Evolutionist: You’re Misrepresenting Natural Selection

_{Cornelius Hunter

December 25, 2011

Intelligent Design}

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How could the most complex designs in the universe arise all by themselves? How could biology’s myriad wonders be fueled by random events such as mutations? Read more

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Elizabeth: I have made an explicit reasoning in my post 11.1 that is independent from what Bozorghmehr may have said, or from what he may be, and of which I take full responsibility. Can you please comment on that? Unless you think that I am a crank too :)gpuccio_{December 30, 2011
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Elizabeth: Let's say, more correctly, that the trensition has a dFSCI of 150 bits. A1 would be the existing protein that "evolves" to A2. A2 would be a new protein, with a new function, a naturally selectable new function. A2 would differ from A1 of 150 bits of functional information. The best way to imagine that is that A2 differs from a! in 35 AAs that must necessarily change exactly to the new value for the function to emerge. As this is not usually the case, we can apply a Durston style computation, attributing to each site that changes an informational value in Fits that corresponds to the reduction in uncertainty that each AA site implies. So, at the two extremes, if one site must necessarily have one aminoacid, its Fit value will be 4.32 The function implies a complete reduction of uncertainty at that site. If instead any AA can stay at that site, its Fit value is 0 (no reduction of uncertainty is implied by the function). And similarly for all intermediate possibilities. The sum of all Fit values at the changing sites gives the dFSCI of the transition. When the starting protein (A1) is totally unrelated, as is the case for new basic protein domains, the total dFSCI of the new proteon can be approximated by the Durston method applied to its protein family.gpuccio_{December 30, 2011
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Elizabeth: Microevolution is a random variation in the range of what a biological system can achieve, that gives a functional selectable result. Some forms of antibiotic resistance are microevolution, and they are well documented. A single aminoacid change can confer antibiotic resistance and be selected, in the presence of the antibiotic. That is well known, and observed. One aminoacis is about 4.32 bits of information. That is in the range of routine variation in a bacterial culture. 150 bits corresponds to about 35 AAs. A transition requiring 35 AAs to confer a new function has never been onserved to occur in any biological context.gpuccio_{December 30, 2011
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Elizabeth, Your position can't even explain the existence of HOX genes. So stop using what you need to explain in the first place. Your position can't explain cellular differentiation. That said I linked to the differences between the two plans- prokaryote and eukaryote. A single-celled organism has a body and therefor a body-plan. I cannot help it that you are not a biologist and don't have the knowledge required to follow along.Joe_{December 30, 2011
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Elizabeth: If you remembered the definition of dFSCI, that I have patiently discussed with you many times. you would know that dFSCI refers to the total information necessary to get a function. If your 1 bit increases are functional and selectable, then show them. If they are not, then the probabilistic barrier remains the same.gpuccio_{December 30, 2011
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Elizabeth, You have it all bass-ackwards. We don't have to say what prevents anything. YOU have to demonstrate what allows it. That means you have to produce POSITIVE evidence for what you claim can/ did happen. The edge of stochastic processes appears to be set at two new protein-to-protein binding sites. So that would be one categorical boundary. Good luck getting over it...Joe_{December 30, 2011
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Elizabeth: Again, I am not asserting that. I am asserting that eukaryotes have new cellular organization. Early eukaryotes are, I suppose, your personal dream. I will be happy to comment on them as soon as you let me make their acquaintance.gpuccio_{December 30, 2011
