Wednesday, August 27, 2014

Michael Behe's final thoughts on the edge of evolution

We've been having an interesting discussion about chloroquine resistance and the Edge of Evolution. It began last month when Michael Behe started bragging that his "prediction" had been confirmed by a recent paper [A Key Inference of The Edge of Evolution Has Now Been Experimentally Confirmed]. It didn't take long for Casey Luskin to jump on the bandwagon [So, Michael Behe Was Right After All; What Will the Critics Say Now?]. Luskin demanded an apology from Behe;s critics.

It turns out that Behe and Luskin are wrong and the recent results published by Summers et al. (2014) actually refute most of Micheal Behe's calculations. PZ Myers pointed out that Behe's critics were mostly1 right when they criticized the original calculations in The Edge of Evolution [Quote-mined by Casey Luskin!].

Behe responded by issuing a challenge [An Open Letter to Kenneth Miller and PZ Myers] where he said ...
Talk is cheap. Let's see your numbers.

In your recent post on and earlier reviews of my book The Edge of Evolution you toss out a lot of words, but no calculations. You downplay FRS Nicholas White's straightforward estimate that -- considering the number of cells per malaria patient (a trillion), times the number of ill people over the years (billions), divided by the number of independent events (fewer than ten) -- the development of chloroquine-resistance in malaria is an event of probability about 1 in 1020 malaria-cell replications. Okay, if you don't like that, what's your estimate? Let's see your numbers.
I responded to the challenge [Taking the Behe challenge!]. I pointed out that these calculations are very difficult because there are many variables and many unknowns. I tried my best but, as it turns out, Behe wasn't satisfied. Now he's given us his final word on this topic [Drawing My Discussion with Laurence Moran to a Close].

Why is this important? Well, in a certain sense, it's not important because the main point in Behe's book is that some evolutionary scenarios are so improbable that they will not occur in lineages leading to large multicellular animals (like humans). That's because the population sizes are far too low—unlike the situation with malarlia parasites that have huge populations, fairly short generation times, and higher mutation rates. Nobody questions this point. It's true that the probability of many complex, specific, evolutionary pathways is so low that they are never going to happen in some species.

On the other hand, it's important because Behe describes something he calls a "chloroquine-complexity cluster" (CCC) that represents the probability of a cluster of mutations arising that confers chloroquine resistance. It's equal to 10-20—a number based on a guesstimate by Nicholas White (White, 2004). His earlier estimate was 10-19 where he says that "the estimates for chloroquine and artemisinin are speculative" (White and Pongtavornpinyo. 2003). Only ten chloroquine resistant strains have been detected.

There are many factors that affect the development of chloroquine resistant strains and only one of them is the frequency of mutation to resistance. White (2004) gives us a table that is quite revealing ....

A lot of different things have to happen before a chloroquine resistant strain becomes established. The combined probabilities, according to Nicholas White is 10-20. Behe uses this number as his estimate of the rate that the resistant genotype occurs (item #1 in the Table). This error has been pointed out to Michael Behe several times and here's how he responds in his latest post.
It takes chutzpah to deride a value calculated by one of the world's foremost malariologists -- a Fellow of the Royal Society, who lives and works in the middle of malarious regions of the world, who reasons deeply and quantitatively about the development of drug resistance -- as a "guesstimate." White's calculation was based on intimate knowledge of many details of the biology and epidemiology of the parasite.

Malaria is a horrendous scourge, and so is followed closely by international health organizations. In this age of easy and rapid sequencing, one would expect independent strains of malaria to be detected quickly by the many researchers in the area. If Professor Moran has any actual evidence that a large number of de novo origins of malaria have gone undetected, we would all love to see it. Otherwise it's reasonable to assume that the number so far identified is close to the number that have in fact arisen.
Keep in mind that Behe's calculations are critically dependent on the idea that the probability of the mutation occurring is 10-20. That's where he gets his CCC and that's the number he uses to discuss the probability of similar mutations during the evolution of complex species.

If it turns out that White's guesstimate incorporates a number of other factors then Behe's calculations are incorrect. Let's see what this famous malariologist says about whether parasites carrying the resistence genotype will automatically be detected as Behe says. I quote from page 1089 of White's 2004 paper.
Even if the resistance-bearing parasites do establish themselves in the anopheline mosquito, they must still be transmitted to a susceptible recipient for resistance to spread. In areas where the majority of the population is immune, the individual probability of propagation is reduced, as inoculation in a subsequent mosquito-feeding event often does not result in an infection capable of being transmitted (i.e., an infection generating sufficient gametocytes for onward transmission).

In high-transmission areas, where malaria-associated illness and death are largely confined to young children, the chance of a drug encountering large numbers of parasites in a semi-immune host is confined to the first few years of life. The net result is considerable reduction in the probability of de novo selection and subsequent transmission of a resistant parasite mutant in high-transmission compared with low-transmission areas. Historically, chloroquine resistance emerged in low-transmission areas, and antifol resistance has increased more rapidly in low-transmission than in high-transmission areas.
So, the expert that Michael Behe quotes says unequivocally that in high transmission areas a great many of the newly mutated organisms will not become established as a drug resistant strain. So it's reasonable to assume that the number detected is NOT close to the "number that have in fact arisen" as Behe claims. Somebody has chutzpah but I don't think it's me.

In my response to the Behe challenge, I tried to show some different calculations that gave different values for the mutation rate to chloroquine resistance. My guesstimates assume that at least two independent mutations are required and I arrive at double mutation rates that are much closer to 10-20 even if both mutations are neutral on their own. What this means is that chloroquine resistant individuals should be even rarer than Behe or White estimate.

I don't know how to explain this. It's a very complicated scenario and many of the estimates could be off by an order of magnitude.

One of the points of contention is whether the pathway to chloroquine resistance must involve a single mutation that is deleterious. If so, this would lower the probability of a resistant strain arising in the first place because the parasite with the first single mutation will likely die before the second mutation occurs.

This is where the data in the Summers et al. (2014) paper becomes relevant. They have a nice figure showing how the chloroquine resistant stains arose from a series of strains that acquired different mutations. The seven resistant strains are underlined (e.g. GB4). If you look at the group of strains on the left, you will see that there are two possible mutational routes to strain D32, which is not significantly resistant to chloroquine in the field even though it carries two essential mutations in the PfCRT gene.
In one pathway, the mutation N75E occurs first giving rise to strain D39 and then the K76T mutation occurs in that strain creating D32. The order of the mutations is reversed in the other pathway. In either case, the first mutation has no effect on the chloroquine uptake while the addition of the second mutation produces a significant effect.

It is important for Behe's argument that the "first" mutation is deleterious and he claims that the K76T mutations is, in fact, deleterious on its own. He says ....
Close your eyes and envision a pathway to a malaria parasite that has four mutations. The first mutation is deleterious, the second rescues the first and makes the parasite marginally chloroquine resistant. Subsequent steps are all beneficial by dint of either improving chloroquine resistance or of stabilizing the structure of the mutated PfCRT, which is required for malaria survival. Once a parasite can survive at least marginally in the presence of chloroquine, further mutations can be added one at a time (no longer two at a time) in each cycle of infection because the population size (1012) greatly exceeds the inverse of the mutation rate.

In the argot of chemical kinetics, getting beyond the deleterious mutation is the "rate-limiting step." After that hurdle is passed further mutations can be added singly -- the way Darwinists like -- and comparatively rapidly. Since they would be added rapidly, they would be difficult to detect in the wild. Hence the pattern described by Summers et al. fits the scenario I described perfectly.
Assuming that Behe is correct about the K76T strain (this is not certain), then the pathway N75E → K76T → strain D32 does not have an intermediate that is "rate-limiting" because the K76T mutation is never present on its own. It seems to me that ALL the pathways have to have a deleterious intermediate in order for Behe's scenario to make sense. In other words, both N75E and K76T have to be deleterious.

This neutral pathway to resistance has been observed. There's a strain in the wild called 106/1 that contains several different allelic variants in the PfCRT gene but it's sensitive to chloroquine. That strain becomes full-blown resistant to chloroquine in a single step when it acquires the K76T mutation (Cooper et al. 2007). Contrast this with Behe's explanation that requires two mutations to occur together in a single infected individual before you can get a resistant parasite.

Isn't that strange? Am I missing something?

As I said above, this quibbling about chloroquine resistance isn't very important to Behe's main complaint about evolution. We can all agree that some pathways are improbable and if he wants to use 10-20 as a point of departure then that's fine by me. Let's just make sure he describes it accurately and let's make sure he isn't claiming to have made an important prediction that was subsequently verified.2

But that's exactly what happened. Behe and his supporters (I called them sycophants, but Behe says that's childish) made it into a big deal by claiming that recent published results confirmed Behe's predictions. The implication here is that if Behe was so right about the science of chloroquine resistance then it's likely that he's right about the improbability of evolution.

As it turns out, he's wrong on both counts.

Let's look at how Behe describes his main thesis in his latest post. Keep in mind that this is his final position after seven years of debate and discussion since his book was published.
I wrote in my last post that I had cited chloroquine resistance in Edge as a likely example of the two-mutation phenomenon, and that Summers et al. recently "confirmed" that it did need two mutations to pump chloroquine. Moran responds, "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."

I'm afraid it is he who is playing the ingénue. There's a big difference between simply requiring serial additive mutations for some maximal effect and requiring multiple mutations before you get an effect at all. The first is a run-of-the-mill, gradualist Darwinian scenario: one mutation comes along, helps a bit, spreads in the population by selection, which increases the base from which the second mutation may arise; the second appears, helps a bit more, spreads, and so forth. Lather, rinse, repeat.

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.

How Much Does that Hurt?

Enormously. For most species, missing even one such baby step increases the required population size/waiting time by a factor of millions to billions. If even one step in a long and relentlessly detailed evolutionary pathway is deleterious, then a Darwinian process is woefully impaired. If several steps in a row are deleterious, you can kiss the Darwinian explanation goodbye.
I'm afraid Michael Behe is confusing me with some of his other critics. I never suggested that chloroquine resistance could arise by stepwise addition of two mutations where each one added a little bit of resistance and was, therefore, favored by natural selection.

I am not a Darwinist and I don't usually rely on adaptationist explanations for complex phenomena with low probabilities. I'm not a big fan of natural selection. In fact, I think I've mentioned other mechanisms on this blog. I think I've even talked about things like Neutral Theory and population genetics and tried to get IDiots to understand how neutral alleles and deleterious alleles can contribute to evolution.

It's sad that Intelligent Design Creationists keep referring to Darwinism and "Darwinian magic" because it confuses their readers. If Behe is simply objecting to a strict Darwinian process as an explanation of chloroquine resistance then I completely agree with him. It seems pretty clear to me that the pathway to a chloroquine resistant strain involved neutral alleles and possibly even slightly deleterious ones.

That's easily explained by modern evolutionary theory but not by the kind of Darwinism that Behe describes. Is that what this is all about? Is Behe's entire point just an argument in favor of random genetic drift and evolution by accident?


1. The debate gets a little complicated because some of Behe's critics really did misinterpret Behe's calculation and proposed a silly scenario for chloroquine resistance that doesn't agree with the data. There were, in fact, several reviews of Michael Behe's book that completely missed the mark. That's embarrassing.

2. I have a small stack of papers from prominent journals that propose multiple mutations behind chloroquine resistance. They were published BEFORE Behe's book appeared in 2006.

Cooper, R.A., Lane, K.D., Deng, B., Mu, J., Patel, J.J., Wellems, T.E., Su, X. and Ferdig, M.T. (2007) Mutations in transmembrane domains 1, 4 and 9 of the Plasmodium falciparum chloroquine resistance transporter alter susceptibility to chloroquine, quinine and quinidine. Molecular microbiology 63:270-282. [doi: 10.1111/j.1365-2958.2006.05511.x]

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. published online April 11, 2014. [doi: 10.1073/pnas.1322965111]

White, N.J. (2004) Antimalarial drug resistance. The Journal of clinical investigation 113:1084-1092. [doi:10.1172/JCI21682]

White, N. J. and Pongtavornpinyo, W. (2003) The de novo selection of drug-resistant malaria parasites. Proceedings of the Royal Society of London. Series B. Biological Sciences 270, 545-554.[doi: 10.1098/rspb.2002.2241]

216 comments :

  1. "If Behe is simply objecting to a strict Darwinian process as an explanation of chloroquine resistance then I completely agree with him"

    But that is exactly the point. Creationists like Behe and his ilk always refer to Darwinism, even after it is pointed out to them that modern evolutionary theory is greatly removed from Darwinism. They simply don't want to hear this.

    In fact, I suspect that authors at UD and other creationist sites have been instructed to use terms such as Darwinism as an intentional strategy.

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    1. Larry:

      A few points:

      (1) The number that Behe uses, 1 in 10^20 comes from the section of White's paper entitled: "Genetic basis of antimalarial drug resistance," while your extensive quote from White's paper comes from the section: "The central role of immunity in preventing the emergence and spread of resistance in high-transmission settings." This is a little like comparing 'apples and oranges.'

      (2) Here' what White wrote early-on in the "central role of immunity" section:
      In low-transmission areas, where infections are acquired infrequently (e.g., less than three times a year), the majority of malaria infections are symptomatic and selection of resistance therefore takes place in the context of specific antimalarial treatment. Relatively large numbers of parasites in an individual encounter antimalarial drugs. In higher-transmission areas the majority of infections are asymptomatic and these are acquired repeatedly throughout life. Symptomatic and sometimes fatal disease occurs in the first years of life, but thereafter malaria becomes increasingly likely to be asymptomatic. In areas of higher malaria transmission, people still receive antimalarial treatments throughout their lives, as the term malaria is often used to describe any type of fever, and most treatment is given empirically without microscopy or dipstick confirmation. But these inappropriate treatments for other febrile illnesses are largely unrelated to the peaks of parasitemia, which reduces the individual probability of resistance selection (8).

      What he's basically saying is that CR is going to develop in "low-transmission" areas because infected individuals in these areas are symptomatic, and so are given chloroquine early on. Hence, the parasites have something to fight against; something that doesn't happen so much in the high-transmission areas, because some kind of immunity already exists, and, because they remain asymptomatic until the population density of the parasite is quite high within them, fewer parasites are exposed to the chloroquine. But this only means, as I said above, that we would expect the CR parasites to emerge from the "low-transmission" area.

      (3) The list that White provides giving factors that determine the "probability of selection of de novo antimalarial drug resistance" also contains the same factors that White talks about in his paper when he discusses why the "in vitro" rate of CR is higher than the "in vivo" rate. This is probably why the rate is 1 in 10^12 ""in vivo" and not, say, 1 in 10^8, which is a figure that accords more with that of the parasite mutation rate.

      (4) Atovoquine resistance is also 1 in 10^12 in actual populations and not in the lab, and White points out that the AR involves only 'one' mutation. Again, we see that "in vivo", because of all the various effects, even AR is 1 in 10^12. This means that CR, involving two mutations present in the same parasite, is 1 in 10^20. If you want, you can say that "technically" we only need 10^16 replications to find the "Promised Land." But Behe's point still stands. 6 million years of the chimp/human divide, with even an average population of 10 million chimps, won't buy you a 2 a.a. change. Something else is going on. Why not admit that it's "design"?

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    2. But Behe's point still stands. 6 million years of the chimp/human divide, with even an average population of 10 million chimps, won't buy you a 2 a.a. change. Something else is going on. Why not admit that it's "design"?

      Yeah, it couldn't be anything like genetic drift, or all mutations not being vanishingly unlikely, or the central fact that when you look at the chances of *one particular* evolutionary path occurring, you're looking at the wrong thing (i.e., your probability math will be wrong), now could it?

      Watch, Lino, I'll use Behe's Evolutionary Probability Calculation to prove you don't exist:

      - Probability of your parents marrying each other (number of people on Earth when they met): 1 in say, 5 billion. Probability of each of their sets of parents marrying: about 1 in 3 billion. So right away it's 1 in 4.5 x 10^27 odds against you being here and we've only gone back a couple generations.

      See how easy that was? I can prove *anything* is impossible, just by using Dr. Behe's version of probability math!

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    3. Funny, judmare, but all you've demonstrated is that the "true believers" in evolution can make numbers do anything they want them to. That's the problem. Then the numbers become meaningless. And you end up knowing nothing.

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    4. "But Behe's point still stands. 6 million years of the chimp/human divide, with even an average population of 10 million chimps, won't buy you a 2 a.a. change."

      Well, we didn't evolve from chimps, but anyway. This is the quintessential IDiot point, and it commits the same basic fallacy we have been trying to knock into their thick skulls since the beginning. There's no use trying to calculate the odds of two specific mutations, that will always give a ridiculously low number.

      Do it, go to the Lenski experiment, pick the starting clone of the experiment and compare it's genome with any one of the latest sequenced strains. It will have over 600 mutations. Now calculate the odds, at the beginning of the experiment, that those 600 specific mutations would happen. You're going to get a smaller number than 2 specific mutations in the human genome.

      What does that number mean then? Nothing, it's the same basic fallacy, the bridge hand fallacy over and over again. Why are they so impervious to this simple principle?

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    5. Lino, you are not getting it.
      "Funny, judmare, but all you've demonstrated is that the "true believers" in evolution can make numbers do anything they want them to. That's the problem. Then the numbers become meaningless. And you end up knowing nothing"
      This is EXACTLY what Behe is doing with his numbers. Don't you see that?

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    6. Something else is going on. Why not admit that it's "design"?

      What, leap straight from the probability of 2 specific aa changes in a particular selective regime, straight over the combined probability of beneficial 2-aa changes somewhere and the very significant roles of Drift and Recombination, to a conclusion of Design? That would be a little hasty. Jibes about 'true believers' in evolution conveniently ignore the fact that there are reasons to consider evolution capable of making change unaided. Stick the telescope to your good eye.

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    7. Very good, Lino Di Ischia. You've just reaffirmed exactly the same flaws in Behe's arguments that Larry identified, only you don't realize it. Do you really think that the exact same factors that limit the expression of of CR in P. falciparum also apply to every single novel trait that has arisen in humans and chimps since their divergence from a common ancestor?

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    8. curiously Allen, just how did organisms acquire the ability to 'utilize' drift and recombination???

