Friday, August 22, 2014

Understanding Michael Behe

Michael Behe has tried to explain where I'm going wrong and why evolution is highly improbable [Guide of the Perplexed: A Quick Reprise of The Edge of Evolution]. He lists a number of bullet points that are supposed to explain his argument. Let's look at each one ...
  • If the development of some particular adaptive biochemical feature requires more than one specific mutation to an organism's genome, and if the intermediate mutations are deleterious (and to a lesser extent even if they are neutral), then the probability of the multiple mutations randomly arising in a population and co-existing in a single individual so as to confer the adaptation will be many orders of magnitude less than for cases in which a single mutation is required.
This is correct. The probability of any single mutation occurring is equal to the mutation rare, which is about 10-10. The probability of an additional specific mutation occurring is also 10-10. The combined probability of any two specific mutations occurring is 10-20.
  • The decreased probability means either that a much larger population size of organisms would be required on average to produce the multiple mutations in the same amount of time as needed for a single mutation, or that for the same population size a multiple-mutation feature would be expected to require many more generations to appear than a single mutation one.
This is correct. It refers to the probability of the specific double mutation occurring and not to whether it becomes fixed in the population.
  • In The Edge of Evolution I cited the development of chloroquine resistance in the malaria parasite Plasmodium falciparum as a very likely real-life example of this phenomenon. The recent paper by Summers et al. confirms that two specific mutations are required to confer upon the protein PfCRT the ability to pump chloroquine, which is necessary but may not be sufficient for resistance in the wild.
This is a little bit misleading and possibly a little bit disingenuous. Everyone understood that chloroquine resistance was rare and that it almost certainly required multiple mutations. Behe developed an explanation based on the idea that two mutations were required and one of them, by itself, had to be very deleterious. This is because he used an incorrect value for the mutation rate that was several orders of magnitude too low. He based his calculations on the assumption that the two mutations had to arise in a single infected patient.

The recent paper by Summers et al. (2014) shows that seven of the chloroquine resistant strains that have been observed have at least four mutations and some of them are relatively neutral. This refutes and discredits the scenario that Michael Behe put forth in his book.

The reason why Behe's statement is disingenuous is because he uses the word "confirms" and because his sycophants are promoting the idea that Behe made "predictions" that have recently been confirmed [A Pretty Sharp Edge: Reflecting on Michael Behe's Vindication] [So, Michael Behe Was Right After All; What Will the Critics Say Now?].
  • The best estimate of the per-parasite occurrence of de novo resistance is Nicholas White's value of 1 in 1020. This number is surely made up of several components, including: 1) the probability of the two required mutations identified by Summers et al. coexisting in a single pfcrt gene; 2) the value of the selection coefficient (which can be thought of as the likelihood that the de novo mutant will successfully reproduce in a person treated by chloroquine and be transmitted to another person); and 3) the probability of any possible further PfCRT mutation needed to confer chloroquine resistance in the wild coexisting in the same gene with the other mutations.
As we all know by now, the "guesstimate" by Nicholas White refers to the possible frequency that a chloroquine resistant strain will be detected someplace in the world. This is a far cry from the probability that the correct mutations will actually occur. Behe's entire argument is based on the idea that 10-20 is the probability that two specific mutations will occur.
  • The known point mutation rate of P. falciparum, combined with the apparent deleterious effect of the required mutations occurring singly, suggests that component 1 from the previous bullet point will account for the lion's share of White's estimate, probably at least a factor of 1 in 1015-1016 of it. The other factors would then account for 1 in 104-105. These values are somewhat flexible, accommodating the uncertainty in our knowledge of the exact values in the wild. In other words, a decrease in our best estimate of the value of one factor can be conceptually offset relatively easily without affecting the argument by supposing another factor is larger, to arrive at 1 in 1020.
As I explained in a previous post, the actual mutation rate in P. falciparum is 2.5 × 10-9. Thus, the probability of two specific mutations is 6.25 × 10-18 [Taking the Behe challenge!] [Flunking the Behe challenge! ]. Typical eukaryotic mutation rates are closer to 10-20. The probability of the two mutations occurring is getting close to Nicholas White's estimate of the frequency of the chloroquine resistant strain being detected.

But, according to Michael Behe, there's a 10,000 (104) fold difference between the probability of the mutations occurring and their actual frequency. This is important because he attributes that difference to the fact that both of the two mutations are deleterious on their own. In other words, whichever mutation occurs first, that individual is likely to be eliminated by natural selection before the second mutation can occur. (Actually, he only says that one of the mutations has to be deleterious but that's a mistake.)
  • Any particular adaptive biochemical feature requiring the same mutational complexity as that needed for chloroquine resistance in malaria is forbiddingly unlikely to have arisen by Darwinian processes and fixed in the population of any class of large animals (such as, say, mammals), because of the much lower population sizes and longer generation times compared to that of malaria. (By "the same mutational complexity" I mean requiring 2-3 point mutations where at least one step consists of intermediates that are deleterious, plus a modest selection coefficient of, say, 1 in 103 to 1 in 104. Those factors will get you in the neighborhood of 1 in 1020.)
Summer et al. (2014) showed conclusively that this calculation is wrong. They showed that among the seven strains analyzed there were multiple pathways to resistance and that a minimum of four mutations were required for effective resistance. The showed that one mutation (K76T) was essential in all strains. All strains had one of two additional mutations that seemed to be required early on, N75E or N326D.

There were at least four paths to resistance ....
WT → K76T → K76T + N75E
WT → K76T → K76T + N326D
WT → N75E → N75E + K76T
WT → N326D → N326D + K76T
The presumed evolutionary path to most of the resistant strains did NOT involve any intermediates that were less fit than the wild type. Strains carrying single mutations were detected in the wild.

Recall that Behe's calculation of the mutation rate is too low by a factor of at least 100 in spite of the fact that he references the accepted mutation rate. The recent data by Summer et al. refutes three of Behe's assumptions: (a) that only two mutations are required to account for the appearance of resistant strains, (b) that a resistant parasite had to arise from wild type within a single infected individual, and (c) that one or more of the individual mutations are deleterious on their own.

Other than that, his calculations and his "predictions" are perfect!!!!
  • Any adaptive biological feature requiring a mutational pathway of twice that complexity (that is, 4-6 mutations with the intermediate steps being deleterious) is unlikely to have arisen by Darwinian processes during the history of life on Earth.
It is true that any specific set of 4-6 mutations is extremely unlikely. Nobody disputes that any more than they dispute the probability of a specific hand of bridge being dealt in the next deal. That's only going to happen once in 1028 tries. It's impossible that you will see it in your lifetime. But you still get to play bridge.

The flaw in Behe's argument is that he assumes that the tape of life will always play the same movie. In other words, every organism we see today must be the product of an extraordinary set of mutations and fixations that had to play out just the way they did. For example, let's say that the difference in needle clusters between red pine and white pine are determined by a single gene. Let's say that three specific mutations are required to change from a cluster of two needles to a cluster of five needles. One hundred million years ago you could calculate that the probability of three specific mutations is about 10-30. It's highly improbable, just like the specific bridge hand.

When such a triple mutation arises we recognize that it was only one of millions and millions of possible evolutionary outcomes. There was no a priori requirement that Earth contain red pines and white pines just as there's no a priori requirement that you get a specific hand in the next deal.

This is hard for IDiots to understand since they begin with the assumption that humans are the designed outcome of the history of life on Earth and they assume that evolutionary theory has to explain why the tape of life will always play out in the same manner every time.

They can't conceive of an alternative history that didn't have Homo sapiens or white pine trees. If they are right, then Behe's argument makes sense. Evolution can't do that. But all the evidence we have indicates that they are wrong, and Gould is right1. Behe's argument makes no sense in the light of evidence of evolution.

There is an edge of evolution and it rules out design in favor of accident and contingency.


I call this experiment "replaying life's tape." You press the rewind button and, making sure you thoroughly erase everything that actually happened, go back to any time and place the past—say, to the seas of the Burgess Shale. Then let the tape run again and see if the repetition looks at all like the original. If each replay strongly resembles life's actual pathway, then we must conclude that what really happened pretty much had to occur. But suppose that the experimental versions all yield sensible results strikingly different from the actual history of life? What could we then say about the predictability of self-conscious intelligence? or of mammals? or of vertebrates? or of life on land? or simply multicellular persistence for 600 million years?
Stephen Jay Gould, "Wonderful Life" pp48-50

Summers, R. L., Dave, A., Dolstra, T. J., Bellanca, S., Marchetti, R. V., Nash, M. N., Richards, S. N., Goh, V., Schenk, R. L., Stein, W. D., Kirk, K., Sanchez, C. P., Lanzer, M. and Martin, R. (2014) Diverse mutational pathways converge on saturable chloroquine transport via the malaria parasite’s chloroquine resistance transporter. Proceedings of the National Academy of Sciences. [doi: 10.1073/pnas.1322965111]

187 comments :

  1. The lesson to be learned here is that scientific theories are not scientifically tested by repeating experiments and such, theories are now judged by a publicity contest where the most important thing is how well a researcher uses strawmen and religious stereotypes to deceive the general public.

    This is a link to theory that has to be ignored

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    1. Larry describes experimental results; asshole says "scientific theories are not scientifically tested by repeating experiments and such." WTF is up with that.

      What's the point of doing experiments and explaining the results to IDiots in baby-talk if they're just going to say no experiment was done.

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    2. What can't be ignored is that evolutionary efforts could not produce the sexual mating process to create a progeny, rather it took intelligence to create and the ability to create a he and a she to function together wherein one bears the offspring with anatomically placed organs to do so. This follows on to the inability of "scientists," although highly imaginative, to prove how life began here. Nor disprove how man's intelligence functions separately - not being seen, measured, or weighed - each controls what he/she thinks.

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    3. tobewan: "What can't be ignored is that evolutionary efforts could not produce the sexual mating process to create a progeny"

      "Evolutionary efforts"? What the hell does that mean? Apparently IDiot is saying, "No intelligent being has ever created male and female; therefore, an intelligent being created male and female."

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    4. tobewan: "it took intelligence to create and the ability to create a he and a she to function together wherein one bears the offspring with anatomically placed organs to do so."

      I see, an intelligent being must have done it, because intelligent beings never could do it. Yes. This whole "male and female parts fit together" is quite popular with Ray Comfort droolers.

      Now let me understand this. You're saying that it's a prediction of intelligent design that male and female parts fit together. Right? So, since it's a prediction, if there were, say, a species where male and female parts don't fit together, that would falsify Intelligent Design. Am I right?

      Anybody here like to take a flying guess at some species where male and female parts don't fit together? Name one, you falsify intelligent design once and for all. Care to take a guess which one I'm thinking of?

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    5. tobewan, you are mistaken in thinking that sex requires a 'he' and a 'she'. Sex is a cellular transaction, simply involving the fusion of two genomes and their ultimate reduction back to haploidy. That one is larger and one smaller, and are produced by different somas with complementary arrangements of parts, in many species, is but one of many possible modes. Ancestral sex was almost certainly isogamous, and unicellular. To get from that state to any modern one requires no leap of faith.

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    6. In fact, some ciliates do this without two separate genomes. The cell undergoes a duplication of its chromosomes, and the undergoes meiosis, all without meeting another cell.

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    7. Larry writes:

      This is hard for IDiots to understand since they begin with the assumption that humans are the designed outcome of the history of life on Earth and they assume that evolutionary theory has to explain why the tape of life will always play out in the same manner every time.

      Those IDists who believe in the One, True God (not all IDists are theists; some, in fact, are atheists---what about that fact Larry?), do, in fact, believe that Life is "designed."

      However!!! this does NOT preclude the possibility that the Creator (to use Darwin's term) did, in fact, use Darwinian mechanisms to bring about the diversity of life---one simply has to point to Ken Miller. (And, certainly, the vast majority of IDists accept what is termed "microevolution," and, hence, that 'some level of diversity' is certainly due to Darwinian mechanisms.)

      So, Larry, your claim is simply not correct.

      Let me, however, point this out. If you do NOT believe that Life is "designed," then, ipso facto, you're obliged to believe that non-random (Darwinian) processes were involved. So you see, Larry, as you point your finger at IDists, you have four fingers pointing back at you, to use a wearying modern turn of phrase (but, which, nonetheless, is very true).

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  2. It's also worth considering what the mutation rate in a given organism is when under intense selective pressure and how much that adaptive response mutation rate with stress induced mutagenesis might differ from more typically measured values.

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  3. Whimple, you better watch your use of word like "stress induced mutagenesis" because from what I learned belief in such things makes you a science denying creotard IDiot who needs to go get an education.

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    1. Actually, there is some evidence that stress induced mutagenesis, or more precisely relaxed DNA replication proofreading happens in some prokaryotes. So whimple brings up a plausible point.

      It's when you vomit nonsensical, indefensible blather like

      "The lesson to be learned here is that scientific theories are not scientifically tested by repeating experiments and such, theories are now judged by a publicity contest where the most important thing is how well a researcher uses strawmen and religious stereotypes to deceive the general public."

      that you might attract some ridicule.

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    2. Chris B, so are you are you saying that when whimple brings up "stress induced mutagenesis" it's a plausible point but where I bring up "stress induced mutagenesis" I "vomit nonsensical, indefensible blather" even though I did not say anything at all about it yet?

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    3. You did not bring up stress induced mutagenesis. Whimple did. You were mocked for your other gobbledygook comment #1.

      Everybody knows about Cairnsian mutation, aka "Fred." Increasing the ERROR RATE is something your Designer would never do if randomness destroys "information."

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    4. Diogenes, the theory you are trashing explains why "Increasing the ERROR RATE is" NECESSARY.

      You once again proved to be a scientifically dysfunctional hypocrite.

