Annoying creationists

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kleinman said:
Only an evolutionist would think it is arrogant to show how mutation and selection works in reality.
Only a creationist would be arrogant enough to believe that he is the only person alive who knows how mutation and selection actually works.
kleinman said:
I’ve never said that selection intensity does not affect the evolutionary process. In fact I have said the exact opposite and posted citations which show this. If you want to accelerate evolution such as done in the laboratory to identify the mutations that appear in a population from a particular drug, you use a sub-lethal concentration of the drug and increase the concentration until you obtain a resistant population. But nothing affects the evolutionary process as does the number of selection conditions. That is the dominant parameter in the mathematics of mutation and selection. Reality reflects this fact as well. So, barrister, you don’t have the science, mathematical or empirical data to support your claim. What do you have left to argue with?
Logic, and that's all I need!

Your comments above suggest that if we conduct an experiment with one very strong therapeutic drug, and an infinity of other drugs administered in homeopathic quantities, that the evolutionary result will be "profoundly slow," to use your expression. But if we conduct the same experiment with one very strong drug and no other drugs, then the evolutionary result will be accelerated to the maximum possible.

Or to put it in mathematical terms: what is the intensity multiplier value that must accompany each selective pressure, that you contend is "the dominant parameter in the mathematics of mutation and selection?"

The above is what everyone here is concluding from your posts, so if the above is not representative of your position, now is your opportunity to explain exactly how selective a pressure must be, relative to any other selective pressure found in the same environment, before that pressure contributes to the "confounding" of the evolutionary process.
 
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That's a very interesting link that concludes pretty much what I've said for some time: ignorance breeds confidence.

I dunno, seems like it may be a horse & cart/chicken & egg situation. I mean, are they overconfident becauase of their ignorance? Or, are they ignorant because they are prone to overconfidence, and assume they don't need to learn?

Or perhaps it's more like a snake eating it's own tail: they're overconfident so don't learn, which increase their ignorance, which makes them more confident, which convinces them they don't need to learn...

I think this study needs to be extended a bit :)
 
I dunno, seems like it may be a horse & cart/chicken & egg situation. I mean, are they overconfident becauase of their ignorance? Or, are they ignorant because they are prone to overconfidence, and assume they don't need to learn?

Or perhaps it's more like a snake eating it's own tail: they're overconfident so don't learn, which increase their ignorance, which makes them more confident, which convinces them they don't need to learn...

I think this study needs to be extended a bit :)
No, I'm confident that we know all there is to know about it.....oh crud.:p
 
To quote Huxley's remark on Darwinism: "How extraordinarily stupid of me not to have thought of that."

But can you explain it to kleinman?


Yes and no.

Normally I'm very good at explaining all kinds of things to all kinds of people. This is partly due, I think, to my association with developmentally disabled people, some of whom I've known since my own early childhood -- that is, for more than 40 years. This calls for an unusual combination of patience and creativity. If I've explained something 100 different ways, and they still don't get it, I'll try my damndest to come up with way 101. Given creativity without patience, one would likely give up too soon. Given patience without creativity, one can only repeat the same explanations that didn't work before.

I have managed (mostly in the original EvolutionIsDead thread) to explain a few things to Alan, including a little bit about what probabilities are (and hence, why they cannot exceed 1). My track record is better than most on that score.

The problem is, my explanations, however creative and patient, can do no good if Alan does not pay attention to them. Getting a point across to someone with, for instance, Down's Syndrome, one might encounter stubbornness, hostility, confusion, and prejudice comparable to or far in excess of Alan's. But in the end the Down's Syndrome guys want to get it right. They want to understand. If you have to explain something 47 times, they'll pay attention to the 47th explanation.

Once Alan showed that he was willing to respond to me without actually paying attention to what I wrote, I stopped addressing him. How can one engage in written discourse with someone who does not read? All the patience and creativity in the world won't help. Trying to offer a better explanation is as useful as pushing harder on a rope.

Absent the delusional pipe-dream of educating him, he ceases altogether to be annoying.

Respectfully,
Myriad
 
So in other words once kleinman stops trying to "get one over" the "evolutionists" he'll be able to learn why he's wrong.

But until he learns why he's wrong he's not going to stop doing that.

Yep. It's a vicious circle alright.
 
