Is There Enough Time For Humans to Have Evolved From Apes? Dr. Ann Gauger Answers

_{Denyse O'Leary

November 5, 2012

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The study talks about how long it takes to get two specific mutations in the same pre-specified regulatory sequence. Gauger wants that to be a speed-limit for human evolution, but hasn’t actually argued as to why it should be.
1- Because not any ole mutational accumulation will do it 2- The changes required themselves require an ordered sequence or they do not work. The muscular-skeleton- nervous system is coordinated. You just can't grow a leg bone without having all the supporting stuff.Joe_{November 17, 2012
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No specificity required:
ATP synthase is a molecular machine used in the production of chemical energy. It is constructed from over 40,000 atoms each in a specific place and performing a specific function. - David S. Goodsell, The Machinery of Life
Any old change will do. But just try living without ATP.Mung_{November 17, 2012
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Eric:
I thought your beef with Gauger was that you don’t think specific mutations are required to get to humans.>
Thank God no evolutionist has ever published a paper on what specific mutations might be required to get to an eye. After all, just any old changes would have sufficed.Mung_{November 16, 2012
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The study talks about how long it takes to get two specific mutations in the same pre-specified regulatory sequence. Gauger wants that to be a speed-limit for human evolution, but hasn't actually argued as to why it should be.wd400_{November 16, 2012
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wd400 @117: Doesn't the study talk about how long it takes to get specified mutations in a particular population? I thought your beef with Gauger was that you don't think specific mutations are required to get to humans.Eric Anderson_{November 16, 2012
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wd400:
The reason I haven’t answered you’re comments about fixation and substitution is there is nothing there – if you want to try again please do, but substitution and fixation are the same thing.
Not always. A fixation is always a substitution but a substitution is not always a fixation. The references have been provided that say all mutations are substitutions and we already know that not all mutations become fixed.Joe_{November 16, 2012
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Sure, but you don't do that by plucking numbers from studies without considering their assumptions in the way Gauger haswd400_{November 16, 2012
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wd400 @114: Good. So I presume you also acknowledge that someone can take an interest in, and ask, the following scientific question on its own merit, without resorting to hypothetical discussions about what evolution could have done in some other alternate universe or timeline: "Given the existence of system x, what can we infer is the most likely explanation for the origin of this system x?"Eric Anderson_{November 16, 2012
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With Intelligent Design evolution, evolution is searching for a particular something. And there still isn't any evidence that any amount of mutational accumulation can account for all the physical differences between humans and chimps. The premise of common ancestry is still unscientific.Joe_{November 16, 2012
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Eric, Sure. Mung, Obviously. Evolution isn't "searching" for a particular something. When the speciation process that separated us from chimps started there were many possible outcomes for the descendant populations. Selection means we only navigate between a small subset of those possible forms.wd400_{November 15, 2012
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wd400:
(1) and (2) are related.
But you do acknowledge that these are logically separate questions, and that answering "No" to the first one does not mean that the answer to the second one is also "No," correct?Eric Anderson_{November 15, 2012
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wd400:
What mung said, basically
Except for the Ideal and the Forms part, I bet. :) There are no unsubstantiated forms just waiting to be found, there is no finding going on in evolution, no searching. It's just pure dumb luck that these "forms most beautiful" are there waiting to be "found."Mung_{November 15, 2012
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Eric, (1) and (2) are related. But if you want to skip that and get on to (2), there aren't many systems that only work exactly as they are now. The only one I can think of off the top of my head are a couple of residudes in ribosomal RNAs that are conserved throughout life. For everything else, even quite basic reaction like the kerb's cycle, very divergent proteins perform the same role. PaV, It would take you 10 secs to google "lactase persistence" and realise what you've said about it doesn't make any sense. It's science because we know lactase persistence is an adaptation that has arisen several times, and every time (it seems) a different mutation gave rise to the phenotype. The reason I haven't answered you're comments about fixation and substitution is there is nothing there - if you want to try again please do, but substitution and fixation are the same thing. There are certainly cases in which very specific mutations are required (the Bt toxin resistance being the shining example), so that requires the same amino acid residue (which can probably arise from different DNA mutations). If you'd like to tell me what that has to do with human evolution I'd love to know.wd400_{November 15, 2012
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wd400:
For that to be relevant to human evolution you have to think most of our evolution involved waiting for these super-specific mutations. That seems unlikely when you think about something like lactose persistence, which has many different alleles giving the phenotype, that seems like a faulty assumption.
