Annoying creationists

[Dr Adequate]

Kjkent1, K172 may be able to digested nylon because of a microevolutionary process but you have no mathematical or empirical evidence that it arose spontaneously from the primordial soup. Wow, you managed to combine the strawman and moving the goalposts into a single exquisitely stupid manoeuvre. It's like watching you do a pratfall into a custard pie.

[kleinman]

Wow, you managed to combine the strawman and moving the goalposts into a single exquisitely stupid manoeuvre. It's like watching you do a pratfall into a custard pie, or something.
Now Adequate, if you want to see something exquisitely stupid look at these totally contradictory statements about selection pressures and evolution.
Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
And
More optimisation takes more time. This is what my model shows.
http://forums.randi.org/images/smilies/doglaugh.gif

[joobz]

When I post my citations, I quote from them on the thread.[/quote]Yes you do, but not for honest reasons. Stop dodging the questions. you are simply flooding the thread. Maybe others still enjoy watching you make a mockery of yourself, but I've had enough. Either honestly address the many critiques that have been made, or I will be forced to report your spamming/flooding posts.

Now why don’t you tell us what the selection pressures are and the target genes from your citation about Madagascar rainforests and show us how these combination selection pressures accelerate evolution.Stop dodging my questions. I will not take the bait.

[Dr Adequate]

When I post my citations, I quote from them on the thread. I let the data from ev and the quotes from citations make my points. Except that they don't, which is, of course, why you have, on the contrary, put such an enormous (albeit futile) effort into lying about their significance.

And we all know this, because we've read the thread, so why lie about this apart from ... I don't know ... whatever strange satisfaction the act of untruth gives you?

[Dr Adequate]

Now Adequate, if you want to see something exquisitely stupid look at these totally contradictory statements about selection pressures and evolution. If I want to see stupid, then yes, your claim that those two statements are contradictory does indeed gladden my heart.

I've a feeling that I could see even stupider stupid if you ever attempted to explain why you think that they're contradictory, but for now I shall settle for the ridiculous spectacle of you reciting your idiocy over and over again.

[kleinman]

When I post my citations, I quote from them on the thread.Yes you do, but not for honest reasons.
Really joobz, perhaps you want to say that the scientists as the National Institute of Health are being dishonest when they say that antibiotic resistance is an example of evolutionary adaptation of the microbes. Here it is in their words.
http://www.niaid.nih.gov/factsheets/antimicro.htm (http://www.niaid.nih.gov/factsheets/antimicro.htm)
Since antibiotics and other antimicrobial drugs first became widely used in the World War II era, they have saved countless lives and blunted serious complications of many feared diseases and infections. The success of antimicrobials against disease-causing microbes is among modern medicine's great achievements. After more than 50 years of widespread use, however, many antimicrobials are not as effective as they used to be.

Over time, some bacteria have developed ways to circumvent the effects of antibiotics. Widespread use of antibiotics is thought to have spurred evolutionarily adaptations that enable bacteria to survive these powerful drugs. Other microbes such as viruses, fungi, and parasites have developed resistance as well. Antimicrobial resistance provides a survival benefit to microbes and makes it harder to eliminate infections from the body. Ultimately, the increasing difficulty in fighting off microbes leads to an increased risk of acquiring infections in a hospital or other setting.

Diseases such as tuberculosis, gonorrhea, malaria, and childhood ear infections are now more difficult to treat than they were just a few decades ago. Drug resistance is an especially difficult problem for hospitals harboring critically ill patients who are less able to fight off infections without the help of antibiotics. Heavy use of antibiotics in these patients selects for changes in bacteria that bring about drug resistance. Unfortunately, this worsens the problem by producing bacteria with greater ability to survive even in the presence of our strongest antibiotics. These even stronger drug-resistant bacteria continue to prey on vulnerable hospital patients.
And how is this evolutionary adaptation slowed? Why ev shows you how, use multiple selection pressures. Here is another empirical example of this phenomenon.
http://www.aafp.org/afp/980600ap/maenza.html (http://www.aafp.org/afp/980600ap/maenza.html)
The primary goal of antiretroviral therapy for human immunodeficiency virus (HIV) infection is suppression of viral replication. Evidence indicates that the optimal way to achieve this goal is by initiating combination therapy with two or more antiretroviral agents. The agents now licensed in the United States for use in combination therapy include five nucleoside analog reverse transcriptase inhibitors (zidovudine, didanosine, zalcitabine, stavudine and lamivudine), two nonnucleoside reverse transcriptase inhibitors (delavirdine and nevirapine) and four protease inhibitors (saquinavir, ritonavir, indinavir and nelfinavir). Current recommendations suggest that antiretroviral therapy be considered in any patient with a viral load higher than 5,000 to 20,000 copies per mL, regardless of the CD4+ count. Selection of the combination regimen must take into account the patient's prior history of antiretroviral use, the side effects of these agents and drug­drug interactions that occur among these agents and with other drugs as well. Because of the potential for viral resistance, nonnucleoside reverse transcriptase inhibitors and protease inhibitors should only be used in combination therapy. Antiretroviral agents are rapidly being developed and approved, so physicians must make increasingly complex treatment decisions about medications with which they may be unfamiliar.

[quixotecoyote]

According to the search function you've had your combination therapy claim shot down two hundred fifty eight times. This will be two hundred fifty nine. Are you going for a record?

[joobz]

Really joobz,
Yes. you are being truly dishonest and are simply flooding this thread. It's no longer cute or amusing.

[kleinman]

According to the search function you've had your combination therapy claim shot down two hundred fifty eight times. This will be two hundred fifty nine. Are you going for a record?
Quixotecoyote, you supporters of the moth eaten theory of evolution certainly have an imagination. Really joobz,Yes. you are being truly dishonest and are simply flooding this thread. It's no longer cute or amusing.
Don’t you know joobz; I have control over the minds of hundreds of scientists and have convinced them to publish nothing but examples of combination selection pressures slowing evolution. Don’t you find that cute or amusing?
http://forums.randi.org/images/smilies/doglaugh.gif
Let’s give another citation of how mutation and selection actually works, that is simultaneous selection pressures profoundly slow the evolutionary process. You do know that ev shows this mathematically, don’t you?
http://theoncologist.alphamedpress.org/cgi/content/full/6/3/233 (http://theoncologist.alphamedpress.org/cgi/content/full/6/3/233)
As efforts continue to elucidate molecular mechanisms of resistance, current clinical trial efforts will focus on expanding the potential of STI571 by its use in combination therapy regimens. Examples of planned phase I/II trials include escalating high-dose Ara-C following initial therapy with STI571 in myeloid blast crisis and escalating doses of daunorubicin in combination with vincristine and prednisone following STI571 induction for lymphoid blast crisis. These studies are based on in vitro data [17] showing additive effects of daunorubicin and synergistic effects of Ara-C when combined with STI571. The in vitro studies also showed additive benefits when STI571 was combined with interferon. Thus new phase I/II trials in chronic phase patients with these combination therapies (STI571 + interferon and STI571 + low-dose Ara-C) will be initiated with the goal of achieving enhanced cytogenetic response (versus single-agent STI571) that could ultimately result in improved survival.
I like these examples from the field of oncology, after all, Dr Schneider, the author of the peer reviewed and published computer simulation of random point mutations and natural selection must surely understand how mutation and selection works.

Hey quixotecoyote, I have only about 1,000,000 hits left to go through on my search.

[kjkent1]

Kjkent1, K172 may be able to digested nylon because of a microevolutionary process but you have no mathematical or empirical evidence that it arose spontaneously from the primordial soup. So if you want to have a dialog about the number of selection pressures and the effect on the rate of the evolutionary process, present some evidence to substantiate your view.If you don't define "microevolutionary process" and distinguish it from "macroevolutionary process," then how can I or anyone else possibly provide you with evidence that K172's existence is the product of one vis-a-vis the other?

Thus far, your definition has been "big change" and "small change." This is scientifically imprecise. I'm sure you can do better.

[joobz]

Quixotecoyote, you supporters of the moth eaten theory of evolution certainly have an imagination.
Don’t you know joobz; I have control over the minds of hundreds of scientists and have convinced them to publish nothing but examples of combination selection pressures slowing evolution. Don’t you find that cute or amusing?
http://forums.randi.org/images/smilies/doglaugh.gif
Let’s give another citation of how mutation and selection actually works, that is simultaneous selection pressures profoundly slow the evolutionary process. You do know that ev shows this mathematically, don’t you?
http://theoncologist.alphamedpress.org/cgi/content/full/6/3/233 (http://theoncologist.alphamedpress.org/cgi/content/full/6/3/233)

I like these examples from the field of oncology, after all, Dr Schneider, the author of the peer reviewed and published computer simulation of random point mutations and natural selection must surely understand how mutation and selection works.

Hey quixotecoyote, I have only about 1,000,000 hits left to go through on my search.
non-responive derisive language. Your posts are worthless.

[kleinman]

Kjkent1, K172 may be able to digested nylon because of a microevolutionary process but you have no mathematical or empirical evidence that it arose spontaneously from the primordial soup. So if you want to have a dialog about the number of selection pressures and the effect on the rate of the evolutionary process, present some evidence to substantiate your view.If you don't define "microevolutionary process" and distinguish it from "macroevolutionary process," then how can I or anyone else possibly provide you with evidence that K172's existence is the product of one vis-a-vis the other?