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Elizabeth: No. There is your first mistake. There no warrant for the assumption that a new domain has to be advantageous (result in greater reproductive success for its phenotype than for phenotypes lacking the new domain). As long as it does not seriously impair reproductive success there is no reason why it should not “emerge” i.e. appear in one indivudual and be replicated down that lineage. There is no mistake. It's simply you that don't understand the reasoning. I am evaluating the probabilities of a certain final event to happen in a random system. The final event is supposed to be a naturally selectable function, because that would be the event that "stops" the random system and implies a nevessity mechanism (the expansion of the selected trait). Unless and until we get to that result, the system is random. And therefore we can evaluate the probabilities of a subset of states versus all possible states. You have made that mistake many times. You seem to believe that neutral or quasi neutral variation can just happen, and that's enough for you. Nothing could be fartgher from truth. It is obvious that neutral variation can happen, but the problem is, it is random variation, All states have the same probability to be reached by neutral variation. So, neutral variation is a perfectly random system where all unrelated states have the same probability to be reached. But, if you want to defend an algorithm such as neodarwinism, that assumes that NS has an important role to explain how unlikely results are obtained in a random system, then you need to reach naturally selectable results. It's as simple as this. Nope. You just need the subset of sequences that result in a foldable protein that is not disastrously disadvantageous to the phenotype in the current environment. Same mistake as above, and even worse. What you say has no meaning. Why do you need a foldable protein at all? If neutral evolution takes place in a duplicated, inactivated gene, any sequence is neutral. You don't even need the sequence to be an ORF. Any random sequence is certainly not disastrously disadvantageous to the phenotype, if it is not translated. If, on the other hand, the variation applies to a function sequence, any sequence that reduces or looses the original function will be visible to negative selection. See also my post 11.1. Now you are double-counting, by equivocating with the word “function”, by conflating genotype with phenotype. If a protein is made, but has no effect on the reproductive success of the phenotype it doesn’t have a “function” in any relevant sense. It merely exists. And provided the first few generations down that lineage survive, it will exist in sufficiently many copies that it is likely to hang around for a long time. Always the same error. I am discussing the probabilities of reaching a naturally selectable result in a random system of variation, If you cannot understand that, you cannot understand any part of my reasoning. Better to call it P(sequence-that-results-in-a-folded-protein), which may be a tiny subset of all possible sequences, but still may be quite high given the immense number of opportunities for sequence mutations to occur. No. Wrong! A folded protein is not functional and is not naturally selectable. Until a functional selectable result occurs, a foldable protein is not different than a non foldable sequence that is not translated. And why should a foldable non functional protein be translated? If that were the case, all living cells would be repleted of foldable non functional proteins that are not "disastrously disadvantageous to the phenotype". I suppose that's not the case. And we simply do not know how large that subset of sequences is, nor indeed whether some of their precursors also result in reproductive advantage for their bearers. That's really an "argument from ignorance", if I ever so one! Yes, we don't know, because nobody has ever been able to show those precursors, either in the proteome or in the lab. But you can always hope and dream... It isn’t precise at all. It’s wrong in a number of respects (the sequences coding for a new domain don’t have to be currently advantageous to appear, and there is no good reason to assume the precursors of those sequences don’t confer reproductive advantage), and we don’t in any case know the size of the subset of DNA sequences that result in foldable proteins, though we may know roughly the size of the subset that have actually appeared in living things. You are simply misrepresenting my argument. I never said that a sequence has to be "currently advantageous" to appear. That's only your imagination. What I said is that a sequence has to be currently advantageous to be naturally selected, and that up to that point all sequences have the same probability to appear. Is that the same thing, in your opinion? The size of the subset of foldable proteins is interesting, but not relevant. The only relevant subset is the one I defined, the subset of naturally selectable proteins. All the rest is random variation. This exactly the problem Petrushka mentioned, and which IDists tend to dismiss as ignorance because they think