Annoying creationists

[Taffer]

Let’s see if Adebz can tell us what the real meaning of these papers is. Then he might not win the race to be the last evolutionist to understand the real meaning of the mathematics of mutation and selection.

Given that he actually understands what evolutionary theory teaches, I suspect he will understand better then you.

To wit: emergence does not mean evolution.

 

[kleinman]

Annoying Creationists

Of course my response to your post was logical. Evolutionists know that most selection pressures are stabilizing. That is why I quoted this line from an evolutionist written text on genetics. Now if evolutionists learn the mathematics of mutation and selection and come to understand that multiple selection pressures slow the evolutionary process, then we can finally lay the theory of evolution to rest. This is substantiated by an evolutionist written and peer reviewed model of random point mutation and natural selection, the Wikipedia reference on fitness landscape and numerous real examples of multiple selection pressures slowing evolution. I will continue looking for more real examples of how multiple selection pressures slow evolution. You evolutionists can look for examples of where multiple selection pressures accelerate evolution, which would spice up this discussion.

Yawn. You say a lot of words, but none address the challenge at your feet. Show evolution how evolution is impossible mathematically. that's it.

Go back and reread this thread and the related thread on the Evolutionisdead forum. You will find the parametric studies done with ev that show that as you increase genome lengths in the model, the number of generations required for evolving the selection conditions becomes huge as you try to approach realistic genome lengths. If you limit the number of selection conditions in the model to a single selection condition that selection condition can evolve very rapidly even with large genomes. This is exactly analogous to what we see in the numerous real examples which I have posted where multiple directed selection pressures slow the creatures ability to evolve resistance to those selection pressures. The Wikipedia reference on fitness landscape presents the same concept in different terminology. This is how mutation and selection works. Stabilizing selection pressures maintain the status quo and directed selection pressures interfere with each other. There are no directed selection pressures that can evolve reptiles into birds or a primate precursor into humans and chimpanzees. It requires too many directed selection pressures which only two or three are sufficient to slow the evolutionary process profoundly even on HIV which has a very high mutation rate, very short generation times, very large reproduction rates and a very short genome length. You can’t evolve binding sites on a genome the length of a typical reptile in a reasonable number of generations using ev. The problem has nothing to do with only allowing random point mutations; the problem is the three selection conditions. How do you expect to evolve the huge number of genetic differences between reptiles and birds with their much lower mutation rates, much longer generation times, much smaller reproduction rates and much longer genome lengths than HIV? The mathematics is not there to support this. Mutation and selection does not work the way evolutionists allege. I will continue to post references to how mutation and selection actually works.

 

[Dr Adequate]

The red line shows generations to achieve fixation of n alleles acted on by n selection pressures, the n+1^th selection pressure being introduced only after the n^th allele is fixed.

The blue line shows generations to achieve fixation of n alleles acted on by n selection pressures simultaneously.

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

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

 

[Dr Adequate]

Go back and reread this thread and the related thread on the Evolutionisdead forum. You will find the parametric studies done with ev that show that as you increase genome lengths in the model, the number of generations required for evolving the selection conditions becomes huge as you try to approach realistic genome lengths. If you limit the number of selection conditions in the model to a single selection condition that selection condition can evolve very rapidly even with large genomes. This is exactly analogous to what we see in the numerous real examples which I have posted where multiple directed selection pressures slow the creatures ability to evolve resistance to those selection pressures. The Wikipedia reference on fitness landscape presents the same concept in different terminology. This is how mutation and selection works. Stabilizing selection pressures maintain the status quo and directed selection pressures interfere with each other. There are no directed selection pressures that can evolve reptiles into birds or a primate precursor into humans and chimpanzees. It requires too many directed selection pressures which only two or three are sufficient to slow the evolutionary process profoundly even on HIV which has a very high mutation rate, very short generation times, very large reproduction rates and a very short genome length. You can’t evolve binding sites on a genome the length of a typical reptile in a reasonable number of generations using ev. The problem has nothing to do with only allowing random point mutations; the problem is the three selection conditions. How do you expect to evolve the huge number of genetic differences between reptiles and birds with their much lower mutation rates, much longer generation times, much smaller reproduction rates and much longer genome lengths than HIV? The mathematics is not there to support this. Mutation and selection does not work the way evolutionists allege. I will continue to post references to how mutation and selection actually works.

