Annoying creationists

[Belz...]

This miscomprehension is not limited to evolution. I think anyone who's ever worked with invertebrates (apart perhaps from insects and invertebrates we eat, such as clams) will sooner or later find that no one can really understand why they do it, unless they are scientists themselves. It's the "stuffed animal syndrome" --- people care about cute animals which can be made into stuffed toys. If they can't, or the animal is in any way ugly, bothersome, slimy or very small, there seems to be no understanding of why anyone would ever want to do any research on them...

They don't ? I've always found ugly things fascinating !!!

And... shrimps are cute!

 

[sol invictus]

In my own model, I continued the simulation to fixation of all alleles. Hence, my own statement of my result was that if the selection pressures are simultaneous, then the rate of evolution (fixations/generation) increases with the number of selection pressures.

I didn't realize you had also done a simulation (I haven't read the entire thread)... in any case, thanks for the comment - your terminology is more precise and less susceptible to distortion than mine.

It is a testimony to the stupidity of Alan Kleinman that he can take my statement "for some n != 0, the average rate of fixation under n + 1 pressures is higher than the average rate of fixation under n pressures" and twist it into "n + 1 pressures evolve faster than n pressures."

Right - so we're all in agreement. I wonder whether I can reproduce your results in my simplistic model.

Question to both of you: does your rate scale as log/n for large n?

 

[kleinman]

Annoying Creationists

Joobz, you just love to speculate and extrapolate from your speculations. Take your list and account for the 150,000,000 base differences between humans and chimpanzees in 500,000 generations and don’t forget to tell us what the selection pressures and target genes for these selection pressures are.

So I guess you two are ready to explain to us what the components of the DNA replicase system were doing before DNA could be replicated. Tell us what the function of helicase and gyrase were. That should be a good story. Joobz, you can tell us this after you show us how ribose can be generated nonenzymatically.

So you can't answer any of my questions?

ETA: pretending your numbers are correct:
~4% difference between genomes over 500,000 generations (since the split is what I assume you are refering to) results in a 0.000008% change per generation. Considering that human genome variablity is somewhere arround 0.08% between individuals, this mutation rate relates to 1/10,000th of the variation between humans. These numbers are far from impossible.

Have you asked any questions? All you have done is post a list of speculations.

So let’s consider your computations and assumptions you have made.
Horribly wrong assumptions in the joobz calculation:
1.) Mutation rate remains constant
2.) Mutation rate is known
3.) Number of selection pressures for all species for all time in all areas is known
4.) Number of selection pressures is constant
5.) Selection pressure magnitude is constant and equal for all pressures
6.) Point mutations are the only mutation/adaptation mechanism
7.) defining selection pressure is unimportant
8.) slow equals stop
9.) Mutation is non-random
10.) And the really, really horrible assumption is that n+1 selection pressures evolve faster than n selection pressures.

Hey joobz, when are you going to take up that $10,000 wager that you can’t prove your claim that my PhD thesis has mathematical or empirical irregularities. Let’s see you put your money where your big mouth is.

Does anyone else notice how Kleinman has been conveniently ignoring my last post?

I’m not ignoring your posts, we are just waiting for you to post your parametric studies of you model which show that n+1 selection pressures evolve more rapidly than n selection pressures. You could also post a real example of your model as well, that would be interesting. Wait a minute you did post the results from your parametric study, here it is:

I also found a set of parameters that brought it down to be lower than for a singly applied pressure but I forgot what it was.

I haven’t made any discovery. All I am doing is reporting the mathematical and empirical facts of how mutation and selection actually works. I haven’t made any discovery. All I am doing is reporting the mathematical and empirical facts of how mutation and selection actually works.

All of which is entirely defeated by fact that ev and all of your citations show faster evolutionary change under the influence of a dominant pressure.

That’s the point member of the bar. A single dominant selection pressure is the only case where you get rapid evolutionary change. Additional selection pressures whether weak or strong slow the sorting/optimization process.

Both ev and reality are consistent -- evolution happens under a dominant selective pressure -- a circumstance which is relatively routine in nature.

So defender of the mathematically illogical and irrational view of mutation and selection, it should be easy for you to tell us what that selection pressure is that transforms reptiles into birds.

If life, and as a result, humans, were 'created' and thus 'intelligently designed', then why did the designer do such a TERRIBLE job at it?

If life, and as a result, humans, were ‘mutated and selected’ and thus ‘evolved’, then why did evolution do such a TERRIBLE job at it?

Hey Shalamar, when was the last time an evolutionist opened a hospital? When you do, I have a suggestion for the name, “The Natural Selection Hospital of the Most Fit”.

