Annoying creationists

[kjkent1]

I think it's just a marvelous coincidence. I verified the generation counts in Kjkent's table, row 8, columns 1 and 2. Then I reran those two cases with a different random number seed (10) and got two different generation counts.

~~ Paul

It would be nice to be able to run all the examples with several different seeds, and then average the results.

kleinman should offer to do that task, in as much as the curret results seem to send his theory of "multiple selective pressures profoundly slows evolution" into the circular file.

 

[Ichneumonwasp]

And since we know, and have provided examples, that in nature multiple selection pressures, at the right level of pressure, actually increase the chance for resistance to develop.

 

[Paul C. Anagnostopoulos]

When I run "serious experiments," I try to run each case with three or four different seeds and take the average. The variance is remarkably high.

~~ Paul

 

[Ichneumonwasp]

Variance in generation counts? Is there a way to adjust variance in the population aside from increasing the mutation rate?

One of the big problems I have with the way Kleinman approaches this mess is his problem with mutation rates. Sure it doesn't match mutation rates elsewhere, but if there is no other means of providing variance within a population, then mutation rate in the model serves the purpose of providing the variation that would natural occur through replication errors.

Or, are replication errors somehow built into the model? Or are they categorized as mutations?

 

[Paul C. Anagnostopoulos]

Variance in generation counts? Is there a way to adjust variance in the population aside from increasing the mutation rate?

Yes, there is great variance in the generation count depending on the random seed. I'm not sure what your second question means.

One of the big problems I have with the way Kleinman approaches this mess is his problem with mutation rates. Sure it doesn't match mutation rates elsewhere, but if there is no other means of providing variance within a population, then mutation rate in the model serves the purpose of providing the variation that would natural occur through replication errors.

I've run a long series of experiments varying only the mutation rate, and the generation count seems to vary linearly with it.

Or, are replication errors somehow built into the model? Or are they categorized as mutations?

The only kind of mutation is point mutations applied to each creature immediately after the best half of the creatures are reproduced.

~~ Paul

 

[articulett]

Dr. Alan Kleinman, when I asked if you were paid for undermining evolution, you dodged the question on the basis that one should have been able to know the answer from reading some other of the 3,510 postings here. It took you more typing to refuse to answer than you would have if you had answered. I'll make it easy for you. If you have been paid, will be paid, or expect to be paid for undermining or attempting to undermine evolution, just answer with a "y" else with a "n".

Thank you, Dr. Kleinman.

I'm sure that Dr. Alan Kleinman will do as most creationists do, and ignore the question. You can take that as an answer in the affirmative.

 

[Dr Adequate]

So, Dr. Alan Kleinamn, not only have you demonstrated your terrible understanding of fundemental scientific principles...but you show utter dishonesty in correcting these errors.

Shall i remind you, Dr. Alan Kleinman, what you have stated that is wrong?

You forgot Lie #5.

Lie #5: Kleinman claims that a wikipedia article which says that evolutionary algorithms are particularly effective at solving a certain kind of optimization problem shows that they aren't. In particular, he claims that this process, which works when there are ... what? ... trillions, quadrillions, quintillions of routes? ... must fail when there are only three.

 

[kleinman]

Annoying Creationists

This paragraph again shows that you don’t understand the mathematics of mutation and selection. Multiple selection pressures do not affect the generations to evolve additively. Multiple selection pressures slow evolution far more than additively. The sorting process is much slower and more difficult when you have multiple selection pressures. Selection pressures do not function synergistically. You can think of this as a database sorting problem. The more sorting conditions you have, the slower the sort goes.

You really are not capable of understanding this, are you? I am discussing with you a real world example that you brought into the discussion. I didn't invent it. You introduced it. You have repeatedly mischaracterized my position. I pointed out your mischaracterizations.

I am not mischaracterizing your position; you just continue to miss the most important point. That point is that multiple selection conditions applied simultaneously slows evolution. This is clearly seen with the use of multiple drug therapy for the treatment of HIV. If you use monotherapy, resistance to that single drug quickly occurs. Now this doesn’t mean that triple therapy eliminates the possibility of resistance, it just slows the process. Drugs with different intensity of selection pressures will affect the rate at which drug resistance can emerge but the underlying mathematics remains the same. For example, a very potent drug which only requires a single base substitution to make that drug ineffective will make the prediction of the behavior of treatment somewhat difficult without collecting a large amount of clinical data or by doing a simulation with a model like ev that is reworked to specifically look at HIV and drug resistance.

You can be a man and admit your mistakes or you can continue to act like this. It is your decision.

