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Author
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Topic: What exactly is ID?
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PaulK
Member Posts: 17828 Joined: 01-10-2003 Member Rating: 2.5
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Re: Flaws of ID
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The only problem is that it is the most important thing. The enzymatic activity obviously depends on the structure of enzymes.
It isn't the most important thing to a flagellum !
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Agaon, wrong. Growth has nothing to do with it. There is an X number of genes needed for ANY single trait on any single living organism. They all grow. Growth has nothing to do with reducing complexity, the information is still there, before, and after the growth.
Unfortunately for you, YOUR measure of complexity CAN be increaded by the processes of growth. That's why Dembski didn't use it in the TDI.
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Human eye is coded by X number of genes before and after it has grown. The amount of information is always the same.
That would be true if we used Dembski's methods as published in TDI. But you say that's wrong and we should use a method which allows the eye to have more of your "information" than the genes.
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Wrong, it's irrelevant. We are not interested at how it works. It's irrelevant to us. Every single body part on the human body grows, so what?
So Dembski's measure of information isn't relevant ? Why not ? We are supposedly discussing Dembski's methods here.
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It is irrelevant how it is formed. The flgellum forming by random chance, or bacteria growing it has the same problem of accounting for the information contained in 50 proteins. We need to account for where the information in those 50 proteins came from. Regardles of how a flagellum comes about.
That's not even in agreement with NFL ! NFL includes the arrangement of the proteins as part of the calculation.
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Flagellum's specification is defined as: "bidirectional rotary motor-driven propeller", and it consists of 50 proteins. Any other flagellum that does not match this pattern or complexity is irrelevant to us, becasue than we would be dealing with another case of CSI.
So your claim is based on the assumption that E Coli is the ONLY bacterium with a "bi-directional rotary propellor" ? And that this must contain 50 proteins even though we know that only 49 are needed for function ? I think that your assertion has some problems. At the least you have to look at other flagella to see if they meet the specification or not !
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What are you talking about? TDI defines the design inference process the same way as in NFL.
So your ideas about how to calculate the complexity DON'T come from NFL and are in direct contradiction to NFL ? Because they completely disagree with TDI !
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Yes, and that's how it's explained in NFL too.
So in fact you KNOW that your complexity calculation is completely wrong and liable to result in a false positive. Because - as you have just stated - NFL tells you as much,
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You are simply saying it! Show me the evidence that it actually works.
The easiest way to do it yourself. Implement a simple well-behaved landscape and see how well a simple hill-climbing algorithm does at finding the peaks. Then try it with a completely random landscape.
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Yes it is problem in general! Why wouldn't it be? Why are human genomes special? What you are basicly saying is that ONLY tested animal experience genetic entropy, and ALL OTHERS do not! Explain why ALL OTHER animals have special genomes that do not deteriorate.
Likely because humans are using technology to counter the disadvantages of a lot of minor genetic problems.
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What the hell does "small" mean anyway? Something that is small is small in relation to something larger than itself and large in relation to something smaller than itself.
Perhaps you should actually try reading the paper to find out what it means by "small" ?
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The point of the papaer is that smaller populations will experience genetic entropy faster than larger ones. And that goes for ALL species. Are you saying that the scientists should ahve tested ALL species on the face of the Earth before you would be convinced that all genomes are deteriorating?
No, I'm saying that since you disagree with the whole theory (while citing a paper that supports the theory) YOU should provide the evidence.
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Didn't you just read what I wrote? Do you simply type in whatever pops into your mind!? Do you understand English language? NATURAL SELECTION CAN'T HELP YOU!!!
I can say it because it's true. Even if you disagree.
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Natural selection selects between MORE AND LESS MUTATED! It doesn't select between mutated and non-mutated. Do you understand what that means? It means that EVERY SINGLE INDIVIDUAL on teh palnet is a mutant and has both deleterious and beneficial mutations. So when sellection occures, those that get selected still pass on their deleterious mutations and this is the cause of accumulation of deleterious mutation in populations!
Wrong! Natural selection selects between more and less fit. Those that have deleterious mutations will be less fit (by definition) and thus less likely to pass on their genes. Proportionately deleterious mutations will tend to do less well and beneficial mutations will do better.
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What exactly did I misunderstand?
That the problem is in using the data that you wish to apply Dembski's method to, to generate the specification. Using other data is fine.
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No need to because you are making no sense.
It makes perfect sence if you understand. But you obviously can't be bothered.
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And which method would that be?
Dembski's CSI of course. The method that we are supposedly discussing.
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And I told you that that is not what I meant.
But since you are busy contradicting yourself that doesn't mean much.
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PaulK
Member Posts: 17828 Joined: 01-10-2003 Member Rating: 2.5
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l
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Than what is?
I would think that the structural elements are rather important.
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No it can't. That's why I said that's not important. the flagellum is coded for by a number of genes, regardless of how it is assembled.
And the information content of the genes depends on how THEY formed.
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And we are using those methods. Which others do you think we are using?
I know that you AREN'T following the method of TDI. Your "complexity" calculation has no basis in TDI whatsoever.
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No, I never in my life said that's wrong. Where the hell did I say it's wrong!? Cite me the part where I said that CSI defined in TDI is wrong!
Then why do you keep insisting on using a "complexity" calculation that is NOT accepted by TDI ?
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What? What the hell are you talking about? What is this my "information" you are talking about? You are making absolutely no sense. I already told you the amount of information stays the same.
The way you measure information it DOESN'T necessarily stay the same.
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Dembski's method is correct and relevat. It is your argument from growth that is irrelevant.
You're contradicting yourself again. The fact that flagella grow IS relevant to Dembski's method (since it controls the configuration of the proteins). Ignoring it is going AGAINST Dembski's method.