      They just happened to stumble upon a 'Powerball moment', I take it??!!

      But how can such 'I really have no F@#$n' idea but dont tell 'em that" 'explanations' be of any use to a scientist??

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    9. actually lutesuite, Behe is well on the way to showing that in fact it is you(pl) that imbibes flawed logic.

      No wonder evolutionary biology is in a funk. Your (pl) intransigence is legendary.

      Carry on.

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    10. "curiously Allen, just how did organisms acquire the ability to 'utilize' drift and recombination???"
      This question is so dumb it boggles the mind. The same way water "acquires the ability to 'utilize'" a mountain slope to form a river at the bottom

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    11. Funny, judmare, but all you've demonstrated is that the "true believers" in evolution can make numbers do anything they want them to. That's the problem. Then the numbers become meaningless. And you end up knowing nothing.

      Lino, just read Arlin's comments, and for further education, the article he linked to in a peer reviewed scientific journal (that cites Behe, by the way). You'll see the opposite of what Behe does, and what I did above - instead of focusing incorrectly on *one individual outcome*, as Dr. Behe does with chloroquine resistance, and as I just did showing it's "impossible" that you exist, Arlin and the paper he cites begin to rigorously evaluate evolutionary probabilities as a whole. They don't focus incorrectly on a single outcome, but instead do the proper thing from a probability math point of view by attempting to take all possibilities into account.

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    12. curiously Allen, just how did organisms acquire the ability to 'utilize' drift and recombination???

      Did I say 'utilize'? Nope. Drift is an inevitable consequence of birth and death. Recombination is probably a side-effect of meiotic crossover, which assists accurate gametogenesis. But they do have long-term consequences. They have significant roles in the progression of an evolutionary trajectory. They permit connection of points in genetic space having deleterious intermediates, because it's not all the 'RM+NS' cartoon that Creationist hacks portray.

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    13. das Kapitalist asked:

      "What do you prefer to be called?"

      judmarc suggested 'Non-IDiots", and here are some other suggestions that may be acceptable to non-IDiots:

      realists
      sane people
      scientists (whether amateur or professional)
      evolutionists
      naturalists
      non-believers in religious fairy tale 'Gods'
      non-creationists
      non-IDiot-creationists

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    14. Judmark: "So right away it's 1 in 4.5 x 10^27 odds against you being here and we've only gone back a couple generations.'

      I think that you may be off by many orders of magnitude on your estimate of probability that Lino exists. You forgot to factor in the fact that one specific ovum out of 400,000 potential ova must have been fertilized by one specific sperm cell out of hundreds of millions available.

      When you include these numbers, there is no way that Lino exists; at least according to Behe's logic.

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    15. Yeah, I was thinking about going there (quarter of a billion sperm each time, say 100 times just to be quite conservative and still use round figures, now we're up to something like 1 in 10^41 without even considering ova; then start multiplying this by ~2,000 generations of modern humans where two people had to find each other among all the humans on Earth at the time...), but I figured just to show how stupid this all becomes without all that explication, taking the chances that two specific people would mate out of the world population at the time over a couple of generations would suffice nicely.

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    16. lutesuite:

      Very good, Lino Di Ischia. You've just reaffirmed exactly the same flaws in Behe's arguments that Larry identified, only you don't realize it. Do you really think that the exact same factors that limit the expression of of CR in P. falciparum also apply to every single novel trait that has arisen in humans and chimps since their divergence from a common ancestor?

      This is exactly what I wasn't saying. Read what I wrote again.

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    17. Allan Miller:

      What, leap straight from the probability of 2 specific aa changes in a particular selective regime, straight over the combined probability of beneficial 2-aa changes somewhere and the very significant roles of Drift and Recombination, to a conclusion of Design?

      Allan, in my calculation in point #4, I used an effective population size of 10 million. Per population genetics, it would take genetic drift 40 million years to "fix" a mutation in such a population, so genetic drift is even worse.

      Are you ready to take the leap yet?

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    18. Dontcha love Mikkel's one-liners. He compares life to a a river.

      Talk about boggling the mind.

      MIkkel hasn't done all that much exploring, has he? Hasn't done that much research on bacterial intelligence, has he?

      Nah. He can't 'see' God, therefore bugs and rivers are the same thing.

      LMAO!!!



      Mikkel the Finn: "This question is so dumb it boggles the mind. The same way water "acquires the ability to 'utilize'" a mountain slope to form a river at the bottom"

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    19. judmarc:

      - Probability of your parents marrying each other (number of people on Earth when they met): 1 in say, 5 billion. Probability of each of their sets of parents marrying: about 1 in 3 billion. So right away it's 1 in 4.5 x 10^27 odds against you being here and we've only gone back a couple generations.

      If your logic is this: there are 10 billion people on earth, and, since you marry one one of them, the odds of marrying another person on this planet is 1 in 5 billion.

      But, may I ask, how many opportunities does each of my parents have, using the above logic, to marry someone? The answer: 5 billion. Hence, the likelihood that they would marry is 5 billion x 1 in 5 billion = 1.0 Should I go on?

      How does a "particular" mutation arrive in some organism's genome? Well, on average, since the odds of that "particular" point mutation occuring is 1 in 10^9 generally, it requires however many generations is needed to arrive at 10^9 mutations being produced using the organism's mutation rate.

      Do you see the parallel between this calculation and my calculation above?

      You're generating meaningless probabilities. Nothing more.

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    20. But, may I ask, how many opportunities does each of my parents have, using the above logic, to marry someone? The answer: 5 billion. Hence, the likelihood that they would marry is 5 billion x 1 in 5 billion = 1.0 Should I go on?

      No, you needn't. That's more than enough to confirm what an absolute imbecile you are.

      I one of your parents had married one of the 5 billion other people who were not your parent, then you wouldn't exist. Or is that too complicated for you?

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    21. Lino,

      But, may I ask, how many opportunities does each of my parents have, using the above logic, to marry someone? The answer: 5 billion. Hence, the likelihood that they would marry is 5 billion x 1 in 5 billion = 1.0 Should I go on?

      Exactly IDiot. By the very same token, the probability that any offspring will carry a bit more than just one mutation is that close to 1. Behe is calculating the probability of a specific outcome, just like judemark was calculating a specific outcome (you). Had your parents married someone else you would not be there. Are you starting to get it now?

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    22. Steve,

      Mikkel's answer was superb, and that you would miss the point only confirms Mikkel's observation that your question is so dumb that it boggles the mind. Evidence thus accumulates that you might be as dumb as your question. Try and use your brain next time if you rather not let us reach that conclusion.

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    23. lutesuite:

      Imbecile: really?

      What are the odds of people getting married? Quite high. What are the odds of them having children? Quite high. What are the odds of my existing? Quite high.

      Now let's look at your numbers: is it realistic to believe that my mother, say, had the choice of any one of 5 billion men? No. And what about her mother? No.

      My parents happen to come from an island where the populations are inbred. And when you go back even a short distance in time, you have populations that don't move around much, so it is rare that outside members are added to the local population. So your numbers are absolutely specious, orders of magnitude off.

      But I'm not going to call you a name. I'll just point this out to you.

      Going on, if, OTOH, what you're getting at is the probability of my having my exact genome, then that's a quite low number.

      Yet you wrote: So right away it's 1 in 4.5 x 10^27 odds against you being here and we've only gone back a couple generations. Notice you said the “odds against [me] being here” and did not say “of you having the exact genome you have." Things like spontaneous abortion rates and the likelihood of lethal genetic defects within my particular lineages would affect the “odds of my being here.”

      Let's look at these things in a different context: contrary to what Mark Perakh has written--and many Darwinist defenders as well--the probability of dealing a hand of bridge is not some huge improbability; it’s actually 1.0. People do it all the time. OTOH, it's only the probability of dealing a particular hand, e.g., a hand that is composed of the ace -through-king of a particular suit, that is quite low, indeed.

      To be more specific, dealing a hand is a quite straight-forward task: you deal all 52 cards to four individuals. Unless you're paralyzed, you can accomplish this. It will happen IMMEDIATELY. “Odds” of accomplishing this task? 1.0

      However, if you sit down and now say to yourself, I'm going to deal out four hands to imaginary people, and reshuffle and deal again, until I deal a hand that is ace-through-king in one suit, this might take you FOREVER. IOW, you’ll likely die before this happens.

      Do you see the difference? In one case, nothing is "specified"ahead of time, while in the other, something is indeed "specified" ahead of time. So, if we start talking about "specific" mutations being needed, then the improbability of these “mutations” being “dealt,” so to speak, via replication now becomes pertinent. It comes into play; and, it is quite low.

      So, to summarize, the odds of my parents having a human child is 1.0. Yet the "odds" of this child having my particular genome is quite low. I hope this is clear now.

      In the case of the malarial parasite, this distinction must be applied. We can't simply look at this a case of one malarial parasite producing any, old offspring it can. UNLESS certain "specified" mutations are present, the parasites will die in the presence of chloroquine, and that particular vector population of malarial parasite will die out if the "specified" mutations are not produced in the replicate. So the odds, if you will, of "having a child with a particular genome" are quite low in the malarial lineage such that in the case of very “specific” mutations needing to be present, the improbability of malarial life continuing on from one generation to the next hangs in the balance and is DEPENDENT on overcoming this improbability.

      This is certainly not the case when it came to my mother and father having me as a child.

      These differences must be respected if we hope to make sense of things.

      Delete
    24. photosynthesis:

      Exactly IDiot.

      I was beginning to think that there was a better caliber of Darwinist posting here. Now I see that it's the same crass tactics as always. You're not interested in understanding things, but thinking yourself to be right. That's a good way to remain blind to things.

      And it wasn't judemarc, it was lutesuite. And look at my response. lutesuite didn't talk about the improbability of my exact genome, but of my existence. These are two entirely different concepts. His numbers in the case of my genome are way off. It's tied up with the whole notion of an "effective" population as opposed to the entire population--something he didn't bother to take into account.

      Delete
    25. This Steve fellow is an excellent front-man for IDiocy, I say let him keep posting. The contrast an only serve us well.

      Delete
    26. Allan, in my calculation in point #4, I used an effective population size of 10 million. Per population genetics, it would take genetic drift 40 million years to "fix" a mutation in such a population, so genetic drift is even worse.

      Are you ready to take the leap yet?


      No, because I actually understand the relevance of drift!

      1) You mean 40 million generations.

      2) Drift fixes neutral mutations at the neutral mutation rate, irrespective of population size. You get just as much neutral change in a large population as a small one. In a steady-state 10 million, each one takes a theoretical 40 million generations, but the larger population is generating more in exact proportion.

      3) See my points elsewhere about effective population size in Plasmodium. Because they go via multicellular hosts, and are sampled, Plasmodium cells do not have effective population sizes anywhere near the cell count, and drift occurs much more rapidly.

      4) My point was not actually about fixation at all, but about the capacity of drift to traverse paths that contain deleterious intermediates, where deterministic selection could not. It is not necessary that the deleterious intermediate be fixed in the population, but merely that it survive in the population for a sufficient period to provide a pool in which the second mutation can occur - either directly, or by recombination between 2 such subpopulations. This is why the mutations don't have to be simultaneous - I think even Behe now accepts that, and therefore, whether he and you realise it or not, he accepts the capacity of drift to create a pool of alleles even if there is no positive selection for them. And such a pool can be sustained even if there is selection against them - particularly if the wider population is not efficiently mixed, or is subject to founder effects ... like these ones.

      Delete
    27. Is Lino actually saying that no matter who his mother or father married out of all the population on the planet HE would be born?

      Delete
    28. Per population genetics, it would take genetic drift 40 million years to "fix" a mutation in such a population, so genetic drift is even worse.

      Why on Earth would the mutation have to be fixed in the population?

      Delete
    29. What are the odds of people getting married? Quite high. What are the odds of them having children? Quite high. What are the odds of my existing? Quite high.

      Hi, Lino. You're still missing it, "it" being the key to why both I and Dr. Behe are, in your words, "generating meaningless probabilities."

      Have a look at your words that I've quoted above, particularly the ones in bold. The mistake that both you and Dr. Behe make, and that I tried to point out with my "meaningless probabilities" is that one cannot, as you and Dr. Behe do, switch between the general ("people" getting married and having "children") and the particular ("my" existing) and simply carry the probability calculations unchanged between them.

      To put it much more simply: The probability that your parents would get married and have children is, as you note, quite high. That is the *general* case. The probability they would marry *each other*, of all the people in the world, and have *you*, of all the possible combinations of their genes, is microscopic. Any time you look at the probability of one very specific event occurring in the entire history of humans, or even life, on earth, you come up with microscopic possibilities, because there are so many alternatives. This is true even of the most prosaic and commonplace events, such as having children, if you restrict the outcome to one specific possibility - you, for instance. And the very same is the case for Dr. Behe using the probability of one very specific sequence of mutations - chloroquine resistance in Plasmodium - as a stand-in for the general case of something that occurs all the time, mutations and inheritance of those mutations at different rates in succeeding generations.

      There are indeed interesting evolutionary issues here - once again I commend to you Arlin's comments and the scholarly article he links to - but they are not regarding whether evolution can be the reason we see so many different forms of life around us. The answer to that has been well settled for a long time, and it's yes. Rather, the interesting stuff is to figure out what the constraints are on evolution, and various ways in which evolutionary events we might expect to be quite rare may actually be less so (you can read about some of these in that very interesting scholarly article, which makes an attempt at quantifying the effects it discusses).

      Delete
    30. @LIno:

      Imbecile: really?

      Really.

      @ Pedro:

      Is Lino actually saying that no matter who his mother or father married out of all the population on the planet HE would be born?

      No. He's saying that it's a really dumb argument to say that, because it is almost impossible that he, himself, would have existed, therefore it is almost impossible that anyone could exist. And he's right, it IS a dumb argument. That's the point.

      However, he thinks it's a really, really good argument to say that, because it is almost impossible that chloroquine resistance could arise in P. falciparum, that means it is almost impossible for any novel trait requiring two mutations to arise in any organism. That's because it's one of his fellow IDiots making the argument. And because Lino is an imbecile.

      Delete
    31. Lino,

      I was beginning to think that there was a better caliber of Darwinist posting here.

      I wouldn't know. I'm not a Darwinist.

      Now I see that it's the same crass tactics as always. You're not interested in understanding things, but thinking yourself to be right. That's a good way to remain blind to things.

      There goes another of my irony meters. Lino, that particular mutations have given rise to chloroquine resistance in Plasmodium does not mean that such is the one and only possible way for that to happen. That particular neutral/semi-neutral/deleterious/advantageous mutations have such and such low probability to being fixed in a population (as in been spread in all of its members), does not mean that the mutations don't exist in any member of the population, that non-fixed mutations exist all over the place makes the case for mutation/drift/selection nicely. You refuse to understand. Maybe evolution is all wrong. But if it is wrong, it's not because of something that would be so obvious. If it was as easy as calculating a probability for an event after-the-fact, we would have abandoned the theory long time ago. But it's simply not so. We don't know how many ways are there to evolve, but we know it's not about very particular outcomes. We have tested the random-mutation/recombination/selection scheme in both the lab and simulations, and it works in both. It's exactly as you say. The probability of your mother marrying is close to 1. But that it would be with your father is a bit less, and that you would be the guy born is close to nothingness. But that's meaningless because there you are. It's a different question whether you would be born or that your mother would have had some children. That is exactly the point those guys are trying to get you to understand and yet you refuse.

      And it wasn't judemarc, it was lute suite.

      Really? Find this:
      judmarc Wednesday, August 27, 2014 10:10:00 PM

      And look at my response. lutesuite didn't talk about the improbability of my exact genome, but of my existence. These are two entirely different concepts.

      So if your mother only had a 15 year old girl that girl would be you?

      His numbers in the case of my genome are way off. It's tied up with the whole notion of an "effective" population as opposed to the entire population--something he didn't bother to take into account.

      His numbers were an oversimplification, but we can play probabilities any number of ways and the exact you would still be quite improbable. The real problem is that the question is not whether you would be born, but whether any person would be born. Then the probability would be huge. Same with evolution. As far as the data shows, there's many avenues for evolutionary outcomes, and after-the-fact probabilities about it are, as you phrase it, meaningless.

      See ya.

      Delete
    32. Lino spewed:

      "Notice you said the “odds against [me] being here” and did not say “of you having the exact genome you have.""

      And:

      "lutesuite didn't talk about the improbability of my exact genome, but of my existence. These are two entirely different concepts."

      NO, for the purpose of lutesuite's points (and points made by others) they are NOT two entirely different concepts.

      Lino, you truly are absolutely imbecilic. You obviously think that the sane, honest, knowledgeable people here are way too stupid to see through your ridiculous distortions of what has been said. For the purposes of what has been said to you, your genome and you are EXACTLY the same thing.

      You're now making some of the same points that have been explained to you numerous times but you're pretending that those points are your original arguments. Throughout this entire debate you have asserted that particular outcomes are extremely improbable but when the improbability of your particular existence was explained to you you distorted what was said and suddenly it's all about the likelihood of anyone's existence in general.

      Because you can't make an honest, intelligent argument you go around and around and around making stupid arguments that contradict what you have asserted previously and you dishonestly ignore the FACT that what you're now asserting has already been explained to you by others in an attempt to get you to understand the improbability of your particular existence (yet, unfortunately, you do exist although you could be a robot like Byers).

      Your assertions are so confused that it's hard for me to believe that anyone could be as imbecilic as you are, but your words are clear and convincing evidence that you really are dumber than a box of rocks.

      Delete
    33. I think that we should stop calling Lino an imbecile. After all, by his own admission, he is not responsible for his low intelligence.

      'My parents happen to come from an island where the populations are inbred."

      That explains so much.

      Delete
    34. Well, in fairness, according to the original medical classication, Lino might well be just moron, rather than imecile, since his language suggests his IQ could be above 50:

      http://en.wikipedia.org/wiki/Imbecile

      At the very least, though he is an IDiot, his parents can proudly say he is not an idiot. That's probably quite an achievement on the island of inbreds from which he hails.

      Delete
    35. Could I make a humble request that we drop the name-calling? Ta.

