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Quote-mined by Casey Luskin!

Once again, Casey Luskin demonstrates that he’s a biological ignoramus. He is much buoyed by a science report that chloroquinone resistance in the malaria parasite requires two mutations, claims that Michael Behe has been vindicated because that’s exactly what he said, and demands an apology from all of Behe’s critics.

Will Ken Miller, Jerry Coyne, Paul Gross, Nick Matzke, Sean Carroll, Richard Dawkins, and PZ Myers Now Apologize to Michael Behe?

No.

Here’s what his critics actually said. We have no problem with the idea that a particular functional phenotype requires a couple of mutations; I can think of lots of examples of that, such as the work of Joe Thornton on corticosteroid receptors. That the malaria parasite needs two mutations was never a point of contention, nor was it particularly worrisome. What was wrong with Behe’s work is that he naively claimed that the two mutations had to occur simultanously in the same individual organism, so that the probability that could happen was the product of multiplying the two individual probabilities. That’s ridiculous.

As Sean Carroll explained:

Behe’s main argument rests on the assertion that two or more simultaneous mutations are required for increases in biochemical complexity and that such changes are, except in rare circumstances, beyond the limit of evolution. .. Examples of cumulative selection changing multiple sites in evolving proteins include … pyrimethamine resistance in malarial parasites (6) — a notable omission given Behe’s extensive discussion of malarial drug resistance.

To show that the activity required two mutations, as the new paper says, is not an issue; it would have to claim that two simultaneous mutations were required, and that the cumulative accumulation of mutations in the population does not happen. And Behe goes further and declares on the basis of his bogus calculations that no evolution, beyond minor changes in a species or genus, occur at all.

So it’s weird to see Luskin announce that I’ve already conceded Behe’s point. No, I have not.

What we’ll probably get is nothing more than PZ Myers’s concession, offered in the context of the rant quoted above:

Fair enough; if you demand a very specific pair of amino acid changes in specific places in a specific protein, I agree, the odds are going to be very long on theoretical considerations alone, and the empirical evidence supports the claim of improbability for that specific combination.

Well, that’s more or less what’s required to generate chloroquine resistance. We’ll gladly take this — i.e., simply being proven right — in lieu of an apology.

Yet if you actually read the post in question, you’ll see that I’m not conceding that Behe is right — I’m explaining that a low probability is not a barrier to evolution.

Yet his argument for this dramatic conclusion is not only weak, it’s wrong. I could, for instance, correctly argue that the odds of getting a straight flush dealt to you in a 5 card poker hand is about 1 in 6×104; we could calculate this with probability theory, and we could also deal lots of poker hands and determine it empirically. No one’s going to argue with that part of the math.

But now, if I were to define a Straight Flush Complexity Cluster (SFCC) parameter and wave it around and claim that “no hand of the same complexity as a straight flush has been dealt by chance in the last ten years of poker games here in town,” that players can only possibly win one hand in 60,000, or worse, that no one has won a poker hand without cheating and stacking the deck, you’d know I was crazy. But that is basically Behe’s entire argument — he claims to have found the “edge of evolution,” and that it is much sharper and steeper and more impassable than anyone but a creationist could believe.

I’m flattered that Luskin thinks a concession from me would be so significant, but he ought to wait until I’ve actually made one before declaring victory.


Ken Miller wrote to second my comments:

With respect to the malaria mutations, your rebuttal is exactly correct. I’m attaching my review of Behe’s book in Nature. The portion of that review that directly deals with Behe’s contention about two mutations is this:

Behe, incredibly, thinks he has determined
the odds of a mutation “of the same complexity”
occurring in the human line. He hasn’t. What
he has actually done is to determine the odds of
these two exact mutations occurring simultaneously
at precisely the same position in exactly
the same gene in a single individual. He then
leads his unsuspecting readers to believe that
this spurious calculation is a hard and fast statistical
barrier to the accumulation of enough
variation to drive darwinian evolution.
It would be difficult to imagine a more
breathtaking abuse of statistical genetics.

