Annoying creationists

[Ichneumonwasp]

Mr Scott, you are confusing several principles. Those principles you are confusing are selection pressures, intensity of selection pressures and extinction. The mathematics is clear; increasing the number of selection pressures slows evolution.

I'm calling you out on this one, Dr. Kleinman. Mr. Scott did not confuse any of those issues in his post. In fact, what he did was distinguish the contributions of each. Then entire thrust of his post, Dr. Kleinman, was to show how it is you that confuses these issues. The mathematics of evolution in the real world (and, no, I am not claiming that he supplied an equation) is quite clear in Mr. Scott's post, Dr. Alan Kleinman -- the number of selection pressures is not the critical element. Rather, it is the intensity of selection pressure that serves as the critical element. As we have demonstrated to you repeatedly, the number of pressures may result in extinction, may result in profound slowing of the evolutionary process, or may result in the development of resistance. The critical determinant of the outcome is not the number of selection pressures, Dr. Kleinman, but the intensity of the total pressure.

 

[Mr. Scott]

Annoying Reality

I'm calling you out on this one, Dr. Kleinman. Mr. Scott did not confuse any of those issues in his post. In fact, what he did was distinguish the contributions of each. Then entire thrust of his post, Dr. Kleinman, was to show how it is you that confuses these issues. The mathematics of evolution in the real world (and, no, I am not claiming that he supplied an equation) is quite clear in Mr. Scott's post, Dr. Alan Kleinman -- the number of selection pressures is not the critical element. Rather, it is the intensity of selection pressure that serves as the critical element. As we have demonstrated to you repeatedly, the number of pressures may result in extinction, may result in profound slowing of the evolutionary process, or may result in the development of resistance. The critical determinant of the outcome is not the number of selection pressures, Dr. Kleinman, but the intensity of the total pressure.

Indeed!

Refuting Dr. Alan Kleinman's own primary example of the impossibility of macroevolution (3-drug HIV treatments) is the article which soundly contradicts Dr. Kleinman's assertion. Please read it!

Based on the UK CHIC cohort study, it is estimated that nearly 40% of HIV-infected patients in the UK have experienced all main classes of antiretroviral drugs and of these 15% are known to have virologically failed all three classes [243].

linkola

So, 15% of these patients' HIV colonies have done something Kleinman asserts is mathematically impossible: macroevolved.

 

[kleinman]

Annoying Creationists

I hope my mathematics is not too obscure. Delphi, if you have any trouble organizing your sock drawer, Paul will help you. He’s very good at the mathematics of sorting socks.

Obscure? Heavens no! Your capacity for mathematical reasoning is abundantly clear. Please, show us more of these "equations." I'm sure they'll further elucidate your "insight" into this complicated subject.

Oh, Dr Schneider has documented his mathematical equations extensively which describes mutation and natural selection in his web site and his peer reviewed publications as well as posting his Pascal version of the ev computer simulation on his web site. You have pointed us to the very helpful Wikipedia reference to the mathematics of the fitness landscape. I’ll point you back to the hundreds of cases run with ev that show that as genome length is increased and realistic mutation rates are use in the model, the number of generations needed to evolve the binding sites becomes too large to support the theory of evolution. And if you look at the behavior of ev when you set two of the three selection conditions to zero, it becomes obvious why mutation and selection becomes an impossible mechanism for macroevolution. Multiple selection conditions cause the rate of convergence of the model to become profoundly slow.

This type of mathematical behavior is seen in numerous applications. Whether it is in database sorting, optimization problems or your example of sorting your sock drawer, the more conditions which you sort on, optimize on or evolve on, the slower the process goes. There are no mathematical examples where this process speeds up as the system becomes more complex. This simple conclusion can be drawn on this complicated subject.

You are making my point. You first sort your socks by color and then put them in pairs. If all the socks are a single color, you don’t have to do the work of the sort, you simply put them in pairs. With a single selection condition, a mutation is determined to be beneficial or detrimental and the ability to reproduce is known. If you have multiple selection conditions, a mutation may be beneficial for one selection condition and detrimental for another selection condition. The total selection process becomes much more complex. Ev shows how difficult this mathematics becomes for satisfying multiple selection conditions when compared to satisfying a single selection condition.

The sock drawer is a silly analogy. What if you have no a priori knowledge that all the socks are the same color? Then you always have to sort them and it takes the same amount of time regardless of the number of colors.

Ok, let’s see how close we can make the sock analogy to mutation and selection. Let’s assume you have no a priori knowledge of the number of colors socks. You start by randomly choosing two socks out of the drawer. If they match, roll them together, if not, start a pile of each color. Continue this process until you finish taking all the socks from the drawer. If the socks are all of one color, your task is finished. If your socks are multiple colored, you have to take the now sorted piles of socks and roll them together. It takes more time and work to match and roll multiple different colors of socks than to match and roll a collection of single color socks. Delphi has come up with very nice, simple example, of why multiple selection conditions slow evolution.

If you think of a “perfect creature” as one which has satisfied all the selection conditions placed on it then this terminology is understandable. You just don’t like when I co-opt anything of yours.

Okay, misuse the term. But then you have to address Kjkent's point that a "perfect creature" arises instantaneously with no selection pressures at all. Don't you see that you're just shooting yourself in the foot?

I’m not misusing your term “perfect creature”, I’m defining for readers of the thread exactly what this term means. This definition is perfectly consistent with Kjkent1’s point that a “perfect creature” arises instantaneously with no selection pressures at all. No selection pressure means there are no mistakes. I’m not shooting myself in the foot; I’m shooting your theory of evolution in the heart.

So what! Define any three selection conditions and evolving the conditions one at a time will occur much more quickly than trying to evolve all three selection conditions simultaneously.

You can't use Ev to demonstrate this. If you turn on one pressure until the mistake count is zero, then turn it off and turn on a second pressure, you won't end up with a creature that distinguishes binding sites from other sites. You'll end up with a creature that performs a different function.

Why don’t you explain to us what the function of mutation and selection is?

There are a couple of interesting numbers in this table highlighted in red. These two cases with two selection conditions actually took more generations to evolve than the three selection condition case. However, the single selection condition cases are able to converge thousands of times more quickly than the three selection condition cases for any of the three selection conditions. It is amazing how quickly a single selection condition can evolve, even on a lengthier genome.

Well then, at least you admit there is nothing special about three or more pressures. Note how even more amazing it is when there are zero selection conditions.

You are missing a point to argue. What you may have is a situation where the two selection case puts the model on a point in the fitness landscape that gives few easy paths to an optimum while adding a third selection condition enables the model to find a path to an optimum. You should not be amazed that zero selection conditions leads to zero mistakes, you have stopped performing mutation and selection under this circumstance.

What you are doing here is extrapolating the rather degraded case of a single selection pressure in Ev to cover the entire real world of evolution. You are claiming there is not a single case of evolution accommodating two selection pressures more quickly than one pressure. You are making a claim about the entire landscape of biochemistry. You have some seriously enlarged gonads there, my friend.

There are many other mathematical situations that exhibit similar behavior to what ev demonstrates. This effect of the “degraded” the behavior ev not only intuitively obvious but also is seen in many similar applications. Why don’t you give us an example of multiple selection conditions that evolve more quickly than a single selection condition? This is the extrapolation you are making.

You've defined a perfect creature as one substantially free of both missed or spurious bindings. If we turn the pressure off that selects for one of these features, then the resulting creature cannot possibly meet the original definition -- it's not the same creature.

Do you think semantics is not going to win this debate little gator? Why don’t you try some mathematics? Why don’t you try to tell us what the purpose of mutation and selection is?

Since natural selection is a restatement of the 1st law of thermodynamics, what selection pressure would lead to the formation of a self replicating ligase?

In case You were wondering 1st law, which states that heat and work are equivilent/interchangable (dE=dQ-dW) is identical to saying that the species best adapted for survival will survive.

If you apply the concept of the first law to natural selection, what you are saying is that the creature that can put more energy toward reproduction than other life activities will be the most successful creature by your theory of evolution. So how do you select for something that does not exist?

The basic approach evolutionists have to ev is that if it shows something that supports your theory it is a valid, if it shows something that contradicts your theory, the model is not valid. You evolutionists are filled with prejudices and biases. But let’s see what Dr Schneider has said about his model:

You may continue to conjure any straw man you wish, but here is, once again, the point:

Dr Schneider’s statements are not my conjectures. He is the author of this peer reviewed and published model of mutation and selection and he believes his model simulates reality. It appears he is going to be that last evolutionist to believe this.

