Uncommon Descent Serving The Intelligent Design Community

The Strongest Arguments Against Design

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In any debate, it is good strategy to acknowledge your opponent’s strongest points up front, effectively taking them off the table. Critics of Intelligent Design have two strong arguments, discussed below, and virtually nothing else. Direct evidence that natural selection or any other unintelligent cause can actually do intelligent things, like design plants or animals, is nonexistent.

  1. The first argument is this: in every other field of science, methodological naturalism has been spectacularly successful, why should evolutionary biology be different? Evolutionary biologists understandably don’t want to be the only scientists at scientific meetings appealing to the workings of an unseen intelligent agent to explain phenomena in their field of study. When we have an approach that has worked so well on so many other problems, we need some powerful justification to switch to another paradigm to attack the problem of evolution, and it is understandable that there is so much resistance to this.But it has long been obvious to the layman that evolution is different, and requires a fundamentally different type of explanation. In recent years, a significant number of scientists have begun to recognize this also. In “A Second Look at the Second Law” I have attempted to express what is obvious to the layman in more scientific terms. A version of this argument written for a more general audience is here. I believe that this argument is the “powerful justification” needed to consider a new methodology in evolutionary biology, and shows why methodological naturalism hasn’t worked, and won’t work.
  2. The second argument is this: there are many things about evolution—the long periods involved, the evidence for common descent, the many evolutionary dead ends, examples of imperfect design—that simply give a strong impression of natural causes. This argument, used repeatedly by Charles Darwin himself in Origin of Species, is basically “a Creator wouldn’t do things this way.” Perhaps a more accurate way of stating the
    argument is, “I wouldn’t have done things this way if I were the Creator.” But, in fact, it does look a lot like the way we humans create things now, though testing and improvements over time. In fact, the similarities actually go beyond that, as brought out in my Mathematical Intelligencer article A Mathematician’s View of Evolution and, more briefly, in this video.Many people feel silly attributing the development of each species directly to God, yet understand that a completely unintelligent process could not possibly have produced the magnificent species we see today. Darwin wrote, in a letter to Sir John Herschel, “One cannot look at this Universe with all living productions and man without believing that all have been intelligently designed; yet when I look to each individual organism, I can see no evidence of this.” This paradox has left many looking for a compromise, such as
    “theistic evolution.”

    At the end of the “Epilogue” of my Discovery Institute Press book In the Beginning… I attempted an explanation for why a Creator might indeed “do things this way.” But of course it is only speculation, and although I often find that explanation reasonable, sometimes it does not even seem convincing to me. Perhaps a more obvious explanation is, our Creator creates through testing and improvements (sometimes trying modifications that don’t work out so well) for the same reason we create this way: it is probably the only way any intelligent agent could create things. If the only other intelligent agents we have experience with cannot create perfect designs by snapping their fingers, why would we assume our Creator could do this?

    I believe the evidence for design in the origin and development of life is scientific and overwhelming. Speculation as to what the designer might be like, or might have been thinking (or should have been thinking, as Darwin often argued ) is of course theology, not science. But I also have a purely scientific resolution of this paradox that I find quite satisfactory. It is simply: “evolution may leave an impression that it is an entirely natural process, but it isn’t.”

Comments
KF: I haven't been ignoring your reply to me here, and I certainly don't mean to blow you off, I just haven't had time to reply properly (I have a reply about half written...). I also desperately owe gpuccio a reply in that discussion.
GD: Pardon, but I think something is seriously wrong with how you are thinking about thermodynamics matters. The relevant context for thinking related to the point that design thinkers and theorists raise, is not the classical, macro-level variables [P, T, V etc], but the micro-scale, microstates view, wherein many microstates are compatible with given sets of macro-observable state variables.
Actually, both classical thermodynamics (the macro-only view you describe) and statistical mechanics (which includes the micro view) give essentially the same results. There are subtle differences, but for the sorts of things I'm criticizing Professor Sewell's work on they're fully equivalent.
For brief instance, the point of the 2nd law is that the direction of spontaneous change is dominated by where the bulk of microstates lies, i.e. towards increasing disorder.
