“There is no controversy”

_{William Dembski

May 22, 2008

Evolution}

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“There is no controversy.” “There should be no controversy.” “It’s okay to expel those who pretend that there is a controversy.” “Academic freedom does not apply where the scientific consensus says there is no controversy.” …

The Washington Post has a ridiculous editorial that elevates evolutionary theory to the same status as gravitational theory and the truths of mathematics (go here).

Meanwhile, the Altenberg meeting coming up this summer brings together biologists who see the contemporary state of evolutionary theory as in upheaval (go here). Yes, the field is in disarray, but there is NO CONTROVERSY. What, are we living in a Kafka novel?

Comments

Frosty122585, To the best of my knowledge all this information is true to the level of peer reviewed studies, save for Dr. Ross's mathematical speculation that similarity may in actuality be closer to 85 to 90%. Yet even in that case my respect for Dr. Ross previous work in scientific apologetics warrants that his claim be taken with a due amount of respect. as a side note on June 1st, a new book is coming out from Reasonstobelieve.org The Cell's Design: How Chemistry Reveals the Creator's Artistry by Fazale Rana Editorial Reviews Armed with cutting-edge techniques, biochemists have unwittingly uncovered startling molecular features inside the cell that compel only one possible conclusion--a supernatural agent must be responsible for life. Destined to be a landmark apologetic work, The Cell's Design explores the full scientific and theological impact of these discoveries. Instead of focusing on the inability of natural processes to generate life's chemical systems (as nearly all apologetics works do), Fazale Rana makes a positive case for life's supernatural basis by highlighting the many biochemical features that reflect the Creator's hallmark signature. This breakthrough work extends the case for design beyond irreducible complexity. These never-before-discussed evidences for design will evoke awe and amazement at God's creative majesty in the remarkable elegance of the cell's chemistry. From the Back Cover The scientific evidence of design just got stronger. Armed with cutting-edge techniques, today's biochemists have uncovered startling molecular features inside the cell that can compel only one reasonable conclusion--a supernatural agent must be responsible for life. Destined to be a landmark apologetic work, The Cell's Design explores the scientific and theological impact of these discoveries. Instead of focusing on the inability of natural processes to generate life's chemical systems (as nearly all apologetics works do), Fazale Rana makes a positive case for life's supernatural origin by highlighting the many biochemical features that reflect the Creator's signature. This breakthrough book extends the case for design beyond irreducible complexity. These never-before-discussed evidences will evoke awe and amazement at God's creative majesty in the remarkable elegance of the cell's chemistry. "In Darwin's day, a living cell was thought to be quite simply--for all practical purposes--little more than a microscopic blob of gelatin. Rana lays out what contemporary science has learned about the cell's design, and he poignantly and provocatively shows that it is the handiwork of not only an Intelligent Designer but specifically the God revealed in Scripture."--Hank Hanegraaff, president, Christian Research Institute; host, Bible Answer Man broadcast "Fazale Rana's welcome sequel to Origins of Life makes a significant contribution to the growing scientific literature pointing to intelligent design."--Kenneth Boa, president, Reflections Ministries Fazale Rana is vice president of research and apologetics at Reasons To Believe. He is the coauthor, with Hugh Ross, of Origins of Life and Who Was Adam?bornagain77_{May 24, 2008
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Bornagain77 at 115 wrote,
"Whereas, Dr. Hugh Ross states the similarity may in actually be closer to 85% to 90%. Secondarily, at the protein level only 29% of genes code for the exact same amino acid sequences in chimps and humans (Nature, 2005). As well, our DNA is 92% similar to mice as well as 92% similar to zebrafish (Simmons PhD., Billions of Missing Links). So are we 92% mouse or are we 92% zebrafish? Our DNA is 70% similar to a fruit fly; So are we therefore 70% fruit fly?"
Is this all really true? I haven't studied this in depth. BTW thanks to you Bornagain for such a magnificent post!Frost122585_{May 24, 2008
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dmso4 Linking evolution and gravity as equally well tested theories is crap made up by evolutionists. You don't hear physicists saying the gravity is as well tested as evolution. The day you do is the day you can take seriously any claim the evolution is as well tested as gravity.DaveScot_{May 23, 2008
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dmso, I have a comment in moderation, so to shortly reiterate what is waiting; You have a suggestive genetic similarity which you presume to be inserted by a virus long ago in some hypothesized common ancestor. Yet I disagree that it is conclusive proof for evolution (a long way from it). The fact in the previous study I cited, that all lines of mammal studies show essential "base level developmental" function for ERV's (your term) should give you a clue that these ERV's are not being slowly incorpoated into the genomes in regards to functionality i.e. they do not display an increasing level of functionality but display consistent functionality in early developmental stages of mammals. A very anti-Dawinian fact. That said, genetic sequence similarities are nororiously weak lines of evidence: Naturalists always try to establish scientific validity for evolution by pointing to suggestive similarities while ignoring the foundational principle of science (genetic entropy; conservation of information) that contradicts their preconceived philosophical bias. For example, naturalists say that evolution is proven true when we look at the 98.8% similarity between certain segments of the DNA in a Chimpanzee and compare them with the same segments of DNA of a Human. Yet that similarity is not nearly good enough to be considered “conclusive” scientific proof. For starters, recent preliminary comparisons of the complete genome of chimps and the complete genome of man yield a similarity of only 96%. As well, the December 2006 issue of PLoS ONE reported that human and chimpanzee gene copy numbers differ by a whopping 6.4% (Hahn). Whereas, Dr. Hugh Ross states the similarity may in actually be closer to 85% to 90%. Secondarily, at the protein level only 29% of genes code for the exact same amino acid sequences in chimps and humans (Nature, 2005). As well, our DNA is 92% similar to mice as well as 92% similar to zebrafish (Simmons PhD., Billions of Missing Links). So are we 92% mouse or are we 92% zebrafish? Our DNA is 70% similar to a fruit fly; So are we therefore 70% fruit fly? Our DNA is 75% similar to a worm; So are we 75% worm? No, of course not!! This type of reasoning is simple minded in its approach and clearly flawed in establishing a solid scientific foundation on which to draw valid inferences from! Clearly, we must find if the DNA is flexible enough to accommodate any type of mutations happening to it in the first place. This one point of evidence, (The actual flexibility of DNA to any random mutations), must be firmly established, first and foremost, before we can draw any meaningful inferences from the genetic data we gather from organisms!! Fortunately we, through the miracle of science, can now establish this crucial point of DNA flexibility. The primary thing that is crushing to the evolutionary theory is this fact. Of the random mutations that do occur, and have manifested traits in organisms that can be measured, at least 999,999 out of 1,000,000 (99.9999%) of these mutations to the DNA have been found to produce traits in organisms that are harmful and/or fa^tal to the life-form having the mutation! (Gerrish and Lenski, 1998, Bataillon, 2000, Elena et al, 1998). "I have seen estimates of the incidence of the ratio of deleterious-to-beneficial mutations which range from one in one thousand up to one in one million. The best estimates seem to be one in one million (Gerrish and Lenski, 1998). The actual rate of beneficial mutations is so extremely low as to thwart any actual measurement (Bataillon, 2000, Elena et al, 1998). Therefore, I cannot ...accurately represent how rare such beneficial mutations really are." (Sanford; Genetic Entropy page 24) The fate of competing beneficial mutations in an asexual population (Philip J. Gerrish & Richard E. Lenski) "Clonal interference is not the only dynamic that inhibits the progression of beneficialmutations to fixation in an asexual population.Asimilar inhibition may be caused by Muller’s ratchet (Muller, 1964; Haigh, 1978), in which deleterious mutations will tend to accumulate in small asexual populations. As shown by Manning and Thompson (1984) and by Peck (1994), the fate of a beneficial mutation is determined as much by the selective disadvantage of any deleterious mutations with which it is linked as by its own selective advantage." Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations? (Thomas Bataillon) Abstract ......It is argued that, although most if not all mutations detected in mutation accumulation experiments are deleterious, the question of the rate of favourable mutations (and their effects) is still a matter for debate. Bergman (2004) has studied the topic of beneficial mutations. Among other things, he did a simple literature search via Biological Abstracts and Medline. He found 453,732 “mutation” hits, but among these only 186 mentioned the word “beneficial” (about 4 in 10,000). When those 186 references were reviewed, almost all the presumed “beneficial mutations” were only beneficial in a very narrow sense- but each mutation consistently involved loss of function changes-hence loss of information.” Trying to find an actual "hard" number for the "truly" beneficial mutation rate is, in fact, what Dr. Behe tried to do in his book "The Edge of Evolution". Dr. Behe states in Edge of Evolution on page 135. Generating a single new cellular protein-protein binding site (in other words, generating a truly beneficial mutational event that would explain the generation of the complexity we see in life) is of the same order of difficulty or worse than the development of chloroquine resistance in the malarial parasite. That order of difficulty is put at 10^20 replications (births) of the malarial parasite, by Dr. Behe. Thus, the actual rate for "truly" beneficial mutations, that would account for the complexity we see in life, is far in excess of one-hundred-billion-billion mutational events. Thus, this one in a million number, that is often bantered about for “truly” beneficial mutations, is actually far, far too generous for the evolutionists to be using for their hypothetical calculations. In fact, from consistent findings such as these, it is increasingly apparent that Genetic Entropy is the overriding foundational rule for all of biology, with no exceptions at all, and that the belief in "truly" beneficial mutations is nothing more than wishful speculation on the naturalists part that has no foundation in empirical science whatsoever: The foundational rule of Genetic Entropy for biology can be stated something like this: All adaptations away from a parent species for a sub-species, which increase fitness to a particular environment, will always come at a loss of the original integrated complex information in the parent species genome. Professional evolutionary biologists are hard-pressed to cite even one clear-cut example of evolution through a beneficial mutation to DNA that would violate the principle of genetic entropy. Although evolutionists try to claim the lactase persistence mutation as a lonely example of a beneficial mutation in humans, lactase persistence is actually a loss of a instruction in the genome to turn the lactase enzyme off, so the mutation clearly does not violate genetic entropy. Yet at the same time, the evidence for the detrimental nature of mutations in humans is clearly overwhelming, for doctors have already cited over 3500 mutational disorders (Dr. Gary Parker).bornagain77_{May 23, 2008
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'da bomb' ?RRE_{May 23, 2008
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Computational CSI at the protein level is the bomb.RRE_{May 23, 2008
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gpuccio: well, I guess what I'm having trouble with is exactly how you determine just how impossible evolution via mutation and selection is, but I'll keep working on my toys :) . Thanks for trying to explain, anyway.Venus Mousetrap_{May 23, 2008
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Bennith Karlow (#90): In principle, it is not difficult to apply the EF. Let's take a single protein, for example. The first step would be to assess he presence of function. That is not a computational task, but rather a logical adn empirical one. Function must be described in a specific context, and it can de assessed as present or absent (values 0 or 1), or measured (for instance, in the case of an enzyme, you can measure its specific activity). Even in that case, you will have to set a minimum value of function which satisfies your concept of specification. The computational step is the second one, which is easy and difficult at the same time. It is easy to compute the search space: that does not even require anything more than a calculator, because it is equal to 20^(length of the protein in aminoacids). That would be great enough for any protein longer than 116 aminoacids, becuase that would overcome Dembski's UPB. Most protein are much longer than that. But the problem is that we are not looking for a single solution, but for a set of functional solutions. We know that many sequences, not necessarily strictly similar, may have the same structure and give the same function, even in different degrees. We have many examples of that in protein families. The fact is, nobody can really compute the subset of the search space which has the specified function, because of two different difficulties: a) we have not enough understanding of the laws of biophysics to be able to anticipate how a protein sequence will fold, and if will have a funtion or not. That is still vastly beyond our understanding. b) The only other way of knowing, that is to really explore the search space and measure the function, is absolutely impossible for the same reason why it is impossible even to nature itself: the search space is simply too big. Now, that should not discourage us, because there are other ways to approach the problem. The fact that the specific subset of solutions with a specific function must really be very tiny in comparison with the whole search space is intuitive enough (it's the same order of reasons why in the second law of thermodinamics the thermal equilibrium space is infinitely bigger than the sum of all specific, ordered spaces). I really believe that a satisfying theoretical approach to that computation will be found, with time. In the meantime, what we can do is to approach the problem empirically from the existing evidence. The best way I have found, up to now, is Abel and Trevors approach to protein families, which you can find in their paper: "Measuring the functional sequence complexity of proteins" easily available online. Another approach could come from protein engineering: as we are partially succeding in creating new function through guided random serach and function measurement, that should give us an idea os the real ratio between functional space and search space. In all cases where that ration is lower than 1:10^150, CSI has been formally demonstrated. And please, take notice ythat such a computation pertains simply to the first level of CSI: that implicit in a single protein. Computing CSI in systems of proteins is certainly more difficult, but it can be done, and it is obvious that the values of complexity become extremely higher there. In other words, if most single functional proteins probably exhibit CSI, any functional system of many proteins will certainly exhibit astounding levels of CSI.gpuccio_{May 23, 2008
