What exactly is ID?

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Which, of course, I did not argue against.

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Than what's your point? That the enzyme got a new function, but that we do not know about it?

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Simply denying the facts is hardly a road to productive discussion. If I am incorrect and Dembski did calculate the probability of P(D*) you need to demonstrate that.

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D* is the "bidirectional rotary motor-driven propeller" which consists of 50 proteins. Which have a probability of forming into that specific pattern of about 1:10^2954.

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I already did that. You need to calculate the number of proteins that are no more than 20% different from each of the 50 used in the E Coli flagellum.

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Fine. Explain how in detail.

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No. D* is the specification considered as an event. So it is ANY "bidirectional rotary motor-driven propeller" however many - or few - proteins are involved.

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Yes, but what is the complexity of this particular specification? It's 50 proteins. Please tell me how do you intend to calcualte the probability of a specification without knowing the complexity.

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Of course, the Caputo case involved nothing more than the Democrats taking first position on the ballot far more often than expected. There was no other pattern to the results.

​

In fact your objection has nothing to do with detachability at all. All you are saying is that D* is much wider than E. But that is the reason WHY we need to use P(D*) - because P(D*) CAN be much higher than P(E) and thus the SPECIFIED information may be only a tiny fraction of the whole.

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And that is why nobody would care if Democrats won 21 and Republicans 19 time the ballot.

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Which rules out your claim:

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How does it rule it out.

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Because Dembski's method relies on detecting the input of information from a designer (as opposed to natural sources). Let me be clear, I am claiming that the operation of a fully automated process cannot be used to reliably detect design because it has a high probability of producing its output. It is certainly possible that the process itself might be designed and if it is, that you might - in principle - be able to use Dembski's method to detect it with reasonable reliability. (While Dembski's method has a number of problems, if the practical difficulties could be overcome, it might be usable as a decent argument for design - when applied correctly).

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But there is no input from natural sources. Because natural sources have no teleology. They are constrained by deterministic natural laws. Therefore, any information they transmit, was originally inputed by an intelligence.

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So what you mean is that the alleles for hair colour and eye colour are neutral and the frequencies aren't changing much through selection or drift, and ask why that isn't the case for sickle-cell. The answer is that sickle-cell trait (heterozygous for sickle-cel) is quite strongly advantageous in malarial areas and mildly deleterious elsewhere, while the homozygous state is strongly deleterious everywhere.

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Except that that is teh case. Just like blue eyes and blond hair is kept at a certain frequency, so is sickle cell. And every other gene.

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If you only want to talk to people who are convinced by your claims regardless of how poor your evidence is, then I suggest that you go to a creationist-run forum. I've already told you what sort of evidence you would need to produce. And any reasonable person would agree.

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No, you do not care what Is how you you are sticking to your faith.

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Obviously you have not understood the position I am putting forward at all. I have not said that natural selection is perfect or that there is no noise. What I have said is that beneficial mutations have a greater chance of spreading - and the more beneficial they are the better their chances. And that deleterious mutations have a lower chance of spreading - and the more deleterious they are, the less their chances (in the extreme case of causing sterility or death before reproductive maturity, NO chance). This fact has to be taken into consideration, rather than simply shrugging it off.

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And yes, I will again say that I know that. But, there is so much noise that regardless of beenficial and deleterious mutations, they do not get spread around as much as they would if there was no noise. So in reality, when we take the effects of noise into considerations, we almost always have genetic drift, as opposed to positive selection working. Meaning, beneficial and deleterious mutations are equally likely to spread through the population.

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No, it is the exact opposite of genetic entropy. Genetic entropy supposedly degrades the fitness of the population until it is forced into extinction. In the Spiegelman monster case, mutations improved the population radically, to the point where the "monster" drove all other populations into extinction.

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NO! How many tiems do I have to say that geentic entropy does not always have to equal loss of fitness?The point is that the chain got shorther. Because of mutations. And the more time went by, it got shorter and shorter. The longer ones died out. And only the shortest were left. Clearly demonstrating that evolution does not work. You can't get a human from RNA chains by this process becasue they are losing not gaining complexity.

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Only if you use your own crazy version of it, rather than one which has any relevance to actual biological function of the changing molecule! Alowing that CSI is represented in this system the specification surely resides with the genetic sequences allowing the production of Streptomycin with a structure allowing it to bind to ribosomal elements, not the other way around. You might argue that the change in the ribosomal element effectively reduces the information content of the streptomycin biosynthesis sequences, but I don't see how you can argue that it represents a loss of information for the ribosomal sequence.