Kotatsu, once you understand that mutation and selection is simply a sorting/optimization problem, you will understand why this process can not transform large numbers of genes simultaneously. I harbor no ill will toward you or anyone else. I just think your ideas are illogical and irrational. They don’t make mathematical or empirical sense.

Do you have any useful response to my two longer posts? I mean the one about polyploidisation giving rise to common descent in a way we can actually measure and infer more easily than (random point) mutation and selection, and the elaboration of the dinosaur-to-bird evolutionary scenario I provided you with? If at any point in either of those two posts I am unclear or too technical --- I understand, for instance, if the polyploidisation post may be too convoluted for someone who has never specifically studied the area --- I would be happy to provide more details and explain it in simpler terms. Just say the word. Also: if you have problem accessing the papers I cite, I would be glad to send them to you. I wouldn't want to just copy and paste, sinc ethat could lead to allegations of cherry picking; far better for you to read the papers in full and get the whole picture.

Kotatsu, why don’t you tell us how polyploid genes are transformed into new genes? Once you figure out it requires mutation and selection then you can study how mutation and selection actually works.

Perhaps you think because humans and chimpanzees have the same insulin might make evolutionists think we arose from a common ancestor but then you have to show why humans and chimpanzees have different preproinsulin.

I don't know anything about this protein. I went to NCBI. I got the sequence for human preproinsulin. I blasted (searched) it against the NR database (all the non redundant DNA we know of in the whole world.) Here are the first three hits:

Delphi, I already did the search and the results are already posted on this thread. So, there is diversity between human and chimpanzee preproinsulin but no diversity in the insulin of humans and chimps. Since you claim that humans and chimps came from a common ancestor, do care to show us how this happened?

I haven’t made any discovery.

Thank you. At last you admit the truth.

But unlike you, I don’t perpetuate a myth that has led to the premature deaths of millions of HIV sufferers and others suffering from diseases that are subject to the principles of mutation and selection. Adequate, you have abandoned your profession as a mathematician and embraced an illogical and irrational belief system.

What you do claim Adequate is that n+1 selection pressures evolve more rapidly than n selection pressures.

What a silly lie. I claim no such thing.

Sure you have Adequate, don’t you remember what you said about your silly graph? Here, let me remind you.

All other features and parameters of the two models are identical. The model is designed so that the relative advantage of n+1 new genes over n (when selection is acting) is the same for all n, i.e. each new allele carries the same advantage.

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.

And then I asked you for a real example of your model and you said this:

So far as I know, no-one has done the experiment.

Adequate, read on and I’ll post more citations which show the exact opposite of what you claim. Reality shows that combination selection pressures profoundly slow the evolutionary process. Adequate, how did you manage to get the mathematics of mutation and selection so wrong?

Here are some more examples of how mutation and selection actually works, and it works like Dr Schneider’s ev program works. Combination selection pressures profoundly slow the evolutionary, sort/optimization process.
http://www.blackwell-synergy.com/doi/full/10.1111/j.1469-0691.2006.01492.x

Although mutational resistance can be selected in vitro, it may not represent the most prevalent resistance mechanism in clinical isolates of a particular species. For example, chloramphenicol-resistant mutants of Staph. aureus have 23S rDNA mutations and may be cross-resistant to linezolid [44], but most clinically significant chloramphenicol resistance in this species is mediated by acetyltransferase enzymes [45]. However, in certain species, mutation is the main, or sole, cause of clinical resistance problems. One of the best examples is Mycobacterium tuberculosis. Resistance to all therapeutic agents in this species is mediated by mutations: i.e., rifampicin resistance in rpoB; isoniazid resistance in katC, inhA, oxyR, ahpC and furA; streptomycin resistance in rrs and rpsL; pyrazinamide resistance in pncA; ethambutol resistance in embB; and fluroquinolone resistance in gyrA and gyrB[46]. The treatment of tuberculosis requires combination therapy to tackle a difficult pathogen that causes prolonged disease [46,47]; monotherapy is not an option because of the very real risk of resistance emerging. Combination therapy decreases, but does not eliminate, this risk, which is influenced by the frequencies of mutation to resistance for each individual agent, and by the number of bacteria at a focus of infection [46].

