Are mutations enough to explain natural selection?

I had some spare time this afternoon and wanted to address Eximus’ post. Frankly the responses Eximius received were completely bogus.

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But surely most mutations (apart from the odd useful macromutation) wouldn't help an organism so much that it increases its chances of survival or reproduction.

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The vast majority of mutations fall in this category.We’ve debated here many times whether or not there are any mutations that add new, useful information to a population. Evolutionists struggle to provide examples, and of those provided I have yet to see a provocative one. Yet there should be a myriad of water-tight examples for evolution to be true.

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For example, if a mutation gave a bird a slightly longer wingspan, the bird might fly more efficiently and catch more food, but does this ensure that the gene for long wing is passed on more than the gene for short wing? A bird that caught 9 fish a day would probably reproduce just as much as a bird that caught 10 fish a day.

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This is a good point.

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Gzus: Sure, the bird that caught 9 fish would survive just as the bird that caught 10, but that's a positive step. the important fact is that 'bird 10' survives, hence his mutated gene survives. he breeds with the other birds until the gene becomes common among the population.

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This is simply nonsense. You start by agreeing with Eximius that there is no selective value, then you turn around and say there *is* selective value!

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Gzus: The important fact is that 'bird 10' survives, hence his mutated gene survives. he breeds with the other birds until the gene becomes common among the population.

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Again, this is nonsense, followed by this nonsense:

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Coragyps: If that one-meter-further flight resulted in 0.01% more of the possums that could do it surviving to breed, the trait (assuming it's heritable, of course) would take over surprisingly soon.

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First, if the mutation is neutral (which part of Gzus agrees is ) then the odds it survives and fixates in a population is equal to its initial frequency, according to evolutionists. So in a population of 100,000, the odds are 1 in 100,000 it will survive and fix. You both act as if it’s unity.What if it does have a selective value? Evolutionists typically consider the odds of a beneficial mutation surviving to be 1 in 50. This is an underestimate because this assumes an atypically high selective value of .1 (Gaylord Simpson believes the average positive selection value is .01). Using the more reasonable selective value the odds are 1 in 500.But that is not the only problem. The rate at which a mutation can fix in a population is governed by its capacity for reproduction. Using all kinds of favorable assumptions, the renowned evolutionist Haldane showed that in vertebrates, at most just 1 beneficial mutation could fixate in a population once every 300 generations! The only way to reduce this number is to increase the selective value, but when you do this the burden on reproductive capacity increases! Haldane showed you had to keep the selective value low to prevent species extinction.Where does all this lead? To one inescapable conclusion: Evolution is one big fairytale. Sources:
Theoretical Aspects of Population Genetics, Kimura & Ohta, 1971, p 3
Evolutionary Genetics, Maynard Smith, 1989, p 161-162
Evolutionary Biology, Douglas Futuyma, 1998, p 298
Haldane, The Cost of Natural Selection, 1957, p 520-521

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Zhimbo: Are you telling me that the %chance of an organism successfully passing on a new neutral mutation is inversely proportional to the population size?

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No. I’m talking about the probability the mutation (or allele) survives and becomes fixed in the population.

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Zhimbo: While "unity" is certainly too high, just how did you get the 1/100,000 figure? Actually, I know how you calculated it -it's the inverse of the population size - but why do you think this calculation is valid? You have sources at the end of your post, so I assume you got this from one of them...care to elaborate?

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It’s a standard pop genetics equation. Fixation probability = initial frequency of allele (see Futuyma, p 300). If there are 100,000 organisms in a population, a new single mutation has a frequency of 1 in 100,000. This also is its odds of reaching 100% frequency over time.

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Originally posted by Fred Williams:
The only way to reduce this number is to increase the selective value, but when you do this the burden on reproductive capacity increases!
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That's what I don't understand. Please help me out.
I apologise if this seems like a stupid question because it's obvious that most of the people on this forum have a greater understanding of this than me but I really want to understand how this works.