You have a computer model (Dr. Schneider's model, so that you will stop harping on trivial minituae as though you are making a point). You claim this computer simulation models the reality of evolution in all its particulars. You have argued that the intersection of this simulation and reality is the behavior of HIV in the presence of triple therapy. You argued that three selection pressures in ev demonstrate that evolution cannot occur on a realistic time scale. You have been shown with the very example you cite as the intersection of reality and your computer model that what you think the model proves is incorrect. The model does not win in this situation. Reality does. And since the model was not intended to simulate this issue, I'm not the least surprised.

So you think that when ev shows that its multiple selection conditions slows evolution profoundly is “trivial minituae” and that the use of combination therapy for the treatment of HIV to slow the evolution of resistant strains of the virus is “trivial minituae”. I will take this “trivial minituae” any time over your contorted interpretation of reality as you attempt to fit these observations to your ridiculous theory.

For the nth time, I am not claiming anything about ev except that it was designed to show one thing -- that information can increase in a very simple model of mutation and selection. That is all that the model was designed to do and that is what it does.

You are in denial Ichneumonwasp. This is what Dr Schneider designed ev to do:

Variations of the program could be used to investigate how population size, genome length, number of sites, size of recognition regions, mutation rate, selective pressure, overlapping sites and other factors affect the evolution.

This sentence is from the peer reviewed and published paper Ev Evolution of Biological Information written by Dr Schneider and was published in Nucleic Acids Research.

It is abundantly clear that Dr Schneider designed his model for more than the one thing you have suggested. When you investigate the other features of his model, it shows the theory of evolution to be mathematically impossible. The number of generations required to evolve binding sites with realistic genome lengths and mutation rates becomes huge, too huge to support the theory of evolution. The reason the number of generations becomes huge is that multiple selection conditions slow the evolutionary process. The model also shows that increasing population does not markedly accelerate the evolutionary process as evolutionists like to claim.

There is no conspiracy to quell the demons of ev. Your entire argument depends on ev modelling the reality of evolution in all its particulars (not just one aspect of reality -- information gain -- as it was designed to do). When it fails to model all of evolutionary reality, reality wins, not the model. The model only goes so far as it can explain anything in the real world. It's the same with all models. The only thing I have denied is the ability of ev to do what you said it does. It simply does not model what you propose. Your own, hand-picked, example -- the only real-world example you have offered -- demonstrates this fact.

I like the way Dr Schneider argues this point:

A good simulation does not attempt to simulate everything; only the essential components are modeled. For the issue at hand, the form of the genetic code is not relevant; information measured by Shannon's method is more general than that.

With respects to my “hand-picked example”, there are numerous examples of the use of combination therapy to slow the evolution of resistant strains of microbes, HIV and TB happen to be the most obvious and there are numerous examples of the use of monotherapy and the evolution of multidrug resistant strains of microbes such as Gonorrhea, MRSA, pseudomonas being obvious examples. I suspect that a similar pattern would be seen with the use of herbicides and pesticides.

Dr Schneider’s model shows important essential relationships between genome length, selection conditions, mutation rates and population. If you take the time to study the model, you will find that genome length and the number of selection conditions are the dominant variables in the mathematics of mutation and selection.

How nice. Need I remind you, again, that the model does what it was designed to do and not what you argue it does. Nothing else in this argument matters. You can argue till you're blue in the face and your fingers cramp at the keyboard that ev models important relationships between genome length, selection conditions, mutation rates, and population and we will all sit back and say "Well, yeah, that is how it is designed, so tell us something we don't know." What it doesn't model is the reality of triple therapy for HIV under all treatment conditions. If you have no real-world analogy, then the model is useless for that purpose. Dr. Schneider provided his real world analogy for what the model was created to do -- demonstrate the emergence of information under Darwinian conditions.

Again, let’s see what Dr Schneider intended for his model which was published in the peer reviewed journal, Nucleic Acids Research.

Variations of the program could be used to investigate how population size, genome length, number of sites, size of recognition regions, mutation rate, selective pressure, overlapping sites and other factors affect the evolution.

You are not going to win this debate by misinterpreting what Dr Schneider’s intentions are for his model. I happen to believe that Dr Schneider properly modeled mutation and selection. This is seen by the evolutionary consequences of the use of combination therapy for the treatment of infectious diseases.

Well Paul, you have your own model of the mathematics mutation and selection which reveals something about genome lengths and selection pressures and you dismiss it out of hand because it doesn’t agree with your world view. Dr Schneider thinks that ev models reality, you used to think this until you finally studied the behavior of the model.

And that is utter BS and another prime example of your penchant for misrepresenting others' arguments. I have yet to see Paul once claim that ev does not model something of reality. He has maintained that ev did its job -- demonstrating an increase in information. That is what Dr. Schneider claims as well -- repeatedly from the quotes you have provided of him. I have yet to see anyone but you claim that ev models all aspects of the evolutionary landscape. You have specifically stated that it predicts the inability of evolution to occur on a realistic time scale if three selection pressures are applied. Your example for this in the real world -- HIV triple therapy -- when all the information about it is considered, actually shows the opposite. Unless you can show some real-world example of how this model that you think explains what occurs in the real world functions, then I'm afraid that your argument is dead in the water. Otherwise, all you have is a model that does nothing but sit in the corner.

Well, you can squirm around and try to find a way to reinterpret the many quotes of Dr Schneider but only an extremely prejudiced and biased reader will find your contorted interpretations acceptable.

What makes you think the mathematics of real-world evolution of drug resistance is any different than from the mathematics of any other mutation and selection process?

First, I never said it was. The "mathematics" of real-world evolution of drug resistance shows that three selection pressures does not stop the process and does not slow it to the point that evolution cannot happen on a realistic time scale. That is what the HIV triple therapy story tells us.

However, the three selection pressure does slow evolution, that is what ev shows and that is what this example shows.

But, there is no question, whatsoever, that different mechanisms play into resistance with different organisms. I am not aware of any lateral transfer of information amongst viruses (there probably is some example of this, though), but there is clear lateral transmission of information in bacteria through plasmids. That is an entirely different mechanism from random mutation and selection and a process that dramatically speeds "evolution".

Lateral transfer of information can not and does not increase the information in the gene pool. Neither does recombination without error.

Ichneumonwasp, this is not my model of mutation and natural selection. This is the peer reviewed and published model of mutation and natural selection, written by Dr Tom Schneider, head of computational molecular biology and the National Cancer Institute.

Wow, really? Please leave the rhetoric at home. We all know the facts here.

The fact is you alleged this was my model when you said the following:

Either Kleinman must give up his model or give up his example. Either way it looks bad. Give up the example and he doesn't have a real world link for the model, and it becomes a nice abstraction of uncertain provenance (at least as far as the full range of evolutionary pressure/history/etc., which is what you have said all along).

This is Dr Schneider’s model and it very nicely explains why combination therapy is useful in slowing the evolution of resistant strains when treating HIV.

This model shows that three selection pressures simultaneously slow the evolution process for each of the conditions.

The model was designed to show increases in information. It performs that task.

Every time you say this, I will post Dr Schneider’s statement that appeared in his peer reviewed publication about his model. Hopefully you will get the hint and either abandon your useless argument and acknowledge what his model shows or at least come up with a more sensible argument.

Variations of the program could be used to investigate how population size, genome length, number of sites, size of recognition regions, mutation rate, selective pressure, overlapping sites and other factors affect the evolution.

It shows that three selection pressures slow the evolutionary process. Well, so does reality. Yes, of course. But that has not been your argument until very recently. If your only argument is that three selection pressures (potency held constant) slow evolution, then we all agree. Yes, for one particular definition of "evolution" -- defined as increased variability in a population -- three pressures, potency held constant, slows evolution.

If you read this thread carefully, you will see that I told Paul that the reason the generations for convergence were increasing so rapidly with increasing genome length was the effect of increased spurious binding in the nonbinding site region of the genome. It was only when I became aware that you could set weight factors to zero that I could show that multiple selection conditions was what was slowing evolution in ev.

If you think that varying the potency of selection pressures will somehow overcome the effect that multiple selection pressures slow evolution, you need to show this.