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What got changed, the ribosome or the streptomycin? Obviously the ribosome. Therefore, it is the one that lost specificty.

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My example is better because it relates to actual deleterious functional effects to the ribosome, which the various informational metrics involving functionality we have discussed would probably all identify as a loss of functional information. Of course there is a counter-argument that we need to be able to calculate the potential gain of functional information that the resistance phenotype represents in order to determine if the informational change has led to a net loss or gain of information.

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I don't care which one is better. Both are fine. You can stick to your example as being better, it's all the same to me. Both show beneficial mutations increasing genetic entropy by degrading biological functions.

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This type of claim seems provable, is it not? Sequence of an ancestor and current of any given species and a genetic loss should be apparent. The larger the gap from ancestor to present species should reveal a larger genetic loss. This sounds like a simple case of adding up the "bits" and Genetic Entropy becomes quite obvious.

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As a matter of fact, I already posted a link which compared 110 mammalian species and how their genetic information kept accumulating slightly deleterious mutations. So yes, it's observable, and it's a well known fact.

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I guess it is equally false whatever you're talking about.

​

If you really know damn-all about thermodynamics, I suggest that you study thermodynamics.

​

Stop me if I'm going to fast for you.

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I'm listening. Explain what's wrong with my description.

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As I have told you, there is nothing in genetics, least of all the existence of the genome, which implies that one can construct a refrigerator without a power source.

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But genomes still do not degrade right? There is no genetic entropy?

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No I am not.

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Listen carefully.

​

Your fantasy of "genetic entropy", which you cannot define, has nothing to do with the theory of thermodynamics. If you called it "genetic weight", it would have nothing to do with the theory of gravity. If you called it "genetic electrical charge", it would have nothing to do with Maxwell's equations.

​

The fact that you have chosen to describe your vague and nebulous fantasy in terms that have real meaning in a real science does not magically mean that your daydream has anything to do with that science.

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This just shows you do not know, you actually still don't know what gentic entropy is supposed to be. It's teh deterioration of genetic information in the genome. Just like any otehr medium that has information embedded in it. Like a CD. Copying it enough times, over and over again, to a new CD, and than take that one and copy it again, and this is going to add few mistakes here and there. Over enough time, enough information will be lost and the CD won't be useful anymore becasue you won't be able to read anything from it.

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I know that you are not telling the truth, because I have read what Sanford has to say.

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Your error is a different error from Sanford's error. He may be completely wrong --- in fact, let's not beat about the bush, he is --- but he is nowhere near being as hopelessly, ludicrously wrong as you are.

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Very well, let's see what Sanford has to say about that...

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The sensitivity of this observational network is such that even if only one mutation out of a million unambiguously creates new information (apart from fine-tuning), the literature would be owerflowing with reports of this happening. Yet I am not convinced there is one crystal-clear example of a known mutation which unambiguously created information. There are certainly many mutations which have been described as beneficial, but most of these mutations have not created information, but rather have destroyed it. For illustration some of us (like me) would view a broken car alarm as "beneficial". However, such random changes, although they might be found to be "desirable", still represent a breakdown and not the creation of a new functional feature. Information decreases. This is the actual case, for example, in chromosomal mutations that lead to antibiotic resistance in bacteria, cell functions are routinely lost. The resistant bacterium has not evolved. In fact it has digressed genetically and is defective.

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John C. Sanford - "Genetic Entropy & The Mystery of The Genome" page 17.

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Of course we don't. This is why you are unable to produce any evidence for your fantasies.

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This article claims you can't invoke beneficial mutations to save the mopulation. Even the large mammalian populations.

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In many vertebrates Ne approximately 10(4), while G approximately 10(9), so that the dangerous range includes more than four orders of magnitude. If substitutions at 10% of all nucleotide sites have selection coefficients within this range with the mean 10(-6), an average individual carries approximately 100 lethal equivalents. Some data suggest that a substantial fraction of nucleotides typical to a species may, indeed, be suboptimal. When selection acts on different mutations independently, this implies too high a mutation load. This paradox cannot be resolved by invoking beneficial mutations or environmental fluctuations.

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Contamination of the genome by very slightly deleterious mutations: why have we not died 100 times over? - PubMed

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Then why can you not quote Sanford saying the same thing as you are?

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Oh, oh, I know. Because his trash is different from your trash.

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I just did, above. I can't wait to see what you have to say to that...

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Because it works exactly like I think it does. Which is why there are species that are not extinct.

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No, they are not extinct YET. But it seems that they will follow those that are extinct.