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Venus Mousetrap (#91): "I tried to be as clear as I could, but it was a hypothetical example. What were you having trouble with, exactly?" You were clear enough to put yourself into trouble! The problem is exactly that: it was a hypothetical example, and it was false, because it did not take into account the problem of statistical and computational resources, which is exactly the main point of ID. And yet you boldly stated: "This isn’t speculation. People do this. It’s my hobby." Which didn't sound hypothetical at all! You say: "I can’t evolve a specific program, because I’d have to specify it in advance, which is the same as putting in the information directly." That's the only thing you have got right. "Evolution doesn’t work that way - indeed, Dawkins is still getting laughed at for his Weasel because people believe he was demonstrating evolution." Evolution as you conceive it doesn't work at all. Dawkins is still getting laughed at because he fully deserved it. "But I can specify a goal which can be met by a subset of all possible programs - for example, find the most food, avoid dying, etc." If you specify a goal, and then in some way measure that function, you are only doing what Dawkins did in the weasel example, or what is being done in protein engineering. NS is not supposed to act that way. NS cannot know in advance what to measure. Indeed, NS does not measure anything. The idea is that RM is creative enough to generate new function which is selected for its intrinsic advantage in the environment (reproductive advantage), and not because someone measures a pre-specified function and, if present, even in minimal form, fixes it. That is called intelligent selection. In other words, your GA should work this way to be valid: your 500 bit program, generated by random noise, should be functional enough to survive, reproduce itself, and generate new, different programs, for its own strength, that is by spontaneously utilizing the implicit resources of your PC environment (or of any other environment). The only necessary thing is that you must not incorporate in the environment exactly the kind of function you want to evolve. To be even more clear, the "evolved" function must be strong of itself, and not be "recognized" by an intelligent, pre-specified system of measurement. That's how it is supposed to work in reality. "I’m also not sure why you’re having trouble seeing how some non-essential code in an organism could change its function via mutation and selection. I mean, I can’t make it clearer than that. Code mutates. Does something else good. Repeats." Here is your fundamental error. The whole point of ID is here, and you have not understood it. You should know that not everything can be computed. Some problems are so complex that they elude finding an algorithmic solution. Finding a functional solution by random search is exactly one of them, if the search space is big enough, so that the ratio between the functional set of solutions to be found and the whole search space is lower than 1:10^150, and if your search algorithm does not incorporate any knowledge of the result to be found, which are exactly the criteria fixed by Dembski, and which I requested of you and your "hypothetical" example. "Anyhow, I can’t meet your request, yet. I’ve been working on it for some time." In the previous point, I have tried to explain to you why there are sound theoretical reasons why you will never be able to meet my request. So, may be you can use your time better, if you want. Anyway, if you should succeed, please let me know. "But there isn’t much point, is there? There seems to be a default barrier in the ID circle against GAs… no matter what they are, the very act of coding them is declared to be sideloading of active information." No. I will be honest with you. I have read that kind of objections here at UD, and I don't agree with them. I will accept as valid a GA, even if it is coded by someone, provided that it respects my conditions. The only thing I really want is that it satisfies the points I have already specified, especially that no specific information about the result to be obtained must be included in the code. In other words, what you can do is set up any kind of generic computer environment, which includes any kind of rules of random variation of existing information, and "evolve" in that context, by that random variation, some information with CSI (more than 500 bit long and functional), which has not been specifically searched and measured by the program. That's all I ask. If you succeed, I will never hold against you the fact that the whole environment was intelligently coded. That's a promise! So, to cite your words: I tried to be as clear as I could: what are you having trouble with, exactly?gpuccio_{May 23, 2008
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dmso74, I found the book, took an hour to find it, and see fig 7.5. I will read the chapter and then ask questions.jerry_{May 23, 2008
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dmso74, Your Evidence itself is loaded with all sorts of presumptions , the main presumption being that evolution is true in the first place and thus this evidence cooborates it. I refer you to a leading expert, Dr. John Sanford, who in Genetic Entropy 2005, explains exactly why such "insertion" mutations are bogus. As for myself, I will address your genome sequence similarity being proof of evolution scenario: naturalists don’t ever seem to get it. Although the evidence in the fossil record, extensive research into selective breeding, as well as all other lines of evidence that are scrutinized, is overwhelmingly against them, they never seem to question the fact they may be viewing the evidence from the wrong overall perspective to begin with. Naturalists always try to establish scientific validity for evolution by pointing to suggestive similarities while ignoring the foundational principle of science (genetic entropy; conservation of information) that contradicts their preconceived philosophical bias. (Kariofocus: mathematical refutation of open system argument by evolutionists) http://www.angelfire.com/pro/kairosfocus/resources/Info_design_and_science.htm#thermod (Dr. William Demski's math for Conservation of Information) http://cayman.globat.com/~trademarksnet.com/T/ActiveInfo.pdf For example, naturalists say that evolution is proven true when we look at the 98.8% similarity between certain segments of the DNA in a Chimpanzee and compare them with the same segments of DNA of a Human. Yet that similarity is not nearly good enough to be considered “conclusive” scientific proof. For starters, recent preliminary comparisons of the complete genome of chimps and the complete genome of man yield a similarity of only 96%. As well, the December 2006 issue of PLoS ONE reported that human and chimpanzee gene copy numbers differ by a whopping 6.4% (Hahn). Whereas, Dr. Hugh Ross states the similarity may in actually be closer to 85% to 90%. Secondarily, at the protein level only 29% of genes code for the exact same amino acid sequences in chimps and humans (Nature, 2005). As well, our DNA is 92% similar to mice as well as 92% similar to zebrafish (Simmons PhD., Billions of Missing Links). So are we 92% mouse or are we 92% zebrafish? Our DNA is 70% similar to a fruit fly; So are we therefore 70% fruit fly? Our DNA is 75% similar to a worm; So are we 75% worm? No, of course not!! This type of reasoning is simple minded in its approach and clearly flawed in establishing a solid scientific foundation on which to draw valid inferences from! Clearly, we must find if the DNA is flexible enough to accommodate any type of mutations happening to it in the first place. This one point of evidence, (The actual flexibility of DNA to any random mutations), must be firmly established, first and foremost, before we can draw any meaningful inferences from the genetic data we gather from organisms!! Fortunately we, through the miracle of science, can now establish this crucial point of DNA flexibility. The primary thing that is crushing to the evolutionary theory is this fact. Of the random mutations that do occur, and have manifested traits in organisms that can be measured, at least 999,999 out of 1,000,000 (99.9999%) of these mutations to the DNA have been found to produce traits in organisms that are harmful and/or fa^tal to the life-form having the mutation! (Gerrish and Lenski, 1998, Bataillon, 2000, Elena et al, 1998). "I have seen estimates of the incidence of the ratio of deleterious-to-beneficial mutations which range from one in one thousand up to one in one million. The best estimates seem to be one in one million (Gerrish and Lenski, 1998). The actual rate of beneficial mutations is so extremely low as to thwart