If you read the entire thread, you would see that I do admit my mistakes. The case of HIV demonstrating that multiple drug therapy (selection pressures) slows the evolution of resistant strains is not one of my mistakes. Now be a scientist and mathematician and understand why what I am saying here is not a mistake.

You can discuss the ev model all you wish with the others. As I have repeated to you now, I think, seven times, we (you and I) are discussing HIV triple therapy. There is no sense in relying on ev to explain your position. We are discussing this real world issue. The interaction with ev occurs later.

You are having a difficult time understanding why multiple drug therapy is used to treat HIV, TB and should have been used to treat Gonorrhea, MRSA, pseudomonas and a variety of other multiple drug resistant microbes. If you understood the mathematics of mutation and selection that is demonstrated by ev and nicely described in Delphi’s Wikipedia reference to fitness landscape, you would better understand this argument. Dr Schneider’s model does accurately simulate an important real world phenomenon, which is multiple selection pressures slow evolution. His mathematics is not trivial but it is understandable.

Are you ready to apologize and move ahead with the discussion, leaving all the name calling and obfuscation behind?

I owe no apology here and stop being a cry baby.

Dr. Alan Kleinman, when I asked if you were paid for undermining evolution, you dodged the question on the basis that one should have been able to know the answer from reading some other of the 3,510 postings here. It took you more typing to refuse to answer than you would have if you had answered. I'll make it easy for you. If you have been paid, will be paid, or expect to be paid for undermining or attempting to undermine evolution, just answer with a "y" else with a "n".

I am under no obligation to answer every stupid question raised by you evolutionists. However, in an attempt to stop your incessant whining, I will answer your stupid question. I have not been paid; I will not be paid and do not expect to be paid for revealing the truth about your dumb ass theory of evolution. One reason I do this thread is because I enjoy annoying thin skinned, whining, crybaby evolutionists by using their own mathematical model to prove your theory is hogwash. This is not my primary reason though for doing this thread. That reason is none of your business.

Thank you, Dr. Kleinman.

Anytime Mr Scott (unless it is a stupid question).

The only thing that Ichneumonwasp has shown here is that reducing the selection pressure speeds up the evolutionary process. This is what ev shows and this is what I have contended for pages on this thread. Ichneumonwasp is making my point.

Dr. Alan Kleinman, that is not what you have contended for pages. You contended that the number of selection pressures slowed evolution. I even asked you directly if that was your hypothesis, and you stated that it was.

Excuse me. When someone is in noncompliance with their HIV treatment, they are reducing the number of selection pressures as well as the intensity of the selection pressures. Were you not the one who said that if the intensity of the selection pressure was sufficient, it causes extinction? What happens when you reduce the intensity of this selection pressure?

Yes, Dr. Alan Kleinman, I would like to know as well. Have you been paid for this?

Are these the best questions that you thin skinned, crybaby evolutionists can come up with?

While you are at it, could you also address the issue of continually referring to the mathematical modelling of "evolution" as it relates to the real world in your very specific example of HIV triple therapy. Since the very question at hand is whether or not the mathematical model is effective for examining this question, why do you continue to dodge questions about HIV triple therapy and drug resistance in the real world? Do you fear that resistance developing in HIV strains indicates that this model does not relate to all real world examples of evolutionary change? Is that the problem, Dr. Kleinman?

Apparently you took dumbbell mathematics in your premed courses so it is taking time to bring you up to speed on the mathematics of mutation and selection. We can start with the principle that multiple selection conditions slow the evolutionary process. You can ask why and you could ask that I demonstrate this to you with the ev model and I could answer that I have already done this but since you are not up to speed on this mathematics, I will repeat it again for you if you are interested.

Why are you doing that, Dr. Alan Kleinman?

It is enough for you to know that I enjoy annoying people who believe in a dumb ass theory and try to pass it off as science. Since you are a physician, you might appreciate the diagnostic criteria for evolutionism; they have denialophila, hyperextraplopia, speculitis and amathematica sciencea.

In case nobody has pointed this out previously, Dr. Alan Kleinman has previously had problems with ev. He got taught a lesson by the folks at Panda's Thumb.

Delphi, you really need to lay off the sterno. Why don’t you post a quote from this link where I was taught a lesson about ev? You are really scraping the bottom of the barrel looking for some way to respond to what ev is showing.

Per Kleinman's request, I have some data from ev. The attached table is based on running ev with all defaults, except that I limited the population to eight (8) creatures, and I changed the mistake weights and genome length as indicated in the table.

You haven’t label your selection pressures.

