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What Behe Actually Said

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For those who are interested in what Professor Behe actually said in Dover (instead of the distortions of his testimony in Judge Jones’ opinion), click on “more.”  [Thank you to tribune7 for sussing this out].

 More...

Q. I just want to make a point clear. You said there were two examples where those who claim that irreducible complexity does not work or is not a valid explanation, they use experimental evidence, and that was the blood clotting system and the lac operon. How does the immunity system, is that experimental evidence or is that a theoretical claim?
A. No, this is mostly a theoretical claim. There is no experimental evidence to show that natural selection could have produced the immune system. And I think that’s a good example of the different views that people with different theoretical frameworks bring to the table.
If we could show the next slide. Professor Miller shows this slide from a reference that he cited by Kapitonov and Jurka, and he has titled Summary, Between 1996 and 2005, each element of the transposon hypothesis has been confirmed. He has this over this diagram.
But again, as I mentioned previously, whenever you see diagrams like this, we’re talking about sequence data, comparison of protein, sequences, or gene sequences between organisms. And such data simply can’t speak to the question of whether random

mutation and natural selection produced the complex systems that we’re talking about.
So Professor Miller — so, in my view, this data does not even touch on the question. And yet Professor Miller offers as compelling evidence. And one more time, I view this as the difference between two people with two different expectations, two different theoretical frameworks, how they view the same data.
And I’d like to take a little bit of time to explain why such studies do not impress me. And I’ll do so by looking at one of the papers that Professor Doolittle — I’m sorry, Professor Miller, that’s his name, cited in his presentation, Kapitonov and Jurka, that was published this year.
I just want to go through, and just kind of as a quick way to show why I am not persuaded by these types of studies. I want to excerpt some sentences from this study to show what I consider to be the speculative nature of such studies.
For example, in this excerpt, the authors say, something indicates that they may be important. This may indicate. It may be encoded. It might have been added. If so, it might have been derived. Alternatively, it might have been derived from a separate unknown transposon. It was probably lost. And we have a lot more of those, one more slide at least.
It says, we cannot exclude the possibility. In any case, the origin appears to be a culmination of earlier evolutionary processes. If so, this might have been altered. Again, without going into the detail of the article, I just wanted to emphasize those phrases to point out what I consider to be the very speculative nature of such papers.
Here’s what I view to be the problem. The sequence of the proteins are there. The sequence of the genes are experimentally determined. And the question is, what do we make of that information? People like Professor Miller and the authors of this paper working from a Darwinian framework simply fit that data into their framework.
But to me, that data does not support their framework. It does not offer experimental evidence for that framework. They’re simply assuming a background of Darwinian random mutation and natural selection and explaining it — or fitting it into that framework, but they’re not offering support for it.
Q. Dr. Behe, is there another paper that scientists point to for the support that the immune system can be explained by this Darwinian process?
A. Yes, there is. There is one more that I have to discuss. Here is a recent paper, again the year 2005, by Klein and Nikolaidis entitled The Descent of the Antibody-Based Immune System by Gradual Evolution. And on the next slide is an excerpt from the initial part of their discussion where they say, quote, According to a currently popular view, the Big Bang hypothesis, the adaptive immune system arose suddenly, within a relatively short time interval, in association with the postulated two rounds of genome-wide duplications.
So these people, Klein and Nikolaidis, are going to argue against what is the currently popular view among immunologists and people who study the immune system on how that system arose.
Q. And what is the Big Bang hypothesis that’s referred to here?
A. Well, that’s kind of a label that they put on to kind of indicate the fact that the immune system appears in one branch of animals, the vertebrates, and any obvious pre-cursors or functional parts of such a system do not appear to be obvious in other branches of animals.
So it seems like the immune system arose almost complete in conjunction with the branching of vertebrates from invertebrate.
Q. Do scientists acknowledge that or treat that as a problem for Darwin’s theory?
A. Well, in my experience, no, nobody treats such a thing as a problem for Darwin’s theory.
Q. Do you consider it a problem?
A. I certainly consider it a problem. But other scientists who think that Darwinian evolution simply is true don’t consider much of anything to be a problem for their theory.
Q. Why do you consider it a problem?
A. Because the — as Darwin insisted, he insisted that adaptations had to arise by numerous successive slight modifications in a very gradual fashion. And this seems to go against the very gradual nature of his view.
Q. Now has this paper been held up by scientists as refuting claims against intelligent design?
A. Yes, it has. As a matter of fact, Professor Miller cited it in his expert report, although he didn’t refer to it in his testimony. Additionally, I attended a meeting on evolution at Penn State in the summer of 2004 where one of the authors, Juan Kline, spoke on his work, and he interpreted it in those terms.
Q. Now we have some quotes, I believe, from this paper that you want to highlight?
A. Yes. Again, I want to pull out some excerpts from that paper just to show you why I regard this as speculative and unpersuasive. For example, they start with, by saying, quote, Here, we sketch out some of the changes and speculate how they may have come about. We argue that the origin only appears to be sudden. They talk about something as probably genuine.
It probably evolved. Probably would require a few substitutions. It might have the potential of signaling. It seems to possess. The motifs presumably needed. One can imagine that a limited number. It might have been relatively minor. Quote, The kind of experimental molecular evolution should nevertheless shed light on events that would otherwise remain hopelessly in the realm of mere speculation. They’re talking about experiments that have yet to be done.
Next slide, I have even more such quotations. These factors are probably genuine. Nonetheless. They might have postdated. Nevertheless. Albeit. It seems. This might have been. These might represent. They might have been needed. This might have functioned. This might have. And this might have contributed.
So again, this is just a shorthand way of trying to convey that, when I read papers like this, I do not see any support for Darwin’s theory. I read them as speculative and — but nonetheless, people who already do believe in Darwin’s theory fit them into their own framework.
Q. Now Dr. Miller cited numerous papers in his testimony to support his claims on irreducible complexity, the type III secretory system, and so forth. Have you done a review of those papers and have some comments on them that you prepared slides for?
A. Yes, I did. I went through many of the papers that Professor Miller cited, as many as I could, and simply, as a shorthand way of trying to indicate or trying to convey why I don’t regard any of them as persuasive, I simply did a search for the phrases, random mutation, which is abbreviated here in this column, RM, and the phrase, natural selection.
Random mutation, of course, and natural selection are the two elements of the Darwinian mechanism. That is what is at issue here. And so this is, you know, this is, of course, a crude and perhaps shorthand way, but nonetheless, I think this illustrates why I do not find any of these papers persuasive.
When I go through the papers that Professor Miller cited on the blood clotting cascade, Semba, et al, Robinson, et al, Jiang and Doolittle, there are no references to those phrases, random mutation and natural selection.
