Annoying creationists

[Foster Zygote]

Wow! It's like I wandered back into this thread just as the Death Star was blowing up.

 

[kjkent1]

I don't think Ev's model is rich enough to demonstrate something like the divergence of chimp and humans.

~~ Paul

I understand completely, but that won't stop kleinman from jumping all over your comments. I'm sure that the upcoming dialog will be fascinating.

 

[articulett]

We don't even know all the changes that resulted in the differences between us and chimps from what I know, since I don't think we yet have a full accounting of any ape genome, nor do we have a full appreciation for differences in exon/intron sites and how intron mutations might affect expression. Heck, even silent exon mutations can produce altered folding of proteins so that new functions are gained or old functions may be lost. If we want a full account of the differences, then we need a full view not only of the genetics but also of the proteomics.

Actually we have sequenced the chimpanzee in 2005, and last year we found a particularly interesting "hot spot". http://www.sciam.com/article.cfm?articleID=00023D61-9116-14E3-911683414B7F0000

In addition to the protein known to be involved with language--and another one involved with brain growth--there is much interest in certain genes that are expressed at different times in brain development during humans (including the fetal period). When and how often particularly genes are expressed may play a more important role in the differences between apes and humans than the actual genes themselves.

http://www.sciencedaily.com/releases/2006/11/061113180219.htm


--and we've also recently sequenced the genome of the rhesus monkey too.

http://www.sciencedaily.com/releases/2007/04/070412141025.htm

And you are correct. There are many, many factors that go into making a genome what it is...which is, of course, why Kleinman's point mutation model (which is a popular nonsensical argument among creationist) is only good for obfuscating and not for understanding anything.

Also, it's not just our intelligence that has made us rise above other apes (in our own minds at least), it's the fact that we cooperate and learn from each other, and genes involved in these traits promise to be important too...just as they are in our closest kin:

http://www.newscientist.com/article/dn11542-bonobos-join-forces-to-outdo-chimps.html

Besides, the math model has been "solved", but Kleinman ignores this:
http://www.medicalnewstoday.com/medicalnews.php?newsid=61885

http://www.scienceagogo.com/news/20070029220033data_trunc_sys.shtml

In the past, mathematical models of evolution have focused largely on how populations respond to single mutations, the random changes in single nucleotides on the DNA chain. Other theories have focused on recombination, the process that occurs in sexual selection when the genetic sequences of parents are recombined.

The new mathematical model, developed by Rice's Michael Deem and visiting professor Jeong-Man Park, attempts to find out how HGT changes the overall dynamics of evolution. In comparison to existing models that account for only point mutations or sexual recombination, Deem and Park's model shows how HGT increases the rate of evolution by propagating favorable mutations across populations.

Published in Physical Review Letters, the new model shows how HGT compliments the modular nature of genetic information, making it feasible to swap whole sets of genetic code - like the genes that allow bacteria to defeat antibiotics. "We have developed the first exact solution of a mathematical model of evolution that accounts for this cross-species genetic exchange," said Deem. "We know that the majority of the DNA in the genomes of some animal and plant species - including humans, mice, wheat and corn - came from HGT insertions. For example, we can trace the development of the adaptive immune system in humans and other jointed vertebrates to an HGT insertion about 400 million years ago. Life clearly evolved to store genetic information in a modular form, and to accept useful modules of genetic information from other species."


I apologize for thinking you are a creationist--but Kleinman has been told everything that you have said before--many times--he can't hear it...and that is what I referred to when I said that no explanation will ever work for a creationist--whatever conundrum makes evolution "untrue" for them, is a conundrum that no amount of explaining or evidence can ever address. They NEED to believe that their question has not been answered. Really. It's insane, but it's true. And it's true of every creationist who has come to this forum. They don't have the same conundrums--but they all have an inability to understand the answers to their questions--or even why their questions are bad questions.

 

[Ichneumonwasp]

I apologize for thinking you are a creationist

Was that directed at me?

Actually we have sequenced the chimpanzee in 2005, and last year we found a particularly interesting "hot spot". http://www.sciam.com/article.cfm?art...1683414B7F0000

Thanks. I wasn't aware that we were that far along with any other ape genome.

 

[Ichneumonwasp]

Each creature is scored for number of mistake points (missing binding sites, spurious bindings within gene, spurious bindings outside gene). Then the creatures are sorted by mistake points. The creatures are compared in pairs: the best and worst, next best and next worst, etc. If the better one has fewer mistakes, it survives and replicates, killing the worse one. If there is a tie, it is broken according to a tie breaking parameter; the default is to keep both creatures.

So fitness is simply inversely proportional to the number of mistake points.


~~ Paul

Good, thanks. So, the model is well constructed for the determination of information gain and not very helpful for real world natural selection. Like I said several times before, I am very sure all this has been covered earlier and I just do not want to read this entire thread, but how in the world could something like this continue for so long when the model itself cannot answer the issues that Kleinman proposes?

This looks to me like the strawman of strawmen; Behe on steroids; Dembski on PCP; Philip Johnson set loose in a boy's refectory with a bottle of Crisco and no nightwatchman.

 

[Paul C. Anagnostopoulos]

Good, thanks. So, the model is well constructed for the determination of information gain and not very helpful for real world natural selection. Like I said several times before, I am very sure all this has been covered earlier and I just do not want to read this entire thread, but how in the world could something like this continue for so long when the model itself cannot answer the issues that Kleinman proposes?

Hey, it's a thread on the James Randi forum. It has a life of it's own. Kleinman's goalpost used to be in a different place: He was simply claiming that Ev demonstrates that not enough time has passed to evolve transcription factor binding sites on huge genomes using only point mutation. Unfortunately, we agreed, so his goalpost has evolved since then.

This looks to me like the strawman of strawmen; Behe on steroids; Dembski on PCP; Philip Johnson set loose in a boy's refectory with a bottle of Crisco and no nightwatchman.

Sig material! But as a moderator, I must refrain.

~~ Paul

 

[Ichneumonwasp]

I have half a mind to insist that Kleinman publish this idea. Immediately. How can he keep such all-important ideas away from the reading pulic? But, please, tell me where it will be published. I want to witness the public burning with my own eyes.

The ev model isn't even in the same ballpark as to how triple therapy affects HIV. They are completely different. Now that I have a better idea how the program works, I'm absolutely flabbergasted by the inanity of it all.

Ev did its job. Let it rest.

 

[articulett]

I have half a mind to insist that Kleinman publish this idea. Immediately. How can he keep such all-important ideas away from the reading pulic? But, please, tell me where it will be published. I want to witness the public burning with my own eyes.

The ev model isn't even in the same ballpark as to how triple therapy affects HIV. They are completely different. Now that I have a better idea how the program works, I'm absolutely flabbergasted by the inanity of it all.

Ev did its job. Let it rest.

In my earlier reply, I implied I had once thought you were a creationist, but I had actually confused you with someone else with a long screen name I couldn't quite remember. I apologize. Your replies are fantastic as already noted.

