by a 1-point mut. Of course, if a mut that confers resistance also lowers general fitness enough, it will not work, as it will be unable to compete otherwise. There is a further context of implied high incidence of use of the relevant drug, so that there is an effective selection pressure.

    A double mut can be had all at once in one cell, or in close succession in a patient or population of patients. The first option is obviously very rare. The second and third imply a context in which the first mut does not radically redefine the parasite population, i.e. it remains rare, and is not eliminated (e.g. by being fatal to the parasite). So, in that context, close sucession is effectively simultaneous and it is reasonable to analyse on p(A AND B) in all three cases.

    A_B’s objection pivots on conflating that with P(B |A), which implies in effect mut A once it appears is quickly so dominant that the situation is diverse.

    This scenario is inconsistent with the reported observations on Chloroquine resistance.

    I add, the problem with involved exchanges in a polarised situation, is that it is likely for a chain of successive side tracks to emerge. The second order exchange on tossing two dice is a first example, and the attempt above to want to say that going into details on the implied pattern changes the situation is another.

    I suggest you read and respond to Behe, as clipped above, and that you address as well the distinction between the “intersection” probability P(A AND B) and the conditional one P(A GIVEN B is already in hand).

    Those will be first steps to addressing the actual matter in hand.

    KF

  102. 102
    kairosfocus says:

    ouch on italics

  103. 103
    wd400 says:

    You seem to be attacking your own misunderstanding of what I have said. I’ll repeat one more time:

    1. The method AB mentioned is a perfectly reasonable way of explaining why the specific result if 1/6th. That’s all I wanted to say.

    2. You can’t square the probability of getting one mutation in one generation to find the probability of getting two mutations eventually.

    It’s remarkable to me that anyone would spend any time arguing those propositions. I’m certainly not going to spend any more time defending the obvious.

  104. 104
    kairosfocus says:

    WD400, the probability of getting two dice to sum to 7, depends on the probabilistic behaviour of both. And, in a joint mutation situation as implied, the result can boil down to the probability of two effectively independent events of similar probability “simultaneously” — meaning without any significant population culling and shifting between that would materially change the pop patterns. In particular without eliminating A or moving A to massive over-representation. And in the end, any model brought up needs to account for the epidemiological evidence of extreme pop sizes and growth rates [10^12 parasites in ONE infected individual’s blood, mut rates 10^-8, perhaps ten origins of Chloroquine resistance over some decades, a contrasting drug where a one point mut would pop up resistance in jut three patients]. And playing at dismissal games only shows what is wrong. Just to begin, do you accept that P(A AND B) is distinct from P(B | A)? That is one root of error. Second, do you accept that two effectively independent events A and B will occur jointly with P(A AND B) = P(A) * P(B)? [If you do, then kindly tell us why you speak in terms of “squaring” when it is actually such a multiplication, under relevant circumstances that makes roughly independent events a reasonable “good enough for govt work” model? If you think P(A) significantly affects P(B) kindly explain how, consistent with the reported epidemiological facts or better warranted facts on Chloroquine resistance. KF

  105. 105
    Querius says:

    Nicely and patiently explained, Kairosfocus! A-B and wd400, please consult the following:
    http://www.mathsisfun.com/data.....ndent.html

    And notice when they state

    You can calculate the chances of two or more independent events by multiplying the chances.

    And that’s all that Behe did. His hypothesis was that two or more mutations were necessary. The following paper examines historical evidence that seems to prove Behe right:

    http://www.pnas.org/content/111/17/E1759

    Thus, the scientific method indicates that the science is settled until someone can come up with a scientifically plausible alternative explanation to the observed data. This has not been done.

    The objection regarding the mathematical difference between calculating simultaneous versus sequential events is not credible—there is no difference as even A-B now admits. And I’d hope that wd400 would be willing to admit that you multiply rather than square probabilities (thus, the probability of rolling a 6 on a 6-sided dice followed by a 6 on a 7-sided dice is 1/6 * 1/7). I’ll leave the answer as an exercice to wd400. 😉

    One can argue that one of the deleterious mutations can be passed to subsequent generations and might survive until a second one (or a third or fourth) appears that together confer chloroquine resistance, but a few generations of malaria is not significant when dealing with a period of ten years of malarial reproduction!

    Behe’s point in all this was to show where several (not one-by-one as Darwin proposed) changes were needed to confer an advantage, and that these multiple changes are extremely unlikely to produce an irreducibly complex structure.

    Mung,
    The reason that casinos pay out 4 to 1 for rolling a seven is that this is how they shave the payouts in their favor. They should be paying 6 to 1 if they were fair.

    And if casinos were seeing the kind of miraculous probabilities that Darwinists depend on, they’d quickly toss the person out as a cheater.

    http://nypost.com/2012/08/21/a.....-to-blame/

    -Q

  106. 106
    Mung says:

    kf:

    …then kindly tell us why you speak in terms of “squaring” when it is actually such a multiplication, under relevant circumstances that makes roughly independent events…

    You mean P(A) * P(B) is not equal to P(A)^2?