Then, later on, I wrote:

“Behe obtains his probabilities by considering
each mutation as an independent event, ruling
out any role for cumulative selection, and
requiring evolution to achieve an exact, predetermined
result. Not only are each of these
conditions unrealistic, but they do not apply
even in the case of his chosen example. First,
he overlooks the existence of chloroquine resistant
strains of malaria lacking one of the
mutations he claims to be essential (at position
220). This matters, because it shows that there
are several mutational routes to effective drug
resistance. Second, and more importantly, Behe
waves away evidence suggesting that chloroquine
resistance may be the result of sequential,
not simultaneous, mutations (Science 298,
74–75; 2002), boosted by the so-called ARMD
(accelerated resistance to multiple drugs)
phenotype, which is itself drug induced.”

I hope these quotes are useful to you and your readers. As usual, Luskin is playing the “pretend” game of taking a new scientific paper and telling folks that it presents a “problem” for evolution. Ain’t life grand?

Best Wishes,

Ken

Comments

  1. Gerard O says

    The dope might even improve your performance. I assume you mean Sean B. Carroll, not Sean M. Carroll, although he probably knows more biology than Luskin.

  2. raven says

    Yeah Behe was just demonstrably, factually wrong.

    A few minutes at the National Library of Medicine turned up a malaria resistance genotype that required 5 mutations.

    Five. Five is greater than 2.

    Evolution occurs in a stepwise fashion, not often in a simultaneous fashion.

  3. Nerd of Redhead, Dances OM Trolls says

    Have these idjits ever built some as simple as a doghouse? It isn’t “poof”, the doghouse is there. It is start with this piece of wood, add another, and another, and you continue until you have a frame. Keep adding boards to the frame. Walls and roof appear. The walls need paint and the roof some shingles. Very piecemeal in how you go about it, and the order in which some things are done can be interchanged without effecting the final result. Now, if each board/paint/shingle is a mutation, how many are required?

  4. raven says

    Infect Dis. 2014 Jan 1;209(1):130-9. doi: 10.1093/infdis/jit415. Epub 2013 Aug 6.

    Ordered accumulation of mutations conferring resistance to sulfadoxine-pyrimethamine in the Plasmodium falciparum parasite.

    Mita T1, Ohashi J, Venkatesan M, Marma AS, Nakamura M, Plowe CV, Tanabe K.
    Author information Abstract

    BACKGROUND:

    Monitoring the prevalence of drug resistant Plasmodium falciparum is essential for effective malaria control. Resistance to pyrimethamine and sulfadoxine increases as mutations accumulate in the parasite genes encoding dihydrofolate reductase (dhfr) and dihydropteroate synthase (dhps), respectively. Although parasites are exposed to these antifolate drugs simultaneously, it remains virtually unknown whether dhfr and dhps mutations accumulate along interrelated paths.

    METHODS:

    We investigated the order of step-wise accumulation in dhfr and dhps by cumulative analyses using binomial tests in 575 P. falciparum isolates obtained from 7 countries in Asia and Melanesia.

    RESULTS:

    An initial step in the accumulation of mutations preferentially occurred in dhfr (2 mutations), followed by 1 mutation in dhps. In a subsequent step, mutations were estimated separately for 5 dhfr/dhps-resistant lineages identified using 12 microsatellites flanking dhfr and dhps.

    Among these lineages, we found 3 major mutational paths, each of which follows a unique stepwise trajectory to produce the most highly resistant form with 4 mutations in dhfr and 3 in dhps.

    CONCLUSIONS:

    The ordered accumulation of mutations in dhfr and dhps elucidated here will assist in predicting the status and progression of antifolate resistance in malaria-endemic regions where antifolate drugs are used for intermittent preventive treatment.

    There you go.

    “Among these lineages, we found 3 major mutational paths, each of which follows a unique stepwise trajectory to produce the most highly resistant form with 4 mutations in dhfr and 3 in dhps.”

    Here is an example of malaria drug resistance to sulfadoxine-pyrimethamine that requires 7 mutations.

    All you need to know that Luskin and Behe are wrong is to be able to count to at least 7. Anyone with a normal complement of fingers could do it.