This is the increasing-entropy form of the second law, which only applies to isolated systems (and that's true in both classical thermo and stat mech). Entropy decreases (changes not dominated by where the bulk of microstates lies) in open system are entirely common and unremarkable.
(Cf my nanobots in vats thought exercise here to see what this is getting at. Rivers running downhill, or water evaporating from surfaces is simply misdirected, as order is not what is to be explained, but functional, complex, specific organisation.)
I was discussing Sewell's claims, which are about order & disorder, not functional organization. Your arguments, which do relate to functionality, complexity, and organization, are quite different than Sewell's. To quickly address your argument, though, I believe that you are making two mistakes: the first is precisely that thermo and stat mech are about order and disorder (and energy), and have very little to say about functionality, complexity, and organization. Entropy is a function of how unconstrained the precise state (technically, the microstate) of a system is -- it doesn't matter if the constraints on it are functional, or the simple constraints of order (e.g. in a crystal). To borrow from Abel's terminology, thermo and stat mech don't distinguish between ordered complexity and functional complexity; and since the laws of thermodynamics certainly allow for the production of ordered complexity (e.g. crystals), I don't see how they can forbid the production of functional complexity. Second, your argument that "...from the statistical perspective, the second law obtains from dominance of the space of possibilities by clusters of states near what is called equilibrium. The direction of spontaneous change is strongly towards such clusters..." is almost exactly what I refuted above in my discussion of the uphill phases of the hydrologic cycle. The second law requires that isolated systems and those with equilibrium boundary conditions will move toward equilibrium; it makes no such requirement for systems with nonequilibrium boundary conditions (like earth), and it is entirely normal for such system to move far away from equilibrium. The earth's water is an example of this: sunlight drives it far from equilibrium, and keeps it there.Gordon Davisson
December 14, 2011
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There are at different ways to be a false negative. The object could have a function but not be complex enough: it could still be designed, but we cannot say. Or we could not be able to understand the code or the function in the object.
I'm told the code itself is completely arbitrary. That is to say there is an intermediate function that translates the symbols into some chemical result. So it would seem that unless you have the reader/translator function, you cannot tell a random sequence from a meaningful one. My question is, in real DNA, assuming the existing cell machinery, can you discriminate a sequence that is just one base pair from being functional from one generated by a random sequence generator? You don't seem to be answering the question. I'm not sure what question you are addressing, but it isn't mine. In practical terms, it would seem that a sequence that can become functional with one change has more of something than a purely random sequence. But can you spot the almost functional sequence without doing the chemistry?Petrushka
December 14, 2011
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Doesn’t exactly explain why this/these “designer(s)” left the rest of the mammalian class with such comparatively weak structures.
They seem to working just dandy though. But I do like your strawmen, they are getting funnier and more desperate sounding...Joe
December 14, 2011
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Doveton- RE vision systems- The reason why the designer(s) did not give us the vision of hawks or cephalopods is because we have the ability to duplicate their vision. Humans do not need it but can haz it if they want.