  107. 107
    Querius says:

    Apparently not, Mung. But I’m afraid you have a lot of arguing and abuse ahead of you! 😉

    -Q

  108. 108
    kairosfocus says:

    Mung (HT Q and attn WD400 and A_B):

    With 2 x 6-sided fair dice tossed, odds of A = 4, B = 3 [let’s suppose A red + B green) = 1/6 * 1/6 = 1/36

    This holds whether or no we hold both in the cup and toss “at once” or if we toss one then the other.

    Now suppose instead it is A and C, C being 7-sided.

    Odds (speaking loosely, strictly “probability, per Bernoulli-Laplace indifference principle”) of A = 4 and C = 3 are now 1/6 * 1/7.

    In neither case have we “squared” the odds of tossing A with value 4.

    Now, let us shift to, IF A = 4, then we toss C not B. We now have imposed a sequence with a conditionality. Event E2 is NOT independent of E1. P(E2 = 3 | E1 = 4) = 1/7, and P(E2 = 3 | E1 != 4) = 1/6. That is, we have a situation where E1 affects E2, and E2 is NOT independent of E1.

    We can make a second shift, tossing C first, and defining the sum of values as the outcome S; then, we toss A.

    Here, We can have a situation with A = 7 (odds 1/7) and on that happening P(S = 7 | C = 7) = 0, but P(S = 7 | C !=7) = 1/6 for each of the six diverse cases C = 1, 2 . . . 6.

    This toy situation will help us understand conditional probabilities and independent events. Also, how a step by step goal-directed procedure (an algorithm) may incorporate designed in randomness.

    That is, chance and design can appear in the same situation. And in fact games of chance in a House are carefully designed to cumulatively give profit to the house based on the theory of sampling a population. Here, in a situation where we have reasonably good probability models.

    Actuarial math, the math of insurers, deals first with uncertainty and tries to convert it into risk with statistical techniques designed to capture the patterns and properties of relevant populations. But as this implies assumptions on stability, there are always walk-away clauses. Here, in a suspiciously timed event, insurance companies repudiated their coverage just about two weeks before the fatal hos volcanic ash flows of June 25, 1997. It turns out that at just about the same time, the lead scientists at the Observatory communicated a letter of warning to the Civil Authorities; a letter that (leaked to a key activist) later featured in the Commission of Inquiry.

    I infer design, with 50-50 epistemic, subjective conditional probability that one of the scientists or someone in the Emergency Dept had a retainer to an insurance company.

    Those odds can be then re-weighted based on further info through Bayesian revision. And, weights may be acquired through expertise calibrated expert elicitation. (Which was introduced here AFTER June 25, 1997. Along with a lot of other things. Let’s just say, HM Governor at the time later testified to HoC that HMG was a year behind the curve of events and that had GBOP 10 mn been spent on building shelters etc in the North and SHV had not gone to full dome building and destructive Merapian Pyroclastic flow events, there could easily have been a different inquiry on the wasting of GBP 10 mn. In 1976 – 77, next door in Guadeloupe the W lobe was evacuated for about a year for an eruption that did not significantly go beyond phreatic explosions which have much less hazardous potential, with IIRC cost US$ 700 mn and a major public scientific quarrel on inter alia whether the island lobe would blow up and sweep the region with tidal waves from Venezuela to Miami or thereabouts; they had to have a big conference to settle the quarrel, which led to rescinding the evacuation, successfully. That possibility popped up again in our case, but the emphasis was now on the “consensus” of the scientists. Saved GBP 10 mn at first, but 14 lives by official count were found to be lost with contributory negligent responsibility of HMG and GoM. And, I can go on and on, the lessons of history are written in blood, sweat and tears.)

    KF

  109. 109
    kairosfocus says:

    F/N: As a test for the hyp utter ignorance in a Google era, let us do a search under the provided clue, Bayes, first five hits (filling my screen without scrolling) . . . all Wiki:

    Bayes’ Theorem

    Thomas Bayes [includes visible ref that he was a Presbyterian Minister]

    Bayesian Probability

    Bayesian

    Bayes [a disambig. page]

    In addition, RH column provides context and initial remarks.

    WD400’s remarks intending to dismiss my remarks as incomprehensible, a la MF’s tactic, falls apart on even basic due diligence.

    KF

  110. 110
    kairosfocus says:

    BTW, why is Wikipedia so dominant in Google rankings — and what does that point to given its own significant bias and misrepresentation problems? Mind you, in all fairness, on basic math, physics etc Wiki can be quite good enough. But once PC issues come up, watch out. KF

  111. 111
    kairosfocus says:

    F/N: Did a Bing, no 3 is SEP on Bayes Th, and 4 and 5 (screenful) are dictionaries. I clip SEP:

    Bayes’ Theorem is a simple mathematical formula used for calculating conditional probabilities. It figures prominently in subjectivist or Bayesian approaches to epistemology, statistics, and inductive logic. Subjectivists, who maintain that rational belief is governed by the laws of probability, lean heavily on conditional probabilities in their theories of evidence and their models of empirical learning. Bayes’ Theorem is central to these enterprises both because it simplifies the calculation of conditional probabilities and because it clarifies significant features of subjectivist position. Indeed, the Theorem’s central insight — that a hypothesis is confirmed by any body of data that its truth renders probable — is the cornerstone of all subjectivist methodology . . . .