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    5. Intelligent Design says that random mutations destroy "information" (of a kind they won't define and can't compute), but they all say random mutations decrease it.

      So why would the omniscient Designer build in a system to greatly accelerate RANDOM mutations and thus intentionally decrease "information" (of the kind IDiots won't define and can't compute)?

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    6. Gary, you didn't bring up stress induced mutagenesis, and then not say anything about it yet....whatever that means.

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    7. The term comes from the scientific literature, is perhaps best characterized in E. coli and is essentially a molecular panic button that can be pressed to compromise the fidelity of DNA replication more or less globally. It has nothing to do with "directed" or "designed" mutations. I simply point out that the 10^-10 mutation rate being discussed has the potential to be a functionally smaller value, which if anything removes some of the logical justification of Behe's argument.

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    8. D: "So why would the omniscient Designer build in a system to greatly accelerate RANDOM mutations "

      Probably for the same reason that he created dinosaur bones and buried them.

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    9. The "stress" is caused by "confidence" being zero. The specific memory location(s) a given stress acts upon are sometimes generalized using the phrase "mutation hotspots".

      From theory:

      A behavior qualifies as intelligent behavior by meeting all four circuit requirements for this ability, which are: [1] body (or modeling platform) with motor muscles (proteins, electric speaker, electronic “write” to a screen) to control, [2] memory addressed by sensory sensors where each motor action and its associated confidence value are separate data elements, [3] confidence (central hedonic, homeostasis) system that increments (stored in memory) confidence value of a successful motor action else decrements the confidence value, [4] guess new memory action when associated confidence level sufficiently decreases (and if not prerandomized motor data then when first addressed). For flagella powered cells reversing motor direction can produce a tumble to a new heading direction, guess where to go.

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    10. Gary,

      That uh, material is not a theory. I even explained to you what a theory is. It's an attempt to define "intelligence" broadly enough to be non-falsifiable and include all biology. Also, it has nothing to do with increasing the rate of random errors.

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    11. Diogenes, your science stopping opinion of what a theory is or isn't is just another pompous cop-out.

      You do NOT have a computer model for (technology willing) any (intelligent or not) behavior and obligatory Theory of Operation that explains how it works, for modeling the behavior of matter on up.

      You are NOT the judge of what is intelligent or not. Nor or you even experienced enough in any field that might make it possible for you to systematically qualify "intelligence" using a working model of your own like the ID Lab.

      The Theory of Intelligent Design operationally defines "intelligence" according to the basic systematics found in basic cognitive science. Please spare us your generalization filled operational definitions you got from a dictionary or WikiPedia that are useless for this level of scientific work.




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    12. The "ID lab". ROTFLMAO! Didn't that only exist on a blue screen?

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    13. Gary: "You do NOT have a computer model ..."

      Since when was a computer model necessary for a theory? What computer model did Copernicus have? Or Galileo? Or Newton? Or Einstein? Or Oppenheimer? Or Darwin? The list is endless.

      Computer models are simply a tool. The output of these "models" must be tested against observations and experiments to mean anything. Could you provide us with a list of peer reviewed papers that have tested your "models" or are the the intellectual equivalent of PacMan and Donkey Kong (but with poorer graphics)?

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    14. Acartia Tonsa: Since when was a computer model necessary for a theory?

      It's standard practice:

      WikiPedia - Theory of operation

      A theory of operation is a description of how a device or system should work. It is often included in documentation, especially maintenance/service documentation, or a user manual. It aids troubleshooting by providing the troubleshooter with a mental model of how the system is supposed to work. The troubleshooter can then more easily identify discrepancies, to aid diagnosis of problem.

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    15. It's totally irrelevant. How typical of you. The Wikipedia article doesn't even mention computer models, and it isn't about scientific theories. Gary, are you human? I've seen some bots behave in this weird way.

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    16. Piotr Gąsiorowski: The Wikipedia article doesn't even mention computer models,

      I will bold the word for you:

      A theory of operation is a description of how a device or system should work.

      See the illustration at this link showing the system that can be computer modeled or put on a circuit board for a robot platform or made out of cells or molecules or whatever!

      A SYSTEM

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    17. OK, I can see you are a badly programmed robot.

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    18. Piotr, you think Gary was intelligently designed? You could be right evolution could never produce anything that dysfunctional.

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  4. Michael Behe has repeatedly said that he doesn't really care how you explain the 1 in 10^20 probability, that however you work things out the "bottom line is that ... there's no escaping the horrendous improbability of developing chloroquine resistance". His understanding is garbled in many ways that you have been explaining, but it seems to me that even before you get into the population genetics, his statement that development of chloroquine resistance is 'an event of probability 1 in 10^20', the basis of his argument, is nonsensical.

    I've thought up a little analogy to explain:

    1. Michael Behe has cited that chlorquine resistance appears about once per decade, and that during this time 10^20 malaria cells grow (something like 10^12 cells per person times 10^8 people). Taking these numbers at face value I would accept the following statement: Over the time that 10^20 malaria cells come into existence, there is one "development" (mutation + fixation) of chlorquine resistance.
    2. Michae Behe incorrectly reinterprets this statement to say that "the acquisition of chloroquine resistance is an event of statistical probability 1 in 10^20". He is interpreting evolution as a random sampling over 10^20 independent trials (one trial per individual), one of which succeeds.

    This is sort of like observing that over the course of human history Australia has been 'discovered' by humans once, and concluding that "the discovery of Australia is an event of statistical probability 1 in 10^11" (the number of people that have ever existed). Similarities between these arguments include:
    * The cells that grow after the double mutant first appears are counted, just as all the people living today are counted
    * The development of resistance is a per-cell probability, just as discovering Australia is a per-person probability
    * Each individual has an independent probability of success (as opposed to building on previous accomplishments)
    * In reality, the random walk that people actually took to get to Australia is vaguely like the random mutational walk of malaria

    Michael Behe then tries to justify the 10^20 number by arguing it can be derived by multiplying the 2 single mutations probabilities and the fixation probability on a *per individual* basis (indeed this would make sense if each individual represented an independent random trial), and extrapolates from this that any 4-point mutation, in any protein in any organism anytime, appears once per 10^40 organisms, more than the number of organisms that ever existed. Similarly, the probability of discovery of both Australia *and* Antarctica must be 1 in 10^22!

    So my challenge to Michael Behe is this: My estimate of 10^11 comes from assuming an exponential human population growth since 50,000 BC. If you think my route to the 10^11 isn't reasonable, go ahead, calculate it a different way. However you compute it, remember the bottom line is that the discovery of Australia is an extremely improbable event. It's so improbable that the naturalist explanation for the discovery of the continents cannot be true, as the number of human beings required to discover even two continents is far more than have ever existed.

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  5. The flaw in Behe's argument is that he assumes that the tape of life will always play the same movie. In other words, every organism we see today must be the product of an extraordinary set of mutations and fixations that had to play out just the way they did. For example, let's say that the difference in needle clusters between red pine and white pine are determined by a single gene. Let's say that three specific mutations are required to change from a cluster of two needles to a cluster of five needles. One hundred million years ago you could calculate that the probability of three specific mutations is about 10-30. It's highly improbable, just like the specific bridge hand.

    .....

    This is hard for IDiots to understand since they begin with the assumption that humans are the designed outcome of the history of life on Earth and they assume that evolutionary theory has to explain why the tape of life will always play out in the same manner every time.

    They can't conceive of an alternative history that didn't have Homo sapiens or white pine trees. If they are right, then Behe's argument makes sense. Evolution can't do that. But all the evidence we have indicates that they are wrong, and Gould is right1. Behe's argument makes no sense in the light of evidence of evolution.


    That's the key point.

    They are in effect shooting themselves in the foot with such arguments, as they undermine human inevitability, but are too blind and ignorant of evolution to understand it. Just as it's Darwin they are trying so hard to debunk (even though what Darwin said is pretty much irrelevant to 21st century biology), they still see the process as a progression with humans as its pinnacle, and its inevitable result.

    But that's what happens when you spend decades cherry picking from the literature instead of actually reading and understanding the whole of it

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  6. Typo Alert: 0.0625 x 10^-20 = 6.25 x 10^-22, not 10^-18. And I think you are being much too kind to Behe to say that he is a "maybe a bit disingenuous." He flagrantly deep-sixed the word "simultaneous" when he started crowing about how he was right that two mutations were required. IIRC, biologists reviewing Edge of Evolution conceded his point that two simultaneous mutations might be beyond natural selection's reach, but pointed out that it doesn't matter because that's not how evolution works. And the new results on malaria have confirmed Behe's critics, not Behe's "prediction."

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    1. Ted Lawry says,

      Typo Alert: 0.0625 x 10^-20 = 6.25 x 10^-22, not 10^-18.M

      Thanks. I fixed my arithmetic errors.

      And I think you are being much too kind to Behe to say that he is a "maybe a bit disingenuous."

      Don't mistake sarcasm for kindness. :-)

      However, I do tend to cut Behe a lot of slack because he's really trying to find genuine defenses of Intelligent Design Creationism and most of his misconceptions are actually misconceptions as opposed to lies. The reason we're still debating irreducible complexity and the edge of evolution is because there's some truth to the biochemistry he describes. It's not that easy to show where he goes wrong.

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    2. Larry said,
      "and most of his misconceptions are actually misconceptions as opposed to lies...."
      But the error of assuming what happened was inevitable has been brought up for several years and IDers continue to ignore it. Behe to his credit has followed with the obvious counter-argument - that the number of possible other-outcomes is rather small. He brought this up in regards to a result from the Thornton lab but again made the same mistake of extrapolating to generalities from a specific example and ignoring the same principle of contingency at a different level

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  7. Hi Larry,

    Just wanted to express my appreciation and gratitude to you for continuing the debate. It's helping me get a better understanding of the issues involved.

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    1. Thanks. Writing these posts also helps me to understand the issues.

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  8. It is difficult to understand how well educated men & women can argue over minute things & mutational chances to the 10th, 20th, & 30th power, when all that is necessary to look up from their powerful microscopes and see what has been given us to enjoy - men and women - who, in order to propagate our human race, must mate and do as we were told, "multiply and fill the earth." When will we cease to squabble about these tiny microscopic items and appreciate together all that we've been given, and the giver.

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    1. I think the human race has done enough propagating for now. It's all getting a little out of hand.

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    2. ""multiply and fill the earth." "

      I guess god never studied ecology.

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    3. Acartia TonsaSaturday, August 23, 2014 11:00:00 AM
      ""multiply and fill the earth." "

      I guess god never studied ecology.


      I have said this many times - the single most important reason why religion has to be completely eradicated ASAP, and this should have happened a long time ago, is that if it does not happen, the species is basically doomed. And it's because of the attitude codified in those words - it is not the real root cause of the problem, but it provides a convenient justification for it.

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    4. Georgi wrote:

      "I have said this many times - the single most important reason why religion has to be completely eradicated ASAP, and this should have happened a long time ago, is that if it does not happen, the species is basically doomed. And it's because of the attitude codified in those words - it is not the real root cause of the problem, but it provides a convenient justification for it."

      According to many estimates, the Earth is able to sustain 20 billion people... How could ecological issues in the world today be related to religion...?

      Maybe this is the real issue...?

      "The world has enough for everyone's need, but not enough for everyone's greed.”― Mahatma Gandhi

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    5. Whose estimates?

      The long-term sustainable level according to people I trust a lot more is at most a billion or two, and that's without really taking into account the depletion of non-renewable resources. If you take that into account, it is significantly less.

      The fact is that we are deeply into overshoot at present at 7 billion, and we are on at this point almost unavoidable path to global civilization collapse, with the corresponding consequences for the long-term future of the species (it is a very useful exercise to revisit the Fermi paradox in the light of what's going on this planet right now).

      You can sustain 20 billion living subsistence-farming lifestyle for some time, but that's a highly unstable arrangement in the long term.

      First, subsistence-farming lifestyles are in general unsustainable - look at what the very poor, low-per-capita-footprint people of Haiti did to their environment.

      Second, you need high levels of education to develop and sustain the ecological literacy needed to prevent entering overshoot. Higher levels than what is achieved in the highly developed industrialized countries of the world today, as evidenced by the fact that so few people pass through their educational systems understanding these issues. Of course, we have a problem with how dysfunctional the education system is, but the fact remains that you have to have a good grasp of a great many fields to properly understand the relationship between humans and their environment and how the way you should overcome you innate biological urges if you don't want your inclusive fitness to go to zero a few generations down the line.

      Which reminds of the deep irony here - an absolute prerequisite for achieving sustainability is a full and proper understanding of evolution and how the behavior of humans (and all other species) is shaped by the process. But it tends to be the same people who are deeply resistant to the idea that there is a sustainability crisis and that evolution even happened, as you just demonstrated...

      Which beautfully makes my point

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    6. I forgot to list that: you need relatively high levels of living standards in order to achieve those levels of education and understanding I was talking about. That means you need to spend your childhood and youth reading books and thinking about them. If you are forced to work the fields instead, that simply does not happen.

      Which, BTW, is one of the deep sources of the problem - historically the only people who had the leisure time to engage in high culture were people who did not have to work the land. So our high culture ended up, being dominated by the concerns of people disconnected from the land, which can be argued to be a significant contributing factor to why our culture is so divorced from ecological reality. Practically none of the great works of art and philosophy deals with these issues, and the worldview expressed in them is completely disconnected from them. And by having subsequent generations study those works, we indoctrinate them in that worldview, and thus the problem propagates itself...

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    7. Did I miss your point or you didn't elaborate on the religion-ecology issue...?

      Can you be specific...?

      Thanks,

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    8. Classic creationist move - ignore everything that was said and then demand more...

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    9. Georgi,

      I'm not a creationist...