Aren't you simply giving an opinion here? That is, 'in your opinion' it is unlikely that "super-specific" mutations must lead the way forward. I say this because the only evidence you give for this view is that there are many 'alleles' giving rise to lactose persistence (whatever that might be). But, given that lactose is how young mammals are fed for the most part, this might simply be some kind of pleitropic effect intended to make sure that various genetic pathways lead to what is absolutely essential for organisms to survive (they will die off if their young all die off). Of course this is a guess on my part, just as your view is a guess on your part. Then how does this become science? Having pointed out the 'guesswork' involved here, let me now point out that in Behe's "Edge of Evolution" two "super-specific" mutations were required to overcome chloroquine resistance. Not just any old mutation would do. Well, hadn't the malarial parasite been around for hundreds of thousands of generations? Shouldn't there have been all kinds of 'neutral mutations' at the ready? So, why did it take so long for it to develop resistance? The only explanation is the need for "super-specific" mutations to arise. [[In your responses so far, let me note that you haven't addressed the point I've made that "substitution" is used instead of "fixation" because we're dealing with 'neutral' loci. You want to claim that 'neutral' loci become, basically, 'conserved' loci. But how? Why? And in what kind of a time-frame?]] Let me also point out a recent study which showed that insects feeding on the leaves of a plant that typically develops a specific kind of fungus on its leaves, developed the very same mutations for overcoming the poisoning effect of the fungus. This "super-specificity" is made clear by the fact that the very same sequence and location occurred even across the boundary of different "orders"(!) of the insects. I suspect that increasingly inexpensive whole genome analysis techniques will soon uncover lots and lots of these "super-specific" mutations, all of which demonstrate the need for having to "wait" for specific mutations if you want to move from functional A to functional non-A. So, wd400, you have your opinion, based on something that is susceptible to various interpretations, and I have an opinion that holds up to what today is being revealed by science. Why, then, ask me to let go of my view? Isn't yours the one that is incompatible with science?PaV_{November 15, 2012
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Mung, I note your sarcasm; wd400, I note your lack of it. Pretty ironic, the two responses. :) I'm not talking about a hypothetical future wherever the winds of evolutionary whim might take us. I'm talking about actual organisms and systems that we know exist. wd400, from your response I take it, though, that it is your position that no specific mutations were required to get any of the organisms or biological systems that we see today? So, back to your alleles example in #105, it doesn't really matter whether we are talking about several possible allele forms with minor point changes between them. We might as well be talking about the mammalian eye, the bacterial flagellum, the Krebs cycle, DNA itself. No specific mutations were required to produce these systems? Is that really your position? Please note that the following are two very different questions, and please make sure you are not conflating the two: (i) Did evolution have to produce this particular system? (ii) In order to get to this particular system (which we know exists), are specific mutations required?Eric Anderson_{November 14, 2012
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What mung said, basicallywd400_{November 14, 2012