So, the same old lies and no actual math?

 

[Dr Adequate]

Let’s see if Adebz can tell us what the real meaning of these papers is.

Sure. They mean what they actually say, none of which supports stupid lies like the following:

Then he might not win the race to be the last evolutionist to understand the real meaning of the mathematics of mutation and selection. Of course my response to your post was logical. Evolutionists know that most selection pressures are stabilizing. That is why I quoted this line from an evolutionist written text on genetics. Now if evolutionists learn the mathematics of mutation and selection and come to understand that multiple selection pressures slow the evolutionary process, then we can finally lay the theory of evolution to rest. This is substantiated by an evolutionist written and peer reviewed model of random point mutation and natural selection, the Wikipedia reference on fitness landscape and numerous real examples of multiple selection pressures slowing evolution. I will continue looking for more real examples of how multiple selection pressures slow evolution. You evolutionists can look for examples of where multiple selection pressures accelerate evolution, which would spice up this discussion.

We all know you're lying, kleinman. 'Cos you've babbled out these lies before, remember? And we showed you up as a liar, remember?

 

[Taffer]

[qimg]http://img514.imageshack.us/img514/3974/genegraphhx4.jpg[/qimg]

The red line shows generations to achieve fixation of n alleles acted on by n selection pressures, the n+1^th selection pressure being introduced only after the n^th allele is fixed.

The blue line shows generations to achieve fixation of n alleles acted on by n selection pressures simulataneously.

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

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

Wonderful. QED.

 

[Dr Adequate]

Wonderful.

Elementary.

I told kleinman this would happen several pages back, on the basis of probability theory.

But thanks.

 

[Dr Adequate]

I've updated the graph to show the effects of recombination.

The red line shows generations to achieve fixation of n alleles acted on by n selection pressures, the n+1^th selection pressure being introduced only after the n^th allele is fixed.

The blue line shows generations to achieve fixation of n alleles acted on by n selection pressures simultaneously.

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

The green line shows simultaneous selection pressures with the same parameters, but with recombination between successful organisms.

Note how with simultaneous selection pressures, with or without recombination, the rate of evolution (fixations/generation) increases with the number of selection pressures.

Note that recombination also increases the rate of evolution.

---

I should have mentioned, perhaps, that each data point is the average of 10,000 trials.

 

[joobz]

Well, that should about sum it up.

The goal post was, multiple "directional" selection pressures slow evolution, which means evolution is impossible.

DR. A. demonstrated, mathematically, that multiple "directional" selection pressures can indeed speed up evolution, which means evolution is possible.

Ok, Kleinman, this is done with. It is now time for you to explain how Noah's ark was mathematically possible.

 

[kleinman]

Annoying Creationists

Adebz is trying to do his mathematics by gif and awe. At least this brainwashed, prejudiced and biased evolutionist is trying. What he is trying to do is be the last evolutionist to understand the mathematics of mutation and selection. He thinks that a graph that does not include genome size, mutation rate, population, description of selection pressures, real examples of what he is trying to demonstrate, and a derivation of the model with assumptions used is somehow going to convince anyone reading this thread that multiple selection pressures accelerates evolution. Wait, it does convince Taffer. So we still have a horse race, its Adebz and Taffer neck and neck to be the last evolutionists on this thread to understand the mathematics of mutation and selection.

To wit: emergence does not mean evolution.

Taffer tries to make a point using semantics.

Here is another link which discusses the attempted extinction of mosquito larve and can be found at http://faculty.ucr.edu/~walton/bacteria.htm . Note that this author does not use the word emergence in describing the evolution of resistance to these selection pressures.