      "You can sustain 20 billion living subsistence-farming lifestyle for some time, but that's a highly unstable arrangement in the long term"

      I guess the long-term unsustainability of 20 billion people on Earth is religion's fault; or even better-creationists....

      BTW: Why did you preform classic atheistic move - ignore everything that was said on the origins of life...? I guess you have a lot of faith...?

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  9. Behe's a coward for posting at ENV which permits no comments, and for not showing up here to argue "face to face" so to speak; probably the Discovery Institute doesn't permit him to.

    But I wanted to update you all on the output of my simulations of evolution of chloroquine resistance, which are much more elaborate than they were last time I reported results. On Behe's theoretical value of 10^20 (many IDiots here keep insisting that 10^20 is an empirical number, like somebody checked 10^20 parasites under the microscope, instead of stupidly multiplying two big numbers, the larger of which is irrelevant to evolution), I commented before that this must be off by many orders of magnitude because the effective population size of Plasmodium cannot be a trillion per patient as Behe assumes. Most of the trillion parasites in a patient will be killed by drugs or die with the patient and not pass on their genes; thus, each time the infection passes via mosquito from one patient to the next, the population passes through a severe bottleneck of about 10-30 parasites per patient, with all other alleles being lost. Behe wants to apply the case for Plasmodium to that of mammals by scaling down population size etc., but complex animals have approximately constant population sizes at least compared to the extreme changes in the population size of Plasmodium. At the start of each round of infection, only 10-30 parasites go into the next patient's liver to start the infection so only 20-60 alleles maximum get passed on to the next replication. Since Behe is using a factor of a trillion per patient, his figure of 10^20 parasites needed to evolve chloroquine resistance could in principle be too high by about 10^10 (10^12 / 10^2).

    Next, there's the question of the number of replications per patient. If a patient started with 1 parasite and that scaled up to 1.1 trillion, it would take 40 replications; but this is not relevant to the evolution of transmitted alleles, because most of the gametocytes that go into the mosquito to start the next round of infection, come from the generation of parasites that leave the liver before they start infecting erythrocytes. That population, which I'll call "early infectors", has size 100,000 to 300,000, and if the patient started with 10 to 30, the parasites went through 14 or 15 replications in the liver before most of the gametocytes were produced. These reduces the number of replications.

    In the previous simulation I reported, I simulated a single sick patient with the parasite replication 40 times. In my later simulations I have tried to simulation multiple rounds of infection in sequential patients with the infection passing from one patient to the next. To make a long story short, I simulate starting a patient off with 16 parasites (I like factors of two) and then after 14 replications in the liver, the population I call "early infectors" has size= 262,144; I assume this population produces all the gametocytes passed into the mosquito and thus into the next patient. So far I've ignored the sexual recombination of Plasmodium in the mosquito.

    To infect the next "patient", I copy from the previous "patient" the fractions of each single mutant and the double mutant (relative to all parasites) from the previous patient's "early infector" generation (replication 14, after leaving the liver, size= 262,144), but in the next patient I whack the population size of parasites down to 16.

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    1. Recall that the equations I reported before iterate up the fractions of each kind of single mutant and double mutants (not integer counts), and to get the actual counts of each kind of mutant I multiply its fraction of the parasite population times the parasite population size in that iteration (which doubles for each replication, but gets whacked down to 16 at the start of the next patient.) The previous equations I reported were recursive, giving the fraction for replication #k in terms of the fractions at replication #k-1. I recently solved thsee recursive equations to get closed-form equations and I will post the closed-form equations below. You can plug them into Matlab or something (yeah I'm sure you will.)

      So anyway, the infections passes from patient to patient, and the number of patients is (approximately) the number of replications / 14 (it's approximate because patient #1 starts with 1 parasite.) Thus I iterate up. I want a count of all parasites that were evolving to compare with Behe's 10^20 figure.

      But what's our terminating condition-- how do we decide when the double mutants are "established"? Obviously, the occurrence of one double mutant out of hundreds of thousands late in an infection is not likely to be established; it will most of the time get killed by drugs or die with the patient. So how many double mutants do I need before I declare them "established" in the population? Conceptually this was very difficult for me because again, my equations are in terms of fractions of all parasites, not integer counts. To get a count of parasites I did the following.

      I focused on the "zeroth generation" of parasites, population size 16, which come straight from the mosquito to start the infection of the next patient., As I wrote above, Behe's figure of a trillion parasites per patient is unrealistic because most of them will be killed by drugs or die with the patient and not pass on their alleles. If you want to somehow get a lesson that you can apply to the evolution of complex animals (by scaling down population sizes), then since complex animals have approximately constant population sizes, you should focus on the minimum population size in a round of infection, which would be 16.

      Then my termination condition is phrased as: given a fixed population of patients on chloroquine at the start of a new round of infections (which I set at 6 million patients, see below), after how many rounds of infection will at least 50 patients receive at least one double mutant in the "zeroth generation" of parasites straight from the mosquito? (I'll justify the figures of 6 million and 50 below.) Obviously if the double mutant is present in a patient's initial infection straight from the mosquito, there is a higher chance of it becoming established in his body. Moreover, if 50 patients get at least one double mutant from the mosquito bite in round of infection #i, then (let's say) definitely 50+ patients will get a double mutant in round of infection #i+1, and more than that in round of infection #+2, etc. and thus the double mutant population is sure to be established.

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    2. I fixed the number of patients in each round of infection at 6 million because Wikipedia says the number of malaria patients per year is 220 million; I estimate the time from the start of one round of infection to the start of the next at a month, because the parasite spends two weeks in the liver; I guess that 1/3 of all malaria patients get chloroquine; thus 220 million / (12*3) = ~ 6 million.

      I require that there be at least 50 patients with one double mutant in their "straight from the mosquito" generation because in population genetics, there's a general rule (for constant population size) that a mutation with selection coefficient s typically must occur independently 1/2s times before it starts to become fixed in the population. A common selection coefficient s is about 1%, and 1/2(0.01) = ~ 50, so 50 dispersed double mutants in the "zeroth generation" should guarantee that the double mutation will get established.

      OK so I computed this for three conditions relating to the single mutants. I define:

      sa = selection coefficient for single mutant a;
      sb = selection coefficient for single mutant b;
      sd = selection coefficient for double mutant ab, which I typically set to 0.01;

      1. Both single mutants neutral: sa = sb = 0.

      2. One single mutant neutral, one single mutant lethal, sa = 0, sb = -1. I call this "pseudo-malaria" because Summers et al. proved experimentally that Behe was wrong: chloroquine resistance does not really have to go through any lethal single mutants.

      3. Both single mutants lethal, sa = sb = -1. I call this "Sad Pterosaur" because creationist are fond of saying intermediates are all impossible in principle and imagining intermediates would die; in Duane Gish's book Dinosaurs by Design there's a drawing of a sad "evolutionary" pterosaur which looks like it will die because its wings are in-between a leg and a wing, and has the function of both-- er, sorry I meant neither.

      So here are the results:

      1. Both single mutants neutral: sa = sb = 0. Terminating condition reached after 120 rounds of infection (10 years if one round of infection takes a month) and 1685 replications. Total number of parasites 5.3 x 10^15. Note that for the number of parasites per patient, I used the figure of 262,144 for the "early infectors" straight from the liver, and multiplied it by two, to capture the earlier generations before the 262,144. (So that's a half million per patient, not a trillion.)


      2. One single mutants neutral, one lethal: sa 0, and sb = -1. Terminating condition reached after 125 rounds of infection (~10 years) and 1685 replications. Total number of parasites 5.5 x 10^15.

      3. "Sad pterosaur", an unrealistic model for malaria; both single mutants lethal. I won't report numbers for the double lethal condition because last time I did, sneaky Behe cherry-picked that number and described it falsely to his readers, saying that I'd derived that for malaria! If Behe is going to lie to his readers about what I computed, then I'm not going to tell him what I computed. Trust me, the numbers are not bad.

      In real malaria, unlike my simulations, one single mutation is lethal and one is "deleterious" so it is somewhere between my double neutral and single lethal values. Let's split the difference and say 5.4 * 10^15.

      Thus Behe's figure of 10^20 is off by a factor of 20,000. I'm sure he'll say that 10^15 is "within a stone's throw" of 10^20. Of course Behe squared his number of 10^20 and made it 10^40 without reason, so if we compare those, we must square our figure of 5.4 *10^15 as well. Thus Behe is wrong by a factor of 400,000,000.

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    3. Hi Diogenes,

      I have been trying to understand your calculations, and I have a couple of questions about some of the numbers and results that you discussed in your comments here and in the previous threads.

      1) In the introduction, you said that the typical malaria infection starts with 10 to 30 parasites that invade the liver and start a cycle of 14 to 15 replications before they burst into the bloodstream. Could you please cite a source that discusses this aspect of the Plasmodium life cycle? I'm especially interested in the number of parasites that are transmitted by a mosquito from one patient to another.

      2) The following point is a bit vague to me, could you please elaborate on it? Is this because the infection cannot pass from one patient to the next before the parasites leave the liver (after 14 replications) and start invading erythrocytes in the bloodstream?

      So anyway, the infections passes from patient to patient, and the number of patients is (approximately) the number of replications / 14 (it's approximate because patient #1 starts with 1 parasite.)

      3) How did you derive the total number of parasites in each of the 3 different scenarios that you tested?

      4) At one point in your comment, you say:

      I call this "pseudo-malaria" because Summers et al. proved experimentally that Behe was wrong: chloroquine resistance does not really have to go through any lethal single mutants.

      But then at the end you say:

      In real malaria, unlike my simulations, one single mutation is lethal and one is "deleterious" so it is somewhere between my double neutral and single lethal values.

      I may have missed something, but it sounds to me that the first statement contradicts the second. Could you please elaborate on what you meant by these 2 statements?

      Thanks.

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    4. Just as I thought.

      No response to a direct challenge of Diogenes' smoke and mirrors.

      Tick, tock, tick, tock...........

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    5. Steve, you have never once contributed a single scientific point to any thread on this forum, and moreover, you have attempted to derail threads with endless obnoxious ad hominems and trollish provocation. As usual, anti-evolutionists have no arguments, no calculations, no experiments, just ad hominem insults and quote mines.

      However, it is beyond the beyond when you start referring to my calculations as "smoke and mirrors" and attack my integrity (without evidnce) because I do not reply within X hours. It's August and I'm supposed to be on vacation camping, and the last campsite I was in had poor wi-fi. Now I've stopped back at the house for a few hours to refuel, and I don't have much time to deal with trolls. But so that we're clear, I'm on vacation till Sunday and that's that.

      No doubt Steve is so pathetically desperate to find an "evidence substitute" for his anti-evolution that he'll point to my lack of response for 3-4 days as proof that Intelligent Design is true.

      Those scientists go on vacation! That proves evolutionary theory is doomed. Doomed!

      As for Steve's "smoke and mirrors" crack, you'll be delighted to learn I'm copying some more calculations below-- which Steve will be unable to refute. Skip to the insults, Steve.

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    6. ShadiZ1 asks,

      But then at the end you say:

      "In real malaria, unlike my simulations, one single mutation is lethal and one is "deleterious" so it is somewhere between my double neutral and single lethal values."

      I may have missed something, but it sounds to me that the first statement contradicts the second. Could you please elaborate on what you meant by these 2 statements?


      You're right, good catch, that's a typo. I should have written:

      In real malaria, unlike my simulations, one single mutation is neutral and one is "deleterious" so it is somewhere between my double neutral and single lethal values.

      I have used sd = +0.01 for the double mutant (d), but I haven't done calculations yet with variable values of sa and sb for the single mutants (a,b). Thus I'm treating the neutral/deleterious case as in between neutral/neutral and neutral/lethal and bracketing. The brackets are fairly narrow.

      You ask a couple questions about the malaria lifecycle. I haven't read Nicholas White's articles (cited by Behe) but commenter Steven Lavalle did, so I'm basing my model on his summary, as follows:

      "I would like to mention something about that 10^20 number that shows up in Edge of Evolution. I was puzzled how Dr. Nicholas White could know that number, so I went back and read his articles. He was actually trying to figure out where resistance arises in the population and whether or not it might be worthwhile to concentrate efforts at some aspect of that population. In the model for the infection, about 10 to 30 sporozoites enter the blood stream and enter the liver, where they go through about 15 rounds of replication and emerge as a population 100,000 to 300,000 and begin that 48-hour cycle. " [Steven Lavalle comments, Aug. 11, 2014]

      In my models I've the population of parasites is always powers of 2, so I've set the population of sporozoites that enter the liver straight from the mosquito at 16 = 2^4. Then I have them go through 14 rounds of replication, so 16*2^14 = 2^18 = 262,144 when they exit the liver and enter the erythrocytes. (For patient #1, I start him with 1 parasite so here he would get 18 rounds of replication, but patients #2,3,4 etc. start with 16 sporozoites and get 14 replications.) About 22 more replications brings the population up to 1.1 trillion, but I have ignored then next 22 replications in that patient, for reasons explained below.

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    7. In response to ShadiZ1. Continuing with LaValle's comment:

      The population becomes detectable when they reach about 10^8 and the patient is considered well enough when it falls below 10^8 again. It is not possible to support 10^14 parasites but 10^13 can be supported.
      What Dr. White did is estimate the number of clinical cases in a given time frame [Diogenes notes: apparently 50 years, 1947-1997] and multiply by the higher number, 10^13 - this is the 10^20 figure. Since fewer than 10 cases of resistance had showed up in that period, he reckoned the population size required to allow one resistant strain to emerge at 10^19 parasites.