1) Three selection pressures converge faster than either/both one and/or two, in some, but not all cases. This suggests that if the trends below hold, then kleinman's theory that multiple selective pressures slow evolution in all cases is falsified.

You have demonstrated nothing of the kind. All your cases have three selection pressures. The only thing you have shown is that varying the weights for the selection pressures varies the generations for convergence.

2) There are some VERY weird coincidences where various mistake weights converge, or produce a perfect creature, at "exactly" the same number of generations. As I have suggested previously in this thread, I am suspect of the reliability of ev's random number generation, as the number of generations increases.

Paul might address this issue however I believe Paul and Dr Schneider have compared evjava and evpascal and get identical results using either languages’ random number generator.

Note: as usual, I am not using zero (0) mistake weights, because to do so is to permit perfect creatures to be reported even though Rseq has not approached Rfreq. This is result of ev creating mistakes in the mutation function, and then completely ignoring those mistakes in the selection function. The result is a creature which ev reports as "perfect," but which, in fact, is described by random information. This state violates the fundamental premise of ev: that Rseq ~ Rfreq in all independent living organism -- Therefore, the state is invalid.

You are using an excuse so as not to set two of the three selection conditions to zero because this demonstrates the crucial behavior of the mathematics of mutation and selection. Since you haven’t, I will do it for your G=4096 case.
Generations to perfect creature
Missed binding sites weight=1\166
Spurious binding sites gene=1\572
Spurious binding sites outside gene=1\493
Your best case for three selection conditions was 17,781 generations
What happens if we set only one selection condition weight to 0?
Generations to perfect creature
Missed binding sites weight=1, Spurious binding sites in gene=1\33,942*
Missed binding sites weight=1, Spurious binding sites outside gene=1\643,480*
Spurious binding sites in gene=1, Spurious binding sites outside gene=1\476
* note Rseq->Rfreq in at least two of the three cases where one of the selection conditions was set to 0.
For completeness, I include the case when all three selection condition weights are set equal to one and the generations for convergence=491,071
Clearly, the case in red above has only two selection conditions and takes more generations for convergence to perfect creature than the case for three selection conditions. The question is this an effect of the stochastic properties of the model or that two selection conditions can take more generations to converge than three selection conditions which would refute my hypothesis. So what happens for G=2048?
Generations to perfect creature
Missed binding sites weight=1, Spurious binding sites in gene=1\11,439*
Missed binding sites weight=1, Spurious binding sites outside gene=1\34,768*
Spurious binding sites in gene=1, Spurious binding sites outside gene=1\360
* note Rseq->Rfreq in at least two of the three cases where one of the selection conditions was set to 0.
The generations for convergence for weights of 1 for all three cases for G=2048 is 107,168
How about for G=1024?
Generations to perfect creature
Missed binding sites weight=1, Spurious binding sites in gene=1\5,794*
Missed binding sites weight=1, Spurious binding sites outside gene=1\29,228*
Spurious binding sites in gene=1, Spurious binding sites outside gene=1\102
* note Rseq->Rfreq in at least two of the three cases where one of the selection conditions was set to 0.
The generations for convergence for weights of 1 for all three cases for G=1024 is 43,354
How about for G=512?
Generations to perfect creature
Missed binding sites weight=1, Spurious binding sites in gene=1\2,792*
Missed binding sites weight=1, Spurious binding sites outside gene=1\10,113*
Spurious binding sites in gene=1, Spurious binding sites outside gene=1\36
* note Rseq->Rfreq in at least two of the three cases where one of the selection conditions was set to 0.
The generations for convergence for weights of 1 for all three cases for G=512 is 8,916
Again, a case where two selection conditions take more generations to converge than three selection conditions.
The generations for convergence for weights of 1 for all three cases for G=1024 is 43,354
How about for G=256?
Generations to perfect creature
Missed binding sites weight=1, Spurious binding sites in gene=1\1,441*
Missed binding sites weight=1, Spurious binding sites outside gene=1\1,194*
Spurious binding sites in gene=1, Spurious binding sites outside gene=1\78
* note Rseq->Rfreq in at least two of the three cases where one of the selection conditions was set to 0.
The generations for convergence for weights of 1 for all three cases for G=256 is 2,424
So kjkent1’s argument that you need all three selection conditions for Rseq->Rfreq is refuted. Kjkent1, your argument is a red herring anyway since selection is not based on Rseq->Rfreq. This is only an secondary result. Missed binding sites and one of the spurious binding site conditions gives his condition. However, in two of the five series, two selection conditions take more generations to evolve to the perfect creature than do three selection conditions. Is this an artifact of the stochastic calculation or does this refute my argument? I also have not posted the data when two of the three selection conditions are set to 0. These cases take far fewer generations to converge than either the two or three selection condition cases. I will post this data and expand kjkent1’s series beyond the G=4096 case in order to establish the trends.