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It’s definitely not a stupid question. There is much to the answer, but I will try to give an abridged response. Imagine a mutation that is so vastly beneficial, its selective value is so high, that most of the population without it dies within a few generations. The surviving positive mutant begins to spread through the population, and the population begins to grow back to its initial size. The rate at which the population can return to its initial size is primarily governed by the number of offspring the organisms can produce per generation. Thus, there are a certain number of deaths per generation that must occur to remove those organisms without the mutation. These deaths need to be replenished. How fast they can be replenished depends on the reproductive capacity of the organism. Much of that capacity has to pay for normal genetic deaths, while some excess is available to move the new positive mutation through the population over time. Even some receiving the advantageous mutation will die and need to be paid for (even though they are superior, they may still get hit by a rock, fall off a cliff, be a stuck up prude and not reproduce, get nailed with kryptonite, etc). ALL genetic deaths must be paid for and replinished by new offspring.Conceptually speaking I hope you can now see why increasing the intensity of selection directly impacts the reproductive capacity and its ability to replinish and pay for the deaths.Haldane showed that fitness is roughly e^(-30n^-1), where n is number of generations, and intensity of selection was roughly I = 30n^-1. As you can see, as intensity increases n decreases. This means fewer generations are available to pay the cost, putting a greater burden on reproductive capacity.If you are really interested in this, you should go to a university library and get Haldane’s paper. I would also recommend Walter Remine’s book the Biotic Message, as he dedicates two chapters to this, plus a detailed appendix. Here is a good online discussion of this that covers some of the ground:http://www.bearfabrique.org/Evolution/reminevictoryAlso, my mutation rate article that thumps the notion of man/simian ancestry also deals with this issue: 404 Not Found

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And thus, genetic redundancies defy evolutionism.

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It's a double-edged sword. Your evidence clearly shows selection did not produce the redunancies. Furthermore, such redundancy cries out design!In my field of work, harldy anyone buys non-redundant products anymore because reliability and up-time is so important. More than 90% of our directors are sold with fully redundant components (http://www.mcdata.com).FYI, redundancy is not achieved via simple design, it at least triples the complexity required to make it work.

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Originally posted by schrafinator:
Of course, one doesn't need any knowledge of DNA to understand that evolution occurs.

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LOL!Translation: "Don't bother me with the facts, I've already made up my mind!"

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We've asked here many times for creationists to explain to all us wrong-headed evos how, exactly, we should find these information-adding mutations, should they exist. And have received not a single answer.

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I see your memory is failing you again. I did provide a criteria, you and several others submitted examples. The examples were either bogus or not provocative. I recall your example fell in the bogus category.

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Me: This is an underestimate because this assumes an atypically high selective value of .1 (Gaylord Simpson believes the average positive selection value is .01). Using the more reasonable selective value the odds are 1 in 500.

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Page: Please explain to us all how, exactly, this is an overestimate. Please provide the relevant and up to date documentation as well. Simple assertions do not suffice. By the way - GG Simpson was a paleontologist who died in 1984.

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I provided the opinion of an evolution in far greater standing than you (well, I guess he isn't "standing" anymore).You are the one who believes in the fairytale, so provide evidence that .1 is a typical selective value for new beneficial mutations. Good luck!

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Please explain - with supporting documentation, of course - that Haldane used "all kinds of favorable assumptions." Your mentor, ReMine, made the same claim (which you are obviously just parroting). He was repeatedly and directly asked to justify this claim.

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I thought you said you finally read his book. I guess not.Favorable assumptions include 1) assuming single gene traits (ie ignoring the impact of quantitative traits), 2) assuming beneficial mutation is always dominant

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Perhaps you can carry the torch for Walter and finally provide an explanation for this assertion.
Thanks.

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Perhaps you should really read his book next time, instead of saying you did.

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In other words, the '1667 substitutions' case is a worst case scenario: 1667 is the number of substitutions that could occur in genes which, in their effect on the genotype, are independent (a condition which is not often met in nature).
I'll post more on this when I have more time...

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Interesting. I will be very curious to see this, since I know that multi-gene traits make the 1667 number worse. It is good you do occasionally provide something useful to this debate. Perhaps this will be another complete backfire like that Wu paper you cited!