      So, where where these 10^19 parasites? It turns out that they would probably be in a child under the age of five who was being treated by chloroquine (there is some in nearly every person in some countries). Given the reasoning above, it would also be in a child who had been infected and suffered recrudescence of the infection. That means, as Diogenes pointed out, that you are not calculating the likelihood of a double mutation, but a double mutation in a population of human hosts who actually survived the first attack - and that is a group of people where the death toll from Malaria is the highest.

      The gametocytes, for the most part, come from that first population to emerge from the liver and not the later population. Those later parasites, the bulk of them, are either killed by the treatment or die with the patient.
      [Steven Lavalle comments, Aug. 11, 2014]

      This answers the question you asked:

      The following point is a bit vague to me, could you please elaborate on it? Is this because the infection cannot pass from one patient to the next before the parasites leave the liver (after 14 replications) and start invading erythrocytes in the bloodstream?

      [Me]: "So anyway, the infections passes from patient to patient, and the number of patients is (approximately) the number of replications / 14 (it's approximate because patient #1 starts with 1 parasite.)"


      So to answer your question, as LaValle says, "The gametocytes, for the most part, come from that first population to emerge from the liver and not the later population" so to "infect" the next patient, I take a "sample" of the parasite population when it leaves the liver (sample from a total population of 262,144) and not when the patient dies with 1.1 trillion parasites. Taking a "sample" means the following: recall that my equations describe the fractions of each single mutant and the double mutant, not total counts; I get the total counts by multiplying the fractions resulting from my equations times the current parasite population size -- so to put a "sample" from patient #i into patient #i+1, I just copy over the fractions of single & double mutants from patient #i after he's had 14 replications (that is, when his population goes from 16 to 262,144) and use those fractions to start the next patient; but patient #i+1 starts with a population of 16.

      This means in practice that I just let my fraction equations iterate up as though nothing happened, but I manually whack the population size from 262,144 back down to 16 to start the next round of infection. Thus the number of rounds of infection is (approximately) = number of replications /14. There's no need to mess with the fractional equations, just let them iterate up.

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    8. ShadiZ1 asks: "How did you derive the total number of parasites in each of the 3 different scenarios that you tested?"

      As I explained above, first I define "zeroth generation" as the first generation from the mosquito into patient #i, that, parasite population = 16. Then I fix the number of patients on chloroquine in each round of infection at 6 million (= 220 million patients / year * (1 year/12 months) * (1/3 [? guessing?] of all patients are on chloroquine.) Then I ask, among the six million new infections, in their "zeroth generation" of parasites, how many replications will it take before there are 50 independent double mutants?

      If fdk = fraction of double mutant (d) at replication k,

      Then the total count of double mutants will be, when "zeroth generation" parasite population is 16 per patient,

      Total # of double mutants in zeroth generation =
      (6,000,000 patients) *(16 parasites / patient) * fdk >= 50

      Or

      1/ fdk <= (6,000,000 patients) *(16 parasites / patient) / 50

      For which k (replication) will this be true? Call this k'. It is typically in the low thousands.

      Then the number of rounds of infection is approximately k' / 14 (technically, (k'-4)/14).

      To get how many parasites total: first ask, how many parasites were involved in each patient before it produces alleles (gametocytes) that go into the next generation? Short answer: 262,144 *2 (including all the ancestors of the parasites that leave the liver.)

      Thus the total number of parasites that contribute to evolution is

      (6,000,000 patients)* (262,144*2 parasites / patient) * (k'-4) / 14

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    9. I'm on vacation, wife wants me to cook breakfast. I'll have to copy in my recursive and closed-form equations later. For now, you can check out the recursive form of my equations from my previous comment. Just plug them into Microsoft Excel and iterate them up. (Note that these early versions do not allow variable values of selection coefficients sa, sb for the single mutants. I'll copy in more complete closed-form equations later. Have to cook now as the wife is giving me the eye.)

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  10. I don't really understand what the alternative to evolution is supposed to be in this case. If it is intelligent design, that would have to mean that there is an unknown, powerful intelligence out there that is sufficiently hostile to us humans to be motivated to help malaria along by giving it resistance to our medicine. (And, it could be added, it is at the same time powerful enough to do genetic engineering to harm us indirectly but not powerful enough to do anything more damaging.)

    Now apart from the fact that there is no evidence for the existence of such an intelligence, is that really what these guys want to argue for?

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    1. Yes, I've read it this way too before, but I think he's really saying that this is the best evolution can do unaided. He is essentially arguing that only large populations can evolve 'useful double mutants' in the time available; small populations need husbandry. There are, of course, fixation, selection, recombination and the multi-dimensionality of the entire genome to consider. I don't think this 2-locus model is adequate for the task being set it.

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    2. Behe's entire case is based on the (correct) idea that chloroquine resistance can arise by completely natural processes involving mutation, selection, and population genetics.

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    3. Of course, but when you extrapolate to the evolvability of small eukaryote populations, you can't just ignore the contribution to probabilities of the other genes, and the actual mechanistic environment.

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    4. Allan Miller said:

      I think the human race has done enough propagating for now. It's all getting a little out of hand.

      Indeed. That's one of the the things that should be the duty of an intelligent designer to take care of. Must be dead by now, like Behe, IIRC, once suggested. Everything points to nature going it's own way with no regard for designers.

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    5. @Allan Miller

      I was responding to Alex SL, not to you. I didn't see the comment you submitted six minutes earlier.

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    6. Okay, then I definitely missed something. I thought that Behe was saying that evolution can't produce something like chloroquine resistance to promote ID.

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    7. No, Behe is saying that evolution did (and regularly does) produce chloroquine resistance, but could not produce anything of similar complexity (whatever he meant by that) in a much smaller population, e.g. the average multicellular eukaryote, nor could it produce anything of much greater complexity even in the largest populations.

      So god isn't on the hook for chloroquine resistance. He is however responsible for Plasmodium in the first place, and thus has some 'splainin' to do. So far he has not appeared to 'splain, and none of his friends have managed to do it for him. What we know is that god is a really good guy and therefore malaria must be all for the best in this best of all possible worlds. Clear now?

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    8. Here's another way in which Behe may see it:

      Everything in 'God's creation' was perfect until the 'Fall'. After the 'Fall' the designer-creator-yhwh-jesus-holy-ghost (aka 'God') inflicted diseases/parasites and lots of other bad stuff on all living things as deserved punishment. Malaria is an example of that bad stuff. But, since 'God' is a merciful, benevolent, forgiving guy, he allows some drugs to cure malaria in some people. However, 'God' also causes resistance to drugs in some people because punishment in general is deserved by all living things and specific punishments are especially deserved by certain people. It's all part of 'God's plan' and that plan should never be questioned. 'Praise the Lord'.

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    9. maleria, a danger marker that says "warning: better not hang around here. Stick and move. Get and go. Just sayin'...creation was a pisser for me to get off the ground. Please have a listen. A little coop will go a long way, so kindly piss off when you see that big, fat mosquito marker I put out there, wouldya? Please????"

      ....but why should humans listen to 'those puny gods'.....f@#k that, I'm going in anyway and I'll do what I please, thank you!!!

      ...atheism in a nutshell.

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    10. A little coop will go a long way, so kindly piss off when you see that big, fat mosquito marker I put out there, wouldya? Please????"

      ....but why should humans listen to 'those puny gods'.....f@#k that, I'm going in anyway and I'll do what I please, thank you!!!

      ...atheism in a nutshell.


      Near as I can tell from this, your "scientific" theory is that God is telling humans not to go places where there are fatal diseases, which is everywhere. (Curious, why didn't you include natural disasters? Do they have weather where you live? Lightning? Why are you still there?)

      And then something about Africans being atheists? As far as I know, the vast majority of Africans are Christian or Muslim.

      So that's your big scientific comment, eh? Enlightening.

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  11. You go far away on vacation. What are the chances you will see your friend Kelly Ann from fourth grade? Very small. But what are the chances you will see someone you know? Still very small, but far higher than of seeing Kelly Ann. And what are the chances that someone there on vacation will see someone they know? Still very small but far higher still.

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  12. I wonder if anyone can point me to some reading on current knowledge about replaying the tape. Presumably we expect land creatures to evolve but what kinds and pathways are possible? How long should it take? How about flying creatures? I would guess flight has evolved independently several times: birds, bats, and butterflies. What does this tell us about replaying the tape? How do replaying-the-tape ideas combine with new discoveries about exoplanets to say something, anything, about the possibilities for alien life?

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    1. The key question is whether eukaryotes (or something equivalent) evolve or not. If you notice, no prokaryote has ever made much progress beyond the single-cell level of organization, and one idea for why this is so is that the evolutionary pathways available to them are limited by the great strength of purifying selection in those lineages. The evolution of eukaryotes is what made complexification possible.

      However, the evolution of eukaryotes seems to have been a unique, one-off event. If it hadn't happened, life on Earth would most likely still be prokaryotic and single-celled. The origin of multicellular organisms might well be an inevitable consequences of the appearance of eukaryotes, as evidenced by the fact that it has happened so many times in so many different lineages. If I was a creationist, it would not be the Cambrian I would focus on, it would be the origin of eukaryotes. However, this is not such a sexy topic, as first, ordinary people need fossils of macroscopic creatures to relate to a topic, single-celled organisms don't do it for them, and second, it is highly unlikely that they creationists have any real understanding of the very deep phylogeny of life.

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    2. Extinction events are probably the closest we will get at replaying the tape on a large scale. However, I could envision numerous bacterial experiments to test the concept. And I would be very surprised if many have not already been conducted.

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  13. Excellent post, Larry. The best one on this issue.
    Creationists and theistic evolutionists commit the same fallacy when they claim that the universe is fine-tuned for life. They cannot imagine how all the highly improbable parameters ended up just right in order to enable life.

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    1. I agree, an excellent and clear explanation even for a layperson like myself. That Behe, who is an expert in this field, does not seem able to follow Larry's argument raises two possibilities: Behe is an incompetent who has nonetheless somehow managed to obtain a highly coveted tenured position in his academic field. Or Behe is a highly dishonest con man.

      And even beyond all the detailed refutation of Behe's statistics, there remains a basic fundamental question that he refuses to even acknowledge: His claim is that chloroquine resistance has resulted as the result of magical intervention by some supernatural being such as the god of Catholicism. What evidence does he have for this?

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  14. Hi Larry,

    Hi re-read your post, and a few points come to mind:

    (1) To be honest, I don't understand all the math. It sounds as if you're saying that Behe's calculations are wrong, but that 1 in 10^20 is about right, so I'm a bit puzzled.

    (2) You wrote: "The presumed evolutionary path to most of the resistant strains did NOT involve any intermediates that were less fit than the wild type. Strains carrying single mutations were detected in the wild."

    Were each of the three mutations found individually in the wild?

    (3) The second major point in your post -- that just as there are all sorts of winning bridge hands so there are all sorts of evolutionary pathways -- seems to have been covered in the second part of Behe's post here: How Many Ways Are There to Win at Sandwalk?

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    1. To #3, Bilbo: Behe just repeats there the same error Larry has already addressed. He is working on the assumption that a particular set of mutations that lead to chloroquine resistance is the only winning hand in the "game" of evolution. But there is a large nnumber of other winning hands that have occurred, even in the single organism P. falciparum. So his analogy has no bearing on biological reality.

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  15. Hi Lutesuite,

    You've either misunderstood or misrepresented Behe's argument. He wrote:
    I agree with this, too. Happily, the tacit hypothesis -- that very many possible-but-unrealized complex biochemical systems could have been made by random mutation/selection -- can actually be tested, but only to a degree. To the extent it can't be tested, it is unfalsifiable. To the extent that it can be tested, in my view, it has already been falsified.

    Now you do make a claim that if true would falsify Behe's claim: But there is a large number of other winning hands that have occurred, even in the single organism P. falciparum.

    Could you provide an example or two of the other winning hands that have occurred in P. falciparum?



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    1. The whole Plasomodium thing is such a straw man that I don't even understand why we are discussing it in such detail.

      So resistance against one compound can only evolve through a very specific set of mutations in one protein in one species. OK, What relevance does this have to the larger questions of whether evolution occurred and whether it did so unguided and undirected? It has close to zero relevance.

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    2. Hey Bilbo,

      Did you ever figure out whether Richard Dawkins is a Eugenicist?

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    3. Could you provide an example or two of the other winning hands that have occurred in P. falciparum?

      Every single genetic trait it possesses that helps it to function.

      That statement you quote from Behe is nonsense, anyway. If a claim has been falsified only to a small degree, then it has not been falsified.

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  16. Georgi: So resistance against one compound can only evolve through a very specific set of mutations in one protein in one species. OK, What relevance does this have to the larger questions of whether evolution occurred and whether it did so unguided and undirected? It has close to zero relevance.

    Behe accepts and even argues for common descent in EoE, so evolution is not the issue for him. The issue for him is whether it happened by random or non-random mutations. If the evolution of chloroquine resistance is a typical example of what must happen in order for most of evolution to occur, then it might be relevant. I think the question then becomes, how many ways are there to win (evolve)? If just about any combination of mutations will result in a "new" (a loaded term) feature, then Professor Moran and the majority of biologists are correct, that random mutations can account for most of evolution. If it turns out that only a small number of combinations of mutations will result in new features of any kind, then that would seem to at least strengthen Behe's position. Behe's argument at this point is that what evidence we do have indicates that only a small number of combinations of mutations will usually work.

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    1. And once again this is an example of failure to understand the process of evolution as it happens in real life. There is no progression towards some predetermined outcome (or set of outcomes) in evolution, all that is required is that some organisms survive and reproduce, and that's a vast space to be explored.