Don’t be silly Mr Scott; your example supports my contention. Single selection conditions can quickly evolve, the more selection conditions imposed, the slower the evolutionary process proceeds. Multiple selection conditions slow evolution.

Alan Kleinman, you are the one being silly. You've said point blank that more than one mutation in response to selection pressure enters the realm of macro-evolution, and that 3-4 was definitely macroevolution, and that macroevolution was mathematically impossible. When you made these statements, you did not offer the caveat that these adaptations must be simultaneous. Indeed, such mutations are usually sequential* even when simultaneous pressures are present. They can and will happen when the intensity of one or more selective pressures is sufficient to supply pressure but not so great as to cause extinction, like the sweet spot in which evolution runs at maximum speed when antibiotic compliance is weak.

There may be a “sweet spot” in which evolution runs at maximum speed and I think you may be correct with this assertion, but you need to demonstrate this mathematically and that it accelerates evolution sufficiently to make your theory possible. You have a really big problem though; you have never described the selection process that would evolve a gene from the beginning. And now you have to describe two selection processes that would evolve two genes from the beginning and that there is some optimum pressure that would allow these two conditions to evolve simultaneously.

*Parallel mutations can be combined when cells exchange genetic material. even cells of different species can "share notes" on selective pressure adaptations. I have a photo of cells caught in the act in my library I will look up. Even pandas and people can combine adptatations to varying selective pressures via sexual congress, thus speeding evolution far beyond what Ev currently models.

What??????? How do different species “share notes” via sexual congress?

It really is silly of you, Dr. Kleinman, to suggest that point mutations as modeled by the Ev simulation, and point mutations alone, suggest an upper limit on the rate of evolution. No such assertion can be justified and is as far away from "mathematic proof" as can be. The genetic and geographical records prove that evolution is indeed fast enough to account for the diversity of life on Earth. The process is just too complex to model with today's computers, Dr. Kleinman. Please stop spreading your hoax the Ev disproves evolution. Quite the contrary is true. You embarass even the creationist community.

As I have said from the earliest posts on this thread, if you think you have some other mechanism of mutation or any other mechanism that would accelerate evolution, put that feature into ev and show how it works mathematically. Otherwise all you have is a collection of dumb ass words that you say explains your dumb ass theory. The theory of evolution started without a mathematical basis and your dumb ass words do not substitute for a mathematical explanation. As it stands, ev shows that the theory of evolution is mathematically impossible.

I think it's just a marvelous coincidence. I verified the generation counts in Kjkent's table, row 8, columns 1 and 2. Then I reran those two cases with a different random number seed (10) and got two different generation counts.

There may be more to than a coincidence, row 6, columns 1, 3 and 4 have the same generations for convergence and row 9, columns 1 and 2 have the same generations for convergence.

kleinman should offer to do that task, in as much as the curret results seem to send his theory of "multiple selective pressures profoundly slows evolution" into the circular file.

The next series I am going to run will do a more thorough investigation of 1, 2 and 3 selection conditions since I have already shown that you don’t need all three selection conditions for Rseq->Rfreq and that 2 selection conditions sometimes take more generations to converge than 3 selection conditions. Whether this effect is due to the noise introduced into the data by the stochastic nature of the calculation or whether 2 selection conditions can actually converge more quickly than three selection needs to be established. I believe the former is the cause of this affect but more data is needed to establish the trend.

You have hit upon something peculiar in the behavior of ev. I think running more cases alone may not explain why you get identical generations for convergence despite different weights on the selection conditions. My first guess would be that one of the three selection conditions is controlling the generations for convergence. The problem with that view is your G=2560 has 3 cases with generations for convergence of 200,079 and there is no weight factor that is common to all three cases. It may require tracking which mistakes each generation are driving the selection process.

And since we know, and have provided examples, that in nature multiple selection pressures, at the right level of pressure, actually increase the chance for resistance to develop.

Certainly as Mr Scott has suggested there may be a “sweet spot” where evolution can be accelerated. You have suggested that this curve may be parabolic. However, this rate of evolution will never be as rapid as when a single selection pressure is applied. You have two ways of establishing the rates of evolution. You can collect data in real situations such as the treatment of HIV or you can look at mathematical models to establish this behavior. You are trying to take a single data point on the fitness landscape for HIV to support your argument. I believe the general behavior of ev with 1, 2 and 3 selection conditions and the use of multiple antimicrobials to treat difficult infections and the failure and consequences of using monotherapy to treat MRSA, Gonorrhea, pseudomonas and other multiply resistant microbes will have far more weight in this debate.