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So, you're back to a definition of genetic entropy whereby the increase of this quantity, which you are unable to measure, is not opposed to evolution and is in fact an inevitable consequence of it.

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How is it not opposed to evolution? When did I say that?

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If you tell me falsehoods about what I am claiming, you will not succeed in deceiving me.

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It's not a falsehood. You do seem to think that darwinism equals evolution.

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Like Kimura, I agree that there were things that Darwin didn't know. And, like Kimura, I think that creationism is bullshit.

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Do you also agree with him that darwinism only, can not account for all diversity of life on Earth?

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It's so good that the "genetic meltdown" in Sanford's fantasies does not in fact happen.

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What about those links I posted that actually showed the genetic meltdown occure?

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... of this stuff called "evidence"

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Which is?

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Well, if you want to fantasize that one day this genetic meltdown will take place, feel free. But this fantasy does not contradict the actual history of life on Earth.

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Are you saying that my idea of genetic entropy is that one day all life on Earth will simply just die out at the same time because of genetic meltdown?

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This explanation, while it might be "simple", or even downright retarded, is not congruent with the facts.

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What factsa re you talking about?

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You inadvertently said something true.

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Heritable change is not an "evolutionary mechanism". Heritable change is evolution. Any mechanism by which it takes place is an evolutionary mechanism.

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But this kind of evolution can not be extrapolated to be evidence for a darwinian evolution leading from a single cell to a human.

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Incidentally, do you have any evidence for your claim that the particular evolutionary mechanism involved was a transposon, or is this just something you made up?

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Mybe it wasn't. I don't know if it was. But I do know of cases where bacteria aquired nylon digestion by transposons, so I said that it could be caused by one this time also. It doesn't really matter to my argument if it really happened that way.

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If you wish to retreat into hysterical denial about plain facts in biology, then may I suggest that this board is perhaps the very worst place for you to do so?

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The bacteria couldn't do something. Then they could, as a result of a genetic change. This is evolution.

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If you want to call this evolution than fine. But his is not darwinian evolution, and it doe not lead froma single cell to a human.

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You had to talk gibberish to pretend that I was confused. I am not confused. This is why you couldn't argue with what I actually said, but had to argue with some incoherent trash about televisions which you made up in your head. Because as you well know, you're not going to get anywhere arguing with people about genetics, a subject of which you are pitifully ignorant.

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I never said you are confused. You are nto confused. To be confused you have to know something in teh first place to confuse it with something else. You on teh other hand do not know anything. Therefore, you can't be confused.Edited by Smooth Operator, : No reason given.

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No, we aren't stuck. I've already told you and I'll tell you again.

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Go ahead, use CSI.

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Just use it on something to prove it WAS designed but which we, in no way, have any idea HOW it was designed/created.

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You are using this to demonstrate proof of concept so we can check it against Creationism.

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If Creationism is the _ONLY_ example, then this is not a valid way of evaluating it.

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It's like having a "Zimzom Detector" which is the only thing which detects "Zimzoms". Can't prove it right or wrong.

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Well than, a perfect exmaple if here.http://www.designinference.com/.../2005.06.Specification.pdf

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For a less artificial example of specificational resources in action, imagine a dictionary of
100,000 (= 105) basic concepts. There are then 105 1-level concepts, 1010 2-level concepts, 1015 3-
level concepts, and so on. If bidirectional, rotary, motor-driven, and propeller are basic
concepts, then the molecular machine known as the bacterial flagellum can be characterized as a
4-level concept of the form bidirectional rotary motor-driven propeller.

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We know that the flagellum consists of 50 protein parts. Than we describe it as a "bidirectional rotary motor-driven propeller".

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Next, define p = P(T|H) as the
probability for the chance formation for the bacterial flagellum. T, here, is conceived not as a
pattern but as the evolutionary event/pathway that brings about that pattern (i.e., the bacterial
flagellar structure). Moreover, H, here, is the relevant chance hypothesis that takes into account
Darwinian and other material mechanisms.

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After that, we define all relevat chance hypoteses, which include Darwinian evolution of the flagellum.

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We may therefore think of the specificational
resources as allowing as many as N = 1020 possible targets for the chance formation of the
bacterial flagellum, where the probability of hitting each target is not more than p.

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After that, we take into account the possibility that the flagellum can be perturbed. The number we take in to account is the 20 orders of magnitude. Becasue it could be possible to mutate the flagellum so it would still be functional.And after that we simply look at teh number we get where teh probability of the flagellum forming by chance has been calcualted from NFL. The number we got is 1:10^2954. Therefore, since we know that the universal probability bound is 1:10^120. It means that the flagellum has less chance of forming than the universal probability bound. Which means it was designed.