 

[articulett]

Was that directed at me?

Accidentally...a synaptic misfire. My face is red. Please forgive.

 

[Ichneumonwasp]

Thanks.

It would be funny, though. A creationist neurologist with a screen name Ichneumonwasp.

The comic potential is definitely there................

 

[joobz]

Forgive me, but I'd like to make sure these questions aren't ignored and lost in the page of posts.

Kleinman, Hope you had a great weekend. Here are some questions that need answering:

1.) Why doesn't magnitude matter in modeling?
2.) Why do only point mutations matter?
3.) Why does running a simulation = doing maths?
4.) What is magical about 3 selection pressures?
5.) Which selection pressure posed by Delphi would take less time?
6.) Why do the yeast strains in the paper I posted develop resistance to the multiple selection pressures when you claim it would take too long to occur?
7.) How does the HIV adapt to three selection pressures?
8.) Why is there evidence of a Gonorrhea Superbug?

And some additional questions posed by ichneumanwasp:
7.) Why are you generalizing a model intended only to demonstrate information gain through mutation and selection?
8.) How does this differ from any other post hoc analysis in science -- a type of analysis that is considered useful for future directions in research but extremely dangerous in drawing new conslusions?
9.) On what grounds do you think that ev closely models all realities concerning evolution when even its creators do not?
10.) How can you claim only a fourfold increase in change with increasing population size when you cannot model population sizes on the order of billions to many more as are seen in nature?
11.) Related to the above, in a model with 90% kill off in a population of 60 or so, the remaining population from the selection pressure would be around 6. But a 90% kill off in a population of 1 billion would result in a population size of 100 million. A 99% kill-off results in a population size of 10 million. Are you suggesting that these differences in population size, in which every member generates new mutations, is incapable of producing viable offspring that can escape the selection pressures? I could certainly see only a fourfold increase in changes if you were talking about the difference between a population size of 60 and one of 6000. The difference in population size is not enough to expect new varieties that could escape these pressure, but a population of 10 million?
12.) If you are modelling kill-off rates higher than 99%, then how does this differ from extinction models? How does this relate to natural conditions?

and Finally,
13.) If math or theory are in conflict with reality, which must we change to correct the error?

 

[kleinman]

Annoying Creationists

You kids have a good weekend;

Thank you.

When you get back, remember to answer the following questions.
Why doesn't magnitude matter in modeling?

[/quote]
If you ask an interesting pertinent question, I will always try to answer your questions. Of course magnitude matters in modeling. This is why Dr Schneider’s failure to consider larger size genomes led to inappropriate extrapolations about the rate of information gain by mutation and selection. There are other practical issues that matter about magnitude that must be considered with modeling such as round off error.

How come only point mutations matter?

[/quote]
I haven’t said that only point mutations matter. What I have said is that other mechanisms of mutations will not alter the fundamental mathematics that multiple selection conditions slow the evolutionary process. It doesn’t matter what form of mutation occurs in the mutation/selection cycle. It is the multiple selection conditions which slow the evolutionary process. What type of mutation mechanism do you propose to put into ev which would alter this mathematics?

Why does running a simulation = doing maths?

[/quote]
Dr Schneider did the “maths”. Running a simulation (doing a parametric study) describes the behavior of the “maths”. Dr Schneider did the “maths” properly; he failed to describe the behavior of the “maths” appropriately by using a single set of parameters in the model to draw his conclusions. Are you sure you are an engineer? When you do a simulation, do you do a single case and draw your conclusions based on that single case?

What is magical about 3 selection pressures?

[/quote]
The only thing “magical” about 3 selection pressures is that it causes evolution to proceed more slowly than 1 or 2 selection pressures.

Which selection pressure posed by Delphi would take less time?

[/quote]
Ask Delphi this question then ask him to put his code fragments into ev to produce the data to prove it.

Why do the yeast strains in the paper I posted develop resistance to the multiple selection pressures when you claim it would take too long to occur?

After reading the paper, I know why you didn’t post any quotes from the paper because it supports my argument that multiple selection pressures slow evolution when applied simultaneously. Here is a quote from the paper:

For batch selection, the overnight cultures of chemically mutagenized S. cerevisiae (named as 101) at lateexponential phase were exposed to each of the four

stress conditions separately, as described in Fig. 1.

I added the bold facing. This situation is exactly analogous to using monotherapy to treat HIV or TB. You can rapidly obtain drug resistant strains to single drugs applied in series. These authors used the same strategy to obtain multiple-stress resistant Saccharomyces. You evolutionists continue to give evidence that makes my point.

Your f(x)=y, where x is a vector in your multidimensional functional equation describing a fitness landscape. In this case, the vector x defines points on the surface of the fitness landscape and the selection pressures, x1, x2, x3,… to the number of selection pressures define a direction for the walk on the fitness landscape. y is the fitness of the creature to reproduce. The optimum solution to this equation represents a value y which gives optimum reproduction.

No no no no no no no no! Slow down. We're already way off the tracks.

I’ve always told you evolutionists that I would be patient with you. I’ll go whatever pace you need to go in order to understand the mathematics of mutation and selection.

Fitness only has meaning with respect to a specific genotype. To make this computation even close to reality, x must be a variable length string of characters from an alphabet (like a DNA sequence.) Multiple independent selection pressures could be represented as multiple functions on the genotype, which could then combined to form the organism's overall fitness. The total fitness represents that genotype's ability to produce offspring in a particular enviornment.

You don’t understand the meaning of a functional equation. A functional equation is the implicit notation that a variable is dependent upon one or more independent variables. So, f(x)=y is simply saying that y depends on the value of x (x1, x2, …). If y is the genotype’s ability to produce offspring in a particular environment (selection conditions, the x1, x2, …) then to optimize y, mutations to the genotype which increase y subject to x selection conditions will satisfy that walk on the fitness landscape to the optimum. In words, an organism’s fitness is dependent on the selection conditions.

Unless we're talking about a very trivial fitness function on trivial genomes, describing the surface of a fitness landscape is very difficult. Visualizing it in any meaningful way is almost impossible, as the "distance" between points is proportional to the probability of mutations between two genotypes.

Certainly the fitness landscape is very complex. This is why I contend there is no way to transform a gene from some initial function to some totally different function. That gene must take a path on the fitness landscape such that it is always selected for in order to make the transformation. Your concept of gene duplication to give the raw material to make new genes requires there to be some path on this complex fitness landscape which allows the transformation to be made. Three selection pressures make the transformation of genes on HIV very slow and this situation does not create new genes with new functions.

Unless you are willing to be patient and read carefully without making assumptions, this thread is going to keep repeating itself.

The only thing I am repeating is the mathematics that ev shows and the real examples of this mathematics. The reason I repeat it is that is how mutation and selection works.

Now I understand your logic, if you have a predetermined goal, evolution goes profoundly slow, if you have no goal at all, it goes faster. Wow! How could anyone doubt this kind of logic?