Multidrug therapy is also recommended for Helicobacter pylori infections, typically comprising triple combination regimens, including two of clarithromycin, metronidazole, amoxycillin or tetracycline, plus a proton pump inhibitor [48]. Chromosomal mutations are responsible for resistance of H. pylori to clarithromycin (in 23S rRNA) [49–52], amoxycillin (changes in penicillin-binding protein 1) [53], metronidazole (in rdxA and other genes) [48], tetracycline (in 16S rRNA and other undefined genes) [54,55] and, in vitro, streptomycin (in rpsL) [56].

http://www.journals.uchicago.edu/CID/journal/issues/v41nS4/36160/36160.html

Widespread drug resistance in parasites aggravates the burden of malaria. The extent of the problem is due mainly to the limited armamentarium of drugs used thus far to treat malaria and to policies and practices constrained by limited resources. All drugs in use are affected except, thus far, artemisinin derivatives. The scale and impact of resistance has been underestimated, leading to the continued use of failing drugs, which contributes to the rise in resistance and increased morbidity and mortality due to malaria. Pharmacological, epidemiological, and operational aspects factor the development and spread of resistance. Although the problem is complex, much can be done to reverse the course of events: adopt adequate tests to assess resistance, encourage and sustain development of new drugs, protect drugs against resistance through use of combinations, expand access to prompt and effective treatment, and promote evidence-based policies and sensible practices. The current situation favors the development of sensible strategies to restrain resistance.

and

De novo selection of resistant mutants. Resistance occurs as a result of spontaneously occurring mutations or gene amplification. Drug-resistant mutants are selected in the presence of levels of drug that are inadequate to suppress their growth. Considering the size of the malaria genome (3 × 10^7 bp), the number of parasites in 1 infected individual (10^8-10^12), and the mutation rate caused by replication errors by eukaryotic DNA polymerases (1 in 10^12), parasites with randomly mutated genomes are likely to occur in any infection. However, resistance is considerably rarer in vivo, being influenced by drug type, the underlying resistance mechanism, and the patient's state of acquired immunity. In some cases, there are mutations in the gene encoding the drug target. Single or multiple mutations of the same gene may accumulate, conferring increasing degrees of resistance. The DHFR of biguanide antifolates and the cytochrome b of atovaquone are particularly prone to resistance (per-parasite resistance mutation frequencies are 1 in 10^11 and 1 in 10^12, respectively). In other cases, resistance requires multigenic, independent mutations to be expressed. Typically, this applies to chloroquine (per-parasite resistance mutation frequency is 1 in 10^-19). These features explain why chloroquine was effective for several decades before it was rendered ineffective, whereas antifolates, even in combinations targeting 2 different enzymes (DHFR and DHPS), have a very short useful therapeutic life span.

Critical to what happens next is the number of parasites exposed to the drug and its pharmacokinetic and pharmacodynamic characteristics. Most vulnerable to resistance are those drugs with a slow onset of action (i.e., low killing rates or parasite reduction ratios) and slow elimination profiles (long half-lives), with a long "selective window" (corresponding roughly to the period during which levels are ~20%-80% of the drug's maximum inhibitory concentration) [26]. The antifolate combination pyrimethamine-sulfadoxine, with its long half-life and a resistance that develops through single-point mutations, is particularly prone to resistance

and

Preserving the life spans of both current and future antimalarial drugs is essential. Clearly, a move away from sequential monotherapy is now warranted and supported by evidence and is endorsed by the WHO [56]. The principle of combining drugs with different modes of action is common practice in other areas of infectious diseases, such as tuberculosis and HIV/AIDS, but is very recent in malaria.

and

ACTs are a way to enhance treatment efficacy, prevent or retard the development of drug resistance, and preserve valuable antimalarial drugs. The scientific rationale for using ACTs is sound for several reasons [57, 58]. In general, combining different drugs with independent modes of action will increase the chances of killing parasites and greatly decrease the probability that an infected patient will develop resistance to both drugs. In particular, artemisinins cause a rapid and substantial reduction in the parasite biomass, irrespective of the parasites' resistance to other antimalarials. The remaining parasites are then killed off by high concentrations of the companion drug.

This last citation for this post is for those of you who claim that I only consider point mutations.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1075723

Resistance to antiretroviral drugs is generally conferred by specific amino acid substitutions, rather than insertions or deletions, in reverse transcriptase (RT) of human immunodeficiency virus type 1 (HIV-1). The exception to these findings is the amino acid insertions found in the β3-β4 loop of the RT enzyme in response to treatment with nucleoside reverse transcriptase inhibitors. This insert consists most commonly of two amino acids, but we describe in detail the evolution of a variant with an 8-amino-acid (aa) insert in a patient treated with zidovudine (ZDV) and 2′-3′-dideoxycytidine (ddC). The 24-nucleotide insert is a partial duplication of local sequences but also contains a sequence segment of unknown origin. Extensive sequence analysis of longitudinal patient samples indicated that the HIV-1 population prior to the start of therapy contained not the wild-type amino acid 215T in RT but a mixture with 215D and 215C. Treatment with ZDV and subsequent ZDV-ddC combination therapy resulted in the evolution of an HIV-1 variant with a typical ZDV resistance genotype (41L, 44D, 67N, 69D, 210W, 215Y), which was slowly replaced by the insert-containing variant (41L, 44D, insert at position 69, 70R, 210W, 215Y). The latter variant demonstrated increased resistance to a wide range of drugs, indicating that the 8-aa insert augments nucleoside analogue resistance. The gain in drug resistance of the insert variant came at the expense of a reduction in replication capacity when assayed in the absence of drugs. We compared these data with the resistance and replication properties of 133 insert-containing sequences of different individuals present in the ViroLogic database and found that the size and actual sequence of the insert at position 69 influence the level of resistance to nucleoside analogues.