    The probability of a hypothesis H conditional on a given body of data E is the ratio of the unconditional probability of the conjunction of the hypothesis with the data to the unconditional probability of the data alone.

    (1.1) Definition.
    The probability of H conditional on E is defined as PE(H) = P(H & E)/P(E), provided that both terms of this ratio exist and P(E) > 0.[1] . . . . Here are some straightforward consequences of (1.1):

    Probability. PE is a probability function.[2]
    Logical Consequence. If E entails H, then PE(H) = 1.
    Preservation of Certainties. If P(H) = 1, then PE(H) = 1.
    Mixing. P(H) = P(E)PE(H) + P(~E)P~E(H).[3]

    The most important fact about conditional probabilities is undoubtedly Bayes’ Theorem, whose significance was first appreciated by the British cleric Thomas Bayes in his posthumously published masterwork, “An Essay Toward Solving a Problem in the Doctrine of Chances” (Bayes 1764). Bayes’ Theorem relates the “direct” probability of a hypothesis conditional on a given body of data, PE(H), to the “inverse” probability of the data conditional on the hypothesis, PH(E).

    (1.2) Bayes’ Theorem.
    PE(H) = [P(H)/P(E)] PH(E)

    In an unfortunate, but now unavoidable, choice of terminology, statisticians refer to the inverse probability PH(E) as the “likelihood” of H on E. It expresses the degree to which the hypothesis predicts the data given the background information codified in the probability P . . . .

    Though a mathematical triviality, Bayes’ Theorem is of great value in calculating conditional probabilities because inverse probabilities are typically both easier to ascertain and less subjective than direct probabilities. People with different views about the unconditional probabilities of E and H often disagree about E’s value as an indicator of H. Even so, they can agree about the degree to which the hypothesis predicts the data if they know any of the following intersubjectively available facts: (a) E’s objective probability given H, (b) the frequency with which events like E will occur if H is true, or (c) the fact that H logically entails E. Scientists often design experiments so that likelihoods can be known in one of these “objective” ways. Bayes’ Theorem then ensures that any dispute about the significance of the experimental results can be traced to “subjective” disagreements about the unconditional probabilities of H and E.

    When both PH(E) and P~H(E) are known an experimenter need not even know E’s probability to determine a value for PE(H) using Bayes’ Theorem.

    (1.3) Bayes’ Theorem (2nd form).[4]
    PE(H) = P(H)PH(E) / [P(H)PH(E) + P(~H)P~H(E)]

    In this guise Bayes’ theorem is particularly useful for inferring causes from their effects since it is often fairly easy to discern the probability of an effect given the presence or absence of a putative cause. For instance, physicians often screen for diseases of known prevalence using diagnostic tests of recognized sensitivity and specificity. The sensitivity of a test, its “true positive” rate, is the fraction of times that patients with the disease test positive for it. The test’s specificity, its “true negative” rate, is the proportion of healthy patients who test negative. If we let H be the event of a given patient having the disease, and E be the event of her testing positive for it, then the test’s specificity and sensitivity are given by the likelihoods PH(E) and P~H(~E), respectively, and the “baseline” prevalence of the disease in the population is P(H). Given these inputs about the effects of the disease on the outcome of the test, one can use (1.3) to determine the probability of disease given a positive test.

    Good FYI. KF

  112. 112
    Querius says:

    [The sound of crickets chirping]

    KF, I guess A-B and wd400 musta had a talk with a math professor.

    Apparently, the supposed difference between “simultaneous” versus “sequential” probability calculations is not determined by the number of trials (past one) after all.

    Oh dear. 🙂

    -Q

  113. 113
    wd400 says:

    To be honest, I’m so dumbfounded by the inability of either of you to read what I wrote, and then the way you can actually agree with my point while pretending the difference can be ignored (“good enough for government work”, “insignificant” given the new criterion that the first mutation be strongly deleterious).So I give up.

    If you want to read Durret and Schmidt you can see they derive the expected waiting time for two mutations given a mutation rate, and indeed, it’s considerably shorter that one over the mutation rate squared.

    As for Behe’s claims. None of us know the actual rate at which resitance arises in P. falciparum. Estimating requires many paramaters (the rate of transmission between host->vector->host, the fitness of the first mutation within host, the rate of growth within host, the proportion of cells that are treated….) so it’s silly to claim (as behe has) teh 10^20 number is empirical observation.

    In any case, I’ll repeat what I said in the first post about the PNAS paper

    I never thought the idea that some traits require two mutations was the major claim Behe was making, but if it is then I’ll happily grant. It’s true in this case, and there are probably many other traits that couldn’t arise by single mutations each with a slight fitness increase

  114. 114
    Box says:

    WD400:

    “(…) so it’s silly to claim (as behe has) teh 10^20 number is empirical observation.”