  5. rhaeyga says

    Don’t they have to be simultaneous? Single mutations in PfCRT do not confer CQ resistance nor CQ transport activity. You need at least the 75 and the 76 mutations for CQ transport activity and an additional three mutations for CQ resistance.

  6. barbaz says

    I really fail to understand the following part.

    His argument was based upon an empirically observed data point from public health studies which found that chloroquine resistance arose in about 1 in every 10^20 organisms. […] He called the mutations (whatever they were) that caused chloroquine resistance a “chloroquine complexity cluster” or CCC. Whatever molecular mechanisms may be behind a CCC, empirical data showed that 10^20 cells are required in order to produce one. Behe pointed out that if a trait required the molecular equivalent of two CCC’s before providing any advantage, then that would pose major problems for Darwinian evolution.

    It’s a simple calculation. Behe observed that if 10^20 organisms were required to obtain one CCC, then the square of that amount — 10^40 organisms — would be required to evolve a trait that required two CCC’s before providing any advantage. However, as Behe observed, a total of only 1040 organisms have lived on Earth over the entire history of the planet.

    So, he argues that the resistance occurs only in 1 of 10^20 cells. But as the resistance requires two mutations, the probability for that to happen then is (10^20)^2.

    Can someone explain to me how this is supposed to make sense?

  7. robb says

    a couple weeks ago playing poker I actually flopped a royal flush. I won about $0.50.

    evilution disproved!

  8. Nerd of Redhead, Dances OM Trolls says

    Don’t they have to be simultaneous?

    No. All have to be in place for activity.
    In Lenski’s long term e-coli experiment, there was about 10,000 generations from the time an initial potentiating mutation occurred, until the final one that allowed uptake of citrate. If the mutations are neutral, they can stick around for a while.

  9. Dick the Damned says

    Once again, Casey Luskin demonstrates that he’s a biological ignoramus.

    Are you sure he’s biological, & not robotic.

  10. flippyshark says

    So, he pretty much wants you to admit that God designed the malaria virus. Ah, that perfect Divine Plan.

  11. raven says

    Don’t they have to be simultaneous? Single mutations in PfCRT do not confer CQ resistance nor CQ transport activity. You need at least the 75 and the 76 mutations for CQ transport activity and an additional three mutations for CQ resistance.

    No!!!

    Proc Natl Acad Sci U S A. 2014 Apr 29;111(17):E1759-67. doi: 10.1073/pnas.1322965111. Epub 2014 Apr 11.

    Diverse mutational pathways converge on saturable chloroquine transport via the malaria parasite’s chloroquine resistance transporter.

    Summers RL1, Dave A, Dolstra TJ, Bellanca S, Marchetti RV, Nash MN, Richards SN, Goh V, Schenk RL, Stein WD, Kirk K, Sanchez CP, Lanzer M, Martin RE.

    Author information Abstract

    Mutations in the chloroquine resistance transporter (PfCRT) are the primary determinant of chloroquine (CQ) resistance in the malaria parasite Plasmodium falciparum.

    A number of distinct PfCRT haplotypes, containing between 4 and 10 mutations, have given rise to CQ resistance in different parts of the world.

    Here we present a detailed molecular analysis of the number of mutations (and the order of addition) required to confer CQ transport activity upon the PfCRT as well as a kinetic characterization of diverse forms of PfCRT. We measured the ability of more than 100 variants of PfCRT to transport CQ when expressed at the surface of Xenopus laevis oocytes. Multiple mutational pathways led to saturable CQ transport via PfCRT, but these could be separated into two main lineages. Moreover, the attainment of full activity followed a rigid process in which mutations had to be added in a specific order to avoid reductions in CQ transport activity.

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

    The finding that diverse PfCRT variants are all limited in their capacity to transport CQ suggests that resistance could be overcome by reoptimizing the CQ dosage.

    Read it yourself. I’ve bolded the key points.

    You need 2 PfCRT mutations for low level resistance, 4 for high. PfCRT haplotypes have between 4 and 10 mutations.

    A key point is that they don’t have to be simultaneous. And we now know something about what the mutational pathways are.

  12. says

    You have to understand how their brains work. If there are existing genotypes with multiple mutations, that is not evidence that Behe’s model is wrong. Since it is a given that Behe’s right, those additional mutations confirm that evolution by natural mechanisms is impossible, and that a Designer has been at work right now.