Two Bacillus are currently used for mosquito control in California; however, because Bacillus thuringiensis subsp. israelensis (Bti) is comparatively less effective against mosquitoes inhabiting the organically enriched waters of treatment wetlands, Bacillus sphaericus currently offers a viable alternative for microbial control of mosquitoes in organically-enriched treatment wetlands (Walton et al. 1998). Unlike Bti which contains multiple toxins that limit the potential for the rapid evolution of resistance in mosquitoes, the two toxin precursors in B. sphaericus act as a single toxin following ingestion and partial digestion by mosquito larvae. Bti has been used for nearly 30 years in large-scale mosquito and black fly control programs and resistance had not been detected in mosquito populations in nature that have been subjected to selection from Bti toxins. Nevertheless, mosquitoes, such as the southern house mosquito Culex quinquefasciatus, can evolve resistance to the full complement of Bti toxins when under strong selection pressure in the laboratory. Resistance to Bti was recently detected in a closely related species Culex pipiens in Syracuse, New York (see: Paul et al. 2005. Journal of the American Mosquito Control Association 21: 305-309). In contrast to the findings for Bti, resistance to B. sphaericus has been observed in several places (Brazil, China, France, India and Thailand). Mosquitoes can evolve resistance to B. sphaericus very rapidly (>10,000-fold in 7-8 generations), especially when the mosquitoes commonly found in often polluted urban environments, such as catch basins and wastewater contaminated by human sewage, are routinely exposed to B. sphaericus toxins.

 

[joobz]

Taffer tries to make a point using semantics.

BWA HA HA HA HA HA!!!! Another one for the completely insane irony department, Mr. "directional" selection pressures.

So we so far have
1.) HIV doesn't count (even though it used to be the perfect example) because it uses recombination and therefore disproves Kleinman's theory
2.) Stabilizing pressures don't count because they are already in equilibrium and therefore are no longer a factor (even though deviations from other pressures can result in these pressures becoming a selection force again)
3.) Dr. A's model doesn't count becuase he's using assumptions that demonstrate how multiple pressures speed evolution, and obviously only Klienman is allowed to decide on what is allowed.

 

[Dr Adequate]

Adebz is trying to do his mathematics by gif and awe. At least this brainwashed, prejudiced and biased evolutionist is trying. What he is trying to do is be the last evolutionist to understand the mathematics of mutation and selection. He thinks that a graph that does not include genome size, mutation rate, population, description of selection pressures, real examples of what he is trying to demonstrate, and a derivation of the model with assumptions used is somehow going to convince anyone reading this thread that multiple selection pressures accelerates evolution. Wait, it does convince Taffer. So we still have a horse race, its Adebz and Taffer neck and neck to be the last evolutionists on this thread to understand the mathematics of mutation and selection.

Wow, I've prompted a lot of hysterics, haven't I?

Do you have any questions about the model, or would you rather scream and twitch and froth and lie and babble gibberish?

Hey, why do I even bother asking?

Carry on with the lies and the gibberish.

 

[kleinman]

Annoying Creationists

Taffer tries to make a point using semantics.

BWA HA HA HA HA HA!!!! Another one for the completely insane irony department, Mr. "directional" selection pressures.

Hold on folks, this is really becoming a horse race; joobz is coming along from the outside. Who will be the last evolutionist on this thread to understand the mathematics of mutation and selection? These evolutionists really have heart; none of them are willing to give up on their mathematically impossible theory. Stay tuned for the finish of this thrilling race.

 

[Dr Adequate]

Hold on folks, this is really becoming a horse race; joobz is coming along from the outside. Who will be the last evolutionist on this thread to understand the mathematics of mutation and selection? These evolutionists really have heart; none of them are willing to give up on their mathematically impossible theory. Stay tuned for the finish of this thrilling race.

Rather than speculate on who will be the last person to be fooled by the stupid innumerate gibberish of lies which you have the mendacity to call "the mathematics of mutation and selection", you should instead turn your attention to the question of whether anyone will ever thus be deceived.