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Eric, there is no specific organism B to get to from organism A. There are all these uninstantiated forms out there in Ideal space, any number of which [or none of which] could have been realized as a consequence of changes to the hypothetical common ancestor of chimps and humans and orangutans. Maybe humans, maybe no. Maybe chimps, maybe no. Maybe some combination of the above, or no combination of the above. It could just as easily have been Pooferbibbles and Grambldorps instead. We just can't say. I know it sucks, but that's science. Whatever will be will be.Mung_{November 14, 2012
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wd400 @103: I'm curious. Does your view (i.e., no specific mutations required) apply only to the particular case of chimp-human transition, or do you believe it also holds generally across speciation transitions, namely that there are no specific mutations required to get from organism A to organism B?Eric Anderson_{November 14, 2012
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The math starts with the assumption that the there is a benefit to be had if one particular mutation (right down the the nucleotide position and the actual residue it has to change to) would only arise. For that to be relevant to human evolution you have to think most of our evolution involved waiting for these super-specific mutations. That seems unlikely when you think about something like lactsse persistence, which has many different alleles giving the phenotype, that seems like a faulty assumption.wd400_{November 14, 2012
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wd400: To think this math is relevent you have to think that environmental pressures changed that one, and only one, mutation would provide a fitness benefit and populations had to wait around for that mutation to gain the benifit. That’s question-begging on a grand scale. Can you restate this? I can't change a word around and make sense of it. Unless, . . . should it read: " . . . to think that environmental pressures, by changing that one, and only one, mutation would provide a fitness benefit, and that populations had to wait around for that mutation to gain the benefit."PaV_{November 14, 2012
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PaV, You're out by an order of magnitude on your math - should be 180 000 years. But that's per nucleotide, not the "entire length of the genome" Other than that, you have actually grasped the point. To think this math is relevent you have to think that environmental pressures changed that one, and only one, mutation would provide a fitness benefit and populations had to wait around for that mutation to gain the benifit. That's question-begging on a grand scale.wd400_{November 14, 2012
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wd400:
6.5 million years is 450 000 15yr generations 65 mutations * 450 000 gens * 2 lineages = 56 million fixed differences 56 million positions in a 3.2 billion base genome is ~ 1.7% divergence (actually greater than the observed difference).
Let's put this into perspective: your calculation tells us that there is a 1.7% chance that a 'neutral' mutations has occurred at any location along the length of the genome in 6.5 million years. But the location where this 'fixation' takes place must be, by definition, 'neutral.' This means that if a particular 'neutral' location had an A as a base, 6.5 million years later, there is a less than 2% chance that it will now have a T, or C, or G instead. Yet, it remains a 'neutral' location. So, . . . who cares if it's a T, or C, or G, or if it's still an A: any way you look at it, it's a 'neutral' mutation; i.e., a location where 'selection' is not taking place. This paves the way for what you say next:
Gauger is just playing the silly “over specify the target” game creationists of all ilks enjoy. It’s true that waiting for co-ordinated mutations in a very small specified region would take a long time if the first didn’t have a selective advantage. That might be a problem if you thought humanity was the goal of evolution and only very narrowly defined pathways could lead to us. But that’s not evolutionary biology’s position, so it doesn’t really matter.