How can that be, combination therapy still works with HIV yet this virus does mutations other than point mutations?

Well, someday you evolutionists will learn how mutation and selection actually works. You could start with a study of Dr Schneider’s ev computer simulation of the process, then these hundreds of citations I have and will continue to post more will make sense to you. Then you will understand that Adequate’s claim that n+1 selection pressures evolve more rapidly than n selection pressures is nothing more than irrational and illogical thinking that if perpetuated will cause the unnecessary premature death of millions of people suffering from diseases subject to the principles of mutation and selection.

 

[sol invictus]

Sure you have Adequate, don’t you remember what you said about your silly graph?

Kleinman, surely you know the meaning of the word "rate"?

No one has said that the time required for n+1 mutations is less than the time for n. What has been said is that the RATE at which those mutations occur increases with n. As I have shown, and you agreed, that is true even in the simple model that you yourself proposed.

I'm sure you're capable of understanding that simple distinction.

 

[delphi_ote]

Delphi, I already did the search and the results are already posted on this thread. So, there is diversity between human and chimpanzee preproinsulin but no diversity in the insulin of humans and chimps.

By "diversity" you mean a few amino acid substitutions?! You realize the number of DNA mutations that requires is on the order of 10s, right? Is this really your argument? You don't understand how mutation could change a handful of amino acids over the course of millions of years?

This is officially the dumbest thing you've said in this entire thread.

 

[kleinman]

Annoying Creationists

Sure you have Adequate, don’t you remember what you said about your silly graph?

Kleinman, surely you know the meaning of the word "rate"?

No one has said that the time required for n+1 mutations is less than the time for n. What has been said is that the RATE at which those mutations occur increases with n. As I have shown, and you agreed, that is true even in the simple model that you yourself proposed.

I'm sure you're capable of understanding that simple distinction.

If you are talking about Dr Schneider’s peer reviewed and published model of random point mutations and natural selection, what it shows is that the ability of a system to sort and optimize is strongly dependent on the number of optimization conditions. The greater the number of optimization conditions, the more difficult for the sorting of mutations for each of the optimization conditions.

I’m sure you’re capable of understanding that simple distinction. Now what Adequate and rocketdodger are alleging is the exact opposite, that the greater the number of optimization conditions, the faster the sort occurs.

Adequate said this:

All other features and parameters of the two models are identical. The model is designed so that the relative advantage of n+1 new genes over n (when selection is acting) is the same for all n, i.e. each new allele carries the same advantage.

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.

And then I asked you for a real example of your model and you said this:

So far as I know, no-one has done the experiment.

And rocketdodger said this:

The model is just a quick and dirty simulation of mutation and selection. It shows that additional selective pressures do not hinder the sorting mechanism like you claim it does. In particular, adding more and more pressures can easily bring the time to fixation per pressure down to within 200% of the time to fixation for a singly applied pressure. I also found a set of parameters that brought it down to be lower than for a singly applied pressure but I forgot what it was.

We all wait for you evolutionists to post a single real example of your irrational and illogical thinking. On the other hand, I continue to post citation after citation which shows that evolution by mutation and selection is profoundly slowed when you have more than a single selection pressure targeting a single gene.

 

[kjkent1]

That’s the point member of the bar. A single dominant selection pressure is the only case where you get rapid evolutionary change. Additional selection pressures whether weak or strong slow the sorting/optimization process.

Yes, that "is" the point. Ev shows different convergence times when altering its mistake weights. Convergence appears to be normally distributed with the mean average at the point where all three selection pressures are equal. This is a clear indication that even the three selection pressures found in ev have different intensities.

You claim that convergence is much more rapid with only one pressure active. Assuming that pressure disabled is the negative extreme, and single pressure enabled is the positive extreme, then it is reasonable to assume that as relative intensity increases, generation time to convergence approaches the mean average.

So, it's not sufficient to simply state that multiple pressures confound evolutionary progress. The relative intensity of those pressures must be considered.

Also, ev's selective mechanism treats the weights as linear. That is, an n+1 mistake weight is 1 unit more selective than an n mistake weight. But, is this how real life selective pressures function? It could be that certain selective pressures are exponentially more powerful than others. I doubt that there's any research in this area, which means no way to know.