they’ve dealt with it. You haven’t. We have dealt with it, and we will continue to deal with it. Because it is an importnant problem, and we believe it has to be dealt with. That does not mean that the problem is completely solved, obviously. Darwininsts, if they were scientifically honest, should deal with it with the same urgency (some, indeed, have tried, with terrible methodology and false results). Because the problem is fundamental for their own theory. Instead, most darwinists, including you, just try to hide behind the supposed impossibility to solve the problem, so that their wrong theories may conrinue to be believed for some more time. The problem can be solved, and we have a lot of indications about what the solution is. And the solution is exactly what ID has shown. You have pre-defined the target as those DNA sequences that result in foldable proteins that form part of modern functional proteins, and assume that that small target comprises the only possible target, forgetting that there may be a vast set of DNA sequences that would also result in protein domans, and another vast set of proteins comprised of those domains that, in some alternative universe, might also prove to confer reproductive advantage in some alternative biosphere. Wow! Have you lost your mind? I have done nothing like that. I have defined a subset as (I quote myself): "That means that we have to look for a specific subset of P(F) (the subset of folded proteins), the subset of folded proteins unrelated at sequence level to already existing proteins in the proteome, with a new fold and a specific new biochemical function. Let’s call that P(NUFF), for New Unrelated Folded and Functional. Then we have to look for an even smaller subset of that, the NUFF that are naturally selectable in that context, IOWs that can confer, by themselves, a reproductive advantage in the context of the living being where the transition is supposed to happen (prokaryotes, I suppose, or a symbiosis of them). Let’s call that P(NUFFNS)." Where in that is the concept you attribute to me? Just to be precise, "those DNA sequences that result in foldable proteins that form part of modern functional proteins? Why do you put in my mouth things I have not said? I will not comment about the "alternative universe" and "alternative biosphere" part, just out of respect for you. I believe you must be really desperate to use those arguments. And anyway, what in the world does an alternative universe have to do with the probabilities of a selectable function arising in a specific biological context, such as my example of prokaryotes transitioning to eukatyotes? And this, to repeat, is the fundamental error at the heart of ID: to look at what exists, and say: what exists must be a tiny subset of what might exist (correct), and is also the only subset possible that could result in life (incorrect) and is therefore extremely improbable. Which is fallacious, because based on a false premise. Wow again! Where have I, (or ID, for what I know), ever said that "what exists is the only subset possible that could result in life"? I hyave never said that, I am really sure of that. For the simple reason that I don't believe it, and I usually don't say things I don't believe. But I have sais a lot of times that already existing information and complexity poses huge constraint to what can be useful in that context. IOWs, if you have to find something useful in an existing strain of bacteria, your options are radically limited, and the possibilities that other forms of life based on fire and lithium could possibly exist in another galaxy are scarcely a help! Quite apart from the fallacy that only sequences that confer reproductive advantage on the phenotype can be replicated, Totally invented fallacy. I never said that. and the fallacy that a sequence that confers a new advantage can have had no precursors that also conferred an advantage (in some different way). Totally invented fallacy. I certainly said, and say, that those precursors have never been shown. And I have said many times that science is note made on "mere possibilities". It usually needs some facts, you know? And the general confusion between genotype and phenotype. What confusion? I have no confusion about that. That is a serious accusation. Please, detail it.gpuccio_{December 30, 2011
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Also, why can't macroevolution, by your definition, consist of, for example, 150 microevolutionary steps of 1 bit increase in dFSCI each? What I'm trying to get at here is what the categorical boundary is supposed to be that divides microevolution from macroevolution?Elizabeth Liddle_{December 30, 2011
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A molecular transition to a new function implying more than 150 bits of dFSCI.