Thus far, your definition has been "big change" and "small change." This is scientifically imprecise. I'm sure you can do better.
I’m glad to see you are paying attention. I thought this was a good time to again visit the microevolutionary/macroevolutionary terminology debate again.

Paul and other evolutionists have said that there is no difference between a microevolutionary and a macroevolutionary process. That view holds that a population simply accumulates microevolutionary steps until you achieve a macroevolutionary change. Ev shows mathematically how difficult it is to sort mutations for more than a single selection condition. The hundreds of real examples of mutation and selection that I have posted show that evolving more than a single genetic system at a time becomes an extremely difficult process for all but the most rapidly reproducing large populations, with the shortest genomes. A delineation for the microevolutionary process (which I believe occur and have posted many examples) and a macroevolutionary process (which I don’t believe occur and which no examples have been posted) is determined by the number of genetic systems which can evolve in a mutation/selection process.

[Dr Adequate]

C'mon, kleinman, you're not even posting fresh crap.

We all know that none of your endless citations of real science support your dotty fantasies.

[kjkent1]

I’m glad to see you are paying attention. I thought this was a good time to again visit the microevolutionary/macroevolutionary terminology debate again.

Paul and other evolutionists have said that there is no difference between a microevolutionary and a macroevolutionary process. That view holds that a population simply accumulates microevolutionary steps until you achieve a macroevolutionary change. Ev shows mathematically how difficult it is to sort mutations for more than a single selection condition. The hundreds of real examples of mutation and selection that I have posted show that evolving more than a single genetic system at a time becomes an extremely difficult process for all but the most rapidly reproducing large populations, with the shortest genomes. A delineation for the microevolutionary process (which I believe occur and have posted many examples) and a macroevolutionary process (which I don’t believe occur and which no examples have been posted) is determined by the number of genetic systems which can evolve in a mutation/selection process.You're not being scientifically precise, Alan. You've just defined macro vis-a-vis micro evolution via a new undefined term: "genetic systems". Furthermore, you require some unspecified number of evolved systems.

What is an evolved genetic system, how many are required to turn microevolution into macroevolution?

I'm simply asking for you to define your terms with precision, because your definitions may permit you to draw a conclusion that would not be reached by others in the scientific community.

[Belz...]

The vast amount of empirical data that demonstrates the opposite, Belz, the moths got to your theory of evolution and there is nothing left but holes.

Cute dodge. Answer the question:

What about the moths ? And the nylon-eating bacteria ? And the dogs and cats ? And humans ?

Don’t you know joobz; I have control over the minds of hundreds of scientists and have convinced them to publish nothing but examples of combination selection pressures slowing evolution. Don’t you find that cute or amusing?

And yet you've forgotted to MAKE them understand how evolution my mutation and selection REALLY works! Or do you have a evil twin brother who's blocking you ?

[Belz...]

I’m glad to see you are paying attention. I thought this was a good time to again visit the microevolutionary/macroevolutionary terminology debate again.

Sure, Klein. Anything you say.

[Belz...]

You're not being scientifically precise, Alan.

Actually he's not being scientific. At all.

[kleinman]

Paul and other evolutionists have said that there is no difference between a microevolutionary and a macroevolutionary process. That view holds that a population simply accumulates microevolutionary steps until you achieve a macroevolutionary change. Ev shows mathematically how difficult it is to sort mutations for more than a single selection condition. The hundreds of real examples of mutation and selection that I have posted show that evolving more than a single genetic system at a time becomes an extremely difficult process for all but the most rapidly reproducing large populations, with the shortest genomes. A delineation for the microevolutionary process (which I believe occur and have posted many examples) and a macroevolutionary process (which I don’t believe occur and which no examples have been posted) is determined by the number of genetic systems which can evolve in a mutation/selection process.You're not being scientifically precise, Alan. You've just defined macro vis-a-vis micro evolution via a new undefined term: "genetic systems". Furthermore, you require some unspecified number of evolved systems.
Ok, let’s try to make this more precise. Do you hold to the view “one gene-one polypeptide”?
What is an evolved genetic system, how many are required to turn microevolution into macroevolution?
An evolved genetic system is set of enzymatic processes which are at a local optimum on the fitness landscape. An example of such a genetic system is the Krebs cycle. A microevolutionary change to such a system occurs when a single selection pressure is targeted to a single gene in the system whereas a macroevolutionary change to such a system occurs when a single selection pressure is targeted to multiple genes in the system or multiple selection pressures are targeted to multiple genes in the system. Now it is clear that according to this definition, microevolutionary processes occur regularly as seen with antimicrobial and cancer resistance. Macroevolutionary processes on the other hand are much more difficult to accomplish. Depending on the life forms, evolution by mutation and selection processes targeted against more than a single gene are seen only on very rapidly reproducing, huge populations with very short genomes. Demonstrating this type of macroevolutionary process on smaller populations of more complex life forms with much lower reproductive rates and much longer genomes is not observed, at least I haven’t seen any examples presented here.

This is the mathematical and empirical barrier to the massive transformation required to metamorphose reptiles into birds or humans and chimpanzees from a primate precursor. By the way, a friend of mine showed me a report that now says that humans and chimpanzee genomes are only 95% similar. Do you want to do the arithmetic for what is 5% of 3 billion? You have to account for these 150 million base differences in only 500,000 generations.
I'm simply asking for you to define your terms with precision, because your definitions may permit you to draw a conclusion that would not be reached by others in the scientific community.
I hope the above definitions give a sense of the differences between macro and microevolution. What is clear from the mathematics of ev and the empirical evidence is that the greater the number of selection conditions the more difficult it is for the population to evolve to these multiple selection conditions.
The vast amount of empirical data that demonstrates the opposite, Belz, the moths got to your theory of evolution and there is nothing left but holes.Cute dodge. Answer the question:

What about the moths ? And the nylon-eating bacteria ? And the dogs and cats ? And humans ?
You should talk with joobz; he doesn’t think I’m cute. I suspect he thinks I’m annoying.

Sure I’ll explain your examples to you. Moth populations can change colors depending on the environment but those color changes are not due to mutation and selection, it is due to recombination and natural selection. Alleles are selected for that give the moth color advantage. What you probably don’t know is that recombination without error can not increase information in the gene pool and recombination and natural selection can and does cause lose of information (alleles) from the gene pool.

Kjkent1’s example of the nylon-eating bacteria is a case of a single selection pressure acting on a single gene (polymerase) enabling the bacteria to cleave the nylon polymer. This is simply and example of a microevolutionary process. Now if you can demonstrate that these bacteria can evolve to multiple selection conditions simultaneously and do it more rapidly than single conditions selecting sequentially, then you would have some evidence for your viewpoint.

Dogs and cats, these are classic examples of recombination and selection. This type of sorting process is much easier than mutation and selection. Recombination and selection sorts alleles, not mutations. Recombination and selection enables the creation of Chihuahuas and Great Danes in only about 10,000 generations. But both are still dogs. Again, I remind you that recombination without error can not increase information in the gene pool.

And humans, I refer you above to my discussion with kjkent1. Now that the evidence is presenting that humans and chimp genomes differ by 150,000,000 bases, you are going to have a very difficult time explaining these differences in only 500,000 generations. Mutation and selection simply does not have the speed to accomplish this huge number of transformations in so few numbers of generations. The mathematics and empirical evidence is simply not there to support such huge differences in so few numbers of generations. Oh, do want to try to describe the selection pressures which would accomplish these huge numbers of transformations.
You're not being scientifically precise, Alan.Actually he's not being scientific. At all.
Why Belz, do you want me to use your scientific standard, no mathematical basis to your argument and no empirical evidence to support your viewpoint?

I’ll stick with the mathematics of ev and other mathematical models which show that multiple selection pressures profoundly slow the evolutionary process and the vast amount of empirical evidence which supports this mathematics. Hey, why don’t I give you another citation which supports my “unscientific” viewpoint?
http://en.wikipedia.org/wiki/Combination_therapy (http://en.wikipedia.org/wiki/Combination_therapy)
In contemporary usage, the expression combination therapy most often refers to the simultaneous administration of two or more medications to treat a single disease, but the expression is also used when other types of therapy are used at the same time.

Conditions treated with combination therapy include tuberculosis, leprosy, cancer, malaria, and HIV/AIDS.

Combination therapy may seem costlier than monotherapies in the short term but causes significant savings: lower treatment failure rate, lower case-fatality ratios, slower development of resistance and consequently, less money needed for the development of new drugs.
How could that be, Wikipedia states that combination therapies slows the evolution of resistance, they certainly are not being scientific. Belz, you better edit that Wikipedia definition and get them into the scientific realm.

[Belz...]

You should talk with joobz; he doesn’t think I’m cute.

Neither do I. I was refering to your dodge, remember ?

Moth populations can change colors depending on the environment but those color changes are not due to mutation and selection

:boggled:

it is due to recombination and natural selection.

Recombination of what ? Genes code for colour. How can you explain colour variation without mutation of that gene ???

Kjkent1’s example of the nylon-eating bacteria is a case of a single selection pressure

How the hell can you tell how many selection pressures there were ? In fact, how do you define "selection pressure" in the singular ?

