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Mark, This is What all the Fuss is About

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

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

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

Fair question, to which gpuccio aptly responds:

Mark:

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

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

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

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

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

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

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

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

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

Comments
BA77
But don’t feel too bad Moran, we are ALL really, really, stupid when it comes to trying to understand the unfathomed complexity of even the simplest of cells!
The more I try to understand the mechanisms behind the cell fate determination, intrinsic asymmetric mitosis, timely centrosome segregation, precise spindle checkpoints, cell polarization, extrinsic or intrinsic factors, signaling pathways, the whole nine yards, mind-boggling, overwhelming, I feel more and more stupid, completely ignorant. In my many years working on engineering design software development I never ever felt this way. Looking back at those years, now it seems like my work was so easy and simple. Now for every outstanding question that gets answered, new questions are raised. Unending revelation of the ultimate reality. Then when I talk to friends biologists and ask them to help me with understanding all that, everyone and their cousins look at me with wide open eyes and confess they don't understand that either. We are approaching a major 'told you so' moment in science. Someone said, long ago, that He will make us feel this way, realizing our limitations to comprehend everything, and swallowing our ridiculous pride. It's not too late to humbly admit we are studying and trying to understand an amazing creation. But we are free to continue in our foolishness going back to our vomit too. It's up to each of us to decide.Dionisio
August 15, 2014
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#29 Jerry   I think there is a misunderstanding between us.  Of course I know that new alleles have to arise naturally. I also understand that in this particular case it took a lot of generations to get to a fairly simple change. But it doesn’t follow that a more complex change such as new allele should take proportionally more generations.  There are so many other factors to take into account. That is why I wrote:
As far as I can see everyone seems to agree that the mutations required for chloroquine resistance are extremely improbable and this is born out by the rarity of such resistance in the wild. So what?
On the original thread I had a brief but interesting discussion with the polite and intelligent Gpuccio about the factors that might make a difference (of course he did not agree with me but I don’t think he found my position either wilfully obstructive or pathetic). I expect you were not aware of that – (which is quite understandable – no one can read everything that is posted) – and that may account for the misunderstanding.Mark Frank
August 15, 2014
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Yes, there is another possibility- some hybrid of naturalistic evolution, ID, and creation is true. Let us take advantage of every opportunity to advance knowledge and understanding, with sincere and honest dialogue, and brotherly love. Amen?littlejohn
August 15, 2014
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Larry Moran 30 Stupid, not in the least. Blinkered by a priori materialist assumptions, yes. Just as many brilliant minds believed in the Ptolemaic system of epicycles because of an a priori commitment to circular orbits.anthropic
August 15, 2014
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But don't feel too bad Moran, we are ALL really, really, stupid when it comes to trying to understand the unfathomed complexity of even the simplest of cells! “Although the tiniest living things known to science, bacterial cells, are incredibly small (10^-12 grams), each is a veritable micro-miniaturized factory containing thousands of elegantly designed pieces of intricate molecular machinery, made up altogether of one hundred thousand million atoms, far more complicated than any machine built by man and absolutely without parallel in the non-living world”. Michael Denton, “Evolution: A Theory in Crisis,” 1986, p. 250. The Cell as a Collection of Protein Machines “We have always underestimated cells. Undoubtedly we still do today,,, Indeed, the entire cell can be viewed as a factory that contains an elaborate network of interlocking assembly lines, each which is composed of a set of large protein machines.” Bruce Alberts: Former President, National Academy of Sciences; “To grasp the reality of life as it has been revealed by molecular biology, we must first magnify a cell a thousand million times until it is 20 kilometers in diameter and resembles a giant airship large enough to cover a great city like London or New York. What we would see then would be an object of unparalleled complexity,…we would