 

[Dr Adequate]

Here is another link which discusses the attempted extinction of mosquito larve and can be found at http://faculty.ucr.edu/~walton/bacteria.htm . Note that this author does not use the word emergence in describing the evolution of resistance to these selection pressures.

Heh heh. You didn't read that, did you?

It has nothing to do with your halfwitted fantasies, you silly little man.

 

[kleinman]

Annoying Creationists

Here is another link which discusses the attempted extinction of mosquito larve and can be found at http://faculty.ucr.edu/~walton/bacteria.htm. Note that this author does not use the word emergence in describing the evolution of resistance to these selection pressures.

Heh heh. You didn't read that, did you?

Sure I did, that’s why I can post quotes like this from the link:

Unlike Bti which contains multiple toxins that limit the potential for the rapid evolution of resistance in mosquitoes, the two toxin precursors in B. sphaericus act as a single toxin following ingestion and partial digestion by mosquito larvae.

And

In contrast to the findings for Bti, resistance to B. sphaericus has been observed in several places (Brazil, China, France, India and Thailand). Mosquitoes can evolve resistance to B. sphaericus very rapidly (>10,000-fold in 7-8 generations), especially when the mosquitoes commonly found in often polluted urban environments, such as catch basins and wastewater contaminated by human sewage, are routinely exposed to B. sphaericus toxins.

Single selection pressure gives rapid evolution of resistance.

Unlike Bti which contains multiple toxins that limit the potential for the rapid evolution of resistance in mosquitoes, the two toxin precursors in B. sphaericus act as a single toxin following ingestion and partial digestion by mosquito larvae.

And

Bti has been used for nearly 30 years in large-scale mosquito and black fly control programs and resistance had not been detected in mosquito populations in nature that have been subjected to selection from Bti toxins. Nevertheless, mosquitoes, such as the southern house mosquito Culex quinquefasciatus, can evolve resistance to the full complement of Bti toxins when under strong selection pressure in the laboratory. Resistance to Bti was recently detected in a closely related species Culex pipiens in Syracuse, New York (see: Paul et al. 2005. Journal of the American Mosquito Control Association 21: 305-309).

Multiple selection pressures slow evolution of resistance. In this case, it goes from 7 to 8 generations for the single selection pressure to 30 years for multiple selection pressures.

Now if you read your URLs that you post, you would be able to quote from them (if they had anything worthwhile to quote to support your position).

And Adebz surges into the lead. Who will win this race to be the last evolutionist to understand the mathematics of mutation and selection?

 

[Mr. Scott]

Annoying Complexities of Real World Evolution

Multiple selection pressures slow evolution of resistance. In this case, it goes from 7 to 8 generations for the single selection pressure to 30 years for multiple selection pressures.

Well, it's quite obvious that the intensity of selection pressures strongly affects the evolution of traits like resistance to antibiotics. A case in point is non-compliance with medication, which is known to encourage resistant populations.

I think we have another unchallenged assumption: that selection pressures are constant and numerous on long time scales in nature.

Why are we assuming this? In nature populations of creatures like primates go through periods of intense selection pressures and periods of little or no selection pressure. There are occasional droughts, food shortages, space shortages, breakouts of infections and predators, and so on and so forth. Individuals will break off from a colony and start other colonies, sometimes in hostile territory with one or more intense selection pressures, sometimes in environments where food is plentiful and selective pressures are absent. Separate colonies will have meetings of individuals which have developed advantageous traits separately and mate to combine them, resulting in parallel, not serial evolution.

And, all those factors not modeled at all in Ev, a simplified model intended only to prove information gain which creationists had previously claimed could not occur.

Another unchalleneged assumption: that an infectious agent like gonorrhea reproduces in a homogeneous environment, as if in a petri dish. Multiple environments with multiple intensities and types of selective pressures in the same organism will resulted in multiple directions of evolution, and cells re-converging after such individual evolutions are known to exchange DNA and combine resistances - as long as selective presures are not so intense as to cause extinction.

All that, again, is not modeled by Ev.