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What's your point?
My point is that appealing to Dembski does you no good if you keep disagreeing with him all over the place.
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No. I gave the possibility of 20% change, which means 20% of increase in probability of the flagellum forming.
So your ACTUAL specification is "no more than 20% different than the E Coli flagelum" which is an obvious fabrication.
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LOL! Show me one statement in NFL that contradicts any statement in TDI.
I said that YOUR statements disagreed with TDI. I leave it to you to say whether they come from NFL.
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No.
Does NFL agree with TDI or not ? Because neither your use of specification or complexity calculation are sanctioned by TDI.
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No, that would be a designed algorithm. Evolution is supposed to be non-designed.
Actually it is very like a simple hill-climbing algorithm. And we all know that simple things can occur naturally.
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LOOOLOOOOL! I can't believe you said that!!! That just means that natural selection is USELESS!!! And that we need INTELLIGENT INTERVENTION to remove the deleterious mutations from our genomes.
No. If you actually understood what I said you would realise that STOPPING the intelligent intervention that is reducing the effectiveness of natural selection would be enough.
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Why don't you tell me since you seem to be so smart.
Because I'm not going to do you work for you. Especially since you have such difficulty understanding what I say.
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What drugs are you using? I'm the one who gave you the link to that paper. You are the one who is disagreeing witht he paper not me!
The problem is that I'm not disagreeing with the paper at all.
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But you have no evidence for it. Unlike what I showed you. I showed you a paper that has actually done experiments and has shown genetic entropy to casue extinction.
A paper that specifically says that it is working with small populations....
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NO!!!!!!!!!!!!!!!!!! ALL INDIVIDUALS ARE MUTANTS!!!! Which part of ALL INDIVIDUALS ARE MUTANTS do you have hard time of understanding!? Those who are less fit have MORE DELETERIOUS MUTATIONS!
Those who are "fit" ALSO HAVE DELETERIOUS MUTATIONS!!! ALL INDIVIDUALS HAVE DELETERIOUS MUTATIONS!!! And even if you select the fit ones, their deleterious mutations keep spreading through the population.
And you are ignoring recombination. As well as the fact that life seems to keep on going withot succumbing to genetic entropy.
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This isn't even English!? What's your first language?
I think that you mean that it is above your reading grade, since there is nothing wrong with it. Is English YOUR first language ?
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CSI is not a method it's a definition of information.
It is certainly not a definition of information ! Edited by PaulK, : No reason given.
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PaulK
Member Posts: 17828 Joined: 01-10-2003 Member Rating: 2.5
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Re: l
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Structural elements are the proteins which function by the laws of biochemistry. When the structure of proteins gets changed enough their biochemical properties change too. Which leads to loss of biological functions. Which is what Axe's work shows.
So what you are saying is that the actual structure of the flagellum has no relevance beyond it's ability to catalyse chemical reactions.
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Obviously it doesn't. If by chance a word "HOUSE" was formed by droping of ink on a piece of paper, would it's informational content been any different than if the exact same word was written by a person? No obviously not.
Again your failure to understand Dembski's method is obvious. According to TDI the information content of an object is based on the probability of it forming without design. So if you want to know the information content of the genes you have to consider how they might have formed. Or in short, you don't get to ignore explanations just becuase you don't like them or because you can't calculate the probability.
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Than tell em how do we calculate the complexity of an object according to TDI.
Calculate the probabiliy of it forming without design. That's it. (For the flagellum the observed probability of an E Coli bacterium growing one without any sign off a designer stepping in seems to be quite high...)
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But that is simply not true. You just keep saying it.
You don't actually know what TDI says, do you ?
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How does it change? Give me an example.
Your measure of complexity is based on random assembly. So your estimate of, say, the information content of a salt crystal would be very high because of the ordered structure. Your estimate of the information in the sodium and chlorine ions in a pool of salt water, and for the sunlight drying out the pool would be rather lower.
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No becasue the final flagellum is always in the same configuration regardless of if it has grown or assembled in any other way.
Unfortunately for you that means that growth is the MOST relevant explanation since it is the non-design explanation with the highest probabiliy, You might even be able to legitmately ignore all the others (you can certainly ignore random assembly !).
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Explain how exactly am I disagreeing with him.
Haven't I provided enough examples ?
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It's an estimate based on Axe's work.
Like I said, it's a fabrication. Axe didn't even LOOK at flagella, let alone consider the differing possible structures or numbers of proteins they might use. You are explicitly limiting the specification to variations of the E Coli flagellum, using variatiosn of the same 50 proteins. That is NOT the specification you said you were using and it is a clear fabrication.
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Yes, you are. You said that genetic entropy is not a problem for "large" populations.
Here's the first sentence of the abstract:
The accumulation of slightly deleterious mutations in populations leads to the buildup of a genetic load and can cause the extinction of populations of small size
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RECOMBINATION IS JUST SHUFFLING OF ALREADY EXISTING GENES!!!! It doesn't even remove the deleterious ones. It just puts them on another spot in the genome. They still stay where they were.
I guess you disagree with the paper you cite:
...mechanisms such as recombination to ameliorate genetic loads may have been in place early in the history of life.
Of course, understanding recombination might help you...
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LOL! YES IT IS! The full name Is: "Complex Specified Information"! Yes it's a definition of information! Why the hell are you debating me when you are so clueless about the topic!? You don't even know what you're attacking!
And here we see your poor understanding of English. In the real English language the term "Complex Specified Information" would refer to a specific subset of information - that which is "specified" and "complex". It cannot therefore be a definition of information. (And of course, in English you must be able to substitute the definition for the word, so "Complex Specified Information" would be "Complex Specified Complex Specified Complex Specified..." LOL indeed !)