find ourselves in a world of supreme technology and bewildering complexity.” Michael Denton PhD., Evolution: A Theory In Crisis, pg.328 “Each cell with genetic information, from bacteria to man, consists of artificial languages and their decoding systems, memory banks for information storage and retrieval, elegant control systems regulating the automated assembly of parts and components, error fail-safe and proof-reading devices utilized for quality control, assembly processes involving the principle of prefabrication and modular construction and a capacity not equaled in any of our most advanced machines, for it would be capable of replicating its entire structure within a matter of a few hours” Michael Denton PhD. Evolution: A Theory In Crisis pg. 329 “a one-celled bacterium, e. coli, is estimated to contain the equivalent of 100 million pages of Encyclopedia Britannica. Expressed in information in science jargon, this would be the same as 10^12 bits of information. In comparison, the total writings from classical Greek Civilization is only 10^9 bits, and the largest libraries in the world – The British Museum, Oxford Bodleian Library, New York Public Library, Harvard Widenier Library, and the Moscow Lenin Library – have about 10 million volumes or 10^12 bits.” – R. C. Wysong ‘The information content of a simple cell has been estimated as around 10^12 bits, comparable to about a hundred million pages of the Encyclopedia Britannica.” Carl Sagan, “Life” in Encyclopedia Britannica: Macropaedia (1974 ed.), pp. 893-894 HISTORY OF EVOLUTIONARY THEORY – WISTAR DESTROYS EVOLUTION Excerpt: A number of mathematicians, familiar with the biological problems, spoke at that 1966 Wistar Institute,, For example, Murray Eden showed that it would be impossible for even a single ordered pair of genes to be produced by DNA mutations in the bacteria, E. coli,—with 5 billion years in which to produce it! His estimate was based on 5 trillion tons of the bacteria covering the planet to a depth of nearly an inch during that 5 billion years. He then explained that,, E. coli contain(s) over a trillion (10^12) bits of data. That is the number 10 followed by 12 zeros. *Eden then showed the mathematical impossibility of protein forming by chance. "It has become clear in the past ten years that the concept of design is not merely an add-on meta-description of biological systems, of no scientific consequence, but is in fact a driver of science. A whole cohort of young scientists is being trained to “think like engineers” when looking at biological systems, using terms explicitly related to engineering design concepts: design, purpose, optimal tradeoffs for multiple goals, information, control, decision making, etc. This approach is widely seen as a successful, predictive, quantitative theory of biology." David Snoke*, Systems Biology as a Research Program for Intelligent Design OT: podcast: "David Snoke: Systems Biology and Intelligent Design, pt. 1" http://intelligentdesign.podomatic.com/entry/2014-08-11T17_19_09-07_00 podcast: David Snoke: Systems Biology and Intelligent Design, pt. 2 http://intelligentdesign.podomatic.com/entry/2014-08-13T16_30_01-07_00bornagain77
August 15, 2014
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We must be really, really, stupid. LOL, surely you don't think you are going to get disagreement on UD do you?bornagain77
August 15, 2014
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In order for naturalistic evolution to take place, new alleles have to arise naturally. These calculations show that just simple modifications of current alleles to reach a new function seem out of reach of naturalistic processes. Let alone of de novo functional alleles. Thus, it is impossible for naturalistic evolution to take place and one must look for an alternative explanation. If you do not understand this then you should go to lurker status till you understand the basic issue.
Isn't it amazing that thousands of evolutionary biologists over the past one hundred years don't understand this simple explanation? We must be really, really, stupid. Or is there another possibility?Larry Moran
August 15, 2014
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So help this poor pathetic person understand the relevance of the point.
In order for naturalistic evolution to take place, new alleles have to arise naturally. These calculations show that just simple modifications of current alleles to reach a new function seem out of reach of naturalistic processes. Let alone of de novo functional alleles. Thus, it is impossible for naturalistic evolution to take place and one must look for an alternative explanation. If you do not understand this then you should go to lurker status till you understand the basic issue. But, you have been here longer than I have and I first came here over 8 years ago. How could you not understand what it is all about. Thus, my two alternatives. You do not have to agree but you have to know. If you know, willful obstruction is the diagnosis. If you do not know this, then the word "pathetic" is appropriate.jerry
August 15, 2014
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Does 4 instead of 2 not lower the odds considerably? Want to some math around that?
The odds of the first two mutations are about one in 10^18, since you need both before selection can start to act on them. Mutations 3 and 4 have odds of about one in 10^9 because selection can act at each step.JoeCoder