But, clearly, intensity is a very important factor, and you are discounting that factor to zero, by claiming that multiple selective pressures confound evolution. The fossil record shows otherwise.

So defender of the mathematically illogical and irrational view of mutation and selection, it should be easy for you to tell us what that selection pressure is that transforms reptiles into birds.

Behold, oh, obsessive-compulsive overconfident insulter of others who have reasonable counterarguments, The geologic record shows what selective pressures were at work throughout history. It is those pressures in concert with unpredictable mutation events which caused the transformation from one species to another.

And, the proof of this is the fossil record, which shows that such transformations took place during the same time that the geologic record shows the selective pressures which were at work.

Had there been a massive global flood only 6,000 years ago, we would see an entirely different geological record, and almost certainly an entirely different fossil record, too.

We all wait for you evolutionists to post a single real example of your irrational and illogical thinking. On the other hand, I continue to post citation after citation which shows that evolution by mutation and selection is profoundly slowed when you have more than a single selection pressure targeting a single gene.

LOL! A day without kleinman's narcissism is like a day without sadness. Regardless, we have posted many citation which have disposed of your arguments. You just don't like them. And, as you view yourself as the sole arbiter of what is and is not true, you continue to misrepresent the facts -- said facts which may easily be witnessed by anyone with the energy to review this thread.

 

[rocketdodger]

Kleinman, you pathetic fool. You resort to quoting obsolete statements in order to disguise your stupidity?

Yes, I forgot the settings I used in a run -- so f---ing what? In a post since then, which I know you have read since you responded to it you idiot, I gave you the exact settings I used to get a set of results that prove you wrong.

Then, you claim my results must not be typical of even my own simulation, because they show you are wrong. In post #6516 I explicitly address all of the issues you brought up. Instead of responding to that, and admitting that you really are wrong, you blow a smokescreen by quoting statements made by Adequate and me that are no longer relevant.

The issue, Kleinman, is not that we have shown evolution speeds up under more selective pressures. We can't claim that, because nobody has actually tried to enumerate the selective pressures acting on populations. Duh. The issue is that both Dr. Adequate and I have shown you sorting algorithms, modeled on the general mechanism of mutation and selection, that are not always confounded by additional sorting conditions. It is this simple -- you have claimed time and time again that ALL sorting algorithms are confounded by additional sorting conditions. We have shown this to be untrue.

Both Adequate and I have studied our algorithms. Our results are not anomalies. We have shown you that all of the issues you claim could "affect" the results are in fact non-issues because we either already account for them or they would in fact not affect the results.

That is actually more than we need to do, because you have no proof at all of your own claim. All you have are studies featuring only a few pressures, and a program that features at most three pressures. You claim to have done parametric studies. How can you do a parametric study on the effects of adding selective pressures when the very program you are touting caps the number at 3? My parametric study of my program shows that for a genome of any appreciable size the threshold number of pressures where additional pressures start increasing the average fixation rate is well over 10. Do you have any data that can refute this? No, you don't. So until you can actually show me and everyone here why my algorithm is not a sorting algorithm, your theory is baseless.

Of course you will respond with some rubbish that has nothing to do with this, in order to dodge the issue once again. Don't you see how pathetic your debate tactics are? Given that you think you are actually right, it makes you look like an a--. Have we dodged ANY of the issues you bring up? NO. Have we ever mangled your words into something you don't actually mean? NO. If you are right about evolution, then why are you the one using the unfair debate tactics? One would think it would be the other way around.

 

[kleinman]

Annoying Creationists

That’s the point member of the bar. A single dominant selection pressure is the only case where you get rapid evolutionary change. Additional selection pressures whether weak or strong slow the sorting/optimization process.

Yes, that "is" the point. Ev shows different convergence times when altering its mistake weights. Convergence appears to be normally distributed with the mean average at the point where all three selection pressures are equal. This is a clear indication that even the three selection pressures found in ev have different intensities.

You claim that convergence is much more rapid with only one pressure active. Assuming that pressure disabled is the negative extreme, and single pressure enabled is the positive extreme, then it is reasonable to assume that as relative intensity increases, generation time to convergence approaches the mean average.

If you doubt my claim, set any two of the three weights for the selection pressures to zero and verify that the number of generations for convergence is far smaller than when trying to converge all three conditions simultaneously. This is true beyond a shadow of a doubt.

So, it's not sufficient to simply state that multiple pressures confound evolutionary progress. The relative intensity of those pressures must be considered.