Doesn't exactly explain why this/these "designer(s)" left the rest of the mammalian class with such comparatively weak structures. Did this/those "designer(s)" expect us to make up the difference for them too? If so, why not leave the entire animal kingdom with the same visual system and have their one tool make correct all of them? But I will give you credit here Joe - at least you tried to provide an explanation for a given phenomenon.Doveton
December 14, 2011
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DrREC, You obviously don't have any clue as to what I say. Youyn would think that you would have learned by now but nope, you press on putting words into my mouth. Pathetic...Joe
December 14, 2011
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Petrushka: The answer to your point was in the following part of the post I have pasted here. To keep the complete flow of the reasoning, I will paste here again the whole post, including the comment (by Gordon Davisson) to which I answer: "I discussed some general problems with this approach earlier, but let me take a closer look at this particular argument. I think it’s pretty clear that evolutionary processes can produce increases in dFSCI, at least if your measure of dFSCI is sufficiently well-behaved. Consider that there exist point mutations that render genes nonfunctional, which I assume that you’d consider a decrease in dFSCI. Point mutations are essentially reversible, meaning that if genome A can be turned into genome B by a single point mutation, B can also be turned into A by a single point mutation. Therefore, the existance of point mutations that decrease dFSCI automatically implies the existance of point mutations that increase dFSCI. Ah! Now we are coming to something really interesting. I must say that I have really appreciated your discussion, and this is probably the only point where you are explicitly wrong. No problem, I will try to show why. Please go back to my (quick) definition of dFSCI in my post number 9 here. I quote myself: “No. The dFSCI of an object is a measure of its functional complexity, expressed as the probability to get that information in a purely random system. For instance. for a protein family, like in Durston’s paper, that probability is the probability of getting a functional sequence with that function through a random search or a random walk starting from an unrelated state (which is more or less the same).” Well, maybe that was too quick, so I will be more detailed. a) We have an object that can be read as a digital sequence of values. b) We want to evaluate the possible presence of dFSCI in that object. c) First of all we have to explicitly define a function for the digital information we can read in the object. I we cannot define a function, we cannot observe dFSCI in that object, It is a negative. Maybe a false negative. There are at different ways to be a false negative. The object could have a function but not be complex enough: it could still be designed, but we cannot say. Or we could not be able to understand the code or the function in the object. d) So, let’s say that we have defined a function explicitly. Then we measure the dFSCI for that function. e) To do that. we must measure the functional (target) space and the search space. Here various possiblities can be considered to approximate these measures. For proteins genes, the best way is to use the Durston method for protein families. f) The ratio of the target space to the search space if the complexity of our dFSCI for that object and that function. What does it express? As I said, it expresses one of two things, which are more or less equivalent: f1) The probability of obtaining that functional sequence from scrtach in a purely random system: IOWs, for a protein gene, the probability of obtaining any sequence that produces a protein with that function in a system that builds up sequences just adding randomly nucleotides. f2) The probability of obtaining that functional sequence through a random walk. That is more relevant to biology, because the usual theort for genes is that they are derived from other, existing sequences through variation. But the important point, that IO have explicitly stated in my previous post, is that it expresses “the probability of getting a functional sequence with that function through … a random walk starting from an unrelated state. Starting from an unrelated state. That’s the important point. Because that’s exactly what happens in biology. Basic protein domains are unrelated states. They are completely unrelated at the sequence level (you can easily verify that going to the SCOP site). Each basic protein domain (there are at least 2000) has less than 10% homology with any other. Indeed, the less than 10% homology rule bears about 6000 unrelated domains. Moreover, they also have different structure and folding, and different functions. So the question is: how does a new domain emerge? In the example I cited about the human de novo gene, it seems to come from non coding DMA. Many examples point to transposon activity. In no case a functional, related precursor is known. That’s why dFSCI is a good measure of the functional information we have to explain. Let’s go to your argument. You say: “Consider that there exist point mutations that render genes nonfunctional, which I assume that you’d consider a decrease in dFSCI.” No. That’s wrong. We have two different objects. In A, I can define a function and neasure dFSCI. In B, I cannot define a function, and dFSCI cannot be measured. Anyway, I could measure the dFSCI implicit in a transition from B to A. That would indeed be of one aminoacid (about 4 bits). And so? If you have a system where you already have B, I will be glad to admit that the transition from B to A is of only 4 bits, and it is perfectly in the range of a random system. IOWs. the dFSCI of that specific transition is of only 4 bits. But you have to already have B in the system. B is not unrelated to A. Indeed, you obtained B from A, and that is the only way you can obtain exactly B. So, can you see why your reasoning is wrong? You are not using the concept of dFSCI correctly. dFSCI tells us that we cannot obtain that object in a purely random system. It is absolutely trivila that we can obtain that object in a random system starting from an almost identical object. Is that a counter argument to dFSCI and its meaning? Absolutely not. For instance, if you can show that a basic protein domain could have originated from an unrelated state thorugh an intermediate that is partially related and is naturally selectable(let’s say from A to A1 to B, where A and B are unrelated, A1 is an intermediate between A and B, and A1 is naturally selectable), , then we are no more interested in the total dFSCI of B. What we have to evaluate is the dFSCI of the transition from A to A1, and the dFSCI of the transition from A1 to B. The assumption is that A1 can be expanded, and its probabilistic resources multiplied. Therefore, if the two (or as many as you want) transitions have low dFSI, and are in the range of the biological systems that are supposed to generate them, then the whole system can work."gpuccio
December 14, 2011
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If you go one step further, 'evolution' did not know, it was making a human, and that a human could make it own clothes, build binoculars, or make a car so he can get around faster. So we really should be all hairy, have better eye sight, and be faster and stronger. And there are no almost humans or ex-humans. The tiny steps that separate us, from animals. It almost looks like we were designed to be like we are! http://patternsofcreation.weebly.comMrDunsapy
December 14, 2011
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"The reason why the designer(s) ".... For a group that chastises "bad design" arguments and says we can't infer the will of the designer, you seem to know a lot about the design plans when you want to. Threads 7 and 8 also.DrREC
December 14, 2011
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1- Understanding development is not the same as undersatnding its evolution.