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PaulK
Member Posts: 17828 Joined: 01-10-2003 Member Rating: 2.5
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Re: l
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Relevance to what?
To the functioning of the flagellum in allowing the bacterium to move. Isn't that obvious ? Are you really going to tell me that the whip is catalysing chemical reactions rather than acting as a propellor ?
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That doesn't answer my question. Is teh informational content the same or not?
Actually it does answer your question, if you understood it. The point is that you have to deal with the origins - in fact all the possible origins - to calculate the information. The information is the same - but you can't even calculate it without considering origins.
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And that's what Dembski did. Your point is?
Oh, wait, your point is that it grows. Yeah, I know it grow, and agaon, that's irrelevant because you still need to account for those 50 proteins one way or another. The fact that the flagellum grow is a whole another piece of machinery and a whole lot of new information. So if you think that the probability has increased, it didn't. Because now you have to account for the information that grows the flagellum. Which actually is besides the point.
That is exactly what Dembski FAILED to do, True the information of the genes has to be accounted for, but neither you nor Dembski have made any honest attempt to measure that.
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Which information? CSI? No. Because salt crystals do not have an independently given pattern. They have no specification, therefore they have no CSI.
Utterly, utterly wrong. The cubic shape of a salt crystal and the organised lattice of sodium and chlorine that make it up is a perfect example of a specification. It is the information content that is low, because the probability of slat forming crystals is high.
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LOL! That's like saying that cars are NOT designed becasue they are assembled by machines. Cars are designed and so are the machines that assemble them. The same goes for the flagellum and the machinery that assembles it.
It's Dembski's method, not mine. And of course Dembski is content to allow false negatives in his method so failures of that sort are not significant. And certainly no excuse to change the method in a way that would make it more susceptible to false positives.
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He didn't need to! His woork was on protein in general. We extrapolate this finding on the flagellum becasue it's also made of proteins.
You're right that Axe didn't need to - but you do. And therefore you can\t rely on Axe's work.
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Yes, that mean that smaller populations are more at risk of experiencing the genetic meltdown. If you actually understood what is happening you would know that the same thing goes for any population. But if the population is larger, more time will be needed for the effect to happen. If you disagree, please expalin what is a "large" population, and how can tehy escape genetic meltdown.
Your understanding of the English language fails again. "...can cause the extinction of populations of small size" implies that the risk is only significant to small populations.
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The papers clearly says that it MAY, which means they are assuming, and it says AMELIORATE, which means it reduces, not removes the effect.
In other words they agree with me ! Combine that with the fact that they think that larger populations will NOT be driven to extinction by genetic entropy and we see that your interpretation of the paper is thoroughly at odds what what it actually says.
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I don't care what you say, Dembski defined it as "Complex Specified Information". Because it's complex and specified. Yes, it is a subset of what information is. Because there are a lot of definitions of information.
Go ahead and blame Dembski all you like. It hardly makes ID look good.
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PaulK
Member Posts: 17828 Joined: 01-10-2003 Member Rating: 2.5
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Re: l
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The propellers motion is a subset of catalysing chemicals. How the hell do you think the flagellum get's it's power?
Even if they work by catalysis (and I would want to research that !) the proteins which provide the power are not in the whip.
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Let's go for the third time. Is the informational content the same or not?
If you are having problems understanding my answers, perhaps you should ask for clarification. BEcause there are some important points there.
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Well duuuuh!!!? It's 50 proteins! That is the informational content!
That's not the base 2 log of a probability, so obviously it isn't Dembski's information content.
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What does it specify?
The structure of a salt crystal, obviously ! If you want to know what the specification would be, simply read up n the descriptions of the structure.
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If it has high probability, than that pattern is not attributed to design but to regularity - i.e. natural law.
Almost right - it is because of natural laws that the probability is high. That is you have to include the natural law explanation when measureing the information of salt crystals.
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But in this case Dembski would claim that cars are designed even if they were assembled by machines. Becasue information was needed in the first place to program the machines to construct cars, and to build the machines themselves.
But he can't do it by ignoring the presence of the machines. He has to work on the origins of THAT information. (Which os a No, it means small populations wii die out sooner than large populations. Explain to me why exactly would large populations not die from genetic entropy. WHY?
[/quote] We know for a fact that life has been around for a long time without going extinct, which strongly indicates that it is not so big a problem as you think. Your picture simply illustrates your assumptions. You offer no reason as to why the numbers should come out as you say. Also it seems that you don't even allow for the effects of beneficial mutations to counter the effects of detrimental mutations. Which makes your picture "stupid and illogical". And the numbers are just made up, to (and way too high). The difference between large and small populations is that natural selection is more effective in large populations. (It's statistics, chance effects are always greter in small samples). Natural selection will tend to make detrimental genes less common, and beneficial genes more common (rememebr it is the individuals with the best mix of genes in each generation that contribute most offspring).
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No, they don't. They said genetic recombination will SLOW DOWN genetic entropy, and you said that it will HALT IT. Big difference.
Except that I didn't say that it would halt it.
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Wrong. They never said that.
As I pointed out, they clearly impilid that large populations could not be driven to extinction by genetic entropy.
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I'm not blaming him, I'm blaming you becasue you misrepresent everything.
Except that you DID try to blame Dembski for your own silly mistake. And it certainly isn't my fault that you tried to say that CSI was a definition of information.
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PaulK
Member Posts: 17828 Joined: 01-10-2003 Member Rating: 2.5
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Re: l
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It doesn't matter where they are. They are doing their job soemhow and are providing power to the flagellum.
That doesn't even make sense. The proteins that make up the whip don't have the job of providing power to the flagellum, any more than the blades of a propellor have the job of providing power to the propellor.
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So, what's the answer. Please do clarify.