The establishment of the true behavior of mutation and selection goes beyond proving whether the theory of evolution is true or not. The proper understanding of this mechanism of mutation and selection impacts the treatment of infectious diseases.

Variance in generation counts? Is there a way to adjust variance in the population aside from increasing the mutation rate?

Ichneumonwasp, you are behind the curve on the way ev works. Each of the parameters in ev has unique effects on the generations for convergence. Increasing populations decreases the generations of convergence at a decreasing rate as you increase population, increasing mutation rate decreases the generations for convergence to a point where the generations for convergence starts to increase. The major factor which increases the generations for convergence is the genome length which increases at an increasing rate as you lengthen the genome. There has been a lot of data posted on this thread and the Evolutionisdead forum which shows this.

One of the big problems I have with the way Kleinman approaches this mess is his problem with mutation rates. Sure it doesn't match mutation rates elsewhere, but if there is no other means of providing variance within a population, then mutation rate in the model serves the purpose of providing the variation that would natural occur through replication errors.

The way I have approached this mess is by doing a systematic parametric study of the behavior of ev. I have done hundreds of cases investigating how mutation rates, population, genome length, binding site width affect convergence of this model. This data has all been posted but evolutionists are all over the map discussing other issues including whether I am being paid to destroy the theory of evolution.

Or, are replication errors somehow built into the model? Or are they categorized as mutations?

Paul, do you want to explain to Ichneumonwasp how your model works? Never mind, I see on your next post that you do explain these points.

Dr. Alan Kleinman, when I asked if you were paid for undermining evolution, you dodged the question on the basis that one should have been able to know the answer from reading some other of the 3,510 postings here. It took you more typing to refuse to answer than you would have if you had answered. I'll make it easy for you. If you have been paid, will be paid, or expect to be paid for undermining or attempting to undermine evolution, just answer with a "y" else with a "n".

Thank you, Dr. Kleinman.

I'm sure that Dr. Alan Kleinman will do as most creationists do, and ignore the question. You can take that as an answer in the affirmative.

Articulett, if you read above you will see I answered this stupid question. So when you evolutionists whine about how long this thread is, you only have yourselves to blame. Do you have any more stupid questions and wrong suppositions to those questions? The only one who has offered less discussion of the mathematics of ev than you is Adequate. You have an excuse because you have no training in mathematical sciences. Adequate has no excuse; he just has nothing to offer on the topic. He has even run out of jpeg and gifs. I am happy for Adequate because he seems to have found a purpose in life. Otherwise, we can get back to the mathematics of mutation and selection and the proof of your dumb ass theory as a collection of hogwash. As icing on the cake, we will get some idea of how mutation and selection works with the treatment of infectious diseases.

 

[delphi_ote]

Excuse me. When someone is in noncompliance with their HIV treatment, they are reducing the number of selection pressures as well as the intensity of the selection pressures.

They're taking the same number of drugs in both cases. You defined the number of drugs taken as the number of selection pressures.

Were you not the one who said that if the intensity of the selection pressure was sufficient, it causes extinction? What happens when you reduce the intensity of this selection pressure?

Dr. Alan Kleinman, it is dishonest to pretend the opposite of your contention is what you were arguing for all along.

 

[kleinman]

Annoying Creationists

Excuse me. When someone is in noncompliance with their HIV treatment, they are reducing the number of selection pressures as well as the intensity of the selection pressures.

They're taking the same number of drugs in both cases. You defined the number of drugs taken as the number of selection pressures.

Really, how many drugs are people taking when they are noncompliant with their treatment?

Were you not the one who said that if the intensity of the selection pressure was sufficient, it causes extinction? What happens when you reduce the intensity of this selection pressure?

Dr. Alan Kleinman, it is dishonest to pretend the opposite of your contention is what you were arguing for all along.

What I have been arguing is that increasing the number of selection pressures slows evolution. I have not argued how the intensity of selection pressures affects evolution. This is an argument that has been raised by kjkent1, Mr Scott and Ichneumonwasp. I suspect that the intensity of selection pressures has a non-linear affect on the rate of evolution. The number of selection pressures and the intensity of selection pressures are independent variables in this system. Once the general effect of multiple selection pressures is established then the effects of intensity of selection pressures can be investigated. From the data I have already obtained from ev, I believe the number of selection pressures is more important than the intensity of the selection pressures unless the intensity of the selection pressure is sufficient to cause extinction.