Now if you can demonstrate that these bacteria can evolve to multiple selection conditions simultaneously and do it more rapidly than single conditions selecting sequentially, then you would have some evidence for your viewpoint.

I don't need evidence to support strawmen theories to which I don't subscribe.

Dogs and cats, these are classic examples of recombination and selection.

Again, RE-combination of what ? Dogs used to be wolves, and I'd like to know how you think the fox terrier evolved from a wolf through the generations without mutation.

This type of sorting process is much easier than mutation and selection.

Define "easier".

Recombination and selection sorts alleles, not mutations. Recombination and selection enables the creation of Chihuahuas and Great Danes in only about 10,000 generations.

Exactly how does it do that if the genes are identical ? It's an honest question, here.

But both are still dogs.

Subjective opinion. Many races of dogs won't or can't breed with other races.

Again, I remind you that recombination without error can not increase information in the gene pool.

And yet we have dogs that vary in size...

And humans, I refer you above to my discussion with kjkent1. Now that the evidence is presenting that humans and chimp genomes differ by 150,000,000 bases

Who asked the question about chimps ? I asked about humans, human variety.

you are going to have a very difficult time explaining these differences in only 500,000 generations.

Then please explain how chimps and humans are related. Oh no, wait. Chimps aren't our ancestors, so why would you have to ?

Mutation and selection simply does not have the speed to accomplish this huge number of transformations in so few numbers of generations. The mathematics and empirical evidence is simply not there to support such huge differences in so few numbers of generations.

That's just another way to word your previous claim.

[Belz...]

Why Belz, do you want me to use your scientific standard, no mathematical basis to your argument and no empirical evidence to support your viewpoint?

That's not even a sentence.

I’ll stick with the mathematics of ev and other mathematical models which show that multiple selection pressures profoundly slow the evolutionary process

Of course you will. Otherwise you'd have to admit that, outside of the ev model, the "mathematics" do not support your thesis.

and the vast amount of empirical evidence which supports this mathematics.

While we're on the subject of blueberries...

How could that be, Wikipedia states that combination therapies slows the evolution of resistance, they certainly are not being scientific. Belz, you better edit that Wikipedia definition and get them into the scientific realm.

Oh. My. God.

If Wiki says it, I'm sold.

[joobz]

Ok, let’s try to make this more precise. Do you hold to the view “one gene-one polypeptide”?

An evolved genetic system is set of enzymatic processes which are at a local optimum on the fitness landscape. An example of such a genetic system is the Krebs cycle. A microevolutionary change to such a system occurs when a single selection pressure is targeted to a single gene in the system whereas a macroevolutionary change to such a system occurs when a single selection pressure is targeted to multiple genes in the system or multiple selection pressures are targeted to multiple genes in the system. Now it is clear that according to this definition, microevolutionary processes occur regularly as seen with antimicrobial and cancer resistance. Macroevolutionary processes on the other hand are much more difficult to accomplish. Depending on the life forms, evolution by mutation and selection processes targeted against more than a single gene are seen only on very rapidly reproducing, huge populations with very short genomes. Demonstrating this type of macroevolutionary process on smaller populations of more complex life forms with much lower reproductive rates and much longer genomes is not observed, at least I haven’t seen any examples presented here.

This is the mathematical and empirical barrier to the massive transformation required to metamorphose reptiles into birds or humans and chimpanzees from a primate precursor. By the way, a friend of mine showed me a report that now says that humans and chimpanzee genomes are only 95% similar. Do you want to do the arithmetic for what is 5% of 3 billion? You have to account for these 150 million base differences in only 500,000 generations.

I hope the above definitions give a sense of the differences between macro and microevolution. What is clear from the mathematics of ev and the empirical evidence is that the greater the number of selection conditions the more difficult it is for the population to evolve to these multiple selection conditions.

You should talk with joobz; he doesn’t think I’m cute. I suspect he thinks I’m annoying.

Sure I’ll explain your examples to you. Moth populations can change colors depending on the environment but those color changes are not due to mutation and selection, it is due to recombination and natural selection. Alleles are selected for that give the moth color advantage. What you probably don’t know is that recombination without error can not increase information in the gene pool and recombination and natural selection can and does cause lose of information (alleles) from the gene pool.

Kjkent1’s example of the nylon-eating bacteria is a case of a single selection pressure acting on a single gene (polymerase) enabling the bacteria to cleave the nylon polymer. This is simply and example of a microevolutionary process. Now if you can demonstrate that these bacteria can evolve to multiple selection conditions simultaneously and do it more rapidly than single conditions selecting sequentially, then you would have some evidence for your viewpoint.

Dogs and cats, these are classic examples of recombination and selection. This type of sorting process is much easier than mutation and selection. Recombination and selection sorts alleles, not mutations. Recombination and selection enables the creation of Chihuahuas and Great Danes in only about 10,000 generations. But both are still dogs. Again, I remind you that recombination without error can not increase information in the gene pool.

And humans, I refer you above to my discussion with kjkent1. Now that the evidence is presenting that humans and chimp genomes differ by 150,000,000 bases, you are going to have a very difficult time explaining these differences in only 500,000 generations. Mutation and selection simply does not have the speed to accomplish this huge number of transformations in so few numbers of generations. The mathematics and empirical evidence is simply not there to support such huge differences in so few numbers of generations. Oh, do want to try to describe the selection pressures which would accomplish these huge numbers of transformations.

Why Belz, do you want me to use your scientific standard, no mathematical basis to your argument and no empirical evidence to support your viewpoint?

I’ll stick with the mathematics of ev and other mathematical models which show that multiple selection pressures profoundly slow the evolutionary process and the vast amount of empirical evidence which supports this mathematics. Hey, why don’t I give you another citation which supports my “unscientific” viewpoint?
http://en.wikipedia.org/wiki/Combination_therapy (http://en.wikipedia.org/wiki/Combination_therapy)

How could that be, Wikipedia states that combination therapies slows the evolution of resistance, they certainly are not being scientific. Belz, you better edit that Wikipedia definition and get them into the scientific realm.
non responsive, derisive language

Do you care to actually discuss anything, or will you continue to use baiting langauge?

here is why your model, your theory, your argument is wrong.
1.) You don't know the mutation rate for all species for all time.
2.) Mutation rate isn't constant
3.) You don't know the number of selection pressures for all species for all time.
4.) Number of selection pressures isn't constant
5.) Point mutations aren't the only mutation adaptation mechanism
6.) Ill defined concept of what a selection pressure is
7.) slow most definitely doesn't equal stop.

You can't make these points go away. They kill your theory.

PS: You've avoided answering this 12 times now.

[Paul C. Anagnostopoulos]

Again, I remind you that recombination without error can not increase information in the gene pool.
Well that depends on how you define "recombination error," doesn't it?

chromosome: ... promoter ju/nk ... gene ...

chromosome: ... ge/ne ... gene ...

recombination: ... promoter june ... gene ...

Is that an error? I don't know, but it looks like we might have a new gene named June.

~~ Paul

[kleinman]