The answer is that the information content is described by possible origins, not by the structure of the thing itself. Anything with the same set of possible origins, with the same probabilities for each has the same information.
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Than that would be log2p(10^2954) for the whole flagellum. And if we include Axe's work, than we have log2p(10^2363).
Wrong on both counts. Even if you have mathematically calculated the correct probability of the gene sequences forming by pure chance then it still isn't the correct probability even for those genes forming. Nor do you have a valid specification (it's an obvious "fabrication" in Dembksi's terminology). And you've misapplied Axe's figures, too.
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Can you specify that structure without observing the event that forms the structure? If not, than it's not a specification.
Obviously we can. Any regular geometric structure can be described without reference to an object actually having that structure. (Try looking for "face-centred cubic lattice" for a start).
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Yes, and we do. And that is why salt crystals are not designed.
Exactly my point.
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LOL, no, you ASSUME it's been here for a long time. Care to show me any evidence for that? And even if it was. It would just mean that it takes longer for the meltdown to occur.
No, we have evidence that life has been around a long time. You may have heard of fossils. And if meltdown takes that long it isn't much of a problem.
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Name me ONE assumption.
One obviously silly one is that the effects of beneficial mutations can't counter the effects of detrimental mutations. (By definition they can, and often will).
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Which number exactly do you have problems with?
The number of detrimental mutations per generation. It looks way too high.
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LOL! How in God's name would that help you? For God's sake, it doesn't matter if you evolve wings or infra red vision, or you evolve te ability to run 200 km/h, if you are sterile or still born!!!
Obviously those beneficial mutations will be useles if you're dead or you can't pass on your great evolved traits! Please think before you speak!
In other words you are not considering ALL detrimental mutations (which is ANY mutation that reduces fitness) rather you are considering a small subset, so that an accumulation of 30 (or whatever) produces a fitness of zero which cannot be countered by any beneficial mutations. So, you seem to have your own idea of genetic entropy, and you are going to have to significantly reduce the number of detrimental mutations per generation to fit your model to reality. Let us try it more simply. A detrimental mutation is any mutation that reduces fitness. A beneficial mutation i any mutation that increases fitness. (Where "fitness" is defined as reproductive success). Obviously an increase can offset a decrease.
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You see? This is the effect of genetic entropy on you. You can't say anything that has any grounding in reason. Of course they are made up! I even said so at the start. I made them like that to demonstrate how genetic entropy leads to genetic meltdown. Did you expect me to make a picture representing 10.000.000 generations?
If you are talking about what happens in large populations, with lower mutation rates over longer timespans then you are going to have to take account of those things somehow. Saying that you can't put them in your diagram is just a cop-out.
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And the best aprt is, you did not explain how a larger population will fix this. Please do. Make a picture or explan how by increasing the population will you make the genetic entropy go away. Go on, do it, or shut up already.
Actually, I did. In large populations, over a long timescale - especially in sexually reproducing species - we can look at the fate of individual alleles, without worrying too much about the individuals that carry them. Those alleles which cary detrimental mutations will tend to decline and disappear. Those that carry beneficial mutations will tend to spread and replace mutated and unmated versions of the gene. The whole idea of genetic meltdown relies on detrimental mutations accumulating faster than natural selection can remove them. In small populations, because chance effects are more significant this situation is far more likely to occur. In larger problems statistics favour selection over chance.
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Again... SO THE HELL WHAT!?
How does that help you? How does that FULLY STOP genetic entropy? It doesn't! It just slows it down, but it doesn't stop it! Even the best offspring have deleterious mutations and they pass them on to their offspring, and the deleterious mutations still accumulate. Which means that the geentic entropy still exists, and at aslower pace is still leading to a genetic meltdown.
Because natural selection will remove deleterious mutations, genetic entropy will be stopped whenever the rate of removal equals the rate at which new detrimental mutations are introduced to the population. You might like to consider the fact that the best offspring will typically have FEWER deleterious mutations than their parents, for a start. How does that fit with your idea of inevitable accumulation ?
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PaulK
Member Posts: 17828 Joined: 01-10-2003 Member Rating: 2.5
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Re: l
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I never said they do. But the flagellum is powered by something.
Unfortunately you did say that. Remember that you are arguing that ALL of the proteins in the flagellum act as enzymes, and must act as enzymes for the flagellum to work. We're still waiting to see some sensible argument for that - let alone any evidence.
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That's wrong.
OK, so Dembski;s wrong. There goes the whole CSI argument.
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Of course it is, because the structure is what is important.
Dembski says otherwise. The information content is measured by the probability of non-design explanations producing the pattern. (That is how CSI is meant to ELIMINATE non-design explanations, so it is an essential part of Dembski's method).
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No it's not. A fabrication is something that is just read of the event that exhibits a pattern
You just managed to contradict yourself again. Your specfication is directly read off of the E Coli flagellum.
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We can describe a "bi-drectional rotary propeller motor" without looking at the flagellum first. Therefore, it's a specification.
Unfortunately that's not the specification that you are actually using. Rememebr that you have to calculate the probability of ANYTHING matching the specification coming about by non-design processes. Which means that you have to go look at all those other flagella.
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Explain how.
Simple. The figure of 20% change doesn't mean that there is a fixed 20% of the gene that CAN change. Which is what you would calculate if you just multiplied the sequence length by 0.8 (which is what you did). It means that a lot more of the protein CAN change, just so long as the total change isn't more than 20%.
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Than describe the snowflake. What is it's pattern called.
Why, exactly ?
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No, your point is that I was supposed to say that they were designed.