That would be an evasion.
What am I evading? Be specific. And hurricanes do NOT evolve. But to understand hurricanes we sure as hell have to understand much more than wind. And what work are you talking about? What work demonstrates a vision system can arise in a population that never had one?Joe
December 14, 2011
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Both MathGrrl and Lizzie are wrong. Ya see the complexity part was taken from Dembski, as was everything else. One clueless person supporting two other clueless people does not make you less clueless.Joe
December 14, 2011
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1- Understanding development is not the same as undersatnding its evolution.
That would be an evasion. I'll take that as you agree that you have a false dichotomy.
2- In order to undersatnd its evolution you have to understand A) Its origin B) The origin of eukaryotes C) the origin of metazoans and cellular differentiation
Your opinion that such is required is erroneous. Your argument is no different than insisting that in order to understand the evolution of hurricanes, we must first understand the evolution of air molecules. While the latter might actually help explain some expects of hurricane evolution better, not knowing such does not preclude understanding the larger evolutionary processes at work.
That said all you have are generalizations that cannot be tested.
The work done in the area demonstrate otherwise.Doveton
December 14, 2011
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Just out of curiosity, is there any conceptual problem with functional sequences arising out of non-functional sequences.
No. A well written GA should be able to do thatJoe
December 14, 2011
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BTW in a common design scenario I would expect to find similar HOX genes (ie control mechanisms) for similar structures. The funny part about control mechanisms is that your position can't explain them but they make very good sense in light of design.Joe
December 14, 2011
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Doveton- RE vision systems- The reason why the designer(s) did not give us the vision of hawks or cephalopods is because we have the ability to duplicate their vision. Humans do not need it but can haz it if they want.Joe
December 14, 2011
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Complex specified information is a specified subset of Shannon information. That means that complex specified information is Shannon information of a specified nature, ie with meaning and/ or function, and with a specified complexity.
Sorry, but both Mathgrrl and Lizzie noted this is not a rigorous mathematical definition and does not match Dembski's definition of CSI. You'll have to come up with something new.Doveton
December 14, 2011
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1- Understanding development is not the same as undersatnding its evolution. 2- In order to undersatnd its evolution you have to understand A) Its origin B) The origin of eukaryotes C) the origin of metazoans and cellular differentiation That said all you have are generalizations that cannot be tested.Joe
December 14, 2011
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Not so much. Archaeology in part compares human artifacts of unknown origin to artifacts of known origin to provide an explanation about the unknown culture.
That is how we develop our knowledge of cause and effect relationships.
Forensic science certainly relies heavily upon the analysis of cause and effect since it’s main focus is providing an explanation for the cause of some crime being investigated. However, the here is being able to evaluate someone’s claim that something is designed. We don’t have to know what caused the design (as ID proponents are so fond of noting) in order to evaluate whether the claim of design has merit.
Exactly.
SETI, otoh, is not looking to identify the cause of radio (or other electo-magnetic) transmissions.
I didn't say they were.
Rather, SETI is focused upon evaluating transmissions from a very narrow frequency range. Signals in that range are not known to occur naturally.
Yes, because of our knowledge of cause and effect- that is how we know what signals will not occur naturally. Thanks, 3 for 3 for me. As for my remark about DNA, again obviously you don't understand how the vision system develops and you think someone can just design one and install it anywhere.