      Delete
    36. Allan Miller wrote:

      "Could I make a humble request that we drop the name-calling? Ta."

      You can't be serious...!?

      Name calling, especially "IDiot" is the best ammunition the stubborn evolutionists/atheists have when they have no arguments or scientific evidence...against creationist...

      Delete
    37. judemarc: (Part 1)

      We have tested the random-mutation/recombination/selection scheme in both the lab and simulations, and it works in both. It's exactly as you say. The probability of your mother marrying is close to 1. But that it would be with your father is a bit less, and that you would be the guy born is close to nothingness. But that's meaningless because there you are. It's a different question whether you would be born or that your mother would have had some children. That is exactly the point those guys are trying to get you to understand and yet you refuse.

      The malarial parasite is a really straight-forward experiment that tests for the powers of NS and genetic drift to solve a life-or-death situation. The selection coefficient is hence: 1.0. All we have to do is wait till these genetic mechanisms find a solution, look at the solution, and then generate number associated with this process. Behe has done this. The bottom-line is that it took 10^20 replications of the parasite for CR to arise, and the minimum number of mutations for this to arise is 2.

      Those are all the numbers you need to know.

      As to simulations, Behe and Snoke did a simulation. And their numbers from that simulation support the result of the CR developing in P. falciparum.

      The numbers above are facts. You can deny their meaning if you like. That is your choice.

      As to me understanding the distinction between the odds of my parents marrying and my existence, and the probability of my genome existing, this misunderstanding on the part of Darwinists is where the problem lies.

      (Part II follows)

      Delete
    38. (Part II)

      Mark Perakh has written that the probability of a bridge hand ace-through-kind in one suite is the same as the odds of any other bridge hand. All this means is that the number of permutations of a 52 card deck dealt into four hands are so many, and that each “hand” is equivalent to any other because in the set containing all these permutations each “hand” only appears “once.”
      Then we have Darwinists coming along and saying (similar to what you said above in the quote): Well, see the probability of any of these “hands” is really, really low. Yet there you are. You’ve been dealt a “hand.” There it is.
      But this is nonsense. To help us see this, all we have to do is ask this question: what is the probability that the ‘hand’ you will be dealt the next time you play bridge will fall outside of the set of all permutations of a 52 card deck dealt four ways? The answer is zero. Hence, the probability that your hand will fall within this set is 1.0.
      By definition, the probability that a mutation will occur somewhere along the length of a genome is 1.0. But the odds of a mutation occurring at particular point along the length of that genome is 1 divided by the length of the genome.
      Similarly, the “odds” of a bridge hand turning up is 1.0. The “odds” of a particular bridge hand—no matter which one you specify from within the set of all permutations—is 1 divided by the total number of permutations in the set. You could, e. g., “specify” the 2,4,10, J of Clubs, the 3,8,J,Q of Hearts, etc. All that matters is that within that set of all permutations, you put a circle around one of them, and then try and “hit” that ‘circle’ when you deal. All of this is likewise true of the genome and “specific” mutations along its length. This is an error in thinking that Darwinists continue to make, and continue to insist on. But all their protestations given, it still doesn’t make it true.
      Now, as to Behe’s work, no one contests that the odds of a particular mutation showing up is around 1 in 10^8. No one disagrees with this. Behe’s contention is that, based on the example of a well-studied real-life adaptational process, more than one ‘step’—here a ‘step’ is a particular mutation being present somewhere along the length of the genome—is required in the case of CR. That is, the adaptational pathway from no resistance to resistance requires two such ‘steps,’ not just one. Simple probability calculations tell us that the chance of this occurring should be in the ballpark of 1 in 10^16, thus requiring 10^16 replications. It turns out to be 10^20 replications that are needed. Again, we’re in the ballpark with these figures. They line up with one another.
      Darwinists simply don’t want to accept what these numbers mean. Again, that’s your prerogative.

      Delete
    39. judmarc:

      Lino, just read Arlin's comments, and for further education

      But on this thread, Arlin's comments are nowhere to be found. So you'll have to indicate where they are.

      Delete
    40. lutesuite:

      Pedro poses the question:Is Lino actually saying that no matter who his mother or father married out of all the population on the planet HE would be born?

      And lutesuite answers:
      No. He's saying that it's a really dumb argument to say that, because it is almost impossible that he, himself, would have existed, therefore it is almost impossible that anyone could exist. And he's right, it IS a dumb argument. That's the point.

      However, he thinks it's a really, really good argument to say that, because it is almost impossible that chloroquine resistance could arise in P. falciparum, that means it is almost impossible for any novel trait requiring two mutations to arise in any organism. That's because it's one of his fellow IDiots making the argument. And because Lino is an imbecile.


      lutesuite, try and keep up.

      You’ve managed to completely misunderstand the argument.
      judmarc, OTOH, has understood it, and agrees.

      The point is this: that I, a human being exist, is not that an improbable an event. That I have the particular genome I have is a very improbable event. judmarc did not make that distinction sufficiently clear, and I took advantage of that to make my point.

      Pretend you’re in a science lab at UC Berkeley. In that lab there are 100 rabbits being used for an experiment. One of the rabbits has a litter. Would you say that the probability of that rabbit existing is 1 in 10^27? No. It is a very likely event.
      You could, however, say that the probability of that rabbit having its particular genome is 1 in 10^27 (these are just numbers to throw around, not actual computations). Has the fog cleared?

      If you were near me and called me an imbecile, I would likely punch you in the nose. Don’t take advantage of the distance between us to make such ignoble remarks.

      Delete
    41. the whole truth:

      NO, for the purpose of lutesuite's points (and points made by others) they are NOT two entirely different concepts.

      Consult my response to lutesuite, especially the last part.

      Delete
    42. The point is this: that I, a human being exist, is not that an improbable an event. That I have the particular genome I have is a very improbable event. judmarc did not make that distinction sufficiently clear, and I took advantage of that to make my point.

      Then why did everyone else understand that was what I said? Come on, Lino, it is not necessary to make erroneous statements about what others have said.

      Delete
    43. Arlin's comments are in the Understanding Michael Behe thread here at Sandwalk on August 25th at 7:41 am. The scholarly article he cites is at http://mbe.oxfordjournals.org/content/27/6/1404.full.pdf+html

      Delete
    44. Lino: By definition, the probability that a mutation will occur somewhere along the length of a genome is 1.0

      In which area is your ignorance greater, maths or biology?

      Delete
    45. Lino the imbecile wrote:

      Pretend you’re in a science lab at UC Berkeley. In that lab there are 100 rabbits being used for an experiment. One of the rabbits has a litter. Would you say that the probability of that rabbit existing is 1 in 10^27? No. It is a very likely event. You could, however, say that the probability of that rabbit having its particular genome is 1 in 10^27 (these are just numbers to throw around, not actual computations).

      Right. And why would someone then say that, because the chance of a rabbit having a particular genome is 1 in 10^27, therefore the chance of any rabbit existing with any genome at all is 1 in 10^27? You know, like you and Michael Behe are arguing with regards to any trait that requires two mutations? The best explanation I can give is that the two of you are imbeciles. Or maybe just morons, it's hard to tell.

      Delete
    46. Lino writes:

      Now, as to Behe’s work, no one contests that the odds of a particular mutation showing up is around 1 in 10^8.

      Here, once again, is where you and Behe are wrong. The math for evolution is very much like the math for a lottery. The odds against a particular person winning the Powerball lottery, are, like the odds against a particular mutation occurring and becoming fixed in the population, quite large (in the case of the Powerball, 175 million to 1).

      Yet someone wins the Powerball every few weeks; and similarly, some mutations occur and become fixed in populations of various life forms so routinely and reliably that scientists can speak of and write about "molecular clocks."

      Such a "molecular clock" has been worked out for the evolution of humans from a common ancestor with apes. It does not require any sort of speedup; the usual mutation rate works just fine. Yet if you looked at the complete mutational path between the ancestor and humans of a particular bit of the genome over millions of years, you could justifiably say that particular path was vanishingly unlikely. Now read this last part very carefully: Since it can be true both that any particular mutational path of any length is very unlikely, and that evolution in general is quite routine, the former statement is not a logical disproof of the latter.

      Understand?

      Delete
    47. Allan Miller wrote:

      "Could I make a humble request that we drop the name-calling? Ta."

      Quest

      You can't be serious...!?

      Name calling, especially "IDiot" is the best ammunition the stubborn evolutionists/atheists have when they have no arguments or scientific evidence...against creationist...


      Jesus Christ Quest! I and numerous others have written post after multi-paragraphed post detailing objections to Behe's argument, with not a whisper of bile. You haven't addressed one single word of it. No arguments my arse!

      Delete
    48. The malarial parasite is a really straight-forward experiment that tests for the powers of NS and genetic drift to solve a life-or-death situation. The selection coefficient is hence: 1.0.

      Not having chloroquine resistance is lethal? That can't be right. I think you might need to take another look at what a selection coefficient represents.

      All we have to do is wait till these genetic mechanisms find a solution, look at the solution, and then generate number associated with this process. Behe has done this. The bottom-line is that it took 10^20 replications of the parasite for CR to arise, and the minimum number of mutations for this to arise is 2.

      Well, one could perhaps agree arguendo that something of the order of 10^20 genome replications occurred between CR strains reaching detectable levels. But if genome replications are what we are counting, multicellular eukaryotes can also toss off that kind of number in a few million individuals. Most of them, it is true, don't get out of the multicellular individual. But, by jingo, the same is true of the vast bulk of P falciparum cells! You see the point? Say there are a million individuals infected with 10^200 P. falciparum apiece, making a mahoosive global population of 10^206. Is that the number that we should be using for effective population size, or is it not actually somewhat closer to a million? A mosquito only extracts a few parasite cells, remember.

      As to simulations, Behe and Snoke did a simulation. And their numbers from that simulation support the result of the CR developing in P. falciparum.

      Well, I suppose we'll have to take your word for it!

      Delete
    49. Lino,

      You, Behe, and other IDiots are the ones claiming that "particular" mutations are extremely improbable, and you are the one who is playing the 'me and my genome aren't the same thing and judmarc didn't make that clear' game.

      Neither judmarc nor luitesuite nor anyone else needed to make that distinction because no one in their right mind has taken what was said to you about the improbability of your existence as needing any distinction between you and your genome.

      I've been thinking about why you would play your 'me and my genome aren't the same thing' game, even though any alleged distinction between you and your genome is irrelevant to the original point about the improbability of your existence. Beside the fact that you IDiots are chronically dishonest, astoundingly ignorant, thoroughly deluded, malignantly narcissistic, and absolutely imbecilic, there's something else behind the childish game you're playing here, isn't there?

      I think that what you really believe is that your body is just a run of the mill human body and that your 'specially created soul' is what makes you you. You believe that your genome (or body) is not you and that a 'clear distinction' should be made between you and your genome (or body or anything else physical/material about you). The points about the improbability of your existence focused on the particular you in toto, and you won't get away with trying to irrelevantly differentiate you from your genome.

      The bottom line is that, with all things considered, your existence or any other particular person's existence is extremely improbable yet you and billions of other particular persons do exist. The thing is, you and they are only 'particular' once you or they actually exist.

      Do you have any evidence to show that your chosen, so-called 'designer-god' did anything to cause you, in particular, to exist? Do you have any evidence to show that your chosen, so-called 'designer-god' did anything to cause malaria, any mutations (multiple or otherwise), and CR in some people but not in others?



      Delete
    50. Guys,

      Lino just takes a few sentences and tries some trick to pretend not to get it because otherwise he would have to concede the point(s). He's so close to having to admit his mistake, that all left to him is this game. He even called me lutesuite to add confusion to the conversation and then tried to make more contortions about Behe's numbers. Anything before acknowledging that he understands.

      I am not wasting more explanations on this Lino the imbecile. He could not care any less about explanations.

      Delete
    51. lutesuite,

      Right. And why would someone then say that, because the chance of a rabbit having a particular genome is 1 in 10^27, therefore the chance of any rabbit existing with any genome at all is 1 in 10^27? You know, like you and Michael Behe are arguing with regards to any trait that requires two mutations? The best explanation I can give is that the two of you are imbeciles. Or maybe just morons, it's hard to tell.

      Exactly. And then Lino says that you deserve a punch in the nose for an "ignoble remark," when he's the one insisting on being an imbecile time and again.

      Delete
    52. Quest,

      Name calling, especially "IDiot" is the best ammunition the stubborn evolutionists/atheists have when they have no arguments or scientific evidence...against creationist...

      Wow, so all those explanations here are invisible? Are you really that dumb? Try and read what we wrote this time around. You guys earn the name-calling. You deserve it for your hard work at trying not to understand any explanations.

      Delete
    53. Allan Miller,

      Could I make a humble request that we drop the name-calling? Ta.

      You could. That does not mean that I will honor your request though. These guys are truly asking for it. They insist, and not as humbly as you make your request. They insist with particular arrogance and gusto.

      Delete
    54. Allan, I think that I understand the reason for your request but I agree with photosynthesis (the IDiots ask for it). Also, when I write something like this:

      "Beside the fact that you IDiots are chronically dishonest, astoundingly ignorant, thoroughly deluded, malignantly narcissistic, and absolutely imbecilic, there's something else behind the childish game you're playing here, isn't there?"

      I see it as accurately and honestly describing IDiots, not as name calling. If I or someone else were to call them ugly, smelly dorks, that would be name calling, although the dork part would still be accurate. I would love it if open, honest, civil discussions/debates could always take place between evolutionists and IDists but IDists behave in ways that deserve to be pointed out and strongly condemned.

      Delete
    55. photosynthesis/twt - it's up to you, obviously. I'm no saint, and find the obtuseness frequently displayed as frustrating as anyone. But it gives them an excuse to misdirect, to pretend they haven't seen the scientific points among the cat-calls. As Quest nicely illustrated above. Though I don't kid myself that calm debate is any more successful! ;)

      Delete
    56. I am not wasting more explanations on this Lino the imbecile. He could not care any less about explanations.

      I'd only like him to explain how he figures out that the probability of a mutation occurring somewhere along the length of a replicated genome is by definition 1.0.

      Delete
    57. On the topic of insulting IDiots, this is not something I engage in just for fun and without careful consideration. It is actually a deliberate decision I have made for reasons elaborated upon by Sam Harris here:

      http://sandwalk.blogspot.ca/2013/03/on-effectiveness-of-ridicule-and-mockery.html

      Delete
    58. The really funny thing about LIno's inability to grasp the analogy is that it isn't really an analogy at all. Behe's argument involves the evolution of genes, and the analogy involves the evolution of genomes, which are nothing more than collections of genes. So somehow it is no problem for collections of tens of thousands of genes to come into being thru naturalistic processes alone, but for a single gene to arise requires Magic. LOL!

      A further analogy to explain Behe's fallacy: We could calculate the odds of a genome arising that encodes for an albino hermaphrodite who is 7 feet tall and has twelve toes, or we could even make the empirical observation that no such individual has been shown to exist, and therefore argue that the odds of such an genome arising are next to impossible. But by following Behe's and LIno's logic, we would have to then conclude that it is also virtually impossible for a brown-haired man whose height is 5'9" and who has the usual complement of 10 toes to exist.

      Delete
    59. judmarc:

      Then why did everyone else understand that was what I said? Come on, Lino, it is not necessary to make erroneous statements about what others have said.

      I think it should be very clear that everyone understood you as referring to my uniqueness, rather than to my general humanity. In my response to you, I was pointing out this lack of clarity so that I could go on to make remarks concerning how probability is sometimes misapplied when it comes to these kinds of discussions.

      You understood immediately the distinction I was making; but, others didn't get it, and slammed me in indelicate ways.


      Delete
    60. the whole truth:

      You, Behe, and other IDiots are the ones claiming that "particular" mutations are extremely improbable, and you are the one who is playing the 'me and my genome aren't the same thing and judmarc didn't make that clear' game.

      Neither judmarc nor luitesuite nor anyone else needed to make that distinction because no one in their right mind has taken what was said to you about the improbability of your existence as needing any distinction between you and your genome.


      You've succeeded in misunderstanding the distinction I've made. Is that my fault?

      Did a news item get written the day I was born to the effect: "Against all odds, less than 1 in 10^27, a married couple have a newly born so!"

      Do I have to answer this question for you? It is, of course, "no." That married couples have children is NOT an improbable event. Isn't this obvious?

      The only thing highly improbable, is that within the configuration space that spans the human genome, in this respect I am highly improbable. But, of course, I've admitted that.

      What judemarc was trying to get at was the improbability of my being born from the particular mother I had and the particular father. But you can't simply say that my mother had all 4 billion people, alive when she was young, to chose from. She was restricted to those she could and would encounter. The probabilities involved are very different than what judemarc had calculated.

      But the real point of all of this, the point I wanted and did make, is that there are so many Darwinists that say, "Oh, the odds of winning the lottery are really small, yet someone always wins."

      I've demonstrated the error in this, an error that is related to the point that judemarc was making.

      Read my posts. Counter my arguments. But don't continue in your shameful rants about what and who IDists are.

      If you have something logical to say, fine, then add to the discussion. But just because you can't put your mind around a subtle point doesn't mean the vitriol must begin.

      Delete
    61. judemarc: (Part I)

      Yet someone wins the Powerball every few weeks; and similarly, some mutations occur and become fixed in populations of various life forms so routinely and reliably that scientists can speak of and write about "molecular clocks."

      This is the very argument I am disputing. Mark Perakh has made it. And I consider it to be bogus. This is exactly what all of this is about in my estimation.

      When population geneticists work out probabilities of a particular mutation arising and then the number of generations within which this "particular" mutation will arrive, they're actually doing a "likelihood" calculation. That is, if there are X number of mutations expected per individual, in a population of size Y, with a mutation rate per individual per generation of Z, then the "particular mutation" is 'expected' to arise in XYZ.

      The "odds" of any particular Powerball lottery ticket winning is 1 in 175 million. But, if you sell 175 million tickets, the "likelihood" of a winning ticket is 1.0.

      No one disputes this. Most IDists, and Behe in particular, fully accept that after 10^8 mutations have taken place in a population, then somewhere within that population is an individual who has a "particular mutation" at a particular location along the length of its genome. This is not in dispute.