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Except that sequence wasn't evolved to have specificity to streptomycin. If I shape my hand to fit into a particular hand hold when climbing a rock have I suddenly increased the rock's 'information' because I have specified my hand to fit it? You seem to be saying that as soon as the full streptomycin biosynthesis pathway had evolved the specified information content of the ribosomal genes jumped despite there being no change in its sequence, we might consider that information to have been 'free' since it only served the function of the antibiotic rather than the ribosome. I don't see why this is more logical than me suggesting that it can lose that binding specificity without losing information content. All you seem to be doing is highlighting why your conflation of the specificity in CSI and binding specificity is meaningless when you don't actuslly look at the functional biological context.

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It doesn't matter if it lost affinity specifically to streptomycin. It probably can bind to something else too. The original structure is the original information content. Now, if it loses the affinity, to anything, it got degraded, and it lost information.

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Once again you are making up a system where things can't help but 'degenerate' because you are defining any change from the initial state as degeneration. Would you consider any mutation which increased binding affinity to anything to therefore represent an increase in information/CSI? Even if the subsequent binding served no functional purpose for the mutated protein?

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You can't gain CSI by one mutation. You would have to gain at least 400 bits. Yet information can be lost by one mutation.

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You are just showing us why these creationist/ID measures of information divorced from actual considerations of function are totally useless. They are just ad hoc measures based on arbitrarily selected starting points and in many cases arbitrary criteria for what constitutes a gain or loss of information.

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What exactly is arbitrarily in my starting point. The ribosome is not arbitrary in any way.

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Remember the Durston et. al FSC measure we discussed, where they base their estimates essentially on conservation, totally regardless of actual functionality beyond very crude classification. Their method means that any novel mutation which allows the maintenance or even improvement of function for a protein nevertheless would represent a loss of FSC. There is no possible route in their approach which allows a novel mutation to produce an increase in functional information.

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I see no reason why a bunch of mutations couldn't build a fully functional ATP synthase. I mean, it won't happen. But if it did, it would be an increase in FSC for sure.

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My point is that we do not know whether the mutated enzyme had no function or if it did. That is what I said. Perhaps you should try harder to remember just what you are arguing against ?

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We know it lost one. It's an observable, empirical, fact! And we are going to stick with that. Unless you think we should invent imaginary functions just for the sake of the argument?

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In other words, your real "specification" is the E Coli flagellum plus near variants of it. And as I have pointed out, this is a fabrication. (The probability calculation is wrong, too, but that isn't important now).

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WHY!? Why the hell is it a fabrication? If it can be described without looking at the event E, than it's not a fabrication. And yes, it can be described in such a way, therefore, it's a specification.

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Since actually doing the calculation would be a complete waste of time, why exactly do I need to explain how to do it ? After all, I don't care whether you do it or not.

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If you do not want to show me what calculation I should do, than don't bother me with it anymore.

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If D is "bidirectional rotary motor-driven propeller" then it makes no mention of 50 proteins. That is just an unspecified detail read off the event (i.e. fabrication). The "complexity"(or rather the information content) is calculated from the probability (it's -logmax(P(D|H)) over all possible explanations H). That's Dembski's method.

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Which comes out at 1:10^2954, as I have mentioned for a trillion times already. With simply applying this here equation.χ = —log2[120^10 ϕ s(T)P(T|H)]

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Obviously if the information was only input in the creation of the first E Coli (or it's ancestor) it cannot also be input in the ordinary operation of the growth mechanisms.

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The first growth mechanism was designed together with the first bacteria.

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Natural sources do not produce Complex Specified Information in Dembski's sense (or rather they almost certainly do not, even if Dembski were entirely right). However we cannot work out if something is Complex Specified Information by Dembski's method without looking into its origin. By Dembski's definition, natural sources can and do generate information, even complex information and specified information (because his measure of information is simply an measure of improbability).

​

So, without applying Dembskis method to this information, we cannot work out whether it is CSI or not. And if it is not CSI - if the specified part of the information (D*) is not complex - then, according to Dembski, it could have a natural source.

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Basicly what you're saying is that we can't know if something is CSI if we do not know how it arises. Why?

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Even if it is the case that the frequencies are constant (and I'm far from certain of that), it isn't the same sort of selection as applies to sickle-cell.

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Than what kind of selection is operating on sickle cell? Is it some magical one? Obviously it's not. It's the same as the one that is operating on any other gene frequency. Why would this one be special?