I would doubt it, since that's not what I said. I said that if there is no goal, then the concept of the speed of evolution makes no sense.

So let’s look at what you said again.

As Mercutio and others have tried to tell you, this statement assumes that there is a predetermined goal toward which evolution is heading. Only then does the concept of the "speed of evolution" make any sense. Ev has a predetermined goal. Real life does not.

It certainly looks like you said that that real life does not have a predetermined goal toward which evolution is heading.

To be clear: It makes sense to look at an evolved function and ask how long it took, and through which steps it evolved. What doesn't make sense is to look forward and ask how long it will take for something interesting to happen, when that something is not predefined.

I understand why you take this view. Your own model shows that when you use it to look forward and ask how long it will take; it shows your belief system to be mathematically impossible. Paul, your prejudices are showing.

Paul, what you have done is to adopted Cyborg’s cruft theory of evolution.

Kleinman, it may surprise and disappoint you to hear it, but there was no particular reason evolution had to end up creating you. As predetermined goals go, there's nothing special about humans. Could be that the "predetermined goal" was banana slugs, and we are just one of millions of misses. Sure, you may feel that you are a "perfect creature"; e coli feel the same way about themselves, and if it came to a vote they'd win.

So tell us Mercutio, did all these living things come about by mutation and selection or mutation and no “predetermined goal”. If you take this second view, do you want to explain it to us mathematically?

In your world, does evolution require every creature to have a separate, predetermined pathway "from the beginning"?

Well, it appears in your world it appears that mutation and selection can not have a predetermined pathway, otherwise your theory is mathematically impossible. This is why you evolutionists have transformed the field of biology into a mushy soft collection of unrealistic extrapolations deficient of any mathematical foundation.

There are a number of news reports today about the verification of a gonorrhea "super bug" resistant to all but one of its useful classes of antibiotics. Seems it has aquired resistance to all four (4) previous classes, as explained in the following quote:

Over the years, gonorrhea has become resistant to a number of antibiotic classes starting with sulfa, then penicillin and the tetracyclines before fluoroquinolones.

Of course this has happened; single selection pressures (monotherapy) can quickly evolve drug resistant strains. If you do a little more investigation you will find MRSA, pseudomonas and a variety of other microbes are displaying the same behavior that ev models. Joobz’s paper shows this same phenomenon to other types of selection stresses.

Dr. Kleinman's mathematics must therefore be incorrect, since the real world is not consistent with his prediction.

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.

The gonorrhea super bug Neisseria gonorrhoeae is now on its fifth antibiotic class -- the only one we now have to treat it. Now, Dr. Kleinman has repeatedly claimed that three is the threshold of mutations against selection pressures for microevolution, at which point the life form can no longer survive, as exemplified by the HIV virus. He's also asserted that the threshold between 2 and 3 adaptations is the threshold between micro and macro evolution, and that macroevolution is mathematically impossible.

He realy said these things?! What a riot!

What really is a riot is that you said this:

There are plenty of examples of A-life evolving. I think Ev rankles the IDers because it is a model of actual life, and also because Schneider is fairly good at advertising it.

And then you said this:

To be clear: It makes sense to look at an evolved function and ask how long it took, and through which steps it evolved. What doesn't make sense is to look forward and ask how long it will take for something interesting to happen, when that something is not predefined.

So how long does it take to evolve binding sites on an e coli size genome?

Triple therapy provides a profoundly (potently) selective pressure on HIV, as witnessed by significant reductions in viral load (I trust that I needn’t reference this phenomenon). But current triple therapy is effective only if compliance is nearly perfect (95+%) – if the selection pressures are kept in place and viral reproduction is kept to a bare minimum. When compliance is reduced to 80%, then enough viral replication occurs that new strains emerge and resistance develops. This level of compliance provides the same three selection pressures but still allows enough viral reproduction so that natural variability can produce resistant strains. So, by definition of selective pressures, 80% compliance with a triple therapy protocol constitutes three selection pressures that are less potent than triple therapy with 95+% compliance. The important factor is not the number of selection pressures but the potency of the selection pressures.

I was hoping to do this mathematically, but you've done it brilliantly with an empirical result. I couldn't hope to get this point across more clearly than you just did. Your post utterly demolishes kleinman's multiple selection pressures mistake hypothesis. He needs to read this until he understands it, and the rest of us need to keep him focused on it until he does.

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.

In short, from my limited understanding of the workings of the program, it cannot be used the way that Kleinman is trying to use it.

Sensible people concluded this some 90 pages ago.

Why cyborg, it is nice to have you back. Do you know that Paul has adopted your cruft theory of evolution?

Kleinman is, however, an Energizer bunny, he just keeps on going on, and on, and on, and on, and...

That’s because you are such an encouragement to me.

I don't think anyone linked drug compliance to the selection pressure's potency yet. This adroit argument demolishes kleinman's hypothesis in a straightforward way. There's nothing subtle about it. Putting the same population under the same number of selection pressures while varying the potency can increase or decrease the rate of adaptation. Clearly adaptation is independent of the number of selection pressures.

Certainly changing the potency of selection pressures changes the rate of adaptation but you are wrong when you say adaptation is independent of the number of selection pressures. Your own Wikipedia link to fitness landscape should make that clear to you.

If anything would convince kleinman he's mistaken, it would be this incontrivertible evidence.

The incontrovertible evidence you and your fellow evolutionists have been posting supports what ev is showing and what I am contending.

So, if we accept your assumptions, for argument's sake, then what sort of numbers would you input into ev to show kleinman that the sort of changes he says are impossible, are actually very reasonable?

I don't think Ev's model is rich enough to demonstrate something like the divergence of chimp and humans.

However, ev is rich enough to demonstrate what multiple selection pressures do to the rate of evolution. Multiple selection pressures profoundly slow the rate of evolution.

Wow! It's like I wandered back into this thread just as the Death Star was blowing up.

Now don’t get hit by any pieces of the theory of evolution as it is vaporized by ev.

I don't think Ev's model is rich enough to demonstrate something like the divergence of chimp and humans.

I understand completely, but that won't stop kleinman from jumping all over your comments. I'm sure that the upcoming dialog will be fascinating.

I was really hoping it will be annoying rather than fascinating.

Each creature is scored for number of mistake points (missing binding sites, spurious bindings within gene, spurious bindings outside gene). Then the creatures are sorted by mistake points. The creatures are compared in pairs: the best and worst, next best and next worst, etc. If the better one has fewer mistakes, it survives and replicates, killing the worse one. If there is a tie, it is broken according to a tie breaking parameter; the default is to keep both creatures.

So fitness is simply inversely proportional to the number of mistake points.

Good, thanks. So, the model is well constructed for the determination of information gain and not very helpful for real world natural selection. Like I said several times before, I am very sure all this has been covered earlier and I just do not want to read this entire thread, but how in the world could something like this continue for so long when the model itself cannot answer the issues that Kleinman proposes?