Q. Some of your indications on this slide, you have 0 with asterisks and some without. Is there a reason for that?
A. Yes. The papers that have asterisks, I scanned by eye. I read through them visually. Ones that do not have an asterisk, I was able to do a computer search for those phrases because they are on the web or in computer readable form. I have a number of other such tables.
On the next one are references that Professor Miller cited on the immune system. And again, none of these references contain either those phrases, random mutation and natural selection. There were a couple more references on the immune system that Professor Miller cited, and they didn’t contain those phrases either.
In references for the bacterial flagellum and the type III secretory system, there was one paper by Hauch, a review in 1998 that did use the phrase natural selection. However, that phrase did not occur in the body of the paper. It was in the title of one of the references that Hauck listed.
And on the next slide, I think there are papers cited by Professor Miller on common descent of hemoglobin. And again, those phrases are not there. I think there’s another slide or two, if I’m not mistaken. This is the one on what he described as molecular trees, Fitch and Margoliash, from 1967. And I didn’t find the phrase there either. So again, this is a shorthand way of showing why I actually considered these off-the-point and unpersuasive.
Q. So all these papers that are being used to provide evidence for Darwin’s theory of evolution, in particular, the mechanism evolution of natural selection, yet they don’t mention random mutation or natural selection in the body of the works?
A. That’s correct.
Q. Could you summarize the point then, Dr. Behe, that you are making with, referring to these studies and the comments you made about the speculative nature of some of these studies?
A. Yes. Again, much of these studies, in my view, are speculative. They assume a Darwinian framework. They do not demonstrate it. And certainly, you know, certainly scientists should be free to speculate whatever they want. You know, science usually starts with speculation, but it can’t end with speculation.
And a person or, and especially a student, should be able to recognize and differentiate between speculation and actual data that actually supports a theory.

Q. Is this — so you’ve done work in this area with the histone H4 and the molecular clock?
A. Yes, uh-huh. I’ve written this commentary in 1990 in a journal called Trends in Biochemical Sciences, commenting on the work of somebody else who experimentally took an organism called yeast into the lab and altered its histone H4 and actually chopped off a couple amino acids at the beginning portion of that protein.
And when he looked, it seems that it didn’t make any difference to the organism. The organism grew just as well without those mutations, which is surprising, which is not what you would expect if all of those residues were critical for the function of that protein, histone H4.
Later on, in the year 1996, I and a student of mine, Sema Agarwal, we were interested in this problem of histone H4 and molecular clock, and so we experimentally altered some amino acid residues into protein and changed them into different amino acids, with the expectation that these might destroy the function of the protein. But it turned out not to.
These positions, these amino acids could be substituted just fine, which is unexpected, and which kind of complicates our interpretation of the molecular clock hypothesis. So there are two complications; complications upon complications.
One, we would expect the number of mutations to accumulate with generation time, but it seems to accumulate, for some unknown reason, with absolute time. And the second is that, proteins accumulate mutations at different rates. We would expect that it would have to do with how vulnerable they are to mutations, and mutations might destroy the function of one protein that evolved slowly, but that is not experimentally supported.
Q. Now has this problem been discussed in the scientific literature?
A. Yes, this has been continuously discussed ever since the idea of the molecular clock hypothesis was first proposed in the early 1960’s by two men named Emile Zuckerkandl and Linus Pauling. And here are a couple of papers which deal with the difficulties of the molecular clock hypothesis.
Here’s a recent one, Gillooly, et al, published in the Proceedings in the National Academy of Sciences, entitled The Rate of DNA Evolution, Effects of Body Size and Temperature on the Molecular Clock. In this publication, they say that, in fact, the size of an organism and temperature can affect how fast or how slow this clock might tick.
Francisco Ayala has written on this frequently. Here’s one from 1997. And I should say, Francisco Ayala is a very prominent evolutionary biologist. He wrote an article in 1997 entitled Vagaries of the Molecular Clock. And I think the title gets across the idea that there are questions with this hypothesis.
And in 1993, a researcher named Tomoka Ohta published an article in the Proceedings of the National Academy of Sciences entitled An Examination of the Generation-time Effect on Molecular Evolution in which she considers exactly that complication that the textbook Voet and Voet pointed out, this generation-time effect.
You know, why shouldn’t organisms that reproduce more quickly accumulate more mutations. I have another slide just from one more recent paper. This paper by Drummond, et al, is entitled Why Highly Expressed Proteins Evolve Slowly. And it’s referring to the sequence evolution that I’ve been discussing.
It was published in the Proceedings of the National Academy of Sciences, and this was from an online version. This is so recent that I don’t think it has yet appeared in print. The point I want to make with this is that, these people treat this question as a currently live question.
They start off by saying, a central problem in molecular evolution is why proteins evolve at different rates. So that question I was trying to illustrate with histone H4, why does one protein tick faster and another one tick more slowly, that’s still — that is still unknown.
And I think I will skip the rest of this slide and go to the next slide and just point out a couple words here. Drummond, et al, say, Surprisingly, the best indicator of a protein’s relative evolutionary rate is the expression level of the encoding gene.
The only point I want to make with this is that, they are reporting what is a surprise, what was not expected, which was not known, you know, 40 years ago, which has only been seen relatively recently. And they say, quote, We introduce a previously unexplored hypothesis, close quote.
And the point I want to emphasize is that, here in this paper published, you know, weeks ago, that they are exploring new hypotheses to try to understand why proteins have the sequences that they do.