You should talk with joobz; he doesn’t think I’m cute.Neither do I. I was refering to your dodge, remember ?
Now Belz, you need to remember what the title of the thread is.
Moth populations can change colors depending on the environment but those color changes are not due to mutation and selection http://forums.randi.org/images/smilies/mazeguyemotions/boggled.gifit is due to recombination and natural selection.Recombination of what ? Genes code for colour. How can you explain colour variation without mutation of that gene ???
Belz, you need to go back and read about Mendelian inheritance. There is a nice description of this process in Wikipedia on this page http://en.wikipedia.org/wiki/Mendelian_inheritance (http://en.wikipedia.org/wiki/Mendelian_inheritance)
Kjkent1’s example of the nylon-eating bacteria is a case of a single selection pressureHow the hell can you tell how many selection pressures there were ? In fact, how do you define "selection pressure" in the singular ?
If you know of other selection pressures in knkent1’s example, feel free to tell us what they were.
Now if you can demonstrate that these bacteria can evolve to multiple selection conditions simultaneously and do it more rapidly than single conditions selecting sequentially, then you would have some evidence for your viewpoint.I don't need evidence to support strawmen theories to which I don't subscribe.
You can only wish that the theory of evolution was made of straw, with Dr Schneider’s ev model of random mutation and natural selection and the empirical evidence which shows how mutation and selection actually works, your theory is left only with moth holes.
Dogs and cats, these are classic examples of recombination and selection.Again, RE-combination of what ? Dogs used to be wolves, and I'd like to know how you think the fox terrier evolved from a wolf through the generations without mutation.
Well Belz, if you think that the fox terrier evolve from the wolf by mutation and selection, why don’t you tell us which genes mutated and the loci of these mutations because the examples which I present define the genes being mutated and often times describe the exact loci where the mutations occur. You keep making vague arguments assuming they are true while I argue from mathematical precision with precisely defined genes, mutations and loci. If you examine dog breeding carefully, you will find that the process is driven by recombination and selection, not mutation and selection but don’t let that stop you from proving to us that dog breeding is a mutation and selection process.
This type of sorting process is much easier than mutation and selection.Define "easier".
Recombination and selection is the sorting of alleles which gives a far smaller search space than mutation and selection which is sorting mutations in a huge search space. In the case of recombination and selection, finches with narrow beaks that can access insects in small spaces breed to give offspring with narrow beaks. Finches that need short stout beaks that are capable of breaking nut shells breed to give beaks that can do this task. Don’t confuse the rapidity that recombination and selection can transform a population with the extremely slow process of mutation and selection.
Recombination and selection sorts alleles, not mutations. Recombination and selection enables the creation of Chihuahuas and Great Danes in only about 10,000 generations.Exactly how does it do that if the genes are identical ? It's an honest question, here.
Again, you need to go back and study some Mendelian genetics. Different combinations of alleles change the way the genes are expressed. Take your moth case for example. Let’s say you have two alleles for the color of the moth, one allele gives a black moth and is dominant and the other allele gives a white moth but is recessive. If the moth is in an environment where being black exposes the moth to a predator, that black allele will be selected against and ultimately that allele can be lost. In the case of dogs, breed the largest dogs you have and you will get larger offspring, breed the smallest dogs together and you will get smaller offspring. These morphological changes are not due to mutation and selection; these changes are due to recombination and selection. You are selecting for alleles with particular properties and you start to see the results of this selection in the next generation.
But both are still dogs.Subjective opinion. Many races of dogs won't or can't breed with other races.
Nope, genetically they are homologous. I have never heard anyone use the term “race” when speaking of dogs, but hey, use any term you like.
Again, I remind you that recombination without error can not increase information in the gene pool.And yet we have dogs that vary in size...
Certainly, and these variations can occur very rapidly but the mistake you are making is that you are not going to transform a dog into a cat (or a reptile into a bird) by recombination and selection.
And humans, I refer you above to my discussion with kjkent1. Now that the evidence is presenting that humans and chimp genomes differ by 150,000,000 basesWho asked the question about chimps ? I asked about humans, human variety.
Oh, yes, quite correct Belz, there is a wide variety of humans but all are homologous (except for occasional instances of chromosomal aberrations).
you are going to have a very difficult time explaining these differences in only 500,000 generations.Then please explain how chimps and humans are related. Oh no, wait. Chimps aren't our ancestors, so why would you have to ?
Belz, if you are going to propose that humans and chimps are related, you are going to have to account for all the genetic differences. You have about 150,000,000 base differences and about 500,000 generations to account for these differences. In addition as each gene is compared on a base by base, you will have to explain all the differences between the human and chimp gene. The theory of evolution is for you to prove, I am just pointing out to you the huge mathematical barrier to your explanation.
Mutation and selection simply does not have the speed to accomplish this huge number of transformations in so few numbers of generations. The mathematics and empirical evidence is simply not there to support such huge differences in so few numbers of generations.That's just another way to word your previous claim.
The difference is that I have a peer reviewed and published mathematical model of random point mutation and natural selection which shows how slow the mutation and selection process is and a massive amount of empirical evidence which substantiates this mathematical finding.
Why Belz, do you want me to use your scientific standard, no mathematical basis to your argument and no empirical evidence to support your viewpoint?That's not even a sentence.
That’s strange; my grammar checker doesn’t have a problem with this sentence. Perhaps the problem is that you have no mathematical basis for your theory of evolution by mutation and selection and you have no empirical evidence to support your viewpoint.
I’ll stick with the mathematics of ev and other mathematical models which show that multiple selection pressures profoundly slow the evolutionary processOf course you will. Otherwise you'd have to admit that, outside of the ev model, the "mathematics" do not support your thesis.
That’s not the case Belz; I have posted citations from other mathematical models that show the same thing that Dr Schneider’s model shows. Even joobz citation Varying environments can speed up evolution substantiates my claims. If you understood that evolution by mutation and selection is simply an optimization problem. This type of mathematical problem is well known in mathematics. It is also well know that the more conditions you try to optimize on simultaneously the slower the process proceeds. This is why ev can easily converge a single selection condition even on longer genomes which will not converge all three conditions simultaneously. I’ll give you some empirical examples below which demonstrate this effect.
and the vast amount of empirical evidence which supports this mathematics.While we're on the subject of blueberries...
What you don’t realize is that your theory of evolution is in a jam.
How could that be, Wikipedia states that combination therapies slows the evolution of resistance, they certainly are not being scientific. Belz, you better edit that Wikipedia definition and get them into the scientific realm.Oh. My. God.

If Wiki says it, I'm sold.
Well then, in that case, let’s look at a couple of examples of simultaneous versus sequential selection pressures; the first is from the Proceedings of the National Academy of Science.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=24062 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=24062)
Exposure to 3TC of HIV-1 mutant strains containing non-nucleoside reverse transcriptase inhibitor (NNRTI)-specific mutations in their reverse transcriptase (RT) easily selected for double-mutant viruses that had acquired the characteristic 184-Ile mutation in their RT in addition to the NNRTI-specific mutations. Conversely, exposure of 3TC-resistant 184-Val mutant HIV-1 strains to nine different NNRTIs resulted in the rapid emergence of NNRTI-resistant virus strains at a time that was not more delayed than when wild-type HIV-1(IIIB) was exposed to the same compounds. The RTs of these resistant virus strains had acquired the NNRTI-characteristic mutations in addition to the preexisting 184-Val mutation. Surprisingly, when the 184-Ile mutant HIV-1 was exposed to a variety of NNRTIs, the 188-His mutation invariably occurred concomitantly with the 184-Ile mutation in the HIV-1 RT. Breakthrough of this double-mutant virus was markedly accelerated as compared with the mutant virus selected from the wild-type or 184-Val mutant HIV-1 strain. The double (184-Ile + 188-His) mutant virus showed a much more profound resistance profile against the NNRTIs than the 188-His HIV-1 mutant. In contrast with the sequential chemotherapy, concomitant combination treatment of HIV-1-infected cells with 3TC and a variety of NNRTIs resulted in a dramatic delay of virus breakthrough and resistance development.
And
Because the enormous virus replication dynamics and virus plasma load in vivo exceed by several orders of magnitude those present in cell culture experiments (18, 19), it is expected that the mutations that emerge during such an intensive virus replication may easily counteract any potentially decreased mutation rate resulting from the higher fidelity of the mutant RT. Moreover, if our observations on the accelerated breakthrough of 184-Ile mutant virus in the presence of NNRTIs can be extrapolated to man, it would seem contraindicated to successively use 3TC and NNRTIs. Such procedure (sequential therapy) may even precipitate virus breakthrough. Also, it has been shown that ratios of CCID50 to p24 are at least four times higher in culture fluids of peripheral blood mononuclear cell and MT-4 (5) or CEM cells (personal observations) infected by the 184-Val HIV-1 mutant than in cells infected with HIV-1/IIIB (wild type). One should therefore avoid giving the virus the opportunity to convert into a more infectious form upon treatment with 3TC as a single agent.
And
Because we found that 3TC is inhibitory to NNRTI-resistant HIV-1 strains, and, vice versa, NNRTIs efficiently inhibit 3TC-resistant viruses (10), the marked suppressive effect noted with the combination of 3TC and NNRTIs may be attributed to a complementary suppression of the NNRTI- and 3TC-specific resistance mutations by 3TC and NNRTIs, respectively. Instead of using 3TC and NNRTIs in sequential order, our studies indicate that 3TC should be simultaneously combined with the NNRTIs. This strategy should be aimed at delaying as long as possible the emergence of drug-resistant virus strains.
Let’s see what the scientists at the University of Chicago have to say about simultaneous versus sequential selection pressures.
http://www.journals.uchicago.edu/cgi-bin/resolve?id=doi:10.1086/322655&erFrom=-1660962831312921427Guest (http://www.journals.uchicago.edu/cgi-bin/resolve?id=doi:10.1086/322655&erFrom=-1660962831312921427Guest)
Individuals coinfected with human immunodeficiency virus 1 (HIV-1) and hepatitis B virus (HBV) often receive treatment with an antiretroviral regimen including lamivudine. Lamivudine monotherapy for HBV may lead to drug-resistant mutations in a significant number of patients. The virological and biochemical responses of 8 patients coinfected with HBV/HIV-1 treated with both lamivudine and famciclovir were studied. Patients exhibiting HBV viral rebound at 1 year were analyzed for the emergence of HBV polymerase mutations. Only 1 patient had no prior exposure to lamivudine. Addition of famciclovir to the treatment regimen resulted in a median fall in HBV DNA level of 0.33 log10 at 3 months and an overall rise in HBV DNA level of 3 log10 at 12 months. The only patient in whom durable viral suppression and HBV e antigen seroconversion were noted began receiving lamivudine and famciclovir simultaneously. HBV polymerase gene sequencing identified resistance-associated mutations in 6 of 7 patients with viral rebound. Sequential nucleoside analogue therapy is unlikely to be successful in achieving long-term suppression of HBV replication, and combination therapy should be considered at treatment initiation.
Note that ev shows that single selection pressures evolve far more easily than simultaneous selection pressures. Belz, if you ever worked with optimization problems, this result would be obvious to you.