    WD400, since you stubbornly refuse to read the article I linked to in post #59, I will quote from it here:

    Behe cites his source that spontaneous resistance to chloroquine occurs in one in every 10^20 malaria cells. It’s from a review article published in the prestigious Journal of Clinical Investigation entitled, “Antimalarial drug resistance” (Vol. 113(8) (April 2004)). The author, Nicholas J. White, holds two doctorates and is an esteemed researcher in his field. As White’s bio states:

    Professor White has contributed to over 500 peer reviewed scientific publications and has written over 30 book chapters. He is a full Professor at Mahidol University and also Oxford University. He is a member of several WHO advisory panels, and is on the International Editorial Advisory boards of several international journals including The Lancet and the Journal of Infectious Diseases.

    White’s article states precisely what Behe claims it does: “the per-parasite probability of developing resistance de novo is on the order of 1 in 10^20 parasite multiplications.” Suffice to say, this kind of author wouldn’t print such a statement in this type of article in this journal if it were a “mere guess.” Behe roughly outlines how White performs this calculation as follows:

    “Nicholas White of Mahidol University in Thailand points out that if you multiply the number of parasites in a person who is very ill with malaria times the number of people who get malaria per year times the number of years since the introduction of chloroquine, then you can estimate the odds of a parasite developing resistance to chloroquine is roughly one in a hundred billion billion. In shorthand scientific notation, that’s one in 10^20.” (Behe, Edge of Evolution, pg. 57.)

    To re-produce the calculation:

    Instances of chloroquine resistance in the past 50 years: Less than 10 (White, 2004). To be generous, we’ll say 10 per 50 years, or 1 instance of chloroquine resistance per 5 years.
    /
    Total malaria cells that exist each year: approximately 10^20 cells per year. (White, 2004; White & Pongtavornpinyo, 2003).
    ———————————————————————–
    = 1 instance of chloroquine resistance per 5 x 10^20 malaria cells, or roughly speaking, 1 instance of chloroquine resistance per 10^20 malaria cells

    Even science writing that has been simplified for public consumption in The New Criterion cannot fairly characterize the 1 in 10^20 statistic as “a mere guess.” It’s the result of real-world studies of malaria behavior in response to chloroquine and reproducible calculations, as reported in review articles by leaders in the field in one of the world’s top medical journals. It was anything but “a mere guess.”

  115. 115
    Querius says:

    wd400,

    Ironically, a friend of mine and I were discussing yesterday how in astrophysics, “close to within a couple of orders of magnitude,” is actually pretty good! This is true when dealing with very large and very small numbers. For example, the temperature of the core of the sun is given as 27 million degrees. When asked whether that’s in degrees Celcius or degrees Kelvin, the correct answer is, “It doesn’t matter.”

    1. The objection to Behe’s math was that he calculated the probability of multiple mutations on the assumption that the mutations were of necessity “simultaneous.” In fact, the binomial theorem doesn’t make a distinction between simultaneous and sequential events (as long as they are independent).

    2. Behe claimed only that the mutations needed to coexist in the same organism at the same time to confer immunity. The mutations themselves didn’t have to be “simultaneous.” The complications from adding a few generations when compared to trillions doesn’t make a significant difference. Whether each of the mutations has the same probability and whether immunity requires 2, 3, or 4 mutations does make a difference.

    3. Behe’s estimates were confirmed empirically by an independent group. The math was easy: the product of the probability of event A and the probability of event B is the probability of both occurring (squaring one of them works only when A and B are equal).

    You wrote:

    I never thought the idea that some traits require two mutations was the major claim Behe was making, but if it is then I’ll happily grant. It’s true in this case, and there are probably many other traits that couldn’t arise by single mutations each with a slight fitness increase

    Yes, the probabilities of multiple mutations resulting in a trait was indeed exactly what Behe was arguing, and you are happily granting him this point. The problem that Behe pointed out in The Edge of Evolution wasn’t that he doesn’t believe in microevolution (which he does believe in), but that traits arising from many multiple mutations are far too improbable (when multiplied out) to account for macroevolution within the time available. Behe was brave enough to make a prediction, and the later observations seem to support him.

    And that’s the point of the hysterical outcry against him. You might want to read his book sometime. It’s not as outrageous as some would lead you believe.

    -Q

  116. 116
    bornagain77 says:

    Purposeful Design at the Foundation of Life – Michael Behe, PhD – video
    https://www.youtube.com/watch?v=I7pRD73PAaE
    This is Michael Behe’s presentation at Christ’s Church of the Valley from Sunday, July 6, 2014.

  117. 117
    Querius says:

    [More crickets chirping]

    Well, I suppose if I had a desire to annoy and humiliate AB and wd400, I could simply bring in some more probability calculations to any controversy.

    Or even worse, I can just imagine it now . . .