Any assertion that any process proven to occur in real world evolution that Ev doesn't model is unimportant needs to be backed up with mathematical proof, or else, Ev cannot be considered mathematical proof evolution can't account for the origin of species.

Keinman's primary thesis is: Considering only processes modeled by Ev, evolution is to slow to account for the genetic and geological records. I don't think there is any disagreement if stated as such.

 

[kleinman]

Annoying Creationists

Multiple selection pressures slow evolution of resistance. In this case, it goes from 7 to 8 generations for the single selection pressure to 30 years for multiple selection pressures.

Well, it's quite obvious that the intensity of selection pressures strongly affects the evolution of traits like resistance to antibiotics. A case in point is non-compliance with medication, which is known to encourage resistant populations.

I hear and read this type of terminology when evolutionists talk about selection pressures. Do you want to enumerate and elaborate on the variables that determine the intensity of selection pressures?

I think we have another unchallenged assumption: that selection pressures are constant and numerous on long time scales in nature.

Give us some examples of this. Do you propose that a selection pressure doesn’t have to be present long enough for at least some individuals in the population to have adapted to that pressure, for example antibiotic resistance?

Why are we assuming this? In nature populations of creatures like primates go through periods of intense selection pressures and periods of little or no selection pressure. There are occasional droughts, food shortages, space shortages, breakouts of infections and predators, and so on and so forth. Individuals will break off from a colony and start other colonies, sometimes in hostile territory with one or more intense selection pressures, sometimes in environments where food is plentiful and selective pressures are absent. Separate colonies will have meetings of individuals which have developed advantageous traits separately and mate to combine them, resulting in parallel, not serial evolution.

Rapid adaptation occurs by recombination and natural selection, not mutation and natural selection. Recombination and natural selection is what Darwin was observing when he reported on the differences in finch beaks. Recombination and natural selection works with selection of alleles, small populations and small numbers of generations. This is where Stephen Gould’s hypothesis of punctuated equilibrium has application. However, the mathematics of mutation and selection shows it is a far slower mechanism of adaptation that requires much larger populations and much more generations to accomplish its task. Recombination without errors does not increase information in the gene pool; recombination with natural selection can reduce the information in the gene pool.

And, all those factors not modeled at all in Ev, a simplified model intended only to prove information gain which creationists had previously claimed could not occur.

Add any feature you want to ev, whether it is recombination, any or all forms of mutations and show us how your theory works mathematically. Show us how these mechanisms overcome the problem for your theory that multiple selection pressures slow evolution.

Another unchalleneged assumption: that an infectious agent like gonorrhea reproduces in a homogeneous environment, as if in a petri dish. Multiple environments with multiple intensities and types of selective pressures in the same organism will resulted in multiple directions of evolution, and cells re-converging after such individual evolutions are known to exchange DNA and combine resistances - as long as selective presures are not so intense as to cause extinction.

All that, again, is not modeled by Ev.

Add this feature to ev and show us mathematically how the theory of evolution works.

Any assertion that any process proven to occur in real world evolution that Ev doesn't model is unimportant needs to be backed up with mathematical proof, or else, Ev cannot be considered mathematical proof evolution can't account for the origin of species.

I haven’t asserted that they are unimportant; I assert that they won’t overcome the fact that multiple selection pressures slow evolution. This is what is discussed in Delphi’s Wikipedia reference to the fitness landscape and the numerous real examples of multiple selection pressures that I have posting on this thread. These real examples are not limited to random point mutations. Joobz pointed out that HIV does recombination. Certainly rodents use recombination. Any mechanism of mutation or recombination is available to these creatures discussed in the links presented here.

In fact, here are more examples of how multiple selection pressures slow evolution. These are not examples derived from a mathematical model; they demonstrate what is shown in the ev mathematical model.