Not exactly. My point was that just calculating the probability of a structure forming without taking into account non-chance processes (which is what you are doing) is wrong and against Dembski's method - using salt crystals of an example. ANd you have agreed with me that you DO have to take into account the regularities that cause salt crystals to form when calculating the information. Now you have to apply that to the flagellum;
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Do fossils come with dates attached to them?
They come with evidence that allows us to work out the dates.
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And again, I ask you, how does the effect of beneficial mutation counter the effect of deleterious mutation when an individual is either sterile or stillborn.
It doesn't., of course. But if you take that approach you are going to have to revise your figures on deleterious mutations downwards to take into account the fact that you are only counting a subset of them.
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And once more, what would ahve changed if I set the rate of mutations to 5 per generation, and the threshold to genetic meltdown to 5000 deleterious mutations. What would change EXCEPT the numbers of generations that would ahve to pass untill teh geentic meltdown occures?
Your estimate of the rate of deleterious mutations appearing would be even sillier.
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The same thing happens as in my diagram. Only in more generations.
Perhaps you would like to provide some evidence for that.
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No they won't. You arte simply asserting this. How would they disappear if the parents pass them on to their offspring.
In asexually reproducing creatures, the lineage dies out, or a new mutation occurs which replaces the deleterious mutation or makes it no longer deleterious or genetic material from elsewhere comes in to do the job. In sexually reproducing species, of course, the mutations are NOT necessarily passed on to the offspring.
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Which is an observed fact.
But ONLY in certain circumstances, and always involving low populations.
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Where is your evidence for that statement?
Basic statistics. Chance variations have less overall effect on large numbers of trials.
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Where is the evidence for that?
Basic arithmetic. Take a number. Add another number to it. THen take away the second number. And you're back with the first number again ! Isn't that amazing !
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No, becasue they inherit their parent's deleterious mutations and add their own.
Wrong. In a sexually reproducing species the average offspring will inherit half of each parent's deleterious mutations. The best offspring will - by definition - inherit less than that. And since they needn't add any of their own then they can easily end up with fewer deleterious mutations than their parents.
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PaulK
Member Posts: 17828 Joined: 01-10-2003 Member Rating: 2.5
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Re: Flaws of ID
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If you are using the book of Genesis then yes. If you are using history itself, the trend for intelligent design is up for sure! We knew nothing about punctuated equilibrium or irreducible complexity or CSI 20, 30, or 40 years ago. The gaps in neo-Darwinism are growing and one of the predictions of ID says those gaps will continue to grow.
Punctuated Equilibria is more than 30 years old. Irreducible complexity (as a prediction of evolutionary theory) is even older. CSI is just a partly-baked idea beset with serious - and likely insurmountable practical problems. The only "use" of it is bluffing the way Smooth Operator is (trying) to do. On the other side we have ID increasingly failing to do what it was originally meant to do (get creationism into schools). It doesn't look so good for ID.
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PaulK
Member Posts: 17828 Joined: 01-10-2003 Member Rating: 2.5
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Re: Flaws of CSI
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We have gone at this before PaulK. Please show me a link of some scientific work which proves CSI has insurmountable practical problems.
Since nobody has ever managed to apply it to a non-trivial case, there musty be some problem. Why hasn't the ID movement come up with a single valid example of CSI in biology in all the years since Dembski published ?
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Information: (this is just one definition) "The attribute inherent in and commiunicated by alternative sequences or arrangements of something that produces specific effects."
Unfortunately that's not the information in CSI.
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I believe the information in crystals is not CSI. It is specified in order to produce a specific effect but since it is "redundant", it is not CSI.
It's specified but low information because the probability of the crystal forming is high.
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So what we are looking for is the "exact" place where information becomes CSI or not? Is this not the problem or the essence of the controversy here? Then again, why should I be that naive to think it boils down to this?
Well you're completely wrong. The biggest problem is calculating the probabilities. Since the information measure is the negative base 2 logarithm of the probability of the specification being met without a designer without those calculations you haven't got anything. ANd nobody knows a sensible way to do those calculatione for any living thing. That's why all we see is bluff, instead of real examples.
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PaulK
Member Posts: 17828 Joined: 01-10-2003 Member Rating: 2.5
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Re: Flaws of CSI
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Dembski applied it to the flagellum. See the following link.
You mean that Dembski completely screwed up his own method. What better proof that it is unusable, if even it's inventor can't even come close to getting it right.
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Am I the only one who consistently gets the impression that you twist things around in certain ways? Do you do it to preserve your fragile viewpoints?
You're not the first person to falsely accuse me. But of course I am twisting nothing, simply reporting the truth.
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In other words, we need to test what the designer would or could have done? Yes, fragile indeed.
Since I never said any such thing it seems that you are the one who is "twisting things around". Perhaps it is your viewpoint that is fragile.
| This message is a reply to: | | | Message 265 by traderdrew, posted 12-22-2009 4:53 PM | | traderdrew has not replied |
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PaulK
Member Posts: 17828 Joined: 01-10-2003 Member Rating: 2.5
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Message 287 of 1273 (540282)
12-23-2009 9:59 AM
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Reply to: Message 286 by Percy
12-23-2009 9:49 AM
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Re: Why the Proposed Connection Between CSI and Intelligence is Bunk
In fact the CSI MAY be different (and probably is) but it isn't so easily calculated. CSI is the probability of the specification being met without design. Simply trying to generate the probability of the sequence forming by simple random assembly is wrong because it lacks a valid specification AND because it ignores other ways in which it could have formed.
| This message is a reply to: | | | Message 286 by Percy, posted 12-23-2009 9:49 AM | | Percy has seen this message but not replied |
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PaulK
Member Posts: 17828 Joined: 01-10-2003 Member Rating: 2.5
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Re: l
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Enzymatic activity is a subset of protein activity. Enzymatic activity depends on teh structure of the proteins. Therefore, if we know what amount of change will affect the catalysis, the same amount will affect whatever the flagellum is doing.