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I was not aware that a population's goal would be to return to its original size.

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I never claimed it was a goal. It's a quite reasonable baseline when considering a population's fitness. Also, as big a problem large populations pose for evolution, it's in an even worse conundrum in small populations because genetic drift will move the far more common deleterious mutations to fixation at a greater clip. Savvy?

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Actually, increasing the selective value would have no impact on the reproductive capacity of the organism at all.

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This shows what little you really know about Haldane's Dilemma. Where is Haldane, a pop geneticist in high regard, wrong, and you right? Like you love to often say, "simple assertions" don't mean dit.

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What happens if we start out with a population of 100,000, a neutral mutation occurs, spreads to, say, 5% of the population, and then an environmental shift occurs, making that previously neutral mutation selectively beneficial. After the elimination of those lacking the mutation, the resulting 5000 member population occupies a new niche.

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As mentioned earlier, the problem becomes even greater for the evolutionist fairytale lover, because small populations mean those new harmful mutations that enter the scene at a far greater clip than beneficial ones will now have an increased probability to fix in the population due to genetic drift. For those siphoned by selection, new offspring are needed to replace them. Thus, an increased burden on reproductive capacity. That is why Haldane assumed a large population. Small ones don't work. You'll de-evolve from a snail to a pile of dirt real quick!

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So, in a large population, the chance for any INDIVIDUAL mutation to fixate becomes small, but there MORE mutations available per generation.
So...what's the problem?

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Several. Haldane’s estimate of 1 beneficial mutation per 300 generations is an average over the entire population.Also, for every new beneficial mutation, there is going to be some greater number of new harmful mutations. So if you crank up the mutation rate, you also crank up the genetic load which keeps you from moving forward (it likely will lead to deterioration). Evolutionists have to assume fanciful tales of extremely efficient, almost omniscient, selection to cull the tide of harmful mutations.

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You don't have a problem with my analysis of the increase of genetic variability through the accumulation of neutral mutations, then.

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I would disagree with your wording of this. Neutral mutations don’t increase *variability*, the variability is already present. Only if the neutral mutation is a gene duplication could one suggest *variability* increased per se, but you and I know that is not what you were referring to. I would say *any* kind of mutation that becomes established will increase genetic *diversity* of a population.

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Haldane did NOT estimate the rate of beneficial mutations to be 1 in 300 generations; rather - unless you're referring to some other 300 generation estimate - that's the time for a SUBSTITUTION of a gene that becomes disadvantageous (e.g. due to an environmental change).

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No it isn’t. I have the paper right in front of me. See pg 514, 4th paragraph.

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Also, I'm not sure what specific point you're making with this conservative estimate of beneficial mutations, anyway.

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Because life cannot be the result of evolution of neutral traits. Beneficial mutations are absolutely essential and you need tons of them. Of course evolutionists of late have been avoiding this by acting as if they are not part of, or required by, their theory. It’s frankly pretty silly!

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Speciation, for example, only requires neutral mutations (or other genetic change).

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Speciation is a subjective term, and it does not require neutral mutations. Regardless, speciation has long been part of the creation model so it doesn’t really aid your argument.

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I wasn't aware that selection against harmful mutations was controversial; even creationists usually grant this.

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Yes, in fact a creationist [Blythe] came up with natural selection before Darwin did. Selection is primarily a conservation mechanism.

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Perhaps you could point out an example of what you're talking about when you talk about "tales of ... almost omniscient" selection. I mean, in the scientific literature, presumably population genetics.