You might ask whether Paul is speaking for himself or for the author of the computer model because the author of the model said the following:
Dr Schneider said the following in response to a critique of ev written by Royal Truman. This quote is taken from Dr Schneider’s web site at:
http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/truman/

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.

And Dr Schneider said the following:
http://www.lecb.ncifcrf.gov/~toms/paper/ev/blog-ev.html
The following are Dr Schneider’s responses to a critique of his paper Evolution of biological information by Dr Stephen E Jones.

Stephen E. Jones[/URL]"]"Schneider's paper is misleadingly titled: "Evolution of biological information". But it is just a *computer* simulation. No actual *biological* materials (e.g. genomes of nucleic acids, proteins, etc) were used, nor does Schneider propose that his simulation be tested with *real* genomes or proteins

Actual biological materials were used to determine the original hypothesis. Read the literature: Schneider1986

Stephen E. Jones[/URL]"]It only becomes *real* biological information and random mutation and natural selection, when the simulation is tested in the *real* world, using *real* DNA, proteins, with *real* mutations and a *real* environment does the selecting. It is significant that Schneider does not propose this, presumably because he knows it wouldn't work.

You are very bad at reading my mind, I have considered doing this experiment. Given the right conditions, it WILL WORK. Do you have th gumption to do the experiment yourself? That's the way real science works! FURTHERMORE, if you read the literature, you will recognize that related experiments have been repeatedly done for 20 years. Look up SELEX.

Stephen E. Jones[/URL]"]In the rest of the paper he uses the single word "selection". I take this as a tacit admission that his model is not a simulation of *real* biological natural selection.

No. A rose is a rose by any other name. Selection is selection whether it be natural (generally meaning the environment of earth), breeding (by humans usually, though perhaps some ants select their fungi), SELEX or in a computer simulation. Of COURSE it is a simulation of natural selection! The paper would not be relevant to biology and would not have been published in a major scientific journal if it were not!

Stephen E. Jones[/URL]"]Schneider lets slip that there is another unrealistic element in his (and indeed all) computer simulations in that it (they) "does not correlate with time":

So? Run the program slower if you want. Make one generation per 20 minutes to match rapid bacterial growth. THIS WILL NOT CHANGE THE FINIAL RESULT!

Stephen E. Jones[/URL]"]Well, when Schneider's simulation is actually tested with *real* "life" (e.g. a bacterium), and under *real* mutation and natural selection it gains information, then, and only then, would "creationists" be favourably impressed. But if they are like me, they would already be impressed (but unfavourably) that Schneider does not mention in his paper that his simulation should now be so tested in the *real* "biological" world.

1. The simulation was of phenomena in the "real" world.
2. Dr. Jones is invited yet again to do an experiment.

The following is a response Dr Schneider made to a statement made by David Berlinski.

David Berlinski[/URL]"]Where attempts to replicate Darwinian evolution on the computer have been successful, they have not used classical Darwinian principles, and where they have used such principles, they have not been successful.

The ev program disproves this statement since it uses classical Darwinian principles and was successful.

The previous statements are clear that Dr Schneider believes that ev simulates the real world. Paul believed this until he saw the true behavior of ev.

Good, thanks. So, the model is well constructed for the determination of information gain and not very helpful for real world natural selection. Like I said several times before, I am very sure all this has been covered earlier and I just do not want to read this entire thread, but how in the world could something like this continue for so long when the model itself cannot answer the issues that Kleinman proposes?

Hey, it's a thread on the James Randi forum. It has a life of it's own. Kleinman's goalpost used to be in a different place: He was simply claiming that Ev demonstrates that not enough time has passed to evolve transcription factor binding sites on huge genomes using only point mutation. Unfortunately, we agreed, so his goalpost has evolved since then.

The only thing that has moved in this discussion is your (d)evaluation of ev. We still have the same goalposts. Ev shows that the theory of evolution is mathematically impossible and we now have the explanation of why it is mathematically impossible. Multiple selection conditions profoundly slow the evolutionary process.

This looks to me like the strawman of strawmen; Behe on steroids; Dembski on PCP; Philip Johnson set loose in a boy's refectory with a bottle of Crisco and no nightwatchman.

Sig material! But as a moderator, I must refrain.

Just because you are a moderator on this forum doesn’t mean you don’t reveal your prejudices and biases. In fact they reveal how sloppy you are as a mathematician and scientist. If the mathematics interferes with you belief system, you simply claim they don’t apply. You defend this by saying that without direction, evolution proceeds more quickly. Put that feature in ev and show us the mathematical proof of you theory.

I have half a mind to insist that Kleinman publish this idea. Immediately. How can he keep such all-important ideas away from the reading pulic? But, please, tell me where it will be published. I want to witness the public burning with my own eyes.

The ev model isn't even in the same ballpark as to how triple therapy affects HIV. They are completely different. Now that I have a better idea how the program works, I'm absolutely flabbergasted by the inanity of it all.

Ev did its job. Let it rest.

Ev is an excellent model of mutation and selection and how multiple selection conditions affects evolution. Just because Paul has gone into denial mode about what ev represents, we still have the author’s own statements about the model. If you studied ev a bit, you would comprehend my arguments.

1.) Why doesn't magnitude matter in modeling?
2.) Why do only point mutations matter?
3.) Why does running a simulation = doing maths?
4.) What is magical about 3 selection pressures?
5.) Which selection pressure posed by Delphi would take less time?
6.) Why do the yeast strains in the paper I posted develop resistance to the multiple selection pressures when you claim it would take too long to occur?

Already answered at the beginning of this post.

7.) How does the HIV adapt to three selection pressures?

Much more quickly with monotherapy than with triple drug therapy.

8.) Why is there evidence of a Gonorrhea Superbug?

Gonorrhea has been treated with monotherapy for years.

And some additional questions posed by ichneumanwasp:
7.) Why are you generalizing a model intended only to demonstrate information gain through mutation and selection?

Shouldn’t this be 9.)? I did this at Dr Schneider’s suggestion. He did this in email communications with me and he suggested this publicly in his publication on ev. The only thing I am generalizing from his model is that multiple selection conditions profoundly slow the evolutionary process. This is a general mathematical principle for mutation and selection no matter what the mechanism of mutation is. There are numerous real examples of the phenomenon including the ones you are raising here.

8.) How does this differ from any other post hoc analysis in science -- a type of analysis that is considered useful for future directions in research but extremely dangerous in drawing new conslusions?

Ev demonstrates a fundamental principle of mutation and selection. It shows why a Gonorrhea Superbug can arise so quickly. It also explains why so many other resistant strains of microbes arise because of the use of monotherapy. What is so dangerous about showing the theory of evolution to be mathematically impossible? It is simply a dumb theory that has failed to explain properly how mutation and selection works.

9.) On what grounds do you think that ev closely models all realities concerning evolution when even its creators do not?

Read Dr Schneider’s quotes that I have posted above and you will understand that the creator of the model believes his model simulates reality. I agree with him, he has properly modeled mutation and selection.