Thanks. That needs a fair bit of unpacking though. First of all, do you mean that you mean by "molecular transition" a series of changes in a DNA sequence (let's call the starting sequence A1 and the "new" sequence A2) where A2 confers enhanced reproductive success on the phenotype relative to A1, and where the A2 has 150 more bits of dFSCI than the A1? Second, if so, how do you define A1 and A2? Third, how do you compute the dFSCI of each sequence?Elizabeth Liddle_{December 30, 2011
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Elizabeth: First of all, you need to give an operational definition of “macroevolution”, otherwise I cannot even begin to evaluate your assertion. A molecular transition to a new function implying more than 150 bits of dFSCI.gpuccio_{December 30, 2011
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First of all, on what grounds do you assert that early eukaryotes had "new, completely new, cellular organisation"? Your argument is, again, circular. You assert that there is a non-stepwise change, then defy evolutionists to explain it by step-wise changes. First demonstrate that the change must have been non-stepwise, otherwise there is no explanandum.Elizabeth Liddle_{December 30, 2011
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Well, in that case be specific. You have been challenging Darwinists for ages to explain the origin of "new body plans" by which most of us assumed you meant, well, something to do with body plans, i.e. cell differentiation in multicellular organisms, for which hox genes are crucial. Turns out you meant "new cell type", which has nothing to do with cell differentiation. If you want to have a technical discussions, it helps to be precise in your language.Elizabeth Liddle_{December 30, 2011
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I would like to add, for clarity, that the probability that is pertinent for the analysis of a specific instance of neo darwinian “explanation” can be defined with much greater detail. For instance, let’s say that we are analyzing the credibility of the neo darwinian explanation for the emergence of a basic new domain at some point in natural history, let’s say at the emergence of eukaryotes.
OK
In that case, the probability we have to consider is the probability of a new domain that is naturally selectable in that context.
No. There is your first mistake. There no warrant for the assumption that a new domain has to be advantageous (result in greater reproductive success for its phenotype than for phenotypes lacking the new domain). As long as it does not seriously impair reproductive success there is no reason why it should not "emerge" i.e. appear in one indivudual and be replicated down that lineage.
That means that we have to look for a specific subset of P(F) (the subset of folded proteins), the subset of folded proteins unrelated at sequence level to already existing proteins in the proteome, with a new fold and a specific new biochemical function. Let’s call that P(NUFF), for New Unrelated Folded and Functional.
Nope. You just need the subset of sequences that result in a foldable protein that is not disastrously disadvantageous to the phenotype in the current environment.
Then we have to look for an even smaller subset of that, the NUFF that are naturally selectable in that context, IOWs that can confer, by themselves, a reproductive advantage in the context of the living being where the transition is supposed to happen (prokaryotes, I suppose, or a symbiosis of them).
Now you are double-counting, by equivocating with the word "function", by conflating genotype with phenotype. If a protein is made, but has no effect on the reproductive success of the phenotype it doesn't have a "function" in any relevant sense. It merely exists. And provided the first few generations down that lineage survive, it will exist in sufficiently many copies that it is likely to hang around for a long time.
Let’s call that P(NUFFNS). That is the tiny subset of probability we are looking for if we want to believe in a darwinian explanation of the emergence of a single new basci protein domain in the course of natural history (an event that took place at least 2000 times in natural history).
Better to call it P(sequence-that-results-in-a-folded-protein), which may be a tiny subset of all possible sequences, but still may be quite high given the immense number of opportunities for sequence mutations to occur. And we simply do not know how large that subset of sequences is, nor indeed whether some of their precursors also result in reproductive advantage for their bearers.
Just to be precise…
It isn't precise at all. It's wrong in a number of respects (the sequences coding for a new domain don't have to be currently advantageous to appear, and there is no good reason to assume the precursors of those sequences don't confer reproductive advantage), and we don't in any case know the size of the subset of DNA sequences that result in foldable proteins, though we may know roughly the size of the subset that have actually appeared in living things. This exactly the problem Petrushka mentioned, and which IDists tend to dismiss as ignorance because they think they've dealt with it. You haven't. You have pre-defined the target as those DNA sequences that result in foldable proteins that form part of modern functional proteins, and assume that that small target comprises the only possible target, forgetting that there may be a vast set of DNA sequences that would also result in protein domans, and another vast set of proteins comprised of those domains that, in some alternative universe, might also prove to confer reproductive advantage in some alternative biosphere. And this, to repeat, is the fundamental error at the heart of ID: to look at what exists, and say: what exists must be a tiny subset of what might exist (correct), and is also the only subset possible that could result in life (incorrect) and is therefore extremely improbable. Which is fallacious, because based on a false premise. Quite apart from the fallacy that only sequences that confer reproductive advantage on the phenotype can be replicated, and the fallacy that a sequence that confers a new advantage can have had no precursors that also conferred an advantage (in some different way). And the general confusion between genotype and phenotype.Elizabeth Liddle_{December 30, 2011
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Evolutionary theory asserts what is wrong. In no way macroevolution is microevolution over longer timescales. That’s pure imagination, and bad imagination all the way. At molecular level, we have simply no example of macroevolution. Do you understand that? No example. We have no molecular model of one single macorevolutionary transition that could realistically be explained by the neo darwinian model of RV + NS. That’s why I think that your statement is false. It is against logic. It is against evidence. It is against facts. It is against mathematics and statistics. It is against engineering. And there is not a single empirical support of it. Is that enough?