  13. Kevin Kehres says

    HIV resistance to antiretrovirals is the same paradigm. One mutation is rarely enough to cause the whole regimen to fail — but stepwise mutations resulting in multi-drug resistance were pretty common in the days before triple-drug therapy.

  14. Nick Gotts says

    So, he pretty much wants you to admit that God designed the malaria virus. – flippyshark@12

    It’s not a virus, but a protozoan. Not that this affects your point.

  15. monad says

    I’ve often thought that if you really wanted to claim things were too complex to evolve – well, there aren’t any real examples, but some of the best to try from would be parasites with their elaborate life cycles, mind control, etc.

    Generally people don’t, though, because it would argue for a rather different designer than the one they want. So kudos to Luskin on this. Maltheists will be glad to know he agrees with them: life has a designer, and it likes malaria much more than it likes us.

  16. flippyshark says

    Thank you, Nick. My scientific ignorance is boundless, but hanging out here ameliorates that somewhat.

  17. raven says

    So, he pretty much wants you to admit that God designed the malaria virus. – flippyshark@12

    True. Most of the fatalities from malaria, over a million a year are…children.

    Luskin’s and Behe’s god is a child killing monster.

    Since gods are sockpuppets created by humans, that is telling us nothing about the gods but a lot we didn’t want to know about Luskin and Behe.

  18. Mobius says

    So Luskin thinks that drug resistance in the malaria parasite is Intelligently Designed, presumably by his God. Who supposedly loves mankind. Which is why He made it harder for mankind to control malaria parasites. Which are one of the great banes of mankind in tropical environments.

    This all makes me wonder if Luskin has even two working neurons.

  19. esmith4102 says

    The irrefutable fact “Casey Luskin demonstrates that he’s a biological ignoramus” before his demand for an apology is unchanged after his silly and uninformed demand.

    Wow, talk about a worthless waste of time! Except, that is, to the Clowns at the Discovery Institute.

  20. consciousness razor says

    So, he argues that the resistance occurs only in 1 of 10^20 cells. But as the resistance requires two mutations, the probability for that to happen then is (10^20)^2.

    Can someone explain to me how this is supposed to make sense?

    I’m trying to figure that out too.

    If the observed rate is actually 10^20, from which orifice is he getting the idea that the probability is the square of that? Assuming they’re equal, shouldn’t we instead figure each factor is roughly √(10^20) or 1 in ten billion, not equal to the total itself? I mean, even that is a stupid calculation, but at least it doesn’t seem completely fucking backwards. The observation of 10^20 is already taking both into account, not each of them separately. Am I missing something here?

  21. Rich Woods says

    @conscousness razor #22:

    Am I missing something here?

    Only that Behe doesn’t understand probability and/or arithmetic any more than he understands biology.

  22. spamamander, internet amphibian says

    @18

    I like to think that the fact that folks like us KNOW we are ignorant and seek to change that fact puts us a step above the unwashed masses. ;)

  23. rgmani says

    Maybe I am completely missing something here but if it is impossible to evolve drug resistance that involves two or more mutations (as Behe and Luskin seem to be suggesting), doesn’t it mean that pretty much every case of drug resistance is some kind of miracle wrought by God. Does it mean that every so often God snaps his fingers and makes yet another drug of ours ineffective?

    I thought the ID types have long since conceded that drug resistance could evolve – dumping it along with a bunch of other things in the “micro-evolution” bucket. Is Behe suggesting now that *any* useful change, no matter how small, requires a miracle?

    – RM

  24. addicted44 says

    @20

    God obviously created the Malaria virus to allow humans the free will to be born in a region where malaria is prevalent.

    Are you some sort of commie who hates FREEdUMB?

  25. says

    @consciousness razor #22

    I think the argument goes like this:
    Mutation rate is 1 in 10^20. That is the probability that any one mutation occurs at given time. Therefore it is the probability of one specific CCC mutation occuring at any given time. Therefore probability of two specific CCC mutations occuring at the same time is 1 in (10^20)^2. I think that is mathematically correct.