If a particular location on the genome is critical, then 'selection' is at work; very likely---in the vast majority of cases---by eliminating a harmful mutation, but, possibly by 'selecting for' a beneficial mutation. So, what about this particular location? Well, the probability of getting a, let us say, 'favorable' mutation at this particular location is 1/size of the genome, which is, approx, 3 x 10^-10/generation. (assuming a genome size of 3.5 x 10^9 nucleotides). Now the 'effective' population size comes into play, and then the expected time for fixation. Ignoring the time of fixation, we can use an average population size of 100,000, with a mutation rate of 100/genome/generation. Thus, per generation, there are 100 x 100,000 possibilities that a 'particular' location receives a SNP (or equivalent). But there is a 3 x 10^-10 chance that it will miss. The numbers show that the time for 'hitting' this particular location is, on average, 3 x 10^-3 chance of 'hitting' this location per generation. Hence, given a 20 year generation time, this means (3 x 10^3) x 20 years/generation = 6 x 10^4 years are needed to 'hit' this particular spot. And what if the mutation is the 'wrong' mutation? Then what? Well, there's a one in three chance of it being the 'right' mutation, so we'll have to multiply by 3, giving us 1,800,000 years to get our 'beneficial' mutation at some particular location. To get another 'specific' and 'beneficial' mutation along the length of the genome This is Ann Gauger's basic argument. And wd400, you simply want to dismiss it out of hand. Your argument is that 'any old' mutation will do. You say: "How do we know it has to be at this exact location, and this particular base? Who says this has to be so?" The answer is that 'genetics' says it must be so. We don't have 100,000 humans with completely random genomes. They're constrained for the most part. And genetics (negative selection) determines these constraints. To hand-wave the obvious away--that is, that mutations at 'specific' locations are needed--is to have a rather silly attitude towards the whole enterprise here. Just because the numbers don't work out using traditional population genetics methods, doesn't mean you can just pretend otherwise. ========================== Now, as to the question of "substitution," there is a great equivocation that takes place in genetics. Substitution is at once the 'substitution' of one nucleotide for another, AND, the fact that 'neutral' mutations are 'substituted' for at the same rate as the mutation rate. Now, the point I was making above accounts for this equivocation: i.e., it is 'silly' to talk about the 'fixation' of a 'neutral' mutation since it matters not one twit (by definition) what nucleotide base you happen to have at a 'neutral' location along the genome. So, it is better to simply call it a 'substitution.' (As in: "one is as good a substitute as another")PaV_{November 14, 2012
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Just how long will these Darwinists continue to stretch their elastic theory just to keep it alive? Don't they realise how the basic premises of their theory are being dealt one death blow after another. Now I often like to step away from all the noise and look at the big pattern. And the way I see it is that Darwinism has been on a state of retreat covered by a smokescreen of unproven assertions, wishful extrapolations, fossil interpretation games, ad-hoc explanations, and an endless bile of just-so stories. Ever since the time of Darwin who believed that variation within a gene pool was "unlimited" and so natural selection alone could account for evolution, that was shown to be false and so the basic premise of Darwinism at the time was done for. But the crafty Darwinists came together and decided to appeal so something called "mutations", and since then we are required to believe that such rare accidents of nature could behave like a magic wand that could endow creatures with brand new novelties of functions and design. And so Darwinism survived the first death blow by administering such a crafty "CPR" and was born anew: Neo-Darwinism. Then came the embarrassingly huge amount of gaps in the fossil record so they said to themselves: you know what, let's just claim that evolution sometimes works in quick bursts of rapid change that leave no traces behind and give it a fancy name "punctuated equilibrium". How convenient! And now we have all this incredible research done by ID scientists demonstrating to Darwinists what should've been already obvious: your precious mutations DON'T WORK, they cannot create the wealth of brand new information novelties that you dream of. And even if we give them a generous benefit of the doubt and wait for mutations to get lucky enough to MAYBE start working, they would take too long to be able to account for the proposed relatively rapid human divergence, let alone the Cambrian explosion which is still crying and begging for an adequate Darwinian explanation to wipe off the tears. So if this is not a death blow then what is? But of course the crafty Darwinists are so determined on keeping their