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No problem. Do a search on truncation selection. The only time this fairytale is brought up is to deal with the cost of harmful mutations. Otherwise no one would dare suggest such a kooky mechanism. See my article: 404 Not Found

Scott, I will say you are consistently reliable in giving the audience a good dose of irony!In your virtually content-less post, you write: You are a real broken record.The point I made was entirely on topic, and entirely valid. You, on the otherhand, repeated many of your old tired standbys that have nothing to do with the debate, ones you always bring in when you can’t rebut my arguments. I counted no less than 5 this time. Very good! Here they are:1) Perhaps the same ones that "informed evos" use to remove SNPs from single sequences prior to performing phylogenetic analyses? (going on 2 years old)
2) If he isn't deleting guestbook posts, he is engaging in these false witness claims (6 months old)
3) Oh - inability to support your claims noted, Moderator 3 (almost 1 year old)
4) the Rice et al. paper - you remember, the one that you accused the authors of dishonesty (almost 1 year old)
5) He can also use oil of Hyssop with its "50% antibacterial" (I dunno, 5 months old?)LOL!Speaking of the Rice paper, don’t you remember I already refuted their misleading claims?
404 Not Found OK, now to your one substantive question in that otherwise entirely worthless post:

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Me: I will be very curious to see this, since I know that multi-gene traits make the 1667 number worse.

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Page: You know this, do you? Amazing. How about explaining it all to us?

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Sure, my young apprentice. Say a new beneficial mutation occurs that impacts a quantitative trait. Say this trait is controlled by 5 genes. In order for one offspring to inherit the precise combination of genes, 2^5 offspring would be needed. That’s 32, for my math-deficient young apprentice. Normally, the reproductive barrier is already a burdensome 50%. But this makes the hurdle 97%!Now granted this is worse case. In my example, the beneficial mutation may work well with a combination of the other 4 genes. But surely there are going to be combinations where the phenotypic expression is not going to be recognizable by natural selection. So the actual barrier falls somewhere between 50% and 97% in the example I gave above. Since Haldane is assuming sing-trait genes, he is assuming 50% all of the time. This is clearly a favorable assumption for his model.Savvy?

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Page: But it is strange that the only person that seems to think that a demonstration of a principle of sexual recombination/evolution in a laboratory environment is "misleading" is a creationist electrical engineer.

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Of course you know I did not say the above was misleading. What I said is misleading is their claim that recombination is an advantage to evolution:

The author’s conclusion essentially is that beneficial mutations have a better chance of fixation in a sexual species over an asexual species, because the high level of harmful mutations in an asexual species wreak greater havoc than they do in a sexual species. If there were not such a powerful current of harmful to slightly harmful mutations at work, then beneficial mutations would clearly proliferate more easily in an asexual species. But the authors fail to emphasize this fact, so the reader can easily be left with the impression that recombination is an advantage to evolution (as happened to Dr Page). It is NOT per se an advantage to evolution. It is only an advantage when contrasted to asexual reproduction in a harmful mutation environment. Recombination remains an "enigma" to evolution.

Link: 404 Not Found

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Fred Hoyle wrote in his last book that 'Haldane's dilemma' is "an illusion."

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What is it about Hoyle’s argument that convinces you it’s an illusion?

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You say:
"In order for one offspring to inherit the precise combination of genes, 2^5 offspring would be needed. That’s 32..."
emphases mine.
Please explain - dumb it down for us non-math folk - how it will take 31 other offspring to provide one with the 'right' combination.

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Say daddy has 5 genes that contribute to a trait: A, B, C, D, E. Mommy has a different gene version at each respective locus: A`, B`, C`, D`, and E`. Say some phenotype is advantageous with the combination A, B`, C`, D, E. The odds of getting A with the first offspring is .5. The odds of getting A & B` is .5 x .5 = .25 (1 in 4), The odds of getting A, B`, C` is .5 x .5 x .5 = .125 (1 in 8), etc. To get 5 is 2^5 or 1 in 32. So on average one out of every 32 offspring will inherit the precise combination (thus 32 offspring are needed to have an even chance).

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I heard on the news the other day that the odds of winning the powerball lottery here is something like 1 in 165 million (or something like that). Yet somebody won.

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This is a meaningless statement. It appears you are headed directly toward a very common fallacy in statistics. See the Fallacies & Traps chapter in Forgotten Statistics (or any other stats book that covers the traps).

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As Williams the elctrical engineer creationist 'explains' it, it sounds an awful lot like he thinks that 31 non-beneficient 'offspring' will have to be born for the 32nd to possess the desired mutant.
That makes no sense whatsoever to me, and it should make no sense to anyone else.
Each conception is an independant event. Therefore, assuming Williams numbers are correct (there is little reason to do so, based on his past performances) each conceptus has a 1 in 32 chance of possessing the mutant.
Now, that could very well be the first born, could it not?