August 15, 2014
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JoeCoder It is true that Larry Moran's calculations take him to 10^18 and I guess in a mathematical sense he could say "the probability is much higher" but that is not what I'm alluding to....... Larry said;
He also doesn’t admit that you probably need FOUR mutations in order to get effective chloroquine resistance.
Larry makes Behe's point here about the difficulty and then tells us that he's wrong!!!!! Dies 4 instead of 2 not lower the odds considerably? Want to some math around that?Andre
August 14, 2014
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True and humans have a fixation with the malaria parasite in the wild. So that's something. ;)Joe
August 14, 2014
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Joe:
As for fixation, well when has that ever been observed in wild populations of the malaria parasite?
All the time Joe, all the time. But it's the allele that does not confer chloroquine resistance that gets fixed! :)Mung
August 14, 2014
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I thought his point about mutations was to show how difficult they were to get specific combinations of, let alone be able to get beyond the Edge of two new protein-protein binding sites.Joe
August 14, 2014
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Joe @22 I'm on Behe's side, Edge of Evolution was actually one of my favorite books, and I think Behe was right on many his points. But because two mutations confer only very weak chloroquine resistance, those two mutations would have to occur hundreds of times before they spread far enough to be detected. So it's probably closer to 10^18 than to 10^20. I think that's close enough and if you swap that number into Edge, the rest of Behe's arguments aren't significantly affected. And it still means the reviewers were wrong in their bickering that a simultaneous mutation was significantly less likely than a stepwise one through neutral space, or saying that selection at each step.JoeCoder
August 14, 2014
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Dr Behe got his numbers from peer-review. The numbers are not as Behe said, they are as Behe cites. When your numbers appear in peer-review Behe will consider them- or even if you send him an email once you hammer it all out.Joe
August 14, 2014
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wd400 I'm sure I've made some mistakes in my comments here too! Thanks for all of your past contributions to UD. Even though I'm an ID person I generally look forward to seeing your comments on a thread.JoeCoder
August 14, 2014
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We cross posted JoeCoder, So just to clarify I wan't assuming the population didn't grow. The 30 is the is the number of ways you can get one success and 29 failures in 30 trials ("30 choose 1"), It would work if each cell was one experiment to itself, but doesn't here because they share some of the divisions.wd400
August 14, 2014
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Andre I don't think that's what Dr. Moran is saying. It looks like it takes less than 10^20 for the mutation to appear, and probably pretty close to 10^18 -- which itself is close to the inverse square of the mutation rate. But because it's only very weakly beneficial, it must appear multiple times before selection will cause it to spread. And it must spread at least to a population in the millions before the third and fourth single-step mutations have a good probability of arising. So IMHO, while it takes less than 10^20 to appear (as Behe said), it still likely takes around 10^20 to appear and be headed toward fixation. Which at the end of the day is all that matters in studying chloroquine resistance. But if there's a two-step mutation that is strongly beneficial, it will take less than 10^20 to fix in the population.JoeCoder
August 14, 2014
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JoeCoder, Ha, seems Diogenes and I made the same mistake by different routes. p = 30 * u *(1-u)^29 is from the biomial distribution, which would apply if each cell went through 30 cell divisions all by itself, but doesn't count here since all cells share some history with each other. You approach is right (though I'd stress the number of cell divisions, not the number of cells that have existed, ,which is slipery with daughter cells anyyway). Ignoring the starting population you end up with 2^(N+1)-2 trials so 5 single mutants after 30 gens.wd400
August 14, 2014
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Strange that Dr Behe flat out states that more than 2 mutations are required. As for fixation, well when has that ever been observed in wild populations of the malaria parasite? With stochastic processes, such as natural selection and drift, specific combinations of mutations are beyond the reach of all species.Joe
August 14, 2014
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Sorry the above should say "So your result of 80.5 single mutants..."JoeCoder
August 14, 2014
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wd400 I think I see the problem in your math now, the error (30) is in bold:
E = 2^30 * (30 * (2.5e-9) * (1-2.5e-9)^29)