Of course we can't know anything of the sort. Different properties may be tolerant of differing amounts of change.
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Explain why
YOU SAID SO! It is really very simple. If Dembski's measue of information is wrong - and you said that it was - the whole thing falls apart.
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Yes, and that means that you have to measure the informational content that is expressed in the structure you are looking at. Int his case the flagellum
Well obviously to do the calculation you must do the calculation. What we mustn't do is to do a different calculation that will very likely produce an inflated result.
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No, because we have a description called "bidirectional rotary motor-driven propeller", that is independent of the flagellum.
But you aren't using that specification in your calculations. What you are using is based directly on the actual structure of the E Coli flagellum. So it is a fabrication.
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And how exactly are those otehr flagella different than this one? They aren't. That is why we are talking about the same thing.
You're just assuming they aren't different. Why don't you give me a source that actually supports your claim ?
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You said it's a specification. That means that it has an independently given pattern. So go on, describe it,a nd tell me it's pattern.
I didn't say anything about snowflakes. You introduced them to the discussion for no apparent reason demanding that I give a specifciation. Therefore - since the reason is a complete falsehood - I decline.
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No, because there are no regularities in flagellum's formation.
So we are back to assuming that flagella CAN'T grow. Sorry, but you are wrong. There must be regularities underlying the process of growth. Otherwise it would require an intelligent designer individually assembling each one as Dembski proved.
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Really? Show me that evidence.
This is not the place for a detailed discussion of geology. Let's just say that by a numhber of methods (mainly radiometric dating, but others too) geologists have worked out dates for the depoition of many strata.
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Than why the hell did you bring it up int he first place!? Yes, I know it doesn't help you. That's what I've been telling you all along.
Because you forgot to mention that you were only considering a subset of deleterious mutations. When we consider the whole set of deleterious mutations it DOES help, because many disadvantages may be offset by other advantages (this is even true in the case of single mutations, such as sickle-cell).
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If I'm only counting a subset of all deleterious mutations, I would have to increase the number if I wee to take into account all of them.
No. Your estimate is for ALL deleterious mutations, but you ignore a lot of them so you have to reduce the number (which was too high in the first place).
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The rate isn't important. I could ahve picked any number. Nothing would ahve changed.
That is also wrong. Because the slower the rate that dleterious mutations enter the gene pool, the lower the rate of removal that natural selection has to achieve to counter it.
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1+1=2. 1+2=3. Does by your logic 1+3=2, or 1+4=1? No obviously not. The more mutations, the faster the genetic meltdown occures. The larger the population, the slower the genetic meltdown occures. But it's still inevitable. It doesn't matter what numbers you include, the end is the same. Only differnece is how long will it take. A deterministic process has always got the same end result.
In other words, your evidence that deleterious mutations must inevitably accumulate to the point of genetic meltdown is your assumption that such must be the case.
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It's possible that that happens sometimes. But that's not the rule. The rule is that mutations accumulate.
So you keep saying, but simply repeating the claim does not make it true. In fact in a large population rare events will occur, and natural selection can work with those rare events to spread the benefits through the population.
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No, in all circumstances and in all populations
NONE of the papers makes that claim.
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This here model shows that even large populations accumulate slightly deleterious mutations. Which are the worst because they do not get removed by natural selection.
By definition even a slightly deleterious mutation is "visible" to natural selection, and may be removed by it. And, of course, the less deleterious the mutation, the lower it's contribution to genetic meltdown. As for the quote, it simply states that a fragmented population is more like several small populations than one large one. Hardly a surprise - or something that helps your argument.
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No. I'm not talking about statistics. I'm talking about evidence from nature.
Well, if you assume that the whole field of statistics is fundamentally wrong, how about the fact that genetic meltdown of a large population has NEVER been observed ?
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No. It is true that because of sexual recombinations teh offspring will on average inherit only half of their parents mutations. That is true. But they do, and they have to add their own. That is just how it goes. All people have their own mutations.
It seems then that the rate DOES matter. Unless the average is well over 1 it is entirely possible that the The vast majority of which will be neutral. Then there are the benefical mutations. Then there are the deleterious mutations which only carry a normal disadvantage. When we have eliminated all the mutations which your model ignores, how many are left ?
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As you can see here, about 175 (nearly) neutral mutations are introduced in every single person born. And as I said before. These are the worst possible mutations becasue they have such a small effect on fitness that they do nto get selected out. Yet they still destroy genetic information, and sccumulate in the genome.
If they are neutral then they aren't deleterious. By definition.
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PaulK
Member Posts: 17828 Joined: 01-10-2003 Member Rating: 2.5
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Re: l
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We know that if we change enough of the structure, the proteins become worthless in any way.
No, we don't because Axe didn't test for all possible functions. Worse still your claim is that you know HOW MUCH you can change the structure by without even considering what the function is.
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But I never said it was wrong.
I told you what Dembski's measure of information is. You say it's wrong. You want to use a different measure. Seems pretty clear that you are saying that Dembski's measure is wrong.
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A fabrication is when an observed pattern does not match any other pattern.
Wrong. A fabrication can still match other patterns - in fact you demonstrated exactly how to create such a fabrication. Just add a range of variation to the actual event. So long as the pattern cannot be determined independently of the event it is a fabrication.
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And we never did that. I increased the chance of the flagellum forming as much as I could.
That's simply false. You didn't even increase it by enough to allow for the variations in structure that you allowed. There is a big difference between allowing any variation, so long as the result is at least 80% similar, and simply counting only 80% of the protein.
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You are the one who is claiming they are different. And if they are different, they are irrelevant to our discussion.