That, quite simply, has not been your argument through this incredibly long series of posts. You have argued that evolution is so profoundly slowed that it could never account for significant change in realistic time frames. Have you changed that argument?

Taffer seems to think that I haven’t changed my argument, you think I have. The only thing I have changed in my argument is to give an explanation why ev evolves so slowly with long genomes.

While single selection conditions evolve much more rapidly. This is exactly what we see when combination therapy is used for treating HIV and TB and what results with monotherapy with the treatment of MRSA, Gonorrhea, pseudomonas and cancers as well. So it is not my model to give up and my examples work just fine, thank you.

We have never debated whether single selection conditions evolve more rapidly than three selection conditions. I don't even see the point in arguing that. Why do you bring this up? No one that I am aware of has contended the opposite position, so what is your point? Is this simply another attempt to misrepresent my position? Should I repeat all the other instances of your attempts to misrepresent my position, Dr. Alan Kleinman?

You are not the only evolutionist I am discussing these issues with. You sometime take quotes addressed to Paul, Mr Scott or others and assume I am addressing responses to you. Mr Scott raised the issue of super bug Gonorrhea; I have just incorporated it into the discussion. I am under no obligation to restrict my discussion with you to only what you want to talk about. If I did that, you have already attempted to reinterpret what Dr Schneider’s intent is for his model and there would be no discussion at all. You evolutionist just like to whine. You think you can frame a mathematical discussion this way but it doesn’t work.

I am not accusing you of creating the model. I am accusing you of using the model for ends it was not designed. Such post-hoc analysis may be useful in science to suggest future research but is notoriously unreliable in arriving at conclusions.

Well, here we go again:

Variations of the program could be used to investigate how population size, genome length, number of sites, size of recognition regions, mutation rate, selective pressure, overlapping sites and other factors affect the evolution.

Not only has Dr Schneider invited this type of analysis with his model publicly through his peer reviewed and published paper on his model, he also personally invited me to do this type of analysis in direct email communication with me. Ichneumonwasp, stop whining that the result of this type of analysis shows your theory is mathematically impossible. It does show how mutation and selection works and this is useful for understanding how to address the evolution of drug resistance when treating infectious diseases.

Dr Schneider modeled the mathematics. The reason you haven’t seen any data is you haven’t read this thread or the Evolutionisdead forum where this discussion started. Here is some new data for you.

That isn't what I asked for. I said that you had not provided data for the mathematics of ev. As in an equation. I have seen plenty of data from individual runs. You continue to harp on the mathematics of ev. Show me the mathematics of it. Show me the equations and let's apply them to the real world and see how they work. If the mathematics of ev models all aspects of the evolutionary landscape then we may continue to discuss it as an accurate model of the evolutionary landscape. If it doesn't, then we scrap it for that purpose and admit that it did it's job -- it showed that information can increase under Darwinian conditions of mutation and natural selection.

There is no need for me to reiterate Dr Schneider’s derivations here. Read his publications and you can find the equations he used to derive his model. In addition, Dr Schneider modeled enough of the evolutionary landscape to describe the mathematics of mutation and selection. Again, Dr Schneider has well said:

A good simulation does not attempt to simulate everything; only the essential components are modeled. For the issue at hand, the form of the genetic code is not relevant; information measured by Shannon's method is more general than that.

Other mutation mechanisms will not change the mathematical fact that increasing the number of selection pressures slows the evolutionary process.

Why would an evolutionist want to scrap a peer reviewed and published model of random point mutation and natural selection?

Mr Scott, you are confusing several principles. Those principles you are confusing are selection pressures, intensity of selection pressures and extinction. The mathematics is clear; increasing the number of selection pressures slows evolution.

I'm calling you out on this one, Dr. Kleinman. Mr. Scott did not confuse any of those issues in his post. In fact, what he did was distinguish the contributions of each. Then entire thrust of his post, Dr. Kleinman, was to show how it is you that confuses these issues. The mathematics of evolution in the real world (and, no, I am not claiming that he supplied an equation) is quite clear in Mr. Scott's post, Dr. Alan Kleinman -- the number of selection pressures is not the critical element. Rather, it is the intensity of selection pressure that serves as the critical element. As we have demonstrated to you repeatedly, the number of pressures may result in extinction, may result in profound slowing of the evolutionary process, or may result in the development of resistance. The critical determinant of the outcome is not the number of selection pressures, Dr. Kleinman, but the intensity of the total pressure.

You aren’t going to accusing me of misrepresenting what you have said, are you?

You have just focused the argument when you said that “the number of selection pressures in not the critical element”. Ev shows that the number of selection pressures is critical in slowing the evolutionary process. What are the critical parameters in the mutation and selection process of evolution? As it stands now, the mathematics of ev shows that genome length and the number of selection conditions are the dominant parameters in the mutation and selection process.

So, 15% of these patients' HIV colonies have done something Kleinman asserts is mathematically impossible: macroevolved.

Mr Scott, the James Randi Educational Forum pussy cat, this is not what I have asserted. What I have asserted is that multiple selection conditions slow the evolutionary process and the use of combination therapy for the treatment of HIV nicely demonstrates this. In addition, this is not a demonstration of macroevolution. What gene has evolved from the beginning? What new function has evolved for these already existing genes?

 

[kjkent1]

Do you think semantics is not going to win this debate little gator? Why don’t you try some mathematics?

I'd tell you to screw off, but that would indicate that you'd succeeded in annoying me.

I'm one of the only persons on this thread who has actually done any experiments using ev to back my position. As for mathematics, you haven't produced any -- you just fall back on "Dr Schneider did the math already." Well, you've extrapolated ev to do everything but wash dishes at this point, so don't bother suggesting that I do anything, at least until you've actually done something yourself, other than cry the same unending river of nonsense.

Why don’t you try to tell us what the purpose of mutation and selection is?

There's no purpose to mutation and selection. "Life is a process of matter that occurs under suitable conditions and evolves while those conditions persist." -- Phillip Wylie.

It has been scientifically established that all independent life forms have a genetic sequence wherein Rseq ~ Rfreq. So, if you mess with ev and produce a perfect creature that doesn't exhibit this state, or that doesn't continue to drift towards that state, then what you've produced is crapola. You may as well pour sand on the floor and call it a sand castle.

 

[Ichneumonwasp]

You aren’t going to accusing me of misrepresenting what you have said, are you?

As should be immediately obvious to anyone who can read I was accusing you of misrepresenting Mr. Scott's position, Dr. Alan Kleinman, since that is precisely what you did. Since you did not answer any of the charges, I assume that you agree to have misrepresented his position as well?

You have already admitted that you misrepresented my position, Dr. Alan Kleinman.

You seem to have a penchant for misrepresentation.

As it stands now, the mathematics of ev shows that genome length and the number of selection conditions are the dominant parameters in the mutation and selection process.

There is no reason to repeat the virtual lack of information in that long post, Dr. Kleinman. So, tell me now, since you have not done so in the past when I have asked, what is the equation that models the dominant parameters in the mutation and selection process? Tell me this mathematics that you continually claim so that we can all examine it and decide if it fits with the reality we see around us. Tell me this equation for evolution, Dr. Kleinman.

 

[kleinman]

Annoying Creationists

Do you think semantics is not going to win this debate little gator? Why don’t you try some mathematics?

I'd tell you to screw off, but that would indicate that you'd succeeded in annoying me.

Oh, go ahead and say it. We all know how annoyed all you evolutionists are that anyone would dare challenge your belief system.

I'm one of the only persons on this thread who has actually done any experiments using ev to back my position. As for mathematics, you haven't produced any -- you just fall back on "Dr Schneider did the math already." Well, you've extrapolated ev to do everything but wash dishes at this point, so don't bother suggesting that I do anything, at least until you've actually done something yourself, other than cry the same unending river of nonsense.

Really? Paul did you read this? Myriad, did you read this? kjkent1 is the only one who has actually done experiments using ev to back his position. You need to read this thread more carefully and the thread on the Evolutionisdead forum and then you wouldn’t make statements like this. But why should I expect an evolutionist to read anything carefully?

Why don’t you try to tell us what the purpose of mutation and selection is?

There's no purpose to mutation and selection. "Life is a process of matter that occurs under suitable conditions and evolves while those conditions persist." -- Phillip Wylie.

So mutation and selection has no relationship to fitness and reproduction?