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It could, but the average hurdle is nevertheless 1 in 32 (as opposed to 1 in 2 to inherit a trait controlled by a single mutated gene). Thus, for species that do not commonly produce 32+offspring, the already low frequency of beneficial mutations is reduced further since most new beneficial mutations will never even make it to the 2nd generation.Multigene families are common and probably average more than 5 genes. This would have a major impact on Haldane’s cost, and in turn makes the 1 in 300 substitution rate unrealistically too high.

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And is offset by his ocnstant population size requirement, which you conveniently have decided not to duscuss anymore.

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I’d love to duscuss (sic) it, I have stated that it is at worst a favorable assumption and at best a NULL assumption. If you think a shifting population size somehow lessens the substitution rate, I’d love to hear how.

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Hmm - didn't Haldane offer several models for different types of alleles, such as recessives and such? Why, yes - yes he did!

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What’s your point? The cost to fix recessives is exponentially higher!

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But surely, you remember the FGF-3 receptor gene?
Surely you have heard of the HOX genes and other developmental regulatory genes?
Genes whose expression during development influences and/or directs morphological development?
How do they fit in?

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Very badly. My understanding is that copying errors to HOX genes are far more likely to cause harm than copy errors to non-HOX genes. Thus, the cost required to pay for lethals increases (more offspring to account for these genetic deaths), increasing the overall substitution rate. Methinks you are attempting a red herring?

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Surely you must know that many if not most evolutionary biologists now consider these genes to be much more important than genes that control or influence single traits?

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Exactly my point. And don’t call me Surely.

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Haven't read it. Have you?

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Yep. But it is not an easy read. If you check it out you will see what I mean. It will take some digging to really begin to understand where he is going. I just haven't had the time because it would be a significant effort (ie dusting off Calc 3 and Diff Equation books). Maynard Smith is an evolutionist who has gone through it and admits it is not convincing. The one thing I recall is that Hoyle estimated the rate would be more like 10 generations instead of 300.

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You do not seem to realize that conceptions are independant events.

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Yes. I also realize you are equivocating/hairsplitting again. Your comment about the lottery already clued me in you were heading to a big, black, fallacy hole. To your defense it is an *extremely* common fallacy. My point remains that the reproductive hurdle goes from 50% to somewhere between 50 and 97% (using my example). Haldane assumes 50%. A very favorable assumption for his model, one that we have learned in the years since his model is grossly unrealistic.

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...you had me convinced at one point that you actually knew what you were talking about.

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I did? When?

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Do you have any clue what a multi-gene family is?

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Yes. I meant multi-gene (quantitative) traits, as I wrote several times earlier. I "miswrote" when I said "family" in my latest post. Perhaps you will save this "gaffe" in your "Williams" file? I suspect I have "multi-family" on the brain from reading all those posts between you and Peter, you know, the ones where you are taking one devastatingly severe whoopin'!

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100,000 starting pop.
5% have a beneficial mutant after origination and drift.
Environemtal shift occurs.
5,000 are left, all those with the beneficial allele.
New population size of 5000.
Cost already paid.
Savvy?

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I can't count the times this has been shown to be bogus. Small populations will invariably reduce the fitness of the species because genetic drift works against selection. That is, the spread of mutations is driven by randomness and not selection, and thus the far more prevalent deleterious mutations will spread more than they would in a much larger population where selection can work. Do you seriously think reducing fitness is good for evolution. Don't feel bad, you are not alone. Many on this board and elsewhere have implied the same thing! Doesn't it get tiring defending the indefensible? "Alice really did see a rabbit, doggonit!"

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I am planning (again) to wind down my 'net activity.

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Yea, right, when have I heard this before! Actually, I do say this in good humor. I don't know how many times I've told myself to "wind down my net activity", only to find myself back on the boards a couple weeks later. Good luck on your attempt, maybe you will be more successful than I.