If you were using the specification of a "bi-directional propellor" then any flagellum that meets that specification is relevant. If it is irrelevant simply for being outside the range of variation that you allow, then it simply proves that you are using a fabrication
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You are the one who brought them up and claimed they have a spcification. Well, what's their specification?
I did not bring snowflakes up, nor did I claim that they had a specification.
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I'm not talking about growth. I'm talking about accounting for the information that is used to build aflagellum. Flagellum's growth does not account for it. Flagellum's growth is the expression of already existing information. What we need to do, is account for how that information comes about in the first place.
Of course BECAUSE flagella grow you cannot use the organisation of the proteins in the flagellum to calculate the complexity - as Dembski does - since that growth relies on regularities. And to calculate the information needed to grow the flagellum you need to calculate the probability of that arising, considering all possible explanations. Which you refuse to do.
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How can I both ignore and include all mutations at the same time?
Oh it's really, really simple. When you want to count how many occur you use all of them, because you want a high number. When you want an excuse for ignoring the possiiblity of beneficial mutations offsetting the effects of deleterious mutations you decide to ignore all those deleterious mutations that CAN be set by beneficial mutations. It's all very transparent.
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Does that completely halt genetic entropy?
If the rate of removal at least exceeds the rate at which new deleterious mutations are introduced then genetic entropy HAS halted. And the lower the rate of deleterious mutations, the easier that is to achieve.
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No, it's math. Math is proof. It's not a assumption. If it's an assumption that 1+1=2, than you're insane.
It is your assumption that 1+1=2 accurately describes the situation.
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Natural selection will work better in larger than in smaller populations. But it will NEVER be perfect. Therefore geentic entropy will always occure.
Since my argument does not require that natural selection be perfect, your conclusion is premature.
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It doesn't have to, you have have common sense to extrapolate. If small populations have more problems with genetic entropy, than larger populations will have less problems. But tell me how does that mean that some populations will have no problems whatsoever with genetic entropy
The papers don't say that large populations simply have less problems. They say only that meltdown sometimes occurs in small populations. Extrapolating that to the idea that large populations are liable to meltdown is simply not justifiable from the text of the papers.
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No. By definition they are effectively neutral. They have such a smalle ffect that natural selection sees them as being neutral.
Of course this is wrong. Because the effect and natural selection "seeing them" are the same thing. You cannot have one without the other
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Becasue there was not enough time!
If we only have theory to go on, then I for one will trust the theories of actual experts over those offered by creationists.
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It matters to what!?!!? To slow down geentic entropy? Yes, it obviously does! That's what I've been saying from the start. But it does not matter to stopping genetic entropy. Becasue to stop it, population would ahve to be infinite in size. Which we know is not true.
You've not proven any such thing.
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Why should we eliminate any mutations? Almost all degrade the genome. Even beneficial ones.
So you are saying that we should use a double standard in counting mutations because in your opinion (an opinion without objective support) all mutations "degrade" the genome in some way you haven't even described. Hardly a scientific attitude.
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NOOOOOOOO!!!. You are clueless about this topic!!!! They are called NEAR NEUTRAL! Or Slightly deleterious. Why? Becasue they have such a small effect on reproduction that they are invisible to natural selection. They are spread around by genetic drift. In other words, by random chance.
On the contrary, it is you who does not understand. To be completely invisible to natural selection a mutation must be absolutely neutral. The most you can say of a nearly neutral mutation is that genetic drift has a larger effect on its spread than natural selection. Of course, in larger populations drift is weaker than in smaller populations. So again we see that population size matters.
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PaulK
Member Posts: 17828 Joined: 01-10-2003 Member Rating: 2.5
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Re: l
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He mutated the Beta lactamase protein to se when will it lose it's function. What other functions does it have except this one?
I don't know. And neither do you. Nor do you know if the mutated versions developed other functions. And the reason that you don't know is that Axe didn't do the tests to find out.
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Whatever you said is not what Dembski said. You can't even tell the difference between the specification and a fabrication, so why would I trst you. I don't believe anything you say. You claim to have read TDI. If you really did, can you give me the definition of spceification, exactly it was written in TDI?
Of course the truth is that we don't disagree on the definition of a specification. You know as well as I do that the specification that you are using is a fabrication since it's main basis is the actual event. Since I am away from home without my copy of TDI I cannot give exact quotes at present. But since the definition is not a point of contention that hardly matters.
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How can it be wrong? Dembski himslef said it that way?
Dembski says that a pattern has to be definable independantly of the actual event. His seperability criterion. Your "specifcation" is not and cannot be defined independantly of the event. Thus it is not a valid specification.
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I increased the chance by 20%, what more was I supposed to do?
fortunately your attempt was not THAT bad, but it still grossly overestimated the complexity. What you need to do is to work out how many sequences are no more than 20% different.
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They are irrelevant because of the difference in their complexity. We are than dealing with totally different machines. Which have more or less CSI. If they have the same complxity, than calcualting flagellums CSI is the same as calcualting their CSI.
In other words they are irrelevant because you are NOT using the specification of a "bi-directional propellor". So that specification (which is valid by Dembski's criterion) is also irrelevant. It's introduction is nothing more than an attempt to pretend to be following Dembski's method - because you know that you are using a fabrication.
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Than what did you bring up? Salt crystals, that's the same.
We discussed the specification of a salt crystal. If you want to claim that snowflakes are the same, that's your claim. I don't have to support anything you say.
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We are setting aside that now. You see that doesn't help you. Becasue of two reasons. First is that growth does not create information itself. It only unpacks the already existing information. So yes, we do have to calculate the whole structure when it's funished. And second, you would have to account for the information of the growth information and mechanisms. Which means that this reduces teh probability of the flagellum nd the growth mechanism arising without design. This goes totally against your claim.