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Which means that all you are really doing is pointing out the weakness of drift in large populations. Remember, it was you who introduced sickle-cell as an example of a beneficial mutation (and even claimed that it was spreading), so comparing it to neutral mutations really misses even your own point.

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Well it did spread didn't it? It is irelevant if it is considered a neutral, a deleterious or a beneficial mutation. And it is also irelevant which mechanism has spread it. A certain population in Africa has this mutation fixed in.

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This is the same noise that - according to you - is having absolutely no effect on the frequency of hair or eye colour. Which means that it isn't going to have much effect against selection either.

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It affects everything. Including genes for eyes, and red blood cells.

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For that to be true, the effect of drift would have to be so strong as to completely overwhelm selection. To be entirely true it would mean that there were no advantageous or deleterious mutations at all. All mutations would be strictly neutral. A completely sterile individual would - on average - have the same number of offspring as the best and most fertile member of the population. Obviously that cannot be the case.

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No it wouldn't. Just is some cases. I'm not saying that positive selection is non-existent. It's here. But it's not as effective as you think it is.And you completely miss the point. It doesn't matter if a certain individual gets a super beneficial mutation, and another gets a super deleterious, but non-lethal mutation. Because of teh noise, the one with the super deleterious mutation can on average get selected by teh natural selection, and the one with the super beneficial one, not get selected.You are totally misunderstanding my point. I'm not saying that the drift is cause by a large amount of neutral mutations. But by other traits that natural selection selects also. The individual will get selected according to:1.) Environmental variation.
2.) Interaction of the environment with the genotype.
3.) Epigenetics
4.) Epistasis.
5.) Dominance.
6.) Homeostasis and cyclic selection.
7.) Genetics.So all this traits get evaluated before an individual gets selected for. It's obvious that just because a particual individual has a beneficial mutation, that doesn't mean that such an individual will on average get selected for by natural selection. Becasue that is only one trait, there are 6 more others to evaluate before it gets selected.

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The number of times you say it, doesn't matter. Genetic entropy IS a cumulative loss of fitness, leading to mutational meltdown and extinction.

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But every single mutation that increases genetic entropy does not have to automatically cause loss of reproductive fitness.

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Aside from the fact that that is going well beyond what the experiment can reliably tell us, it isn't even relevant to the real point. You claimed that it was evidence that genetic entropy increases. And it isn't. The monster beat genetic entropy.

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How could he have beat the genetic entropy if he WAS CONSTANTLY DECREASING IN SIZE!!!!!!?????!?!!?!?!?!

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However, the evidence indicates two things. First, compensatory mutations arise which ameliorate the effects of slightly deleterious mutations:

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Sometimkes they do. I already addressed that. It's possible for that to happen. But it does not happen ALWAYS, or even on average. And if it doesn't. Than the only thing that is happening is that genetic entropy is slowing down, but not stopping. And if it is nto stopping, that just means that it will take more time for the genetic meltdown to happen.

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So the first mechanism to overcome genetic entropy are mutations which increase fitness. That is, beneficial mutations.

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Which on average destroy genetic information, still causing genetic entropy.

quote:

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The second mechanism is negative selection. That is, those with the highest deleterious mutation rate are selected against. This ongoing process stops Muller's ratchet.

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No because of the noise. Just becasue somebody has the highest amount of deleterious mutations, that does not mean such an individual will be selected against on average. Even if they do, others are still mutated, and they spread their mutations through the population, constantly increasing entropy. Yes, even if the worst ones always get selected out. And as your source says, it limits the effect. It does not stop it.

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In order for this to be an accurate analogy you need a source of selection.

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Whichever CD has te most un-damaged information gets copied again.

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Would a gain in specificity be a gain in specified information?

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Yes, but not in complex specified information, unless it was 400 nucleotide change.

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Would a gain in function be an increase of specified information?

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Both in specified and in complex specified information, yes.

quote:

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That may look familiar since you copied it onto your post as well.

​

You CAN NOT use Creationism as an example of something which is NOT CREATIONISM to test against CREATIONISM.

​

I was EXTREMELY specific in my request. Give us something OTHER THAN CREATIONISM which demonstrates design without knowing mechanism so we can VALIDATE your claim about Creationism.

​

And the _ONLY_ example you can come up with is...

​

Creationism. Again.

​

Is Creationism the only thing that the magical wizard designed? Is it the only thing that CSI (or any other method) can determine was designed?

​

If so, CSI is just another Zimzom Detector.