 

Comments
Sorry about commenting on a semi-old post, but I wanted to get my thoughts straightened out a bit. First, a thank you to Joseph for an answer that made me think a bit. If Joseph is still reading this thread (not likely, I know) I'd like to know if the idea of counterflow can be applied to the bacteria that eats nylon. Nylon is a material that was obviously designed by humans (since we know the individuals who did so) and can't be found in nature (barring its introduction by humans). Wouldn't that seem to make the ability of the nylon-eating bacteria artificial? Was it intelligently designed? How? Was there some other (non-evolutionary) mechanism?Monimonika
August 22, 2006
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minlay: "I see, so you don’t feel that it’s necessary to demonstrate the actual EXISTENCE of the one doing the designing, or provide any evidence for it whatsoever. This is not how science proceeds." Joseph: "Nice goal post move. No one said the designer has to still exist. The data we do have says at least one did exist but that data did not come with a time stamp." I didn't say the designer had to still exist, just that it had to at one point. I'm assuming the data that you have is the empirical argument we've been discussing, meaning you don't have any independent evidence of the existence of a designer. Joseph:"the ONLY way to make ANY determination about the designer in the absence of direct observation or designer input is by studying the design in question. THAT is a fact of life." So what determinations have you been able to make regarding the designer based on studying the design?minlay
August 18, 2006
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Me: "Do you see IDists trying to develop testable models to explain the origins of IC biological systems?" By Joseph: "Yes, IDists say they originated by design. The process and the designer are separate questions." But you haven't even described the process of design for IC biological systems. All you said was the word 'design'. What process are you referring to? Joseph again: "How does one test ID? By the concepts of IC and/ or CSI." Can you be more specific here? Can you describe an actual experiment that an ID researcher could perform to test whether or not an IC biological system could originate by intelligent design? Joseph: "How does one falsify ID? By showing that either can arise in the absence of an intelligent agency." Unfortunately, that would not falsify intelligent design. It's entirely possible an IDer could have used evolution to create an IC object. Or that the IDer created the object in a way indistinguishable from evolution. Or that evolution could have created the object, but didn't, and the IDer did. It would make the IC to ID inference worthless, but it wouldn't falsify ID. Incidently, we've already shown that IC systems CAN arise in the absence of intelligent agency. Any hypothetical model will do that. What we haven't shown (in the opinion of the IDists) is that IC systems HAVE arisen in the absence of intelligent agency. Again, this goes back to the logical vs. empirical argument of IC. There is no logical barrier to the evolution of IC objects by "Darwinian" evolution.minlay
August 18, 2006
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To Monimonika, Counterflow does very nicely. Counterflow being that which nature could not or would not do if left to operate freely. Therefore if we see an insulin producing sequence in bacteria we would be correct in inferring it was put there by an intelligent agency. That would also apply to GMF. All that would take is to "know" what a plant's, for example, genome should be and compare that to what we have in front of us (the suspected modified plant). ------------------------------------------------------------------------------------ Minlay: Do you see IDists trying to develop testable models to explain the origins of IC biological systems? Yes, IDists say they originated by design. The process and the designer are separate questions. Minlay: No, and the reason is that it would require some hypotheses about the nature and capabilities of the designer. Reality demonstrates that the ONLY way to make ANY determination about the designer or the process in the absence of direct observation or designer input is by studying the design in question. What part of that don't you understand? For example what could you tell about the Wright Brothers just by studying the jets of today? Could you deduce how they produced their first plane? First you detect the design, then you study it. THAT is ID- detection AND understanding. Evolutionists insist on making evolution and abiogenesis separate questions even though life's origins directly impacts its subsequent evolution- if life didn't arise from non-living matter via unintelligent, blind/ undirected (non-goal oriented) processes there would be no reason to infer its subsequent diversity arose via those types of processes. AND we don't even know if mutations can allow for the range of change required if all of life's divesity owed its collective common ancestry to some unknown population of single-celled organisms which just happened to have the ability to asexually reproduce. BTW thanks for your long response. I will get back to you on that... How does one test ID? By the concepts of IC and/ or CSI. How does one falsify ID? By showing that either can arise in the absence of an intelligent agency.Joseph
August 18, 2006
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Joseph, I'm trying to avoid the point-by-point response technique, because it only takes a few exchanges from each of us before our posts become unreadible. If there are points you really want me to address that I didn't, please reiterate them. As for the lamprey question, I just haven't gotten around to it, but I don't like feeeling like I'm being coerced to answer any particular question (see DaveScot), so I usually tend to ignore them. Joseph's questoin: "Just how can one test or falsify the premise that the human immune system “evolved” from the lamprey’s via unintelligent, blind/ undirected (non-goal oriented) processes?" The lamprey's immune system may not be the best system to use for this example, because about 2 years ago, we discovered evidence that they have their own version of the adaptive immune system that's quite different than ours. I don't know how long ago we diverged from the extant lamprey, but let's say 500 million years ago. That's a lot of time for them to evolve their own system. So I'm just going to use a generic jawless vertebrate that existed after the lamprey/jawed vertebrate split. Since you're not going to argue the details of how we think the immune system evolved, I'll just focus on the "unintelligent, blind/undirected (non-goal oriented) process. However, here's the basic model that I'll be working with. In a jawless vertebrate, a transposon containing the RAG-1 and RAG-2 genes, and flanked by recombination signal sequences (RSSs), integrated into an antigen receptor gene, near the point on the gene that encodes the antigen binding pocket. During the development of the lymphocytes that express this gene, as the gene becomes transcriptionally active, so does the RAGs, which then undergo a second transposition reaction, removing the transposon, and leaving the gene slightly different than when it entered. This only happens in a subset of lymphocytes (because of the randomness of the transposition reaction), but in every lymphocyte it happens to, it leaves the antigen receptor gene slightly different, creating a diversity of antigen receptor genes, and increases the types of antigens that these genes can bind. As the population of jawless vertebrates is exposed to pathogens in their environment, the one animal bearing this unique antigen receptor has a competitive advantage, being able to fight off infections from a broader range of pathogens. Eventually it's offspring take over the population, and a new system emerges. That's the basic model. Each sentence in that description I can back up using evidence from the 58 papers originally referenced. Now your issue seemed to be not that this sequence of events occured, but rather whether or not it could be accounted for by the evolutionary mechanisms mainstream scientists recognize. To that end, there are certain predictions that a system of random mutation and natural selection makes. One is that genes will continuously mutate, and the mutations in essential regions of genes will likely be detrimental (though not always!), whereas mutations in non-essential, or non-coding regions will be effectively neutral. So if we compare sequences of organisms within those genes, the prediction is that coding regions will have fewer differences than non-coding regions, and essential coding-regions will have fewer differences than non-essential regions. There's also the issue of silent mutations, which don't affect the protein sequences, and non-synonymous mutations, which do. In addition, there is the issue of time. Organisms which diverged from humans longer ago will have more differences in their genetic sequence than organisms which diverged more recently. Taken together, what this means is that there's a range of possible sequences that we expect to find in any given lamprey gene. Since this is a probablistic argument, we expect that if examine ALL the lamprey genes and compare them to their homologues in humans, we will find a bell curve, with some genes being more similar (just due to probability), and some genes being more dissimilar. The mean value or peak of that curve will have a percent similarity to humans that's inversely proportional to the predicted age (based on fossil records and