10.)How can you claim only a fourfold increase in change with increasing population size when you cannot model population sizes on the order of billions to many more as are seen in nature?

I have run simulations with a 10,000 fold increase in the population and it shows that the decrease in the generations for convergence occurs at less than an additive rate with increasing population. It is easy to understand why this occurs when you understand that doubling population less than doubles the probability of an appropriate mutation occurring at a particular locus. Paul is supposed to be running a population series now but does not seem to be posting any data. I have run and posted several population series and they all show the same mathematical behavior I’ve described here. Once I get a computer with more memory, I will run population cases with >10^6 creatures but the trends are already established.

11.) Related to the above, in a model with 90% kill off in a population of 60 or so, the remaining population from the selection pressure would be around 6. But a 90% kill off in a population of 1 billion would result in a population size of 100 million. A 99% kill-off results in a population size of 10 million. Are you suggesting that these differences in population size, in which every member generates new mutations, is incapable of producing viable offspring that can escape the selection pressures? I could certainly see only a fourfold increase in changes if you were talking about the difference between a population size of 60 and one of 6000. The difference in population size is not enough to expect new varieties that could escape these pressure, but a population of 10 million?

The selection pressures are independent of population sizes. Dr Richard has already said that with HIV, you are producing 10^9 viruses/day yet triple therapy still slows evolution. Complex creatures don’t reproduce at this rate and have much smaller populations. The fundamental mathematics of mutation and selection makes it impossible for any macroevolutionary process to occur.

12.) If you are modelling kill-off rates higher than 99%, then how does this differ from extinction models? How does this relate to natural conditions?

Increasing the kill off rate only slows the mathematics of mutation and selection further, you reduce population and that is the only parameter that accelerates evolution (for a given set of selection conditions).

If math or theory are in conflict with reality, which must we change to correct the error?

The mathematics of ev is consistent with reality. We have at least five real examples of what ev is demonstrating mathematically, including your example.

 

[joobz]

After reading the paper, I know why you didn’t post any quotes from the paper because it supports my argument that multiple selection pressures slow evolution when applied simultaneously. Here is a quote from the paper:
Originally Posted by Evolutionary engineering of multiple-stress resistant Saccharomyces cerevisiae
For batch selection, the overnight cultures of chemically mutagenized S. cerevisiae (named as 101) at lateexponential phase were exposed to each of the four

Originally Posted by Evolutionary engineering of multiple-stress resistant Saccharomyces cerevisiae
stress conditions separately, as described in Fig. 1.


I added the bold facing. This situation is exactly analogous to using monotherapy to treat HIV or TB. You can rapidly obtain drug resistant strains to single drugs applied in series. These authors used the same strategy to obtain multiple-stress resistant Saccharomyces. You evolutionists continue to give evidence that makes my point.

I should have known you'd move the goal post again. So we now play the game of "a stress is what I call a stress".

Let's look at what you said earlier (keeping your derisions and ad homs in tact) about a chemical stressor example I gave:

I wonder if you ever considered what happens chemically when you use chemically active chlorine or iodine as a disinfectant. This is an example of large number of multiple selection pressures. Chlorine and iodine combine chemically to large number of sites on a wide variety of biological molecules including proteins, DNA and other crucial molecules necessary to support life. These chemical additions of these large chemically active groups change the conformation of huge number of biological molecules simultaneously which is why these chemicals are effective disinfectants.

Now, in that paper, they included an ethanol stress, an oxidative stress (in the form of hydrogen peroxide), a heat stress and a freeze-thaw stress. Each of these gross scale stresses actually represents a variety of independantly functioning stresses. By your own admission, the hydrogen peroxide (Which functions identically similarly to the chlorine or iodine) is a multi stress event in and of itself.

I refuse to allow you to move this goalpost.

Your theory has been refuted. Your math holds no logic. You are floundering in your foolishness.

 

[kjkent1]

Kleinman:

None of the evidence, real world or mathematical, proves that all selective pressures are of equal force and effect. Nor does the evidence prove that multiple selective pressures are of additive power, extending without limit.

How do you know that the curve of selective pressures doesn't level off in its effect?

How do you know that "all" selective pressures interfere with each other?

How do you know that some selective pressures don't negate or aid each other?

You keep insisting on adherence to sound science -- maybe you should follow your own policy. Right now, you can modify the relative weight of the selective pressures in ev, and the results will alter the number of generations necessary for Rseq -> Rfreq. Missed bindings, spurious bindings inside, and spurious bindings outside display different selective pressures.

So, we know for a fact that all selective pressures are not equal.

And as we can't test some other pressure, not found in ev, we can't conclude that selective pressures restrict evolution without limits. I submit that the effect of many selective pressures will center around a mean, and likely are normally distributed. My own experiments with ev show the appearance of this behavior even with only three pressures.

I have yet to see you provide any contrary proof.

PS. You don't annoy me. You're far too predictable to do that.

 

[kleinman]

Annoying Creationists

I should have known you'd move the goal post again. So we now play the game of "a stress is what I call a stress".

Who are you quoting? Are you whining because I pointed out in your paper that they were applying selective pressures one at a time?

I wonder if you ever considered what happens chemically when you use chemically active chlorine or iodine as a disinfectant. This is an example of large number of multiple selection pressures. Chlorine and iodine combine chemically to large number of sites on a wide variety of biological molecules including proteins, DNA and other crucial molecules necessary to support life. These chemical additions of these large chemically active groups change the conformation of huge number of biological molecules simultaneously which is why these chemicals are effective disinfectants.

Now, in that paper, they included an ethanol stress, an oxidative stress (in the form of hydrogen peroxide), a heat stress and a freeze-thaw stress. Each of these gross scale stresses actually represents a variety of independantly functioning stresses. By your own admission, the hydrogen peroxide (Which functions identically similarly to the chlorine or iodine) is a multi stress event in and of itself.

So let’s consider each of the selective pressures. Do you consider an ethanol stress as a large number of multiple selection pressures? Consider how these authors applied this stress. The used slowly increasing levels of ethanol alone without the other selective pressures applied at the same time. Once they had strains of their yeast that could tolerate an elevated level of ethanol, the then applied the next selection pressure.

Now consider their use of hydrogen peroxide, you are probably not aware of the enzyme superoxide dimutatase. By slowly increasing the concentration of hydrogen peroxide they are selecting strains that are better producers of this enzyme. You are not evolving this enzyme de novo; you are simply producing strains of the yeast that are good producers of this enzyme. The heat stress and freeze-thaw stress are multiple selection stressors but consider that these authors limited these stresses in order to produce viable yeast. Why don’t you write to these authors and ask them what would happen if they applied all for of their stressor conditions at the same time rather than one at a time.

I refuse to allow you to move this goalpost.

I neither need to nor want to move the goalposts. I’m just waiting for you evolutionists to get to the ball park.

Your theory has been refuted. Your math holds no logic. You are floundering in your foolishness.