any actual measurement (Bataillon, 2000, Elena et al, 1998). Therefore, I cannot ...accurately represent how rare such beneficial mutations really are." (Sanford; Genetic Entropy page 24) The fate of competing beneficial mutations in an asexual population (Philip J. Gerrish & Richard E. Lenski) "Clonal interference is not the only dynamic that inhibits the progression of beneficialmutations to fixation in an asexual population.Asimilar inhibition may be caused by Muller’s ratchet (Muller, 1964; Haigh, 1978), in which deleterious mutations will tend to accumulate in small asexual populations. As shown by Manning and Thompson (1984) and by Peck (1994), the fate of a beneficial mutation is determined as much by the selective disadvantage of any deleterious mutations with which it is linked as by its own selective advantage." http://myxo.css.msu.edu/lenski/pdf/1998,%20Genetica,%20Gerrish%20&%20Lenski.pdf Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations? (Thomas Bataillon) Abstract ......It is argued that, although most if not all mutations detected in mutation accumulation experiments are deleterious, the question of the rate of favourable mutations (and their effects) is still a matter for debate. http://www.nature.com/hdy/journal/v84/n5/full/6887270a.html High Frequency of Cryptic Deleterious Mutations in Caenorhabditis elegans ( Esther K. Davies, Andrew D. Peters, Peter D. Keightley) "In fitness assays, only about 4 percent of the deleterious mutations fixed in each line were detectable. The remaining 96 percent, though cryptic, are significant for mutation load...the presence of a large class of mildly deleterious mutations can never be ruled out. " http://www.sciencemag.org/cgi/content/abstract/285/5434/1748 ” Bergman (2004) has studied the topic of beneficial mutations. Among other things, he did a simple literature search via Biological Abstracts and Medline. He found 453,732 “mutation” hits, but among these only 186 mentioned the word “beneficial” (about 4 in 10,000). When those 186 references were reviewed, almost all the presumed “beneficial mutations” were only beneficial in a very narrow sense- but each mutation consistently involved loss of function changes-hence loss of information.” Trying to find an actual "hard" number for the "truly" beneficial mutation rate is, in fact, what Dr. Behe tried to do in his book "The Edge of Evolution". Dr. Behe states in Edge of Evolution on page 135. Generating a single new cellular protein-protein binding site (in other words, generating a truly beneficial mutational event that would explain the generation of the complexity we see in life) is of the same order of difficulty or worse than the development of chloroquine resistance in the malarial parasite. That order of difficulty is put at 10^20 replications (births) of the malarial parasite, by Dr. Behe. Thus, the actual rate for "truly" beneficial mutations, that would account for the complexity we see in life, is far in excess of one-hundred-billion-billion mutational events. Thus, this one in a million number, that is often bantered about for “truly” beneficial mutations, is actually far, far too generous for the evolutionists to be using for their hypothetical calculations. In fact, from consistent findings such as these, it is increasingly apparent that Genetic Entropy is the overriding foundational rule for all of biology, with no exceptions at all, and that the belief in "truly" beneficial mutations is nothing more than wishful speculation on the naturalists part that has no foundation in empirical science whatsoever: The foundational rule of Genetic Entropy for biology can be stated something like this: All adaptations away from a parent species for a sub-species, which increase fitness to a particular environment, will always come at a loss of the original integrated complex information in the parent species genome. Professional evolutionary biologists are hard-pressed to cite even one clear-cut example of evolution through a beneficial mutation to DNA that would violate the principle of genetic entropy. Although evolutionists try to claim the lactase persistence mutation as a lonely example of a beneficial mutation in humans, lactase persistence is actually a loss of a instruction in the genome to turn the lactase enzyme off, so the mutation clearly does not violate genetic entropy. Yet at the same time, the evidence for the detrimental nature of mutations in humans is clearly overwhelming, for doctors have already cited over 3500 mutational disorders (Dr. Gary Parker). "Mutations" by Dr. Gary Parker http://www.answersingenesis.org/home/area/cfol/ch2-mutations.asp Mutations: The Raw Material for Evolution? http://www.icr.org/articles/print/3466/ “It is entirely in line with the accidental nature of naturally occurring mutations that extensive tests have agreed in showing the vast majority of them to be detrimental to the organisms in its job of surviving and reproducing, just as changes accidentally introduced into any artificial mechanism are predominantly harmful to its useful operation” H.J. Muller (Received a Nobel Prize for his work on mutations to DNA) “Mutations, in summary, tend to induce sickness, death, or deficiencies. No evidence in the vast literature of heredity change shows unambiguous evidence that random mutation itself, even with geographical isolation of populations leads to speciation.” (Lynn Margulis - Acquiring Genomes [2003], p. 29). “But there is no evidence that DNA mutations can provide the sorts of variation needed for evolution… There is no evidence for beneficial mutations at the level of macroevolution, but there is also no evidence at the level of what is commonly regarded as microevolution.” Jonathan Wells (PhD. Molecular Biology) "The neo-Darwinians would like us to believe that large evolutionary changes can result from a series of small events if there are enough of them. But if these events all lose information they can’t be the steps in the kind of evolution the neo-Darwin theory is supposed to explain, no matter how many mutations there are. Whoever thinks macroevolution can be made by mutations that lose information is like the merchant who lost a little money on every sale but thought he could make it up on volume." Dr. Lee Spetner (Ph.D. Physics - MIT) Man has over 3 billion base pairs of DNA code. Even if there were just a 1% difference of DNA between monkeys and humans, that would still be 30 million base pairs of DNA difference. It is easily shown, mathematically, for it to be fantastically impossible for evolution to ever occur between monkeys and man, or monkeys and anything else for that matter. Since, it is an established fact that at least 999,999 in 1,000,000 of any mutations to DNA will be harmful and/or fatal, then it is also an established fact that there is at least a 999,999^30,000,000 to one chance that the monkey will fail to reach man by evolutionary processes. The monkey will hit a dead end of harmful/fatal mutations that will kill him or severely mutilate him before killing him. The poor monkey barely even gets out of the evolutionary starting gate before he is crushed by blind chance. This would still be true even if the entire universe were populated with nothing but monkeys to begin with! This number (999,999^30,000,000), is fantastically impossible for any hypothetical beneficial mutation to ever overcome! Worse yet for the naturalists, mathematician William Dembski PhD. has worked out the foundational math that shows the mutation/natural selection scenario to be impossible EVEN IF the harmful/fatal rate for mutation to the DNA were only 50%. The naturalist stamps his feet again and says that symbiotic gene transfer, cross-breeding (yes they, desperately, suggested cross-breeding as a solution), gene duplication and multiplication of chromosomes, alternative splicing etc .. etc .. are the reasons for the changes in DNA between humans and apes. They say these things with utmost confidence without even batting an eye. Incredibly, this is done in spite of solid evidences testifying to the contrary. Indeed, even if a hypothetical beneficial mutation to the DNA ever did occur, it would be of absolutely no use for it would be swallowed in a vast ocean of slightly detrimental mutations that would be far below the culling power of natural selection to remove from a genome! “The theory of gene duplication in its present form is unable to account for the origin of new genetic