[kleinman]

1.) You don't know the mutation rate for all species for all time.
2.) Mutation rate isn't constant
3.) You don't know the number of selection pressures for all species for all time.
4.) Number of selection pressures isn't constant
5.) Point mutations aren't the only mutation adaptation mechanism
6.) Ill defined concept of what a selection pressure is
7.) slow most definitely doesn't equal stop.
1.) There is a huge amount of empirical evidence available for mutation rate available. Speculate whatever mutation rate you want and show us that it contradicts my hypothesis.
2.) If you think there is some variable mutation rate that will contradict my hypothesis, speculate what that rate is and prove it and give us a real example of this.
3.) We do know what selection pressures are now. If you think there were some selection pressures that existed in ancient history that do not exist now, speculate whatever selection pressure you want and show that it contradicts my hypothesis and give us a real example of this.
4.) If you think you can vary the number of selection pressures and contradict my hypothesis, speculate what this variation in selection pressures is and show that it contradicts my hypothesis and give us a real example of this.
5.) If you think that other forms of mutations will contradict my hypothesis, speculate which form(s) of mutation(s) will do this and give us a real example of this.
6.) My examples give specific selection pressures and target genes to these selection pressures; your example is the “Madagascar rainforest”. Don’t confuse your ill defined concept of what a selection pressure is with my mathematically precise examples.
7.) All I have to do is show that multiple selection pressures slow evolution enough to make it mathematically impossible, even though you don’t believe in extinction.
We’ll see if joobz will put any meat on his bare bones speculations of how mutation and selection works. I doubt he will do any better than his speculations on abiogenesis.
Again, I remind you that recombination without error can not increase information in the gene pool.Well that depends on how you define "recombination error," doesn't it?
Well, let’s see how you define it.
chromosome: ... promoter ju/nk ... gene ...

chromosome: ... ge/ne ... gene ...

recombination: ... promoter june ... gene ... Is that an error? I don't know, but it looks like we might have a new gene named June.
Paul, are you going to put this logic in ev and show us how this solves the problem of combination selection pressures profoundly slowing evolution? BTW, it’s September.

[joobz]

1.) There is a huge amount of empirical evidence available for mutation rate available. Speculate whatever mutation rate you want and show us that it contradicts my hypothesis.
Correct data exists and shows mutation rates aren't constant. Your assumption is invalid. Therefore any speculation on the impossible nature of evolution is invalid.
Xu, et al. relationship between the rate of molecular evolution and the rate of genome rearrangement in animal mitochondrial genomes. J Mol Evol. 2006 Sep;63(3):375-92

Even within species across different populations this rate is not constant and within mitochondria.

Graffelman, Et al. Variation in estimated recombination rates across human populations Hum Genet. 2007 PMID: 17609980

This fact becomes even more complicated by the fact that rate of mutation can determine the relative development of non-encoded DNA.

Knibbe, Et al. A Long-Term Evolutionary Pressure on the Amount of Non-Coding DNA. Mol Biol Evol. 2007 PMID: 17709335


2.) If you think there is some variable mutation rate that will contradict my hypothesis, speculate what that rate is and prove it and give us a real example of this.
see above.

3.) We do know what selection pressures are now. If you think there were some selection pressures that existed in ancient history that do not exist now, speculate whatever selection pressure you want and show that it contradicts my hypothesis and give us a real example of this.can you provide a list for all pressures?

did you remember to include plate tectonics?

Derek E. Wildman, Monica Uddin, Juan C. Opazo, Guozhen Liu, Vincent Lefort, Stephane Guindon, Olivier Gascuel, Lawrence I. Grossman, Roberto Romero, and Morris Goodman"Genomics, biogeography, and the diversification of placental mammals" PNAS 2007 104: 14395-14400
...Crown placental mammalian diversification appears to be largely the result of ancient plate tectonic events that allowed time for convergent phenotypes to evolve in the descendant clades

4.) If you think you can vary the number of selection pressures and contradict my hypothesis, speculate what this variation in selection pressures is and show that it contradicts my hypothesis and give us a real example of this.
I have already. You've ignored it. Allow me to repost it.

Robert E. Dewar and Alison F. Richard Evolution in the hypervariable environment of Madagascar PNAS 2007 104: 13723-13727
We show that the diverse ecoregions of Madagascar share one distinctive climatic feature: unpredictable intra- or interannual precipitation compared with other regions with comparable rainfall. Climatic unpredictability is associated with unpredictable patterns of fruiting and flowering. It is argued that these features have shaped the evolution of distinctive characteristics in the mammalian fauna of the island. Endemic Herpestidae and Tenrecidae and members of five endemic primate families differ from closely related species elsewhere, exhibiting extremes of "fastness" and "slowness" in their life histories. Climatic features may also account for the dearth of frugivorous birds and mammals in Madagascar, and for the evolutionary prevalence of species with large body mass.

5.) If you think that other forms of mutations will contradict my hypothesis, speculate which form(s) of mutation(s) will do this and give us a real example of this.
I have already, you ignored it.

Bisharat N et. alInfect Genet Evol. 2007 Jul 20 The evolution of genetic structure in the marine pathogen, Vibrio vulnificus.

Cooper TF. Recombination Speeds Adaptation by Reducing Competition between Beneficial Mutations in Populations of Escherichia coli. PLoS Biol. 2007 Aug 21;5(9):e225

Leavis HL, et al. Insertion sequence-driven diversification creates a globally dispersed emerging multiresistant subspecies of E. faecium. PLoS Pathog. 2007 Jan;3(1):e7.

6.) My examples give specific selection pressures and target genes to these selection pressures; your example is the “Madagascar rainforest”. Don’t confuse your ill defined concept of what a selection pressure is with my mathematically precise examples.


Again, you defined yourself into a unrealstic hole. Nature doesn't need to worry about such definitions. A single stress, like oxiditive stress can impact several proteins and transcription factors. In other words, it can act upon several target genes at once. As a result, developing resistence against such a pressure is evolution against multiple selection pressures.
Since, biology can adapt to these types of conditions, you have multiple real world examples of evolution against multiple selection pressures.


7.) All I have to do is show that multiple selection pressures slow evolution enough to make it mathematically impossible, even though you don’t believe in extinction.
How does this rambling (Which containes a false statement and a strawman) address the fact that slow doesn't equal stop. All of life is under "multiple selection pressures", yet life isn't extinct. Therefore, multiple selection pressures do not ultimately lead to extinction.(the only stop condition). If genes are allowed to progress from generation to generation, you can be sure that adaptation will occur.



We’ll see if joobz will put any meat on his bare bones speculations of how mutation and selection works. I doubt he will do any better than his speculations on abiogenesis. derisive language noted.
Please realize, that it is also obvious that I have ALREADY answered and provided meat to my argument. It isn't speculation, but rather supported fact. Your argument is busted.

[Dr Adequate]

Hey, why don’t I give you another citation which supports my “unscientific” viewpoint?
http://en.wikipedia.org/wiki/Combination_therapy (http://en.wikipedia.org/wiki/Combination_therapy)

How could that be, Wikipedia states that combination therapies slows the evolution of resistance... ... which, as we know, does not support your unscientific viewpoint.

You're not fooling anyone, kleinman.

Hello?

[kleinman]