---

I gave you the example that I find good enough. If you don't think it's good enough, than explain why. That would be like me saying you can't give me evidence for evolution if it comes from an evolutionist source and is evidence for evolution. Do you have evidence for evolution which is not evidence for evolution? You do understand that you are asking me for something that is impossible?

quote:

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That it's wrong. It's as though you said: "The Second Law of Thermodynamics says that there's a unicorn in my backyard playing the trombone".

​

Well, no it doesn't.

​

Pace Percy, I don't think that I have to teach you a beginner's course in thermodynamics to explain to you why that is not what the Second Law of Thermodynamics says.

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I'm still waiting for a detailed explanation, and I'm not going to leave it like that. I gave you all the explanations, quotes, and what not you saked for.

quote:

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If we use Sanford's definition, then genetic entropy does not occur except in very small populations.

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Sanford says that ALL life is experiencing genetic entropy. I say so too. Now, explain in detail, how exactly is my definition different to his.

quote:

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No it doesn't.

​

This is why you can't quote any part of that article that supports your fantasies.

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LOL? I quoted the part where it said just that. Did you not see it? Here is the quote again.

quote:

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In many vertebrates Ne approximately 10(4), while G approximately 10(9), so that the dangerous range includes more than four orders of magnitude. If substitutions at 10% of all nucleotide sites have selection coefficients within this range with the mean 10(-6), an average individual carries approximately 100 lethal equivalents. Some data suggest that a substantial fraction of nucleotides typical to a species may, indeed, be suboptimal. When selection acts on different mutations independently, this implies too high a mutation load. This paradox cannot be resolved by invoking beneficial mutations or environmental fluctuations.

---

Read the last statement in the quote. It says:"This paradox cannot be resolved by invoking beneficial mutations or environmental fluctuations."

quote:

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Yes, according to you this might happen if we wait ten billion years.

​

But even if this daydream was true, it would not contradict reality.

---

And what is reality? Show me this reality you are talking about. You are saying evolution can work miracles. Well than, show me where has evolution done anything.

quote:

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If your definition of increase of genetic entropy includes every event that biologists claim has taken place, then you are not arguing against biology.

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And I'm not arguing against biology. When did I say I am? I'm arguing against evolution, particualry darwinian one.

quote:

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Where did Kimura write that "darwinism only, can not account for all diversity of life on Earth"?

​

Actually, that's an unfair question, since the moderators have decided that your repeated and ridiculous untruths about Kimura are off-topic. I suggest that if you want to tell blatant, absurd, and libelous falsehoods about Kimura, you should start a new thread.

---

I gave you a quote where he said that darwinism is like any dogma that is drilled into people at young age, and is championed by all the elite, so an average personw ill come to think it's true.And that quote was from his book "The Neutral Theory of Evolution", which is opposed to darwinism. Because darwinism claims that positive selection brought about all the diversity of life on Earth. As opposed to neutral theory, which claims that genetic drift caused the majority of diversity, and the positive selection had only a minor role.Read the website I quoted from. It's an anti-darwinian, pro-neutralist website.

quote:

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Your links showed strong experimental evidence that genetic meltdown does not occur except in populations which have been artificially reduced in size.

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So if a population of that size existed in nature would it undergo a genetic meltdown? Yes it would. Therefore, genetic entropy exists, it leads to a genetic meltdown, and a small population could have never evolved into anything else. Becasue it was small from the start.

quote:

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On the 649th post of this thread you refer to a link that may or may not be on this thread. Message 115. The link does not appear to be what you claim it to be however, why exactly do you think this paper has any impact at all on evolution?

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Please read carefully.

quote:

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Furthermore, because in the course of mammalian evolution body size tends to increase and, consequently, Ne tends to decline, evolution of mammals toward large body size may involve accumulation of slightly deleterious mutations in mitochondrial protein-coding genes, which may contribute to decline or extinction of large mammals.

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Just a moment...Notice what the article claims. It says that during the course of mammalian evolution, teh body size had increased. Therefore, the accumulation of slightly deleterious mutations increased also. And than they finish it off by saying that this could contribute to the extinction of large mammals.

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Your task was to come up with an example of design without mechanism APART from the one you are claiming so that we can use it to check your claim AGAINST.

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Do you not understand why presenting the EXACT same thing as something to check itself against fails? Really?

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If you don't have ANY examples of ANYTHING which was designed without mechanism APART from Creationism than your argument is over. You have nothing.