So in other words once kleinman stops trying to "get one over" the "evolutionists" he'll be able to learn why he's wrong.

But until he learns why he's wrong he's not going to stop doing that.

Yep. It's a vicious circle alright.


Actually, most (if not all) creationists will NEVER learn that they are wrong. This is because they aren't open to logic, or more importantly, CHANGE. They are SO set in their ways and beliefs that NO amount of proof, evidence, logic, or reasoning will EVER change their set ways. IOW, it's almost always completely useless to even make the attempt.


Cheers,
DrZ
 
A question for Paul:

Can you describe precisely how Kleinman is misusing Ev that leads him to believe it disproves macro evolution? Even though this is probably covered somewhere in the 6608 postings here, it's become too difficult to search out. A summary would especially help newcomers to the thread.

S
 
Mr. Scott said:
Can you describe precisely how Kleinman is misusing Ev that leads him to believe it disproves macro evolution? Even though this is probably covered somewhere in the 6608 postings here, it's become too difficult to search out. A summary would especially help newcomers to the thread.
I don't know how precise I can be, since Kleinman's mathematical proof of the impossibility of evolution by point mutation and natural selection is somewhat lacking in actual math.

At first, Kleinman ran some experiments with Evj that demonstrate that larger genomes take longer to evolve a "perfect creature" than do smaller ones. A perfect creature is defined as one with zero mistakes, when all the mistake points (New dialog, Advanced) are equal. For some reason, he decided that when we extrapolate to the real world, there hasn't been enough time to evolve humans, or leopards, or flagella, or something. This in spite of the fact that he has no idea which biological features evolved when, on what size genomes, with what size populations, or under the influence of what sorts of mutations.

After awhile, Kleinman discovered the mistake points feature, which I had added at the behest of another Creationist. That's when he got into the whole "multiple selection pressures" thing. No amount of repetition can convince him that different functions are being evolved when one or two mistake points are set to zero, and so comparing the times to evolve a perfect creature are problematical. In particular, the concept of a perfect creature doesn't even make sense unless all mistake points are nonzero.

Since then, the multiple selection pressures thing has evolved from a simple "three pressures stop evolution" to the extraordinarily baroque concept that you see today.

Finally, we have had an ongoing backstory discussion about Rcapacity.

~~ Paul
 
So in other words once kleinman stops trying to "get one over" the "evolutionists" he'll be able to learn why he's wrong.

But until he learns why he's wrong he's not going to stop doing that.

Yep. It's a vicious circle alright.
Most creationists only feel the need to be wrong about biology, maybe a little geology and astronomy ... kleinman finds that he can only defend his fantasies by incomprehension of simple English and by failing grade-school math --- and he's willing to go the extra mile.

It's lucky for him that he didn't start doing this when he was at school, or he'd still be resitting the seventh grade.
 
Annoying Creationists

Adequate said:
Are you listening carefully?
Adequate said:

(1) With simultaneous selection pressures the [size=+4]rate of evolution (fixations/generation) increases with the number of selection pressures. [/SIZE]

(2) More optimisation takes more [size=+4]time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.
[/SIZE]
Ladies and Gentlemen: We interrupt our regularly schedule discussion for this important announcement. An evolutionator and his clones have time traveled from Skeptiwikiland to the here and now James Randi Educational Forum. It is their goal to evolutionate the annoying creationist. The evolutionator has accomplished this time travel by increasing the number of routes he can take, even though most of his routes lead to no where. He has accomplished this by increasing the speed of his space zeppelin to 40 furlongs per fortnight from its normal travel speed of 20 furlongs per fortnight. Not only has the evolutionator been able to increase his speed by increasing the number of routes, he has been reduce his fuel consumption by 1.3 gallons per furlong. Beware of the evolutionator! Now back to our regularly scheduled discussion, the funeral for the theory of evolution.

Sure Adequate, I’m listening carefully. I love your quote above. And your use of font size and color are strikingly convincing. Hey Adequate, I was listening to CNN this weekend and they mentioned “an obscure Internet message board”. I wonder if you can guess which “obscure Internet message board” was mentioned?
Kleinman said:
Only an evolutionist would think it is arrogant to show how mutation and selection works in reality.
kjkent1 said:
Only a creationist would be arrogant enough to believe that he is the only person alive who knows how mutation and selection actually works.
Oh, I’m not the only one, check out the citations below.
Mr Scott said:
A question for Paul:
Mr Scott said:

Can you describe precisely how Kleinman is misusing Ev that leads him to believe it disproves macro evolution? Even though this is probably covered somewhere in the 6608 postings here, it's become too difficult to search out. A summary would especially help newcomers to the thread.