holy theory on life support by telling themselves: you know what, let's just say that mutations work much faster by appealing to developmental mutations. And so we are going in circles again with Darwinists who forgot all the generations of fruit flies that did not yield any fruitful result through developmental mutations. So what's next? Maybe in the near future we'll hear about "super" mutations that could literally transform a species over night. But in the end Darwinists have no shortage of "wise guys" who would suddenly jump at you and say: there is nothing wrong with scientists correcting themselves. But the reality is that such a true statement is being used to disguise false premises that keep getting blown one by one through scientific evidence that is rejected or downplayed by those who call themselves "scientific". Just what would it take to refute Darwinism in the elastic minds of Darwinists? It is ironic that such a theory that always had survival of the fittest at its core is in fact no longer fit to survive without all these patch-works and repairs that only serve to delay, not prevent, and inevitable collapse.Shogun_{November 14, 2012
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wd400 wants to use math, but unfortunately for wd400 math requires proof. And even more unfortunate is the fact that population genetics is not amendable to proof.Joe_{November 13, 2012
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wd400 @93: I've never accused you of not playing straight. There is a paradigm issue that needs to be addressed (as I've said and will revisit again below), and we all understand there are lots of caveats and exceptions and specific anomalies that could be discussed with the calculations, but overall I believe you've been sincerely explaining the calculations and I think it has been helpful. ----- So it is fair to say that if we look at a current individual's genome, in theory we can trace each locus within the genome back through its own "family line" to some progenitor. In theory any two or more loci could be traced back to the same exact progenitor, but they might just as readily have come from two different progenitors (though, ultimately, all would presumably have to trace back to the universal common ancestor, so we end up with something of a reverse-hourglass shape for the genetic lineage map -- an interesting topic for another time). In any event, for purposes of the present discussion going back only 6M years, we could expect to have a number of progenitors at that first generation. So that brings us back to one of the key issues at the start of this thread: are coordinated changes needed? Let's assume that our first generation progenitors 6M years ago consisted of 26 individuals A-Z. Now each of these individuals went merrily along its way, producing offspring with somewhere between 40-65 mutations/generation. Now at some point in this process an individual in lineage A received a genetic mutation that would ultimately after many generations become part of, say, a gene controlling pelvic structure, thus allowing humans to walk upright. How did the rest of this critical gene come about? Well, there must have been other mutations, either in line A or another line, that, when taken together with other mutations, eventually resulted in the gene in question. And this is key: Regardless of whether evolution could have taken any number of hypothetical paths, once a specific structure is in process in the actual biological realm, the remaining parts or instructions for that structure -- by definition -- have to have been coordinated, or the structure would not have come about. Stated in the simplest example with a nucleic sequence for a protein: once an organism receives that first point mutation in a nucleotide that ultimately will lead to a particular protein, all other mutations in the nucleotide sequence must be coordinated, or -- again by definition -- the protein will not exist. As soon as we are on the path to building any structure we are no longer in the realm of "anything goes." Thus, the realization that evolution is contingent is of no help in answering the question on the table. We know certain structures exist. The salient question is: "What is the most likely explanation for the structure in question?" It is quite apparent to anyone willing to ask that question that everything had to come together just right in order for the structure to exist. So then we can get back to discussing the astronomical probabilities of mutations being accidentally coordinated and whether there might be a better explanation for the coordinated complexity we see. Stating that evolution is contingent is not an answer; it does not in any way change the awful probability calculations; it is simply a reassertion of faith in chance.
So that brings us back to one of the early questions on this thread: at what point and in what instances do we need coordinated (or specified, if you will) mutations to get to humans (as opposed to a simple additive model of unspecified mutations along a lineal descent line)?
Well, yeah, that’s the question Gauger is begging.