It has been scientifically established that all independent life forms have a genetic sequence wherein Rseq ~ Rfreq. So, if you mess with ev and produce a perfect creature that doesn't exhibit this state, or that doesn't continue to drift towards that state, then what you've produced is crapola. You may as well pour sand on the floor and call it a sand castle.

Is that what you’ve proven with ev? So ev showing that multiple selection conditions slows the evolutionary process has nothing to do with reality?

You aren’t going to accusing me of misrepresenting what you have said, are you?

As should be immediately obvious to anyone who can read I was accusing you of misrepresenting Mr. Scott's position, Dr. Alan Kleinman, since that is precisely what you did. Since you did not answer any of the charges, I assume that you agree to have misrepresented his position as well?

Do you evolutionists ever quit whining?

You have already admitted that you misrepresented my position, Dr. Alan Kleinman.

So let’s see, what is your position now? You have finally come to the conclusion that multiple selection conditions slow evolution however you don’t think this is a dominant parameter in the mathematics. You’ve got it half right now.

As it stands now, the mathematics of ev shows that genome length and the number of selection conditions are the dominant parameters in the mutation and selection process.

There is no reason to repeat the virtual lack of information in that long post, Dr. Kleinman. So, tell me now, since you have not done so in the past when I have asked, what is the equation that models the dominant parameters in the mutation and selection process? Tell me this mathematics that you continually claim so that we can all examine it and decide if it fits with the reality we see around us. Tell me this equation for evolution, Dr. Kleinman.

You evolutionists whine if I don’t respond to your posts and now you whine when I do respond to your posts. Dr Schneider has clearly explained how he intended to use ev to study the parameters in the mathematics of mutation and selection. When you do study these parameters, it is clear that genome length and the number of selection conditions dominate the mathematics.

Ichneumonwasp, since you seem to have difficulty in grasping the fact that multiple selection conditions slows and dominates the mathematics of evolution as demonstrated by the real cases of the treatment of infectious diseases with combination therapy, here some other examples of how multiple selection conditions slow evolution.

Here is an example from Wikipedia:

Tankmixing pesticides is the combination of two or more pesticides with different modes of action. This practice may improve individual pesticide application results in addition to the benefit of delaying the onset of or mitigating existing pest resistance.

You can find this quote at http://en.wikipedia.org/wiki/Pesticide

How about for herbicides, does the use of multiple herbicides slow evolution?
Here is something from Iowa State:

The evolution of herbicide resistance within a weed population is based on selection pressure. The more frequently a herbicide is used, the more pressure placed on a weed population, and the sooner resistance will appear at a troublesome level in the population. Using alternative modes of action can reduce the potential for selecting resistant weeds by placing different selection pressures on weed populations. In a system relying only on glyphosate, a weed possessing a trait allowing it to survive glyphosate will rapidly increase in frequency. But if a second herbicide is used with glyphosate, this alternative herbicide may kill the weed with the glyphosate resistant trait and prevent it from increasing within the weed population. Theoretically this approach is sound and can reduce the potential for herbicide resistance.

You can find this quote at http://www.weeds.iastate.edu/mgmt/2004/combination.shtml

How about rodenticides, does the use of multiple rodenticides slow evolution?
Here is something from German researchers:

Coumatetralyl (Racumin ) has been known since 1957 as a multiple dose anticoagulant and has been used successfully over many decades. In the seventies and especially the eighties, rats developed an increased resistance to anticoagulants in certain regions of Central Europe. Also, the addition of vitamin K to animal feed (especially to chicken feed) has reduced the efficacy against rats and mice in farm buildings. Combinations of anticoagulants with different types of vitamin D are generally described to increase the efficacy of action against rodents. It was found that especially the combination of coumatetralyl with cholecalciferol (vitamin D3) could overcome the above mentioned problems. Cholecalciferol causes hypercalcemia and, therefore, has a different mode of action compared to anticoagulants. The combination of these active ingredients leads to an obvious increase in efficacy against rodents, even under difficult conditions. The formulation with optimal rodenticidal efficacy contains 0.04 % coumatetralyl and 0.025 % cholecalciferol mixed in rolled oats.

You can find this paper at http://72.14.253.104/search?q=cache:rHo5amSD9IAJ:digitalcommons.unl.edu/cgi/viewcontent.cgi%3Farticle%3D1047%26context%3Dvpc16+combination+rodenticide+resistance&hl=en&ct=clnk&cd=4&gl=us

Multiple selection pressures slow evolution in all types of life forms and all types of circumstances. This is what ev reveals and this is what is seen in reality. This is how the mathematics of mutation and selection works. Multiple selection conditions slow the evolutionary process. If the potency of the selection pressures is sufficient, you get extinction. If the potency of the selection pressures is not sufficient to cause extinction, the evolutionary process is slowed.

So Paul, you proposed that the appearance of oxygen is the selection pressure that led to the evolution of hemoglobin gene. Is that a weak or potent selection pressure? Did the genes which code for the enzymes of the Krebs cycle evolve at the same time? When did the insulin gene evolve? How about all the genes which code for structural proteins? Did all this evolution you proposed that occurred evolve simultaneously? Or did all the genes required for living creatures come about one at a time?

Mutation and natural selection can not and does not do what you evolutionists allege. Ev shows how mutation and natural selection works and it can not accomplish a macroevolutionary process. Your theory is mathematically impossible.

 

[Ichneumonwasp]

Ichneumonwasp, since you seem to have difficulty in grasping the fact that multiple selection conditions slows and dominates the mathematics of evolution as demonstrated by the real cases of the treatment of infectious diseases with combination therapy, here some other examples of how multiple selection conditions slow evolution.

So, I see Dr. Alan Kleinman that you once again wish to misrepresent my position. Why, Dr. Kleinman, have you chosen your entire rebuttal again to consist solely in a misrepresentation of my position? Since I have repeatedly argued that multiple selection pressures (potency held constant) slow the evolutionary process (for one definition of evolution), why do you insist on stating that I have difficulty understanding this fact? Why do you persist, Dr. Alan Kleinman, in misrepresenting what I have said? Why, even when you admitted that you had misrepresented what I had earlier said on this very topic, do you insist on again misrepresenting my position in exactly the same way? Why do you engage in this behavior, Dr. Alan Kleinman?

And why have you not provided the mathematics of evolution, Dr. Kleinman? We are all waiting.

 

[kleinman]

Annoying Creationists

Ichneumonwasp, since you seem to have difficulty in grasping the fact that multiple selection conditions slows and dominates the mathematics of evolution as demonstrated by the real cases of the treatment of infectious diseases with combination therapy, here some other examples of how multiple selection conditions slow evolution.

So, I see Dr. Alan Kleinman that you once again wish to misrepresent my position. Why, Dr. Kleinman, have you chosen your entire rebuttal again to consist solely in a misrepresentation of my position? Since I have repeatedly argued that multiple selection pressures (potency held constant) slow the evolutionary process (for one definition of evolution), why do you insist on stating that I have difficulty understanding this fact? Why do you persist, Dr. Alan Kleinman, in misrepresenting what I have said? Why, even when you admitted that you had misrepresented what I had earlier said on this very topic, do you insist on again misrepresenting my position in exactly the same way? Why do you engage in this behavior, Dr. Alan Kleinman?

Quit whining and look at the quotes and links to pesticides, herbicides and rodenticides. These examples are analogous to what is seen with combination therapy for treating HIV, TB and other infectious diseases, that is that multiple selection pressures slow evolution.

And why have you not provided the mathematics of evolution, Dr. Kleinman? We are all waiting.

Read this thread, the thread in the Evolutionisdead forum on this topic and Dr Schneider’s publications. The mathematics and parametric studies are available for everyone to read who want to understand the mathematics of mutation and selection. If you have trouble reading this information I’ll help explain it to you. Then you will understand why your theory is mathematically impossible.

 

[Ichneumonwasp]

No whining here, Dr. Kleinman. Just simple honest questions that you have not answered. Why, Dr. Alan Kleinman, do you persist in misrepresenting my position in exactly the same way that you earlier admitted to be an instance where you misrepresented my position? Why do you persist in that behaviour, Dr. Kleinman? I would really like an answer, Dr. Alan Kleinman.

Read this thread, the thread in the Evolutionisdead forum on this topic and Dr Schneider’s publications. The mathematics and parametric studies are available for everyone to read who want to understand the mathematics of mutation and selection. If you have trouble reading this information I’ll help explain it to you. Then you will understand why your theory is mathematically impossible.

