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.
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.
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.
Why don’t you explain to us what the function of mutation and selection is?
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.
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.
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?
You haven’t read this thread very carefully, if you had you would have seen that I called the theory of evolution “dumbass”.
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?
In one breath, you evolutionists complain that I’m always moving the goalposts and in your next breath you complain I haven’t changed my argument one bit. Would you evolutionists make up your mind?
Are you sure you mean “wonder” or did you mean to say “wander”? Wonder means to speculate.
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.
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.
You are in denial Ichneumonwasp. This is what Dr Schneider designed ev to do:
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.
I like the way Dr Schneider argues this point:
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.
Again, let’s see what Dr Schneider intended for his model which was published in the peer reviewed journal, Nucleic Acids Research.
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, 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.
However, the three selection pressure does slow evolution, that is what ev shows and that is what this example shows.
Lateral transfer of information can not and does not increase the information in the gene pool. Neither does recombination without error.
The fact is you alleged this was my model when you said the following:
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.
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.
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.
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.
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.
Well, here we go again:
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.
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:
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?
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.
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?
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