The second point IS my claim. It help me because it shows that what you SHOULD be attempting to do is to apply Dembski's method to the mechanisms underlying the growth of the flagellum - instead of doing completely the wrong calculation on the flagellum structure or the genes.
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As I just said above, This does not help you in any possible way. This would just increase the amount of information, and decrease the chance.
If you can't work out why the fact that you are going against Dembski's method helps me, then you would have to be very stupid.
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You don't get it. I'm not saying that two deleterious mutations may not act as a beneficial, unlike where one deleterious mutation would just be deleterious. I'm saying that that does not help you because that still leads to degradation of genetic information in the genome, which leads to genetic entropy.
Of course you are writing complete nonsense. The question is whether a reduction in fitness in one respect may be offset by an increase in fitness in some other respect. Obviously it is possible for that to occur.
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Completely WRONG! This is why you fail to understand what genetic entropy is, and how it works. Genetic entropy is NOT about beneficial VS deleterious mutations! It's about accumulation of ANY mutations.Beneficial mutations still degrade genetic information and cause genetic entropy.
Your assertion that beneficial mutations lead to genetic meltdown and extinction is just your opinion. YOu won't find it in any scientific study. And of course, the fact that the comment you were responding to did not even mention beneficial mutations. Instead it talked about the REMOVAL of deleterious mutations which would obviously act against accumulation.
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Yes it does. Becasue if mutations can't be eliminated 100%, they will logically accumulate!
Of course that's wrong. To prevent accumulation all that is required is that the rate of removal equals the rate of entry. Natural selection simply needs to be efficient enough that the balance point is reached before genetic meltdown occurs.
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Look at this picture. This is from a paper by Motoo Kimura. He has shown that some mutations are nearly neutral. They are in the shaded area. They have such a small effect on fitness that they do not get selected, and they keep accumulation in the population.
I have already answered that point. By definition the effect on fitness is the same as the force of selection against the mutation. Complete invisibility to selection is complete neutrality. The fact that selection against them is weak means that many will accumulate before the balance point is reached. However, because the effect on fitness is equally weak that is not necessarily a problem - a population can tolerate many without suffering a major loss of fitness.
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In otehr words, you already made up your mind and you don't care what anyone who des not agree with you has to say...
No. It means that I trust the opinion of people who know what they are talking over the opinion of people who don't - and don't care.
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PaulK
Member Posts: 17828 Joined: 01-10-2003 Member Rating: 2.5
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Re: l
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It ws totally useless. It didn't do anyting. If it did, that we would have seen some changes.
How exactly can you "see" functions without testing for them ?
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Use google.books. You have the TDI and NFL there.
Even if that is true it doesn't change the fact that we aren't arguing over the definition. You just refuse to apply it.
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Than expalin to me me what is my specification. How is this "my" specification different than Dembski's?
Of course you haven't bothered to actually give your specification. All I know is that it includes either the protein or the gene sequences for the 50 proteins in the E Coli flagellum, modified by a factor that is supposed tollow for the 20% variation allowed by Axe.
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What is that supposed to mean?
It mean that you have to calculate the number of sequences that are no more than 20% different from each of the 50 proteins or genes (whichever Axe used) that make up the E Coli flagellum. Or you could do the sensible thing and give up - because even if you include the correct factor the whole calculation doesn't do you any good anyway.
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Yes, I am using that specification. I clearly pointed out to you that the differenceis in the complexity. If there is some other flagellum composed of more or of less proteins, than it's adifferent amount of CSI
You are wrong again. If TDI really is on google books you ought to read and understand it. Then you might not keep making so many mistakes. Or maybe not, because you will find sections of it harder to read than anything I've written. Anyway, you can't have CSI without a specification. The information content belongs to the specification not the particular event. So if the only valid specification you have includes both flagella - as is the case - then the only CSI you have is the same for each.
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Yes, tehy are the same. Both are produced by natural laws. Both have no specification, both are not designed.
Salt crystals DON'T have the form of a face-centred cubic lattice ? This will be news to a lot of crystallographers.
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No, that's a side event. That is a totally different event. That even does NOT account for the origin of flagellum's information. It only account for the expression of that inforamtion. It's origin is somewhere else.
So we have to go to the origins of the origins of the mechanisms that grow the flagellum now ? That's OK by me. Produce your specification and get calculating.
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How am I going against his method?
By not using a valid specification, nor taking all possible explanations into account. Both are mandatory in TDI.
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NO IT'S A FCAT! I just gave you an example! Sickle cell is a BENEFICIAL mutation! Yet id degrades the information in the genome by making red blood cells less efficient!
One example - especially where the beneficial nature of the mutation is highly qualified - is not sufficient to prove a universal claim. Especially when the claim itself is so vague and wooly.
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You answered it, but you were wrong! Natural selection is not perfect. It is affected by noise. By non-hereditary noise. Which increases genetic drift. Therefore, mutations that are nearly neutral, meaning slightly deleterious are still invisible to natural seelction.
The only way that the can be truly invisible is to have no effect. That is a simple fact. By definition any deleterious mutation reduces fitness. By definition lower fitness means that the average number of offspring will be lower. And lower fitness individuals producing fewer offspring IS natural selection.
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The graph shows just that. If you disagree with it, show me the one that agrees with you.
The graph shows no such thing. All it shows is that there are many more nearly neutral mutations then strongly deleterious mutations. That doesn't contradict my views in the slightest. In fact it's exactly what I predicted.
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So you do not trust Motoo Kimura, becasue he is ignorant and he doesn't care?
At the present time I have no reason to think that Motoo Kimura agrees with your ideas of genetic entropy. If you could produce a genuine quotation which showed that he did I would take the idea a lot more seriously.
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