Yes Paul, explain to all the newcomers how I am misusing the ev mutation and selection sorting algorithm and that what ev really shows is how a human genome can evolve in a billion years based on the rate of information gain on a 256 base genome.
Paul said:
I don't know how precise I can be, since Kleinman's mathematical proof of the impossibility of evolution by point mutation and natural selection is somewhat lacking in actual math.
Paul, I’m using the data from your own computer model. Is their some lack of math in your model? Dr Schneider said that it includes the essentials.
Paul said:
At first, Kleinman ran some experiments with Evj that demonstrate that larger genomes take longer to evolve a "perfect creature" than do smaller ones. A perfect creature is defined as one with zero mistakes, when all the mistake points (New dialog, Advanced) are equal. For some reason, he decided that when we extrapolate to the real world, there hasn't been enough time to evolve humans, or leopards, or flagella, or something. This in spite of the fact that he has no idea which biological features evolved when, on what size genomes, with what size populations, or under the influence of what sorts of mutations.
That’s hundreds of experiments I have run and posted the results from ev and longer genomes taking longer to evolve to a “perfect creature” than do smaller ones is a bit of an understatement, in fact it is a huge understatement. The evolution of the same binding sites on Dr Schneider’s single published case of G=256 which takes less than 1,000 generations takes hundreds of millions of generations on a G=100k by your own estimate. Dr Schneider had no problem estimating the evolution of a human from his model let alone leopards, flagella or any other complex biological system.
Paul said:
After awhile, Kleinman discovered the mistake points feature, which I had added at the behest of another Creationist. That's when he got into the whole "multiple selection pressures" thing. No amount of repetition can convince him that different functions are being evolved when one or two mistake points are set to zero, and so comparing the times to evolve a perfect creature are problematical. In particular, the concept of a perfect creature doesn't even make sense unless all mistake points are nonzero.
I didn’t discover the “mistakes points feature” in ev. Kjkent1 pointed it out for me, thank you kjkent1. What I was looking for was the parameter which was causing ev to evolve so slowly for all but the tiniest genomes. It was the “mistake point feature” which reveals why the sorting process becomes so profoundly slow with all but the tiniest genomes. Set two of the three selection conditions to zero and the remaining selection condition sorts very rapidly, even with small populations. This extremely simple mutation and selection sorting/optimization algorithm demonstrates exactly how the mutation and selection process works. It is the number of selection conditions which dominates the mathematical and empirical behavior of the mutation and selection sorting/optimization process. Hundreds of empirical examples of mutation and selection verifies what Dr Schneider’s computer model shows.
Paul said:
Since then, the multiple selection pressures thing has evolved from a simple "three pressures stop evolution" to the extraordinarily baroque concept that you see today.
If you mean that I am decorating the hypothesis that combination selection pressures profoundly slow the evolutionary process with hundreds of real examples of mutation and selection then your use of the word “baroque” is appropriate. Since you evolutionists have yet to produce a single example of n+1 selection pressures evolving more rapidly than n selection pressures, how would you describe your architecture, plain, how about nonexistent?
Paul said:
Finally, we have had an ongoing backstory discussion about Rcapacity.
That’s a fitting “backstory” for the theory of evolution since ev converges to a local optimum, it just doesn’t happen to be a “perfect creature” local optimum for longer genomes. Those are the routes that Adequate’s space zeppelin takes when he makes his excursion from Skeptiwikiland to the James Randi Educational Forum.