No. First of all, you need to give an operational definition of "macroevolution", otherwise I cannot even begin to evaluate your assertion. You seem to be implying something like "irreducible complexity", in which case your argument would be circular.Elizabeth Liddle_{December 30, 2011
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Bozorghmehr is a crank with no training in biological science who somehow managed to get his phoney papers past inadequate peer-review. He's an internet troll who was so successful he moved on to trolling scientific journals. I sometimes suspect he's an atheist sockpuppet.Elizabeth Liddle_{December 30, 2011
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tjguy: The paper is exactly right. Let's just comment very simply the problems of the duplicated gene mechanism as a neodarwinian tool. It's complete nonsense. The simple truth is that NS acts as negative selection to keep the already existing information. We see the results of that everywhere in the proteome: the same function is maintained in time and in different species, even if the primary sequence can vary in time because of neutral variation. So, negative NS conserves the existing function, and allow only neutral or quasi neutral variation. In that sense it works against any emergence of completely new information from the existing one, even if it can tolerate some limites "tweaking" of what already exists (microevolution). I suppose that darwinists, or at least some of them, are aware of that difficulty as soon as one tries to explain completely new information, such as a new basic protein domain. Not only the darwinian theory cannot explain it, it really works against it. So, the duplicated gene mechanism is invoked. The problem is that the duplicated gene, to be free to vary and to leave the original functional island, must be no more translated and no more functional. Indeed, that happens very early in the history of a duplicated gene, because many forma of variation will completely inactivate it as a functional ORF, as we can see all the time with pseudogenes. So, one of the two: a) either the duplicated gene remains functional and contributes to the reproduction, so that negative NS can preserve it. In that case, it cannot "move" to new unrelated forms of function. b) or the duplicated gene immediately becomes non functional, and is free to vary. The important point is that case a) is completely useless to the darwinian explanation. Case b) allows free transitions, but they are no more visible to NS, at least not until a new functional ORF (with the necessary regulatory sites) is generated. IOWs, all variation from that point on becomes neutral by definition. But neutral variation, while free of going anywhere, is indeed free of going anywhere. That means: feedom is accompanied by the huge rising of the probability barriers. As we know, finding a new protein domain by chance alone is exactly what ID has shown to be empirically impossible. IOWs, the neo darwinian "explanation" is silly and wrong.gpuccio_{December 30, 2011
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material.infantacy and Petrushka: I would like to add, for clarity, that the probability that is pertinent for the analysis of a specific instance of neo darwinian "explanation" can be defined with much greater detail. For instance, let's say that we are analyzing the credibility of the neo darwinian explanation for the emergence of a basic new domain at some point in natural history, let's say at the emergence of eukaryotes. In that case, the probability we have to consider is the probability of a new domain that is naturally selectable in that context. That means that we have to look for a specific subset of P(F) (the subset of folded proteins), the subset of folded proteins unrelated at sequence level to already existing proteins in the proteome, with a new fold and a specific new biochemical function. Let's call that P(NUFF), for New Unrelated Folded and Functional. Then we have to look for an even smaller subset of that, the NUFF that are naturally selectable in that context, IOWs that can confer, by themselves, a reproductive advantage in the context of the living being where the transition is supposed to happen (prokaryotes, I suppose, or a symbiosis of them). Let's call that P(NUFFNS). That is the tiny subset of probability we are looking for if we want to believe in a darwinian explanation of the emergence of a single new basci protein domain in the course of natural history (an event that took place at least 2000 times in natural history). Just to be precise...gpuccio_{December 30, 2011