I see, Dr. Kleinman. I have read this thread. You have not provided the equation. It should be quite easy to cut and paste it here for me to examine if you've already provided it. Please Dr. Kleinman, show me this equation. Show me the equation that proves evolution is impossible. We all need to know this information. It would be ground-breaking info. You would do us all a terrible disservice to withhold it. Please show me the equation, Dr. Kleinman.

 

[kleinman]

Annoying Creationists

Quit whining

No whining here, Dr. Kleinman. Just simple honest questions that you have not answered. Why, Dr. Alan Kleinman, do you persist in misrepresenting my position in exactly the same way that you earlier admitted to be an instance where you misrepresented my position? Why do you persist in that behaviour, Dr. Kleinman? I would really like an answer, Dr. Alan Kleinman.

And I have answered your question. If you want to have an understanding of the mathematics of mutation and selection, you will have to study Dr Schneider’s work. Before I started this public discussion, I studied Dr Schneider’s papers for several months and spent a lot of time studying his web site which includes more information and glossaries to his terminology. If you want to have some understanding of what Dr Schneider has done, read these resources. Once you have done this, you can look at the Evolutionisdead forum on this topic and read this thread and you will find the parametric study done with this model. You haven’t done your homework and you complain when you don’t understand Dr Schneider’s mathematics and my parametric study done with his mathematics. You then whine and say that I don’t show you the mathematics. There is no need to repost Dr Schneider’s work on this thread. There is only need for you to read what is already out there. Why don’t you start here http://nar.oxfordjournals.org/cgi/content/full/28/14/2794

Read this thread, the thread in the Evolutionisdead forum on this topic and Dr Schneider’s publications. The mathematics and parametric studies are available for everyone to read who want to understand the mathematics of mutation and selection. If you have trouble reading this information I’ll help explain it to you. Then you will understand why your theory is mathematically impossible.

I see, Dr. Kleinman. I have read this thread. You have not provided the equation. It should be quite easy to cut and paste it here for me to examine if you've already provided it. Please Dr. Kleinman, show me this equation. Show me the equation that proves evolution is impossible. We all need to know this information. It would be ground-breaking info. You would do us all a terrible disservice to withhold it. Please show me the equation, Dr. Kleinman.

If you read this thread, it is clear that you don’t understand the mathematics that Dr Schneider has presented nor understand the parametric studies done with ev. I have cut and pasted the link to Dr Schneider’s paper above. Read that link and if there is something you don’t understand in his paper, ask and we will see if we can give you an explanation. It may help if you download Dr Schneider’s paper Information Theory Primer. You can find this document at http://www-lmmb.ncifcrf.gov/~toms/paper/primer/primer.pdf Once you read these two documents, you will have in introduction to Dr Schneider’s mathematics of the evolution of binding sites by mutation and selection.

Once you have this introduction, you will start to understand what the parametric study shows from the computer simulation based on this mathematics Dr Schneider developed.

Prepare yourself, because his mathematics shows that mutation and selection is a profoundly slow process and the reason why it is slow is that multiple selection conditions interfere with the evolution process. This is what is seen in reality with combination therapy for treatment of infections, combination pesticides, combination herbicides and combination rodenticides. Welcome to the world of hard mathematical science, not the mushy soft pseudoscience that forms the basis for the theory of evolution.

 

[Ichneumonwasp]

And I have answered your question.

Gosh and gee willikers, Dr. Kleinman, no you haven't. The question was, "Why do you continue to misrepresent my position when you have already admitted that you recognize that you are misrepresenting my position?" You haven't answered that question, Dr. Kleinman? Why haven't you answered that question, Dr. Kleinman?

If you want to have an understanding of the mathematics of mutation and selection, you will have to study Dr Schneider’s work.

Oh, yes, if I want to understand the mathematics behind ev, that is so true. But that isn't the other question that I asked, Dr. Kleinman. I asked for your equation of evolution. You have told me that you have the mathematics of evolution. We have already demonstrated that ev does not cover the entire spectrum of evolution. You, however, insist that you have the mathematics of evolution. It should be easy for you to cut and paste it here. Why don't you do that, Dr. Kleinman? I'm asking nicely.

I'm reading Dr. Schneider's paper now, Dr. Kleinman. I expect that you can have cut and pasted all the relevant data concerning the mathematics of evolution by the time I return. You can do that can you not, Dr. Alan Kleinman?

Once again, I'm not asking for any of the runs of ev. I am asking for the mathematics behind evolution. Please share.

 

[kjkent1]

Oh, go ahead and say it. We all know how annoyed all you evolutionists are that anyone would dare challenge your belief system.

You should try defining evolutionist, before you use it to attribute a belief system to me. I don't "believe" in anything. Everything is subject to change on the basis of subsequent evidence.

I'm one of the only persons on this thread who has actually done any experiments using ev to back my position.

Really? Paul did you read this? Myriad, did you read this? kjkent1 is the only one who has actually done experiments using ev to back his position. You need to read this thread more carefully and the thread on the Evolutionisdead forum and then you wouldn’t make statements like this. But why should I expect an evolutionist to read anything carefully?

Apparently, as a creationist, you read considerably less carefully than I do, because you've just misquoted me -- as emphasized above. Anytime you want to apologize, you just go right ahead with yo bad sef!

So mutation and selection has no relationship to fitness and reproduction?

You asked what "purpose" evolution had. Now, you're asking about a "relationship to fitness and reproduction." Huge difference. Practice your word use.

Is that what you’ve proven with ev? So ev showing that multiple selection conditions slows the evolutionary process has nothing to do with reality?

I've already demonstrated that multiple selection conditions act to create an average result, likely the product of a normal distribution of possible outcomes, which is, as of yet, unproven, because ev only has three selective conditions to test. But the results definitely center around a mean.

You, on the other hand, have simply claimed that evolution is slowed without bounds by multiple selection conditions. You haven't provided a shred of actual proof.

 

[Ichneumonwasp]

OK, read it. Funny, that paper seemed to concern gain of information in biological systems modelled by a computer program, not to provide the mathematics of the entire evolutionary landscape. But, you're such a nice feller' Kleinman, I'm sure that you will guide me. Please tell me the equation of evolution. Please, oh please.

I already knew that Rsequence approaches Rfrequency, so I am sure that you have much more information to impart. Please tell me how it all works.

Oh, can we speak in population sizes of multibillions just for kicks? These puny populations of 64 just don't do it for me. Show me how it works in the real world, why doncha'?

ETA

This is what is seen in reality with combination therapy for treatment of infections, combination pesticides, combination herbicides and combination rodenticides.

Ah, dang, I'm afraid you left out the effects of certain triple therapy regimens in your hand-picked example -- HIV treatment -- where 95+% compliance results in fairly rapid development of resistance. And since your examples demonstrate quite plainly that potent selection pressures dramatically reduce variability, I must ask you one simple question: why are you proving the theory of evolution for us? I mean, we'd be in a right bloody mess if strong selection pressures didn't diminish variability and slow the process. We couldn't explain anything without that. No extinctions, no populations near the brink. Thank you, Dr. Kleinman, for proving to me so completely how correct and prescient Darwin was by use of these examples. I'm wondering, though, why you are arguing my case for me, since this is what I have been screeching for the past four weeks now. Potent pressures slow one definition of the word evolution by reducing variability. I'm sure Richard Dawkins will be so relieved, since he has argued this for decades.

When are you going to show me this elusive equation for evolution?

And, oh yeah, I forgot to mention again -- why are we so focused on a computer model that demonstrates the development of information through mutation and natural selection when nature clearly shows your conjecture about this model to be wrong (need I repeat the story of HIV triple therapy -- your hand picked example -- again?)?

 

[kleinman]

Annoying Creationists

And I have answered your question.

Gosh and gee willikers, Dr. Kleinman, no you haven't. The question was, "Why do you continue to misrepresent my position when you have already admitted that you recognize that you are misrepresenting my position?" You haven't answered that question, Dr. Kleinman? Why haven't you answered that question, Dr. Kleinman?

Sure I have answered your question; you are just a poor misunderstood evolutionist that has been ganged up on by an annoying creationist.

Have I asked you the following question? What were the components of the DNA replicase system doing before the DNA replicase system existed? In particular what were Gyrase and helicase doing before DNA could be replicated? This question relates to irreducible complexity.