You have refuted nothing; all you have shown is that with careful application of single selection pressures you can breed yeasts with particular properties to survive in particular environments. Now if you show that all their selection pressures can be applied simultaneously and you are able to breed this yeast as quickly as with single selection pressures then you would have a point.

None of the evidence, real world or mathematical, proves that all selective pressures are of equal force and effect. Nor does the evidence prove that multiple selective pressures are of additive power, extending without limit.

I’ve never said that all selective pressures are of equal force and effect. What I have said is that when you have multiple selective pressures, the multiple pressures slow the evolutionary process. You have played with the weighting factors for the different mistakes in ev and see that it changes the generations for convergence but none of the weight factors have such an extreme effect as when setting the value to 0. If you think changing the weights on the selection conditions in ev will allow larger genomes to converge, do some examples for us.

I also don’t believe that selection pressures are additive. Two selection pressures that alone might otherwise have minimal impact on the reproduction of a creature, when combined have a marked affect on the ability of the organism to reproduce. Triple antiviral agents for the treatment of HIV are an example of this. One agent has minimal effect on the reproduction virus while three agents together profoundly affect reproduction of the virus. The effect of the three agents is more than three times the affect of any single agent.

How do you know that the curve of selective pressures doesn't level off in its effect?

The curve for selective pressures is easily bracketed. At one extreme you have very mild selective pressures that have virtual no effect on the reproduction of the creature while at the other extreme, you have selective pressures that cause extinction. All other selective pressures fall with the range of these two selective pressures.

How do you know that "all" selective pressures interfere with each other?

That is the mathematical principle that is demonstrated by ev and is well described by Delphi’s reference to Wikipedia and the fitness landscape. You are requiring multiple stress conditions to be overcome simultaneously. This is mathematically and physiologically more difficult than overcoming a single selection condition at a time.

How do you know that some selective pressures don't negate or aid each other?

You may be able to come up with peculiar selective pressures that might do something like you suggest but in general this is not what the mathematics suggests.

You keep insisting on adherence to sound science -- maybe you should follow your own policy. Right now, you can modify the relative weight of the selective pressures in ev, and the results will alter the number of generations necessary for Rseq -> Rfreq. Missed bindings, spurious bindings inside, and spurious bindings outside display different selective pressures.

So, we know for a fact that all selective pressures are not equal.

Nothing affects convergence in ev like shutting off two of the three selection pressures. If you think you can markedly change the generations for convergence by simply varying the weights without setting any to zero, do some examples on a 32k or 64k genome and show us.

And as we can't test some other pressure, not found in ev, we can't conclude that selective pressures restrict evolution without limits. I submit that the effect of many selective pressures will center around a mean, and likely are normally distributed. My own experiments with ev show the appearance of this behavior even with only three pressures.

What ev is showing is that each additional selection pressure slows the evolution process. This is a general mathematical principle that does not matter what the selection pressure is. Read Wikipedia on fitness landscape. They say the same thing I am saying but using different terminology.

I have yet to see you provide any contrary proof.

Well, we have the mathematics of ev and we have numerous examples of how multiple selective pressure slow the evolution of resistant strains of microbes. Too bad you can’t see this proof. I’ll look for more examples of this and I’m sure you evolutionists will come up with more examples, like joobz example of developing multiple stress resistant yeasts by applying single pressures at a time.

PS. You don't annoy me. You're far too predictable to do that.

I’ll have to work on that.

 

[joobz]

Now consider their use of hydrogen peroxide, you are probably not aware of the enzyme superoxide dimutatase. By slowly increasing the concentration of hydrogen peroxide they are selecting strains that are better producers of this enzyme.

you can't help but be wrong can you?

Superoxide dismutase (SOD), whether you are talking about copper/zinc SOD or manganese SOD, catalyzes the conversion of Superoxide INTO hydrogen peroxide. It doesn't catalyze the degradation of H2O2. Catalase is the enzyme that degrades hydrogen peroxide. As well as (to lesser extents) the family of glutathione peroxidases.

SOD blocks injury as result of direct oxidation from superoxide, (such as the peroxidation of lipids), but not from hydrogen peroxide. Hydrogen peroxide can still generate hydroxyl radicals through fenton chemistry.

So, yes, hydrogen peroxide IS a multiple stressor. As is ethanol: Ethanol results in changes in membrane fluidity, alterations in membrane potential, and the generation of acetaldehyde.

 

[kleinman]

Annoying Creationists

Now consider their use of hydrogen peroxide, you are probably not aware of the enzyme superoxide dimutatase. By slowly increasing the concentration of hydrogen peroxide they are selecting strains that are better producers of this enzyme.

you can't help but be wrong can you?

Superoxide dismutase (SOD), whether you are talking about copper/zinc SOD or manganese SOD, catalyzes the conversion of Superoxide INTO hydrogen peroxide. It doesn't catalyze the degradation of H2O2. Catalase is the enzyme that degrades hydrogen peroxide. As well as (to lesser extents) the family of glutathione peroxidases.

I stand corrected here master of alchemical engineering. It is the family of peroxidases that decompose the peroxides. But the point is that the paper you provided describes the application of H2O2 as a single selection pressures in slowly increasing concentration to select yeasts which produce enzymes that decompose this oxidizer. That is unless you are arguing that the numerous proteins and other molecules which are damaged by H2O2 are all evolving to new forms that are not affected by H2O2.

SOD blocks injury as result of direct oxidation from superoxide, (such as the peroxidation of lipids), but not from hydrogen peroxide. Hydrogen peroxide can still generate hydroxyl radicals through fenton chemistry.

So, yes, hydrogen peroxide IS a multiple stressor. As is ethanol: Ethanol results in changes in membrane fluidity, alterations in membrane potential, and the generation of acetaldehyde.

So you are arguing that all the molecules which would be harmed by H2O2 and ethanol are all evolving to new forms which are resistant to the damage these chemicals would do. I think you and Delphi both need to lay off the ethanol.

 

[Ichneumonwasp]

Ev is an excellent model of mutation and selection and how multiple selection conditions affects evolution.

How does Ev model HIV triple therapy? Ev selects based on "mistakes" gained through a mutation process. Are you suggesting that HIV is selected by triple therapy solely by the development of mistakes in its genome? Ev is an excellent model of mutation and selection related to the development of information. It does not model HIV selection with triple therapy.

HIV triple therapy works by inhibiting viral replication, not by selecting out mistakes. Selection pressures in the real world either limit reproduction or kill. Ev models, from what I can tell, killing. There are clear Darwinian pressures in place, but what constitutes a "defect" is arbitrarily designed. A "mistake" in nature depends upon context, not upon a pre-defined decision of an investigator.

As to Dr. Schneider's comments, he is correct from what I can tell in what you have provided, but those comments are not applicable to this issue. His point was that his model employed Darwinian selection pressure. It does. It doesn't mimic what occurs in all situations, though, and certainly does not mimic the mechanism by which HIV triple therapy works. His model was designed for a particular purpose -- modelling mutation and selection as it relates to information gain.