    However, that a given probability is low does not equal it is impossible, even if those mutations had to occur simultaneously. And backtracking from any event that has happened already and concluding, that it is improbable therefore it could not have happened by accident is statistical stupidity par excellence.

    What I find most amusing is the fact, that catholic Behe is arguing for “Ingelligent designer” who right now designs pathogens resistant to current cures in order to kill humans. To square that with the idea of loving God requires some pretty impressive mental gymnastic.

  26. busterggi says

    Don’t get too cocky PZ, you could outhink Luskin even if you were dead so a few drugs don’t make any difference.

  27. Amphiox says

    What I find most amusing is the fact, that catholic Behe is arguing for “Ingelligent designer” who right now designs pathogens resistant to current cures in order to kill humans. To square that with the idea of loving God requires some pretty impressive mental gymnastic.

    To be fair to Behe, IIRC correctly, he actually has addressed this point. He actually did state that he believes that an Intelligent Designer deliberately designed malaria resistance that kills children and that theologians would have to deal with that “fact”.

    I’m not sure this puts him in better a light though…

  28. Crimson Clupeidae says

    So, according to the IDiots:

    1. At one point in the not too distant past, CQ was the best treatment for malaria, with a high (nearly 100%?) effectivity.
    2. Now, some strains of malaria are resistant.
    3. Therefore, sometime in the easily recordable/searchable recent history, GOD in all his glory and magnificence appeared on earth, probably as an impressively huge wise old man with a beard (I’ve seen Monty Python, I know how this works, dammit!).
    4. There were, presumably, hundreds of thousands of witnesses, at least.
    5. Therefore, ID is proven true, and evolution turns out to be false after all.

    Checkmate atheists! (I know, needs more exclamations….)
    Since only the first two points of the above list seem to be true, and we know about genetic drift and random mutation, we can investigate and figure it out.
    Science is waaaaaay more interesting (and even more correct). :)
    That’s what annoys me so much about these hucksters. They always retreat to ‘we don’t try to explain how gawd does it, but we just know it can’t be evilution’… Meanwhile, real scientists figure out how it actually occurs. If they really wanted to show their position is scientifically accurate, wouldn’t they want to at least try to catch god the designer in action?

  29. rhaeyga says

    Don’t forget that Behe probably also believes in Satan, who might be a bioterrorist

  30. raven says

    To square that with the idea of loving God requires some pretty impressive mental gymnastic.

    Not really.

    The god of love is a modern invention.

    The fundies tossed it along with a lot of great ideas from the modern era, i.e. democracy, vaccines, modern medicine, equality, freedom, peace etc..

    Their god is a moral monster and intellectually, not the brightest bulb on the tree.

    Really, among the real victims of the fundie xians are satan and the demons. Their job was stolen and they’ve become redundant and unemployed.

  31. unclefrogy says

    in reading these discussions I try to guess what is it that the creationists are missing in all of it.
    as a metaphor humans being made out of the mud the lower dregs of earth kind of works OK as we are the result of a long chain of events and ancestors starting with simple self-replicating molecules “mud”
    It is plain to me that they are trying to fit what science reveals into there chronology and it does not fit at all it makes no sense. They fail to see the population instead of just the singe individual they can not grasp the implications of the time involved and the interconnectedness of all of life on earth.
    it is whistling past the grave yard of death, it is failing to understand that we are not something separate but were are made up of all of the lesser things of the very earth we stand upon.
    It is completely ego driven.
    reality is not a debate that can be won with rhetorical points no matter how far you torture logic.

    uncle frogy

  32. consciousness razor says

    Mutation rate is 1 in 10^20. That is the probability that any one mutation occurs at given time.

    That’s real data? And they’re both the same, just by coincidence? Or is it a theoretical prediction based on a bunch of assumptions about what the rate “ought to be”?

    Therefore it is the probability of one specific CCC mutation occuring at any given time. Therefore probability of two specific CCC mutations occuring at the same time is 1 in (10^20)^2. I think that is mathematically correct.