      One of the common arguments that Darwinian evolutionists employ is the one you've made: the lottery is a highly improbable event, and someone wins; ergo, just because something is improbable doesn't mean it won't happen. IDists argue that Darwinian evolution is too improbable. And so, they're wrong.

      Yet, what is he likelihood of a bridge hand being dealt? 1.0
      Why? Because the probability of dealing a hand is 1.0.

      If you now consider the configuration space of all permutations of bridge hands, then the probability of any one of those hands being dealt is 1 divided by the total number of permutations in the configuration space.

      If you deal a bridge hand a total number of times equal to the total number of permutations in configuration space, then the "likelihood" of arriving at any one of those hands is 1.0. Just put a circle around any one of those hands in configuration space; then, after a total number of bridge hands equal to the total number of 'bridge hands' in configuration have been dealt, this 'circled' hand will, on average arise---maybe right away, maybe a lot later, but, on average, it will arise.

      The ID position that Dr. Dembski has laid out involves probabilities of 1 in 10^500. This is equivalent to buying just one ticket in each lottery held, and then winning the Powerball lottery 5 x 10^481 times in a row. Are you willing to admit these are insuperable odds?

      I suspect you'll answer: "no." Because otherwise Darwinism comes to an end.

      Delete
    62. judemarc: (Part II)

      Behe takes a different approach.

      If we are to use the 'bridge hand' example as analogous to Behe's malarial parasite analysis, we would find these parallels:

      (1) the "dealing of a hand" is tantamount to a "replication"
      (2) the "mutated genome" is tantamount to the actual hands dealt out
      (3) the "bridge hand" that is being sought is one of the two mutations that confer CR
      (4) the "probability of any given bridge hand" is tantamount to the "probability of a particular mutation arising," which is the genome size divided by the mutation rate.
      (5) the "likelihood" of the sought after "bridge hand" actually arising, which is the number of hands dealt x the improbability of any given hand [(4) above] is tantamount to the "number of replications of the malarial parasite" x "probability of a particular mutation arising."

      What's so hard to see about this?

      Now, what Behe was arguing was that CR could NOT arise without TWO "particular mutations" being present.

      Well, then, what is that equivalent to this in the analogy I've given?

      The equivalent is "dealing enough hands so that a 'circled' hand in the configuration space" arises, and then "dealing enough hands so that another ‘circled’ hand in the configuration space” arises.

      In terms of the malarial parasite: it’s waiting for ONE particular mutation to arise—the likelihood of which is 1 in 10^8, and then waiting for ANOTHER particular mutation to arise, the first “chosen” completely independently from the first (i.e., the selection of the first had no effect on the selection of the second)—the likelihood of which, since they’re independent events, is also 1 in 10^8.

      What is the “likelihood” of both “hands” being dealt? = What is the “likelihood” of both “particular mutations” arising? = The number of replications x genome size/mutation rate.

      For it to be “likely” for these “two particular mutations” to arise then it will take, on average, (1 x 10^8) x (1 x 10^8) = 1x 10^16 replications to occur.

      What do we see? Per White’s calculation, we see 10^20 replications being needed. That’s well above the 10^16 needed using the “likelihood” approach. And, of course, White documents in his review article the other factors at play that cause more replications to be needed.

      Now, none of this should be controversial.

      Delete
    63. judemarc: (Part III)

      But, it becomes controversial the moment that Behe points out that any evolutionary path involving more than ONE “particular mutation” arising, as in the case of the malarial parasite, then this pathway becomes very unlikely. And, if two, separate (and, thus, independent) “two particular mutation”steps are necessary, then, effectively, this pathway is completely beyond the reach of neo-Darwinian evolutionary mechanisms.

      Now the controversy. But not because of the concepts involved. And not because of the numbers (if White had arrived at smaller numbers of replications being needed, then the numbers would matter). Only because it throws the whole neo-Darwinian structure into question.

      And we’re discussing this here now because Summers, et. al., have published a study that demonstrates
      TWO “particular mutations” are needed in order for CR to arise (Yes, more mutations are needed to get the malarial parasite up to snuff, but this is completely irrelevant to the finding that, at a minimum, TWO particular mutations must arise to have CR).

      I hope people think about all of this.

      N.B.
      [[What we don’t see, however, is one of malarial parasites—of which there are hundreds of millions of lineages, vectors, if you will, throughout the human population—that arrived at CR faster.
      What can we infer from this?

      Well, I said above that “on average” it should take 10^16 replications to arrive at the two needed CR mutations. If, according to Darwinists, there are all kinds of things happening—neutral drift, recombination, invisible forces that can work magic—then why didn’t CR develop with fewer replications? Can all of you here answer this question honestly?]]

      Delete
    64. Piotr:

      I'd only like him to explain how he figures out that the probability of a mutation occurring somewhere along the length of a replicated genome is by definition 1.0.

      I did not say "particular" mutation. I said "a mutation"--as in a mutation of kind. And every genome that I know of 'mutates' when it replicates. Maybe you know of an exception.

      Delete
    65. Piotr:

      " . . .--as in a mutation of "any" kind." Sorry.

      Delete
    66. the whole truth:

      I see it as accurately and honestly describing IDiots, not as name calling. If I or someone else were to call them ugly, smelly dorks, that would be name calling, although the dork part would still be accurate.

      What is it you see as "accurately and honestly describing IDiots"?

      This:

      Beside the fact that you IDiots are chronically dishonest, astoundingly ignorant, thoroughly deluded, malignantly narcissistic, and absolutely imbecilic, there's something else behind the childish game you're playing here, isn't there?"

      Think about this:

      Your nose tells you what smells. Your eyes tell you what is ugly. And this, you consider wrong in saying about others. But when it comes to qualities that, at best, you can only 'tentatively' be accurate in, this you consider to be "accurate and honest" and plenty OK to say about others.

      Delete
    67. Not just an imbecile, but a tediously long-winded imbecile.

      Lino, by Behe's and Dembski's (and your) "logic," a game or bridge could never occur because the odds against each possible combination of hands being dealt is so low as to be practically impossible.

      So why can people still play bridge?

      That you still cannot follow this argument, despite the many times it has been explained to you, demonstrates why you so richly deserve the appellation "imbecile."

      Delete
    68. Well, I said above that “on average” it should take 10^16 replications to arrive at the two needed CR mutations. If, according to Darwinists, there are all kinds of things happening—neutral drift, recombination, invisible forces that can work magic—then why didn’t CR develop with fewer replications? Can all of you here answer this question honestly?

      The answer is provided in White's paper, and has been summarized in Larry's post. You know, the one you're responding to right now. Unfortunately, it seems the explanation sailed right over your imbecilic head.

      Delete
    69. Lino: I did not say "particular" mutation. I said "a mutation"--as in a mutation of kind. And every genome that I know of 'mutates' when it replicates. Maybe you know of an exception.

      So you haven't given it any thought. It isn't anything advanced, its just elementary maths. You'd like to overthrow modern biology by talking about mutations and probabilities, but it's painfully clear that you have no grasp of anything. What makes you so sure that a mutation (of any kind) has to happen when a genome gets replicated? For simplicity, let's focus on the haploid genome of Plasmodium falciparum. Do you think at least one mutation happens every time it's replicated? Well, of course you do, because you say that the probability of a mutation equals 1.0 "by definition". Definition of what?

      Do you know how to compute this probability? It isn't what you say it is. If not, what makes you think you are qualified to handle anything more complex?

      Delete
    70. Lino said:

      "I think it should be very clear that everyone understood you as referring to my uniqueness, rather than to my general humanity."

      And:

      "What judemarc was trying to get at was the improbability of my being born from the particular mother I had and the particular father."

      Lino, from the very start I understood that judmarc (or lutesuite or whomever first brought it up (I don't remember)) was referring to you in particular, your "uniqueness" as you now put it. YOU are the one who tried to confuse the point by playing your 'me and my genome are not the same thing' game, and since then you've been asserting things (as though they're your original idea) that I and and especially others have been trying to get across to you all along. You STILL don't (or won't) get it.

      If anyone here who isn't an IDiot thinks that I'm mixed up, please let me know.

      Delete
    71. lutesuite:

      Lino, by Behe's and Dembski's (and your) "logic," a game or bridge could never occur because the odds against each possible combination of hands being dealt is so low as to be practically impossible.

      So why can people still play bridge?


      What does it mean when I write: "The probability of dealing a bridge hand is 1.0"?

      Can you understand this? If you understand this, then you'll understand perfectly why people are able to play a hand of bridge.

      Delete
    72. "For it to be “likely” for these “two particular mutations” to arise then it will take, on average, (1 x 10^8) x (1 x 10^8) = 1x 10^16 replications to occur."

      But that caluclation makes some assumptions. It assumes at least these things:

      1. The two mutations must be simultaneous, in the same individual on the same chromosome.

      2. Either mutation alone is lethal.

      We know from studies of the genetics and population genetics of P. falciparum that these assumptions are wrong.

      "What do we see? Per White’s calculation, we see 10^20 replications being needed. That’s well above the 10^16 needed using the “likelihood” approach. And, of course, White documents in his review article the other factors at play that cause more replications to be needed"

      White's calculation is not based on mutation rates, and is unrelated to the 10^16 figure. It also makes some bad assumtions.

      We have been over this ground many times.

      Delete
    73. lutesuite:

      The answer is provided in White's paper, and has been summarized in Larry's post. You know, the one you're responding to right now. Unfortunately, it seems the explanation sailed right over your imbecilic head.

      Have you read White's paper?

      He gives reasons for the difference between the probability of developing CR via "in vitro" malarial parasites and "in vivo" malarial parasites. He also gives reason for why, overall, the probability is as high as it is.

      This does nothing in the least to detract from the question I have posed. Would you now like to give an answer to it?

      Delete
    74. Lino asked/said:

      "What is it you see as "accurately and honestly describing IDiots"?

      This:"

      Beside the fact that you IDiots are chronically dishonest, astoundingly ignorant, thoroughly deluded, malignantly narcissistic, and absolutely imbecilic, there's something else behind the childish game you're playing here, isn't there?"

      "Think about this:

      Your nose tells you what smells. Your eyes tell you what is ugly. And this, you consider wrong in saying about others. But when it comes to qualities that, at best, you can only 'tentatively' be accurate in, this you consider to be "accurate and honest" and plenty OK to say about others."

      I didn't say that "ugly, smelly dork" is wrong, I said that it is name calling. Whether name calling is wrong or not is a matter of opinion. Since I can't see and smell you I can't accurately and honestly say whether you're ugly and/or smelly. I don't have to see you or smell you to know that how I described you IDiots above is accurate and honest. There's nothing tentative about it.

      Delete
    75. Chris B:

      But that calculation makes some assumptions. It assumes at least these things:

      1. The two mutations must be simultaneous, in the same individual on the same chromosome.

      2. Either mutation alone is lethal.

      As to (1): we've gone over this a couple of posts back. Simultaneous does not mean that they happen at the same time. It only mean that they have to be simultaneously "present". IOW, ONE mutation alone is not sufficient to acquire CR.

      As to (2): the parasite is not looking for a "lethal" mutation. It is the chloroquine that is 'lethal,' and, unless the mutations are found, the chloroquine will kill the billions of parasites present in the host so that the parasite cannot be passed on via a mosquito bite.

      As to White's paper, in the section on the genetics behind the malarial parasite he writes this:

      The genetic events that confer antimalarial drug resistance (while retaining parasite viability) are spontaneous and rare and are thought to be independent of the drug used. They are mutations in or changes in the copy number of genes encoding or relating to the drug’s parasite target or influx/efflux pumps that affect intra-parasitic concentrations of the drug (Table (Table1).1). A single genetic event may be all that is required, or multiple unlinked events may be necessary (epistasis). As the probability of multi-genic resistance arising is the product of the individual component probabilities, this is a significantly rarer event. P. falciparum parasites from Southeast Asia have been shown to have an increased propensity to develop drug resistance.

      Chloroquine resistance in P. falciparum may be multi-genic and is initially conferred by mutations in a gene encoding a transporter (PfCRT) (13). In the presence of PfCRT mutations, mutations in a second transporter (PfMDR1) modulate the level of resistance in vitro, but the role of PfMDR1 mutations in determining the therapeutic response following chloroquine treatment remains unclear

      So White, knowing that atovoquine resistance develops readily and involves ONE mutation (and, which, “in vitro” needs around 10^8 replications to develop), clearly is talking about the need for a second “genetic event” for CR to arise in P. falciparum. And, he says that since they are independent, the “probability” of “multi-genic resistance” (like CR, which we now know requires, at minimum, two mutations) is the PRODUCT of the individual component probabilities.

      It is complete intellectual dishonesty to blithely say that the probability of a SNP is directly related to genome size and mutation rate, and then, when it no longer serves to buttress the prevailing paradigm, to then say that we have no idea what this probability might be.

      Hence, using White’s number, and rounding down, Behe used 1 in 10^8. No one disputes this kind of number---except when some prevailing idea—wrong as it may be—is threatened.

      Using 10^8, then the 1 in 10^16 is simply the PRODUCT of this “multi-genic” event where the probabilities are multiplied. The only way around this level of improbability is if something unusual happens in eukaryotic cells, because this 1 in 10^16 figure requires 10^16 replications “on average.” Now, if something unusual was going on, it is possible that CR would develop in the P. falciparum more quickly. But it doesn’t.

      So, any explanation why nothing happens quicker? If not, then Darwinism is left to live with these numbers.

      Delete
    76. Some imbecile named "Lino" spews ignorantly:

      He gives reasons for the difference between the probability of developing CR via "in vitro" malarial parasites and "in vivo" malarial parasites.

      That's right, he does, doesn't he? So, then, you have the answer to your question. That is, if you actually understand what he has written there.

      Behe doesn't. Do you?

      Helpful hints: What are the factors that White identifies? Are they all restricted only to the mutation rate? Do the exact same factors that White identifies as influencing the frequency with which chloroquine resistance occurs apply to every single novel trait that could possibly arise in every single species of organism that has ever existed on earth? Is the probability that chloroquine resistance will evolve in P. falciparum the same thing as the probability that some genetic trait requiring two mutations will arise in some species, sometime, somewhere? (That is to say, are the odds that you would have been dealt the exact bridge hand you hold the same as the odds that someone would be dealt a bridge hand of some sort?)

      Think hard about those last two questions, Lino They're very important.

      Delete
    77. Piotr:

      Do you know how to compute this probability? It isn't what you say it is. If not, what makes you think you are qualified to handle anything more complex?

      I might not. I suspect that per the definition of probability you would use, the probability would never rise to the level of being 1.0. Instead, it might be 0.999999999. You know there's a difference between the mathematical content of ideas, and the ideas themselves. The ideas are what's important. The numbers lead us in the right direction.

      But, again, do you know of any organism that does not mutate to some degree when it reproduces, whether sexually or asexually. If you do, then I will revise down my "1.0" number accordingly.

      Delete
    78. Lino, let's face it, you are mathematically illiterate. You should not discuss probabilities because you simply don't understand them. You have no idea what the actual probability is (hint: nowhere even close to 1.0). If such an elementary calculation boggles your mind, how can you know who is right and who is wrong in this dispute? You accept Behe's numbers because you are in the same camp, not because you understand his argument.

      By the way: it was you who said "by definition", so I asked you what you meant by that. Don't bother to answer. It's obvious that you didn't mean anything in particular.

      Delete
    79. the whole truth:

      YOU are the one who tried to confuse the point by playing your 'me and my genome are not the same thing' game, and since then you've been asserting things (as though they're your original idea) that I and and especially others have been trying to get across to you all along. You STILL don't (or won't) get it.
      Let me repeat myself: on the day of my birth, the N.Y. Times did not run an article titled: “Married couple give rise a son.” That humans give birth to humans is straightforward. That rabbits give birth to rabbits, or that peacocks give birth to peacocks, is nothing surprising or highly improbable.
      If the “probability” of my being born is, per judemarc (IIRC) is 1 in 10^27, then that would mean that for the “likelihood” of a person being born to a married couple, 10^27 couples would be needed. But, then, where did they come from if a birth is so rare an “event.”??

      Can you answer that?

      You can then look back at the event that judemarc likely had in mind when he made his remark, and that is: what are the odds that I was born of the mother and father from which I was born—which is not the same as either of the two ways of looking at this I’ve already mentioned.

      Then you calculate something along the lines of an effective population. Let’s start with this: unless you meet someone and have dialogue with them, there will be no marriage. Then think of the years that a woman is fertile. Then think of how many people that person might run into during those years. This would be an upper limit on the set of possible spouse’s for that person. You would get a completely different number, incredibly smaller than, the one that judemarc was calculating. He agreed to this.

      Let’s say that the “odds” of my mother marrying my father are very low, but not fantastically low. Then the point I keep making is that the “odds” of my parents having a “son”—and if you deny that I am their son then you’re denying reality is, on average 1 out of 2.

      The “odds” of being dealt a “Bridge hand” in a game of Bridge is 1 out of 1. Unless you quit.

      What Darwinists do is to substitute the probability of this hand, as determined by its configuration space, for the probability of getting a hand of cards in a game of Bridge, and then announcing: “Look, this highly improbable event happens over and over again. So much for probability arguments.” They fail to see that it is only when a ‘hand’ is specified ahead of time that these probabilities take on any meaning.

      If we now turn to the case of the malarial parasite, we find that Nature has specified TWO mutations ahead of time if the lethal effects of chloroquinone are to be overcome. And, the probability of “finding” each of these mutations, on average, is 1 in 10^8, giving a total probability for “finding” these two mutations of 1 in 10^16.

      Everyone here seems to want to deny this rather straightforward analysis.

      Delete
    80. Piotr:

      Can you name one genome that you know of that doesn't mutate when it reproduces?

      Give an example. Or I will assume that there are no such examples.

      And all of this because I used the word "definition"? What about Behe's analysis. What about the fact that CR doesn't arise within any one human individual?

      Does that mean nothing. Are you simply pushing out your chest and saying: "I am a much better biologist and mathematician than you"?

      What does that prove? I'm wouldn't be surprised at all that you're a better mathematician and biologist than I am. So what? Use that knowledge to counter my arguments and not just nit-pick.