cladistics) that the organism diverged from humans. In other words, the further ago the two organisms diverged, the smaller their average percent similarity of homologous genes will be. A potential falsifier of "Darwinian" evolution is if the average percent similarity of homologous genes for lamprey vs. human is greater than that for mouse vs. humans. Also, I should point out that because lamprey diverged from humans at the same time it diverged from mice, we also predict that the percent similarity of lamprey vs. humans will be the same as lamprey vs. mice (or lamprey vs. any jawed vertebrate). The same idea applies to every other genome we have sequenced, and so a phylogeny can be made of all the genomes sequenced, and "Darwinian" evolution predicts that these phylogenies should match the phylogenies we've made using traditional methods (fossils records, cladistics). I would guess that these phylogenies don't match 100% of the time, and I would argue that in those cases the fossil record is wrong, and so another prediction of "Darwinian" evolution is that in cases where they don't match, the fossil record will be found to be in error. It is a necessary condition of common descent that all organisms are contained within one "true" phylogeny, though we don't necessarily know exactly 100% what that phylogeny is. Note that for those who do not believe in common descent, there is absolutely no requirement for anything to fit in a phylogeny. So to answer your question, we can test whether or not the model of how the human immune system evolved from lamprey or better yet tunicate immune systems by analyzing the sequence data and seeing if it falls within our predicted ranges. It should also be noted that intelligent design makes NO sequence predictions, and therefore all sequences are equally likely. Here are some other ways to test the model. We should be able to generate a pathway for each of the major steps in the evolution of the immune system (after the initial transposon insertion I described above). There are a number of features that we must take into account. In humans, there are actually 7 genes that can undergo V(D)J recombination: TCRalpha, TCRbeta, TCRgamma, TCRdelta, and Igkappa, Iglambda, and IgH (heavy chain). If "Darwinian" evolution is true, than all of these genes should have evolved from a single antigen receptor, and therefore all 7 should be able to fit a phylogeny. Furthermore, a phylogeny should be possible for EVERY organism that has a V(D)J recombination system. For example, while mice are similar to humans, there are some key differences in their genomic organization. Furthermore, all sharks, fish, birds, and reptiles should also each fit into their own individual phylogeny, and the phylogenies of each should match (to the extent that their systems are similar). For example, if mammals and birds both contain Igkappa and Iglambda genes (which they do), then their common ancestor (reptiles) at one point contained both Igkappa and Iglambda genes. Since the Igkappa and Iglambda genes are quite similar to each other, then the prediction is they were once a single gene in one of our ancestors. The timing of their divergence (via gene duplication) should match between birds and mammals, and their split should be consistent with all the other phylogenies. So if there is only a single Igkappa/Iglambda gene in reptiles, then there should not be a distinct Igkappa or Iglambda gene in any of the predecessors of reptiles (amphibians, fish, sharks). My basic point is that there are a LOT of rules to make the phylogenies consistent with each other. However, a lot of what I described applies to the notion of common descent, not necessarily "Darwinian" evolution, but the sequence data is very Darwinism-specific. That the two are highly interwoven is a consquence of our current evolutionary theory. There have been a few roadblocks discovered along the way. One example is that intially there were thought to be two random insertions of the RAG transposon into an antigen receptor gene. One split the gene into V and J segments, and a second one split it again into V, D, and J. Because some genes have only V and J, while others have V, D, and J, if all of these genes evolved from a single gene then there had to have been two transposon insertions, at totally different times. This wasn't a very feasible model. However, later on we discovered that an errant recombination reaction could actually create a novel gene segment, which would explain how a D segment was created through non-intelligent means and without appealling to another transposition reaction. Here's a second example. Not all recombination signal sequences are the same. Some have a 12 base pair gap, and others have a 23 base pair gap. Only RSSs with a 12 bp gap can rearrange with RSSs with a 23 bp gap (this is called the 12/23 rule). In some genes, the V segments have a 12 bp gap, and in other genes the Vs have a 23 bp gap. This is totally inconsistent with common descent via "Darwinian" evolution, but of course it would be easy for an IDer to flip the RSSs. However, a few years later, it was discovered that another type of errant recombination could flip the RSSs. Again, a major problem for the evolution of this system (via "Darwinian" evolution) was solved. So here is another prediction of "Darwinian" evolution. For every situation that would appear to falsify the proposed pathway, a novel mechanism will be found to explain it. It's happened twice so far. So what I've presented here (which was contained within the 58 references all along!) is a model for how the adaptive immune system could have evolved. The model is detailed (it could easily fill a book, just for the adaptive part), and testable (as I have shown above). And a major point in its favor is that there are researchers out there that are actively testing it. It's one thing to propose an experiment, and another thing entirely to conduct one. Where is the actual ID research on the origin of any IC system? So here we have a situation where the pro-evolution side is actively studying the origin of this system via evolution using the scientific method (i.e. developing and testing models), and is achieving real tangible results. And on the ID side, no one is proposing an actual model, no one is conducting research on an ID model for any IC system, and certainly no one has produced any actual results to support ID. So let me turn this question back to you: Describe a model for the origin of any IC biological system by intelligent design, and show how this model is testable and/or falsifiable.minlay
August 18, 2006
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Me: “Clearly no archaeologist is going to propose that a rock shaped like an arrowhead was intelligently designed, if the arrowhead was found in a sediment that’s 10 million years old. … For example, an archaeologist might examine an arrowhead-shaped rock for evidence of chipping, of a type of technique he/she knows that tribes (that existed at the time the arrowhead was created) commonly used.” Sorry for the sloppy wording, I wasn't trying to imply in the first sentence that the arrowhead-shaped rock had evidence of chipping, just that it was SHAPED like an arrowhead, nothing more. I'm not sure if any evidence of manufacturing would be left on a 10 million year old piece of rock. However, in monimonika's scenario: "It could be that there existed a tool-making creature prior humans", the study of this model would proceed by a) looking for evidence that such a creature existed, b) hypothesizing what method the creature used to create the arrowhead and looking for other objects that contain similar manipulations, c) hypothesizing what the function of the arrowhead-shaped rock was (somehow I doubt that creatures 10 million years ago hunted with bow and arrow), and looking for objects that may complement such a function. Essentially what I'm describing is a series of testable models to explain the origin of that arrowhead. I still think it's highly unlikely that anyone would think a 10 million year old rock was intelligently designed just because it bore the shape of an arrowhead, but if they found real evidence of manipulation, that's how I think they might proceed. Do you see IDists trying to develop testable models to explain the origins of IC biological systems? No, and the reason is that it would require some hypotheses about the nature and capabilities of the designer.minlay
August 18, 2006
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Oh, and one more thing. I have to call on an error by Minlay in comment #88: "Clearly no archaeologist is going to propose that a rock shaped like an arrowhead was intelligently designed, if the arrowhead was found in a sediment that’s 10 million years old. ... For example, an archaeologist might examine an arrowhead-shaped rock for evidence of chipping, of a type of technique he/she knows that tribes (that existed at the time the arrowhead was created) commonly used." I have to side with Joseph on this one. If an archaeologist found an arrowhead-shaped rock with evidence of chipping/modifications in sediment that's 10 million years old, then the finding would be picked up and studied like crazy, with multiple theories (here, "theory" means guesses) on how it came to be the way it is. It wouldn't be tossed aside. Of course, there would be more digging for other clues and arrowhead-shaped rocks, which would take time and would, hopefully, lead to a better and better set of explanations (which, depending on the evidence, may also include "sheer coincidence" as a possiblity). Just one arrowhead-shaped rock (with evidence of modifications) would not be enough to solidly claim anything, of course. The main point is that, it will all depend on what we can conclude from the evidence surrounding the may-be arrowhead-rock. It could be a coincidence. It could be that there existed a tool-making creature prior humans (evidence of which should turn up in other forms Monimonika