information” Ray Bohlin, (PhD. in molecular and cell biology) “Evolution through random duplications”... While it sounds quite sophisticated and respectable, it does not withstand honest and critical assessment” John C. Sanford (PhD Genetics; inventor of the biolistic “gene gun” process! Holds over 25 patents! In addition to the gene gun, Sanford invented both pathgen derived resistance, and genetic immunization. If you have eaten today you have probably eaten some food touched by his work!) The human genome, according to Bill Gates the founder of Microsoft, far, far surpasses in complexity any computer program ever written by man. The data compression (multiple meanings) of some stretches of human DNA is estimated to be up to 12 codes thick (Trifonov, 1989)! No line of computer code ever written by man approaches that level of data compression (poly-functional complexity). Further evidence for the inherent complexity of the DNA is found in a another study. In June 2007, a international team of scientists, named ENCODE, published a study that indicates the genome contains very little unused sequences and, in fact, is a complex, interwoven network. This “complex interwoven network” throughout the entire DNA code makes the human genome severely poly-constrained to random mutations (Sanford; Genetic Entropy, 2005; page 141). This means the DNA code is now much more severely limited in its chance of ever having a hypothetical beneficial mutation since almost the entire DNA code is now proven to be intimately connected to many other parts of the DNA code. Thus even though a random mutation to DNA may be able to change one part of an organism for the better, it is now proven much more likely to harm many other parts of the organism that depend on that one particular part being as it originally was. Since evolution was forced, by the established proof of Mendelian genetics, to no longer view the whole organism as to what natural selection works upon, but to view the whole organism as a multiple independent collection of genes that can be selected or discarded as natural selection sees fit, this “complex interwoven network” finding is extremely bad news, if not absolutely crushing, for the population genetics scenario of evolution (modern neo-Darwinian synthesis) developed by Haldane, Fisher and Wright (page 52 and 53: Genetic Entropy: Sanford 2005)! http://www.genome.gov/25521554 BETHESDA, Md., Wed., June 13, 2007 -" An international research consortium today published a set of papers that promise to reshape our understanding of how the human genome functions. The findings challenge the traditional view of our genetic blueprint as a tidy collection of independent genes, pointing instead to a complex network in which genes, along with regulatory elements and other types of DNA sequences that do not code for proteins, interact in overlapping ways not yet fully understood." http://www.boston.com/news/globe/health_science/articles/2007/09/24/dna_unraveled/?page=1 "The science of life is undergoing changes so jolting that even its top researchers are feeling something akin to shell-shock. Just four years after scientists finished mapping the human genome - the full sequence of 3 billion DNA "letters" folded within every cell - they find themselves confronted by a biological jungle deeper, denser, and more difficult to penetrate than anyone imagined." Naturalists truly believe you can get such staggering complexity of information in the DNA from some dead process based on blind chance. They cannot seem to fathom that any variation to a basic component in a species is going to require precise modifications to the entire range of interconnected components related to that basic component. NO natural law based on blind chance, would have the wisdom to implement the multitude of precise modifications on the molecular level in order to effect a positive change from one species to another. Only a “vastly superior intelligence” would have the wisdom to know exactly which amino acids in which proteins, which letters in the DNA code and exactly which repositioning of the 25 million nucleosomes (DNA spools) etc .. etc .. would need to be precisely modified to effect a positive change in a species. For men to imagine blind chance has the inherently vast wisdom to create such stunning interrelated complexity is even more foolish than some pagan culture worshipping a dead stone statue as their god and creator. Even if evolution of man were true, then only God could have made man through evolution. For only He would have the vast wisdom to master the complexity that would be required to accomplish such a thing. Anyone who fails to see this fails to appreciate the truly astonishing interwoven complexity of life at the molecular level.bornagain77_{May 23, 2008
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F2XL: you're taking the model far too literally. All it's supposed to show is that divergence is probabilistically inevitable if you isolate two populations. I could have just said it but I felt an illustration would be easier. This notion of harmful mutations is interesting however. You seem convinced that harmful mutations will build up and up... I know about this little crazy idea called selection which I'm told stops that happening, but then, I was going for an amechanistic description of macroevolution. However, the definition seems to have moved on from speciation to 'large morphological changes' now, so I guess that means that there no longer is a species barrier. My apologies, I was working from an older definition of the term. but why is everyone so sure that even small mutations don't accumulate, or that functions can be fluid over time? You all keep saying it, and even that page of Arguments you don't want to hear says it, but the fact is that even slightly beneficial mutations can give a population the edge. It's a matter of statistics. I tried to explain with my idea of the spinning flagellum that keeps building functionality onto its new forms, and I get told that's a highly improbable indirect Darwinian pathway. Uh, no, highly improbable would be the direct pathway where it all forms at once. Indirect is the stupid, aimless, and easy way which only cares about the function of the moment, and the possibilities open at those times.Venus Mousetrap_{May 23, 2008
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Jerry
I will want to explore just what are its capabilities given a gene pool.
There are simulations of particular situations that illustrate that sort of thing that can be run, even in excel which you can get for free via openoffice. I can post you some links if you like but it's all easy to find via google. Patrick, I also wanted to ask you do you think it would be possible to implelemt some sort of limited design detection, via the EF, in a computer program of sorts? It seems like a worthwhile project, even if only ever with the possiblity of limited sucuess.Bennith Karlow_{May 23, 2008
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Patrick
The “default barrier” is against the absurd claims made by Darwinists
Perhaps it's time to get down and dirty and name and shame the Dariwinists? Maybe picking a specific claim made by Darwinists, one of the more absurd ones and showing how it is in fact absurd when viewed under the ageis of ID is the way to go? Show them no mercy. After all, once the claim has been shown to be untrue then if they continue to make it they are patently, provably dishonest and you can claim the moral highground.Bennith Karlow_{May 23, 2008
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Patrick: that's not even slightly basic, unless search biases and transmission functions are well known in ID. But it turns out I actually agree with you. :) I have no problem with the idea that life was wilfully and intelligently placed to evolve over millions of years. The problem I have is with people denying the power of random mutation and natural selection to create novelty, when it is intuitively obvious to me that it can. I've even tried to explain the process. I'll let you know when I've cracked it for real. :)Venus Mousetrap_{May 23, 2008
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It’d be nicer if you could tell me where, in my hypothetical machine code example, that side-loading is occuring. Is it the act of deciding what the code should be, and arranging a genetic toolkit for organisms to build themselves?