But, there is a much larger issue. Suppose everything that Dr. Schneider said is wrong. Suppose that it is dead wrong. What then? You mean we should actually look at how the model works and how it actually relates to HIV and our use of triple therapy? We should not make bare appeals to authority? We should care about evidence and reasoning? Fancy that.

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.

If I am making your point how is it that you couldn't realize that fact for the past two weeks? Please tell me what we have been discussing, because I am still making exactly the same point that I have been making all along -- that it is the potency of selection pressures that makes a difference in the real world and not the number of selection pressures (of course multiple selection pressures add together at the very least if potency is kept stable).

That or you have no idea what my point is now or has been in the past.

To say that increasing selection pressure (potency not number) slows evolution is like saying 1+1=2. That is the friggin' definition of selection pressure, as I have argued for two weeks.

So, let's go back over the argument again. The evidence offered demonstrates that it is not the number of pressures that is critical (you have repeatedly argued that it is the number and not the potency that is critical). With the exact same number of selection pressures, different triple therapy protocols and/or different medication schedules (80% vs 95+%) produce different results. When the potency of the selection pressure is reduced more virions are produced and variability is able to increase -- consequently, resistance develops more easily.

You cannot argue (successfully) that there is a synergistic effect such that the three selection pressures "kill" the reverse transcriptase. Multidrug resistance develops, and the reverse transcriptase works in the resistant strains. You cannot argue that three pressures are critical because there are three pressures in all three situations (actually many more, but that is beside the point, since we can play your way and you still lose) -- triple therapy with profound selection pressure and 95+% compliance (currently used triple therapies), triple therapy with 80% compliance and consequently lessened pressure (resistance develops), older triple therapies with less profound selection pressure with 95+% compliance (resistance develops).

So, what is your solution to this impasse?

What ev is showing is that each additional selection pressure slows the evolution process.

We can continue repeating the same arguments over and over. Everyone knows that the evolutionary process is slowed by the addition of selection pressures, if the new selection pressures produce independent effects. The additional pressures will be either additive or synergistic. But the important point is not the number but the total potency of the selection pressure. If all selection pressures are weak even a large number of them will not produce much of an effect -- take HIV triple therapy at a compliance of 20-30%. Resistance may develop, but it is harder to produce resistant strains at that level of compliance. At 80% compliance -- more selection pressure -- resistance develops more easily with triple therapy. That level provides enough pressure and enough room for viral replication so that resistence may develop in HIV. At 95+% compliance, the selection pressures are so profound that not enough viral replication can occur, so variability is reduced, so resistance does not develop. At lower compliance levels not enough selection pressure is created to drive the process as easily. Resistance is still possible, but it develops more slowly. So, no, it is not a simple arithmetical relationiship. More of parabola really, with little tails on the ends and a nice path running down the middle. Ni.

It's all three selection pressures, according to your definitions, but different potencies.

 

[kleinman]

Annoying Creationists

Ev is an excellent model of mutation and selection and how multiple selection conditions affects evolution.

How does Ev model HIV triple therapy? Ev selects based on "mistakes" gained through a mutation process. Are you suggesting that HIV is selected by triple therapy solely by the development of mistakes in its genome? Ev is an excellent model of mutation and selection related to the development of information. It does not model HIV selection with triple therapy.

What ev models is the evolution of binding sites based on three selection conditions (Paul might call this two selection conditions). One selection condition is that a binding site must occur where it is expected to occur otherwise this is considered a mistake. A second selection condition is that a binding site must not be identified in the region of the gene associated with the binding site otherwise that is considered a mistake and the third selection condition is that a binding site must not be identified outside the binding site region of the genome otherwise that is considered a mistake. Paul calls the last two selection conditions the identification of spurious binding sites and will sometimes call these two selection conditions a single selection condition. What happens as you lengthen the genome length parameter in the model, it becomes more and more difficult to satisfy all three selection conditions and evolve the binding sites in the model. If you set any two of the three selection conditions to zero, the remaining selection condition will rapidly evolve satisfying that selection condition no matter how long the genome. The analogy of the ev model and the use of triple therapy for the treatment of HIV is that you are forcing the HIV virus to satisfy three selection pressures imposed by the triple drug therapy. This delays the evolution of resistant strains of the virus. It is this mathematics which ev simulates and which the use of triple selection conditions on the HIV virus demonstrates in reality. If you attempt to use monotherapy on the HIV virus, it quickly can evolve to that single selection condition. This is demonstrated mathematically in ev by setting two of the three selection conditions to zero.

HIV triple therapy works by inhibiting viral replication, not by selecting out mistakes. Selection pressures in the real world either limit reproduction or kill. Ev models, from what I can tell, killing. There are clear Darwinian pressures in place, but what constitutes a "defect" is arbitrarily designed. A "mistake" in nature depends upon context, not upon a pre-defined decision of an investigator.

Ev selecting out of mistakes is analogous to preventing replication of the virus. The selection rule in ev only allows the genomes with the fewest mistakes to reproduce. This is done for programming simplicity. If instead of modeling the evolution of binding sites on a random genome, the genetic sequence of HIV could be introduced into the model and random mutations to this genome could be allowed to this sequence based on using different selection conditions imposed by antiviral drugs and then you would get an almost exact simulation of the evolution of HIV virus subject to the selection conditions imposed by antiviral medications rather than the analogous situation of the evolution of binding sites. However the mathematical behavior of these two simulations would be very similar.

As to Dr. Schneider's comments, he is correct from what I can tell in what you have provided, but those comments are not applicable to this issue. His point was that his model employed Darwinian selection pressure. It does. It doesn't mimic what occurs in all situations, though, and certainly does not mimic the mechanism by which HIV triple therapy works. His model was designed for a particular purpose -- modelling mutation and selection as it relates to information gain.

I believe that Dr Schneider modeled the mathematics of mutation and selection correctly. The evolution of resistant strains of HIV would require some modification of Dr Schneider’s selection rules but otherwise, the mathematics is identical. Of course, you evolutionists can try to argue that frame shift mutations, inversions and other forms of mutations would speed up this process but I doubt it. Random point mutations drives this process.

But, there is a much larger issue. Suppose everything that Dr. Schneider said is wrong. Suppose that it is dead wrong. What then? You mean we should actually look at how the model works and how it actually relates to HIV and our use of triple therapy? We should not make bare appeals to authority? We should care about evidence and reasoning? Fancy that.

I happen to think that Dr Schneider modeled the mathematical mechanism of mutation and selection properly. So do the peer reviewers at Nucleic Acids Research. Where Dr Schneider slipped up in his analysis was using a 256 base genome with an extremely high, unrealistic mutation rate in the model to compute a rate of information acquisition by this mechanism. I did tell Dr Schneider that once the real behavior of his model was known that evolutionists would discredit the model. This response of the evolutionist community has been unanimous so far, including his own programmer, Paul.