August 18, 2006
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Comment #89 by Joseph: "Moni: I just wanted to point out a misconception by Joseph here. The method for detecting genetically modified foods is not based on the ID methodology of probabilities. Probabilities is NOT the ONLY ID methodology. Had you known about ID you would have known that. " I apologize for my ignorance, but only if you can please explain this other part(s) of the ID methodology (of detecting intelligent design) that relates to the methodology of detecting genetically modified foods. As said before, detecting GM foods depends upon knowing the sequence of the modified part of the genetic code before going out to look for it. You most likely will not make this particular arguement, but I just want to specify that I will not accept analogies of "parts of biological organisms" to "parts of man-made, non-biological, machinery". Reasons on why I dismiss this analogy approach are: 1) it assumes human intelligence when making distinctions, not necessarily that of a non-human designer, and 2) man-made, non-biological, machinery are built from parts assembled by other beings (humans in this case) rather than being reproduced from each other (plus, they don't grow). Again, I don't believe that you will make this arguement, but I didn't want to read about it from others. Joseph, please tell me what I am missing since I admit that I haven't been following the ID methodology too closely and most likely missed something due to the biased reading of the subject that I encountered early on. Thank you, MonimonikaMonimonika
August 18, 2006
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And while we are waiting: Just how can one test or falsify the premise that the human immune system “evolved” from the lamprey’s via unintelligent, blind/ undirected (non-goal oriented) processes?Joseph
August 18, 2006
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“Minlay: How many of those IC objects whose causes were discovered were biological organisms? Me: Tell us Minlay, what prevents tried-n-true design detection methodology from being used on biological organisms? And yes we can discover genetically modified foods via ID methodology.” Moni: I just wanted to point out a misconception by Joseph here. The method for detecting genetically modified foods is not based on the ID methodology of probabilities. Probabilities is NOT the ONLY ID methodology. Had you known about ID you would have known that. Minlay: To add to Monimonika’s point, with regards to forensics, archaeology, and GM foods, in all those cases, any inference to design takes into account knowledge of the designer, i.e. humans. Irrelevant. Minlay: Clearly no archaeologist is going to propose that a rock shaped like an arrowhead was intelligently designed, if the arrowhead was found in a sediment that’s 10 million years old. Then they have a problem. A major problem. Minlay: With ID, no information about the capabilities, motives, or existence of the designer is even looked for, and therefore no models for how the designer may have created the supposed designs are made. Again if we knew the capabilities of the designer we would NOT have a design inference- design would be a given. also- the ONLY way to make ANY determination about the designer in the absence of direct observation or designer input is by studying the design in question THAT is a fact of life. Also the design inference makes both the designer and the process separate questions- just as Wm. DEmbski explains in "No Free Lunch". Minlay: Without a model, there’s nothing to look for, and therefore there’s no science. We look for CSI and/ or IC. OR we could start with Behe's simple criteria:
"Our ability to be confident of the design of the cilium or intracellular transport rests on the same principles to be confident of the design of anything: the ordering of separate components to achieve an identifiable function that depends sharply on the components.
Joseph
August 18, 2006
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Sorry, I've been busy at work so I haven't had much time to continue this conversation. Joseph: "Tell us Minlay, what prevents tried-n-true design detection methodology from being used on biological organisms? And yes we can discover genetically modified foods via ID methodology." To add to Monimonika's point, with regards to forensics, archaeology, and GM foods, in all those cases, any inference to design takes into account knowledge of the designer, i.e. humans. Clearly no archaeologist is going to propose that a rock shaped like an arrowhead was intelligently designed, if the arrowhead was found in a sediment that's 10 million years old. No forensic scientist is going to propose that a person was murdered using technology that doesn't exist. All design inferences in these fields were made by forming a model of how a designer created the object, then looking for evidence to support that model. For example, an archaeologist might examine an arrowhead-shaped rock for evidence of chipping, of a type of technique he/she knows that tribes (that existed at the time the arrowhead was created) commonly used. With ID, no information about the capabilities, motives, or existence of the designer is even looked for, and therefore no models for how the designer may have created the supposed designs are made. Without a model, there's nothing to look for, and therefore there's no science. (I'll try and address these other points when I have time)minlay
August 17, 2006
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In comment #65 by Joseph: "Minlay: How many of those IC objects whose causes were discovered were biological organisms? Tell us Minlay, what prevents tried-n-true design detection methodology from being used on biological organisms? And yes we can discover genetically modified foods via ID methodology." I just wanted to point out a misconception by Joseph here. The method for detecting genetically modified foods is not based on the ID methodology of probabilities. What it's based on is knowing _in advance_ what the genetically modified string of genetic code looks like and _then_ searching for it. Obviously, unless we know ahead of time what the "intelligent designer" was capable of, this tried-n-true detection methodology does nothing in detecting design in non(human)-modified biological organisms.Monimonika
August 17, 2006
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85: Joseph quoting from Extrapolating From Small Changes: "And when talking about the evolution of the mammalian middle ear bones, we should not forget that we are still basically in the dark in trying to explain how both a mammalian and reptilian zygote actually develops the middle ear and jaw bones, respectively. Without this knowledge, attempts to explain such a transition as a function of a series of small, incremental changes stretched across time are rooted in ignorance." I glad to see that the notion of a "gap" in the fossil record has been abandoned here. Time to move the bar. Also: Ofro: "Second: why random? Because at least in the test tube, transposons behave randomly; there are even commercial kits available that use transposons to deliberately and randomly shift DNA around, such as for the purpose of sequencing long stretches of DNA." Joseph replie: "Again they are random only due to our ignorance. This approach is like trying to figure out the output of a C++ programm by only looking at the ASCII representation of the output." I don't know where the "ignorance" is to be found. I have the DNA sequence in my laboratory notebooks and know where the transposon insertions are. That is an experimental observation not an assertion from ignorance. I am not claiming that I know the exact biochemical/enzymatic mechanism of the process (is that what you mean by your C++ code?). I know the experimental outcome, and that is what I have claimed.ofro
August 17, 2006
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54: Joseph : “So how can changes that do NOT affect functionality at the molecular level produce profound effects at the morphological level?” snip Joseph” It does if we were discussing variations within a population. However we both know we aren’t discussing that.” Ofro: I guess it boils down to your denial that if a species accumulates many mutations over a long time, resulting in changes of morphology as well as inner workings (such as in the nervous system, but could be other organs, too), that this process could result in a related species. Can't deny what has never been demonstrated. Then there is the following to consider: Extrapolating From Small Changes:
If one desires to extrapolate small changes into large changes by simply adding time, one requires independent evidence to justify this move. The problem is that we really don't know how evolution occurs. And when talking about the evolution of the mammalian middle ear bones, we should not forget that we are still basically in the dark in trying to explain how both a mammalian and reptilian zygote actually develops the middle ear and jaw bones, respectively. Without this knowledge, attempts to explain such a transition as a function of a series of small, incremental changes stretched across time are rooted in ignorance. That is, we don't truly understand neither the process of development nor the process of evolution and without such knowledge, there is no reason to think we are on safe ground when employing (1).