      Delete
    81. Piotr:

      Mathematically illiterate. Quite a sweeping statement.

      So the fact that I've taken a full course of calculus, differential equation, advanced differential equations and linear algebra, all of them with the highest marks, means nothing, right?

      Have I taken a class in probability? No. Have I read some books? Yes. Do I work in probability theory every day? No. Do I forget things? Yes.

      When the "odds" of something are 1 in 10^8, no one needs a degree in probability theory to figure that out.

      Again, please supply one example of a genome that reproduces without a mutation forming somewhere along its length. You've raised this possibility, and supply no examples. Why?

      Delete
    82. Lino, yes or no:

      Do you believe that your chosen 'God' designed and created harmful/deadly parasites, bacteria, and viruses?

      Do you believe that your chosen 'God' designed and created mutations that enable harmful/deadly drug resistance in parasites, bacteria, and viruses?

      Do yo believe that your chosen 'God' designed and created harmful/deadly parasites, bacteria, and viruses to righteously punish all living things because the biblical characters adam and eve sinned and their sin was spread into every living thing forever?

      Do you believe that all living things deserve to be punished by your chosen 'God' because of adam and eve's sin?

      Do you believe that you were/are specially created in the image of your chosen 'God'?

      Delete
    83. lutesuite:

      Think hard about those last two questions, Lino They're very important.

      Those last two questions only demonstrate that when faced with the truth, you prefer something else. Can't help you there. You can continue doing that all your life. It's not my problem.

      But what will you do when Darwinian thinking is overthrown simply by the weight of more and more experiments demonstrating the inability of Darwinian mechanisms to explain what is being discovered? It will be a sad day indeed.

      Delete
    84. The whole truth:

      And your questions, what do they have to do with whether or not CR develops in the malarial parasite and how many replications it takes?

      Delete
    85. So the fact that I've taken a full course of calculus, differential equation, advanced differential equations and linear algebra, all of them with the highest marks, means nothing, right?

      Not much if you have forgotten how to use this knowledge. Let's say, it's functional illiteracy.

      Again, please supply one example of a genome that reproduces without a mutation forming somewhere along its length. You've raised this possibility, and supply no examples. Why?

      OK, Plasmodium fulciparum is a good example. The probability that at least one mutation -- any mutation of any kind -- will occur when its genome gets replicated is about 0.04. I'm sure you will agree that it's pretty far from 1.00. On the average, you must wait 25 generations till something happens to its genome. In 96 cases out of 100 the offspring is genetically identical with the parent.

      Delete
    86. Lino, many of the claims that you're now making, e.g. regarding the probability/improbability of a particular person being born to particular parents or just any ol' person being born to any ol' parents, are what I and especially others have been telling you all along.

      This paragraph of yours further demonstrates that you STILL DON'T GET IT:

      "If we now turn to the case of the malarial parasite, we find that Nature has specified TWO mutations ahead of time if the lethal effects of chloroquinone are to be overcome. And, the probability of “finding” each of these mutations, on average, is 1 in 10^8, giving a total probability for “finding” these two mutations of 1 in 10^16."

      You're still on the 'specified mutations ahead of time' kick (a typical IDiotic kick). You obviously believe that the 'uniqueness' or 'particularity' of people (or at least you) and other things (such as mutations) is specified, designed, and created ahead of time by your chosen, so-called 'God'. How far ahead of time, and in the case of CR why are the malarial parasites in only some people resistant to chloroquine? Why not all malarial parasites or none at all? Are the people with those particular, specified, designed, created, chloroquine resistant parasites particularly evil or something?

      Present the evidence that shows that your chosen, so-called 'God' or any other so-called 'God' specifies, designs, and creates people, diseases, mutations, or anything at all (whether 'particular/unique' or not) and explain why your chosen, so-called 'God' specifies, designs, and creates deadly diseases and drug resistance, ahead of time or at any time.

      Delete
    87. Lino asked me:

      "And your questions, what do they have to do with whether or not CR develops in the malarial parasite and how many replications it takes?"

      My questions pertain to what you believe is the 'truthful' alternative to natural evolution and scientific evolutionary theory. Since you are obviously a god pusher and you don't and won't accept that natural evolution occurs and that scientific evolutionary theory is credible then you should be willing to answer questions about your religious beliefs. After all, it's your religious beliefs that you believe are the 'truthful' alternative to natural evolution and scientific evolutionary theory, right?

      Delete
    88. Lino

      Well, I said above that “on average” it should take 10^16 replications to arrive at the two needed CR mutations. If, according to Darwinists, there are all kinds of things happening—neutral drift, recombination, invisible forces that can work magic—then why didn’t CR develop with fewer replications? Can all of you here answer this question honestly?]]

      Here's a brief summary. I trust you will credit me with honesty, and no attempt to invoke 'invisible forces that can work magic' - I think that's Behe's department.

      You are treating P. falciparum as if it were a free-living population in steady state. It isn't. In the infective phase, a mosquito bites a healthy human and injects a few Pf cells - a founder effect. After about 40 generations of doubling, it reaches 10^12. Although a population that large has a good chance of producing a CR mutant, it will only exist in single copy if it happens when it's that large, giving it virtually no chance to get out. The earlier in the cycle, the greater the chance of getting out, but the population size is smaller and so the chance of it happening at that stage exponentially diminishes. The combined probability of CR occurring and getting out will be much less than your intuition determines. It will, nonetheless, be of the order of a double mutant happening in a eukaryote population - the very thing Behe is trying to cast doubt upon with this case. 10 repeats in a few years will do nicely!

      Given the host constraint, overall, CR might be very rare indeed - except for the fact that there is recombination. This has a substantial probabilistic effect on a double mutant, depending upon the map distance of the two components. Of course, recombination isn't guaranteed to rescue things either, and the probabilistic scenario depends upon a mosquito biting individuals with two strains, which itself depends upon the local distribution of those strains. Nonetheless, recombination is much more powerful than serial mutation, so a little makes a big difference.

      Then there is the issue of chloroquine itself. It is not guaranteed to be present in every individual, to exert its maximal selective effect, and many individuals (including virtually all non-human hosts) will not contain any chloroquine at all. This reduces the power of selection to compound those instances that do get out.

      Of couse, whatever the incidence was, you would demand to know why it wasn't something else!

      Delete
    89. Lino says:

      "As to (1): we've gone over this a couple of posts back. Simultaneous does not mean that they happen at the same time. It only mean that they have to be simultaneously "present". IOW, ONE mutation alone is not sufficient to acquire CR."

      Seriously, look up the word simultaneous. It means at the same time.

      If you just mean that the two mutations have to be present at the same time and don't have to arise smultaneously, then the 10^16 caculation is wrong. That is all.

      "As to (2): the parasite is not looking for a "lethal" mutation. It is the chloroquine that is 'lethal,' and, unless the mutations are found, the chloroquine will kill the billions of parasites present in the host so that the parasite cannot be passed on via a mosquito bite"

      Nothing is "looking for a mutation". This statement indicates you do not know how mutations work and don't know what a lethal mutation is.

      Whenever the obfuscatory back and forth talk is rewound and we go to the original very simple calculations that started the conversation, we see that there are fundamental misunderstandings about how evolution works, and that Behe's caculations are worng. Every single time.

      Delete
    90. If you accurately empty a revolver to a target you have six hits. What you do not have is six simultaneous hits, even though they all ended up on the same target.

      Less but still somewhat relevant to the issue at hand, if you adjust your aim between shots the likelyhood of having two or more hits near the center is higher than it would be with six simultaneous shots.

      Delete
    91. Allan Miller: (Part 1)

      Here's a brief summary. I trust you will credit me with honesty, and no attempt to invoke 'invisible forces that can work magic' - I think that's Behe's department.
      I do, indeed, credit you with a straight-forward, honest answer. Thank you.

      AM: You are treating P. falciparum as if it were a free-living population in steady state. It isn't.

      If I understand you here correctly, I assure that I’m not treating it as a free-living population in steady state.

      AM: In the infective phase, a mosquito bites a healthy human and injects a few Pf cells - a founder effect.
      This is exactly why you can’t treat P.falciparum as a “free-living population,” it’s as though a “new” (and separate) population comes into existence with each case of infection (inoculation).

      AM: After about 40 generations of doubling, it reaches 10^12. Although a population that large has a good chance of producing a CR mutant, it will only exist in single copy if it happens when it's that large, giving it virtually no chance to get out.

      This is using White’s numbers. I made a calculation, and base on the need of 10^8 replications to affect a mutation at one of the two sites, and then taking into account the ‘doublings’ that will take place after that, as well as the likelihood of initial suitable mutations taking place along the way at each ‘generation,’ I calculate that there will be 258,000 “particular” mutations that will exist within the host when reaching the 10^12 number of parasites. Since only, on average, one of three mutations will give the desired a.a., effectively we should have 86,000 CR-type mutations.

      If you consider that a mosquito, in one bite, might take up 10 sporozoites, and that at any time millions of people will be affected and being treated with chloroquine, then you have a sample size of 10^7, with the likelihood of one of the sporozoites in the host who is bitten being taken being 1 in 10^12/86,000. This is almost 1. If you had 10 million people being treated with chloroquine, then this would be above 1.0. This means that in any given year a sporozoite will make it into the gut of a mosquito, and, with enough mosquitos biting enough individuals more than once, we should expect that “one” of the two needed mutations will have found itself into a new host and have become a “founding,” a new population. As that population increases with the newly infected host, after 10^8 replications, then mutation “two” should have come upon the scene, and CR would have arisen. So the fact that we don’t see CR arising every other year in some individual means that something else is at play.

      Well, of course, this is what all those other factors are that White was taking into account, factors which make these probabilities less than what we would otherwise expect.

      So far, so good. We’re in agreement roughly.

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    92. Allan Miller: (Part II)

      AM: The combined probability of CR occurring and getting out will be much less than your intuition determines. It will, nonetheless, be of the order of a double mutant happening in a eukaryote population - the very thing Behe is trying to cast doubt upon with this case. 10 repeats in a few years will do nicely!

      I’m not sure what you mean about “10 repeats in a few years will do.” I’m assuming you mean something along the lines of: “Ten instances of CR development over a period of a few years will do nicely in overcoming the ‘combined probability.’”

      I don’t, however, understand what you’re saying about Behe. It’s not my impression that Behe is challenging the idea that neo-Darwinian mechanisms can’t over the “combined probability” of a double mutation in a eukaryotic line, for, after all, the malarial parasite has just done this.

      He’s challenging the ability of the same neo-Darwinian mechanisms to come up with 4 mutations all at once—meaning the presence of all four within the genome of one organism simultaneously. That seems to me something very different. His book was, after all, The Edge of Evolution, and not The Impossibility of Evolution.

      AM: Given the host constraint, overall, CR might be very rare indeed - except for the fact that there is recombination.

      Here I take you to mean CR in a strain of parasites rather than in just one individual here or there.

      AM: This has a substantial probabilistic effect on a double mutant, depending upon the map distance of the two components. Of course, recombination isn't guaranteed to rescue things either, and the probabilistic scenario depends upon a mosquito biting individuals with two strains, which itself depends upon the local distribution of those strains. Nonetheless, recombination is much more powerful than serial mutation, so a little makes a big difference.

      Then there is the issue of chloroquine itself. It is not guaranteed to be present in every individual, to exert its maximal selective effect, and many individuals (including virtually all non-human hosts) will not contain any chloroquine at all. This reduces the power of selection to compound those instances that do get out.


      These are some more of the factors that White addresses and that show up in his Table 1. I have no problems with any of this.

      AM: Of couse, whatever the incidence was, you would demand to know why it wasn't something else!

      We seem to see things very similiarly—at least when it comes to what has happened. It’s the interpretation where we differ. Don’t bother looking—there’s been too much written already—but I’ve already said something to this effect. I don’t think the dispute is about the ‘facts’ but about what they mean. I think these results are devastating for neo-Darwinism, and you don’t think this at all.

      I don’t know where you go from here, but it sure looks like we’re not quibbling over much—‘facts’-wise, at least.

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    93. Lino: He’s challenging the ability of the same neo-Darwinian mechanisms to come up with 4 mutations all at once—meaning the presence of all four within the genome of one organism simultaneously.

      Since nobody proposes that the two/four/... [enter your favourite number] mutations have to occur simultaneously, Behe is fighting a straw man.

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    94. Piotr:

      Since nobody proposes that the two/four/... [enter your favourite number] mutations have to occur simultaneously, Behe is fighting a straw man.

      Yes, that's right. No one does. But does this, all by itself, mean that evolution can, and does, proceed one mutation at a time? Is there never a time when more than one needed mutation must be present within the genome before a "step" can be taken?

      The language in White's paper suggests otherwise. He talks, e.g., about a "multi-genic" event. And Summers' paper documents that unless TWO specific mutations are present, not even minimal pumping out of chloroquine can occur. That is, the parasites will die. So 'both' mutations have to be in place for CR to even begin to develop. How do you address this?

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    95. The language in White's paper suggests otherwise. He talks, e.g., about a "multi-genic" event. And Summers' paper documents that unless TWO specific mutations are present, not even minimal pumping out of chloroquine can occur. That is, the parasites will die. So 'both' mutations have to be in place for CR to even begin to develop. How do you address this?

      And you wonder why we call you an imbecile.

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    96. Not much if you have forgotten how to use this knowledge. Let's say, it's functional illiteracy.

      Though I note Lino did not list anything to do with probability in his math education, I think you are still not correct, Piotr. We've all pointed out to Lino the quite elementary distinction between the chance of any particular sequence of mutations and the chance of evolution occurring. My reading of Lino's responses is that he cannot help but understand this distinction yet persists in responding as if the probabilities of the particular (a specific sequence of mutations) and the general case (evolution) are identical. Thus I think there is a basic lack of intellectual honesty in his responses, and we are (surprise, surprise) wasting our time.

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    97. @Lino Di Ischia
      The language in White's paper suggests otherwise. He talks, e.g., about a "multi-genic" event. And Summers' paper documents that unless TWO specific mutations are present, not even minimal pumping out of chloroquine can occur. That is, the parasites will die. So 'both' mutations have to be in place for CR to even begin to develop. How do you address this?

      Let's see...
      * Not all parasites without CR die when chloroquine is present - this is resistance, not immunity
      * Not all parasites develop with chloroquine present, whether they have CR or not
      * Not all mutations occur with chloroquine present, whether they lead to CR or not

      This could only be a problem if CR was some kind of targeted response against chloroquine, that is, if presence of chloroquine was a necessary trigger to start the mutations leading to CR and any such mutation was actively suppressed otherwise. Since no one except maybe the ID crowd suggests such a scenario, it is safe to assume that one or more of the necessary underlying mutations was already in place before chroloquine was even invented.

      @judmark
      Thus I think there is a basic lack of intellectual honesty in his responses, and we are (surprise, surprise) wasting our time.

      It does look like that, right?

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    98. Lino

      This is using White’s numbers. I made a calculation [...] So the fact that we don’t see CR arising every other year in some individual means that something else is at play.

      I think it's your maths. I don't know what a 'particular' mutation is, but 86,000 CR mutants in every 10^12-cell infection appears to be completely off-beam. 1 in 10^-8 is the mutation rate per base, and I don't know why 1/3rd of mutations occurring would be CR.

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    99. Lino,

      I don’t think this dispute is about the ‘facts’ but about what they mean. I think these results are devastating for neo-Darwinism, and you don’t think this at all.

      Which leads me to suspect that we aren't in agreement about the facts at all.

      If we were in agreement on the facts, I could take it that you accept the following:

      1) The effective population size of Pf is of the order of the effective population size of one of its eukaryote hosts, not the number of Pf cells at any one time.

      2) The substantial reduction in expected instances of the serial double mutant due to 1) being the salient parameter (not 10^20) may be offset by recombination.

      3) The selection coefficient of CR-lacking Pf is nowhere near 1.0 (lethality), and the number of instances of CR we would expect to see must depend on the actual value, which will in turn depend on the extent of chloroquine use in its hosts (including non-humans, where cross-species transmission exists).

      4) The selection coefficient of CR cannot be just assumed to be the same as any other selection coefficient anywhere in nature, and hence these results cannot be extrapolated to cover the whole of evolution.

      If you do, then I’m at a loss to see why this is devastating for neo-Darwinism. A small effective population has thrown up 10 separate instances of the double mutant in a few years. If other mutations can spread simultaneously (they can) then evolution does not appear to come anywhere near stalling at this assumed boundary. If it’s about triple or quadruple mutations, you might like to give an example of one that was too improbable to have happened.

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    100. Allan Miller:

      I think it's your maths.

      How does 86,000 represent a third of the CR mutations? I'm a little lost. What's your point of reference?

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    101. Allan Miller:

      3) The selection coefficient of CR-lacking Pf is nowhere near 1.0 (lethality), and the number of instances of CR we would expect to see must depend on the actual value, which will in turn depend on the extent of chloroquine use in its hosts (including non-humans, where cross-species transmission exists).

      Believe it or not, sometimes I engage in a little hyperbole here and there.

      Yes, if we start considering the level of chloroquine throughout the various parts of the body, the in situ immune response, etc, the selection coefficient is less than 1.0. The main point is that we know we're dealing with something that NS will do something about right away. It won't be a delayed response (comparatively).

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    102. Allan Miller:

      4) The selection coefficient of CR cannot be just assumed to be the same as any other selection coefficient anywhere in nature, and hence these results cannot be extrapolated to cover the whole of evolution.

      But if the selection coefficient is less in other instances, and I think you would agree it would be, then, since NS will be working less efficiently, the result would be than more generations/replicates would be needed than in the malarial parasite instance.

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    103. Allan Miller:

      1) The effective population size of Pf is of the order of the effective population size of one of its eukaryote hosts, not the number of Pf cells at any one time.

      2) The substantial reduction in expected instances of the serial double mutant due to 1) being the salient parameter (not 10^20) may be offset by recombination.

      Is your concern here how various lineages will spread among human populations, and, hence, how CR will spread among the parasites?

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    104. Lino

      How does 86,000 represent a third of the CR mutations? I'm a little lost. What's your point of reference?