My mistake in extending this to all scientists, however your claim regarding biologists not knowing anything about designing still remains your opinion without substantiation. Craig Venter, as an example, would likely have a different opinion.
LoL! You can't even follow along- is Venter one of the biologists that claim our vision system is a poor design?Joe
December 14, 2011
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Right, we just have to have some knowledge of cause and effect relationships.
I don’t see that as a requirement either. Care to explain why you think it is?
That is how it is done in archaeology, forensic science and SETI- to name a few venues.
Not so much. Archaeology in part compares human artifacts of unknown origin to artifacts of known origin to provide an explanation about the unknown culture. In another part, archaeology studies artifacts from two known origins and determines the cultural differences. Forensic science certainly relies heavily upon the analysis of cause and effect since it's main focus is providing an explanation for the cause of some crime being investigated. However, the here is being able to evaluate someone's claim that something is designed. We don't have to know what caused the design (as ID proponents are so fond of noting) in order to evaluate whether the claim of design has merit. SETI, otoh, is not looking to identify the cause of radio (or other electo-magnetic) transmissions. Rather, SETI is focused upon evaluating transmissions from a very narrow frequency range. Signals in that range are not known to occur naturally. Investigating any cause and effect in this case is impractical to say the least of a little value at this point. Bottom line, none of these demonstrate that cause and effect analysis, while certainly useful, is required to evaluate someone's claim of design in nature.
Your response above is incoherent.
That is because you are cluelss.
This response does not make your previous response any more coherent or valid. “the human vision system has to be embedded in something that does not have it, namely the gametes of humans” does not mean anything, aside from not even referencing anything I noted.
So you don’t understand how the vision systems come about?
Irrelevant to your response above and my note that it is incoherent.
As for your claim that scientists don’t know anything about design,
BIOLOGISTS- and only the BIOLOGISTS you were referring to. They sure as heck can’t provide anything to substantiate their claims of a poor design.
My mistake in extending this to all scientists, however your claim regarding biologists not knowing anything about designing still remains your opinion without substantiation. Craig Venter, as an example, would likely have a different opinion.Doveton
December 14, 2011
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There are a number of perfectly valid evolutionary explanations for the vision system out there Joe.
What do you mean by “valid”? There isn’t one that is scientifically testable.
This would your claim without any substantiation against the research performed and published out there in scientific journals and research papers.
Heck we don’t even know the genes responsible- all we know is- Andrea Bottaro said the following over at the panda’s thumb:
Eyes are formed via long and complex developmental genetic networks/cascades, which we are only beginning to understand, and of which Pax6/eyeless (the gene in question, in mammals and Drosophila, respectively) merely constitutes one of the initial elements.
Moving the goalposts. Whether we know the specific development process of the specific genes of eye development in a given species (or multiple species) is not the same thing as having a valid explanation for the evolution of vision. Btw, you do know that a more fundamental understanding of those genes has been gained since Bottaro's comment? http://www.ncbi.nlm.nih.gov/books/NBK10024/ That's the thing about science - unlike ID, it isn't static.
IOW the only evidence for the evolution of the vision system is that we have observed varying degrees of complexity in living organisms, from simple light sensitive spots on unicellular organisms to the vision system of more complex metazoans, and we “know” that the first population(s) of living organisms didn’t have either. Therefore the vision system “evolved”. Isn’t evolutionary “science” great!
That would be an inaccurate summary at best, but it did provide me a chuckle.
I say the above because if Dr Bottaro is correct then we really have no idea whether or not the vision system could have evolved from a population or populations that did not have one.