No. That coordinated mutations are needed is a biological and engineering fact. Gauger is not begging the question. You are avoiding the question.Eric Anderson_{November 12, 2012
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you simply have no 'real world' evidence that it is even possible to fixate mutations on anything like the scale postulated by neo-Darwinism for humans to have evolved from some chimp-like ancestor: Mutations : when benefits level off - June 2011 - (Lenski's e-coli after 50,000 generations) Excerpt: After having identified the first five beneficial mutations combined successively and spontaneously in the bacterial population, the scientists generated, from the ancestral bacterial strain, 32 mutant strains exhibiting all of the possible combinations of each of these five mutations. They then noted that the benefit linked to the simultaneous presence of five mutations was less than the sum of the individual benefits conferred by each mutation individually. http://www2.cnrs.fr/en/1867.htm?theme1=7 The preceding experiment was interesting, for they found, after 50,000 generations of e-coli which is equivalent to about 1,000,000 years of 'supposed' human evolution, only 5 'beneficial' mutations. Moreover, these 5 'beneficial' mutations were found to interfere with each other when they were combined in the ancestral population. Needless to say, this is far, far short of the functional complexity we find in life that neo-Darwinism is required to explain the origination of. Even more problematic for neo-Darwinism is when we realize that Michael Behe showed that the 'beneficial' mutations were actually loss or modification of function mutations not gain of function mutations. Richard Lenski's Long-Term Evolution Experiments with E. coli and the Origin of New Biological Information - September 2011 Excerpt: The results of future work aside, so far, during the course of the longest, most open-ended, and most extensive laboratory investigation of bacterial evolution, a number of adaptive mutations have been identified that endow the bacterial strain with greater fitness compared to that of the ancestral strain in the particular growth medium. The goal of Lenski's research was not to analyze adaptive mutations in terms of gain or loss of function, as is the focus here, but rather to address other longstanding evolutionary questions. Nonetheless, all of the mutations identified to date can readily be classified as either modification-of-function or loss-of-FCT. (Michael J. Behe, "Experimental Evolution, Loss-of-Function Mutations and 'The First Rule of Adaptive Evolution'," Quarterly Review of Biology, Vol. 85(4) (December, 2010).) http://www.evolutionnews.org/2011/09/richard_lenskis_long_term_evol051051.html i.e. The individual 'beneficial' mutations were never shown to be in the process of building functional complexity at the molecular level in the first place! related notes: Response from Ralph Seelke to David Hillis Regarding Testimony on Bacterial Evolution Before Texas State Board of Education, January 21, 2009 Excerpt: He has done excellent work showing the capabilities of evolution when it can take one step at a time. I have used a different approach to show the difficulties that evolution encounters when it must take two steps at a time. So while similar, our work has important differences, and Dr. Bull’s research has not contradicted or refuted my own. http://www.discovery.org/a/9951 Epistasis between Beneficial Mutations - July 2011 Excerpt: We found that epistatic interactions between beneficial mutations were all antagonistic—the effects of the double mutations were less than the sums of the effects of their component single mutations. We found a number of cases of decompensatory interactions, an extreme form of antagonistic epistasis in which the second mutation is actually deleterious in the presence of the first. In the vast majority of cases, recombination uniting two beneficial mutations into the same genome would not be favored by selection, as the recombinant could not outcompete its constituent single mutations. https://uncommondescent.com/epigenetics/darwins-beneficial-mutations-do-not-benefit-each-other/ As pointed out before by Dr. Gauger, the limits for multicellular creatures to fixate mutations is much worse than the strict limits found for bacteria: Experimental Evolution in Fruit Flies (35 years of trying to force fruit flies to evolve in the laboratory fails, spectacularly) - October 2010 Excerpt: "Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles.,,, "This research really upends the dominant paradigm about how species evolve," said ecology and evolutionary biology professor Anthony Long, the primary investigator. http://www.arn.org/blogs/index.php/literature/2010/10/07/experimental_evolution_in_fruit_flies More from Ann Gauger on why humans didn’t happen the way Darwin said - July 2012 Excerpt: Each of these new features probably required multiple mutations. Getting a feature that requires six neutral mutations is the limit of what bacteria can produce. For primates (e.g., monkeys, apes and humans) the limit is much more severe. Because of much smaller effective population sizes (an estimated ten thousand for humans instead of a billion for bacteria) and longer generation times (fifteen to twenty years per generation for humans vs. a thousand generations per year for bacteria), it would take a very long time for even a single beneficial mutation to appear and become fixed in a human population. You don’t have to take my word for it. In 2007, Durrett and Schmidt estimated in the journal Genetics that for a single mutation to occur in a nucleotide-binding site and be fixed in a primate lineage would require a waiting time of six million years. The same authors later estimated it would take 216 million years for the binding site to acquire two mutations, if the first mutation was neutral in its effect. Facing Facts But six million years is the entire time allotted for the transition from our last common ancestor with chimps to us according to the standard evolutionary timescale. Two hundred and sixteen million years takes us back to the Triassic, when the very first mammals appeared. One or two mutations simply aren’t sufficient to produce the necessary changes— sixteen anatomical features—in the time available. At most, a new binding site might affect the regulation of one or two genes. https://uncommondescent.com/intelligent-design/more-from-ann-gauger-on-why-humans-didnt-happen-the-way-darwin-said/bornagain77_{November 12, 2012
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wd400:
I’ve shown you the derivation of the math.