Also, ev's selective mechanism treats the weights as linear. That is, an n+1 mistake weight is 1 unit more selective than an n mistake weight. But, is this how real life selective pressures function? It could be that certain selective pressures are exponentially more powerful than others. I doubt that there's any research in this area, which means no way to know.

But, clearly, intensity is a very important factor, and you are discounting that factor to zero, by claiming that multiple selective pressures confound evolution. The fossil record shows otherwise.

Kjkent1, it is that simple to say that multiple selection pressures confound the evolutionary process. This is how sorting/optimization problems work. Now your claim that the weight factor has a linear behavior is completely wrong. The weight factor has a highly nonlinear affect on the generations for convergence. That is why there is a huge difference between the generations for convergence when you set two of the three selection conditions to zero. If the weight factors were linear, setting two of the three conditions to zero should give a generations of convergence of 1/3 that of converging all three conditions simultaneously, instead, it take many orders of magnitude few generations to converge any one selection condition than all three selection conditions. That also happens to be what the hundreds of real examples of mutation and selection shows.

Now I can understand your desire to change the topic to evolutionist Rorschach tests but since we are talking about the mathematics of mutation and selection and the empirical evidence which shows that the evolutionist interpretation of this evidence is mathematically and empirically impossible.

So defender of the mathematically illogical and irrational view of mutation and selection, it should be easy for you to tell us what that selection pressure is that transforms reptiles into birds.

Behold, oh, obsessive-compulsive overconfident insulter of others who have reasonable counterarguments, The geologic record shows what selective pressures were at work throughout history. It is those pressures in concert with unpredictable mutation events which caused the transformation from one species to another.

And, the proof of this is the fossil record, which shows that such transformations took place during the same time that the geologic record shows the selective pressures which were at work.

Had there been a massive global flood only 6,000 years ago, we would see an entirely different geological record, and almost certainly an entirely different fossil record, too.

Kjkent1, it’s all about what you obsess on. You are obsessing on a mathematically and empirically impossible idea. I’m not surprised that you would want to talk about a flood since the theory of evolution is sinking like the Titanic after hitting an iceberg. Only in this case it is a mathematical and empirical iceberg. Perhaps you would like to set up an orchestra on the deck of the theory of evolution so you could listen to some classical music as the theory sinks to the depths.

We all wait for you evolutionists to post a single real example of your irrational and illogical thinking. On the other hand, I continue to post citation after citation which shows that evolution by mutation and selection is profoundly slowed when you have more than a single selection pressure targeting a single gene.

LOL! A day without kleinman's narcissism is like a day without sadness. Regardless, we have posted many citation which have disposed of your arguments. You just don't like them. And, as you view yourself as the sole arbiter of what is and is not true, you continue to misrepresent the facts -- said facts which may easily be witnessed by anyone with the energy to review this thread.

You find it narcissistic when I post real repeatable and measurable examples of mutation and selection? You evolutionists must hate yourselves. That explains why there are so many of you evolutionists. Misery loves company.

 

[kjkent1]

Kjkent1, it is that simple to say that multiple selection pressures confound the evolutionary process. This is how sorting/optimization problems work. Now your claim that the weight factor has a linear behavior is completely wrong. The weight factor has a highly nonlinear affect on the generations for convergence. That is why there is a huge difference between the generations for convergence when you set two of the three selection conditions to zero. If the weight factors were linear, setting two of the three conditions to zero should give a generations of convergence of 1/3 that of converging all three conditions simultaneously, instead, it take many orders of magnitude few generations to converge any one selection condition than all three selection conditions. That also happens to be what the hundreds of real examples of mutation and selection shows.

Oh, my bovine excretionary friend, you are so mercifully free of the ravages of intelligence.

If you set all three selective weights to 1, the convergence will be identical to setting all three weights to 100, or to any other number. It's only when you set the weights to different numbers that you observe different generational times to convergence. This demonstrates both that the RELATIVE weight is significant, and that the various possible convergence outcomes are normally distributed centering around the mean of all three weights set to the same number.

It should be obvious that in the real world, various selective pressures will exhibit all sorts of different outcomes based on their relative weight. A meteor strike that upsets the global environment and radically changes the air temperature is much stronger than, shall we say, a one year drought that reduces water flow in a river by a few cubic meters per hour.

As for your reflections re narcissism, you really need to spend a little more time praying on the subject. The fact that you don't see just how arrogant you are, clearly must affect your ability to render care to your patients. Everyone makes mistakes, Alan -- even you. And, at the moment, you are making a big one by proclaiming that selective intensity is meaningless to the biological evolutionary process.

 

[Dr Adequate]

I’m sure you’re capable of understanding that simple distinction. Now what Adequate and rocketdodger are alleging is the exact opposite, that the greater the number of optimization conditions, the faster the sort occurs.