If you want to have an understanding of the mathematics of mutation and selection, you will have to study Dr Schneider’s work.

Oh, yes, if I want to understand the mathematics behind ev, that is so true. But that isn't the other question that I asked, Dr. Kleinman. I asked for your equation of evolution. You have told me that you have the mathematics of evolution. We have already demonstrated that ev does not cover the entire spectrum of evolution. You, however, insist that you have the mathematics of evolution. It should be easy for you to cut and paste it here. Why don't you do that, Dr. Kleinman? I'm asking nicely.

Oh no, I did tell you I have the mathematics of evolution, I told you Dr Schneider has the mathematics of evolution. And that mathematics shows that mutation and selection is a profoundly slow process, far too slow to support the theory of evolution. And why is that process too slow? It is too slow because multiple selection conditions slow the evolutionary process. Dr Schneider has done a very good job in doing the mathematics of mutation and selection.

Ev doesn’t need to cover the entire spectrum of evolution. Dr Schneider said it very well when he said the following:

A good simulation does not attempt to simulate everything; only the essential components are modeled. For the issue at hand, the form of the genetic code is not relevant; information measured by Shannon's method is more general than that.

Now if you think that other mechanisms of mutation will alter this fundamental mathematical finding then why do the real examples of multiple selection conditions such as combination therapy for the treatment of HIV and TB, combination pesticides, combination herbicides and combination rodenticides demonstrate this same fundamental mathematical finding? Are these real examples of mutation and selection situations limited to random point mutations?

I'm reading Dr. Schneider's paper now, Dr. Kleinman. I expect that you can have cut and pasted all the relevant data concerning the mathematics of evolution by the time I return. You can do that can you not, Dr. Alan Kleinman?

It’s about time you started reading these papers. You may find that much of his paper is already familiar to you. I have already cut and pasted much of the paper into this thread.

Once again, I'm not asking for any of the runs of ev. I am asking for the mathematics behind evolution. Please share.

Let’s start with something simple. If a mutation is beneficial, it increases the fitness of a creature to reproduce. If a mutation is detrimental it reduces the fitness of a creature to reproduce. If a mutation is neutral, it does not affect the fitness of a creature one way or the other. Dr Schneider’s selection process is based on three selection conditions. Dr Schneider uses a weight matrix to simulate a binding protein. Dr Schneider’s simulation traverses this weight matrix along the genome and looks to see if there is a match to a threshold of this weight matrix. If the weight matrix does not find a binding site where it is expected, that is considered an error. That is one selection condition. If the weight matrix finds spurious binding site in the genome, that is considered an error. That is the second selection condition. If the weight matrix finds a binding site outside the binding site region, that is also considered an error. That is the third selection condition. Paul will sometimes talk of the spurious binding sites in the gene and nonbinding site region as a single selection condition. In that case, you have two rather than three selection conditions in the model. Selection is based on the half of the creatures with the fewest errors (mistakes) being allowed to reproduce with random point mutations occurring based on a rate specified. Once you understand this, we will talk more about what this mathematics shows.

Oh, go ahead and say it. We all know how annoyed all you evolutionists are that anyone would dare challenge your belief system.

You should try defining evolutionist, before you use it to attribute a belief system to me. I don't "believe" in anything. Everything is subject to change on the basis of subsequent evidence.

You mean you don’t believe in your string cheese theory of evolution? Was that just a red herring, string cheese and whine meal that you were serving up?

OK, read it. Funny, that paper seemed to concern gain of information in biological systems modelled by a computer program, not to provide the mathematics of the entire evolutionary landscape. But, you're such a nice feller' Kleinman, I'm sure that you will guide me. Please tell me the equation of evolution. Please, oh please.

And that rate of information gain becomes profoundly slow when you use a realistic genome length and mutation rate. This is what you theory is mathematically impossible. The rate of information gain is profoundly slow for realistic genome lengths and mutation rates. If you read that paper, you would know that Dr Schneider wanted to investigate how these parameters affect evolution. The next question you should ask is why is this rate of information gain so profoundly slow on realistic genomes with realistic mutations rates? The rate of information gain is profoundly slow because of competing selection conditions.

I already knew that Rsequence approaches Rfrequency, so I am sure that you have much more information to impart. Please tell me how it all works.

It doesn’t work because the rate at which Rsequence approaches Rfrequency is profoundly slow on any realistic genome. Why is it so profoundly slow? Because multiple selection condition slow evolution.

Oh, can we speak in population sizes of multibillions just for kicks? These puny populations of 64 just don't do it for me. Show me how it works in the real world, why doncha'?

Well, I have done populations up to 10^6 (the limits of the memory on my computer) and what it shows is that the rate of decrease in the generations for convergence drops dramatically as you increase populations. Why is this happening? This happens because increasing population increases the probability of a proper mutation hitting a proper locus at less than an additive amount. All the data we have on population shows that huge populations will not increase the rate of convergence sufficiently to make your theory possible. Of course you would already know this if you had read this thread.

 

[Ichneumonwasp]

Sure I have answered your question; you are just a poor misunderstood evolutionist that has been ganged up on by an annoying creationist.

So, once again you dodge the question? Why do you persist in misrepresenting my position, Dr. Kleinman, even after you have admitted to doing so in the past? Why do you act like that Dr. Kleinman? Just answer the question, please.

Oh, ganged up, really? I must have missed the gang. What did they look like? I hope they had cool colors and face paint and all that. Did they carry baseball bats and wear uniforms?

Have I asked you the following question? What were the components of the DNA replicase system doing before the DNA replicase system existed? In particular what were Gyrase and helicase doing before DNA could be replicated? This question relates to irreducible complexity.

Oh, sure you have. And I told you then what I will tell you now -- we deal with those issues once we have dealt with your example of HIV triple therapy. You proposed it. I still have yet to hear a straight answer from you about that issue. Does the data from every HIV triple therapy protocol demonstrate your contention that evolution is so slow that it could never have occurred in realistic time periods when resistance to triple therapy forms in both relatively lower potency protocols with 95+% compliance and strongly potent protocols with 80% compliance?

I did tell you I have the mathematics of evolution

Oh, good, then. I was getting a bit worried. What's that equation, now?

Now if you think that other mechanisms of mutation will alter this fundamental mathematical finding then why do the real examples of multiple selection conditions such as combination therapy for the treatment of HIV and TB, combination pesticides, combination herbicides and combination rodenticides demonstrate this same fundamental mathematical finding? Are these real examples of mutation and selection situations limited to random point mutations?

They don't under all treatment conditions, as has been shown you repeatedly. The prime factors determining the relatively rapid development of resistance depends on a combination of potency and variability within the treated population. If potency is so high that variability is kept to a bare minimum, then resistance will develop very slowly. If either potency is less intense or compliance is not complete -- both conditions permitting sufficient population size to allow enough variability -- then resistance develops relatively quickly. That is what the natural data show unequivocally. Any computer model must take each of these issues into account if it wants to describe the natural processes of resistance development -- progress by means of mutation and natural selection.

Let’s start with something simple. If a mutation is beneficial, it increases the fitness of a creature to reproduce. If a mutation is detrimental it reduces the fitness of a creature to reproduce. If a mutation is neutral, it does not affect the fitness of a creature one way or the other. Dr Schneider’s selection process is based on three selection conditions. Dr Schneider uses a weight matrix to simulate a binding protein. Dr Schneider’s simulation traverses this weight matrix along the genome and looks to see if there is a match to a threshold of this weight matrix. If the weight matrix does not find a binding site where it is expected, that is considered an error. That is one selection condition. If the weight matrix finds spurious binding site in the genome, that is considered an error. That is the second selection condition. If the weight matrix finds a binding site outside the binding site region, that is also considered an error. That is the third selection condition. Paul will sometimes talk of the spurious binding sites in the gene and nonbinding site region as a single selection condition. In that case, you have two rather than three selection conditions in the model. Selection is based on the half of the creatures with the fewest errors (mistakes) being allowed to reproduce with random point mutations occurring based on a rate specified. Once you understand this, we will talk more about what this mathematics shows.

Golly jeepers, Dr. Kleinman, I surely did know that you was a nice feller to go off and repeat all that mess that was already covered so well earlier.

Give me the equation, Dr. Kleinman. Stop pussyfooting around the issue. Inquiring minds want that equation.