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material.infantacy: Thank you for explaining it so clearly! Petrushka, please your answer.gpuccio_{December 30, 2011
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Here is an interesting write-up on a study by Bozorgmehr published in Complexity on Dec. 22, 2010 that seems to falsify evolution and show the limits of natural selection: First, here are some quotes from the article. To read the originally write-up, please check out the web address listed at the end of this post. The writer calls says that Bozorgmehr dealt “a falsifying blow to natural selection”. Many arguably “beneficial” mutations have been observed to incur some sort of cost and so can be classified as a form of antagonistic pleiotropy. Indeed, the place and extent of natural selection as a force for change in molecular biology have been questioned in recent years. Moreover, several well-known factors such as the linkage and the multilocus nature of important phenotypes tend to restrain the power of Darwinian evolution, and so represent natural limits to biological change. Selection, being an essentially negative filter, tends to act against variation including mutations previously believed to be innocuous. The idea that natural selection is more permissive with duplicated genes was analyzed by Bozorgmehr. In conclusion, he noted that accidental gene duplication clearly adds to the size of some genomes. “However, in all of the examples given above, known evolutionary mechanisms were markedly constrained in their ability to innovate and to create any novel information, he said. “This natural limit to biological change can be attributed mostly to the power of purifying selection, which, despite being relaxed in duplicates, is nonetheless ever-present.” Then he examined cases of co-option cited by Darwinists, but found, again, that “a proclivity toward functional stability and the conservation of information, as opposed to any adventurous innovation, predominates.”? The various postduplication mechanisms entailing random mutations and recombinations considered were observed to tweak, tinker, copy, cut, divide, and shuffle existing genetic information around, but fell short of generating genuinely distinct and entirely novel functionality. : “Gradual natural selection is no doubt important in biological adaptation and for ensuring the robustness of the genome in the face of constantly changing environmental pressures.” Bad news: “However, its potential for innovation is greatly inadequate as far as explaining the origination of the distinct exonic sequences that contribute to the complexity of the organism and diversity of life.”? He didn’t offer a replacement evolutionary theory, but warned that any new contender must think holistically about the cell (cf. 04/02/2008). “Any alternative/revision to Neo-Darwinism has to consider the holistic nature and organization of information encoded in genes, which specify the interdependent and complex biochemical motifs that allow protein molecules to fold properly and function effectively.” Bozorgmehr did not refer to intelligent design, and did not cite any ID sources, but arrived at the same conclusions about the natural limits to biological change that creationists and ID advocates have been preaching for decades. http://crev.info/2011/01/evolution_by_gene_duplication_falsified/tjguy_{December 29, 2011
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Sure, that is possible, but it doesn't speak too well for the Intelligent Designer. What an inefficient way to make things! Takes forever. Lots of mistakes, death, disease, suffering, bloodshed, etc. I wouldn't be too impressed with such a Designer myself. I prefer an omniscient Designer who knew how to do it right from the beginning and looked back over His creation and said "It is very good." Then later, when sin entered the world, things started to fall apart which explains why we see all the problems in the world today.tjguy_{December 29, 2011
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Ummmm for a single-celled organism the "cell type" is the body plan. A body is a collection of masses...Joe_{December 29, 2011
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"No! Not again. This is really an offense to your own intelligence!"