1.) There is a huge amount of empirical evidence available for mutation rate available. Speculate whatever mutation rate you want and show us that it contradicts my hypothesis.Correct data exists and shows mutation rates aren't constant. Your assumption is invalid. Therefore any speculation on the impossible nature of evolution is invalid.
So let’s look at your correct data.
http://www.ingentaconnect.com/content/klu/239/2006/00000063/00000003/00000246;jsessionid=1ttk8bey8gs9h.alice?format=pri nt&crawler=true (http://www.ingentaconnect.com/content/klu/239/2006/00000063/00000003/00000246;jsessionid=1ttk8bey8gs9h.alice?format=pri nt&crawler=true)
Evolution of mitochondrial genes is far from clock-like. The substitution rate varies considerably between species, and there are many species that have a significantly increased rate with respect to their close relatives. There is also considerable variation among species in the rate of gene order rearrangement. Using a set of 55 complete arthropod mitochondrial genomes, we estimate the evolutionary distance from the common ancestor to each species using protein sequences, tRNA sequences, and breakpoint distances (a measure of the degree of genome rearrangement). All these distance measures are correlated. We use relative rate tests to compare pairs of related species in several animal phyla. In the majority of cases, the species with the more highly rearranged genome also has a significantly higher rate of sequence evolution. Species with higher amino acid substitution rates in mitochondria also have more variable amino acid composition in response to mutation pressure. We discuss the possible causes of variation in rates of sequence evolution and gene rearrangement among species and the possible reasons for the observed correlation between the two rates.
Why joobz, your reference has nothing to do with combination selection pressures and the rate of evolution. In fact, this article has nothing to do with nuclear DNA. Once again, you have proven you don’t read your own citations. Let’s see if your arguments improve. Ah yes, you have another citation which you don’t quote. Let’s see if this has anything to do with combination selection pressures accelerating evolution.
http://www.springerlink.com/content/jjj7331665g7n7t6/ (http://www.springerlink.com/content/jjj7331665g7n7t6/)
Abstract: Recently it has been reported that recombination hotspots appear to be highly variable between humans and chimpanzees, and there is evidence for between-person variability in hotspots, and evolutionary transience. To understand the nature of variation in human recombination rates, it is important to describe patterns of variability across populations. Direct measurement of recombination rates remains infeasible on a large scale, and population-genetic approaches can be imprecise, and are affected by demographic history. Reports to date have suggested broad similarity in recombination rates at large genomic scales and across human populations. Here, we examine recombination rate estimates at a finer population and genomic scale: 28 worldwide populations and 107 SNPs in a 1 Mb stretch of chromosome 22q. We employ analysis of variance of recombination rate estimates, corrected for differences in effective population size using genome-wide microsatellite mutation rate estimates. We find substantial variation in fine-scale rates between populations, but reduced variation within continental groups. All effects examined (SNP-pair, region, population and interactions) were highly significant. Adjustment for effective population size made little difference to the conclusions. Observed hotspots tended to be conserved across populations, albeit at varying intensities. This holds particularly for populations from the same region, and also to a considerable degree across geographical regions. However, some hotspots appear to be population-specific. Several results from studies on the population history of humans are in accordance with our analysis. Our results suggest that between-population variation in DNA sequences may underly recombination rate variation.
Joobz, once again you prove that you don’t read your own citations. This paper is about recombination rates, not mutation rates. But don’t let me stop you from showing how this disproves my hypothesis that combination selection pressures profoundly slow evolution. So let’s see, joobz is 0 for 2, should we see if joobz can go for the strikeout, why not?
This fact becomes even more complicated by the fact that rate of mutation can determine the relative development of non-encoded DNA.
http://mbe.oxfordjournals.org/cgi/content/short/msm165v1?rss=1 (http://mbe.oxfordjournals.org/cgi/content/short/msm165v1?rss=1)
A significant part of eukaryotic non-coding DNA is viewed as the passive result of mutational processes, such as the proliferation of mobile elements. However, sequences lacking an immediate utility can nonetheless play a major role in the long-term evolvability of a lineage, for instance by promoting genomic rearrangements. They could thus be subject to an indirect selection. Yet such a long-term effect is difficult to isolate either in vivo or in vitro. Here, by performing in silico experimental evolution, we demonstrate that, under low mutation rates, the indirect selection of variability promotes the accumulation of non-coding sequences: Even in the absence of self-replicating elements and mutational bias, non-coding sequences constituted an important fraction of the evolved genome, because the indirectly selected genomes were those that were variable enough to discover beneficial mutations. On the other hand, high mutation rates lead to compact genomes, much like the viral ones, although no selective cost of genome size was applied: The indirectly selected genomes were those that were small enough for the genetic information to be reliably transmitted. Thus the spontaneous evolution of the amount of non-coding DNA strongly depends on the mutation rate. Our results suggest the existence of an additional pressure on the amount of non-coding DNA, namely the indirect selection of an appropriate trade-off between the fidelity of the transmission of the genetic information and the exploration of the mutational neighbourhood. Interestingly, this trade-off resulted robustly in the accumulation of non-coding DNA so that the best individual leaves one offspring without mutation (or only neutral ones) per generation.
Strike 3 joobz, there is nothing in this article that addresses my hypothesis that combined selection pressures profoundly slow evolution. When will you read your citations before you post their titles?
2.) If you think there is some variable mutation rate that will contradict my hypothesis, speculate what that rate is and prove it and give us a real example of this.see above.
That’s right joobz, see above because none of your citations show that variable mutation rates overcomes the mathematical and empirical fact that combined selection pressures profoundly slows the evolutionary process.
3.) We do know what selection pressures are now. If you think there were some selection pressures that existed in ancient history that do not exist now, speculate whatever selection pressure you want and show that it contradicts my hypothesis and give us a real example of this.can you provide a list for all pressures?