Ofro: I am not asking for turning a fish into a quadruped. I am only asking about mouse vs. rat or wolf vs. dog. Is there not even the theoretical possibility of that? Wolf/ dog is more of the variations I was talking about. Joseph: “Transposition is a form of random muation? How was that figured out?” Ofro: First, I think there are very few people who would disagree with classifying any change of DNA sequence as a mutation. That is irrelevant. Ofro: Second: why random? Because at least in the test tube, transposons behave randomly; there are even commercial kits available that use transposons to deliberately and randomly shift DNA around, such as for the purpose of sequencing long stretches of DNA. Again they are random only due to our ignorance. This approach is like trying to figure out the output of a C++ programm by only looking at the ASCII representation of the output. Ofro: So if you are challenging the notion that this enzyme system does not have at least a random component in its action, wouldn’t this be something worthwhile for the molecular biologists among the ID crowd to disprove experimentally? Once again- Dr. Spetner discussing transposons: The motion of these genetic elements to produce the above mutations has been found to a complex process and we probably haven’t yet discovered all the complexity. But because no one knows why they occur, many geneticists have assumed they occur only by chance. I find it hard to believe that a process as precise and well controlled as the transposition of genetic elements happens only by chance. Some scientists tend to call a mechanism [I]random[/I] before we learn what it really does. If the source of the variation for evolution were point mutations, we could say the variation is random. But if the source of the variation is the complex process of transposition, then there is no justification for saying that evolution is based on random events." --------------------------------------------------------------------------------------- Karen asks: Anyway, I have a question: if there is an intelligent designer at work, why do we even need an intelligently designed immune system to protect us from intelligently designed pathogens? No one said the design had to be "perfect" or that even if it started out "perfect" that it had to remain that way. Karen: What kind of purpose and morality is inferred from a designer who creates life forms, only to turn around and design parasites, etc. to sicken, torture and kill them? Tell us Karen, what do you know about ID? What would happen on an Earth in which humans did not die? People die and we find out why. It's a discovery process. And that fits in nicely with the premise of "The Privileged Planet".Joseph
August 17, 2006
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DaveScot, " ...and ask what tests were performed to rule out the same programmed process occuring during phylogenesis" I am not an immunology expert and may not be the ideal person to ask, but from what I understand from the field and from your question, I think I can exclude your proposed scheme just by referring to the textbooks (I don’t have any in front of me right now to verify what I am writing). The development of the immune system in the embryo, like so much else in the embryo, follows a fairly specific program that is set up by (what I understand, but again, I am not the expert here) a sequential activation of hox genes, followed by activation of increasingly “lower-level” systems and transcription factors with more specific locational specificity. (Of course there are also many transcription factors that are not location- or tissue-specific). During reproduction, which obviously must happen if you want to progress through any evolutionary pathway, these mechanism play no role, and totally different regulatory pathways are in charge. If hox genes, and all the other pathways that set up the immune system, were involved, this would have been detected even without specifically looking for that. So your proposal of the “same programmed process occuring during phylogenesis” does not work. Perhaps your statement was a bit more general in that some other program exists (or existed) according to which the immune system had no choice but developing during the evolutionary process over many generations. I am not sure how to answer that. I think you are asking for a test of whether some (any?) not-yet-specified programmed process exists which determines the generation of an immune system that had not occurred in previous generations. (Is that a version of genetic front-loading that permits future diversification into many different species?). I can only come up with two possible replies: 1. Considering the amount of work that has been put into learning about the immune system and its possible evolutionary precursors, I would be very surprised that some regulatory pathway should have been overlooked. No matter how biased you may consider scientists to be against directed evolution, if you want to put a negative spin on scientists, you will also accept that a) if a scientist discovers a potentially revolutionary mechanism, he/she will make sure that everybody knows about it, either through the scientific literature or by trumpeting it in the popular press; and b) that there will be a horde of other scientist jumping on it to test and hopefully disprove it. (I am exaggerating a bit, but the essence is there; and this is how the bad stuff eventually is weeded out). In addition, negative results, i.e. the fact that one couldn’t find something one was looking for, are much less likely to be published. Overall, no such proclamation of a regulatory principle or program has ever been made in my knowledge. So my tentative conclusion is that your question may already have been answered, unnoticed by anybody. 2. (I don’t want to sound too antagonistic, so please excuse if I come across as too strong for you) If a proof is required, it is always better to demonstrate the existence of a process/object than to demonstrate its absence. You are essentially asking your scientific opponent to demonstrate the _absence_ of something that you propose as an (competitive) alternative. I would invite scientists on the ID side to put efforts into demonstrating the _presence_ of what you postulate.ofro
August 16, 2006
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ofro Just about anything is possible. It's possible that tiny invisible pixies from Mars are the mechanism responsible for organic evolution. Science is all about narrowing down the list of the possible to a list of the probable. So again I point to the programmed development of the immune system during ontogenesis and ask what tests were performed to rule out the same programmed process occuring during phylogenesis. I'm of the opinion that they are basically the same diversification process at different scales - neither is or was a matter of chance.DaveScot
August 16, 2006
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Karen, You are conflating religion and philosophy with design detection. Inferring design is not inferring moral purpose. If you are concerned rather with the problem of evil as pertains to the God of Christian belief then Bill Dembski's theodicy might be for you. http://www.designinference.com/Charlie
August 16, 2006
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Joseph said: "Just how can one test or falsify the premise that the human immune system “evolved” from the lamprey’s via unintelligent, blind/ undirected (non-goal oriented) processes?" Is someone acually claiming that our human immune system evolved from the lamprey's immune system? My goodness! Anyway, I have a question: if there is an intelligent designer at work, why do we even need an intelligently designed immune system to protect us from intelligently designed pathogens? What kind of purpose and morality is inferred from a designer who creates life forms, only to turn around and design parasites, etc. to sicken, torture and kill them? (For this example I'm assuming there is but one designer.)Karen
August 16, 2006
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54: Joseph : “So how can changes that do NOT affect functionality at the molecular level produce profound effects at the morphological level?” snip Joseph" It does if we were discussing variations within a population. However we both know we aren’t discussing that." I guess it boils down to your denial that if a species accumulates many mutations over a long time, resulting in changes of morphology as well as inner workings (such as in the nervous system, but could be other organs, too), that this process could result in a related species. I am not asking for turning a fish into a quadruped. I am only asking about mouse vs. rat or wolf vs. dog. Is there not even the theoretical possibility of that?ofro
August 16, 2006
