What exactly is ID?

On the Second Law of Thermodynamics
by Means of Mammals and FleasorThe Preservation of Good Ideas in the Struggle for SanityImagine a sealed room with a flea infested panda sitting next to a flealess tiger. Imagine further that the fleas jump from one to the other randomly. Obviously, in the beginning there will be more fleas jumping from the panda to the tiger than vice versa. But as more and more fleas jump to the tiger, some fleas will be jumping back to the panda. Eventually, a situation will be arrived at with equally as many fleas on the panda as there are on the tiger. The fleas keep jumping to and fro, but the situation overall will be in equilibrium. The system (comprised of the panda, the tiger and the fleas) has gone from minimal entropy (i.e. minimal disorder: all fleas on the panda) to maximal entropy (i.e. maximal disorder: fleas equally distributed between both animals).Will there ever again arise a situation in which there are more fleas on the panda than there are on the tiger, or the other way around? If the situation stays exactly as described above then the answer is no, it will never happen. But what if we add some energy to the mixture, what will happen then? Well, let's try. We'll open up the sealed room and set fire to the tiger. The fleas on the tiger don't relish being burnt and jump to the panda more readily. The fleas on the panda no longer smell a fresh tiger nearby, but a smouldering one, and they forego the jump. The result is that the fleas end up, en masse, on the panda. It's amazing what a little heat can do.There is grandeur in this view of science, with its several laws, having been originally thought of by Some Scientists in some form or other; and that, whilst this planet has gone cycling on according to the laws of Another Scientist, from so simple a beginning, endless science most beautiful and most wonderful has been, and is being thought of.

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"Ignorance more frequently begets confidence than does knowledge: it is those who know little, not those who know much, who so positively assert that this or that problem will never be solved by science." - Charles Darwin.

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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.

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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.

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

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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.

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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.

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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.

Smooth Operator's key argument is that both deleterious and beneficial mutations reduce the amount of information in the genome, cause a reduction in function and specificity, and increase genetic entropy. I suggest that both sides keep their posts short and focused on these points.Edited by Admin, : Typo.

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--	Percy
	EvC Forum Director

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.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?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.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.TTFN,WKEdited by Wounded King, : No reason given.

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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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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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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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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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Fine. Explain how in detail.

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

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Exactly - because Dembski was right and the correct probability is P(D*). Which does not permit adding in details that are not in the specification D.

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How does it rule it out.

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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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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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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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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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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. 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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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.

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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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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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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.So since it can't be entirely true, the question is, how close to the truth is it. What is the evidence ? Is it so weak as to have almost no effect - as you claim, or so strong as to completely overwhelm selection - as you claim.

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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?

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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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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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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.

This is such an important point. Unless SO is talking about a totally different concept of Genetic Entropy from Sanford then it must absolutely be about actually deleterious mutations and decreases in fitness. Abstruse notions of beneficial mutations which reduce some unmeasurable notion of information are totally beside the point.TTFN,WK

This relates to Muller's Ratchet."The theory of Muller' Ratchet predicts that small asexual populations are doomed to accumulate ever-increasing deleterious mutation loads as a consequence of the magnified power of genetic drift and mutation that accompanies small population size."--sourceHowever, the evidence indicates two things. First, compensatory mutations arise which ameliorate the effects of slightly deleterious mutations:"Isolates encoding DRSeq3 also show lower ND5 deletion levels, though the difference as compared to those that encode DRSeq1 is not significant (P > 0.10, two-tailed t-test). When considered as groups, mean heteroplasmic deletion levels were higher in tropical-clade isolates (12.1%) as compared to temperate-clade isolates (7.3%), though the difference was not significant (P > 0.9, two-tailed t-test). We also analyzed fecundity variation with respect to the three sequence motifs and found that isolates encoding DRSeq2 displayed significantly elevated fecundity as compared to those encoding DRSeq1 (P < 0.001, two-tailed t-test) — see Figure 4C. Fecundities in isolates encoding DRSeq3 and DRSeq1, however, were highly similar and not significantly different (P > 0.1, two-tailed t-test). The relatively low ND5 deletion proportions and high fecundities associated with isolates encoding DRSeq2 are suggestive of compensatory mutation — in particular, the ND5-2 substitutions are expected to result in reduced interactions of directly repeated sequences in ND5-2 and ND5, thereby resulting in lower ND5 deletion incidences and higher fitness. However, we are again unable to account for the potential effects of nuclear loci."--same source as aboveSo the first mechanism to overcome genetic entropy are mutations which increase fitness. That is, beneficial mutations.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."A decrease in nucleotide substitution rates over time suggests that selection may be limiting the effects of Muller's ratchet by removing individuals with the highest mutational loads and decreasing the rate at which new mutations become fixed."--sourceIn order for this to be an accurate analogy you need a source of selection.Edited by Taq, : No reason given.

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

Another important element in this is the existence of synergystic epistatic effects, where the fitness burden of multiple deleterious mutations is greater than the product of their effects in isolation.TTFN,WK

Try and pay attention, SO.Nuggin wrote: 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.

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. If we use Sanford's definition, then genetic entropy does not occur except in very small populations. I note that your reply was not an answer to anything that I actually said.This leaves me with a problem. How do I converse with someone who is not actually talking to me?I guess I'll just taunt you once again with the fact that you cannot quantify "genetic information" or "genetic entropy". I have already acknowledged the fact that Sanford is wrong. My point is that mistake is different from your mistake.You have quoted him talking halfwitted nonsense about beneficial mutations. Very well then, I admit that he is a stupid liar. But the mere fact that he is a stupid liar does not prove that his definition of "genetic entropy" is in agreement with yours. The mere fact that he is a stupid liar does not in itself prove that you and he are in agreement. No it doesn't.This is why you can't quote any part of that article that supports your fantasies. That your trash is different from Sanford's trash. 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. If your definition of increase of genetic entropy includes every event that biologists claim has taken place, then you are not arguing against biology. You are still telling me blatant falsehoods about my own opinions, and you will never succeed in deceiving me. 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. Your links showed strong experimental evidence that genetic meltdown does not occur except in populations which have been artificially reduced in size. I guess that's why I never in any way said or implied that it could. We are already aware that facts don't affect your arguments. Your statement is of, course, untrue. Here is the post where you said that I was "confused".I find you people hard to understand. Obviously, you need to deny reality --- you're a creationist. But you go further than that --- you gratuitously deny reality. You make false statements when you know that you're going to get caught and exposed.Obviously, everyone reading this thread knows that your statement is false. You know that your statement is false. And, this is the thing that I don't quite understand about people like you --- you know that everyone else knows that your statement is false. You can be absolutely certain, without any shadow of a doubt, that everyone reading this thread will know as a matter of complete certainly that you are not telling the truth.So, why do you do it? This is the question that eats away at me. You know that everyone reading your posts knows that what you are saying is not true. So why bother saying it? The only conceivable function it serves is to let people know that you hate the truth. But surely that is not your objective. It is surely not your goal to persuade people that you should be an object of contempt and mockery.So ... so why do you do it?Edited by Dr Adequate, : No reason given.