      You! Though I didn't say 86,000 represents a 3rd of CR mutations, I just couldn't see where you got 1/3rd from. But I realise now you are looking at a situation where every base has had a mutation, and each base has 3 possible options.

      Your calculation is still off. You need to consider that at the start of an infection there are few cells, and at the end there is a sampling process of the many remaining, and in between there is increase. Consider a population of hosts as a set of empty jars. For simplicity start with one cell in each, ignore chloroquine, and double for 40 generations till you get 10^12, and establish the probability that a random cell drawn from each jar will be a mutant. The mutation will actually occur at a different generation in different jars, and the earlier it happens, the more descendants it will leave, but the less likely it is to happen because at that point the population was smaller. I think the probability of a single random cell being a mutant will be the same for each jar regardless because these factors cancel each other out.

      You can compound this probability up for a larger and larger population of jars, but if you end up with a probability of 1 or more, you've done it wrong.

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    105. Lino Yes, if we start considering the level of chloroquine throughout the various parts of the body, the in situ immune response, etc, the selection coefficient is less than 1.0

      I think you're confusing the selection coefficient in an individual with that in the population at large. I meant the latter. The selection coefficient in an individual is pretty meaningless for evolutionary purposes.

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  2. the only thing i can say is if Mr Moran doesn't like natural selection and so on and says other mechanisms are acting. tHen its a admittance that other mechanisms are needed and yet not established, as far as evolutionism establishes anything, amongst the evolutionist community.
    Why can't a creationist say Mr Moran is uncomfortable intellectually with the usual weight evolutionists give to mechanisms that is claimed to have created biology.?
    I think I got that right.

    The final thing is that mutationism must drive evolution. Behe has well attacked this and regardless of possible errors, or not, the great point is about how unlikely mutationism could create the diversity and complexity of glorious biology.
    I got that right.

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    1. tHen its a admittance that other mechanisms are needed and yet not established, as far as evolutionism establishes anything, amongst the evolutionist community.

      Hi Robert, it's the early 20th century calling - that's when the basic population genetics math and concepts were developed. Sorry if your sources have made it seem to you that genetic drift is not "accepted." It has been, there are simply lively discussions going on about the extent of its role.

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    2. i didn't read that at all. Moran does respect natural selection (if you didn't nothing would hold an organism together) What he does not respect however is that everything must have a selective advantage. Creationists try to play that line by saying everything in evolution must have selective advantage else it could not have evolved. This ignores the neutrality that is possible. Don't call him a darwinian. Call him a modern evolutionary biologist.

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  3. Well Larry, you just don't know when to quit. You could never bring yourself (like your sycophants here) to concede any point to the 'other side'.....doo,do,doo,doo,do.....

    The really amusing thing is your mud wrestlin' verbosity clouds any realization on your part that you had already lost the initiative at the get-go.

    Behe has clearly shown an intimate grasp of the issue, which reduces all of you to quibbling about the probability of various factors (mostly imagined on your(pl) part).

    That's why Behe is public enemy no. 1. Dangerous, that Behe, dangerous.

    Behe 1, Moran and sychos 0.

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    1. Dangerous, that Behe, dangerous.

      If you think so, try reading his cross-examination from the Dover trial. It's been recommended as a literal textbook example for law students to demonstrate how to destroy an opposing expert's credibility through effective cross examination. And have no doubt, Behe's credibility was destroyed. Laughter rang out from attendees at several points, and then of course there's the judge's ruling that tells you all you want to know about how intellectually "dangerous" he thought Dr. Behe was.

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    2. O, no, Steve, is Larry going clickety-clack across your bridge again?

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    3. clearly judmarc, Moran wouldn't be taking up so much time writing...how many posts is it now?....about the Behe, if he wasn't worried about him.

      Behe rattles you all....no question there.

      ...and Behe's unflappable, reasonable demeanor drives you nuts.

      Admit it.

      Kudos to The Behe.

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    4. Love those adjectives. The Inimitable Jeeves, the Unflappable Behe.

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    5. It's ironic that Steve considers himself to be in a position to evaluate the relative merits of the scientific arguments of this discussion while at the same time not being able to make a single argument of whatever nature of his own. It's telling.

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    6. clearly judmarc, Moran wouldn't be taking up so much time writing...how many posts is it now?....about the Behe, if he wasn't worried about him.

      Yes, he's worried about credible boobs learning an incorrect version of settled science.

      Larry also devotes considerable space to real scientists, science writers, and others who get various aspects of biochemistry or evolutionary theory wrong in his opinion; or to issues within those topics and others where, unlike the current discussions with Behe, there are actual scientific controversies.

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  4. Incidentally, the life cycle of the parasite renders its effective population size vastly smaller than if it were free living (I suspect that this point has been made by others). Huge numbers of parasites breed asexually in a host, but then only a small number, if any, are sampled by a mosquito. This is not a million miles from the amplification of gametes in a multicellular eukaryote, followed by sampling. The population size in the latter case is taken as the number of multicellular individuals, not the number of gametes or 'dead-end' cells. The effective mutation rate is a 'vertical' parameter, the number of replications in a cell lineage, not the total number of replications undergone by the entire pool. For a like-with-like comparison, the population size of Plasmodium must be a lot closer to the number of hosts than it is to the number of parasite cells.

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    1. It's smaller than even that, Allan. Only a subset of the asexually produced parasites differentiate into gametocytes in the human host. Only those gametocytes ingested by the mosquito have a chance to infect another human someday. Gamete production and the actual sex part happens in the mosquito midgut.

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    2. Well, it's probably of the order of the number of infected animals at any one time, since an infected individual can be bitten multiple times, and each bite can extract more than one parasite cell, offsetting those individuals who prove to be a dead end (sometimes literally) for a parasite lineage.

      This has been the most interesting thing about this debate. If you account for the bottlenecking caused by hosts and mosquitoes, Plasmodium actually has a population size close to that of the multicellular eukaryotes whose evolution Behe was trying to disprove. He treated Plasmodium as a large-population organism, whereas the effect of bottlenecking is that it causes it to have population genetic parameters that are much closer to those of its hosts. 10^20 becomes irrelevant, just as the wasted gametes and somatic replications in us are irrelevant to evolution.

      So I think Behe shot himself in the foot choosing this particular organism. If Plasmodium is a model for evolution's edge, an effective population of just a few million - the number of hosts, give or take - has managed to do something supposedly difficult about 10 times in just a few years. Evolution in eukaryotic populations of such a size is thus clearly not constrained by this supposed edge.

      In fact, one would wonder how it arose even once, if the double mutant has a likelihood of about 10^18. And the answer, I think, is the contribution to probabilities by recombination. A little goes a long way.

      I wonder if Behe's numerous fans in these threads have a comment on this?

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    3. Plasmo, like lots of other critters have a build in security system that gets triggered under stress. Its a mean fighter and finds a solution in the nick of time..to fight another day. But humans are smarter. They have effective counter-attacks.....because they possess a stronger intelligence.

      Hence, humanity at 7Bills.

      Pisser, that intelligence.....pulls the rug from right under evolution.

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    4. @Allan Miller
      good point, but I wonder whether it makes a difference that the selection step only occurs in the human host, where population sizes are much larger. Intuitively, that should mean that many more mutations would become available in Plasmodium than if it were the size of the host population. Of course, your argument works fine for drift, which indeed should be of the same order as in the host population.

      Oh, and I am not a Behe fan BTW :-)

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    5. Corneel,

      That certainly makes a difference, but the large population in a host is still bottlenecked on exit, and it starts small. If there are (say) 10^12 parasite cells in a late-stage victim (a guess), that gives a fair chance for a double mutant arising at least once in a couple of million victims. But it has to get out. If we assume that everything survives and replicates, you'd get 10^12 chances after about 40 generations of doubling. But the big numbers only arise at the end, so if it happens at gen 40, you have a high chance of it occurring but a minimal chance of it getting out - only 1 cell in 10^12 has it. If it happens at gen 1, every cell will have it, but that's the least likely point for the stochastic mutation to occur, when population numbers are tiny. If it happens in the middle, selection can obviously give it a boost, but it's more the serial selection in successive hosts that is significant.

      But either way, this is actually little different to the situation in the eukaryote's own gametes. There is less selection going on at gamete level, but a huge 'population' exploring mutational space with only a fractional chance of getting out. Once a mutation does get into the next zygote, half of descendant gametes will have it. Likewise, if a CR mutation happens early enough, it could get into a decent percentage of subsequent bites on this victim, and on around the population of carriers.

      I would liken the multicellular individuals to a set of jars, from which aliquots are periodically taken to seed new jars. Whether those aliquots are parasite cells, or the organism's own gametes, we have a huge population in the jar, and a massive notional population multiplying jars by cells, but there's a sampling process going on. The effective population for surviving mutations, and for their selection, is closer to the number of jars than to the total number of cells, in both cases.

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    6. The point about life-cycle bottlenecks limiting the effective population of Plasmodium is indeed fascinating. There's actually little difference between a unicellular parasite and its muticellular host. Behe should have chosen anything but a malaria-type parasite.

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    7. Steve: Pisser, that intelligence.....pulls the rug from right under evolution.

      Not your intelligence, surely.

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    8. Piotr, I take my intelligence over your(pl) pedantry any day of the week.

      Reliance on musings about what 'could' work doesnt' replace what we actually do know what works.

      Behe is arguing on the ground. You're(pl) arguing from remote possibilities.








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    9. Behe is arguing on the ground. You're(pl) arguing from remote possibilities.

      Hah! You could have phrased that a little better; it doesn't put Behe in the best of positions!

      The life cycle of the malaria parasite is not a remote possibility. It's what happens. It makes all the difference in the world between 10^20 free-living cells in a varying-strength chloroquine solution, and 10^20 cells distributed among a few million containers, some of which contain chloroquine. Over at TSZ, I recall you offering the possibility that Lenski's bugs communicate between jars ... maybe you could invoke that here!

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    10. Steve, I've never seen you make a cogent argument, or saying anything coherent, for that matter. You behave like an ordinary troll. If you do have any intelligence, please demonstrate it. I wouldn't be surprised if you are another sockpuppet/clone of the same person who posts as "Quest". Even if you aren't, the similarity (not to say indistinguishability) is intriguing.

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    11. In passing:

      Behe chose the malarial parasite because so much was known about it. Lots of data were available on it.

      I don't think the term "effective population" and asexual reproduction should have a lot in common with one another. It doesn't "take two to tango" with malarial parsites. And let's remember that in any one human infection, upwards of 10^12 replications can occur. That's one heck of a population size!

      I was at first surprised that there were different lineages, strains of malarial parasite. Why? Because I couldn't see how their "independence"---host to mosquito to new host to new mosquito---allowed for any genetic transfer between the parasites. Finding out that there was a "sexual" exchange between various lineages that takes place in the malarial gut helped solve that problem.

      But, then, my question to you who post here is: don't you wonder how such a "life-cycle" developed? How does such a thing come about?

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    12. Lino: "But, then, my question to you who post here is: don't you wonder how such a "life-cycle" developed? How does such a thing come about?"

      Finally, a reasonable question from a creationist. The answer is, yes, scientists, and specifically evolutionary biologists, ask these sorts of questions all the time.

      The difference between these people and creationists is that creationists never ask these questions. In fact, they are told by their various churches that they can't. Rather, they are given an answer (and a wrong one, at that) and told that it is fact and not to be questioned.

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    13. I don't think the term "effective population" and asexual reproduction should have a lot in common with one another. It doesn't "take two to tango" with malarial parsites.

      Lino, we've been over this.

      1) Even asexual organisms have an 'effective population'.
      2) Paramecium falciparum is not an asexual organism. It performs many mitoses in between meioses. That is true of every organism with a sexual step - including us. Mitosis is used for increase. Our cells happen to stay clumped together, Pf don't. Either way, the effective population is down to the amount of variation that can be sustained, and sharp population bottlenecks reduce that variation substantially. It's the cells that survive the bottleneck that count, not the ones that approach it.

      And let's remember that in any one human infection, upwards of 10^12 replications can occur. That's one heck of a population size!

      And let's remember that in one human male upwards of 1.5 * 10^12 replications can occur in the germline alone, in a lifetime. That's one heck of a population size! Now, you will say 'but that's different'. But HOW is it different? Infected humans don't burst, releasing 10^12 Pf into the environment, so the gee-whiz numbers involved in an infection have little evolutionary impact. If there is selection in the host, and variation (separate strains, or a mutation during the progression of a single strain), one variant may have an elevated chance of being sampled. But regardless, the only way out is that a mosquito samples just a few of those 10^12. The rest of the 10^12 die, and contribute nothing to evolution, and so are completely irrelevant, other than to bump up Behe's argument.

      But, then, my question to you who post here is: don't you wonder how such a "life-cycle" developed? How does such a thing come about?

      Sure. I'd hope it wasn't designed though, as such an elaborate means of visiting slaughter and misery does not reflect well on the Designer.

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    14. Lino, on this thread you have made numerous mathematical blunders, and consistently used science jargon incorrectly ("selection coefficient", "likelihood".) You appear to be reading our comments and trying to "guess" how to use jargon by following us, but this strategy only works for people with excellent reading comprehension. To be frank, your reading comprehension is not good enough for you to guess at the meanings of science jargon words by reading what we write. (Your use of "selection coefficient" was painful to read; you appear to think it means probability and you equated it to 1.0. Behe would not approve of this mistake.)

      Now you write:

      And let's remember that in any one human infection, upwards of 10^12 replications can occur. That's one heck of a population size!


      NO. The number of replications is approximately log base 2 of the CHANGE in population size. The # of replications would be ~40 if a patient started with one parasite and ended with 1.1 *10^12. But a patient would more likely start with 10 to 30 parasites, so since 2^4 = 16, subtract 4, the number of replications would be ~35 to 37, not 10^12 as you wrote above, so you are wrong by a factor of ~10^10.

      Again, we have emphasized here that Behe was very very wrong to assume the effective population size is 1 trillion parasites per patient. A more realistic value for effective population size is 10 to 30 per patient, so Behe's 10^20 number was wrong here by about 10^10. Since he squared his 10^20 number to make it 10^40, we should square his error-- his population size estimate was wrong by 10^20.

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    15. But then again, perhaps Lino meant total replication events and not rounds of replication. The latter (on the order of 40) is relevant to counting cumulative mutations for transmission to next patient; the former would be about 10^12, is relevant to total population size, but is not relevant to evolution.

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    16. ,,, perhaps Lino meant total replication events ...

      Could be, as he did state, and I quote, "By definition, the probability that a mutation will occur somewhere along the length of a genome is 1.0" although he has elected not to give the particular definition of replication that shows that.

      As Piotr has mentioned, the probability of mutation for any particular replication for the Plasmodium fulciparum genome is actually somewhat lower. By a factor of 25 or so.

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    18. Assuming a mean mutation rate m of 1.7 x 10^-9 per base pair per generation, and a genome size s of 23 Mbp (both taken from the literature), the probability that no mutation will occur anywhere in the genome during a single replication event must be close to (1-m)^s ≈ 0.96. How many mutations will accumulate after n rounds of replication is a trickier question, since there will be some net negative selection against non-synonymous mutations. Anyway, we can expect to find the first non-identical clone of the ancestral cell most likely after the fourth or fifth round of replication, when the population size grows to something of the order of 25.

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    19. Piotr:

      I've found both the numbers you've used above. Using those numbers, indeed, one would expect most parasites would replicate without mutating. This changes things dramatically, and this certainly would constitute a legitimate, and substantial argument against Behe's interpretation. It seems to me that someone should have challenged me with these numbers a long time ago.

      However, then there are results like this:
      [From: “Mutations in transmembrane domains 1, 4 and 9 of the Plasmodium falciparum chloroquine resistance transporter alter susceptibility to chloroquine, quinine and quinidine," Roland A. Cooper, et.al.]

      In our single-step selection experiments with CQ or QN, the concentration of drug used was rapidly lethal to the drug-sensitive parental 106/1K76 or 106/176I line, preventing proliferation of parasites without adaptive changes. With sufficiently large parasite populations, however, it was possible to select parasite(s) that had incurred a spontaneous point mutation capable of conferring resistance to the media concentration of the drug. Gassis and Rathod (1996) showed that 10^5−10^8 parasites are required to select resistance to atovaquone and 5-fluororotate.

      http://onlinelibrary.wiley.com/enhanced/doi/10.1111/j.1365-2958.2006.05511.x/

      By the 17th round of replication, there are already 10^5 parasites. According to your numbers, not a single mutation will arise until 8 rounds of replication later.

      Do you have an explanation for this discrepancy?

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    20. Diogenes:

      And let's remember that in any one human infection, upwards of 10^12 replications can occur. That's one heck of a population size!

      Did I write "rounds of replication"? No. Perhaps I should have written "replicants," but I think from context you should have been able to figure that out.

      As to selection coefficient, normally they are less than 1.0, much less. But here we're dealing with an environment that is lethal--either the mutations are there or they are not. If they are not, then the parasite won't live and won't "replicate." If you call something a "coefficient," then why would you use it as a 'probability'? There are standard population genetic equations that utilize the selection coefficient "s." Just plug in 1.0 instead of 0.01 or 0.01 etc.

      Why all the side-adventures?

      Delete
    21. Acartia:

      The difference between these people and creationists is that creationists never ask these questions. In fact, they are told by their various churches that they can't. Rather, they are given an answer (and a wrong one, at that) and told that it is fact and not to be questioned.

      You're just erecting a "straw-man." You'd do well to look beyond such suppositions. Remember, just because you disagree with the Darwinian paradigm, this by itself doesn't make you a Creationist. There are atheists who disagree with the paradigm. Why look for easy-way-outs?

      Delete
    22. Piotr:

      There's actually little difference between a unicellular parasite and its muticellular host. Behe should have chosen anything but a malaria-type parasite.

      What do you mean by this comment? Can you elaborate?

      Delete
    23. By the 17th round of replication, there are already 10^5 parasites. According to your numbers, not a single mutation will arise until 8 rounds of replication later.

      No, as I wrote a few posts up the thread, you can reasonably expect the first "mutants" after 4-5 rounds of replication. If you look at a particular lineage, mutations will happen more or less once per 25 generations. I hope it's clear enough.