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76. Joseph: “Transposition is a form of random muation? How was that figured out?” First, I think there are very few people who would disagree with classifying any change of DNA sequence as a mutation. Second: why random? Because at least in the test tube, transposons behave randomly; there are even commercial kits available that use transposons to deliberately and randomly shift DNA around, such as for the purpose of sequencing long stretches of DNA. see http://www.neb.com/nebecomm/products/productE7100.asp So if you are challenging the notion that this enzyme system does not have at least a random component in its action, wouldn’t this be something worthwhile for the molecular biologists among the ID crowd to disprove experimentally?ofro
August 16, 2006
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54: Joseph asks: “So how can changes that do NOT affect functionality at the molecular level produce profound effects at the morphological level?” Ofro's response: “The reason is that the mutations can not only affect a protein’s function but also its expression level. [plus detailed explanation how]“ Joseph's new response: “But the function is not affected.“ You are asking me how there can be a mutation that does not affect functionality, I give you an example, and then you turn 180 degrees and challenge my answer by saying that function is not affected. Sorry, I am at a loss about what you want.ofro
August 16, 2006
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I take it neither NickM or Minlay will even attempt to answer the following: Just how can one test or falsify the premise that the human immune system “evolved” from the lamprey’s via unintelligent, blind/ undirected (non-goal oriented) processes? Typical but still sad...Joseph
August 16, 2006
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Transposition is a form of random muation? How was that figured out? NickM: Um…by studying transposons and transposition. The vast majority of transposon activity isn’t doing much besides reproducing transposons. 3% of the human genome is DNA transposons and fossils of DNA transposons (much of the rest of the genome is other repetitive elements) and doesn’t appear to be doing much besides propagating itself. As far as we know transposition of genetic elements are as random as statements in C++ programs. For example someone who didn’t understand C++ would think that “go to” “if else”, etc. were random events. C++ programmers know better. Again evolutionists rely on our ignorance in order to declare that which is not understood as being random. NickM: Regarding the demand to prove it was “unintentional”, this cannot be done because the hypothesis that a supernatural ID agent miraculously intervened in unspecified ways via mysterious mechanisms cannot be tested or falsified. But ID does NOT say anything about a supernatural ID agent. That is because even that anti-ID position "turtles down" to something beyond nature. Also design is a mechanism. ID can be tested by the concepts of IC and/ of CSI. Either they exist or they do not. All of our experience demonstrates that both only arise via intelligent agencies. Therefore if it is demonstrated, for example, that life can arise from non-living matter via unintelligent, blind/ undirected (non-goal oriented) processes ID would be falsified. NickM: Hypotheses of mysterious supernatural designer intervention are unconstrained and puts no constraints on the data, and therefore no expectations to be tested. All we can say is that the model using specific natural processes has been highly successful when put to experimental test. Way to go Nick! You just proved you can create a strawman and attempt to knock it down! BTW both intelligence AND design are natural processes. And there isn't anything "specific" about RM culled by NS. ------------------------------------------------------------------------------ Joseph: “I don’t have a time-table. Nor do I need one.” Minlay: I see, so you don’t feel that it’s necessary to demonstrate the actual EXISTENCE of the one doing the designing, or provide any evidence for it whatsoever. This is not how science proceeds. Nice goal post move. No one said the designer has to still exist. The data we do have says at least one did exist but that data did not come with a time stamp. “Gee I guess I stand refuted. LoL! But anyway- yes when EVERY time we observe something and X is ALWAYS the cause-> well you know, science and predictions.” Minlay: And EVERY time that designer is human. Wrong. But even if it were true- so what? All we need is the knowledge of what intelligent agencies can do and contrast that knowledge with the knowledge of wjay nature, acting freely, can and cannot do. “Again that they can “evolve” is NOT being debated. They very well could have “evolved” by DESIGN! Read the article “Evolving Inventions” 2003 SciAm.” Minlay: Are you really sure that the ability of evolution is not being debated? Ability of evolution? What is that? The debate is about the ability of mechanisms. Minlay: I have no problem granting the argument that evolution could have been designed, but again, there will have to be evidence for it. There isn't any evidence for the anti-ID position so why do you grant it a free pass? “The logical barrier to the blind watchmaker is obvious- such processes have NEVER been demonstrated to do anything except alter already existing designs.” Minlay: That isn’t a logical barrier, that’s an empirical one. Actually it's both. Minlay: We can easily form hypothetical models for how an IC system could have evolved. Not without breaking many rules. Minlay: Really? Because this whole discussion began with the presentation of 58 articles on the evolution of the immune system. And AGAIN- Not one of those 58 discuss blind watchmaker-type processes! What part of that don't you understand? And if that antic happens again the anti-IDists will be eating crow. Of that I am very sure. BTW beaver dams and lodges are intelligently designed. Nature, operating freely, could not have produced either.Joseph
August 16, 2006
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Now I ask again, in the phylogenetic evolution of the immune system, what tests were performed to discriminate between a preprogrammed sequence of events leading to an immune system and a random sequence of events leading to an immune system?
And that really is the central question, isn't it.Scott
August 16, 2006
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Maybe this will help Nick et al understand the issues. A fertilized human egg cell doesn't have an immune system. The immune system begins to develop during the embryo stage and is fully developed in the fetal stage. There is nothing left to chance in this process. The egg cell contains all the information and mechanisms needed to eventually build a functional, mature immune system. Ontogeny proves that single cells can have a preprogrammed plan of diversification into many different cell types and complex organization. Nothing in the normal course of ontogenesis is due to chance. This is the design model I hold. Now I ask again, in the phylogenetic evolution of the immune system, what tests were performed to discriminate between a preprogrammed sequence of events leading to an immune system and a random sequence of events leading to an immune system? If you can't point to any tests that can and did discriminate between programmed and random evolution of the immune system what justification do you have in saying it was due to chance instead of design?DaveScot
August 15, 2006
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NickM Is it your position that the evolution of the immune system was driven by chance mutations filtered by natural selection? If so, what tests were performed to verify or falsify the assertion that the mutations were generated by chance?DaveScot
August 15, 2006
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Nick Matzke, I have to add, I think we do not serve the cause of science well if we give the impression forensic speculation like evolution should receive the same level of acceptance as operational theories like electromagnetism. Thus, if you want lower standards of acceptance for forensic theories, you should make it clear that forensic theories have far lower threshhold of acceptable proof in your eyes. In other words, you should communicate to your audiences that to get evolution to be accepted requires lowered standards of proof. Salvadorscordova
August 15, 2006
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You have to chose, Sal. Shall we require all science to provide near-infinite detail before any model is accepted? (Like Behe requires for evolution)
That's a leading question with respect to Behe requiring infinite detail. Thus you question is disqualified. I already described what you guys could consider providing just based on basic population thoery in the absence of hard evidence. If it turns out you need unrealistic populaiton resources to achieve your ends, then you might realize your theory is DOA.