Well, I have done populations up to 10^6

Really? Populations approximately 10^-3 lower than what I asked? How very nice. And under what conditions, with what selection pressures, with what error rates?

All the data we have on population shows that huge populations will not increase the rate of convergence sufficiently to make your theory possible.

Well that would appear to be a big problem for your argument. Because the real world shows that when populations are increased by limiting the potency of selection pressures resistance develops. You must excuse me for trusting reality.

 

[joobz]

If you apply the concept of the first law to natural selection, what you are saying is that the creature that can put more energy toward reproduction than other life activities will be the most successful creature by your theory of evolution. So how do you select for something that does not exist?

Oh, you big silly, Dr. kleinman. Of course, evolution must abide by the thermodynamic principles. But your gibberish relates to the first law how? And this explains that natural selection is a restatement of the first law? Really? How?

It seems you've been performing the Kleinman method of debate for so long that you've become completely unable to make a logical thought.

 

[Paul C. Anagnostopoulos]

Ok, let’s see how close we can make the sock analogy to mutation and selection. Let’s assume you have no a priori knowledge of the number of colors socks. You start by randomly choosing two socks out of the drawer. If they match, roll them together, if not, start a pile of each color. Continue this process until you finish taking all the socks from the drawer. If the socks are all of one color, your task is finished. If your socks are multiple colored, you have to take the now sorted piles of socks and roll them together. It takes more time and work to match and roll multiple different colors of socks than to match and roll a collection of single color socks. Delphi has come up with very nice, simple example, of why multiple selection conditions slow evolution.

Ah, so now we're pairing the socks, not just sorting them. I'm not exactly sure how this relates to evolution, but I can certainly pair them as I sort them, avoiding the second pass to pair them. It takes the same time regardless of the number of colors, because the number of selecting, matching, and pairing operations is the same in all cases. The matching operations require more comparisons as the number of colors increases. Perhaps that's what you're referring to.

I’m not misusing your term “perfect creature”, I’m defining for readers of the thread exactly what this term means. This definition is perfectly consistent with Kjkent1’s point that a “perfect creature” arises instantaneously with no selection pressures at all. No selection pressure means there are no mistakes. I’m not shooting myself in the foot; I’m shooting your theory of evolution in the heart.

And no selection pressures means that the function performed by the evolved creatures is different than when there are selection pressures. And so we agree that comparing the number of generations to perfection is a risky business.

Why don’t you explain to us what the function of mutation and selection is?

Evasion noted. Do you agree that the function performed by the evolved creatures depends on the number and type of selection pressures?

You are missing a point to argue. What you may have is a situation where the two selection case puts the model on a point in the fitness landscape that gives few easy paths to an optimum while adding a third selection condition enables the model to find a path to an optimum. You should not be amazed that zero selection conditions leads to zero mistakes, you have stopped performing mutation and selection under this circumstance.

Both mutation and selection continue. It's just that all the creatures have zero mistakes. They're perfect! It's a wonderment!

~~ Paul

 

[Paul C. Anagnostopoulos]

Really? Paul did you read this? Myriad, did you read this? kjkent1 is the only one who has actually done experiments using ev to back his position. You need to read this thread more carefully and the thread on the Evolutionisdead forum and then you wouldn’t make statements like this. But why should I expect an evolutionist to read anything carefully?

Boy howdy!

~~ Paul

 

[Ichneumonwasp]

Sorry, missed this the first time through......

Ev doesn’t need to cover the entire spectrum of evolution. Dr Schneider said it very well when he said the following:

Originally Posted by Dr Schneider
A good simulation does not attempt to simulate everything; only the essential components are modeled. For the issue at hand, the form of the genetic code is not relevant; information measured by Shannon's method is more general than that.

Yes, he did say that. Because ev does not cover the entire spectrum of evolution. Ev deals with information gain in a relatively concise system that uses arbitrary selection pressures and relatively small population sizes, so necessarily small variability. Yet, it still shows information gain.

It does not, as Dr. Schneider says "attempt to simulate everything". For instance it does not simulate the development of resistance in biological entities. You still have no real world example to show three pressures that work like ev. Your assessment of the model does not fit with reality. His model worked quite well for the reality it simulated. It was not designed to do the job you say it does. You have no evidence to demonstrate that it simulates reality in any way outside of information gain. There is considerable evidence already supplied to show that the results you claim for three selection pressures within the model are not seen in the real world. I'm sorry, but again the real world wins.

 

[kleinman]

Annoying Creationists

Sure I have answered your question; you are just a poor misunderstood evolutionist that has been ganged up on by an annoying creationist.

So, once again you dodge the question? Why do you persist in misrepresenting my position, Dr. Kleinman, even after you have admitted to doing so in the past? Why do you act like that Dr. Kleinman? Just answer the question, please.

So what is this position of yours that you continually whine that I am misrepresenting? It can’t be your position that multiple selection pressures slow the evolution process since that is true. It must be your position that multiple selection pressures don’t dominate the mathematics of mutation and selection. You just happen to be wrong in that position. The mathematics of ev shows this and there are numerous real examples that show this.

Oh, ganged up, really? I must have missed the gang. What did they look like? I hope they had cool colors and face paint and all that. Did they carry baseball bats and wear uniforms?

Didn’t you know that creationists have flocked to this web site? At least that’s what evolutionists on this thread have posted. Of course if you had read this thread, you would know this.

Have I asked you the following question? What were the components of the DNA replicase system doing before the DNA replicase system existed? In particular what were Gyrase and helicase doing before DNA could be replicated? This question relates to irreducible complexity.

Oh, sure you have. And I told you then what I will tell you now -- we deal with those issues once we have dealt with your example of HIV triple therapy. You proposed it. I still have yet to hear a straight answer from you about that issue. Does the data from every HIV triple therapy protocol demonstrate your contention that evolution is so slow that it could never have occurred in realistic time periods when resistance to triple therapy forms in both relatively lower potency protocols with 95+% compliance and strongly potent protocols with 80% compliance?

Ok, we can talk about irreducible complexity after you learn the mathematics of mutation and selection.

Oh no, I never said that you couldn’t evolve three selection conditions in realistic periods of time, what I said is that multiple selection conditions slow the evolutionary process. You wouldn’t misrepresent what I have said would you?

I did tell you I have the mathematics of evolution.

Oh, good, then. I was getting a bit worried. What's that equation, now?

It’s not a single equation. Of course if you understood Dr Schneider’s work, I wouldn’t have to explain this to you. You finally read his paper about an hour ago so now that you are an expert on the mathematics of mutation and selection, you now should understand why multiple selection conditions slow the evolutionary process. By the way, what is that selection condition that would evolve a gene from the beginning?

Now if you think that other mechanisms of mutation will alter this fundamental mathematical finding then why do the real examples of multiple selection conditions such as combination therapy for the treatment of HIV and TB, combination pesticides, combination herbicides and combination rodenticides demonstrate this same fundamental mathematical finding? Are these real examples of mutation and selection situations limited to random point mutations?

They don't under all treatment conditions, as has been shown you repeatedly. The prime factors determining the relatively rapid development of resistance depends on a combination of potency and variability within the treated population. If potency is so high that variability is kept to a bare minimum, then resistance will develop very slowly. If either potency is less intense or compliance is not complete -- both conditions permitting sufficient population size to allow enough variability -- then resistance develops relatively quickly. That is what the natural data show unequivocally. Any computer model must take each of these issues into account if it wants to describe the natural processes of resistance development -- progress by means of mutation and natural selection.

Since you now are an expert in the mathematics of mutation and selection, you don’t need to run the numbers to prove your point. Just what mutation mechanism is going to speed up the process of evolution? And what is that selection condition that would evolve a gene from the beginning?

Let’s start with something simple. If a mutation is beneficial, it increases the fitness of a creature to reproduce. If a mutation is detrimental it reduces the fitness of a creature to reproduce. If a mutation is neutral, it does not affect the fitness of a creature one way or the other. Dr Schneider’s selection process is based on three selection conditions. Dr Schneider uses a weight matrix to simulate a binding protein. Dr Schneider’s simulation traverses this weight matrix along the genome and looks to see if there is a match to a threshold of this weight matrix. If the weight matrix does not find a binding site where it is expected, that is considered an error. That is one selection condition. If the weight matrix finds spurious binding site in the genome, that is considered an error. That is the second selection condition. If the weight matrix finds a binding site outside the binding site region, that is also considered an error. That is the third selection condition. Paul will sometimes talk of the spurious binding sites in the gene and nonbinding site region as a single selection condition. In that case, you have two rather than three selection conditions in the model. Selection is based on the half of the creatures with the fewest errors (mistakes) being allowed to reproduce with random point mutations occurring based on a rate specified. Once you understand this, we will talk more about what this mathematics shows.