So how does mutation and selection actually work? Here are some more citations which show how.
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=10671334&dopt=AbstractPlus
Patients with plasma viral RNA >50,000 copies/mL, despite a protease-inhibitor regimen, received abacavir, amprenavir, and efavirenz to assess efavirenz-amprenavir drug interactions and to evaluate safety and antiviral response. Patients first received amprenavir with abacavir and other nucleoside analogs. Amprenavir levels were measured before and after adding efavirenz. Patients then received a second protease inhibitor. There was evidence of genotypic and phenotypic resistance at study entry. No patient had study drugs discontinued because of toxicity. Efavirenz decreased the steady-state area under the curve, maximum plasma concentration, and minimum plasma concentration of amprenavir by 24%, 33%, and 43%, respectively. Three of 10 patients had >1.5 log10 viral response to abacavir and amprenavir. All 8 patients who added efavirenz had >0.5 log10 decline in viral load, and this response lasted >24 weeks for 3 of the patients. A combination regimen that included abacavir, amprenavir, and efavirenz was well tolerated and had sustained activity in some patients. Concomitant efavirenz therapy decreases amprenavir concentrations.
http://jvi.asm.org/cgi/content/abstract/71/2/1089
Impaired fitness of human immunodeficiency virus type 1 variants with high-level resistance to protease inhibitors said:
One hope to maintain the benefits of antiviral therapy against the human immunodeficiency virus type 1 (HIV-1), despite the development of resistance, is the possibility that resistant variants will show decreased viral fitness. To study this possibility, HIV-1 variants showing high-level resistance (up to 1,500-fold) to the substrate analog protease inhibitors BILA 1906 BS and BILA 2185 BS have been characterized. Active-site mutations V32I and I84V/A were consistently observed in the protease of highly resistant viruses, along with up to six other mutations. In vitro studies with recombinant mutant proteases demonstrated that these mutations resulted in up to 10(4)-fold increases in the Ki values toward BILA 1906 BS and BILA 2185 BS and a concomitant 2,200-fold decrease in catalytic efficiency of the enzymes toward a synthetic substrate. When introduced into viral molecular clones, the protease mutations impaired polyprotein processing, consistent with a decrease in enzyme activity in virions. Despite these observations, however, most mutations had little effect on viral replication except when the active-site mutations V32I and I84V/A were coexpressed in the protease. The latter combinations not only conferred a significant growth reduction of viral clones on peripheral blood mononuclear cells but also caused the complete disappearance of mutated clones when cocultured with wild-type virus on T-cell lines. Furthermore, the double nucleotide mutation I84A rapidly reverted to I84V upon drug removal, confirming its impact on viral fitness. Therefore, high-level resistance to protease inhibitors can be associated with impaired viral fitness, suggesting that antiviral therapies with such inhibitors may maintain some clinical benefits.
http://www.pnas.org/cgi/content/abstract/93/4/1648
Human immunodeficiency virus type 1 viral background plays a major role in development of resistance to protease inhibitors said:
The observed in vitro and in vivo benefit of combination treatment with anti-human immunodeficiency virus (HIV) agents prompted us to examine the potential of resistance development when two protease inhibitors are used concurrently. Recombinant HIV-1 (NL4-3) proteases containing combined resistance mutations associated with BMS-186318 and A-77003 (or saquinavir) were either inactive or had impaired enzyme activity. Subsequent construction of HIV-1 (NL4-3) proviral clones containing the same mutations yielded viruses that were severely impaired in growth or nonviable, confirming that combination therapy may be advantageous. However, passage of BMS-186318-resistant HIV-1 (RF) in the presence of either saquinavir or SC52151, which represented sequential drug treatment, produced viable viruses resistant to both BMS-186318 and the second compound. The predominant breakthrough virus contained the G48V/A71T/V82A protease mutations. The clone-purified RF (G48V/A71T/V82A) virus, unlike the corresponding defective NL4-3 triple mutant, grew well and displayed cross-resistance to four distinct protease inhibitors. Chimeric virus and in vitro mutagenesis studies indicated that the RF-specific protease sequence, specifically the Ile at residue 10, enabled the NL4-3 strain with the triple mutant to grow. Our results clearly indicate that viral genetic background will play a key role in determining whether cross-resistance variants will arise.
http://aac.asm.org/cgi/content/full/44/3/794?ck=nck
Delavirdine Susceptibilities and Associated Reverse Transcriptase Mutations in Human Immunodeficiency Virus Type 1 Isolates from Patients in a Phase I/II Trial of Delavirdine Monotherapy (ACTG 260) said:
The development of human immunodeficiency virus type 1 resistance to delavirdine (DLV) was studied in subjects receiving DLV monotherapy. Phenotypic resistance developed in 28 of 30 subjects within 8 weeks. K103N and Y181C, which confer nonnucleoside reverse transcriptase inhibitor (NNRTI) cross-resistance, were the predominant reverse transcriptase mutations. P236L, which confers DLV resistance but hypersensitivity to other NNRTIs, developed in <10% of isolates.
And
Delavirdine Susceptibilities and Associated Reverse Transcriptase Mutations in Human Immunodeficiency Virus Type 1 Isolates from Patients in a Phase I/II Trial of Delavirdine Monotherapy (ACTG 260) said:
In vitro passage of HIV-1 in the presence of DLV leads to the emergence of a unique RT mutation, P236L (5). In contrast to Y181C and K103N, P236L confers an increase in HIV-1 susceptibility to other NNRTIs. This observation suggested that cross-resistance to other NNRTIs might not be an inevitable consequence of bis(heteroaryl)piperazine resistance. However, P236L was only rarely detected in patients given DLV in combination with didanosine, and the majority of isolates in these patients had a Y181C and/or K103N mutation (3).
That’s the story of how mutation and selection works. Combination selection pressures profoundly slow a population’s ability to do the sort of beneficial and detrimental mutations. You have too many routes on the fitness landscape that lead to no where. Single selection conditions which target a single gene give relatively rapid sorting of beneficial and detrimental mutations but as soon as you have multiple selection conditions targeting multiple different genes, the sorting process is interfered with by the multiple different selection conditions. That is what ev shows and that is what the hundreds of real examples of mutation and selection demonstrates. Now you evolutionists could overwhelm me with a single empirical example of n+1 selection pressures evolving more rapidly than n selection pressures, alas I suspect we are in for a long wait for that. The failure of you evolutionists to understand this simple principle has and will continue to contribute to the premature death of millions of people with HIV, cancer and other infectious diseases subject to the principles of mutation and selection.
 