    AB and wd400 are standing at the pearly gates, hoping for admittance. St. Peter finally comes and tells them, “Ok, I have just one question to ask you that will determine whether you go to heaven or hell. Here it is. If you roll three 6-sided dice, one after the other, what are the odds that you will roll at least one 5 spot? 😉

    -Q

  118. 118
    wd400 says:

    Querius,

    You were shown to be wrong and then just going on about being within a few orders of magnitude and repeated a bunch more wrong stuff (you’ve not even grasped what the “binomial theorem” is, or what the new paper presented, for instance). So why would anyone bother?

  119. 119
    bornagain77 says:

    wd400, I know that you pride yourself on understanding evolution and scoffing at us poor IDiots who don’t have a clue as to how evolution REALLY works. So, if I could beg your patience for poor ole ignorant me, could you please show us the empirical evidence of unguided processes creating a molecular machine that far outclasses anything man has ever made?

    Bacterial Flagellum – A Sheer Wonder Of Intelligent Design – video
    http://tl.cross.tv/61771

    Biologist Howard Berg at Harvard calls the Bacterial Flagellum

    “the most efficient machine in the universe.”

    Michael Behe on Falsifying Intelligent Design – video
    http://www.youtube.com/watch?v=N8jXXJN4o_A

    Orr maintains that the theory of intelligent design is not falsifiable. He’s wrong. To falsify design theory a scientist need only experimentally demonstrate that a bacterial flagellum, or any other comparably complex system, could arise by natural selection. If that happened I would conclude that neither flagella nor any system of similar or lesser complexity had to have been designed. In short, biochemical design would be neatly disproved.-
    Dr Behe in 1997

    Or wd400, if you are a bit short on empirical evidence, (which you are), could you at least show us the math as to how long we will have to wait for a flagellum to appear de novo? Perhaps a ballpark figure? A year? two years? 100 million years? 2 billion years? 20 billion years? 20 trillion years???? etc… Never???

    The numbers I’m getting don’t look good for you.

    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) –
    per ENV

    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.
    Per pathlights

    “So there we have it. The amount of time currently available for life to evolve is of the order of time N (billions of years), but according to Chaitin’s toy model, Darwinian evolution should take at least time N^2, or quintillions of years. That fact troubles Chaitin, and it should. But at least he has the honesty to admit there is a problem.”
    Dr. VJ Torley
    http://www.uncommondescent.com.....the-earth/

    A review of The Edge of Evolution: The Search for the Limits of Darwinism
    Excerpt: The numbers of Plasmodium and HIV in the last 50 years greatly exceeds the total number of mammals since their supposed evolutionary origin (several hundred million years ago), yet little has been achieved by evolution. This suggests that mammals could have “invented” little in their time frame. Behe: ‘Our experience with HIV gives good reason to think that Darwinism doesn’t do much—even with billions of years and all the cells in that world at its disposal’ (p. 155).
    http://creation.com/review-mic.....-evolution

    Don’t Mess With ID by Paul Giem (Durrett and Schmidt paper)- video
    https://www.youtube.com/watch?v=5JeYJ29-I7o

    Waiting Longer for Two Mutations – Michael J. Behe
    Excerpt: Citing malaria literature sources (White 2004) I had noted that the de novo appearance of chloroquine resistance in Plasmodium falciparum was an event of probability of 1 in 10^20. I then wrote that ‘for humans to achieve a mutation like this by chance, we would have to wait 100 million times 10 million years’ (1 quadrillion years)(Behe 2007) (because that is the extrapolated time that it would take to produce 10^20 humans). Durrett and Schmidt (2008, p. 1507) retort that my number ‘is 5 million times larger than the calculation we have just given’ using their model (which nonetheless “using their model” gives a prohibitively long waiting time of 216 million years). Their criticism compares apples to oranges. My figure of 10^20 is an empirical statistic from the literature; it is not, as their calculation is, a theoretical estimate from a population genetics model.
    http://www.discovery.org/a/9461

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

    “Phosphatase speeds up reactions vital for cell signalling by 10^21 times. Allows essential reactions to take place in a hundredth of a second; without it, it would take a trillion years!” Jonathan Sarfati
    http://www.pnas.org/content/100/10/5607.abstract

    William Lane Craig – If Human Evolution Did Occur It Was A Miracle – video
    http://www.youtube.com/watch?v=GUxm8dXLRpA

    Quote from preceding video – In Barrow and Tippler’s book The Anthropic Cosmological Principle, they list ten steps necessary in the course of human evolution, each of which, is so improbable that if left to happen by chance alone, the sun would have ceased to be a main sequence star and would have incinerated the earth. They estimate that the odds of the evolution (by chance) of the human genome is somewhere between 4 to the negative 180th power, to the 110,000th power, and 4 to the negative 360th power, to the 110,000th power. Therefore, if evolution did occur, it literally would have been a miracle and evidence for the existence of God.
    William Lane Craig

  120. 120
    bornagain77 says:

    footnote on bacterial flagellum from the Long-Term Evolution Experiment:

    Lenski’s Long-Term Evolution Experiment: 25 Years and Counting – Michael Behe – November 21, 2013
    Excerpt: Twenty-five years later the culture — a cumulative total of trillions of cells — has been going for an astounding 58,000 generations and counting. As the article points out, that’s equivalent to a million years in the lineage of a large animal such as humans.,,,
    ,,,its mutation rate has increased some 150-fold. As Lenski’s work showed, that’s due to a mutation (dubbed mutT) that degrades an enzyme that rids the cell of damaged guanine nucleotides, preventing their misincorporation into DNA. Loss of function of a second enzyme (MutY), which removes mispaired bases from DNA, also increases the mutation rate when it occurs by itself. However, when the two mutations, mutT and mutY, occur together, the mutation rate decreases by half of what it is in the presence of mutT alone — that is, it is 75-fold greater than the unmutated case.
    Lenski is an optimistic man, and always accentuates the positive. In the paper on mutT and mutY, the stress is on how the bacterium has improved with the second mutation. Heavily unemphasized is the ominous fact that one loss of function mutation is “improved” by another loss of function mutation — by degrading a second gene. Anyone who is interested in long-term evolution should see this as a baleful portent for any theory of evolution that relies exclusively on blind, undirected processes.
    ,,,for proponents of intelligent design the bottom line is that the great majority of even beneficial mutations have turned out to be due to the breaking, degrading, or minor tweaking of pre-existing genes or regulatory regions (Behe 2010). There have been no mutations or series of mutations identified that appear to be on their way to constructing elegant new molecular machinery of the kind that fills every cell. For example, the genes making the bacterial flagellum are consistently turned off by a beneficial mutation (apparently it saves cells energy used in constructing flagella). The suite of genes used to make the sugar ribose is the uniform target of a destructive mutation, which somehow helps the bacterium grow more quickly in the laboratory. Degrading a host of other genes leads to beneficial effects, too.,,, –
    http://www.evolutionnews.org/2.....79401.html

    also of note for your favored model of genetic drift wd400:

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

  121. 121
    Querius says:

    wd400,

    You were shown to be wrong and then just going on about being within a few orders of magnitude and repeated a bunch more wrong stuff (you’ve not even grasped what the “binomial theorem” is, or what the new paper presented, for instance). So why would anyone bother?

    Oh puleeze! Neither you nor anyone else showed anything of the sort! Just take a class in probability or get a math major to explain it to you. You have no credibility at all with anyone who’s taken even one math course dealing with probability. And now you proceed to demonstrate your profound ignorance of significant digits in measured values. For example, what’s Avogadro’s number + 1?

    But since you claim that you understand the binomial theorem, go ahead and try to answer my easy question about the three dice—and without help I should add.

    Here it is again: If you roll three 6-sided dice, one after the other, what are the odds that you will roll at least one 5 spot?

    -Q

  122. 122
    kairosfocus says:

    Box, I should thank you for your patience. Someone needs to appreciate it. All I will add is that if anyone does not realise that Behe was talking about multiple muts leading to drug resistance s/he did not read his original work with understanding, or even his recent letter. As I recall, his “edge” was about seven muts, and he spoke of the taxonomic category, the family, as a rough practical threshold. Malaria came in as a pivotal study, where because of reproduction rate, pop size and the long-term interaction with humans (spell that sickle-cell) we have some highly relevant dynamics. 10^20 reproduction events probably covers how many mammals have ever been born. So, blend in mut rate 10^-8 as a sort of generous upper estimate . . . and one is working to a few ords of mag here [an extension to Fermi’s approach of estimation by reasonable numbers, informed by epidemiology] . . . and we are looking at the patterns as already laid out. That is, a double mut model without elim or dominance of mut A leading to joint action of A and B to give resistance becomes reasonable. Once that happens in a context where Chloroquine is in widespread use, additional muts that reinforce the resistance then come in as hill climbing. The double mut challenge is to get to the shoreline of function. And recall, with the mut rates, pop size in ONE patient [10^12 . . . comparable to the number of HUMAN cells in the body, being what 1%, we have a large no of ordinary gut bacteria too], and having the double in hand, increments become very plausible. At this stage, I doubt there will be an explicit admission that P(A AND B) is distinct from P(B | A), that this distinction is relevant to the odds of two dice summing to 7, and that onwards it speaks to the double mut challenge. I will say, that the incident is quite revealing of what we are up against. Sadly revealing. KF

  123. 123
    kairosfocus says:

    PS: BTW, taking mosquito bites as samples/searches, we are also looking at the dynamics of needles in haystacks. If 100 bites is a ml, 1,000 bites is 10 ml out of what a blood volume of 4 – 5 l, say. 10^12 parasites is 250 * 10^6 per ml for 4 l. at 10^4 copies of each possible mut in the 10^12, that is 2.5 per ml, or it takes coming on 100 bites to pass on any given mut if in proportion . . . and here I am applying the random sampling principle that boils down to there must be a sufficient sample size to make capture of a rare item likely enough — which also holds for random walks. Thee are feasible numbers for a serious epidemic. It also points out that keeping the mosquitoes out of biting range is likely to be effective. When one goes instead to very large spaces that are sampled by proportionately tiny searches, then finding needles in the haystack becomes a serious challenge. For FSCO/I on the gamut of our solar system that is like a straw sized single sample to a cubical haystack 1,000 LY across, comparable to the thickness of our galaxy’s central bulge. The implications on the implausibility of capturing something that is naturally rate int eh space of possible configs then jumps out. At least, if you are not challenged to grasp the implications of samples and populations with rare items in them. We already saw the issue of islands of function where the challenge is to get to shorelines of function. But then, there are two distinct types of difficulty with understanding, primary ignorance and interference from a conflicting conceptual system that if held on to with a death grip frustrates understanding.