Here is an article that discusses the treatment of Hepatitis C http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1472602 . Again, these authors report that multiple selection pressures slow the evolution of resistant strains of this virus as reported in this quote:

The effective treatment of HCV infection will likely require multiple antiviral drugs with different resistance profiles to delay the emergence of resistance, as has been shown in human immunodeficiency virus (35). In the present study, treatment with either a thumb or a palm inhibitor alone rendered large numbers of resistant replicon colonies in vitro, a potential indication of the likely rapid emergence of HCV-resistant variants upon initiation of monotherapy. Importantly, by combining two inhibitors binding to the thumb and to the palm sites of the HCV polymerase we observed a greater-than-additive inhibitory effect of replicon RNA replication.

I include the following quote from this paper just for Taffer who thinks that “emergence” somehow does not refer to “evolution”.

Mutants Ile482Leu, Met423Ile, and Met423Val were observed at different sequential passages, illustrating the plasticity and evolution of the quasispecies population in the presence of inhibitor's selective pressure (Table 2).

Here is another paper that discusses combination selection pressures for the treatment of malaria. It is located at http://www.ajtmh.org/cgi/content/full/72/2/163 .

The goal of combination therapy (CT) is to delay the emergence and spread of drug resistance. The strategy is supported empirically by the success of CT in treating tuberculosis and human immunodeficiency virus infections, and by mathematical models.1 The rationale for CT is simple. If two drugs have independent mechanisms of action, mutations that confer resistance to each drug will only rarely co-exist in the same parasite. By this logic, drug combinations should both improve treatment cure rate, and delay the emergence of drug resistance.2

Again, I include the following quote for Taffer so that he know that the emergence of resistance is by evolution.

These equations enable the frequencies of dhfr mutations to be tracked over the time course of the evolution of resistance as described in more detail elsewhere.4

 

[Dr Adequate]

I hear and read this type of terminology when evolutionists talk about selection pressures. Do you want to enumerate and elaborate on the variables that determine the intensity of selection pressures?

Give us some examples of this. Do you propose that a selection pressure doesn’t have to be present long enough for at least some individuals in the population to have adapted to that pressure, for example antibiotic resistance?

Rapid adaptation occurs by recombination and natural selection, not mutation and natural selection. Recombination and natural selection is what Darwin was observing when he reported on the differences in finch beaks. Recombination and natural selection works with selection of alleles, small populations and small numbers of generations. This is where Stephen Gould’s hypothesis of punctuated equilibrium has application. However, the mathematics of mutation and selection shows it is a far slower mechanism of adaptation that requires much larger populations and much more generations to accomplish its task. Recombination without errors does not increase information in the gene pool; recombination with natural selection can reduce the information in the gene pool.

Add any feature you want to ev, whether it is recombination, any or all forms of mutations and show us how your theory works mathematically. Show us how these mechanisms overcome the problem for your theory that multiple selection pressures slow evolution.

Add this feature to ev and show us mathematically how the theory of evolution works.

I haven’t asserted that they are unimportant; I assert that they won’t overcome the fact that multiple selection pressures slow evolution. This is what is discussed in Delphi’s Wikipedia reference to the fitness landscape and the numerous real examples of multiple selection pressures that I have posting on this thread. These real examples are not limited to random point mutations. Joobz pointed out that HIV does recombination. Certainly rodents use recombination. Any mechanism of mutation or recombination is available to these creatures discussed in the links presented here.

In fact, here are more examples of how multiple selection pressures slow evolution. These are not examples derived from a mathematical model; they demonstrate what is shown in the ev mathematical model.

Here is an article that discusses the treatment of Hepatitis C http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1472602 . Again, these authors report that multiple selection pressures slow the evolution of resistant strains of this virus as reported in this quote:

I include the following quote from this paper just for Taffer who thinks that “emergence” somehow does not refer to “evolution”.

Here is another paper that discusses combination selection pressures for the treatment of malaria. It is located at http://www.ajtmh.org/cgi/content/full/72/2/163 .

Again, I include the following quote for Taffer so that he know that the emergence of resistance is by evolution.

So, the same old lies and no math.

How did I guess.

 

[kleinman]

Annoying Creationists

So, the same old lies and no math.

Folks, we are back at our horserace to find out who will be the last evolutionist who understands the mathematics of mutation and selection. And we find that Adebz has surged ahead by a tale.