While you wait for a real example of n+1 pressures evolving faster than n pressures (which we have shown you time and time again, by the way, you genius) we will be waiting for you to show us a real example of whatever it is you claim generated life as we know it.

Do you have a more probable explanation than evolution, Kleinman? We would all love to hear it. You see, the funny thing is, no matter how improbable you think you show the theory of evolution to be, it will still be more probable than whatever nonsense you claim should replace it.
 
That’s the story of how mutation and selection works. Combination selection pressures profoundly slow a population’s ability to do the sort of beneficial and detrimental mutations. You have too many routes on the fitness landscape that lead to no where. Single selection conditions which target a single gene give relatively rapid sorting of beneficial and detrimental mutations but as soon as you have multiple selection conditions targeting multiple different genes, the sorting process is interfered with by the multiple different selection conditions. That is what ev shows and that is what the hundreds of real examples of mutation and selection demonstrates.

No, no, and no. We have shown you over and over, in formal proofs and arguments, why you are wrong here. You have failed to counter even a single argument of ours.

1) We have shown you multiple sorting algorithms that are not always confounded by additional sorting conditions. You have failed to find any evidence that these are not sorting algorithms and show that your argument to the contrary is correct.

2) We have shown you multiple examples, in the real world, of n+1 selective pressures leading to faster evolution than n selective pressures. We have also shown you that every single citation you have given is from a study predicated on this fact. You have failed to provide any argument to the contrary.

3) We have shown you why the conclusions you reached using the ev program are utter nonsense. The programmer himself showed you. As before, you have failed to provide any argument to the contrary.

Your incompetence in mathematics and logic, as well as your complete inability to follow the arguments presented by others, has resulted in the mishmash of nonsensical posts that you contend are proof of your claims. Nobody else thinks so, Kleinman. In fact, your performance in this debate is so pathetic that the majority of us question whether you really are who and what you say you are.
 
I see kleinman is again attacking the stawman. I see you haven't justified your horribly wrong assumptions. Isn't it funny how you are unable to wish reality away?
 
kleinman said:
I didn’t discover the “mistakes points feature” in ev. Kjkent1 pointed it out for me, thank you kjkent1. What I was looking for was the parameter which was causing ev to evolve so slowly for all but the tiniest genomes. It was the “mistake point feature” which reveals why the sorting process becomes so profoundly slow with all but the tiniest genomes. Set two of the three selection conditions to zero and the remaining selection condition sorts very rapidly, even with small populations.
You're welcome, however you continue to misunderstand the effect of setting a mistake count to zero.