That would be incorrect. Aside from your generalization of what constitutes understanding the visual system, your conclusion rests on a false dichotomy. While certainly understanding specific gene development in specific species would be great, and more so understanding the specific evolutionary path between ancestral species, such does not prevent understanding the evolution of the visual system at a more general level. Indeed, it is because of such a general understanding and the ability to make predictions based on that understanding that the PAX6 genes as control mechanisms were investigated in the first place. See: http://www.accessexcellence.org/WN/SUA01/master_eye_gene.phpDoveton
December 14, 2011
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Just out of curiosity, is there any conceptual problem with functional sequences arising out of non-functional sequences. As I recall, I once asked you if you could identify a sequence that is just one base pair from being functional. Could you pick it out from a batch of purely random sequences? What is the dFSCI of a sequence that is just one base pair from being functional?Petrushka
December 14, 2011
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Doveton: For your convenience, I paste here one of the many recent summries of my definition of dFSCI (digital functionally specified complex information) I have given recently here. Just to start the discussion: "Please go back to my (quick) definition of dFSCI in my post number 9 here. I quote myself: “No. The dFSCI of an object is a measure of its functional complexity, expressed as the probability to get that information in a purely random system. For instance. for a protein family, like in Durston’s paper, that probability is the probability of getting a functional sequence with that function through a random search or a random walk starting from an unrelated state (which is more or less the same).” Well, maybe that was too quick, so I will be more detailed. a) We have an object that can be read as a digital sequence of values. b) We want to evaluate the possible presence of dFSCI in that object. c) First of all we have to explicitly define a function for the digital information we can read in the object. I we cannot define a function, we cannot observe dFSCI in that object, It is a negative. Maybe a false negative. There are at different ways to be a false negative. The object could have a function but not be complex enough: it could still be designed, but we cannot say. Or we could not be able to understand the code or the function in the object. d) So, let’s say that we have defined a function explicitly. Then we measure the dFSCI for that function. e) To do that. we must measure the functional (target) space and the search space. Here various possiblities can be considered to approximate these measures. For proteins genes, the best way is to use the Durston method for protein families. f) The ratio of the target space to the search space if the complexity of our dFSCI for that object and that function. What does it express? As I said, it expresses one of two things, which are more or less equivalent: f1) The probability of obtaining that functional sequence from scrtach in a purely random system: IOWs, for a protein gene, the probability of obtaining any sequence that produces a protein with that function in a system that builds up sequences just adding randomly nucleotides. f2) The probability of obtaining that functional sequence through a random walk. That is more relevant to biology, because the usual theort for genes is that they are derived from other, existing sequences through variation. But the important point, that IO have explicitly stated in my previous post, is that it expresses “the probability of getting a functional sequence with that function through … a random walk starting from an unrelated state. Starting from an unrelated state. That’s the important point. Because that’s exactly what happens in biology. Basic protein domains are unrelated states. They are completely unrelated at the sequence level (you can easily verify that going to the SCOP site). Each basic protein domain (there are at least 2000) has less than 10% homology with any other. Indeed, the less than 10% homology rule bears about 6000 unrelated domains. Moreover, they also have different structure and folding, and different functions. So the question is: how does a new domain emerge? In the example I cited about the human de novo gene, it seems to come from non coding DMA. Many examples point to transposon activity. In no case a functional, related precursor is known. That’s why dFSCI is a good measure of the functional information we have to explain." Any inquiries are welcome.gpuccio
December 14, 2011
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doveton:
I notice you didn’t link to this supposedly provided rigorous definition.
CSI- Complex Specified Information. Information- see Shannon, Claude (When Shannon developed his information theory he was not concerned about "specific effects":
The word information in this theory is used in a special mathematical sense that must not be confused with its ordinary usage. In particular, information must not be confused with meaning.- Warren Weaver, one of Shannon's collaborators
And that is what separates mere complexity (Shannon) from specified complexity.) Specified Information is Shannon Information with meaning/ function Complex Specified Information is 500 bits or more of specified information Complex specified information is a specified subset of Shannon information. That means that complex specified information is Shannon information of a specified nature, ie with meaning and/ or function, and with a specified complexity. Now choke on it.Joe
December 14, 2011
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Right, we just have to have some knowledge of cause and effect relationships.
I don’t see that as a requirement either. Care to explain why you think it is?
That is how it is done in archaeology, forensic science and SETI- to name a few venues.
Your response above is incoherent.
That is because you are cluelss.
“the human vision system has to be embedded in something that does not have it, namely the gametes of humans” does not mean anything, aside from not even referencing anything I noted.
So you don't understand how the vision systems come about?