I have not, of course, said that, which is why you cannot quote me saying that.

Adequate said this:

Yes, I said that. Because it's true.

That's why I said it, and why you can actually quote me saying it, and why you can't produce any counterexample.

And then I asked you for a real example of your model and you said this:

Yes, I said that. Because it's true.

That's why I said it, and why you can actually quote me saying it, and why you can't produce any counterexample

We all wait for you evolutionists to post a single real example of your irrational and illogical thinking.

But, alas for you, there are no examples of our "irrational and illogical thinking".

On the other hand, I continue to post citation after citation which shows that evolution by mutation and selection is profoundly slowed when you have more than a single selection pressure targeting a single gene.

We all know that this isn't true, remember?

 

[joobz]

Have you asked any questions? All you have done is post a list of speculations.

Ah, can't find any problems with it can you? How sad for you.

So let’s consider your computations and assumptions you have made.
Horribly wrong assumptions in the joobz calculation:

this should be fun, considering I made none of these assumptions. Here we go:
1.) Mutation rate remains constant
No it doesn't you are correct. I was simply showing that the mutation rate must be equal to or faster than 0.0000085% base/generation change cummulatively. This allows for variation imposed emergence as well. Not very hard to acheive and mutation rate doesn't need to be constant.
2.) Mutation rate is known
I don't know it. I simply gave a change that would be needed. Is an average 0.0000085% base change/generation too fast?
3.) Number of selection pressures for all species for all time in all areas is known
It isn't known. You are correct. Is an average 0.0000085% base change/generation too fast?
4.) Number of selection pressures is constant
it isn't constant. you are correct. I'm glad we agree. Again, Is an average 0.0000085% base change/generation too fast?
5.) Selection pressure magnitude is constant and equal for all pressures
Again, you are correct. it isn't constant. you are correct. I'm glad we agree. Is an average 0.0000085% base change/generation too fast?
6.) Point mutations are the only mutation/adaptation mechanism
You are so right. variation mutations can occur in different individuals and recombine together. This means that the average 0.0000085% base change/generation isn't only in one individual and that varation in population can speed this along. WOW, I'm glad I didn't assume this was the only important method of adaption. That would be stupid. Who would make such a dumb conclusion?
7.) defining selection pressure is unimportant
I do assume this, you are correct. I'm only looking the seperation between human and chimp, and not considering relative selection pressures. I can assume based upon living habits that the protohuman protochimp populations filled different evolutionary nitches. So what bases were being fixed are different. Interestingly, the growth of variations can occur in both the chimp and human populations independantly. This allows for even more rapid seperation between species.
8.) slow equals stop
No obviously, I would never make this dumb statement. After allit 0.0000085% base change/generation is rather slow. But it most certainly isn't a stop.

9.) Mutation is non-random
Nope, I'm counting on it being rather random.

10.) And the really, really horrible assumption is that n+1 selection pressures evolve faster than n selection pressures.
Interestingly, my argument has nothing at all to do with this. Again, Is an average 0.0000085% base change/generation too fast?

Hey joobz, when are you going to take up that $10,000 wager that you can’t prove your claim that my PhD thesis has mathematical or empirical irregularities. Let’s see you put your money where your big mouth is.

Why would I care about what is obviously unimportant and had little to no impact in the scientific community?

 

[Dr Adequate]

Kleinman, surely you know the meaning of the word "rate"?

No one has said that the time required for n+1 mutations is less than the time for n. What has been said is that the RATE at which those mutations occur increases with n. As I have shown, and you agreed, that is true even in the simple model that you yourself proposed.

I'm sure you're capable of understanding that simple distinction.

What in the world makes you sure of that?

He seems to have a real mental block when it comes to math, even the grade-school stuff.

 

[Dr Adequate]

I didn't realize you had also done a simulation (I haven't read the entire thread) ...

Yes, it appears that three of us have independently simulated mutation and selection and got the same results.

Results here.

The function is here; call it from some sort of output routine with pop set as a constant.

... in any case, thanks for the comment - your terminology is more precise and less susceptible to distortion than mine.

Which still doesn't make it kleinman-proof, as you can see --- the man is capable of misunderstanding anything, no matter how precisely stated.

Question to both of you: does your rate scale as log/n for large n?

I didn't think to look. It might be worth checking --- that looks like the sort of thing one might demonstrate directly from probability theory, without this fussing about with simulations.