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Creationism is not a mechanism. How exactly is creationism supposed to be a mechanism?Anyway, your argument is nonsensical how ever you look at it. I'm claiming to have a method of design detection. And when I apply it, you claim that I can't use it because that's "creationism". Well, that's liek saying that you can show me evidence for evolution, except when you use evidence for evolution.How exactly is than somebody supposed to show evidence for evolution, if not with evidence for evolution? And how is somebody show evidence for a working design detecting method, without actually referencing that design detecting method.

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No, that's quite possible. There are a myriad of examples of non-biological evolution which we can demonstrate evolution against.

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The evolution of transportation is one such example - from chariot to wagon to motorized transportation. Off branches would include subcatagories such as dogsleds to snowmobiles, the evolution of various safety features, the appearance and disappearance of fins, etc.]

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Those two things you aer comparing are totally different. And if you want to call the advancement of transportation - "evolution". Than fine by me.But do not, and I repeat, do not try and confuse the mechanism which brought about those changes, with what is going on in nature. The advancement of transportation was brought about by an intelligence. It's a case of intelligent design. Over a more or less large period of time. And no, there is no way to compare this to what you are claiming is going on in nature. You are claiming that NO INTELLIGENCE was there in teh process of biological evolution. You are claiming that natural selection and random mutations did the job all by themselves.So what you are basicly doing is a common bait and switch method. You show me a case of intelligent design (advancement of transportation), you call that evolution, and than you claim that this is evidence for evolution in nature, which is supposed to be a non-intelligent darwinian process.

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This shows CHANGE over TIME while NOT demonstrating mutation. It allows us to verify the change over time aspect of evolution.

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Change over time caused by what? Random mutations, or intelligent input? Obviously intelligent input. The changes were caused not by random changes, but by intelligent changes. This is why this example is not applicable to biological evolution. Unless you want to claim that natural biological evolution is also designed.

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If you want to talk about selection based on non-deliberate variables (ie NOT designed changes) you can look at non-biological software/firmware studies on mini-robots where switches are randomly assigned on/off positions and the best combinations are "bred" together. This has resulted in examples of simple programs which accomplish a goal with less code than those designed by people.

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This is also a great example of intelligent design. Such programs are designed to evolve. Dembski explained this perfectly using the AVIDA program.The changes are more or less random, but the selection isn't. When the selection happens, information is being transmited from the environment into the robots. And this cutoff is called a fitness function. It selects certain robots and removes others. But this fitness function has been designed. So the same amount of information that was in the fitness function fromt he start has been transmited into the robots later on. No new information was created.

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The first and foremost thing which contributes to the extinction of all animals is low population size.

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Since large mammals tend to have lower population numbers over all, it's easier to transition them from "low" population to "no" population (which is the definition of extinction).

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Which is why it so easy for small population to go extinct. Yes, I agree with that. And the same goes for large populations, only not as much, beccause selection is more effective in larger populations. But the same principles apply to all populations.Edited by Smooth Operator, : No reason given.

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That is not in contention. The question is whether the mutated version had NO function. And we do not know that.

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No, that's not the question. That was not the point of the experiment. The point was to show how much mutational load can a enzyme take before it loses it's function. The one function that was known to exist was measured. And it went away after some time. So now we know how much changes can there be on average before a certain function is lost.

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Since the probabilty you are calculating relies not only on the number of proteins in the E Coli flagellum, but also their structure it seems very unlikely that it can be separated to the degree required by Dembski's TRACT condition. But please, if you think otherwise then give the specification.

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The only relevant question is. Does the flagellum describe this pattern: "bidirectional rotary motor-driven propeller"? The answer is - yes. So since we know of other objects that exhibit this pattern, we conclude that it's a specification, and not a fabrication.

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So long as you give me no reason to bring up your error I am happy to stop talking about it.
On the other hand if, for instance, you try to use the result of your erroneous calculation it is perfectly reasonable for me to point out that it is wrong.
(I will add that anyone with even a basic understanding of probability theory should be capable of working out how to calculate the number without too much difficulty).

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I'm willing to do the "correct" calculation. I'm simply waiting for you to tell me what to do.

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As we both know that isn't true. Your calculation is based on using details which are completely absent from the specification "bidirectional rotary motor-driven propeller".

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Let's see what Dembski has to say about that...

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For a less artificial example of specificational resources in action, imagine a dictionary of 100,000 (= 105) basic concepts. There are then 105 1-level concepts, 1010 2-level concepts, 1015 3- level concepts, and so on. If bidirectional, rotary, motor-driven, and propeller are basic concepts, then the molecular machine known as the bacterial flagellum can be characterized as a 4-level concept of the form bidirectional rotary motor-driven propeller. Now, there are approximately N = 1020 concepts of level 4 or less, which therefore constitute the specificational resources relevant to characterizing the bacterial flagellum.