      One of the deepest limitations of creationist/ID thinking (and not just theirs - the truth is that it dominates most of human thought) is the inability to dissociate oneself from anthropocentrism. As strange as it might sounds, we are much better mentally equipped to understand life on other planets should we happen to find it one day than to have an objective view of live of Earth, because of that enormous cognitive bias we have. But if one succeeds in freeing himself from it, a lot of things that are difficult to understand otherwise begin to make much more sense.

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    2. Georgi: And once again this is an example of failure to understand the process of evolution as it happens in real life. There is no progression towards some predetermined outcome (or set of outcomes) in evolution, all that is required is that some organisms survive and reproduce, and that's a vast space to be explored.

      Surviving and reproducing is one thing (though do we know how organisms came to have all the mechanisms that make that possible?). But evolving new features? If any new feature, no matter what direction it would go in, involves too many deleterious (or even neutral?) mutations in a row, then would organisms be able to explore that space? Or would they be stuck on this side of the chasm, unable to proceed any further? And if there are chasms on every side, then are they stuck on islands of function, waiting for the hand of God or somebody to help them across to another function?

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    3. I just explained to you there is no mandate for there to be new features. In fact, the dominant mode of evolution seems to be streamlining due to purifying selection (the reason we don't appreciate that is that we view the process through the prism of our multicellular bias). New features evolve because they can. This is why I will once again say that the Plasmodium resistance to chloroquine is completely irrelevant to the discussion. In less than 10,000 years artificial selection has turned the wolf into bulldog, teosinte into maize (which is quite a dramatic transformation - look at some pictures of the former), the wild Brassica oleracea into cabbage, cauliflower, broccoli, brussel sprouts, etc., I can list many other examples of the sort, a number of which including some quite dramatic transformations.

      "New features" is a creationist buzzwword that has sufficient malleability and vagueness to it to make it a convenient argumentative tool allowing one to constantly move the goalposts every time an example is provided and say "but that's not a new feature".

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    4. Georgi: "New features" is a creationist buzzwword that has sufficient malleability and vagueness to it to make it a convenient argumentative tool allowing one to constantly move the goalposts every time an example is provided and say "but that's not a new feature".

      I agree that "new feature" is a loaded term. So let's try to unpack it. One way would be to define it as requiring more that two protein-protein binding sites (Behe's edge). Another way would be to define it as any feature that required more than four to six deleterious mutations (another way of stating Behe's edge). I don't know if there is an accepted limit to how many neutral mutations can happen. I think Douglas Axe said seven, but I don't know if that number is accepted by most biologists or not.

      Or we could say that for organisms that have smaller population sizes, features that require more than one binding site, or more than two to three deleterious mutations, or whatever the limit of neutral mutations would be for that category of organism.

      So then looking at the examples of new features that you have offered, did any of them exceed those limits?

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    5. Douglas Axe is the last person you should learn your evolutionary biology from (OK, Ken Ham is probably worse).

      What the hell does "how many neutral mutations can happen" mean? There is a mutation rate, there is a genome size, there is some portion of the genome that is strongly constrained, with the rest less so. Where does the number 7 come from???

      Also, small population sizes indeed mean that fewer instances of a particular mutation will occur. But they also mean greater tolerance toward slightly deleterious mutations and a greater role for drift in the process of evolution. Which in turn means more room for constructive neutral evolution and similar processes to take place. Curiously, there is a strongly negative correlation between population size and organismal "complexity" (the recent human population explosion aside), which suggests that these are topics creationists would do well to read more about. And understand them, not quote mine them - someone was claiming that because effective population size in mammals is so low, evolution could not have occurred in that lineage as selection is not a factor (of course, that's not at all what the theory says). Really, there is no reasoning with people like this

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    6. Bilbo, if the alleged designer-god's goal was/is to specially create humans as the pinnacle of design-creation and to design-create the Earth (and the universe) so that it is finely tuned for humans, then what was the purpose of dinosaurs, trilobites, placoderms, ammonites, pterosaurs, and dragonflies with 28 inch wing spans? What was the purpose of designing-creating those animals and all of the other species (plants, animals, etc.) that became extinct before humans existed?

      If you had a time machine and could go ten million years into Earth's future, do you think that there would be any humans still living and that they would be just like humans are now? If you found that humans had become extinct at some point in that ten million years, do you think that other organisms would or could still be living on Earth and evolving, or do you think that when humans end, everything else must end?

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    7. Hi Georgi,

      You might be right about Axe. I wouldn't know. But let's get back to Behe. He admits in EoE that if evolution could be explained as the result of changes occurring one new protein at a time (in whatever direction it occurred), then yes, random mutations would be an adequate explanation for it. He cites the fact that most proteins work in complexes of six or more as a reason to doubt that most of evolution could have occurred just one new protein at a time. Of course, if most of the protein complexes could be explained as having been built up one new protein at a time, then Behe's argument would take a very severe hit from which it could probably never recover. I suspect that at this stage we just don't know enough to answer the question of how most protein complexes came into existence.

      Meanwhile, Behe is willing to grant random mutations the ability at least to evolve new species, possibly new Genera, Families,and Orders, as well. He thinks higher steps on the ladder, such as Classes, Cell Types, and Phyla would have required non-random mutations.

      So it seems to me that there is reasoning with people like Behe. Right now, he says that all the empirical evidence points to random mutations not being able to exceed his edge. The question of whether it ever needed to exceed his edge remains, in my opinion, a question that hasn't been answered, yet.

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    8. Once again we have some severe misunderstandings here:

      1) For people so obsessed with the demise of junk DNA, to say that evolution occurs "one new protein at a time" is very strange. What about regulatory elements? Evolution of form in animals is just as much, if not more, the result of changes in the regulation of otherwise functionally identical proteins as it is of changes in proteins.

      2) The very use of the terms "Class", "Phylum" (and what the hell are Cell Types" doing in your list of steps in the evolutionary "ladder") as having any real biological meaning reveals profound ignorance of 21st century biology. First, those are arbitrary labels. Second, they can only be assigned post-hoc, from our current perspective. You would not have used those labels if you were able to observe those lineages when they initially diverged.

      Stop stuffing your mind with the intellectual excretions of the Discovery Institute, it is not good for you, and read some actual scientific literature instead.

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    9. Hey Bilbo,

      If you "wouldn't know" about the opinions expressed by Douglas Axe, why did you quote him ?

      Are we to assume that you commonly regurgitate the opinions of others that you don't actually understand ?

      Still waiting to hear about the results of your investigations into Richard Dawkins and his dastardly eugenics background.

      By the way, did you know that The ancestors of Richard Dawkins, the atheist campaigner against superstition, intolerance and suffering, built their fortune using slaves, it has been revealed.

      Do try to contain your excitement over this little nail in the coffin of evolutionary biology.


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    10. P.S. It should also be pointed out that you completely evaded the points I made in the previous post

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    11. Hi Georgi,

      Behe isn't one of those people obssessed eith the demise of junk DNA. He also discusses regulatory elements in his book. Have biologists abandoned using taxonomical categories? "Cell types" is a term Behe uses. I would guess that there are different cell types in different Classes. Not sure how reading other literature would answer Behe's challenge. I was hoping Professor Moran would do that in his ongoing discussion with Behe.

      What points did I evade?

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    12. Hi Steve,

      I quoted Axe because he's the only person I know who offered a limit on the number of neutral mutations that we could reasonably expect in an evolutionary explanation, but I was careful to point out that I didn't know if other biologists would accept that. Would you know what number of consecutive neutral mutations would be acceptable?

      I haven't mentioned Dawkins' eugenics on this thread, since it is irrelevant to the discussion.

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    13. "Cell types" is a term Behe uses. I would guess that there are different cell types in different Classes.

      This is why I am telling you to stop ingesting ID/DI junk and start reading some actual science.

      That was a horrifying sentence to read.

      Behe isn't one of those people obssessed eith the demise of junk DNA.

      ID proponents as a whole are.

      Have biologists abandoned using taxonomical categories?

      Largely yes. They might be used as labels but they are not thought of as equivalence classes as they used to be. And these aren't even that recent developments - Hennig died in 1976...

      What points did I evade?

      Pretty much every single one I make.

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    14. A "horrifying sentence"? Who knew I had such powers? But aren't there different cell types?

      I would classify Behe as a maverick in the ID movement. I don't think Larry would put him in the same class as the other ID proponents, either.

      Regarding Phyla, am I mistaken in thinking that the genes that determine phyla do not tolerate much if any mutational change? Wouldn't that mean that at least that classification is not artificial?

      Which points that I evaded are relevant to the discussion?

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    15. There are different cell types. Cell types are not a taxonomic unit.

      Different phyla do not have different genes - it is mostly the same set of developmental regulators with a few differences here and there in terms of the number of members of each families.

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    16. Okay, I'm not sure why Behe put Cell Types after Phyla instead of before it. A good question to ask him one day. Maybe after their done debating.

      Then am I mistaken in thinking that the genes and/or regulators that determine the different phyla do not tolerate much if any mutational change?

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    17. There is no progression towards some predetermined outcome (or set of outcomes) in evolution

      Thanks, Georgi, for saying this so understandably and economically. It's really the key to where the probability math espoused by Behe and other ID folks falls apart. To use my favorite example once again: It's the difference between the 1 in 175 million chance that a particular person (for instance, you) will win the PowerBall lottery versus the fact that someone wins the PowerBall every couple of weeks.

      Evolution is some mutation(s) being fixed in a population or populations of some lifeform(s), not a particular mutation being fixed in a population of a particular lifeform.

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    18. Evolution is some mutation(s) being fixed in a population or populations of some lifeform(s), not a particular mutation being fixed in a population of a particular lifeform.

      To say that a bit better: Evolutionary probabilities are correctly viewed as those of some mutation(s) being fixed in a population or populations of some life form(s), not of a particular mutation being fixed in a population of a particular life form.

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    19. And if there are chasms on every side, then are they stuck on islands of function, waiting for the hand of God or somebody to help them across to another function?

      If one assumes that Behe would be correct and that there was an edge regarding what present ToE could explain, then the best conclusion would be that current ToE was at least partially incorrect and that we were missing something, the same way that Newtonian mechanics missed something, Relativity is known to be missing something (QM), quantum mechanics may be missing something, we definetely miss a completely functional unified theory of physics, etc. There's no reason, if one assumes Behe would be right, that ToE being inadequate would mean God did it. Would you automatically assume that like the IDists?



      Then am I mistaken in thinking that the genes and/or regulators that determine the different phyla do not tolerate much if any mutational change?

      They tolerate the same amount of mutations that any other genes or regulatory sequencences, generaly speaking, tolerate. If something turns up that increases fitness, it may generate a new lineage. If it's neutral, it's neutral. If it's deletrious, fitness goes down.

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    20. Wouldn't that mean that at least that classification is not artificial?

      All taxonomic levels are artificial. They're useful to organize knowledge and expecially to find evolutionary relashionships, but what features you call what are still arbitrarilly defined. For example, the PhyloCode system does NOT use taxonomic ranks.

      Actually, I remember a discussion at Panda's Thumb some years ago on Phyla that was quite interesting. No one seems to agree on how many Phyla there are to begin with, and some biologists even go as far as stating that Phyla is a useless taxonomic level. Coming from Genetics and Microbiology (and with a degree in Geology), I have no vested interest in the matter. Maybe someone here can find the link to that. I seem to remember that some worm group had "recently" aquired a new body plan without much genetic change watsoever, and it kind of undermined the taxonomic position and importance classical taxonomy atributes to Phyla levels. It was a nice discussion.

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    21. Actually, I remember a discussion at Panda's Thumb some years ago on Phyla that was quite interesting. No one seems to agree on how many Phyla there are to begin with, and some biologists even go as far as stating that Phyla is a useless taxonomic level. Coming from Genetics and Microbiology (and with a degree in Geology), I have no vested interest in the matter. Maybe someone here can find the link to that. I seem to remember that some worm group had "recently" aquired a new body plan without much genetic change watsoever, and it kind of undermined the taxonomic position and importance classical taxonomy atributes to Phyla levels. It was a nice discussion.

      The Pogonophora and Vestimentifera (deep-sea worms) used to be considered separate phyla until quite recently but then it turned out both of them belong to the same family of polychaetes...

      Echiura used to be a separate phylum too, but now they are nested within Annelida too based on molecular evidence. The same seems to be true for Sipunculida.

      And speaking of polychaetes, for almost as long as there has been taxonomy, annelids used to be divided into three or four classes - Polychaeta, Oligochaeta, Hirudinea (leeches) plus Archiannelida. Now it's known that's also artificial (PMID: 21368831)

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    22. Thanks for the interesting info. The discussion at Panda's can be found here:

      http://pandasthumb.org/archives/2005/04/down-with-phyla-1.html

      There's a few more articles on the same topic there, so search for "Down with Phyla" in Google.

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  17. Bilbo,

    ///If any new feature, no matter what direction it would go in, involves too many deleterious (or even neutral?) mutations in a row, then would organisms be able to explore that space?///

    Unlikely.
    But unlikely events can still happen by random chance. That's the point you're failing to grasp. Your existence itself is a highly improbable event since several factors spanning several generations had to occur for you to emerge. Even a slightly different sperm fusing with a slightly different egg from the same parents would have produced someone else and not you.
    But here you are!
    Now you're making a post hoc rationalization and asking how all these highly unlikely events fall into place to produce not just you, but any human being for that matter.
    But if you go back in time to before you were conceived, you can see that countless possibilities existed and you're only one among them. There was no apriori requirement to produce you, it just came about by accident.

    This holds true for evolution as well. Chance events can cause evolution to take unlikely routes just as it did in our lives.

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    1. Hi Vimal,

      But even we draw a line on unlikely events. I remember in The Blind Watchmaker, Dawkins talking about the probability of a statue of Mary waving its hand being too small to regard as a serious possibility. If Behe's argument is correct (all the way through), then there have been too many unlikely events for random mutations to be taken seriously.