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Your "equivocating/hairsplitting" charge is a given.

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There is a reason it’s a given. 32 offspring are needed to have an even chance means precisely that. An even chance means 50%. Not 0, not 100%. It follows that 1 offspring yields a 1 in 32 chance, which means there is a chance, and it could be the first offspring. I never said otherwise. In fact, my context has always been that the hurdle worst case is 97%, not 100%. Normally, resorting to such trivial hairsplitting is a clear sign the person engaging in it cannot defend his position, so I am only too pleased to point it out when my opponent engages in it.

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You imply that your "worst case scenario" is more realistic than Haldane's model

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Again, I implied no such thing. In fact I made it clear the multi-gene problem makes the reproduction hurdle lie somewhere between 50 & 97% (in the example I gave). If I had focused on the worst case scenario I would have stuck with 97%, instead of 50-97%. As a reminder, Haldane assumed a hard 50%. We now know that multi-gene traits makes this number higher (by how much we do not know).

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You are misrepresenting my scenario. It starts out as a large population. The selection has already taken place. That is why there are now only 5000 individuals instead of 100,000. Savvy?

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No I’m not. If the selection has already taken place, it means the selection was very intense. This means reduced fitness, which you later admit is not good for evolution. So, you use a mechanism you admit is bad for evolution as a solution for something that is bad for evolution! Man, it’s got to be real frustrating defending such a vacuous fairytale. No wonder you want to cut back your internet time.

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Me: That is, the spread of mutations is driven by randomness and not selection, and thus the far more prevalent deleterious mutations will spread more than they would in a much larger population where selection can work.

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Good thing that sexual recombination works to counter that...

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Yes, it sure does. No creationist disputes this. What we claim (and many evolutionists realize) is that recombination is an enigma for evolution. Recombination merely serves to retard de-evolution. Even Rice showed this, but he tried to pull a fast one by extrapolating this to mean that recombination is an advantage for evolution (even though he also admitted it was an enigma!). He seemed to only fool evolutionists with that sleight-of-hand. If I were you I’d be mad that he snagged you hook, line, and sinker with that illusion. You write: it does get tiring having to read the illinformed (and disinformed) pontificate on matters that they have no business doing so on. I pontificate because it flabbergasts me that you refuse to see that the Rice paper, or specifically your continual reference to it as showing some positive force or advantage for evolution, is utterly bogus beyond words. I am glad you dropped the Wu paper, but as you continue to insist the Rice paper has something to offer evolution, I will continue to point out it has nothing to offer evolution (except for the reminder of the bad news, that recombination is an enigma that actually is counter-evolution). Why don’t you tell us what evidence Rice has uncovered that shows recombination is an advantage for evolution? As I pointed out in our debate, Rice merely showed recombination is an advantage only when contrasting sexual organisms to asexual organisms when harmful mutation rates are high (hardly an advantage to evolution).

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all the while claiming that those that don't agree are inferior somehow.

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I made no such claim. Being wrong on something does not make one inferior.

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Bye, Fred. Hopefully for a long time...

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I’ve never known you to go without giving the last word. What if I keep responding? PS. I'm not positive, but I recall Hoyle also assumed a large, cosntant population size. If I remember I'll check it tonight (the book is at home).

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Peter: P.Borger means 'unused' or 'non-functional' when he says redundant.
PB: PB stated several times that redundant genes are functional openreading frames,
Peter: Apologies for the mis-definition ... all I was trying to do
was point out to Fred that his use of redundant was not
the same as yours ... which still stands.

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I was not giving a definition of redundancy, I was simply pointing out that redundancy cries out design. Regardless, the redundancy I deal with is actually similar to genetic redundancies in that both are functional, and 100% operation is achieved even after knocking one out.If redundancies originated via an NDT process, we would not expect to see similar levels of constraint in the redundant gene as in their corresponding peer. Peter has shown that these redundant genes are equally constrained or nearly so with their corresponding peer (ie not associated with higher rate of change), which is very compelling evidence against NDT and very compelling evidence for intelligent design. As Peter pointed out, you guys need a new paradigm!