You have not shown that it applies to the real world.
You need to tell me what’s wrong with the math, or how the assumptions (only really finite population size) of the math don’t align with real populations.
No, YOU need to demonstrate to us that the math is valid, ie applies to real populations in the real world. If you can't do that, and still push the math, what does that make you?Joe_{November 12, 2012
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Haldane's Dilemma Excerpt: Haldane was the first to recognize there was a cost to selection which limited what it realistically could be expected to do. He did not fully realize that his thinking would create major problems for evolutionary theory. He calculated that in man it would take 6 million years to fix just 1,000 mutations (assuming 20 years per generation).,,, Man and chimp differ by at least 150 million nucleotides representing at least 40 million hypothetical mutations (Britten, 2002). So if man evolved from a chimp-like creature, then during that process there were at least 20 million mutations fixed within the human lineage (40 million divided by 2), yet natural selection could only have selected for 1,000 of those. All the rest would have had to been fixed by random drift - creating millions of nearly-neutral deleterious mutations. This would not just have made us inferior to our chimp-like ancestors - it surely would have killed us. Since Haldane's dilemma there have been a number of efforts to sweep the problem under the rug, but the problem is still exactly the same. ReMine (1993, 2005) has extensively reviewed the problem, and has analyzed it using an entirely different mathematical formulation - but has obtained identical results. John Sanford PhD. - "Genetic Entropy and The Mystery of the Genome" - pg. 159-160 Kimura's Quandary Excerpt: Kimura realized that Haldane was correct,,, He developed his neutral theory in responce to this overwhelming evolutionary problem. Paradoxically, his theory led him to believe that most mutations are unselectable, and therefore,,, most 'evolution' must be independent of selection! Because he was totally committed to the primary axiom (neo-Darwinism), Kimura apparently never considered his cost arguments could most rationally be used to argue against the Axiom's (neo-Darwinism's) very validity. John Sanford PhD. - "Genetic Entropy and The Mystery of the Genome" - pg. 161 - 162 A graph featuring 'Kimura's Distribution' is shown in the following video: Evolution Vs Genetic Entropy - Andy McIntosh - video http://www.metacafe.com/watch/4028086bornagain77_{November 12, 2012
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Human Evolution: A Facebook Dialog - By Ann Gauger - Nov. 12, 2012 Excerpt: PM:Is it also possible that the mechanism that you refer to in your video clip is not the only/main one at play? Biologic: The mechanism I refer to is based on the standard Darwinian model for evolution. Published population genetics estimates for how long it would take to make *and fix* a single base change to a DNA binding site in a 1 kb segment of DNA are prohibitively long—six million years. To get a second mutation in the same DNA binding site would take in excess of 200 million years. Now to go from hominid to human requires many changes, most of them to gene expression patterns. It is much easier to change the DNA binding site than to change the transcription factor’s specificity. And all these mutations must work together and be beneficial to the evolving organism. The window of time available according to the fossil record and phylogenetic estimates is too short for known mechanisms to be sufficient. So do I think there are are other things at play? Yes. http://www.biologicinstitute.org/post/35586805901/human-evolution-a-facebook-dialog?og=1bornagain77_{November 12, 2012
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Joe, I've shown you the derivation of the math. You need to tell me what's wrong with the math, or how the assumptions (only really finite population size) of the math don't align with real populations. If you can't do that, and you still deny the math, what does that make you?wd400_{November 12, 2012
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