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    2. Bilbo, correct me if I'm wrong but you apparently don't accept that 'random' or 'accidental' or 'chance' things occur in nature. Instead, you apparently think that everything, or at least certain things, are designed, created, and directed by an intelligent entity or a particular 'God'.

      If you think that only certain things are designed/created/directed, will you please name at least five things in nature that are not designed/created/directed by the alleged designer or a particular 'God'?

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    3. Bilbo,

      There's a difference between improbable events and impossible events. A statue moving its hand is impossible. But a series of mutations, although improbable, is still possible.

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    4. Hi TWT,

      I think the question of what God did or did not direct in evolution is still to be decided.

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    5. If I remember correctly, Dawkins' point was that quantum mechanics allows for improbable things like a statue waving its hand.

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    6. I'm not sure if Dawkins ever said so (have you got a reference?), but no, quantum mechanics does not allow statues to wave their hands.

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    7. Bilbo said:

      "I think the question of what God did or did not direct in evolution is still to be decided."

      I was talking/asking about what you think.

      You're apparently claiming that there is a "God" but that everyone hasn't decided yet what "God" did or did not direct in evolution. Which so-called "God" are you referring to, what scientific evidence can you present that supports the existence of that so-called "God", who hasn't decided yet, who should make the decision, and on what basis should the decision be made? Also, who should decide which so-called "God" actually exists and on what basis should that decision be made?

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    8. I'm not sure if Dawkins ever said so (have you got a reference?), but no, quantum mechanics does not allow statues to wave their hands.

      Actually, Piotr, it does, but the probability is - well, the phrase "vanishingly unlikely" is entirely inadequate to convey just how improbable it is. But it is not categorically ruled out by quantum mechanics, in contrast to classical mechanics.

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    9. Or to put it less anthropomorphically/teleologically: Quantum mechanics does allow, though at more-than-astronomical levels of improbability, for the hand of a statue to move in a waving motion.

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    10. A spontaneously handvawing statue would have to violate some conservation laws. In order to move, tha hand could borrow the necessary amount of energy ΔE from the fluctuations of the quantum vacuum, but such "Heisenberg uncertainty" in its energy couldn't last longer than Δt = ħ/ΔE. In the case of a macroscopic object, nothing as brief as that could by any stretch of the imagination be perceived as "waving". So, at least according to my understanding of quantum indeterminacy, quantum mechanics rules out such behaviour. ;-)

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    11. I think the question of what God did or did not direct in evolution is still to be decided.

      Or perhaps decide if there's any evidence for god(s) in the first place would be nice.

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    12. In the case of a macroscopic object, nothing as brief as that could by any stretch of the imagination be perceived as "waving". So, at least according to my understanding of quantum indeterminacy, quantum mechanics rules out such behaviour. ;-)

      OK, in terms of being perceived as "waving," I'll agree. Of course this could suggest all sorts of shenanigans these statues may be up to that would be far too quick for us to perceive. :-)

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    13. "OK, in terms of being perceived as "waving," I'll agree. Of course this could suggest all sorts of shenanigans these statues may be up to that would be far too quick for us to perceive. :-)"

      Damn. That explains the virgin birth. Now I am a believer.

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    14. Hi Bilbo,

      "I think the question of what God did or did not direct in evolution is still to be decided"

      By what criteria do we distinguish those things that god directed from those things (s)he did not direct?

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  18. Again, Behe's reasoning succinct.

    To Michael Behe: Go pick one of the bacteria in the Lenski long term evolution experiment with E coli. Compare the genome of the most recent clone to the original ancestral specimen used to start the experiment, then count the number of mutational differences between them.

    Then, please calculate the probability that all those specific mutations would happen. We are talking about a set of over 600 mutations happening in the lineage that lead to that single bacterium.

    What would have been the probability of that set of mutations at the start of the experiment?

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    1. Hi Mikkel,

      What didn't you understand about Behe's answer to Moran, here:

      Where a critic might demur is on the question of how many ways exist to solve an evolutionary problem of that mutational complexity. I think that's due to a confusion about the need for particular mutations versus nonspecific mutations. While comparing the math of chloroquine resistance to mutations that have occurred in the primate line leading to humans, Professor Moran wrote, "Does he really mean that there can't be any examples of two mutations occurring in the same gene since humans and chimps diverged?" No, of course not. That overlooks the requirement for the great specificity needed to build biochemical systems. For example, to achieve chloroquine resistance malaria must at least acquire the mutations K76T plus either N75E or N326D in PfCRT -- two very particular amino acid positions in a very particular gene -- not just any two amino acids in any gene. That of course makes a huge difference to the probability.

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    2. Can't speak for Mikkel, but what I can't understand is how something who considers himself to be a trained scientist could consider that an answer to Larry's question.

      More specifically: What is the basis for Behe's position that there is some mysterious force that prevents beneficial pairs of mutations from arising over time in the same gene, while allowing neutral or detrimental pairs to arise freely? Because that is the position he is taking, whether or not he understands or admits to it. In effect, he believes in some weird form of negative natural selection, in which beneficial mutations are selectively prevented from occurring. Weird.

      You have to understand that ID creationists are almost always saying things that are false. So if you just take their proferred conclusions at face value without actually understanding the falsehoods and flaws in logic necessary for them to reach those conclusions, you are going to end up looking gullible and silly.

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    3. OK, I know I wrote "something" instead of "someone" in the first sentence of that last post. However, in deference to Sigmund Freud, I'm going to leave it as is.

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    4. Bilbo, you didn't understand my point, or how it utterly annihilates Behe's spurious probability calculations. This failing is yours (and Behe's). I have re-stated the above problem in several different ways over the last few weeks in the various posts Larry has made on the subject, I'm running out of new and inventive ways to make the obvious any more obvious.

      At this stage I can only suggest to you, and my intent here is only to convey understanding, not to be an arrogant prick, that you spend some time to try and understand what point I'm trying to make and it's relation to the subject. This requires effort on your part, which I cannot be held responsible for.

      You're welcome to ask questions of course. Thank you.

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    5. lutesuite said/asked:

      "More specifically: What is the basis for Behe's position that there is some mysterious force that prevents beneficial pairs of mutations from arising over time in the same gene, while allowing neutral or detrimental pairs to arise freely? Because that is the position he is taking, whether or not he understands or admits to it. In effect, he believes in some weird form of negative natural selection, in which beneficial mutations are selectively prevented from occurring. Weird."

      Yeah, weird.

      Sin, the fall, satan, demons, the 'Lord's' judgement and punishment, non-repentance, the soon to happen end of days, etc., are likely the degenerative force(s) that Behe imagines and believes in, and to god pushers like Behe it's not mysterious at all that some or all of those things cause negative natural selection and other destructive things that, to him and his fellow god pushers, are ultimately righteous, merciful, forgiving, loving, and divinely benevolent.

      Repent now sinners! 'God's' judgement is upon you! The end is near!

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    6. That overlooks the requirement for the great specificity needed to build biochemical systems.

      Really? How many different species have ever existed on Earth, and in all of these species, how many individuals are absolutely identical genetically and in regulatory RNA/DNA? Those are lots of different ways to "build biochemical systems." And they are only the ones that have actually come into existence; it says nothing about the innumerable other different forms of life that would have been viable if, through contingency, they had ever appeared in the first place.

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  19. When I was an undergraduate at UC Berkeley, a chemistry TA cited a case in a local bridge tournament where each player receive a full suit. The odds of that happening are 1 in 2*10^28, a lot longer then Behe's quoted odds.

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    1. Which by the way are exactly the same odds as those 4 players receiving any 4 specified bridge hands.

      We just happen to attach special significance to full suites.

      Just like numbnuts IDiots attach special significance to their appearance in a completely uncaring universe, in a touching display of christian humility and humbleness.

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  20. Much of this discussion doesn't focus on what's important. Yes, there are a lot of mistakes in Behe's argument, but the general direction of it is interesting. I remember discussing with my advisor in grad school that E. coli might be evolving on the basis of the latest triple mutation (because single nt mutations happen so often that every single one is going to get tried just in one person's gut over the next few days). We can grant Behe that a mutation might occur with a rate of 1E-10, even if he estimates this in the wrong way. Yes, Behe's implicit assumption that there is only one way to generate resistance is illegitimate, but we can still use this as an example.

    Behe’s calculation includes a number of mistakes, but we can ignore all but two of them.

    The larger of the two problems is that Behe makes an estimate for the rate of evolution of 1 complex adaptation in mosquito, and jumps from that to a conclusion about ANY complex adaptation in humans. This is like assuming that over the past million years, the only possible way for humans to adapt by a double mutation would be a specific pair of mutations like the ones in chloroquine resistance.

    That's not the right way to do it. Once we know how many possible mutations there are, we'll want to take that number and calculate the number of unique pairs, which is X(X-1)/2. Then we'll need to make a wild guess about what fraction are beneficial. I'm going to guess 1 in 1000 (but I'll also calculate assuming 1 in a million).

    Now, let's work the numbers.

    In the human genome, there are 2E9 bp, and for each one we could count 7 point mutations (3 substitutions, 1 deletion, 4 insertions-- of which 1/4 are redundant). There are lots of other types of mutations, and the numbers get really huge. The number of sequences of length i is 4^i, thus the number of possible de novo insertions is 4^i * n, where n is the genome size, which is ~ 1E6n for i = 10. A translocation has a point of origin chosen from the length of the genome, it extends up to r bp, and has a point of insertion chosen from the genome, so the count of translocations scales with rn^2! That's insanely large! Maybe we don't want to count these if we think they occur at rates much less than 1E-10 each. But we need to include at least 1.4E10 point mutations.

    The number of double-mutant combinations is then 1.4E10 * (1.4E10 - 1)/2 ~ 1E20. If we assume that 1 in a thousand combinations is beneficial, then we have to count 1E17 (and if we assume 1 in a million, that's 1E14).

    Thus, we have 1E17 (or 1E14) *beneficial* combos each with a rate of 1E-20, so the total rate per person generation is 1E-3 (or 1E-6). In other words, you might have already met someone with a beneficial double mutation. This may seem counterintuitive, but look at it this way. Humans have a mutation rate such that the total genomic rate is about 1 (1.6 according to Drake, et al 1998). Given a Poisson distribution, this means there must be substantial numbers of 0s, 1s, 2s, and increasingly fewer 3s, 4s, etc. You have some double-mutants in your family already. We just assumed that 1 in 1000 (or 1 in a million) are beneficial, so voila! multiple beneficial double mutants just in NYC.

    What about all of human evolution? If humans had a population size of a million for the past million years, that is ~1E11 person-generations, as a rough order-of-magnitude estimate. That's surely an over-estimate. With these numbers, humans have experienced many beneficial double mutations. Even if we assume that only 1 in a million doubles are beneficial, we still get about 1E5 of them in the course of human evolution.

    That solves the biggest problem with Behe's argument. The next problem, still quite significant, is the lack of population genetics. This post is long so I'll address that separately

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  21. Of those millions of beneficial double mutations, most will get lost. We have to take population genetics into account. When we do that, we don't want to frame this in terms of a double-mutation, as if we have to wait for two mutations to happen in one individual. Actually, a mutation could happen in an individual, and the second in the individual's grand-child, even if the first mutation is deleterious (because low-fitness individuals have children and grand-children, just not quite as many as high-fitness ones). If we extend out this line of thinking, the probabilities start to add up, and we discover an important population-genetic phenomenon of "stochastic tunneling", where we can get from 0 --> 1 --> 2, even when 1 is deleterious and never takes over the population.

    And I know this because population geneticists have already looked at this question in some ways, and it is interesting. It is reasonable to ask how adaptations that require multiple mutations can emerge in evolution, and whether we can calculate any limits to that. People like Frazetta or Lynch have addressed it. In fact, Lynch's paper cites Behe (http://mbe.oxfordjournals.org/content/27/6/1404.full.pdf+html ).

    So, we want to reframe this problem in terms of what Lynch calls "complex adaptations," i.e., adaptations that depend on multiple mutations, without restricting it to waiting for a double mutation. Complex adaptations are going to be more likely with more time, and less obviously, with larger population sizes (see Lynch). Humans are at a disadvantage relative to mosquitos and fruitflies and E. coli. At the end of the day, there are going to be some kinds of complex adaptations that are likely in fruitflies but negligible in humans. So, if we take away all of Behe's numbers, and his logic, and just squint a bit and look at the general nature of the conclusion, he is on the right track.

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    1. You have some double-mutants in your family already.

      I knew it.

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    2. Arlin, thanks for your comments and the link. Nice to get into some actual scientific work rather than back-of-the-envelope goal-directed stuff paraded around like it's science. (Though Behe raises an issue of scientific interest, I think you still give him too much credit. If there is "evolution by accident," I think this is "raising valid issues for evolutionary theory by accident" - he pretty much stumbled into this one while doing the usual hollering of "Unpossible!" re evolution without teleology.)

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  22. Replies
    1. But if the first required mutation (or second, or third) doesn't help, or positively hurts, then the gradualist scenario is interrupted. The first mutation does not spread in the population (in fact it's actively kept in check by negative selection), so the number of organisms with the mutation does not increase and can't provide a larger base within which the second mutation can arise. The Darwinian magic is turned off.

      Only if the mutation is clearly detrimental. Otherwise, genetic drift can easily spread it throughout the population (or not, since it's a stochastic process).

      Also, with gene duplication, there is no need for the mutations to occur sequencially, and it's irrelevant if the mutations are deleterious, since one of the copies is working fine (although I don't know if there was gene duplication in any of this observed cases).

      Well, that's the theory. But what if a necessary single amino acid replacement doesn't affect performance at all (because it's neutral), or "affects performance" by making it worse?