dynamics.org/Altenberg/FILES/LeeEEGP.pdf “Both the regression and the search bias terms require the transmission function to have ‘knowledge’ about the fitness function. Under random search, the expected value of both these terms would be zero. Some knowledge of the fitness function must be incorporated in the transmission function for the expected value of these terms to be positive. It is this knowledge — whether incorporated explicitly or implicitly — that is the source of power in genetic algorithms.” That's pretty basic. In order to function, the “evolving holistic synthesis” requires OOL, which is its own separate question. Besides “directed front-loading” (what I’m calling Behe’s hypothesis in order to differentiate it from other variants) there is the potential that ID only holds true in regards to the OOL. Dembski’s recent work shows that in order to find the targets in search space active information is required. This active information IS the design of the system (code, error correction, self-replication, modular components, plasticity in the language conventions, etc), which allows the “evolving holistic synthesis” to function without there being a directly embedded plan. Thus, it’s the initial design of the system that requires intelligent design, not necessarily every step of evolution (although that may be a possibility, via intervention or front-loading). I haven’t had a chance to read Mike Gene’s book but I believe he has the same or similar hypothesis. Dave described it as the design of the system being “transformer-like”. The system is designed to evolve. Still, this hypothesis needs much research and personally I find it unlikely that it is the entire picture. Portions of the system are obviously designed to evolve. I'd think it more likely that biological reality is a combination of specifically foresighted functionality, front-loaded information, and non-foresighted mechanisms that function due to the design of the system. Now do these GAs reflect biological reality? For Darwinists sake, they better not.
If you’re going to assume that every single GA is sneaking it in via the back, then I’m wasting my time, aren’t I?
A GA won't function as intended unless designed properly. Did you miss the entire point of the GA Chess article?
Also, I could be wrong, but wasn’t Dr Marks’ paper on ev found to be in error?
Yes. They admitted it here: http://cayman.globat.com/~trademarksnet.com/Research/EILab/Publications/eev.html Unfortunately that link is down now. What it used to say was:
Thanks to those who pointed to a bug in our software. This paper has been withdrawn. For revised analysis, see HERE.
I don't have a link to the revised analysis on hand. I'll email Bill for it. I remember thinking when that quote first came out that it sounded absurd that a blind search would operate better. I've never known a single decent GA that doesn't operate better than a blind search.
I admire your effort to actually go through the math of ID, but I cannot find any that applies to what I’m talking about.
Right. Observed limitations of GAs capabilities?
I’m also not sure why you’re having trouble seeing how some non-essential code in an organism could change its function via mutation and selection. I mean, I can’t make it clearer than that. Code mutates. Does something else good. Repeats.
You've proven you can write a trial and error program. Programs which are known to have limitations. And how does that provides positive evidence that biological reality operates uniformly in the same manner, capable of overcoming all obstacles it's claimed to?
There seems to be a default barrier in the ID circle against GAs… no matter what they are, the very act of coding them is declared to be sideloading of active information.
The "default barrier" is against the absurd claims made by Darwinists. We know from experience what GAs are capable of, and what their limitations are. Even programs written by Darwinists showcase this.Patrick_{May 23, 2008
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bornagain, I didn’t presume, I looked at the evidence: http://www.retrovirology.com/content/3/1/67 jerry, great! then you have the book. look at fig 7.5 and we can discuss. Don't see a figure 7.5 in the article you site (goes up to four though), but aside from that I've always been told viruses are not categorized as "life." And the links to the Youtube videos that BA has provided, I can remember acting as the thought police for some of the videos by IDbyIllustra, and boy did it get repetitive. I eventually decided it would be better to just read up more on the subject of ID and possibly join up on here then waste time with those people.F2XL_{May 23, 2008
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In science, we call the process of simplification 'modelling'. It's then left to the scientists to decide just how well those models reflect reality. I can agree with what you're saying in the above quotations but if you came here to convince us that speciation is a lot more probable then we had assumed in terms of being a gateway to macro-evolution (e.g. new morphological traits), then this model (to use an odd metaphor) has to be a bit more shiny in the face of reality. In my model I actually made it harder for myself, on purpose. I can totally understand why you would want to do that, I personally do the same thing when it comes to OoL calculations. But this is not what you did. You basically used a small genome (which means that small changes have bigger effects) and you also assumed that a bit changing in this genome size is equivalent or more hard on evolution in this simulator. Taking one of the smallest genomes known to biology from the SAR11, which has 1.3 million base pairs, we can see that if you divided it up into 16 parts in the way your model does, and mutate one part at a time, then your bit mutations are the equivalent to having over 80 thousand point mutations happen at once. Hence, you model doesn't come anywhere near close to reality. No organism can possibly undergo such changes without dying on the spot. It would be like trying to add a whole new chapter to a novel and hope that the randomly generated paragraphs in it actually convey something meaningful the first time. If, for example, I had used strings of a billion bits, and insisted that the same species must be 99% identical, then I could still have run the sim to give the same effect: two populations will diverge while still remaining supposedly the same species themselves. The math hasn’t changed. No it wouldn't, see the above point. That doesn't refute the math. It's the same in both cases. Yes it does. Differences between two species are more similar, but that doesn't make divergence easier. It just means that there is far less room for error; if an organism builds up too many harmful mutations then it would be better off not to drift from the mean. Again, this is a M-O-D-E-L. One which has a lot of room for improvement. It’s an illustration of the math. In real life, it’s even worse because there are more ways for it to change from one generation to the next… but it still remains the same species in its own line of descent. In real life, even the difference between chimps and humans equates to a 60 million base pair gap, not to mention the different genome sizes. And if each change doesn't provide and real benefit then why would we want to believe that a new set of changes will become dominant in a significant portion of the population? You keep saying this, but you’re not explaining why it refutes the math. A large genome has the same problems as a small one (it mutates in all areas) and the high similarity between species actually means they’ll become incompatible more quickly when separated. Larger genomes mean it takes more changes to have any divergence at all. And if you look in the supposed evolutionary history between general primates and humans you will see that the tolerances between making one species into another requires large amounts of information to appear at once without actually harming the organism. It's like trying to get a new paragraph at once in a random fashion, not just ANY mutations will actually go anywhere even in terms of speciation. I'll have to take your word for that since I've not been able to fathom how ID calculates information, but you haven't explained why a dog has to remain a dog. Because it takes a simultaneous appearance of multiple changes all at once for there to be any kind of functional advantage. Are we defining species by their information level now? No, it's still information content. Um… that’s not an answer. That was my answer. Yeah I know. Nope. I wasn't talking about Darwinism, just the accumulation of mutations. In that case what was this supposed to