      I don't think the fact that most replications (in a genome of that size) happen without copying errors is an argument against Behe. I mentioned it only because you had said something that was an obvious blunder. It doesn't matter because Behe's reasoning is sufficiently invalidated by other flaws.

      Delete
    24. What do you mean by this comment? Can you elaborate?

      One part of his argument was that a unicellular organism with a vast population had developed a feature like CR with some difficulty, so a similar feat should be impossible for a multicellular organism with a population that's many orders of magnitude smaller (with fewer opportunities for "pure chance" to produce anything interesting). But the contrast is hardly as sharp he thought it was. All those bottlenecks enforced by the complex life cycles of Plasmodium make its effective population very small in comparison with the number of individuals living at any given time. In fact, it's comparable with the effective populations of many multicellular organisms.

      Delete
    25. Piotr:

      I was reading quickly, and I thought you had written the 25 "round" of replication rather than simply a population size of 25 .

      But with this cleared up, there still remains the dilemna that with a population size as small as 10^5 atovoquine resistance is still seen to arise. And we're told that it is due to a SNP. The numbers we're using here doesn't allow a full sampling of the genome via SNPs when the population size is but 10^5. How is the neede SNP discovered? Any ideas?

      Delete
    26. Piotr:

      All those bottlenecks enforced by the complex life cycles of Plasmodium make its effective population very small in comparison with the number of individuals living at any given time. In fact, it's comparable with the effective populations of many multicellular organisms.

      I see that this would be your fundamental argument contra Behe. Right?

      Delete
    27. One of several. And it isn't "mine"; others have made it before.

      Delete
    28. Lino:
      "t doesn't "take two to tango" with malarial parsites."

      Yes it does. All species of malaria are sexually reproducing organisms. If both a male and a female gametocyte don't make it into the same mosquito, no tango, no oocyte, no baby parasites (so to speak).

      Delete
    29. Lino said to Acartia:

      "You're just erecting a "straw-man." You'd do well to look beyond such suppositions. Remember, just because you disagree with the Darwinian paradigm, this by itself doesn't make you a Creationist. There are atheists who disagree with the paradigm. Why look for easy-way-outs?"

      Lino, playing willfully dishonest games is one of the things that really pisses me off about you IDiot-creationists. You know damn well that you are a creationist and that what Acartia said about creationists is correct. You also know damn well that your religious beliefs are your sole motivation in your dominionist agenda against scientific evolutionary theory (what you IDiots perjoratively label as Darwinism or the Darwinian paradigm).

      You and the other IDiots pretend to be interested in doing and promoting credible science and in following the evidence to wherever it leads but your only actual interest and agenda is in destroying the practice of credible science and replacing it with your version of stifling, willfully uneducated, narcissistic, insane, authoritarian dominionism, and there's obviously no ruse that you IDCs will not employ to try to get away with it.

      It is completely irrelevant if there are any atheists who disagree with the "Darwinian paradigm", and the only reason that you asserted that is because you want to to distract the scientific people here from your REAL motivation and agenda. That's also why you won't answer my questions about your religious beliefs.

      You and the other IDiot-creationists go on and on and on about what you think is wrong with evolutionary theory but you provide NO evidence or an honest, positive, detailed, scientific explanation of your allegedly scientific alternative,

      Who is your chosen designer-god and what positive, scientific evidence can you provide to support its alleged existence and accomplishments? When, where, how, and why did/does your designer-god design, specify, create, intervene, manipulate, modify, build, destroy, or otherwise do all of the things that you claim evolution can't do and evolutionary theory can't explain? I included "why" because you 'God' pushers claim that there's a 'divine purpose' for everything.

      Here are my other questions/requests to you again (I may have missed some):

      Do you have any evidence to show that your chosen, so-called 'designer-god' did anything to cause you, in particular, to exist? Do you have any evidence to show that your chosen, so-called 'designer-god' did anything to cause malaria, any mutations (multiple or otherwise), and CR in some people but not in others?
      --------

      Lino, yes or no:

      Do you believe that your chosen 'God' designed and created harmful/deadly parasites, bacteria, and viruses?

      Do you believe that your chosen 'God' designed and created mutations that enable harmful/deadly drug resistance in parasites, bacteria, and viruses?

      Do yo believe that your chosen 'God' designed and created harmful/deadly parasites, bacteria, and viruses to righteously punish all living things because the biblical characters adam and eve sinned and their sin was spread into every living thing forever?

      Do you believe that all living things deserve to be punished by your chosen 'God' because of adam and eve's sin?

      Do you believe that you were/are specially created in the image of your chosen 'God'?

      ------

      See part two.

      Delete
    30. Part two.

      You're still on the 'specified mutations ahead of time' kick (a typical IDiotic kick). You obviously believe that the 'uniqueness' or 'particularity' of people (or at least you) and other things (such as mutations) is specified, designed, and created ahead of time by your chosen, so-called 'God'. How far ahead of time, and in the case of CR why are the malarial parasites in only some people resistant to chloroquine? Why not all malarial parasites or none at all? Are the people with those particular, specified, designed, created, chloroquine resistant parasites particularly evil or something?

      Present the evidence that shows that your chosen, so-called 'God' or any other so-called 'God' specifies, designs, and creates people, diseases, mutations, or anything at all (whether 'particular/unique' or not) and explain why your chosen, so-called 'God' specifies, designs, and creates deadly diseases and drug resistance, ahead of time or at any time.

      -------

      My questions pertain to what you believe is the 'truthful' alternative to natural evolution and scientific evolutionary theory. Since you are obviously a god pusher and you don't and won't accept that natural evolution occurs and that scientific evolutionary theory is credible then you should be willing to answer questions about your religious beliefs. After all, it's your religious beliefs that you believe are the 'truthful' alternative to natural evolution and scientific evolutionary theory, right?

      Delete
    31. The whole truth:

      You obviously believe that the 'uniqueness' or 'particularity' of people (or at least you) and other things (such as mutations) is specified, designed, and created ahead of time by your chosen, so-called 'God'.

      It is the nature of the chloroquine and the nature of the malarial parasite that requires the presence of two "specific" mutations. This is a battle between P. falciparum and chloroquine. We need not invoke anything else.

      Nonetheless, the fact remains that unless the parasite "finds" these two mutations, it will die. And if CR never develops, then lineage after lineage will die off until there likely would be no malarial parasites. But it manages to ultimately "find" these two mutations.

      If any two mutations would do, then by the 4th or 5th round of replication CR would already develop. I can't see how to interpret this any way differently.

      Delete
    32. The whole truth:

      My questions pertain to what you believe is the 'truthful' alternative to natural evolution and scientific evolutionary theory. Since you are obviously a god pusher and you don't and won't accept that natural evolution occurs and that scientific evolutionary theory is credible then you should be willing to answer questions about your religious beliefs. After all, it's your religious beliefs that you believe are the 'truthful' alternative to natural evolution and scientific evolutionary theory, right?

      You have to be careful to avoid the case of the “pot calling the kettle black.”

      I can believe that God designed, and is the Author of all of Life, and yet still believe that Darwinian mechanisms have been set in motion by this same God in order to bring about diversity of life. This is a position I maintained for many years.

      OTOH, if you begin to look at Darwinian theory, there is simply, IMO, too many things it seems almost impossible to explain. So, why can’t I object to Darwinian theory as faulty science? Why must you assume that the problems I have with Darwinism stem from my religious beliefs.

      In your case, you seem to take this approach to evolution: “Obviously God doesn’t exist. That’s nonsense. So it is crystal clear that evolutionary forces brought life into existence and provided for its diversity." In your case—as opposed to mine—there is no room in your thinking for ANY alternative; whereas I do have a default position.

      Who of us, then, is “freer” to think what he thinks?

      Delete
    33. Piotr:

      What other objections would you raise?

      BTW, I've thought over things, and I see that though the "speed" of mutation is less, this is balanced by there being less of a genome to explore. I imagine the numbers basically balance out, and we arrive at a figure, on average, of needing 10^8 replicates to reach the likelihood of there having been one mutation at every location along the genome's length.

      This makes my basic presentation sound. And, so, some other reason for disagreeing with Behe will need to be raised.

      That's why I'm asking about your objections. It seems that "bottlenecks" are "bottlenecks" for genetic drift, and big 'bottlenecks' will require P. falciparum to rely solely on its mutation rate---something we seem to be seeing.

      Any thoughts?

      Delete
    34. "Nonetheless, the fact remains that unless the parasite "finds" these two mutations, it will die. And if CR never develops, then lineage after lineage will die off until there likely would be no malarial parasites. But it manages to ultimately "find" these two mutations."

      And once again, no one would dispute this. The issue is with extending this single case to general cell biology and body plan evolution of multicellular eukaryotes. There is simply no evidence that simple changes to developmental timings, or general cell biology evolution, should require passing through these kinds of "only possible solution among a vast sea of nonfunctional mutational change", they are imagined, not evident.

      If you want evidence that a multitude of "solutions" exist in phenotypical space, look at the almost absurd diversity of life. There are tens of thousands species of beetles, there are over 11.000 species of Ferns. There are probably more species of microorganisms than every thing else combined.

      Again, the issue is not whether "too unlikely" solutions exist that could not be found in the available time, they do. The issue is extending such a situtation to the general evolution of life, thinking these kinds of obstacles would exist all over the place. Why? What merits this extrapolation?

      "OTOH, if you begin to look at Darwinian theory, there is simply, IMO, too many things it seems almost impossible to explain."

      A viewpoint almost exclusively correlated with religiosity. I don't think you can honestly deny that your religious convictions are fueling your propensity to extend the chloroquine resistance results into thinking this must generally be the case for the evolution of life.

      It actually seems to be the other way around. There is more often than not, some solution within reach. Almost every antibiotic we try eventually lead to some organism developing effective resistance.

      Delete
    35. Mikkel:

      The other side to all of this is this simple reality: if every evolutionary step is just one mutation away from the next, and, if nature's forces are 'blind,' then there is absolutely no direction to evolution, and just as an amoeba can become a fish, per Darwinian thought, there is nothing preventing a fish from becoming an amoeba. If this is so, then how do you explains stasis? How do you explain the fact that we don't see all kinds of intermediate forms, since nothing prevents evolution from going in either direction?

      If you take the position that two a.a.s are needed at the same time, then no barriers exist from one species from becoming another, and vice versa. And there's no explaining stasis.

      This is like wanting to have your cake and eating it too. Either way the Darwinian position is problematic.

      Delete
    36. Mikkel:

      Did the above questions I posed seem in any way motivated by religion?

      Delete
    37. They seem ignorant. That ignorance is probably motivated subconsciously by religion. Instead of a motivation to try to understand, you're motivated to jump at conclusions before you've considered all sides of the argument. As soon as you see some kind of problem, you stop your train of thought entirely. It's like you don't have an internal debate, you're not trying to find flaws in your own reasoning.

      What prevents just random change? Natural selection. Species usually occupy specific niches they're well adapted to, most niches are already occupied, which means that to diverge too much from your niche which you're well adapted to, into anther you're perhaps not that well adapted to, you're going to be at a disadvantage compared to those species already occupying that niche. In such a case one would expect natural selection to preserve the status quo.
      Notice how following large extinction events in the fossil record, we see a lot of evolution and divsersification. That's because large extinctions upset the established niches by killing off many species, this opens up a lot of niches, so that's when we see diversification. After a while, an equilibrium is established again and we start to see stasis.

      This is pretty standard stuff in paleontology and natural history, I'm surprised you've not alighted on this solution yourself. Well actually I'm not, because you're motivated to see flaws and barriers, instead of being motivated to see what kinds of solutions and patterns actual evolutionary biologists and paleontologists have found evidence of.

      Your biases are all the more problematic when you're not aware of them. I really think you should take some time to try to look more deeply into the litterature and see what kinds of thoughts evolutionary biologists and paleontologists have had on these matters. You will find you're rarely the first person to think about these things.

      Delete
    38. The other side to all of this is this simple reality: if every evolutionary step is just one mutation away from the next, and, if nature's forces are 'blind,' then there is absolutely no direction to evolution, and just as an amoeba can become a fish, per Darwinian thought, there is nothing preventing a fish from becoming an amoeba.

      ...says the imbecile who claims to understand probabilities.

      Great question, Lino! How about this one: If there is no direction to lottery winners, how is that we never see all the people who ever won the Powerball lottery winning it again, only in exactly the reverse chronological order? That's a real stumper, isn't it?

      Delete
    39. Lino said:
      "and just as an amoeba can become a fish, per Darwinian thought, there is nothing preventing a fish from becoming an amoeba."

      Evolution doesn't say any of that.Who told you that?

      Delete
    40. Mikkel:

      What prevents just random change? Natural selection. Species usually occupy specific niches they're well adapted to, most niches are already occupied, which means that to diverge too much from your niche which you're well adapted to, into anther you're perhaps not that well adapted to, you're going to be at a disadvantage compared to those species already occupying that niche.

      But the logic being employed here is that evolution is just one mutation away from some other "niche." There's the non-CR parasite, and, some argue, it's only one mutation away from CR.

      So, it would be easy via drift for a species that is being "out-competed" to become what it's competing with. Unless there are barriers keeping one species away from another---some kind of "multigenic event," then reversion will be the rule.

      If you tell me that reversion isn't the rule, then I'll insist that we're dealing with a "multgenic event."

      Delete
    41. Good lord. LIno thinks that a fish is one mutation away from becoming an amoeba.

      He is rapidly departing the category of "imbecile" and heading towards outright idiocy.

      Delete
    42. Speaking of fish, Lino is desperately fishing for something, anything, in the hope of saving face.

      Hey Lino, your responses to me show that when your dishonest, diversionary games are pointed out, you just play more dishonest, diversionary games, and your responses to others show the same thing.

      In addition to the fact that you IDiot-creationists are dishonest, one of the other things that really pisses me off about you is that you obviously think that people who accept natural evolution and scientific evolutionary theory are really stupid and will fall for your dishonesty and diversionary tactics. Your entire impression of yourselves is that you're 'divinely special' and vastly superior to anyone who accepts natural evolution and scientific evolutionary theory, right? You also see yourselves as VASTLY superior to all non-human life forms, don't you?

      You IDCs obviously have no qualms about lying, distorting, quote mining, conveniently ignoring, diverting, distracting, falsely accusing, making things up, and any other deceitful games in your 'war' against science (especially evolutionary theory and evolutionists) because you believe that you're superior and empowered by 'God' which, in your narcissistic, delusional, and unscrupulous mind, makes it not only perfectly okay but also a righteous crusade to push your authoritarian dominionist agenda by any means, no matter how despicable.

      Delete
    43. "But the logic being employed here is that evolution is just one mutation away from some other "niche. There's the non-CR parasite, and, some argue, it's only one mutation away from CR."

      How the hell do you extract this nonsense from what I wrote? No one is claiming it takes a single mutation to switch into a different niche. Seriously, how did you invent this? Nothing I or any one else here have said even remotely implies this.

      There's that strange religious bias clouding your judgement again. Please, please allow yourself some time to think a bit about it.

      Delete
    44. just as an amoeba can become a fish, per Darwinian thought, there is nothing preventing a fish from becoming an amoeba.

      Holy moly, Lino, this is just nonsense. It took billions of years and huge numbers of evolutionary changes for fish to come into existence. The fact that evolution occurs doesn't mean large evolutionary changes occur quickly or often.

      If this is so, then how do you explains stasis?

      Population genetics helps a lot with the explanation for relatively stable populations of species over long periods of time. There was a lot of good work done in this area almost a century ago. You should really read up on it. It is also true that populations that *appear* stable (sometimes called "living fossils" in the popular press) do in fact continue to evolve.

      How do you explain the fact that we don't see all kinds of intermediate forms, since nothing prevents evolution from going in either direction?

      We see lots and lots of intermediate forms. Since no population has absolutely stopped evolving, you can consider every species an intermediate form. But if you are talking about fossils, granting the difficulty of finding things tens of millions of years old, there are plenty of intermediate forms there. Archaeopteryx was found in 1861; more than 150 years later, don't you think it's time to agree with the simple fact that we see intermediate forms in the fossil record?

      It might help (perhaps not you, but someone sincerely contemplating these matters) to think in terms of languages. We see populations of the speakers of various languages coming into being, evolving to relatively stable forms, and passing out of existence. Even the relatively stable forms are constantly changing in small ways. For example, English has been relatively stable for a long period, such that you could probably get by pretty well in a conversation with someone from the 18th century; you'd be OK with someone from the 16th; but go back to the 14th century (Chaucer's time) and you'd be hard pressed to make any sense of English speech or writing at that time.

      And just like evolution, the changes in language don't have a particular overall direction. Some people claim English is "devolving," and certainly words, phrases and concepts are being lost; but new words, phrases, and concepts are constantly being added, too.

      Just like languages, it isn't that species are going "down" some evolutionary ladder that they formerly "climbed." They're just steadily changing, with no overall direction. (As Stephen Jay Gould pointed out, by far the largest biological groups are bacteria and viruses. That's what most life has evolved "into." So much for any overall "upward direction" to evolution.)

      Delete
    45. Mikkel:

      How the hell do you extract this nonsense from what I wrote? No one is claiming it takes a single mutation to switch into a different niche. Seriously, how did you invent this? Nothing I or any one else here have said even remotely implies this.

      There's that strange religious bias clouding your judgement again. Please, please allow yourself some time to think a bit about it.


      Let me start with your last two sentences. Did you think about this remark of mine?

      But the logic being employed here is that evolution is just one mutation away from some other "niche." There's the non-CR parasite, and, some argue, it's only one mutation away from CR.

      Do you not see that your argument is that species are in competition with one another for survival, AND, the non-CR malarial parasite is in an almost absolute struggle for survival, likely even more intense than between species in some locality? And, what is being argued here is that what separates the non-CR from the CR malarial parasites is ONE mutation.

      So, when you ask the question of logic, I'm simply generalizing the situation--there's a parallel between a malarial parasite trying to overcome a lethal dose of chloroquine and a kind of grass that is competing with flowers for soil---and then applying YOUR logic. Where have I gone wrong?

      Delete
  5. I don't know why Behe wasted the time an effort to write "The Edge of Evolution", when he could have made his entire argument in the form of a simple couplet:

    Chloroquine resistance is exceedingly rare.
    And, therefore, it's not possible that human bodies could have no hair.