I know, this is getting old. Nobody's interested in the fact that, of a set of possible outcomes in a sample space, any single one of them coming about has a probability of exactly one. Yet this is what we are hearing as an argument against the improbability of functional specification. This is the same as saying, that for a sample space S, the probability of S occurring is one, or P(S) = 1.0, which is axiomatic, and is irrelevant to the issue at hand. However for an event F in a sample space S, the probability of F occurring is n(F)/n(S). If the set F consists of all potentially functional sequences, then the probability of F occurring is less than one; and the probability never changes (because the size of F doesn't change) regardless of whether it occurred or not at some point in history. To suggest otherwise is also to suggest that any sequence is as good as any other. This cannot possibly be the case. Not all sequences fold, which means that P(F) < 1.0. This alone should suggest that the axiom P(S) = 1.0 couldn't be more irrelevant, and that the set F will remain an unchanging subset -- and a minuscule one at that, given its proportion to S. For a set S, which is a universal set consisting of every possible sequence of length n, there is a subset F which consists of every sequence that results in a folded protein. P(F) = n(F) / n(S) That is, the probability of F occurring is equal to the number of elements in F divided by the number of elements in S. The set F is objectively improbable, unchanging, and contains the subset of all potentially functional proteins. (That is, the size of the subset of functional proteins is bounded by the size of the subset F.) Let's see an end to the "as equally improbable as any other sequence" straw man, which is really just a rehash of Miller's fallacious "cards" analogy.material.infantacy_{December 29, 2011
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Petrushka: Every possible sequence of flipped coins is equally likely or unlikely. Predicting a specific sequence is unlikely, but finding a sequence unlikely after the tosses is pointless. No! Not again. This is really an offense to your own intelligence! You should know very well that finding a sequence that is part of some specific, and extremely unlikely, subset of events is not pointless at all. What do you think the second law is about? Do you pre-specify the unlikely states of a gas molecules? Is it pointless to say that ordered states are too unlikely to emerge spontaneously? Please, answer these points if you really mean what you said in your post. Or just admit that you say some of the things you say for mere propaganda.gpuccio_{December 29, 2011
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Elizabeth: Yes, evolutionary theory asserts that all adaptation is incremental – that “macroevolution” is micro-evolution over longer timescales. There are some other features that we observe over longer timescales, of course, such as speciation (bifurcation of population) and population-level effects, but down any one lineage, its microevolution all the way. If you think this is false, please say why. Evolutionary theory asserts what is wrong. In no way macroevolution is microevolution over longer timescales. That's pure imagination, and bad imagination all the way. At molecular level, we have simply no example of macroevolution. Do you understand that? No example. We have no molecular model of one single macorevolutionary transition that could realistically be explained by the neo darwinian model of RV + NS. That's why I think that your statement is false. It is against logic. It is against evidence. It is against facts. It is against mathematics and statistics. It is against engineering. And there is not a single empirical support of it. Is that enough?gpuccio_{December 29, 2011
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Elizabeth: Hi! Let's see: OK, here is a clue to the problem: what do you mean by “a case of evolution? Please give an example. What about the emergence of basci protein domains? That is a good case of macroevolution, I would say. There are a great many hypotheses specifying what may or may not have happened. Almost any data paper you find on evolution will be a test of a specific hypothesis about what may or may not have happened. What about a credible hypothesis about the above? With a serious analysis of the probabilistic credibility of the random part? Sure, prokaryotic cells and eukaryotic cells are different, but, as I said, we have at least one theory (symbiosis) that might explain that. You must be kidding. Plese, explain all the new protein information in eukaryotes (which is a lot), and the new, completely new, cellular organization. In what way symbiosis would explain that? I am not saying that symbiosis is not a part of the process. It probably is. But to say that it might explain the transition is really the overstaement of the century. And so on, and so on...gpuccio_{December 29, 2011
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Petrushka: Really? What physical laws are violated by mainstream theories of evolution? Now, that's really silly. Why should physical laws be violated? Neo darwinian theory is not about physical laws, it simply violates the laws of logic and the laws of probability and the laws of empirical explanation. Isn't that enough?gpuccio_{December 29, 2011
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Scott, Your argument brought an analogy to mind. Here's an imaginary dialogue between you and an astronomer: Scott: I agree that the theory of gravity holds within our solar system, but extrapolating it to interstellar and galactic scales is unwarranted. Astronomer: What barrier are you aware of that prevents gravity from acting over interstellar distances? Scott: Your error is in assuming that it does. Astronomer: But we see evidence that it does. Scott: Have you ever directly measured the force between two stars? Astronomer: We can't. But stars behave exactly as we would expect if gravity were operating on them. To support your view, we'd have to posit that 1) gravity mysteriously stops working on some scale larger than the solar system, and 2) there is a different, unknown mechanism that makes it appear that gravity is still working on the larger scales! Are you serious? Scott: Game over.champignon_{December 29, 2011
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Evolutionary theory does not posit a difference – that’s another way of saying that it asserts that they are the same. Again, how convenient.