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http://www.designinference.com/.../2005.06.Specification.pdfLet me explain what he is saying here breafly.The ϕs(T) part of the equation describes the specificational resources. That is, the amount of all possible specifications relevant the the specification T that is exibited by the even E. Imagine now a descriptive language D* for which we will say will be English language consisting of aprox. 100.000 words. That's 10^5 basic concepts.Using the definition of CKS information theory The flagellum describes the pattern "bidirectional rotary motor-driven propeller". This patternt consists of 4 basic concepts, that is, 4 words. The total complexity of this specification is thus 10^5 10^5 10^5 10^5 which equals 10^20.This is the complexity of the specification as calculated by Dembski himslef. After that we multiply it by 10^120, and with the probability of the event, and than we get the final number...

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Basically I am saying that we cannot know if something is CSI unless we use the method for working out whether it is CSI or not. Which requires looking at all the possible explanations of how it arose.

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I agree. The problem I have with your interpretation is that you confuse growth mechanisms with high probability events.

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I have already explained this. Firstly the sickle-cell trait is beneficial while hair and eye colour are neutral. So, the frequency of hair and eye colour is dominated by drift, while selective effects dominate in the case of sickle-cell. That is one difference.
Secondly - as I have pointed out more than once - the sickle cell allele is unusual in that the heterozygous state is quite strongly beneficial in malarial areas, while the homozygous state is strongly deleterious even there. Thus selection acts to hold the frequency in balance.

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But this is not a difference. Remember. Mutations are neutral/beneficial/deleterious depending on the environment. Therefore, in some environment, blue eyes could be beneficial, or deleterious. So no, there is no difference, the same natural selection is operating on all traits.In all cases it depends on the environment and the mutations if they will be removed or spread and at which extent. There is nothing special in this case.

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It is not fixed in ANY human population (unless you mean some small and soon to be extinct group). As I have already explained. it can't be, because the homozygous state is strongly deleterious and for it to be fixed the entire population must be homozygous for sickle-cell.

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And while sickle-cell did spread in the past, it is no longer spreading - which was your claim.

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Neitehr are a lot of other traits. So what? Are blue eyes fiex in human population? No obviously they are not. Only a small minority has them. Does that mean they are deleterious? No obviously not.

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This only shows that you badly fail to understand my argument. My argument is not based on individual cases at all. Instead it is based on the long term aggregate effect over all the population.

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That's my argument also. Iw as just making an example on an individual. Are you telling me that other traits that get selected besides genes are not working on the level of population? Are you telling me they do not interfeer with genetic selection on the level of population over a long periods of time? Of course they do! And that is why natural selection is inefficient.

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The monster beat genetic entropy BY decreasing in size. By decreasing in size it increased it's fitness so that it could outcompete all the other variants.

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No, it's the genetic entropy that is causing it's shortness. And the most important question is, how is that chain supposed to evolve into something more complex if it is constantly decreasing? It's not! And that's why evolution doesn't work. If it did, the chain would be getting longer. But it's not getting longer.

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No, that is not what the article says. "consequently, Ne tends to decline" - I realize you missed that part but you missed it again when Wounded King explained what the article actually says, better than I could, above on this very thread. Please read more carefully.

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No I didn't miss that part. What's so special about it? The slightly deleterious mutations keep accumulationg. That is the point of the article, and that's my point. What am I missing?

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***ABE: I just noticed that with PaulK you indicate a decrease in size shows genetic entropy, but you quote an article and argue with me that an increase in size produces "slightly deleterious mutations" and that is an indicator of genetic entropy.

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So do you swing both ways or is there something else afoot?

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No, either increase or decrease in size itself has nothing to do with genetic entropy. Nothing, absolutely nothing. The reduction in size does nto cause geentic entropy, or the decrease. What causes genetic entropy is the degradation of biological functions.

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This is because the gene pool is smaller and allows for less genetic variation as a result of sexual selection.

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More individuals means more variation within the gene pool. This means the organism is less vulnerable to catastrophic change as when creatures with deleterious mutation dies (as it normally does) it has a proportionally large impact on the population.

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As an aside, larger organisms tend to have longer generations so they recover from population catastrophe.

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Okay, I don't really care why this is. My point is simply that it's happening. It's causing genetic entropy. If you consider genetic meltdown a catastrophe, than no, the population is not going to recover.