 

[kleinman]

Annoying Creationists

Kjkent1, it is that simple to say that multiple selection pressures confound the evolutionary process. This is how sorting/optimization problems work. Now your claim that the weight factor has a linear behavior is completely wrong. The weight factor has a highly nonlinear affect on the generations for convergence. That is why there is a huge difference between the generations for convergence when you set two of the three selection conditions to zero. If the weight factors were linear, setting two of the three conditions to zero should give a generations of convergence of 1/3 that of converging all three conditions simultaneously, instead, it take many orders of magnitude few generations to converge any one selection condition than all three selection conditions. That also happens to be what the hundreds of real examples of mutation and selection shows.

If you set all three selective weights to 1, the convergence will be identical to setting all three weights to 100, or to any other number. It's only when you set the weights to different numbers that you observe different generational times to convergence. This demonstrates both that the RELATIVE weight is significant, and that the various possible convergence outcomes are normally distributed centering around the mean of all three weights set to the same number.

So is this how you draw the conclusion that ev treats the selection weights as linear? The convergence of ev is not linear with the weight factors, in fact the behavior is highly non-linear. Setting two of the three weight factors to zero demonstrates this fact. Nothing affects the generations for convergence in ev more than the number of selection conditions. Even when ev fails to evolve all three selection conditions simultaneously, single selection conditions still evolve to convergence with the selection condition.

It should be obvious that in the real world, various selective pressures will exhibit all sorts of different outcomes based on their relative weight. A meteor strike that upsets the global environment and radically changes the air temperature is much stronger than, shall we say, a one year drought that reduces water flow in a river by a few cubic meters per hour.

The principle that you are having difficulty understanding is if you take a given set of selection conditions then add an additional selection condition, it slows evolution of all the selection conditions. This is what ev is showing and this is what the citations I have posted is showing. This is how sorting/optimization problems work. There is nothing linear about the behavior of these problems. They are highly sensitive to the number of selection (optimization) conditions. Even only three selection conditions slow the evolutionary process profoundly as shown in ev and in the real examples of mutation and selection as well.

As for your reflections re narcissism, you really need to spend a little more time praying on the subject. The fact that you don't see just how arrogant you are, clearly must affect your ability to render care to your patients. Everyone makes mistakes, Alan -- even you. And, at the moment, you are making a big one by proclaiming that selective intensity is meaningless to the biological evolutionary process.

Only an evolutionist would think it is arrogant to show how mutation and selection works in reality. 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?

I’m sure you’re capable of understanding that simple distinction. Now what Adequate and rocketdodger are alleging is the exact opposite, that the greater the number of optimization conditions, the faster the sort occurs.

I have not, of course, said that, which is why you cannot quote me saying that.

No problem Adequate, here’s your post again and let’s here you contradict yourself again.

All other features and parameters of the two models are identical. The model is designed so that the relative advantage of n+1 new genes over n (when selection is acting) is the same for all n, i.e. each new allele carries the same advantage.

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.

And then Adequate goes on to say this:

More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.

Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?

And

So far as I know, no-one has done the experiment.

and

and too bad you don’t have any empirical examples of your silly graph ...

As I have explained to you, I produced the model because I've not heard of this precise experiment being done.

Adequate, the only problem I have with what you have said here is determining which is dumber, your silly graph where you claim that n+1 selection pressures evolve more rapidly than n selection pressures or joobz’s speculation of abiogenesis by “cooperative” chemistry.

 

[Dr Adequate]

What you do claim Adequate is that n+1 selection pressures evolve more rapidly than n selection pressures.

What a silly lie. I claim no such thing.

Sure you have Adequate

What a silly lie. I have claimed no such thing.

 

[Dr Adequate]

Adequate, the only problem I have with what you have said here is determining which is dumber, your silly graph where you claim that n+1 selection pressures evolve more rapidly than n selection pressures ...

What a silly lie. I claim no such thing.

 

[rocketdodger]

Yet more posts from Kleinman that contain no logical arguments whatsoever. And he still hasn't responded to the fact that the foundation of his theory has been demonstrated to be untrue (using independently created models, I would add).

Kleinman, how many posts will you make before you actually address the issue of your claim about sorting/optimization algorithms being proven false? Can you show anyone here why the algorithms Adequate and I use are not sorting algorithms?

 

[Belz...]

I see the laughing dog's been brought back into play.

We must be on to something.

 

[Belz...]

Yet more posts from Kleinman that contain no logical arguments whatsoever. And he still hasn't responded to the fact that the foundation of his theory has been demonstrated to be untrue (using independently created models, I would add).

Kleinman, how many posts will you make before you actually address the issue of your claim about sorting/optimization algorithms being proven false? Can you show anyone here why the algorithms Adequate and I use are not sorting algorithms?

Kleinman has a way of wording his theory, though, that seems well-learned to those who don't know better. That's why I was a little unsure at the beginning of this thread, because I couldn't spot anything wrong with his argument.

But once you learn more about the subject, Kleinman's flaws (or lies) become readily transparent.