As for your claim that scientists don’t know anything about design,
BIOLOGISTS- and only the BIOLOGISTS you were referring to. They sure as heck can't provide anything to substantiate their claims of a poor design.Joe
December 14, 2011
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Where exactly is the rigorous mathematical definition of CSI that Mathgrrl/Patrick and Elizabeth Liddle requested?
It has been provided and they choked on it. Where exactly is your position’s rigorous anything?
I notice you didn't link to this supposedly provided rigorous definition. Funny how no one here seems to be able to do that. I'll take your non-response as an admission it's still not been provided. As to your inquiry about my position's rigorous anything, our deal is still in effect. I will provide you with such explanations when/if you provide the valid answers to the questions posed to you. If you wish to break that deal, that's up to you.Doveton
December 14, 2011
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We don’t have to be able to recognize design in nature to evaluate someone else’s claim of design.
Right, we just have to have some knowledge of cause and effect relationships.
I don't see that as a requirement either. Care to explain why you think it is?
As for evaluating the claimed design itself, that’s easy – we merely compare the item that is claimed to be designed against the human approach to designing something similar and against other objects of the same type in nature, taking into account that a “more advanced” designer would have fewer reasons to create shortcuts, use inferior materials, have resource limitations, etc – particular if said “designer” is supposed a god.
I smell a strawman.
Hence the reason that most biologists criticize the claim that the human eye (and any eye actually) is designed.
That is because they don’t know anything about designing.
Given the human engineering approach to such a item, the human eye is objectively a terrible design – particularly in light of the far superior eye “designs” out there in nature that would suit humans far better for the type of activities we engage in (the cuttlefish’s for instance).
Strawman. Ya see doveton the human vision system has to be embedded in something that does not have it, namely the gametes of humans. Not one human engineer could pull that off. IOW all you are doing is providing may ways of how not to argue against ID.
Your response above is incoherent. "the human vision system has to be embedded in something that does not have it, namely the gametes of humans" does not mean anything, aside from not even referencing anything I noted. Care to try again? As for your claim that scientists don't know anything about design, that would be your opinion I guess as you provided no substantiation for the claim.Doveton
December 14, 2011
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That is precisely my modern take on the watchmaker, "the iPod maker". There is innate logic and reasoning programmed into our dna that allows us to recognize design. No one would ever come across an iPod in the forest and just think that all those 0's and 1's just happened to align in a precise pattern that when passed through a DA converter and fed to transducer actually produce Beethoven's 5th Symphony. Actually, forget the o's and 1's that code the symphony, how did the flash memory, DA converter and Transducer get there??!?!?!? Like I said above, it is the "suspension of disbelief" that allows people to live as if there is no Designer, because to accept the Designer, would require you to actually change the way you are living.Ultimately Real
December 14, 2011
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doveton:
There are a number of perfectly valid evolutionary explanations for the vision system out there Joe.
What do you mean by "valid"? There isn't one that is scientifically testable. Heck we don't even know the genes responsible- all we know is- Andrea Bottaro said the following over at the panda’s thumb:
Eyes are formed via long and complex developmental genetic networks/cascades, which we are only beginning to understand, and of which Pax6/eyeless (the gene in question, in mammals and Drosophila, respectively) merely constitutes one of the initial elements.
IOW the only evidence for the evolution of the vision system is that we have observed varying degrees of complexity in living organisms, from simple light sensitive spots on unicellular organisms to the vision system of more complex metazoans, and we “know” that the first population(s) of living organisms didn’t have either. Therefore the vision system “evolved”. Isn’t evolutionary “science” great! I say the above because if Dr Bottaro is correct then we really have no idea whether or not the vision system could have evolved from a population or populations that did not have one.Joe
December 14, 2011
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10:48 AM
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"No one suggests that such a scenario ever happened" I think you just made my point.Ultimately Real
December 14, 2011
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doveton:
Where exactly is the rigorous mathematical definition of CSI that Mathgrrl/Patrick and Elizabeth Liddle requested?
It has been provided and they choked on it. Where exactly is your position's rigorous anything?Joe
December 14, 2011
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Whatever. Descent with modification does not expect a nested hierarchy based on characteristics. And thanks to genetic recombination we wouldn't expect one at the level of genes either.Joe
December 14, 2011
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