Or, instead of omniscience, shall we go with the standard science has successfully used for hundreds of years, namely, testable models and passed tests?
We should go with testable models, but so far the only tests passed are suggestions of similarity. Big deal. It does not settle the issue of what mechanisms were in play for the various reasons I pointed out. You repeat again the equivocation between Darwinism and evolution. The two are not equal. Science should welcome increasing scrutiny of its theories, because its in the presence of anomalies that interesting things are discovered. Behe suspects that Darwinism cannot account for the majority of molecular evolution, and that is highly consistent with initial findings of population genetics. Brian Goodwin, Salthe, others make a good case Darwinism as the mechanism is a bit pre-mature.
Which one is the reasonable standard, Sal?
More leading questions. But as far as good standards, how about the standards which established real scientific theories like: 1. universal gravitation 2. atomic theory of chemistry 3. electro-magnetism 4. thermodynamics 5. celestial mechanics All by design-friendly scientists.scordova
August 15, 2006
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Matt: "What evidence do you have that an intelligent designer even existed 500 million years ago?" Joseph: "I don’t have a time-table. Nor do I need one." I see, so you don't feel that it's necessary to demonstrate the actual EXISTENCE of the one doing the designing, or provide any evidence for it whatsoever. This is not how science proceeds. "Gee I guess I stand refuted. LoL! But anyway- yes when EVERY time we observe something and X is ALWAYS the cause-> well you know, science and predictions." And EVERY time that designer is human. Please give me an example of an intelligently designed IC object that was designed by a non-human designer. I'll give you some starters. Is a spider web intelligently designed? How about a beaver's dam? A bee hive? How about the tiny magnetite crystals that magnetic bacteria can form? This is something I've always wanted to know, but never got a straight answer from the ID crowd. So what predictions can be made from the logical argument you just gave? Can any of these predictions be verified by ID researchers? "Again that they can “evolve” is NOT being debated. They very well could have “evolved” by DESIGN! Read the article “Evolving Inventions” 2003 SciAm." Are you really sure that the ability of evolution is not being debated? I have no problem granting the argument that evolution could have been designed, but again, there will have to be evidence for it. "The logical barrier to the blind watchmaker is obvious- such processes have NEVER been demonstrated to do anything except alter already existing designs." That isn't a logical barrier, that's an empirical one. We can easily form hypothetical models for how an IC system could have evolved. If you want I can give you several simple examples. There are also numerous examples of biological processes that have created novel functions. The ironic thing is that the immune system creates a novel function everytime it is activated by an infection. I don't think you want to argue that the immune system itself is an intelligent agent. I can give you other examples if you're interested. Me: "We certainly have more evidence of that than IDists have that a designer existed back then." Joseph: "If you did we wouldn’t be having this discussion. You can puff out your chest all you want but that will get painful after a while." Really? Because this whole discussion began with the presentation of 58 articles on the evolution of the immune system. Where are the 59 papers on the existence of an IDer?minlay
August 15, 2006
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The detail Behe has asked for has been discussed, and is indeed finite. It is the kind of detail that is required by any other science making claims of a mechanism’s ability to create a result - step by step testable models or experiments showing that the claims are actually being demonstrated, including relevant variables. This is surely not too much to ask of a science whose claims are to be taken as ‘fact’, which are as well-attested to as gravity, and which are as proven as the claim that the Earth revolves around the sun. For the origin of VDJ recombination, evolutionary biologists have the major steps, they have tested them, and they have convincing and widely accepted model for how VDJ recombination evolved by natural processes.* But if hundreds of published research papers are clearly "not enough" for you guys and for Behe (and you are agreeing that the lawyer's characterization was exactly correct), and you still think you get to say cavalierly that there are "no answers" (even though UD folks apparently now accept the transposon answer after we evolutionists taught them about it on these threads!). You demand yet more detail, that every single mutation be reconstructed, even though the main mutations (transposition and rearrangements) account for the major features, and point mutations etc. are uncontroversial "microevolutionary" processes. You also demand that every single ecological interaction, population change, etc. be reconstructed for 500 million years ago, so that you can exactly characterize every selection pressure, even though there is a large amount of work (by Cohn, Gould, and others) showing why natural selection regularly favors receptor diversity. This kind of reconstruction is impossible without a time machine, and probably impossible *with* a time machine (i.e. sequencing the genome of every individual fish that lived between 500 and 450 million years ago). And yet this is what you are demanding. If this standard of "totally complete knowledge" were required in any other science it would kill it. Take the study of flagellum structure. We know that proteins are exported through the based of the flagellum. This is basically 100% certain. However, we know almost nothing about exactly how this protein export occurs. We know that an ATPase is involved and that it interacts with some other proteins -- but we don't know their structure, how exactly they interact, etc. On your logic, no matter much evidence supported the hypothesis of export-through-the base, we couldn't conclude that proteins are exported through the base of the flagellum, until we knew exactly and completely how it happened. Basically, you and Behe are providing an *excuse* for not admitting Behe was wrong when he said scientists had "no answers." We let Behe make his excuse in Court, and the judge accurately recounted the excuse in his opinion. The judge clearly described Behe's opinion that the 58 articles were not detailed enough for him. The judge simply realized, along with everyone accept diehard ID fans, that Behe's infinite-detail criterion was ridiculous. You can keep deluding yourselves all you like, but it just means you will make fools of yourselves again and again against informed opposition. But by all means, keep dreaming that you could save the ID case with legal technicalities and by dismissing piles of scientific evidence by employing absurd and tenditious standards. It will just make it easier for us next time in court. Later, Nick (* Regarding the demand to prove it was "unintentional", this cannot be done because the hypothesis that a supernatural ID agent miraculously intervened in unspecified ways via mysterious mechanisms cannot be tested or falsified. Hypotheses of mysterious supernatural designer intervention are unconstrained and puts no constraints on the data, and therefore no expectations to be tested. All we can say is that the model using specific natural processes has been highly successful when put to experimental test.)Nickm
August 15, 2006
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