      Same answer as above.

      The several mutant proteins they did test in malaria cells were coded by genes carried on plasmids -- meaning that the malaria cells also expressed their own, wild-type, normal, genomic, unmutated gene, which of course could compensate for any missing required activity of a nonfunctional mutant plasmid gene, so they couldn't detect if a mutant protein were deleterious by itself. On the other hand, it was shown years ago that malaria cells constrained to express only mutant K76T PfCRT would not grow in the lab, demonstrating the mutation is indeed deleterious.

      Actually no. It demonstrates that the mutation is indeed deleterious IF there is no other copy in the cell. From Behe, it's not clear to me if those cells "constrained to express only mutant K76T PfCRT that would not grow in the lab" were artificially constrained (e.g. by knocking out other copies that could be functional) or not. Does anyone here know if malaria cells in general carry several copies of the gene in question? If they do, than there is no requirement regarding the order of the mutations, nor with deleterious effects (by Behe's own admission).


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    2. Were there "millions and millions of possible evolutionary outcomes" that could make malaria resistant to chloroquine? I can think of a few possible alternative scenarios. Instead of a chloroquine pump appearing, maybe a chloroquine-degrading enzyme could have arisen, or maybe malaria's membrane could somehow be altered to stop chloroquine from entering the cell, or maybe the cell could become dormant until the chloroquine passed.

      But none of those scenarios happened. Why not? Because any evolutionary pathway leading to those outcomes was even less probable than the pathway that occurred. The odds of 1 in 1020 are not just the probability of PfCRT acquiring the right mutations -- it's the minimum odds of any chloroquine-resistance mechanism arising in P. falciparum. It may very well be the case that there are no other resistance mechanisms that can be reached by malaria.


      I don't quite agree with the second part of Behe's comment. His calculations don't represent the possibility of total outcomes. It's not the individual probability of an outcome that matters here so much as the probability of ANY of them occuring as a response. And his number DOESN'T take that into account. Behe's argument is like saying that since there is an infinitesimal chance of any *particular* person winning the lottery, than no one can win it.

      On the other hand, I think Behe makes a good point, generally speaking. Although the evolutionary history of life can follow multiple, uncountable, and contingent pathways that end in the present day lifeforms, the point is still that there are only a few limited variants of the malaria parasite at present, and those variants constrain whatever the organism can evolve as a response to a particular chemical. I certainly don't believe that there are "millions and millions" of different ways with which *existent* malaria parasite populations can develop resistance to chloroquine.

      In the end, I think Behe does ignore some facts, some mechanisms of TeO, and does seem to think that IF the present ToE is insufficient to explain particular aspects of molecular evolution than that automatically means that some god did it. In my opinion, this last aspect is Behe's major logical flaw (Irreducible Complexity is not even worth mentioning). If ToE was shown to be insufficient for molecular evolution, all it would mean would be that we would need to gather more knowledge, do more research, propose new mechanims based on observation and experimentation, and hopefully get an answer. Newton's orbital mechanics are not stabilized by angels, even if Behe seems to think so.

      Otherwise, I think that Behe occasionaly raises some points that are worth looking at. If only he was honest about the whole thing, instead of wasting his time embarking on a Jihad against "Darwinism", he could actually have made some decent contributions to molecular evolution as a science.

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    3. Otherwise, I think that Behe occasionaly raises some points that are worth looking at. If only he was honest about the whole thing, instead of wasting his time embarking on a Jihad against "Darwinism", he could actually have made some decent contributions to molecular evolution as a science.

      I'm not sure. It seems to me that perhaps an even more fundamental difference than between religion and non-religion is the divide between those who are satisfied with slipshod work as long as it meets their goals, and those who by nature can be happy only with good, thorough, careful work. Behe, it seems to me, is clearly one of the former group, and to me that precludes the possibility of making "decent contributions to molecular evolution as a science."

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    4. I think he's "slipshod work" is a consequence of not actually doing much in the way of increasing scientific knowledge as opposed to missionary work. His job is making converts, as well as finding some solace in the form of gaps so that god may indeed have a role in evolution. I think that if Behe was unbiased by faith and had a genuine interest in molecular evolution the problem you point out would go away.

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    5. If you bother to read Behe's article , be sure to turn off your irony meter before you read the first sentence:

      Ever have a conversation with someone where, try as you might, you just can't seem to get through?

      I'm sure Larry can tell us all about that.

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    6. I think that if Behe was unbiased by faith and had a genuine interest in molecular evolution the problem you point out would go away.

      Hi Pedro - yes, I thought that was where you were coming from. My own point of view is that there are people who are "biased by faith," but whose good, careful scientific work will not allow them to sidestep the fact of evolution (e.g., Ken Miller, Francis Collins).

      There is a whole other level of lack of care and thought necessary to arrive at a difference like the probability calculations Behe makes versus those Arlin, for example, showed here and in the paper he linked to. The latter two are done with an obvious concern to model reality carefully and accurately that contrasts starkly with Behe's.

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    7. I agree, judmarc. But I think it's possible that Behe is not just a case of someone biased by faith and being dishonest to others, but someone who is ultimately being dishonest with himself. I think that makes it much more difficult for him to approach science seriously. I don't want to do cheap psychoanalysis, since that would be unfair to Behe, but it seems like he is desperately grabbing at every potential knowledge gap he can find to fill it with his god, so as to keep his faith out of conflict with the knowledge he has as a biochemist.

      Or maybe he's just a total crook and I'm being to kind.

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    8. If you bother to read Behe's article , be sure to turn off your irony meter[...]

      That goes without saying :)

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    9. Pedro, Pedro,

      I understand your headache, caused by Behe's unflappable reasonableness, logic, and use of actual evidence, is taking its toll on you.

      But bashing Behe ain't gonna relieve the pain.

      A mirror and a commitment to change is a potent remedial coctail.

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    10. Tell me Steve, is that stuff you're taking over-the-counter or does it require medical prescription?

      Delete
  23. My own point of view is that there are people who are "biased by faith," but whose good, careful scientific work will not allow them to sidestep the fact of evolution (e.g., Ken Miller, Francis Collins).

    I don't know about Miller, but there's plenty of shoddy thinking in Collins' "The Language of God" regarding evolution. For example, he thinks the existence of humans defies evolutionary theory, that morals are absolute (sociobiology and comparative ethology be damned), that altruism cannot be explained by evolution, that the universe is fine-tuned and the multiverse is an ad oc concept (when it's in fact predicted by any inflationary scenario), etc. That's scientific shoddiness to me, regardless of his acceptance of evolutionary theory in general. He is a critic of ID and rightly so, but he's guilty on his own for ignoring the inconvenient when it comes to supporting his faith.

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    1. Ah, I haven't read TLOG, so I'll take your assessment "on faith," as it were. ;-)

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    2. Heh. My dear judmarc, take it just as a personal opinion and therefore temporary, until you read it and make up your own. We're not IDiots, after all. :)

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  24. Sandwalk as just been pwned!!!!!!!!!!!!!!

    By Behe of course.

    You are all now officially idiots......with a small d that is.

    Now you've got cooties, to boot.

    Toodalooo!!!!!

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    1. Even me...? I neither totally agree with Behe nor with Moran... What does that make me...? Behe-Moran-tionist...?

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  25. So Moran claims 4 mutations are required to confer "effective" chloroquine resistance (QR).

    Behe argues that 2 mutations are required for chloroquine transport (QT), the mechanism of QR.

    Summers supports Behe, 2 mutations are the minimum required for QT.

    Moran would probably respond that QT is not "effective" QR. But where does Summers support that claim? And why does it matter?

    Behe has already stated that after 2 mutations are achieved to confer QT, third and fourth mutations can be easily added "because the population size (10^12) greatly exceeds the inverse of the mutation rate."

    So where has Moran refuted Behe?

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  26. In other words, a decrease in our best estimate of the value of one factor can be conceptually offset relatively easily without affecting the argument by supposing another factor is larger, to arrive at 1 in 10^20.

    This bit makes me goggle somewhat. A decrease can be conceptually offset easily by supposing ... ? It cuts both ways. We could just as easily suppose in the opposite direction. The reality will be a probability distribution. We don't know where we are in that distribution; we don't have access to all the data. And yet Behe can extrapolate to infer a hard limit on every organism ever, simply by clinging to 10^20, per White, as the number of organisms per actual instance of a specific detected phenotype. It is suspect reasoning.

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    1. No it doesn't cut both ways. 10^20 is an empirical observation from an extraordinarily well studied area of science. 10^20 is the number nature gives us when we observe and measure.

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    2. 10^20 is an empirical observation

      No it isn't. No-one has observed 10^20 cells, nor have they 'empirically observed' the probability distribution. White has simply estimated the number of cells involved given the observed incidence of CR. To regard that as empirical proof of 10^20 is like saying that, if you empirically observe 3 heads in 10 throws, the probability must be 30%.

      Behe thinks you must fiddle with the data to make it fit 10^20. If it doesn't fit 10^20 you just 'suppose' something else needs fiddling with to get it back there. It's not a robust methodology.

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    3. Yes it is. It is based on the observation of the number of times CR emerges and the population size. It is possible the further observations will refine the number but a sufficient amount of data has been collected such that a reasonable argument cannot be made that any refinement will be dramatically different.

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    4. Even if the 10^20 estimate was accurate, it doesn't support Behe's claim. All that figure would represent is the approx. odds of a particular trait appearing in a particular species under a particular set of circumstances. For Behe to then say this represents the exact odds for all traits requiring two mutations in all species under all circumstances is just batty.

      To illustrate with just one factor: If chloroquine had never been synthesized, would that affect the frequency with which the trait is observed? Of course it would. What if chloroquine happened to be a regular part of the diet of all host organisms? Again, the answer is "Of course."

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    5. Oh, and as to the question "So where has Moran refuted Behe?," to save you the trouble of scrolling up:

      The presumed evolutionary path to most of the resistant strains did NOT involve any intermediates that were less fit than the wild type. Strains carrying single mutations were detected in the wild.

      Recall that Behe's calculation of the mutation rate is too low by a factor of at least 100 in spite of the fact that he references the accepted mutation rate. The recent data by Summer et al. refutes three of Behe's assumptions: (a) that only two mutations are required to account for the appearance of resistant strains, (b) that a resistant parasite had to arise from wild type within a single infected individual, and (c) that one or more of the individual mutations are deleterious on their own.


      Behe starts by failing to understand how CR evolved in the malaria parasite, them compounds this error by assuming that, even if he had understood it correctly, this represents the process by which all traits requiring two mutations evolves in all circumstances.

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    6. das Kapitalist Yes it is.

      No it sodding isn't. No-one observed that it took 10^20 cells. No one observed the population size. No one has the probability distribution, or the expected number of times it would emerge if we reran ad infinitum. 10^20 is just White's estimate, and potentially subject to the deviation of a small data set, something to bear in mind when extrapolating. Unless, of course, you're just desperate for Behe to be right, and accuracy doesn't bother you overmuch.

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    7. Miller,

      I am sorry you don't know the definition of empirical. A finding is empirical when it is based on observation rather than theory. White didn't come up with 10^20 based on theory, he based it on the populations size and number of times CR has emerged.

      And no, there is no deviation of small data sets. Malaria is astonishingly well studied with over 17,000 related publications in the last 5 years.

      Like I said, future observations may modify the 10^20, but given the large amounts of data already accumulated on the topic, it is not reasonable to suggest that the number will change significantly enough to have any material impact on Behe's argument.

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    8. Actually, rather than "empirical," this qualifies as a WAG (wild-ass guess), which is then used to do some incorrect probability math. If you want to see real numbers used correctly, please have a look at Arlin's two comments in this thread.

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    9. lutesuite,

      You wrote (quoting Moran I think),

      "Recall that Behe's calculation of the mutation rate is too low by a factor of at least 100 in spite of the fact that he references the accepted mutation rate"

      Wrong. The commonly accepted mutation rate is 2.5 x 10^-9, with some recent publications citing 1.0 - 9.7 x 10^9. Behe uses 10^-8, a higher mutation rate.

      Delete
    10. Larry discusses the mutation rate in his initial response to Behe's "challenge":

      http://sandwalk.blogspot.ca/2014/08/taking-behe-challenge.html

      But, really, that's just a peripheral issue and not worth spending too much time on. Larry's most recent post on the topic, published today, has reemphasized the crucial error Behe makes, which happens to be the idea I have been trying to get thru to you (and which you seem to have ignored in your response to my post).

      In brief, the 10^20 figure that Behe cites from White's paper, and upon which Behe's entire argument hinges, is not the result of frequency of mutation alone. It is determined by at least seven other completely unrelated factors. With that single number dismissed, Behe's entire argument collapses. And he knows this, or should. As Larry also mentions, this has been pointed out to Behe many times already. But why should Behe admit to this, when he knows the churches are still full of IDiotic sycophants like yourself who will keep buying his claims (and his books) no matter how many times they are refuted?

      Delete
    11. das Kapital

      "I am sorry you don't know the definition of empirical. A finding is empirical when it is based on observation rather than theory."

      The observation is that c10 CR strains have been identified. And we can sample infection rates and parasite numbers. But all else is estimate - neither observation nor theory. 1 CR strain per 10^20 replications is not an empirically observed fact. The word 'empirical' appears a lot in ENV-style coverage of this issue. I think you've picked up the misuse from there. And, to repeat, it's probability distribution that's important if you want to use this as a starting point for extrapolation to ... ooh, picking a species completely at random ... humans.

      And no, there is no deviation of small data sets. Malaria is astonishingly well studied with over 17,000 related publications in the last 5 years.