Golly jeepers, Dr. Kleinman, I surely did know that you was a nice feller to go off and repeat all that mess that was already covered so well earlier.

I have to do this because you are so deficient in the mathematics of mutation and selection. I wouldn’t have to repeat this for you if you had read and understood this thread but I’ll be patient with you until you understand this topic.

Give me the equation, Dr. Kleinman. Stop pussyfooting around the issue. Inquiring minds want that equation.

I am giving you the equations of mutation and selection but a prejudiced and biased mind is having a hard time understanding them. But I’ll be patient with you. Did you read Dr Schneider’s primer on information theory?

Well, I have done populations up to 10^6

Really? Populations approximately 10^-3 lower than what I asked? How very nice. And under what conditions, with what selection pressures, with what error rates?

I posted all the parameters used to compute this data with ev. If you had read and understood this thread, you would have seen this data. Do you want me to post the data again (for at least the third time)?

All the data we have on population shows that huge populations will not increase the rate of convergence sufficiently to make your theory possible.

Well that would appear to be a big problem for your argument. Because the real world shows that when populations are increased by limiting the potency of selection pressures resistance develops. You must excuse me for trusting reality.

Certainly if a selection pressure does not cause extinction, a creature may develop resistance to that selection pressure; however there are no selection pressures that will evolve a gene from the beginning. And multiple selection pressures slow the evolutionary process. This is why your theory is mathematically impossible. You can attain microevolutionary changes by mutation and selection but you can not attain the huge number of changes required for macroevolution. It is mathematically impossible.

As you study and learn Dr Schneider’s equations, this will become more apparent to you.

If you apply the concept of the first law to natural selection, what you are saying is that the creature that can put more energy toward reproduction than other life activities will be the most successful creature by your theory of evolution. So how do you select for something that does not exist?

Oh, you big silly, Dr. kleinman. Of course, evolution must abide by the thermodynamic principles. But your gibberish relates to the first law how? And this explains that natural selection is a restatement of the first law? Really? How?

It’s quite simple joobz. If a creature has to expend energy to survive a selection pressure, the creature has less energy available to reproduce.

It seems you've been performing the Kleinman method of debate for so long that you've become completely unable to make a logical thought.

It seems your mind is so prejudiced and biased by the theory of evolution that you have lost the ability to understand simple logic.

Ok, let’s see how close we can make the sock analogy to mutation and selection. Let’s assume you have no a priori knowledge of the number of colors socks. You start by randomly choosing two socks out of the drawer. If they match, roll them together, if not, start a pile of each color. Continue this process until you finish taking all the socks from the drawer. If the socks are all of one color, your task is finished. If your socks are multiple colored, you have to take the now sorted piles of socks and roll them together. It takes more time and work to match and roll multiple different colors of socks than to match and roll a collection of single color socks. Delphi has come up with very nice, simple example, of why multiple selection conditions slow evolution.

Ah, so now we're pairing the socks, not just sorting them. I'm not exactly sure how this relates to evolution, but I can certainly pair them as I sort them, avoiding the second pass to pair them. It takes the same time regardless of the number of colors, because the number of selecting, matching, and pairing operations is the same in all cases. The matching operations require more comparisons as the number of colors increases. Perhaps that's what you're referring to.

Even if you don’t pair the socks, it takes more work to sort multiple color socks. If the socks are all the same color, as you randomly pull the socks out of the draw, the socks all go into one pile. If you have a variety of different color socks, you must decide which pile to put the sock into. That requires more decision making and makes the sort go more slowly.

I’m not misusing your term “perfect creature”, I’m defining for readers of the thread exactly what this term means. This definition is perfectly consistent with Kjkent1’s point that a “perfect creature” arises instantaneously with no selection pressures at all. No selection pressure means there are no mistakes. I’m not shooting myself in the foot; I’m shooting your theory of evolution in the heart.

And no selection pressures means that the function performed by the evolved creatures is different than when there are selection pressures. And so we agree that comparing the number of generations to perfection is a risky business.

The function of the evolved creature is to adapt to the given selection pressures which are affecting that creature’s fitness to reproduce. If you have multiple selection conditions, it takes far more generations for a creature to adapt to these conditions simultaneously. If you subject the creature to the same selection conditions serially, the creature can adapt in far few generations. This is what is demonstrated by the use of combination therapy for treatment of HIV, combination pesticides, combination herbicides and combination rodenticides. This is what is demonstrated with ev.

Why don’t you explain to us what the function of mutation and selection is?

Evasion noted. Do you agree that the function performed by the evolved creatures depends on the number and type of selection pressures?

The function of an evolved creature is to adapt to selection pressures which is affecting the creature’s fitness to reproduce. This is what you do with ev, this is what is shown with combination therapy to treat infectious diseases, this is what is shown with pesticides, this is what is shown with herbicides, this is what is shown with rodenticides. This is how the mathematics of mutation and selection works.

You are missing a point to argue. What you may have is a situation where the two selection case puts the model on a point in the fitness landscape that gives few easy paths to an optimum while adding a third selection condition enables the model to find a path to an optimum. You should not be amazed that zero selection conditions leads to zero mistakes, you have stopped performing mutation and selection under this circumstance.

Both mutation and selection continue. It's just that all the creatures have zero mistakes. They're perfect! It's a wonderment!

They have adapted to the particular selection pressures applied. Your mistakes go to zero for that selection condition when that selection condition is satisfied.

Really? Paul did you read this? Myriad, did you read this? kjkent1 is the only one who has actually done experiments using ev to back his position. You need to read this thread more carefully and the thread on the Evolutionisdead forum and then you wouldn’t make statements like this. But why should I expect an evolutionist to read anything carefully?

Boy howdy!

I just wanted to make sure that you got credit for all your hard work. After all, if it wasn’t for Dr Schneider’s mathematics and your good computer programming skills, it would be much more difficult to prove your theory is mathematically impossible. I appreciate all you have done, now if we can only teach Dr Schneider’s mathematics to Ichneumonwasp, then we will have really accomplished something.

Sorry, missed this the first time through......

Ev doesn’t need to cover the entire spectrum of evolution. Dr Schneider said it very well when he said the following:

A good simulation does not attempt to simulate everything; only the essential components are modeled. For the issue at hand, the form of the genetic code is not relevant; information measured by Shannon's method is more general than that.

Yes, he did say that. Because ev does not cover the entire spectrum of evolution. Ev deals with information gain in a relatively concise system that uses arbitrary selection pressures and relatively small population sizes, so necessarily small variability. Yet, it still shows information gain.

You know what else you missed? The rate of information gain becomes profoundly slow when you use realistic genome lengths and mutations rates. Why does this happen? It happens because multiple selection conditions slow down the rate of information gain. Don’t worry, I’ll help you out with the stuff you miss (which is just about everything when it comes to the mathematics of mutation and selection).

It does not, as Dr. Schneider says "attempt to simulate everything". For instance it does not simulate the development of resistance in biological entities. You still have no real world example to show three pressures that work like ev. Your assessment of the model does not fit with reality. His model worked quite well for the reality it simulated. It was not designed to do the job you say it does. You have no evidence to demonstrate that it simulates reality in any way outside of information gain. There is considerable evidence already supplied to show that the results you claim for three selection pressures within the model are not seen in the real world. I'm sorry, but again the real world wins.

So tell us, what is the difference between the mathematics of the evolution of drug resistance and the mathematics of the evolution of binding sites as done in ev? Or, what is the difference between the mathematics of combination pesticides or combination herbicides or combination rodenticides when comparing this to the multiple selection pressures as used in ev?

Selection pressures are nothing more than stresses put on creatures affecting the fitness of the creature to reproduce. Dr Schneider hit the nail on the head mathematically and the numerous real examples of this with combination therapy of infectious diseases or combination pesticides or combination herbicides or combination rodenticides all hit that nail on the head on how multiple selection pressure slow the evolution of resistant strains to those selection pressures. It just so happens that those nails are in the coffin for the theory of evolution.