prove beyond speciation? And I'm sure the evo-devo people will appreciate the ignorance of their years of research into how new structures form. Indeed, they probably wouldn't want people to be aware that many embryos are self-correcting not to mention the fact that changes in homeotic genes only alters existing body plans, nothing new is ever really generated. The best they can come up with are fruit flies which only survive under laboratory conditions, and are nonetheless, still fruit flies. Having antennae replaced with legs isn't something I would consider to be advantageous. ie. if you can't see how something happened, then it couldn't have happened. Based on the information available to everyone today, that's what we must conclude. And please refer to the FAQ section here to understand why mutations alone don't mean anything. https://uncommondescent.com/index.php/comment-policy/put-a-sock-in-it/ Odd that no one insists on watching the designer overcome them. I suppose you could say the same exact thing with regards to the formation of a car engine, the fact is we don't actually have to SEE a designer overcome such obstacles to know that it's the only plausible explanation. Are you're trying to deny that animals have genomes which mutate? Yet another common tactic, straw man. What I WAS saying was that mutations alone don't typically go anywhere.F2XL_{May 23, 2008
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bornagain, I didn't presume, I looked at the evidence: http://www.retrovirology.com/content/3/1/67 jerry, great! then you have the book. look at fig 7.5 and we can discuss.dmso74_{May 23, 2008
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dmso74, I have read Carroll's book and found nothing in it that pointed to a Darwinian scenario. Now I will admit that some of it got very complex and maybe we can with your help translate it into the vernacular. Carroll's book is what I call the kindergarten - graduate school approach. It starts out and continues in places at a man on the street level but then goes into complex explanations that those only with a graduate degree can understand. It often leaves out the grades in between. But because dinner time is approaching here and I have to go to the super market, I will ask more later on just what natural selection can do. I will want to explore just what are its capabilities given a gene pool.jerry_{May 23, 2008
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Intelligent Design is the only displine of knowledge I know of where most of the students are absolutely convinced that they know more than the teachers do, as well as thinking that the teachers are in need of much needed mental help. You presume that it was inserted and then go prove your case. Whereas I presumed nothing and sought to find function. If it has essential function then the "random insertion loses credibility and Intelligent Design gains credibility. I cited a study that shows essential "developemantal" function. This is hardly condusive to your presumption, yet you are so far down the road with your presumption that you do not find it peculiar at all. You have nothing but a suggestive similarity that does not pan out under scrutiny; Just like all other lines of evidence you will bring forth will be found to have; all fluff and no bite!bornagain77_{May 23, 2008
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bornagain, that is a neat link. just please keep in mind that ervs are not a single entity.. they provide good evidence for common descent of primates not bc primates share any old ervs, but bc we (and not other vertebrates) share the exact same ones in the exact same location in our genomes.. since ervs insert randomly the chances of this happening by accident are around 0. rather, it suggests that they are there bc our ancestors were infected and passed them on to us. the fact that they seem to have taken on new functional roles is, to me, completely fascinating.. there is "addition of new genetic information" right there.. by viral infection! one of the most fascinating bits is that chimps and bonobos (our sister species) seem to have been infected by an ERV that we don't have.. big trouble for common descent, right? nope,we also have a different form of a trim5alpha protein that is resistant to that erv.. chimps have a version that isn't resistant.. but guess what it gives them resistance to that we are sucscptible to? HIV. http://www.sciencemag.org/cgi/content/full/318/5856/1565 sorry that was long, i got excited. any particular reason why you think ervs aren't really ervs? jerry, "The mechanism of micro evolution through natural selection tends to winnow down the gene pool not build it up (please do not bring up that there are other processes that operate, we understand they do.) this is a pretty narrow view of natural selection. if you focus on one trait, then yes, diversity in that trait will tend to decrease if there is strong directional selection. however, stabilizing selection for a homozygous trait, for example, will tend to increase the diversity of alleles. strong directional selection on one trait could also free up other traits to be more variable. the loss of the hyobranchial skeleton in salamanders after the evolution of skin-breathing that freed up chest space for a longer tongue is a good example. "ow I believe evolutionary biology believes that some form of mutations are hypothesized that would dramatically change gene pools and explain how new variants arise that are substantially different from anything that was possible from a previous gene pool. However, such a process has never been demonstrated but only speculated on. The types of mutations that are hypothesized have been demonstrated. However, there are no examples or very few that can be pointed to where a new function for an organism has developed through these mutations. " this is why you HAVE to read "Endless forms most beautiful".. it is all about empirical evidence for small genetic changes causing large phenotypic changes such as in the evolution of the arthropod wing.. it will show you that these are more than hypotheses and speculations now.. i won't pretend that it's all 100% certain, but pretty dang neat nonetheless.dmso74_{May 23, 2008
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dmso74 you stated as a mechanistic hypothesis: from sean carrol’s “endless forms” is my favoite mechanistic hypothesis.. wings in arthropods evolve from reduction in number and exxageration of gill-like features in primitive aquatic nymphs. Well lets look at an anthropod through deep evolutionary time: The Trilobite; If any anthropod should sprout, wings, legs, etc... this should be your baby for it was in the fossil record for over 270 million years since it abruptly appeared at the beginning of the Cambrian Explosion. A Cambrian Peak in Morphological Variation Within Trilobite Species Mark Webster http://www.sciencemag.org/cgi/content/abstract/317/5837/499 Webster compiled morphological data for nearly 1,000 of the 17,000 different species of trilobites, a class of marine arthropods that died out by 250 million years ago, from 49 previously published sources. By tracking different morphological features — the number of body segments, for example — Webster found that trilobite species exhibited more variation during the Cambrian than in later periods, he reported in Science July 27. "Once you go beyond the Cambrian, the diversity of forms within any one species drops off," he says. "Early and Middle Cambrian trilobite species, especially, exhibited greater morphological variations than their descendants. This high within-species variation provided more raw material upon which natural selection could operate, Webster says, potentially accounting for the high rates of evolution in Cambrian trilobites. Such findings may have implications for our understanding of the nature of evolutionary processes, he says. Why the early trilobites were so morphologically diverse is a whole different mystery." Guess what Intelligent Design we know the answer to the mystery! CSI degeneration aka Genetic Entropy i.e. conservation of information! And it gets even better if you go into the actual studies themselves you find all trilobites that branch off the "parent" trilobites species quickly lose variability that is found in the parent stock. Exactly as would be predicted by the Theistic ID mod^el. Now dmso74, I certainly did not see any wings sprouting from these ancient anthropods at any time in their 270 million year history. In fact What is noted is a long slow deterioration within overall group (kind) and even a long slow deterioration within morphological variability of specific species. That is hardly condusive to any of your fanciful notions for evolution.bornagain77_{May 23, 2008