When are you crybaby evolutionists going to learn that questioning my honesty is not a substitute for a good logical argument? I neither need nor want to lie in this debate. I have a good mathematical model written by a devoted evolutionist that refutes your theory just fine, Dr Cunningham.

 

[delphi_ote]

Really, how many drugs are people taking when they are noncompliant with their treatment?

All of their meds, but less than the required dosage.

From the data I have already obtained from ev, I believe the number of selection pressures is more important than the intensity of the selection pressures unless the intensity of the selection pressure is sufficient to cause extinction.

But you were proven wrong on this in the HIV compliance study, Dr. Alan Kleinman. Argue all you like, but you're going to have a very hard time when reality disagrees with you.

I neither need nor want to lie in this debate.

Then stop doing it. While you're at it, stop waffling back and forth on your positions whenever you find it convenient.

 

[Dr Adequate]

I neither need nor want to lie in this debate.

Ironically, you've lied so often about whether you tell lies that this is numbered as Lie #0 in my catalogue of your habitual lies.

 

[kleinman]

Annoying Creationists

Really, how many drugs are people taking when they are noncompliant with their treatment?

All of their meds, but less than the required dosage.

You don’t know this a priori. Sometimes patients will not take a particular medicine because they don’t like the side affect it gives. The form of the noncompliance must be clearly defined.

From the data I have already obtained from ev, I believe the number of selection pressures is more important than the intensity of the selection pressures unless the intensity of the selection pressure is sufficient to cause extinction.

But you were proven wrong on this in the HIV compliance study, Dr. Alan Kleinman. Argue all you like, but you're going to have a very hard time when reality disagrees with you.

You are jumping to a conclusion here. Ichneumonwasp has not shown that despite compliance with multi-drug therapy that drug resistance occurs as quickly as if monotherapy were used.

I neither need nor want to lie in this debate.

Then stop doing it. While you're at it, stop waffling back and forth on your positions whenever you find it convenient.

I’m not lying you silly jack ass. You’ve been whining for pages that I’ve been moving the goalposts when my argument from the very beginning has been that ev shows your theory to be mathematically impossible. Your own Wikipedia link to fitness landscape shows why ev’s convergence is so slow.

You started to describe this problem properly when you said the following:

Unless we're talking about a real population. High enough selection pressure will slow the rate of evolution because the population will die off.

Also, if you think about it, it's possible the earlier mutations in a series of smooth mutations to adapt to one selection pressure might be maladaptive to a different selection pressure. This is possible, but I can't think of a natural case where this is likely.

In the end, the number of selection pressures don't matter. It's the shape of the resulting fitness landscape that matters. We can only really talk about fitness landscape in a concrete way in terms of simulations like ev.

There are two things you got wrong in this quote. The first is that high selection pressures will slow evolution in real populations and simulations because the population will die off and the second is that the number of selection pressures does matter. This is explained in your own Wikipedia link to fitness landscapes.

 

[kjkent1]

You are using an excuse so as not to set two of the three selection conditions to zero because this demonstrates the crucial behavior of the mathematics of mutation and selection.

Kleinman, I don't need an advantage to beat you in an argument.

You are currently arguing that my data is false because I exclude zero mistake weights. Okay, well what about the case where all mistake weights are set to zero. Ev reports a perfect creature in the first generation, every time, and regardless of the genome length.

You can't have your cake and eat it, too, bubba! If mistake weights of zero are valid, then ev proves that a completely random genome can produce a viable life form without selection in the first generation.

And, that is the EXACT definition of your "gene from the beginning."

So, make up your mind. Or is zero selection pressures a "special case," that you get to proclaim as unviable, because it doesn't fit with your personal belief system?

 

[Dr Adequate]

I am happy for Adequate because he seems to have found a purpose in life.

Yes. That's more fun than it sounds, by the way, you should try it some time.

Adequate has no excuse; he just has nothing to offer on the topic.

I exposed the halfwitted nonsense that is Lie #5. I exposed Lie #1 and Lie #2, if it comes to that.

This is why everyone reading this thread knows that you're a liar.

I can see why this throws you into screaming, twitching, hysterical denial.

He has even run out of jpeg and gifs.

Au contraire. I have one right here which fits you to a T.

 

[Ichneumonwasp]

I haven't read the rest, but this caught my eye passing through quickly:

You are jumping to a conclusion here. Ichneumonwasp has not shown that despite compliance with multi-drug therapy that drug resistance occurs as quickly as if monotherapy were used.