    Yeah, that would be fine. I was reading it as though the “CCC” is the whole shebang that produces the effect in question. It’s a “complexity cluster” for fuck’s sake, but now it just means one fucking mutation! Take this quote:

    He called the mutations (whatever they were) that caused chloroquine resistance a “chloroquine complexity cluster” or CCC.

    He waves his hands and says “whatever it is that does it is called X.” But X is apparently not the whole mechanism, whatever it is; each specific mutation is an X #1 and an X #2. I get that the objection about two (not) happening simultaneously makes sense that way, but it’s not very clear what his claim was actually supposed to be in the first place. I mean, I could dig through that paper from ten years ago for the data … but this is already some pretty silly stuff.

    However, that a given probability is low does not equal it is impossible, even if those mutations had to occur simultaneously.

    Yes. Impossible means a probability of zero (or a logical contradiction). That apparently confuses creationists a lot. But extremely unlikely things do tend to make us want some kind of an explanation. The idea that “some magic man wanted that way” is … well … it’s hard to even argue it’s coherent, much less explanatory.

  33. raven says

    Mutation rate is 1 in 10^20. That is the probability that any one mutation occurs at given time.

    WTH!!!

    Mutation rates run around 1 in 10 exp7-10.

    Probabilities are multiplicative.

    If we assume a quite low level of 1 mutation in 10exp10, two simultaneous mutations would be 1 in 10exp20. Which we see often.

  34. barbaz says

    @consciousness razor #31, charly #27

    The blog clearly says
    studies which found that chloroquine resistance arose in about 1 in every 1020 organisms
    That’s “resistance”, not “one required mutation”.

    Yes. Impossible means a probability of zero

    Actually, “impossible” can also mean that it’s too unlikely to happen in the given time frame. If the chance for the resistance to occur actually was 10^-40, that would be hard to explain.

    But apparently, the whole argument boils down to “we take this number from reality and square it. Now it no longer fits into reality, thus god.”

  35. consciousness razor says

    Actually, “impossible” can also mean that it’s too unlikely to happen in the given time frame.

    There’s no such thing as “too unlikely to happen in the given time frame.” (That’s presumably something larger than zero, or else your claim wouldn’t contradict what I said.) If there’s any chance at all that it happens in that time frame, then that’s what the chance is, obviously. It isn’t “impossible,” which means “not possible” or “cannot happen,” because it can happen, namely at some rate greater than zero (or not happening). Of course, if the probability is zero at some place or time, but not others, then you’re still talking about physical impossibility, only in that specific context. But if you think it “actually” means something other than “cannot happen,” I think you’re confused about how people tend to misuse the term or how they talk about it casually.

  36. Matt G says

    When I first got my iPad, I decided I wanted to include science and skepticism quotes in my signature. My very first one was Francis Bacon: “The root of all superstition is that a man sees when a thing hits, but not when it misses.”

  37. evodevo says

    It takes an estimated 2-8 mutations to produce a cancer cell IN THE SAME INDIVIDUAL IN AN OBVIOUSLY LESS THAN INFINITE TIME SPAN . He’s never heard of cancer? He thinks cancer is rare? None of his probability-fantasms make any sense. But then the audience he is writing for isn’t interested in reality anyway.

  38. says

    @raven #35

    WTH!!!

    Mutation rates run around 1 in 10 exp7-10.

    Probabilities are multiplicative.

    If we assume a quite low level of 1 mutation in 10exp10, two simultaneous mutations would be 1 in 10exp20. Which we see often.

    You are right, now I see where I misunderstood the original article and subsequently got confused along with consciousnes razor.

    The probability of occuring of two mutations mentioned in original blog post is 1 in 10^20 , also correctly as a multiplication of two probabilities of 1 in 10^10.

    That makes Behe’s argument even vorse, of course, because 1 in 10^20, despite being very, very high number, does not suddenly look so big given that there are milions of people infected with malaria per year and those pesky protozoans have probably populations in order of 10^10 and higher in each infected individual (my guess , I was not able to find a correct number on casual google search).

  39. raven says

    It takes an estimated 2-8 mutations to produce a cancer cell IN THE SAME INDIVIDUAL IN AN OBVIOUSLY LESS THAN INFINITE TIME SPAN .

    Good point.