did you remember to include plate tectonics?
I see, plate tectonics accelerates evolution, which explains what happens in California every time there is an earthquake. Oh wait, you have a reference.
http://www.pnas.org/cgi/content/abstract/0704342104v1 (http://www.pnas.org/cgi/content/abstract/0704342104v1)
Previous molecular analyses of mammalian evolutionary relationships involving a wide range of placental mammalian taxa have been restricted in size from one to two dozen gene loci and have not decisively resolved the basal branching order within Placentalia. Here, on extracting from thousands of gene loci both their coding nucleotide sequences and translated amino acid sequences, we attempt to resolve key uncertainties about the ancient branching pattern of crown placental mammals. Focusing on 1,700 conserved gene loci, those that have the more slowly evolving coding sequences, and using maximum-likelihood, Bayesian inference, maximum parsimony, and neighbor-joining (NJ) phylogenetic tree reconstruction methods, we find from almost all results that a clade (the southern Atlantogenata) composed of Afrotheria and Xenarthra is the sister group of all other (the northern Boreoeutheria) crown placental mammals, among boreoeutherians Rodentia groups with Lagomorpha, and the resultant Glires is close to Primates. Only the NJ tree for nucleotide sequences separates Rodentia (murids) first and then Lagomorpha (rabbit) from the other placental mammals. However, this nucleotide NJ tree still depicts Atlantogenata and Boreoeutheria but minus Rodentia and Lagomorpha. Moreover, the NJ tree for amino acid sequences does depict the basal separation to be between Atlantogenata and a Boreoeutheria that includes Rodentia and Lagomorpha. Crown placental mammalian diversification appears to be largely the result of ancient plate tectonic events that allowed time for convergent phenotypes to evolve in the descendant clades.
Now how could I have missed this, this article is the perfect refutation of my hypothesis that combination selection pressures profoundly slow the evolutionary process except for one thing, this article has nothing to do with the mathematics of mutation and selection. Strike 4 joobz.
4.) If you think you can vary the number of selection pressures and contradict my hypothesis, speculate what this variation in selection pressures is and show that it contradicts my hypothesis and give us a real example of this.I have already. You've ignored it. Allow me to repost it.We show that the diverse ecoregions of Madagascar share one distinctive climatic feature: unpredictable intra- or interannual precipitation compared with other regions with comparable rainfall. Climatic unpredictability is associated with unpredictable patterns of fruiting and flowering. It is argued that these features have shaped the evolution of distinctive characteristics in the mammalian fauna of the island. Endemic Herpestidae and Tenrecidae and members of five endemic primate families differ from closely related species elsewhere, exhibiting extremes of "fastness" and "slowness" in their life histories. Climatic features may also account for the dearth of frugivorous birds and mammals in Madagascar, and for the evolutionary prevalence of species with large body mass.
Joobz, could you tell us what happens when plate tectonics hits Madagascar? Joobz, strike 5 and 6 because you have swung at this one twice.
5.) If you think that other forms of mutations will contradict my hypothesis, speculate which form(s) of mutation(s) will do this and give us a real example of this.I have already, you ignored it.
So let’s post more than just the title of the article and find out why joobz won’t quote his own citations.
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6W8B-4P7FSFS-2&_user=10&_coverDate=07%2F20%2F2007&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=e34055c7ada18215268c30d904aa27f0 (http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6W8B-4P7FSFS-2&_user=10&_coverDate=07%2F20%2F2007&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=e34055c7ada18215268c30d904aa27f0)
Vibrio vulnificus[/I]"]Multi-locus sequence types (MLST) from a global collection of Vibrio vulnificus isolates were analysed for the contribution of recombination to the evolution of two divergent clusters of strains and a human-pathogenic hybrid genotype, which caused a disease outbreak in Israel. Recombination contributes more substantially than mutation to generating strain diversity. For allelic diversity within loci, the ratio of recombination to mutation events is approximately 2:1. The role of recombination relative to mutation in the generation of new MLST variants of V. vulnificus within the clusters is comparable to that of other highly recombining bacteria such as Neisseria meningitidis. However, across the divide between the two major clusters of V. vulnificus strains, there is substantial linkage disequilibrium, lower estimates for recombination rates and shorter estimates of recombination tract length. We account for these differences between V. vulnificus and N. meningitidis by attributing them to the presence of the unusual genetic structure within V. vulnificus. The reason for the presence of distinct and divergent genomes remains unresolved. Two possible explanations put forward for future study are first, ecologically based population structure within V. vulnificus and second, a recombination donor from a phenotypically differentiated species.
That’s why joobz didn’t quote from this article, it has nothing to do with combination selection pressures and the effects on the rate of evolution, but I do understand why joobz likes this article, it is loaded with speculation. What is that, strike 7? Now wait, joobz has another citation.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1950772 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1950772)
Identification of the selective forces contributing to the origin and maintenance of sex is a fundamental problem in biology. The Fisher–Muller model proposes that sex is advantageous because it allows beneficial mutations that arise in different lineages to recombine, thereby reducing clonal interference and speeding adaptation. I used the F plasmid to mediate recombination in the bacterium Escherichia coli and measured its effect on adaptation at high and low mutation rates. Recombination increased the rate of adaptation ~3-fold more in the high mutation rate treatment, where beneficial mutations had to compete for fixation. Sequencing of candidate loci revealed the presence of a beneficial mutation in six high mutation rate lines. In the absence of recombination, this mutation took longer to fix and, over the course of its substitution, conferred a reduced competitive advantage, indicating interference between competing beneficial mutations. Together, these results provide experimental support for the Fisher–Muller model and demonstrate that plasmid-mediated gene transfer can accelerate bacterial adaptation.
Joobz, when are you going to post a citation which addresses my hypothesis that combination selection pressures profoundly slow evolution? Posting an article which shows that E Coli can adapt by means of plasmids has nothing to do with combination selection pressures. We have gone this far, what else does joobz have to offer except strikes 8, 9, 10,…
http://pathogens.plosjournals.org/perlserv/?request=get-document&doi=10.1371%2Fjournal.ppat.0030007 (http://pathogens.plosjournals.org/perlserv/?request=get-document&doi=10.1371%2Fjournal.ppat.0030007)
Enterococcus faecium, an ubiquous colonizer of humans and animals, has evolved in the last 15 years from an avirulent commensal to the third most frequently isolated nosocomial pathogen among intensive care unit patients in the United States. E. faecium combines multidrug resistance with the potential of horizontal resistance gene transfer to even more pathogenic bacteria. Little is known about the evolution and virulence of E. faecium, and genomic studies are hampered by the absence of a completely annotated genome sequence. To further unravel its evolution, we used a mixed whole-genome microarray and hybridized 97 E. faecium isolates from different backgrounds (hospital outbreaks (n = 18), documented infections (n = 34) and asymptomatic carriage of hospitalized patients (n = 15), and healthy persons (n = 15) and animals (n = 21)). Supported by Bayesian posterior probabilities (PP = 1.0), a specific clade containing all outbreak-associated strains and 63% of clinical isolates was identified. Sequencing of 146 of 437 clade-specific inserts revealed mobile elements (n = 74), including insertion sequence (IS) elements (n = 42), phage genes (n = 6) and plasmid sequences (n = 26), hypothetical (n = 58) and membrane proteins (n = 10), and antibiotic resistance (n = 9) and regulatory genes (n = 11), mainly located on two contigs of the unfinished E. faecium DO genome. Split decomposition analysis, varying guanine cytosine content, and aberrant codon adaptation indices all supported acquisition of these genes through horizontal gene transfer with IS16 as the predicted most prominent insert (98% sensitive, 100% specific). These findings suggest that acquisition of IS elements has facilitated niche adaptation of a distinct E. faecium subpopulation by increasing its genome plasticity. Increased genome plasticity was supported by higher diversity indices (ratio of average genetic similarities of pulsed-field gel electrophoresis and multi locus sequence typing) for clade-specific isolates. Interestingly, the previously described multi locus sequence typing–based clonal complex 17 largely overlapped with this clade. The present data imply that the global emergence of E. faecium, as observed since 1990, represents the evolution of a subspecies with a presumably better adaptation than other E. faecium isolates to the constraints of a hospital environment.
Wait a minute, this article is related to combination versus single selection pressures. The reason Enterococcus faecium has become multi-drug resistant is the use of monotherapy. This is exactly how you accelerate evolution by having single selection pressures. Joobz, I do thank you for another citation which supports my hypothesis that combined selection pressures profoundly slow evolution.
6.) My examples give specific selection pressures and target genes to these selection pressures; your example is the “Madagascar rainforest”. Don’t confuse your ill defined concept of what a selection pressure is with my mathematically precise examples. Again, you defined yourself into a unrealstic hole. Nature doesn't need to worry about such definitions. A single stress, like oxiditive stress can impact several proteins and transcription factors. In other words, it can act upon several target genes at once. As a result, developing resistence against such a pressure is evolution against multiple selection pressures.
Since, biology can adapt to these types of conditions, you have multiple real world examples of evolution against multiple selection pressures.
The only hole I am making here is the one to bury the mathematically impossible theory of evolution. You have yet to post a single real example that contradicts my hypothesis. If you think oxidative stress is an example that contradicts my hypothesis, post it, but you haven’t and you can’t.
7.) All I have to do is show that multiple selection pressures slow evolution enough to make it mathematically impossible, even though you don’t believe in extinction.How does this rambling (Which containes a false statement and a strawman) address the fact that slow doesn't equal stop. All of life is under "multiple selection pressures", yet life isn't extinct. Therefore, multiple selection pressures do not ultimately lead to extinction.(the only stop condition). If genes are allowed to progress from generation to generation, you can be sure that adaptation will occur.
Well, we have gone on joobz strange tour of speculations, none of which have anything to do with combination selection pressures versus single selection pressures, except his single reference to Enterococcus faecium which supports my hypothesis. While joobz is sitting in the rainforest in Madagascar marveling how plate tectonics accelerates evolution, I will continue to post real, measured examples of mutation and selection which show that combination selection pressures profoundly slow the evolutionary process. Here are a couple more real examples with precisely defined selection pressures and their target genes, something which joobz hasn’t posted in any of his examples (for that matter, none of the supporters of the theory of evolution have).
http://www.nature.com/leu/journal/v12/n10/abs/2401158a.html (http://www.nature.com/leu/journal/v12/n10/abs/2401158a.html)
Prompt empiric antibiotic therapy is of critical importance for patients with neutropenic fever. However, a major concern with important clinical consequences is the emergence of bacterial resistance to antibiotics. After using ceftazidime with a glycopeptide as initial empiric therapy for neutropenic fever, we were confronted with a 75% reduced susceptibility rate to ceftazidime of inducible Enterobacteriaceae collected in 1994. The initial empiric therapy was therefore replaced in May 1995 by a combination of cefepime with amikacin, with addition of a glycopeptide after 48 h if necessary. After this change, we observed a significant decrease in reduced susceptibility of inducible Enterobacteriaceae, not only to ceftazidime, but also to amikacin, cotrimoxazole and ciprofloxacin. There was also a decrease in reduced susceptibility of non-inducible Enterobacteriaceae, such as Klebsiella spp, to ceftazidime. The reduction of resistance may be related at least in part to the combined use of cefepime together with an aminoglycoside. This study shows that it is possible to reverse bacterial resistance by modifying the antibiotic regimen used.
This following reference is dedicated to Dr Schneider and his team over at the National Cancer Institute.
http://www.medpagetoday.com/HematologyOncology/LeukemiaLymphoma/tb/6437 (http://www.medpagetoday.com/HematologyOncology/LeukemiaLymphoma/tb/6437)
NEW YORK, Aug. 17 -- A double-barreled initial approach to chronic myelogenous leukemia with both imatinib (Gleevec) and dasatinib (SPRYCEL) may prevent treatment-resistant genetic mutations.
Dasatinib is approved as second-line treatment of chronic myelogenous leukemia with resistance or intolerance to prior therapy including imatinib.

Conventional use of dasatinib only after imatinib fails allows for compound drug-resistant mutations that synergistically increase tumor growth, found Charles L. Sawyers, M.D., of Memorial Sloan-Kettering Cancer Center here, and colleagues.

Frontline kinase inhibitor combination therapy could "substantially improve both the depth and durability of clinical responses," particularly in advanced phases of disease, they wrote online in the Journal of Clinical Investigation.

Furthermore, "it is likely that other cancers being treated with kinase inhibitor therapy will benefit from a similar treatment strategy," they added.

Mutations conferring kinase inhibitor resistance have become increasingly common not just in chronic myelogenous leukemia but also in gastrointestinal stromal tumor and lung cancer. As clinical experience with dasatinib grows, some patients have begun to experience relapse on second-line dasatinib, the researchers said.
Compare the citations I have and continue to post which precisely identify the selection pressures and the targeted genes with joobz’s citations about rainforests in Madagascar and plate tectonics. My citations demonstrate what the mathematics of ev shows, that is combined selection pressures profoundly slow the evolutionary process. Joobz, what do your citations demonstrate? They demonstrate that you haven’t read them.

Now you all have a good weekend and I’ll be back to post more examples next week of how mutation and selection actually works and it works as the mathematics of ev shows, that is combination selection pressures profoundly slow the evolutionary process.

[Dr Adequate]

Now you all have a good weekend and I’ll be back to post more examples next week of how mutation and selection actually works and it works as the mathematics of ev shows, that is combination selection pressures profoundly slow the evolutionary process. Translation into English: kleinman will continue to spam the thread with the same old pointless crap.

Yes, kleinman, we know you will. The limitations of your monomania are depressingly obvious.

You don't need to tell us. We know, kleinman. We know.

[Paul C. Anagnostopoulos]

By the way:


Paul, are you now proposing that there are selection pressures which are not targeted against specific biochemical processes in the organisms?
Yes, selection pressures in nature.


Selection pressures like temperature changes in the environment, which Delphi has suggested is the selection pressure which drove reptiles to evolve to birds, are targeted against many biochemical processes simultaneously.
There is no targeting in nature. Nature does not have a detailed understanding of the biochemical processes of life.

~~ Paul

[Paul C. Anagnostopoulos]

Paul, are you going to put this logic in ev and show us how this solves the problem of combination selection pressures profoundly slowing evolution? BTW, it’s September.
No, I was just addressing your comment that recombination without error cannot increase information.