When a mistake count is disabled, the ev organisms do not evolve to the "perfect creature" contemplated by the software, even though the software reports a "perfect creature." This is because when all three mistake counts are non-zero, "perfect" means a creature absent any missing or spurious bindings -- whereas when either missing or spurious bindings are set to zero, the "perfect creature," contains these errors, because they are not selected against.

If you want to conduct a realistic experiment, then set one or more of the mistake counts to zero, disable the "Stop on perfect creature" setting, and enable the "Stop on Rseq >= Rfreq." You will find that the creatures never converge, i.e., they do not evolve towards anything resembling a real-world genome.

Whereas, if you set the mistake counts to non-zero values -- no matter how disparate, then the creature will eventually converge to Rseq >= Rfreq.

The whole point of ev is to show information gain from a random start as measured by the Rseq ~ Rfreq relationship. Any setting which causes ev to terminate prior to that relationship being reached, is defective, because the final organism has no relationship to the real-world genomes that it supposed to be modeling.

Having said all of the above, I believe that you have demonstrated that "random point" mutation and selection cannot reasonably account for the entire history of evolutionary change. However, as you refuse to acknowledge that anything other than random point mutation exists in the real world, you are intentionally excluding the very evidence which would show you how mutation and selection accomplishes speciation in the generational time available.

Your citations to research shows that heavy selective pressure from multiple sources slows evolutionary change. But, none of those experiments attempt to demonstrate that natural environments do not routinely appear with only one dominant selective pressure. To the contrary, all of the organisms that the research tests exist precisely because those organisms change rapidly in response to a dominant selective pressure -- and the research demonstrates this rapid change by subjecting test organisms to a single dominant pressure, before subjecting the organisms to multiple pressures.

Kleinman, you have not disproved evolution -- you've proved it.
 
Ladies and Gentlemen: We interrupt our regularly schedule discussion for this important announcement. An evolutionator and his clones have time traveled from Skeptiwikiland to the here and now James Randi Educational Forum. It is their goal to evolutionate the annoying creationist. The evolutionator has accomplished this time travel by increasing the number of routes he can take, even though most of his routes lead to no where. He has accomplished this by increasing the speed of his space zeppelin to 40 furlongs per fortnight from its normal travel speed of 20 furlongs per fortnight. Not only has the evolutionator been able to increase his speed by increasing the number of routes, he has been reduce his fuel consumption by 1.3 gallons per furlong. Beware of the evolutionator! Now back to our regularly scheduled discussion, the funeral for the theory of evolution.
And then you wonder why people think that you're insane.

Sure Adequate, I’m listening carefully. I love your quote above. And your use of font size and color are strikingly convincing. Hey Adequate, I was listening to CNN this weekend and they mentioned “an obscure Internet message board”. I wonder if you can guess which “obscure Internet message board” was mentioned?
I'm guessing that it's the same obscure Internet message board that I keep pointing out to you is an obscure Internet message board.

The same obscure Internet message board on which you've spent an entire year and (at a conservative estimate) half-a-million words explaining your ideas to a dozen people, all of whom keep laughing their heads off at your pathetic antics.

I should still be fascinated to know your reasons for doing this, but you're too ashamed to tell me, aren't you?
 
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That’s the story of how mutation and selection works. Combination selection pressures profoundly slow a population’s ability to do the sort of beneficial and detrimental mutations. You have too many routes on the fitness landscape that lead to no where. Single selection conditions which target a single gene give relatively rapid sorting of beneficial and detrimental mutations but as soon as you have multiple selection conditions targeting multiple different genes, the sorting process is interfered with by the multiple different selection conditions. That is what ev shows and that is what the hundreds of real examples of mutation and selection demonstrates. Now you evolutionists could overwhelm me with a single empirical example of n+1 selection pressures evolving more rapidly than n selection pressures, alas I suspect we are in for a long wait for that. The failure of you evolutionists to understand this simple principle has and will continue to contribute to the premature death of millions of people with HIV, cancer and other infectious diseases subject to the principles of mutation and selection.
We know that you're talking bollocks, and if you could ever get your head round grade-school-level math, so would you.

But I don't think that you ever will.
 
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