I think Dr Schneider’s model points to an important principle (besides showing that the theory of evolution is mathematically impossible) of the way microbial infections are treated in general. In general, monotherapy for the treatment of infections is the rule and note how many multiple resistant microbes are appearing. The present view is that doctors are using too many antibiotics and that fewer antibiotics should be used. It may be that serious infection should always be treated with double or triple antimicrobials to prevent the emergence of resistant strains.

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.

If I am making your point how is it that you couldn't realize that fact for the past two weeks? Please tell me what we have been discussing, because I am still making exactly the same point that I have been making all along -- that it is the potency of selection pressures that makes a difference in the real world and not the number of selection pressures (of course multiple selection pressures add together at the very least if potency is kept stable).

That or you have no idea what my point is now or has been in the past.

When you talk about noncompliance with treatment of HIV, you are talking about the missing of doses of one or more medications. Lifting the selection pressures has several benefits for the virus. The first is that the virus can reproduce more rapidly. The second is that if one or more drugs are consistently left out of the treatment plan by the noncompliant patient, it is much easier for the virus to evolve resistance to the remaining drug. Either way, less than therapeutic dosages of medication or the reduction of the number of drugs used accelerates the evolution of resistant strains of the virus.

To say that increasing selection pressure (potency not number) slows evolution is like saying 1+1=2. That is the friggin' definition of selection pressure, as I have argued for two weeks.

Of course increasing selection pressure potency slows evolution, in the extreme case it causes extinction. What you are still having difficulty understanding is that multiple selection pressures no matter what their potency slows evolution for each of the selection conditions.

So, let's go back over the argument again. The evidence offered demonstrates that it is not the number of pressures that is critical (you have repeatedly argued that it is the number and not the potency that is critical). With the exact same number of selection pressures, different triple therapy protocols and/or different medication schedules (80% vs 95+%) produce different results. When the potency of the selection pressure is reduced more virions are produced and variability is able to increase -- consequently, resistance develops more easily.

It is not quite that simple. Increasing the number of selection pressures will always slow the evolutionary process. This is a mathematical fact shown by ev. This is demonstrated by Delphi’s Wikipedia reference to fitness landscape. And this is shown in reality by the use of multiple antimicrobials which delays the evolution of resistant strains of these microbes. Where the mathematics gets more complex is when you have less potent selection pressures which in combination can still cause extinction. This is what is being approached with use of triple antiviral medications for the treatment of HIV. Alone, none of the drugs have the potency to completely stop the virus but in combination, the reproduction and evolution of the virus is almost completely stopped as long as compliance with treatment is maintained.

You cannot argue (successfully) that there is a synergistic effect such that the three selection pressures "kill" the reverse transcriptase. Multidrug resistance develops, and the reverse transcriptase works in the resistant strains. You cannot argue that three pressures are critical because there are three pressures in all three situations (actually many more, but that is beside the point, since we can play your way and you still lose) -- triple therapy with profound selection pressure and 95+% compliance (currently used triple therapies), triple therapy with 80% compliance and consequently lessened pressure (resistance develops), older triple therapies with less profound selection pressure with 95+% compliance (resistance develops).

If you recall, I have never said that these therapies kill the virus or the reverse transcriptase. What these therapies do is slow the reproduction of the virus. This by definition is what fitness is. Unless and until a single selection pressure is developed against the virus that completely stops reproduction of the virus, the only treatment available will be multiple drugs with less than complete prevention of the reproduction of the virus.

So, what is your solution to this impasse?

There is no impasse here. There is only your lack of understanding of the mathematics of mutation and selection. The key point that you don’t understand is that multiple selection pressures slow the evolutionary process. This is what ev shows, this is explained in Wikipedia in the description of the fitness landscape and is shown by the use of multiple drug regimens for the treatment of antimicrobial infection. Compliance with these therapies causes some confusion in the behavior of mutation and selection but the underlying mathematics is clear.

What ev is showing is that each additional selection pressure slows the evolution process.

We can continue repeating the same arguments over and over. Everyone knows that the evolutionary process is slowed by the addition of selection pressures, if the new selection pressures produce independent effects. The additional pressures will be either additive or synergistic. But the important point is not the number but the total potency of the selection pressure. If all selection pressures are weak even a large number of them will not produce much of an effect -- take HIV triple therapy at a compliance of 20-30%. Resistance may develop, but it is harder to produce resistant strains at that level of compliance. At 80% compliance -- more selection pressure -- resistance develops more easily with triple therapy. That level provides enough pressure and enough room for viral replication so that resistence may develop in HIV. At 95+% compliance, the selection pressures are so profound that not enough viral replication can occur, so variability is reduced, so resistance does not develop. At lower compliance levels not enough selection pressure is created to drive the process as easily. Resistance is still possible, but it develops more slowly. So, no, it is not a simple arithmetical relationiship. More of parabola really, with little tails on the ends and a nice path running down the middle. Ni.

Potency of selection pressures does complicate the mathematics but I think you are starting to understand the point. Selection pressures don’t obey the simple addition. Selection pressures are highly non-linear. The only thing you can say in general about selection pressures is that increasing the number of selection pressures slows reproduction and confounds the evolution process.

It's all three selection pressures, according to your definitions, but different potencies.

Again, potencies of selection pressures affect the mathematics and real situations of evolution but the additional selection pressures always slow evolution. That is if kjkent1 doesn’t show us a case where two selection pressures acting simultaneously speed up evolution.

 

[joobz]

I stand corrected here master of alchemical engineering. It is the family of peroxidases that decompose the peroxides. But the point is that the paper you provided describes the application of H2O2 as a single selection pressures in slowly increasing concentration to select yeasts which produce enzymes that decompose this oxidizer. That is unless you are arguing that the numerous proteins and other molecules which are damaged by H2O2 are all evolving to new forms that are not affected by H2O2.

Your factual errors have become quite numerous. You've claimed mastery of thermodynamics, but couldn't argue what thermo really is. Remember the, "Natural selection, which is a restatement of the 2nd law" silliness. You've claimed mastery of mathematics, claiming that magnitude doesn't matter. You've even used F=ma as an example, where we know it breaks down in instances of extreme velocity.
You've reiterated the importance of point selection as the only relavent method of mutation and that all others are of equal weight. Yet, the paper by Deem et. al., presented by Articulett the critical importance of gene transfer argues directly against this point. You claimed that 3 pressures halted evolution, and we have three examples where this isn't true. You claimed that SOD was the primary degrading enzyme of hydrogen peroxide, and this is, again, woefully wrong.

Can you provide evidence of where you have been correct? Because, there seems to be an amazing lack of it.

Wait, I have one, I have terrible grammar/editing skills. Of that point, you have been fully correct.

So you are arguing that all the molecules which would be harmed by H2O2 and ethanol are all evolving to new forms which are resistant to the damage these chemicals would do. I think you and Delphi both need to lay off the ethanol.

gibberish argument