Why do you continue to lie and misrepresent my arguments, Dr. Alan Kleinman? Please answer why you continue to do this?

No one has argued that resistance with triple therapy occurs as quickly as with monotherapy. It doesn't particularly matter for this debate. You have argued that HIV triple therapy slows evolution so profoundly that the process basically stops, implying that resistance cannot develop. I have shown you that resistance does develop, and rather quickly on an evolutionary time scale, when what you call three selection pressures (HIV triple therapy) is employed. This occurs, moreover, in two situations -- approximately 80% compliance with the drug regimen in patients taking the relatively recent therapies that supply profound selection pressure on the virus and nearly perfect compliance (95+%) with earlier triple therapy programs that supplied less profound selection pressures. You cannot argue that it is the particular drugs used since this occurs in both groups. You cannot argue that it is a matter of the first group simply taking one or two drugs at a time because there is a group under less profound selection pressures taking a different triple therapy regimen with nearly perfect compliance. If you want to argue that more selection pressure=slower evolution, then we all agree. Everyone knows this; that's the definition of selection pressure, but it really concerns the potency of the selection pressure and not the number of pressures. Three selection pressures do not stop evolution. They clearly don't slow the process to the point where evolution cannot occur in the time frame of billions of years. This process has occurred in our lifetime, even within the rather shorter lifespan of individuals who carry HIV.

So, please answer me Dr. Kleinman, why do you persist in misrepresenting the evidence and the arguments? Why do you continue to lie so blatantly, Dr. Alan Kleinman?

 

[Paul C. Anagnostopoulos]

What I have been arguing is that increasing the number of selection pressures slows evolution.

Well, except when you were arguing that it stopped evolution.

I’m not lying you silly jack ass. You’ve been whining for pages that I’ve been moving the goalposts when my argument from the very beginning has been that ev shows your theory to be mathematically impossible.

That's the claim, not the goalpost.

You can't have your cake and eat it, too, bubba! If mistake weights of zero are valid, then ev proves that a completely random genome can produce a viable life form without selection in the first generation.

And, that is the EXACT definition of your "gene from the beginning."

So, make up your mind. Or is zero selection pressures a "special case," that you get to proclaim as unviable, because it doesn't fit with your personal belief system?

Alan Kleinman should stop referring to a "perfect creature" in his arguments, since we all agree that is a misleading term when one or more mistake counts are set to zero. Then he would have to explain exactly what is happening when one or more mistake counts are set to zero and a creature evolves with zero mistakes.

~~ Paul

 

[Ichneumonwasp]

I am not mischaracterizing your position; you just continue to miss the most important point. That point is that multiple selection conditions applied simultaneously slows evolution. This is clearly seen with the use of multiple drug therapy for the treatment of HIV. If you use monotherapy, resistance to that single drug quickly occurs.

So, there you go again, Dr. Kleinman, mischaracterizing my position. Since I have not only stated repeatedly that increasing selection pressure slows evolution and have, in fact, provided repeat posting of the relevant passages from previous posts to show you that I have said exactly that, why do you persist, Dr. Kleinman, in arguing that I am saying the opposite? Why do persist in this behavior, Dr. Kleinman?

The case of HIV demonstrating that multiple drug therapy (selection pressures) slows the evolution of resistant strains is not one of my mistakes. Now be a scientist and mathematician and understand why what I am saying here is not a mistake.

Dr. Kleinman, I have never once said that applying multiple selection pressures does not slow evolution (though I am very open to the possibility that there are exceptions). I have never said that the idea of multiple selection pressures slowing evolution is one of your mistakes. Your mistakes in relation to my postings concern:

1. Your insistence that I do not recognize that multiple selection pressures can slow evolution, when I have repeatedly argued that selection pressures added together holding potency constant do slow evolution (which you tried to twist into a complete non-sequitor accusing me of saying that selection pressures have an additive effect, which is not what I said). I further argue that it is the potency of the selection pressures that it important, as should be obvious based on the definition of selection pressure.

2. Your insistence that three selection pressures applied simultaneously so profoundly slows evolution that they essentially stop the process.

You are having a difficult time understanding why multiple drug therapy is used to treat HIV, TB and should have been used to treat Gonorrhea, MRSA, pseudomonas and a variety of other multiple drug resistant microbes.