    ReplyDelete
  6. I know the real reason why Behe decided to "close the discussion". He was losing.

    ReplyDelete
  7. Professor Moran,

    Thanks for your informative contributions to the debate with Professor Behe. I have found it all to be worthwhile and enoyable reading.

    ReplyDelete
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    1. Naaaaa....rhaeyga.

      Behe feels bad for Moran. Moran was gracious enough to admit the math was more than he could handle. The Behe won't clock an opponent on the mat.

      Besides, Behe need not write anything more...what with Moran scooping as much dirt over his pile as he can.

      Delete
    2. You have it all wrong Steve.

      "Behe feels bad for Moran. Moran was gracious enough to admit the math was more than he could handle. The Behe won't clock an opponent on the mat"

      The only thing you have right is that Dr. Moran did admit that the math was very difficult. That's because he is a scientist and not embarassed to admit there are details he can't reliably quantify.

      Behe, on the other hand, calculated the probability that Plasmodium falciparum could eveolve cloroquine resisitance at 1 in 10^20. Do you know how Behe arrived at this figure?

      Behe has been the one on the mat, with regard to the bacterial flagellum, blood clotting, the Dover testimony, and cloroquine resisitance in P. falciparum.

      Your sad, science-free troll bait won't be of interest to Bilbo, who I think is genuinely interested in understanding the complex issues raised in these discussions.

      Delete
    3. It recently struck me that one person who has been conspicuously silent on this issue is Nicholas White himself, which seemed odd as he is the one person who could settle the matter once and for all. This made me wonder if he was even aware of Behe's book.

      Luckily, there is this thing called the "internet" which includes a feature called "email."

      So it turns out that Prof. White was not aware of how Behe was, shall we say, interpreting his research. But he is now....

      Delete
  8. Agreed. With guys like Mikkel on board, its a crap shoot for ID.

    His erudition convinces him that emergent properties of matter allow him to not answer any hard questions. Intelligence emerges from non-intelligence ever so slowly.

    But rest assured, it happens. You can bank on it. At Mikkel Trust Bank, of course.

    That's where Larry happens to bank as well. Whodofthunk?

    ALL the hard question HAVE been SOLVED..............duh.

    Mikkel The Finn: "This Steve fellow is an excellent front-man for IDiocy, I say let him keep posting. The contrast an only serve us well."

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    Replies
    1. Sorry Steve, but your clear stupidity and attempts at "winning" by cheer-leading on Behe is so ridiculous that you make a huge disservice to your cause each time you write something. You should really stop and pay attention instead. Learn something. Read a book. Go to school. Get an education. Do some effort instead of pretending to understand something that's clearly so far from your grasp.

      Delete
    2. Yeah, right photo.

      Plasmo, like other parasites is limited in its defense capabilities. That IS the f#$% reason why we are able to develop defenses against it.

      We can only win the disease war if there in fact IS an edge to evolution.

      Your(pl) pedantic obfuscations don't change this reality.

      ...or would you prefer there is no edge and we all be consumed by a bug with a limitless arsenal.

      You make thinking more complicated then it need be.

      Like the penultimate academicians you(pl) are, you take the long way home so you can enjoy the breeze and falling autumn leaves while you contemplate the complexity of it all.

      Some folks are hungry, want a hot meal and have no time for such pleasantries.




      Delete
    3. Steve again demonstrates that he not only does not understand evolution. He does not even understand the Intelligent Design "theory" he is trying to defend.

      No one denies that there is an "edge to evolution". Just confining discussion to the human species, there are many traits and abilities that we do not possess. We cannot run at 60 mph. We cannot lift 50x our body weight. We can't shoot laser beams out of our eyes. Etc. All of these abilities, it seems, are beyond the "edge of evolution" to produce in a primate species.

      Behe's claim is that things that have actually evolved, such as the bacterial flagellum, are also beyond this "edge", despite the fact that they demonstrably are well within this edge, by simple virtue of the fact that they exist. So in order to support this ludicrous claim, he tries to bamboozle people with false claims and bad math. Luckily for him, there are enough gullible sycophants like yourself around to buy his ridiculous arguments.

      Delete
    4. Steve says: We can only win the disease war if there in fact IS an edge to evolution.

      True but irrelevant to Behe's blunders. Behe's figure of 10^20 was wrong by many orders of magnitude and no IDiot, Steve or otherwise, can save Behe's bad math. Behe put the limits of evolution in the totally wrong place and ascribed it to a phony mechanism which we know from experiments to be absurd: Behe claimed protein binding sites can't evolve, but experimentally we've seen many examples of it happening. So Behe's claims were falsified mathematically and experimentally and his figure of 10^20 (which he squared to make 10^40) is wrong by an astronomically large factor.

      (And who says we're guaranteed to win the war against disease? We're lucky if we just get stalemate.)

      None of you IDiots have the skills to save Behe's bacon, so you resort to endless name-calling and counterfactual declarations of victory. But Behe lost at every step of this argument.

      Delete
  9. Speaking of mutations and evolution, this article is about Ebola, not Malaria, but some of you may find it interesting:

    http://www.nature.com/news/ebola-virus-mutating-rapidly-as-it-spreads-1.15777

    ReplyDelete
  10. I was hoping I wouldn’t have to comment on this thread for many reasons; first off, I know that debates like that are pointless…. Why? Well, the back and forth arguments between professor Behe and professor Moran as well as the numerous flocks of Darwinists comments here seem to prove my argument…
    Just to prove my point, here is professor Moran’s final remark on professor Behe’s final blog on the issue of chloroquine resistance in malaria parasite…
    So, here we go….

    Professor Moran final remarks:
    “I'm afraid Michael Behe is confusing me with some of his other critics. I never suggested that chloroquine resistance could arise by stepwise addition of two mutations where each one added a little bit of resistance and was, therefore, favored by natural selection.”
    So after many years of debates, professor Moran decides to separate himself from other critics of Behe’s claims because…The evidence points in favor of Behe’s critics…possibly…? No.. it’s actually the other way around… just read the following what professor Moran wrote:
    “I am not a Darwinist and I don't usually rely on adaptationist explanations for complex phenomena with low probabilities. I'm not a big fan of natural selection. In fact, I think I've mentioned other mechanisms on this blog. I think I've even talked about things like Neutral Theory and population genetics and tried to get IDiots to understand how neutral alleles and deleterious alleles can contribute to evolution. “
    So…? What is the problem all of the sudden…?
    Professor Moran is not a Darwinist…It turns out NOW, (better now than never) that he is not a big fan of adaptation evolution that explains complex evolutionary changes…Why though…?
    Larry is not a big fan of natural selection that most of the big boys of the gang-Coyne, PZ Myers, Dawkins, etc) like… And they do like natural selection all right…But Larry doesn’t…
    I always give Larry credit for at least trying to be different and more open the “wholly trinity” …
    Larry keeps on going and at least tries to explain why he is not a part of the “wholly trinity” ….he no likes it…
    Larry:
    “ It's sad that Intelligent Design Creationists keep referring to Darwinism and "Darwinian magic" because it confuses their readers. If Behe is simply objecting to a strict Darwinian process as an explanation of chloroquine resistance then I completely agree with him. It seems pretty clear to me that the pathway to a chloroquine resistant strain involved neutral alleles and possibly even slightly deleterious ones. “
    So….What is Larry really saying here…? Larry doesn’t like the strict Darwinian process including the explanation of chloriquine resistance… He, Larry, goes beyond that; He agrees with Behe… why? He doesn’t think that strict Darwinian processes can explain this phenomenon…Meaning natural selection acting on variation….
    So… What is the solution that Larry proposes…? It must be as solid as rock….right? Be the judge for yourself…

    After admitting that Behe was right after all… Larry presents his substitution for Darwinian faith…:
    “ That's easily explained by modern evolutionary theory but not by the kind of Darwinism that Behe describes. Is that what this is all about? Is Behe's entire point just an argument in favor of random genetic drift and evolution by accident?”
    Darwin or Amen whatever you choose to belive….

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    1. I go with contingency. There is not a shred of evidence for your idiotic jesus nor any other god out there. Jesus/Allah/Vishnu/Zeus are all dead gods that deserve zero respect. Only to be believed by the gullible masses. If there is a god, It ain't none of them that I mentioned and thats a fact. We either looking at the eternal shifting forms of energy and matter as our daddy or a deistic god. We have no need of that hypothesis for a god since it has zero supporting evidence from reality. We do not find evidence that minds can exist independently of the brain.Retardation/Down Syndrome/Alzheimer's all attest to Bodiless mind as being pseudoscience only to be believed by abject slaves who so desperately want to believe in a celestial dictatorship

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    2. Quest, follow the link below and read one of the very first Sandwalk blogs, back in 2006.

      http://sandwalk.blogspot.com/2006/11/why-im-not-darwinist.html

      Prof. Moran has been repeating it for ages, and you have just taken notice. Better late than never, I suppose.

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    3. John Locklin wrote:

      "I go with contingency. There is not a shred of evidence for your idiotic jesus nor any other god out there. Jesus/Allah/Vishnu/Zeus are all dead gods that deserve zero respect. Only to be believed by the gullible masses. If there is a god, It ain't none of them that I mentioned and thats a fact. We either looking at the eternal shifting forms of energy and matter as our daddy or a deistic god. We have no need of that hypothesis for a god since it has zero supporting evidence from reality. We do not find evidence that minds can exist independently of the brain.Retardation/Down Syndrome/Alzheimer's all attest to Bodiless mind as being pseudoscience only to be believed by abject slaves who so desperately want to believe in a celestial dictatorship"

      Therefore evolution has to be true... even though everyday there is more and more evidence against it...

      One wise man once said: "...This is a very strange phenomenon; the more evidence there is out there against evolution, abiogenesis and for the universe that had to have the first intelligent cause the more people don't want to hear it. I see the world in 21 century (he said those words in 1980-ties) with more and more compiling evidence against materialistic explanation of the existence of the universe and life, with more and more people refusing to accept. I just don't understand why this is the case but I have a few hunches."

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    4. Quest:
      "Therefore evolution has to be true... even though everyday there is more and more evidence against it...

      No, it doesn't have to be true, but evolutionary theory has stood the test of time and scientific rigor. Everyday there is more evdence for it, not against it.

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    5. Chris B,

      Can you tell me what it would take, from evolutionary prospective, for a chicken to fly again...? The way I see... it's not much..

      So prove to me that ..."...evolutionary theory has stood the test of time and scientific rigor. Everyday there is more evdence for it, not against it..."

      Am I asking for too much...???

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    6. Quest seems to think that Baby Jesus has sent battalions of tiny invisible angels to hold chickens down and prevent them from taking flight, What an idiot.

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    7. Quest,
      Again, I'm not doing your work for you.

      "So prove to me that ..."...evolutionary theory has stood the test of time and scientific rigor. Everyday there is more evdence for it, not against it..." "

      Familirize yourself with some published literature on evolution.

      BTW, chickens can fly. I'll grant that chickens bred for roasting and kept in a pen where they can't stretch their wings, much less fly, their whole lives maybe can't fly. They were bred by artificial selection, which would not be possible if evolution was a failed theory.

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    8. And btw again, Quest,
      "Can you tell me what it would take, from evolutionary prospective, for a chicken to fly again...? The way I see... it's not much"

      Arguments from personal incredulity are not helpful. As for losing and regaining particular traits in species over evolutionary time, evolution is constrained by contingency. Presenting silly hypotheticals and asking evolutionary theory to explain them is not an argument.

      At least you're not bringing up the origins canard again, at least with me.

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    9. Professor Gąsiorowski,

      It is quite indisputable that professor Behe and many, many others are well aware where professor Moran stands on his own version how evolution supposed to have happened... However, I don't think this is the issue here at all …on this thread…

      The Moran/Behe exchange began when professor Moran got agitated with IDers demands for Behe’s critics to apologize to him in view of the new Summers 2014 paper on chloroquine resistance…that seem to have now confirmed Behe’s prediction in his book back in 2007…
      Professor Moran questioned whether that was the case and proposed his OWN CALCULATIONS… though he was not sure if he was right, so he asked for help, (which I think just speaks volumes about professor’s Moran’s humility…, well most of the times… I still think he is a really good guy… ;-)) ,regarding the probability of the chloroquine resistance arising according to Behe’s calculations… Without going into details, because there are too, too many details and too many variables when taken into consideration that can change the accuracy of the calculations (that is one of the reasons why I tend to avoid these kinds of debates…you don’t want to know the second one lol…) I think professor Moran had had many opportunities to present his final stand…. him not being Darwinist and all… He didn’t choose to do that until his final remark, which I’m referring to… Why?
      My view is this: He thought he could question Behe’s calculations; he did…
      But Behe fired back….So did Larry… both of them back and forth…

      However… in the end of this debate I sensed a bit of defeat on professor’s Moran’s side… Correct me if I’m wrong… Here is the quote…:
      Larry: “…If Behe is simply objecting to a strict Darwinian process as an explanation of chloroquine resistance then I completely agree with him. It seems pretty clear to me that the pathway to a chloroquine resistant strain involved neutral alleles and possibly even slightly deleterious ones. “
      I don’t have to present professor Moran’s views on this issue do I…
      My point is that if he was going to end the debate this way; being not Darwinist and all.. he could have argued it at the outset of his first blog on so called Behe’s challenge… he chose to do it…? I don’t know but I can only make an educated guess…

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    10. Anybody else on the board on the chicken evolution issue...? Larry..? Diogenes? I'm about to present the challenge.. You must disagree with me in one way or another....

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    11. Quest sez:

      Correct me if I’m wrong.

      You're wrong.

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    12. Latesuite,

      And your proof is....?

      Well, too bad you don't have any... ;)

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    13. Quest, quoting Larry Moran:

      …If Behe is simply objecting to a strict Darwinian process as an explanation of chloroquine resistance then I completely agree with him. It seems pretty clear to me that the pathway to a chloroquine resistant strain involved neutral alleles and possibly even slightly deleterious ones.

      You don't get irony, do you?

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    14. Irony..? You must be the third or the forth person on this blog who claims to know what Larry thinks and really means...

      However ... in this case irony is rather doubtful... unless it is synonymous with perjury where you come from...

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    15. You must be the third or the forth person on this blog who claims to know what Larry thinks and really means...

      Anyone can do it. It's called "reading comprehension."

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    16. @Quest

      There are lots of people who understand exactly what I mean. They are smart enough to recognize irony and sarcasm when they see it. They are also smart enough to understand modern evolutionary theory.

      You are not one of those people.

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    17. Quest has done us the favour of practically demonstrating the type of cognitive functioning that allows creationism to persist and continue to attract acolytes. LIno's doing a pretty good job, too.

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  11. Larry wrote:"

    If Behe is simply objecting to a strict Darwinian process as an explanation of chloroquine resistance then I completely agree with him. It seems pretty clear to me that the pathway to a chloroquine resistant strain involved neutral alleles and possibly even slightly deleterious ones..."

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    1. Yes, that's what Larry wrote.
      Did you have a point or were you just demonstrating a quotemine?

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    2. So…? What is the problem all of the sudden…?
      Professor Moran is not a Darwinist…It turns out NOW, (better now than never) that he is not a big fan of adaptation evolution that explains complex evolutionary changes…


      All of the sudden? NOW?

      OK. I'll quotemine too. This is LM from more than seven years ago, on this very blog that you so secantially intrude on:

      "While we've known about drift for decades the full scale of it's role in evolution is only now beginning to be appreciated. Most people still don't realize that random genetic drift is by far the most common mechanism of evolution."

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  12. I don’t know why but this morning I feel like opening with

    Hi Larry, you seem to be attractive to Musca domestica, you got quite a swarm buzzing around here. Most of the time they are harmless, but they can be a real nuisance when they are flying around. But they can also transmit diseases, so it is important to get rid of them. House fly control is not always as easy as it sounds. There is often more involved than a fly swatter.

    The old saying “You cant teach a house fly new tricks” is only the tip of the iceberg. You can’t teach them anything. As for instance, it can be pointed out to them time and again but germs like the anthropic principle, fine-tuned universe, origins of life, edge of evolution and many more are stuck to their legs. They are religious as well, their deity is the God-of-the gaps.

    One thing is certain, there are edges to evolution like there are edges to most other things – but there’s no edge to creationism. There are more than 16,000 species of flies in North America. They may posses all the intelligence they need to survive but otherwise qualify as ignorant.

    If it isn’t ID and Demsbki, Luskin, Meyer or Behe, the fossil record, it is YEC and the bible. Or a combination of both, anything goes as long as it is anti science. What they haven’t got and never will, is a theory of Intelligent Design. The most legitimate question of “who did what where and when” is ignored.

    I saved the following from the ARN ID forum man many years ago where I first learned about the existence of ID:

    QUOTE
    From a transcript made at the DDD3 conference in 2002:

    Question from the audience: I’d be interested in hearing you tell us a little bit about what your theory of intelligent design is, as opposed to what evolution isn’t.

    Behe replies: Well, that’s a great question, and I know folks on the other side who are sceptical of intelligent design often get frustrated, but I try to be as conservative as I can and I don’t go out beyond what the data can support because I think overreaching is the bane of theories of design. You say that flagellum looks designed so everything is designed, or that everything that looks complex was designed, or something like that.

    I think the short answer to your question is, for all of those things, I don’t know.

    There not enough data. For the elephant, we have primelephus, the ancestral elephant of the Asian and African elephant, and mammoth. Well, could that happened by random mutation and natural selection? My instinctive answer is sure - it sure looks like it. It doesn’t look like any big deal.

    The more careful answer, the actual answer, is I don’t know - cause I don’t know what’s involved in making one versus the other. I don’t know what molecular changes are necessary to make the small anatomical differences in those different species.

    Suppose one believed that those things could have happened by natural selection, but maybe the origination of mammals needed some extra information - how would that have happened - how would the designer have done that? Would it have been, say, information embedded into nature at the big bang, or whenever nature started, or might it have been manipulations along the way, or some sort of input along the way?

    The short answer is “I don’t know.”
    UNQUOTE

    Indeed, we know.

    If only the rest of them would come out of the closet.

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