    1. Probably that is just a minimum. One sees a lot more mutations by sequencing end stage cancers. Maybe up to 15 contribute to the phenotype.

    2. Cancer will kill 1/3 of the USA population, 100 million people. It’s not rare.

    3. Cancer is evolution in action. Somatic cell evolution to evade growth control, become immortal, move around, set up a blood supply, evade host defenses and chemo etc..

    Behe’s model of mutation in evolution is a strawperson.

  40. monad says

    @40 evodevo: Maybe he thinks cancer is a miracle, something visited on people by the special hand of a designer. I mean, if you’re going to argue antibiotic resistant malaria is like that, why not cancer?

  41. Doc Bill says

    Behe “picked” the value 1 in 10^20 from a review by Nicholas White that provides an estimate of the frequency of occurrence of a “CCC” – a complexity cluster. Unfortunately, I can’t lay my hands on the original reference but someone with Google Fu could track it down. If I recall, the estimate was in a footnote, of all things!

    Behe basically hijacked the number. He can’t derive it. He has no experimental evidence for it. The number doesn’t even pertain to what Behe’s talking about which is what made the entire discussion so maddening.

    Finally, Behe does state in Edge that the plasmodium was designed. Point blank he writes: it was designed.

    What a genius!

  42. chris61 says

    @44 Doc Bill

    There is nothing in the White reference that explains where the number comes from although one can infer that it is based on the number of times in which chloroquine resistance has emerged in the last 40-50 years along some ballpark estimates of how many malarial organisms are present on average in an infected individual and how many individuals are infected per year.

  43. says

    The strong presence of N (nitrogen) in chloroquine, exposed in parallel with the genetic make up of Plasmodium, explains why and how an unicellular organism can, quickly, search and captures chemical elements for re-enforcing itself, evolving resistance – if we considers the Matrix/DNA Theory formula. The debate between these two world views – PZ Myers x Behe – is again the repetition of a eternal natural process of evolution, where every time that Nature develops a new shape of systems, first appears the strong expression of two opposites, creating war, environmental chaos, till both coming to an agreement and creating a third new more evolved and complex world view. It is possible that two sequential mutations occurs inside a population of same species -as want PZ Myers – but, only if there is a natural selector agent acting with a purpose – and this, does not want PZ Myers. It is possible that an invisible creator is acting behind the two sequential mutations for creating a new species – as want Behe – but not under an intelligent abrupte and magical act of a divine God, and so, under a merely genetic process coming from a natural bigger and ancestral system – as does not want Behe… if we see the problem under the Matrix/DNA world view.

    I, myself, got simultaneously, the two species of malaria, Falciparum and Vivax, when at the hell of Amazon jungle doing the research that lead me to the Matrix/DNA worldview ( despite the fact that everyday, at 4:00 PM – the time that the mosquitoes comes from the rivers- I was taking a big capsule of chloroquine, as prevention against the malaria). It was under the mortal fever of malaria that I discovered the Matrix/DNA formula. Before that time I had no conclusions, my mind was a big conflict between atheism and creationism, occurring under the chaos of the salvage jungle, and the final result is a nowaday suspicion that the real thru is neither one, neither other, but something in between.

  44. vecordae says

    To that 10^20 number and the mystery involved with it.

    Here’s a breakdown of Behe’s position: 10^8 is the likelihood of any given gene mutating. For two genes to mutate at the same time and both come up “correct” for chloroquine resistance, the likelihood jumps to 10^16, minimum and 10^20 for certain. However, since the typical population of infecting organisms is only 10^12 and each infestation exists in some sort of isolation (presumably), then the scope of the existing population is so unlikely to produce the correct combination of genes that it is virtually impossible. However, since we see that combination did occur, that means God did it.

    If one were to replace the numbers and population sizes with a single six-sided dice, one can already see the problem:

    1 in 6 is the likelihood of a person rolling a 6 on single die throw. For two dice to roll a 6 at the same time, the likelihood jumps to 1 in 36. However, since you only get two throws, the scope of the dice available is so unlikely to produce two 6’s that it is virtually impossible. However, since you did roll two six’s, that means God did it.

    I hope that clears that up.