You're calculating the odds for 30 generations with each generation having 2^30. Not a population that's growing up from a small number to 2^30 in size. So your result of 268 single mutants is after a cumulative population of 30 x 2^30 = 32 billion cells. Or one mutant arising every 32 billion / 80.5 = 397 million cells. Which is the inverse of the mutation rate we started with, as it should be.JoeCoder
August 14, 2014
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Am i reading this right? Larry Moran says it is even more complicated than what Behe suggests so therefor he is wrong? LOL!!!! thank you for proving Behe's point Larry..... This post is a keeper! This just shows even if the IDIOT is more right than materialists they will cook up a scheme to say..... "You're wrong because its even worse than you claimed" Did a professor just say that? Hahahaha!!!!! Just admit it Larry Behe busted you lot.....Andre
August 14, 2014
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We all agree that some genotypes, like chloroquine resistance in Plasmodium, are extremely rare. That's not an issue. We also agree that such combinations of mutation will be beyond the reach of some species. What we're contesting is the claim that Behe's predictions were recently confirmed. They were not. Behe predicted that only two mutations were required and that the probability of this happening is 10^-20. We said his calculation was wrong. Behe challenged us to come up with our own numbers. We did - to the best of our ability. Turns out that that the probability of two mutations is much higher than Behe claimed but that there's more to the issue than just the occurrence of a mutation. Behe didn't take fixation/detection into account. He also doesn't admit that you probably need FOUR mutations in order to get effective chloroquine resistance. Some of us are still waiting to see if Michael Behe can meet his own challenge. The rest of Behe's argument is as bogus as his calculation of the probability of chloroquine resistance.Larry Moran
August 14, 2014
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Above you can remove the steps of multiplying and then dividing by 23 million to simplify the calculation. But the result it the same.JoeCoder
August 14, 2014
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wd4000, thank you for the friendly feedback, but I think you are wrong :). Specifically here:
p = 30 * u *(1-u)^29
I'm not sure where this formula comes from but I tried plugging some different numbers into it:
2^24 * (24* (2.5e-9) * (1-2.5e-9)^23) = 1
That would mean that a single mutant arises once once the population reaches 2^24=16.7 million in size. Times two would be a total cumulative population of 33 million. Those 33 million cells times u=2.5e-9 times a 23 million base genome size = 1.9 million mutations that would have occurred. 1.9 million / 23 million is 8.2%. That would mean that on average they find the first single-point mutation after only exploring 8.2% of their genome. But that can't be right because you can't find it faster than you can look for it. So I think that must be a wrong result. Are your formulas the correct ones to use in this exercise? Please check my work to see if I'm wrong :)JoeCoder
August 14, 2014
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#3 Jerry
ID in the evolution debate is mainly about the origin of new alleles.
I total agree this is true but I am afraid I don't see the relevance of this remark. It is not a case of wilful insertion of obstructive comments so I guess it must be pathetic. So help this poor pathetic person understand the relevance of the point.Mark Frank
August 14, 2014
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(the above should say the malaria parasite is haploid in humans, it's diploid in other stages. THere are many other subtlties these back of the envelope calculations ignore too)wd400
August 14, 2014
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JoeCoder, You are both wrong :) It's not the sum of the number of cells that have existed that matter, so we don't need to sum the series. Instead, we want to know how many cell divisions have occured. Diogenes has calculated the population size presuming the infection starts form two sporozites, which is indeed 2^30 or about a billion. Seems like he created a complex way of tracking the mutations, but we can't instead use basic probability. We are looking for cells that have acquired exactly one mutation in 30 generations. If we call the mutation rate u the probability this happens is p = 30 * u *(1-u)^29 and the expected number of these from n trials is n.p so E = 2^30 * (30 * (2.5e-9) * (1-2.5e-9)^29) ~ 80.5 Diogenes then multiplies that by 2/3 to get ~53.7. But diogenes has assumed that the infection starts from two sporozites, which is not necessarily the case, and that the malaria paraise it diploid (in fact it's haploid). If an infection started from 10 sporozites, factor in the haploidy and say only one of 3 possible mutations is the right one you'd end up with (10 * 2^30) * (30 * (2.5e-9) * (1-2.5e-9)^29) * 1/3 ~268 single mutants.wd400
August 14, 2014
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willful insertion of obstructive comments just for the hell of it.
Ding! I think you got it.TSErik
August 14, 2014
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