Yes, evolutionary theory asserts that all adaptation is incremental - that "macroevolution" is micro-evolution over longer timescales. There are some other features that we observe over longer timescales, of course, such as speciation (bifurcation of population) and population-level effects, but down any one lineage, its microevolution all the way. If you think this is false, please say why.
Meanwhile, in evolutionary terms of genetic variation and selection it does not fail, but rather does not even attempt to explain the evolutionary transition between any two beak forms, not even the finches.
Yes it does - it does exactly that. The transition between a mean 5.7 mm beak and a mean 5.8 mm beak is a result of the finches with the slightly larger beaks in Generation X being better able to crack open the larger seeds and thus survive to leave more finchlings in Generation Y, who inherit the larger-beak-producing alleles of their parents. That's the explanation. You understand it. I understand it. What is the problem?
So it asserts that the transitions it doesn’t explain are no different from the other transitions it doesn’t explain.
I don't know what you mean. Just keep going. Keep those El Ninos with their big seeds coming. Next year, the mean beak size of Generation Z is 5.9. Then 6.0. Then 6.1, Thenn 6.2. Soon, we have no beaks in the population smaller than 5.8, and some are even 6.5, hitherto unheard of. The population has transitioned to a brand-new beak size.
I can see why someone would have a hard time falsifying that.
Well, for a start, science does not, in fact, proceed by falsification. It proceeds by fitting data to models, and testing those modes against new data. Which has been done, over and over again. You change the environment, and the population adapts - beaks grow, spots shrink, resistance increases. It works - in the field, in the lab, in computer models. It's extremely powerful. And yet people like you insist that somehow we are cheating - failing to explain something that needs to be explained. Well, what is that thing? What is the barrier that you claim that microevolution by means of natural selection from a constantly enriched gene-pool cannot leap? And how do you demonstrate that that barrier is real?Elizabeth Liddle_{December 29, 2011
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How exactly does one understand the probabilities correctly when no one will even attempt to specify what may or may not have happened?
There are a great many hypotheses specifying what may or may not have happened. Almost any data paper you find on evolution will be a test of a specific hypothesis about what may or may not have happened.
I don’t care if Dembski got it wrong. Who got it right?
Nobody. Dembski's mistake was to answer the wrong question. The question he tried to answer is a useless question. It's completely uncomputable.
Use evolution to explain something more than a variation within species. If someone ever bothers to even offer a hypothesis that incorporates the actual mechanics of evolution to explain a case of evolution then we can talk about falsification. Nothing has merited that.
OK, here is a clue to the problem: what do you mean by "a case of evolution? Please give an example. I'd call the Grants' finch beaks "a case of evolution", but you don't. I'd call a speciation event "a case of evolution" but you don't. So what do you call "a case of evolution"?
There is nothing to refute. It is disqualified from the competition by its refusal to show up. The success, failure, or nonexistence of competing explanations is irrelevant. Game over.
The game hasn't even started yet. There is nothing to refute because we apparently aren't even talking about the same thing. What you appear to have is a straw man - a "case of evolution" that bears no resemblance to any phenomenon any evolutionist has ever sought to explain. Can you say what you understand by that term?Elizabeth Liddle_{December 29, 2011
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