No, Dr. Kleinman, I have no such problem. As a physician I am well aware of the reasoning behind the use of multi-drug protocols to limit the development of resistant organisms, as I have repeatedly demonstrated throughout my involvement in this thread. You, however, persist in lying about my position, as you are doing again here. Why do you continue with this egregious behavior Dr. Alan Kleinman? And why do you continue to dodge the simple fact that resistance develops in patients receiving triple therapy protocols, as has been demonstrated to you more than once?

Apparently you took dumbbell mathematics in your premed courses so it is taking time to bring you up to speed on the mathematics of mutation and selection. We can start with the principle that multiple selection conditions slow the evolutionary process. You can ask why and you could ask that I demonstrate this to you with the ev model and I could answer that I have already done this but since you are not up to speed on this mathematics, I will repeat it again for you if you are interested.

Yes, it would be so tempting to sink to your level, Dr. Kleinman. Please explain to me now why you continue to mischaracterize my position and lie about my arguments, Dr. Alan Kleinman?

 

[Ichneumonwasp]

Certainly as Mr Scott has suggested there may be a “sweet spot” where evolution can be accelerated. You have suggested that this curve may be parabolic. However, this rate of evolution will never be as rapid as when a single selection pressure is applied. You have two ways of establishing the rates of evolution. You can collect data in real situations such as the treatment of HIV or you can look at mathematical models to establish this behavior. You are trying to take a single data point on the fitness landscape for HIV to support your argument.

So, now you agree that multiple selection pressures do not stop evolution? OK< then the argument is at an end.

I am not constructing an argument for anything here, Dr. Kleinman. I am arguing against your position that you have stated repeatedly -- that three selection pressures so profoundly slow evolution that the process essentially stops. That the rate of evolution is not as rapid as when one selection pressure is applied is completely beside the point, Dr. Kleinman, since no one has argued that multiple selection pressures will necessarily be faster than one selection pressure in stimulating evolutionary change. We are arguing against your stated position that three pressures will stop evolution.

You now seem to agree with us that evolution continues along, three pressures or no. Your real world example (HIV triple therapy) -- your example, Dr. Kleinman, not mine -- of how three selection pressures demonstrates that evolution is stopped by those three selection pressures is bunk, Dr. Kleinman. So, your insistence that ev serves as a reliable model for the evolutionary process with HIV triple therapy in the real world and demonstrates the actual mathematics of evolutionary change is bunk, Dr. Kleinman.

I believe the general behavior of ev with 1, 2 and 3 selection conditions and the use of multiple antimicrobials to treat difficult infections and the failure and consequences of using monotherapy to treat MRSA, Gonorrhea, pseudomonas and other multiply resistant microbes will have far more weight in this debate.

So, in other words, Dr. Kleinman, when evidence argues against you, you will ignore the evidence?

A computer model that was devised to show the emergence of new information and not mimic all evolutionary conditions is better evidence of how the evolutionary process works than a real world example?

There is only one reason I have harped on HIV, Dr. Kleinman -- because of your insistence that HIV triple therapy serves as the real world example that validates your idea of how ev functions. There are many examples of three and more selection pressures working on organisms in the real world. May we now begin to examine all the other examples of multiple selection pressures not stopping the evolutionary process? There are so many, it is difficult to know where to begin.

Each of the parameters in ev has unique effects on the generations for convergence. Increasing populations decreases the generations of convergence at a decreasing rate as you increase population, increasing mutation rate decreases the generations for convergence to a point where the generations for convergence starts to increase. The major factor which increases the generations for convergence is the genome length which increases at an increasing rate as you lengthen the genome. There has been a lot of data posted on this thread and the Evolutionisdead forum which shows this.

Dr. Kleinman, why do you insist on answering a question not even asked? Paul answered my question briefly and to the point, all the while demonstrating that you do not know how to correlate the results of ev runs with the real world, since you harp on "abnormally high mutation rates". In small populations in the real world variance among organisms cannot be high. That is how current HIV triple therapies slow the evolutionary process, as opposed to earlier triple therapy regimens that permitted high enough population counts, which translates in the real world to increased variability. If one cannot input high populations in ev, the only way to mimic "real world" variability in orgnisms is through increasing the mutation rate. That there are rates that interfere is beside the point, as we all know. Kill organisms or eliminate their ability to replicate, and they do not leave behin progeny.

 

[Ichneumonwasp]

Yes, there is great variance in the generation count depending on the random seed. I'm not sure what your second question means.


I've run a long series of experiments varying only the mutation rate, and the generation count seems to vary linearly with it.


The only kind of mutation is point mutations applied to each creature immediately after the best half of the creatures are reproduced.

~~ Paul

Thanks Paul.