      You misunderstand. Chloroquine resistance is a stochastic process. It has been observed just 10 times. We can't thereby conclude that 10^20 cells is the centre of the probability distribution, particularly given the many uncertainties in the path to observation as a CR strain. What are the error bars, the p values? Further, chloroquine resistance itself is but one phenotype. This is really not enough to infer the probability of ALL dual-mutation phenotypes throughout nature. It is a tiny dataset, however well studied.

      Like I said, future observations may modify the 10^20, but given the large amounts of data already accumulated on the topic, it is not reasonable to suggest that the number will change significantly enough to have any material impact on Behe's argument.

      I don't think anything will have an impact on Behe's argument. It's bogus, and will remain so whatever the issues associated with this particular phenotype. There are two separate issues: the accuracy of the 10^20 figure, and the reasonableness of extrapolation off such a specific pathway to the whole of evolution. Even if the first proves correct, the second remains unjustified. You defend 10^20 come hell or high water, because the numbers have to be large so you can make your leap to the impossibility of Nature. You try and dignify it as an 'empirical' figure, to lend gravitas. But really, it can be anything it likes. We have no reason to accept that whatever it is, everything else is that also, or that nothing else can happen while we watch for our pre-specified CCC.

      Delete
    12. Evern Moran admits 10^20 is a reasonable number. Clearly, it is the best estimate supported by evidence. You are simply hoping for a better number sans evidence for a better number. Which is why you are arguing semantics instead of facts.

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    13. 10^20 is not out of the question, as the total number of parasite replications taking place between detected incidences of CR. But there are numerous reasons why it could be wrong, and many more why it is irrelevant, both to CR, and to eukaryote evolution in general. I'm not 'hoping for a better number' - as I clearly stated in my last paragraph, it doesn't matter a damn what it actually is. But it is important to understand concepts such as probability distributions, and the population bottlenecking I discuss below. None of this is 'semantic' in any sense; where do you get your ideas from?

      These factors are relevant to whether we should accept Behe's Edge. You just accept 10^20 blindly and uncritically, because the bigger the better, and refuse to see the holes in his argument, because - well - he's proved God! Scientifically! Can't argue with that.

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  27. If evidence for random evolution is so strong as modern evolutionists claim it to be why professor Behe needed to write half a dozen articles in which he practically challenged you to present your evidence.

    Is it perhaps because there is none? Why only "arguments" against professor Behe were only stories about "playing Bridge" or all kinds of excuses.

    Professor Moran could you explain to professor Behe your claim that random errors did all the evolution what evidence is based on? Is it based on actual evidence or just on your belief that there can be no designer?

    M. Behe:
    "The bridge analogy is inapt (see my previous post). P. falciparum dies without the needed mutations. It will never play bridge again."

    "And just as those alternative chloroquine resistance pathways are imaginary, Professor Moran's "millions and millions of possible evolutionary outcomes" are imaginary. In the absence of actual evidence that a huge number of relevant unrealized biochemical features could have been built by Darwinian processes, it is illegitimate to arbitrarily multiply probabilistic resources."

    "In the absence of an a priori requirement, science is obliged to investigate whether or not such pathways exist. Right now the evidence we have in hand militates strongly against it.

    This is hard for IDiots to understand.

    See my remark above about name-calling."

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    1. "In the absence of actual evidence that a huge number of relevant unrealized biochemical features could have been built by Darwinian processes"

      Like when HIV couldn't possibly evolve something new, and Abbie Smith of ERV fame had to point out a new gene with a new function had evolved and that a figure in Behe's own fucking book contained the gene?

      Denial of reality is a staple of the IDiot modus operandi.

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    2. Professor Moran could you explain to professor Behe your claim that random errors did all the evolution what evidence is based on? Is it based on actual evidence or just on your belief that there can be no designer?

      Naturalistic processes (evolution) are sufficient to account for the history of life on Earth. There's no need to invoke supernatural beings. If you advance the extraordinary claim that supernatural beings are required then the burden of proof is on you to show that such beings exist and that they are capable of doing what you claim.

      You could start by simply giving us a brief description of your intelligent design scenario. How do you think your gods made humans? Give us dates and actual events. Which god did it? Was it Jesus, Satan, Mary, or did they delegate it to one of the archangels?

      Don't forget to present actual evidence.

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    3. Larry wrote:

      "How do you think your gods made humans?"

      If people knew how God or gods made humans, wouldn't that make them the creators themselves...and pretty much equal to God or gods in that aspect...? How would God or gods be the source of all life then...?

      But, let's flip this scenario around...

      If scientists like you Larry are so sure that ..."Naturalistic processes (evolution) are sufficient to account for the history of life on Earth..." why can't they provide any evidence for the origins of life and evolution or other processes that led to the formation of the "simplest" cell...?

      What makes you so certain that natural processes did it, if there is no evidence for it...?

      Aren't you being hypocritical here...?

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    4. No Mikkal, Behe said in his book that HIV would have a better ability to evolve something new because of its massive population sizes and high mutation rate. Abbie Smith apparently never read Behe's book.

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    5. Re Rasmussen

      It should also be noted that Abbie Smith challenged Behe to a debate about HIV evolution and the cowardly Behe declined on the basis that she was only a graduate student at the time. Of course, the real reason he declined was that Dr. Smith's PhD thesis work was on the evolution of HIV and that she knows more about the subject then he does. Her current employment is in an HIV lab. "Dr." Behe has some chicken feathers where competitive spirit ought to be.

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    6. Re Rasmussen

      It would also not surprise me if one of Behe's unmentioned excuses for declining to debate Abbie Smith was that he was afraid of being shown up by a woman. Possibly a little male chauvinism there.

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    7. Behe's dismissal of the analogy with bridge only shows that he doesn't know what he's talking about. The issue is that, to my understanding, Behe is claiming that his calculation of the probability of 2 simultaneous mutations occurring is 1 in 10^20, and therefore is highly unlikely. My comment about a bridge hand with 4 perfect suits was 1 in 2*10^27, which is even more unlikely then Behe's 2 simultaneous mutations. The issue is probabilities, not the details of bridge vs biology. As a matter of fact, I would be willing to wager then there have been no where near 2*10^27 bridge hands dealt in the entire history of the game. In fact, I would bet that it is totally impossible that all possible bridge hands have been dealt since the beginning of the game.

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    8. "No Mikkal, Behe said in his book that HIV would have a better ability to evolve something new because of its massive population sizes and high mutation rate. Abbie Smith apparently never read Behe's book."

      See, this is why I say reality denial is a staple of the IDiot modus operandi. You needed merely have clicked the link in my previous post.

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  28. "If evidence for random evolution is so strong as modern evolutionists claim it to be why professor Behe needed to write half a dozen articles in which he practically challenged you to present your evidence"

    It's not hard to guess what motivates Behe's "needs" in this context. His religious convictions is what leads him to question what has been shown beyond doubt time and time again. He's also a fellow of an institute working explicitly with sociopolitical goals in mind, him being one among several chief propagandists on that institution. This is what motivates him to keep erecting specious controversies

    "Is it perhaps because there is none? Why only "arguments" against professor Behe were only stories about "playing Bridge" or all kinds of excuses."

    If the fundamental problem with Behe's argument is conceptual in nature, the refutation will necessarily have to expand on that concept. This is not an excuse, it's simply that Behe's making trivial errors in reasoning. That means the issue is not about evidence, but Behe's ability to reason, and the ability of his deluded acolytes to get beyond their predisposition to think everything Behe says is correct and actually try to look at the underlying logic.

    Quick hint: When Behe says "The bridge analogy is inapt" that doesn't mean Behe is automatically correct.

    Can YOU explain why the bridge hand analogy is inapt, in your own words, without just mindlessly copy-pasting Behe?

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  29. It really is amazing how most of the IDiots coming here seem capable of nothing else but linking to, or copy-pasting Behe.

    "Behe spoke - that settles it".

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    1. I referred to them as Behe's sycophants but Behe says that's childish.

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    2. It really is amazing how most of the IDiots coming here seem capable of nothing else but linking to, or copy-pasting Behe.

      Big numbers + big words = willing suspension of disbelief. There's no motivation on the part of the audience to understand the concepts behind the numbers and words, whereas that's exactly what I read science blogs for.

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    3. Funny, as I posted above, you guys haven't refuted Behe at all and here you are patting yourselves on the back.

      Whereas Behe's argument is supported by empirical observations your argument boils down to "hey, there could be another organism that we haven't studied that evolves better."

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    4. No body has made that argument. Rather, the general problem is Behe is over-extrapolating this single case of chloroquine resistance to arguing against general cell biology and body plan evolution of large multicellular eukaryotes.

      Behe's the one imagining cell and body plan evolution is chuck full of these supposedly insurmountable barriers to evolution. He has one single case in one single parasite where the process is slow. Why do you think it is valid to extrapolate this result into a general rule of evolution?

      We seem to have quite good evidence from developmental biology that gene regulatory networks can be reprogrammed rather easily to make significant changes in body plans.

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    5. If evidence for random evolution is so strong as modern evolutionists claim it to be why professor Behe needed to write half a dozen articles in which he practically challenged you to present your evidence.

      Because he never bothered to read the 12 inches' worth of papers and manuscripts piled up in front of him at the Dover trial, perhaps? Each and every one refuted Behe's contention that the immune cascade was irreducibly complex and could not have evolved, and what he said under oath on the stand was that he didn't need to read them because no amount of factual evidence could convince him he was wrong.

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  30. Here it is again, so you guys don't have to scroll up to respond:

    So Moran claims 4 mutations are required to confer "effective" chloroquine resistance (QR).

    Behe argues that 2 mutations are required for chloroquine transport (QT), the mechanism of QR.

    Summers supports Behe, 2 mutations are the minimum required for QT.

    Moran would probably respond that QT is not "effective" QR. But where does Summers support that claim? And why does it matter?

    Behe has already stated that after 2 mutations are achieved to confer QT, third and fourth mutations can be easily added "because the population size (10^12) greatly exceeds the inverse of the mutation rate."

    So where has Moran refuted Behe?

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    1. If the 3rd and 4th mutations can be easily added, then the 1st and 2nd can too. You know, because "the population size (10^12) greatly exceeds the inverse of the mutation rate."

      LOL

      Wasn't Behe's argument supposed to show that the evolution of some things were hard, now suddenly you're arguing it's easy?

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    2. Behe's argument is that where two or more mutations are required to confer a selective benefit, evolution reaches the edge of its creative ability. Where the edge is depends on population size and mutation rate. Where a single mutation will confer a benefit, evolution is easy in large populations like P.falciparum. However, when two mutations are required, and the first mutation is either neutral or slightly deleterious, then it creates a very difficult hurdle. In the case of chloroquine transport in P.falciparum, it takes about 10^20 reproductive events.

      Adding my argument here, not Behe, an evolutionary step requiring 10^20 reproductive events wold not be achievable in mammals because mammals do not have sufficient population sizes and have lower mutation rates.

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    3. Behe's argument is that where two or more mutations are required to confer a selective benefit, evolution reaches the edge of its creative ability.

      Generalizing this conclusion (without ignoring the many other reasons it's wrong) necessarily implies any two mutations one picks have the same probability. This is flatly incorrect, and has been shown to be so in experiments. That is, some mutations are far more likely to occur than others.

      Still don't want to leave this comment without re-emphasizing that the entire enterprise of looking at the likelihood of a *single* particular mutational path will *always* create astronomical numbers against, and in fact the *more* likely it is that evolution generally takes place, the *less* likely Behe's spurious calculation will show any particular pathway to be. As I showed Lino, using Behe's calculation, one can show it's impossible that you exist. Just think of the chances your parents married each other, of all people on Earth; go back to their parents, and their parents...and within just a couple of generations your existence becomes vanishingly unlikely. That's what happens when, like Behe, you do probability math incorrectly.

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    4. Adding my argument here, not Behe, an evolutionary step requiring 10^20 reproductive events wold not be achievable in mammals because mammals do not have sufficient population sizes and have lower mutation rates.

      That is Behe's argument. What, you think he wrote a whole book just to show how God helps the malarial parasite?

      It's interesting that, here your are, purporting to defend Behe's arguments, and you don't even know what those arguments are.

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    5. Adding my argument here, not Behe, an evolutionary step requiring 10^20 reproductive events wold not be achievable in mammals because mammals do not have sufficient population sizes and have lower mutation rates.

      Actually (I made this point in the more recent thread too) this is an erroneous comparison. Because P falciparum is unicellular, you count every replication in your 10^20, and every cell counts towards the population census size. However, because a human being is 'the organism', you only count each separate one.

      But compare and contrast infection and human reproduction. A male produces about 200 million sperm per ejaculate. And ejaculates about ... well, that's none of your damn business(!), but let's say 1.5 * 10^12 cells in a lifetime. Of course actual reproductions are limited by bottlenecking - females are a limiting resource.

      Meanwhile, an individual becomes infected with a small inoculum of P falciparum. These multiple rapidly, and you count every one of these towards your 10^20. They have to multiply greatly, to stand a chance of some of them getting into another mosquito, otherwise the lineage is toast. But if they multiply too much, they kill the host, and the cells get nowhere. There is a severe bottleneck, as the new mozzie can only get a few in a drop of blood, and not every host lives to yield.

      Now, these situations are closely related. There is a bottleneck in both cases, and constraint is provided by the 'bottle' - the human - and not by the number of cells the bottle can hold. You should either count every cell, or every host, in both cases. Counting cells in the one, and individuals in the other, gives a misleading result. CR has arisen 10 times despite the life cycle of Plasmodium rendering its effective population size conditioned most by its host population size, not the cell census size. ie, Plasmodium shows just what a small population can do!

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  31. Repeating a claim without addressing previous replies is a standard IDiot move, usually indicating inability to address those replies. Most IDiots at least take the time to change the words a little.

    ReplyDelete