  124. 124
    kairosfocus says:

    Q: Let’s spot them a hint, it is often helpful to think in terms of P(x) = 1 – P(NOT-x). KF

  125. 125
    bornagain77 says:

    A challenger finally steps into the ring with Dr. Behe (and promptly leaves the ring mumbling incoherently)

    Laurence Moran’s Sandwalk Evolves Chloroquine Resistance – Michael Behe August 13, 2014
    Excerpt: First, a bit of background. As I discussed previously (see here, here, and here) in a new paper Summers et al. show that a minimum of two mutations to the malarial protein PfCRT are needed to confer an ability to pump the antibiotic chloroquine (which is necessary but may not be sufficient for chloroquine resistance in the wild).

    That result agrees with my discussion in The Edge of Evolution and goes a long way toward quantitatively explaining the rarity of the development of resistance. Over at PZ Myers’s blog Pharyngula, he and Kenneth Miller disagreed strongly with me in words, but cited no numbers. I then invited them, since they don’t like mine, to show us their calculations for how frequently chloroquine resistance should arise in the malarial parasite.

    The bad news is that so far neither has responded. The good news is that Laurence Moran, Professor of Biochemistry at the University of Toronto, has done so. Professor Moran is an intelligent, informed, direct, and relatively civil critic of intelligent design who maintains a popular blog, Sandwalk, on evolution-related matters. So his response gives us a great opportunity to see what the best alternative explanations might be.

    Moran begins his own calculation by assuming that the first required mutation is strictly neutral and spreads in the growing population before the second one arises. His straightforward computation leads him to conclude that “What this means is that if you start with an infection by a cell that has none of the required mutations then you will only get the right pair of mutations once in one million infected people.”

    Once in one million infected people…. Since there are a trillion malarial cells in one sick person, then according to Moran’s own calculation there are a million times a trillion malaria cells needed for resistance to arise, which in scientific notation is 10^18. On a log scale that’s a stone’s throw from Nicholas White’s estimate of 10^20 cells per origin of resistance that I have been citing, literally an astronomically large number (there are only a paltry hundred billion, 10^11, stars in our galaxy). So let me just say thank you and welcome aboard to Professor Moran. Unfortunately, he seems not to have realized the import of his calculation at the time, and has shown no enthusiasm for exploring it much after it was brought to his attention by a commenter.

    Right after his calculation Moran writes “We know that the right pair of mutations … is not sufficient to confer resistance to chloroquine so the actual frequency of chloroquine resistance is far less.” Far less? Far less than 1 in 10^18? Now, it’s true that at least four mutations have been found in all known resistant strains of malaria. And it’s true that, although Summers et al. showed two mutations are necessary for pumping chloroquine at a low level, they might not be sufficient for chloroquine resistance in the wild. Nonetheless, a need for further mutations would only make the problem for Darwinism much worse. It wouldn’t make it better. Let me emphasize: Professor Moran’s own reasoning would make the problem much more severe than I myself have ever argued. Yet he doesn’t take any time on his blog to explore the ramifications of his own reckoning. Why doesn’t he think that’s an interesting result? Why not ponder it a bit?

    Moran doesn’t seem to actually have much confidence in his own numbers. He asks the readers of his blog to help him correct his calculations — which is a commendable attitude but makes one wonder, if he’s so unsure of the likelihood of helpful combinations of mutations, whence his trust in mutation/selection? In response to the commenter who alerted him to the huge number of parasites in a million people he writes, “This is why meeting the Behe challenge is so difficult. There are too many variables and too many unknowns. You can’t calculate the probability because real evolution is much more complicated than Behe imagines.” But, again, if he thinks everything is so darn complicated and incalculable, on what basis does he suppose he’s right?

    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.

    Another commenter at Sandwalk didn’t like Moran’s calculation, so came up with his own. Great! The more the merrier! He also assumed the first mutation to be neutral, but kept a more careful accounting of its accumulation through the generations and ended up with a result of one necessary double-mutation per 420 patients. That actually strikes me as a more realistic value for a neutral mutation than Professor Moran’s. Now, at first blush 420 may seem much smaller than Moran’s number of a million patients, but that’s only because we haven’t yet considered the factor of a trillion parasites per patient. When we multiply by 10^12 to get the total number of parasites per double mutation, the commenter’s odds turn out to be 1 in 10^14.6 versus Moran’s 1 in 10^18, again not all that far on a log scale. Either or both of these values can easily be reconciled to White’s calculation of 1 in 10^20 by tweaking selection coefficients or by inferring that a further mutation is needed for effective chloroquine resistance in the wild, as Professor Moran noted.