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dmso74, You are the expert so follow the line of reasoning. The mechanism of micro evolution through natural selection tends to winnow down the gene pool not build it up (please do not bring up that there are other processes that operate, we understand they do.) If a population gets separated from the mother population, then its gene pool is narrower than the original gene pool. If environmental pressures cause the new separated population to change it is probable that the new population's gene pool will be even narrower still. If the population is small enough then genetic drift will fix some alleles. The net result of the process is that the gene pool becomes narrower over time, not broader. It is possible that mutations will cause some of these separated populations' gene pools to increase but this is mainly speculative on how much this has ever happened. If this is the process that is mainly working in the world, then an original gene pool would be the order or class and the families, genera and species would just be refinements of this gene pool over time and not new variants. In other words most species are just a devolving from an original gene pool. There can be some exceptions to this but this is the general pattern that the data supports. Now I believe evolutionary biology believes that some form of mutations are hypothesized that would dramatically change gene pools and explain how new variants arise that are substantially different from anything that was possible from a previous gene pool. However, such a process has never been demonstrated but only speculated on. The types of mutations that are hypothesized have been demonstrated. However, there are no examples or very few that can be pointed to where a new function for an organism has developed through these mutations. By the way Allen MacNeill listed 47 different engines of variation so we accept that these events do happen. We have just never seen anything of consequence result from these processes. Typical Darwinism hypothesizes a process by where single cell organisms become multi celled organism and then builds up to the phyla. But the process we see is that the phyla popped out of nowhere and then the classes and then the orders etc all descended from there. Just the opposite of the Darwinian paradigm. There are no examples of any process that builds up from below. It is all top down. As I said you are the expert who teaches the material and are welcome to elaborate, criticize or present alternatives on what has been offered. We can also talk about specific examples.jerry_{May 23, 2008
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As well, That the ERV's would be found to have essential developemental purpose heavily suggests that ERV's are not a "recent" add on evolutionary featurebornagain77_{May 23, 2008
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dmso74, You presume that ERV's are proof of evolution, yet ID would presume that the sequence similarity in genomes, which you call ERV's, is actually an essential sequence of the genome that has an unknown but essential function. In fact the following study shows that if the "ERV's" (your term) sequence is disabled proper development is retarded. Endogenous retroviruses regulate periimplantation placental growth and differentiation http://www.pnas.org/cgi/content/abstract/103/39/14390 Endogenous retroviruses (ERVs) are fixed and abundant in the genomes of vertebrates. Circumstantial evidence suggests that ERVs play a role in mammalian reproduction, particularly placental morphogenesis, because intact ERV envelope genes were found to be expressed in the syncytiotrophoblasts of human and mouse placenta and to elicit fusion of cells in vitro. We report here in vivo and in vitro experiments finding that the envelope of a particular class of ERVs of sheep, endogenous Jaagsiekte sheep retroviruses (enJSRVs), regulates trophectoderm growth and differentiation in the periimplantation conceptus (embryo/fetus and associated extraembryonic membranes). The enJSRV envelope gene is expressed in the trophectoderm of the elongating ovine conceptus after day 12 of pregnancy. Loss-of-function experiments were conducted in utero by injecting morpholino antisense oligonucleotides on day 8 of pregnancy that blocked enJSRV envelope protein production in the conceptus trophectoderm. This approach retarded trophectoderm outgrowth during conceptus elongation and inhibited trophoblast giant binucleate cell differentiation as observed on day 16. Pregnancy loss was observed by day 20 in sheep receiving morpholino antisense oligonucleotides. In vitro inhibition of the enJSRV envelope reduced the proliferation of mononuclear trophectoderm cells isolated from day 15 conceptuses. Consequently, these results demonstrate that the enJSRV envelope regulates trophectoderm growth and differentiation in the periimplantation ovine conceptus. This work supports the hypothesis that ERVs play fundamental roles in placental morphogenesis and mammalian reproduction. Thus ID's position is validated and your position (materialism) is found wanting once again.bornagain77_{May 23, 2008
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How oft has the mantra been repeated that among biologists there is no controversy that evolution happened, the only dibates are as to how it happened. Well, if nearly every aspect of the how is questioned and often in controversy, then its no big leap to say the entire theory is in crisis and that controversy reigns. We in ID could just as easily say "there's no controversy that intelligent design accounts for many features of the cosmos and certain aspects of biological systems, the only debates are as to how it may have happened" and be done with it. I wonder how that would play in biologic academia!DonaldM_{May 23, 2008
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gpuccio: I tried to be as clear as I could, but it was a hypothetical example. What were you having trouble with, exactly? I can't evolve a specific program, because I'd have to specify it in advance, which is the same as putting in the information directly. Evolution doesn't work that way - indeed, Dawkins is still getting laughed at for his Weasel because people believe he was demonstrating evolution. But I can specify a goal which can be met by a subset of all possible programs - for example, find the most food, avoid dying, etc. I'm also not sure why you're having trouble seeing how some non-essential code in an organism could change its function via mutation and selection. I mean, I can't make it clearer than that. Code mutates. Does something else good. Repeats. Anyhow, I can't meet your request, yet. I've been working on it for some time. :) But there isn't much point, is there? There seems to be a default barrier in the ID circle against GAs... no matter what they are, the very act of coding them is declared to be sideloading of active information.Venus Mousetrap_{May 23, 2008
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gpuccio
Show me how you have created a program of at least 500 bit length from random variation in your computer, with a definite function (I mean a function of the whole problem, not just an incoherent mix of elementary functions)
Interesting stuff. I wonder if Venus will post some sounce. On a somewhat different angle, what do you say to the possiblity that a computer program could be written to implement some aspect of the explnatory filter and detect design? Of course I don't expect a all purpose 100% accurate program by any means, I doubt such a thing is possible, but I believe this might be an excellent group project if performed on a wiki style basis? How about it?Bennith Karlow_{May 23, 2008
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Jerry, a few questions: you accept universal common descent, then? "And the question becomes is micro evolution evolution upwards (species > genera > family > order) or devolution (order > family > genera > species.)" i'm sorry, this does not make sense to me. are you suggesting that evolution is a linear progression in some way from species to orders or vice versa? well my favorite bit from the 29 evidences is the shared ervs among primates.. but of course that's just evidence of common descent, not the mechanisms.. figure 7.5 from sean carrol's "endless forms" is my favoite mechanistic hypothesis.. wings in arthropods evolve from reduction in number and exxageration of gill-like features in primitive aquatic nymphs.. all accompanied by concordant additions of hox gene receptors.. phenotypic subtraction and exxageration by genotypic addition..dmso74_{May 23, 2008
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