    What if the first necessary mutation isn’t neutral? What if — as seems very likely from the failure of malaria cells with one required mutation (K76T) to thrive in the lab — the first mutation is rather deleterious? The commenter estimated that, too (and also added another consideration, a selection coefficient), and came up with a value of one new double mutant per 818,500 patients. Let’s relax the admirable precision a bit and round the number up to a million. That’s the same count Professor Moran got in his (supposedly neutral) calculation, which we saw means there is one new origin per 10^18 malarial parasites — not far at all on a log scale from White’s number that I cited.

    The bottom line is that numbers can be tweaked and a few different scenarios can be floated, but there’s no escaping the horrendous improbability of developing chloroquine resistance in particular, or of getting two required mutations for any biological feature in general, most especially if intermediate mutations are disadvantageous. If a (selectable) step has to be skipped, the wind goes out of Darwin’s sails.
    http://www.evolutionnews.org/2.....88811.html

  126. 126
    wd400 says:

    The idea that you must be right, and I can’t do highschool mats problems is…. strange. Read Durret and Schmidt, who explain one of Behe’s calculations was out by a factor of > 1000 and try again.

    As per the probelm. This is made much easier as we are really calculating the probability of there being no ‘5’s and that’s (5/6)^3

    The general solution for getting more than any k occurrences is


    1 – [Sum(i=0, k) nCi p^i(1-p)^(n-1)]

    Which you’ll see agrees here.

  127. 127
    wd400 says:

    As per the probelm. This is made much easier as we are really calculating the probability of there being no ’5?s and that’s (5/6)^3

    Of course the probability of one or more 5s is therefore 1-(5/6)^3.

    BTW, discussion of the malaria case would be much more precise if you used the expected waiting time for two mutations or specified the time period (number of trials) across which the probability was calculated.

  128. 128
    Mung says:

    Q:

    If you roll three 6-sided dice, one after the other, what are the odds that you will roll at least one 5 spot?

    What if I roll one six-sided die three times simultaneously?

  129. 129
    Querius says:

    kairosfocus and bornagain77—great posts! Also, note that whether one of the required mutations is indeed strictly neutral might be testable because that would make a significant difference in Behe’s calculation. If that were the case, then the apparent experimental results that seem to bear out his calculated estimates would need to be attributed to some other mechanism.

    wd400—yes, there’s only about a 42% chance of rolling at least one 5–spot in 3 rolls. And that’s the same binomial math that Behe and others use to estimate the probability of malaria overcoming a drug, antibiotic resistance, and the time it would take for a multi-step evolutionary advantage to emerge.

    10^20 is such a large number that being off by 1000 doesn’t make that much difference. Ok, so it’s 10^17. With hundreds of trillions of these protozoans reproducing wildly, we can estimate the rate of micro-evolution. For humans with a relatively tiny population of single-digit billions and a pathetic reproduction rate, micro-evolution will be many millions of times slower.

    And that’s what Behe is pointing out as a problem with the current macro-evolution model. If evolution is true, then a different mechanism—don’t ask me what—must be responsible.

    -Q

  130. 130
    Mung says:

    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.

    – M. Behe

  131. 131
    Querius says:

    Mung,

    Try each method a hundred times. You’ll find that it makes no statistically significant difference.

    Hmmm, what do you know. Our resident biologist and statistican seems to have vanished. 😉

    -Q

  132. 132
    wd400 says:

    You should maybe read the paper, Querius.

    Behe’s error was ~1e4 fold for an estimate that was ~1e7.

    Finally, it’s obviously true there is some ‘edge’ to evolution, and that ultra-specific mutational pathways that involve neutral or deleterious intermediates will rarely get fixed by selection in small populations.

    The thing IDers need to prove is that such pathways have been, or are required to be, traversed by such population lineages.

  133. 133
    Querius says:

    wd400,

    Yes, and after going to a bunch of scientific blog sites critical of Behe’s 2007 estimate, I found that they all gave different reasons or estimates for their objections. Hmmm.

    It seemed reasonable to me that calculating the expected prevalence to CQR involves a lot of complicating factors, major and minor, possibly offsetting. So, it seemed to me that relying on statistical data would be a more direct way of estimating CQR resistance rates, since hundreds of millions of individuals are suffering from around a trillion parasites each.

    While I found a lot of fascinating publications, the one that stuck out the most was this on, published in 2010 titled “Prospective strategies to delay the evolution of anti-malarial drug resistance: weighing the uncertainty.”

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

    Tell me what you think of it.

    -Q

  134. 134
    Querius says:

    Oh, and I don’t think it’s up to ID advocates to try to prove anything. In my opinion, ID is a paradigm, not a theory.

    However, amassing evidence for and against the theory of evolution, might very well lead to concluding that the mechanism of mutation is not adequate to explain macro-evolution (i.e. TOE is over the edge), and might spur a hunt for another, heretofore hidden, mechanism.

    -Q

Leave a Reply