~~ Paul

[kleinman]

Now you all have a good weekend and I’ll be back to post more examples next week of how mutation and selection actually works and it works as the mathematics of ev shows, that is combination selection pressures profoundly slow the evolutionary process.Translation into English: kleinman will continue to spam the thread with the same old pointless crap.
We all know your view point Adequate, you expressed this way when you described your graph.
Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
Perhaps you should explain this do these scientists who published this citation.
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=10669360&dopt=AbstractPlus (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=10669360&dopt=AbstractPlus)
Hepatitis B virus (HBV) drug resistance to lamivudine is always accompanied by mutations in the viral polymerase gene at position 550, termed group 1 (M550V with L526M) or group 2 (M550I) mutations. The latter mutation has not been associated with famciclovir resistance. Thus, the addition of famciclovir to lamivudine therapy in persons with group 2 lamivudine resistance may lead to virus suppression. The effect of lamivudine/famciclovir combination therapy on HBV infection was monitored in 5 lamivudine-resistant patients by quantitative polymerase chain reaction and polymerase gene sequencing of serum virus. No patients treated with combination therapy had a decline in HBV load >1 log10. Continual evolution of the viral polymerase was detected in association with virologic resistance to both drugs. Cloning experiments identified the preexistence of these multidrug-resistant virus variants as minority species prior to addition of famciclovir therapy. HBV resistance to lamivudine monotherapy is associated with a complex mixture of variants that limit the efficacy of second-line nucleoside-analogue therapy. First-line potent combination therapy may reduce the emergence of HBV drug resistance.
Adequate, you better hurry out there and tell these scientists they have got it all wrong, that combination selection pressures accelerate evolution.
http://forums.randi.org/images/smilies/doglaugh.gif
You all have a good weekend and I will be back next week if for no other reason than to annoy Adequate, my favorite annoyee.

[joobz]

So let’s look at your correct data.
http://www.ingentaconnect.com/content/klu/239/2006/00000063/00000003/00000246;jsessionid=1ttk8bey8gs9h.alice?format=pri nt&crawler=true (http://www.ingentaconnect.com/content/klu/239/2006/00000063/00000003/00000246;jsessionid=1ttk8bey8gs9h.alice?format=pri nt&crawler=true)

Why joobz, your reference has nothing to do with combination selection pressures and the rate of evolution. In fact, this article has nothing to do with nuclear DNA. Once again, you have proven you don’t read your own citations. Let’s see if your arguments improve. Ah yes, you have another citation which you don’t quote. Let’s see if this has anything to do with combination selection pressures accelerating evolution.
http://www.springerlink.com/content/jjj7331665g7n7t6/ (http://www.springerlink.com/content/jjj7331665g7n7t6/)

Joobz, once again you prove that you don’t read your own citations. This paper is about recombination rates, not mutation rates. But don’t let me stop you from showing how this disproves my hypothesis that combination selection pressures profoundly slow evolution. So let’s see, joobz is 0 for 2, should we see if joobz can go for the strikeout, why not?

http://mbe.oxfordjournals.org/cgi/content/short/msm165v1?rss=1 (http://mbe.oxfordjournals.org/cgi/content/short/msm165v1?rss=1)

Strike 3 joobz, there is nothing in this article that addresses my hypothesis that combined selection pressures profoundly slow evolution. When will you read your citations before you post their titles?

That’s right joobz, see above because none of your citations show that variable mutation rates overcomes the mathematical and empirical fact that combined selection pressures profoundly slows the evolutionary process.

I see, plate tectonics accelerates evolution, which explains what happens in California every time there is an earthquake. Oh wait, you have a reference.
http://www.pnas.org/cgi/content/abstract/0704342104v1 (http://www.pnas.org/cgi/content/abstract/0704342104v1)

Now how could I have missed this, this article is the perfect refutation of my hypothesis that combination selection pressures profoundly slow the evolutionary process except for one thing, this article has nothing to do with the mathematics of mutation and selection. Strike 4 joobz.

Joobz, could you tell us what happens when plate tectonics hits Madagascar? Joobz, strike 5 and 6 because you have swung at this one twice.

So let’s post more than just the title of the article and find out why joobz won’t quote his own citations.
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6W8B-4P7FSFS-2&_user=10&_coverDate=07%2F20%2F2007&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=e34055c7ada18215268c30d904aa27f0 (http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6W8B-4P7FSFS-2&_user=10&_coverDate=07%2F20%2F2007&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=e34055c7ada18215268c30d904aa27f0)

That’s why joobz didn’t quote from this article, it has nothing to do with combination selection pressures and the effects on the rate of evolution, but I do understand why joobz likes this article, it is loaded with speculation. What is that, strike 7? Now wait, joobz has another citation.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1950772 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1950772)

Joobz, when are you going to post a citation which addresses my hypothesis that combination selection pressures profoundly slow evolution? Posting an article which shows that E Coli can adapt by means of plasmids has nothing to do with combination selection pressures. We have gone this far, what else does joobz have to offer except strikes 8, 9, 10,…
http://pathogens.plosjournals.org/perlserv/?request=get-document&doi=10.1371%2Fjournal.ppat.0030007 (http://pathogens.plosjournals.org/perlserv/?request=get-document&doi=10.1371%2Fjournal.ppat.0030007)

Wait a minute, this article is related to combination versus single selection pressures. The reason Enterococcus faecium has become multi-drug resistant is the use of monotherapy. This is exactly how you accelerate evolution by having single selection pressures. Joobz, I do thank you for another citation which supports my hypothesis that combined selection pressures profoundly slow evolution.

The only hole I am making here is the one to bury the mathematically impossible theory of evolution. You have yet to post a single real example that contradicts my hypothesis. If you think oxidative stress is an example that contradicts my hypothesis, post it, but you haven’t and you can’t.

Well, we have gone on joobz strange tour of speculations, none of which have anything to do with combination selection pressures versus single selection pressures, except his single reference to Enterococcus faecium which supports my hypothesis. While joobz is sitting in the rainforest in Madagascar marveling how plate tectonics accelerates evolution, I will continue to post real, measured examples of mutation and selection which show that combination selection pressures profoundly slow the evolutionary process. Here are a couple more real examples with precisely defined selection pressures and their target genes, something which joobz hasn’t posted in any of his examples (for that matter, none of the supporters of the theory of evolution have).
http://www.nature.com/leu/journal/v12/n10/abs/2401158a.html (http://www.nature.com/leu/journal/v12/n10/abs/2401158a.html)

This following reference is dedicated to Dr Schneider and his team over at the National Cancer Institute.
http://www.medpagetoday.com/HematologyOncology/LeukemiaLymphoma/tb/6437 (http://www.medpagetoday.com/HematologyOncology/LeukemiaLymphoma/tb/6437)

Compare the citations I have and continue to post which precisely identify the selection pressures and the targeted genes with joobz’s citations about rainforests in Madagascar and plate tectonics. My citations demonstrate what the mathematics of ev shows, that is combined selection pressures profoundly slow the evolutionary process. Joobz, what do your citations demonstrate? They demonstrate that you haven’t read them.

Now you all have a good weekend and I’ll be back to post more examples next week of how mutation and selection actually works and it works as the mathematics of ev shows, that is combination selection pressures profoundly slow the evolutionary process.
derisive language noted. Too bad it doesn't work as a replacement for intelligence.
by your argument, if it's not point mutation, it doesn't count as evolution?
i understand now, you live in the world that only one form of mutation and adaptation matters. interesting, too bad reality is completely unbound by your dumb ideas.

[Belz...]

Now Belz, you need to remember what the title of the thread is.

Yes, and you're a prime example of it.

Belz, you need to go back and read about Mendelian inheritance.

Unless there exists a lot of variation in the first place, there can't be much variation due to inheritance, can there ? Where does this variation come from, Klein ?

If you know of other selection pressures in knkent1’s example, feel free to tell us what they were.

Since this isn't a response to my question, I'll take it that you don't have a clue what selection pressures were at work.

You can only wish that the theory of evolution was made of straw

Are you an automatic post-generator ? You saw the word "straw" and made up a reply without actually making it relevant. What you said was a strawman, Klein. It's a shame that you never adress other people's points. I never said multiple pressures accelerated evolution. You did, via your strawman.

your theory is left only with moth holes.

You should stop thinking that you're really clever and actually say something of substance, for a change.

Well Belz, if you think that the fox terrier evolve from the wolf by mutation and selection, why don’t you tell us which genes mutated and the loci of these mutations because the examples which I present define the genes being mutated and often times describe the exact loci where the mutations occur.

Argument from ignorance. Well hidden, but that's what that is. _I_ was the one asking you a question, Klein. You have no interest in having an honest debate. Now all you're doing is playing the mirror/rebound argument game.

You keep making vague arguments assuming they are true while I argue from mathematical precision with precisely defined genes, mutations and loci.

Really ?

Then perhaps you can answer your own question and tell me which genes differ between a fox terrier and a wolf ?

If you examine dog breeding carefully, you will find that the process is driven by recombination and selection, not mutation and selection but don’t let that stop you from proving to us that dog breeding is a mutation and selection process.

Again, please explain how recombination can lead to variation if that variation is not created by mutation in the first place. Please.

Nope, genetically they are homologous.

Then you also believe that tigers and lions are the same species ?

I have never heard anyone use the term “race” when speaking of dogs, but hey, use any term you like.

You know, if you weren't so damn ignorant, it would help a lot. Sorry to burst your bubble, but in French we say "race" because we don't have a direct word for "breed", and I didn't want to repeat "breed" three times in the same sentence. I thought you wouldn't mind, but I forgot that any word that doesn't suit you is a good reason to derail the argument.

The theory of evolution is for you to prove

Klein, if we were debating physics, you'd say that Newtonian physics is for me to prove. You're the one with an unorthodox idea. You prove YOUR theory.

I am just pointing out to you the huge mathematical barrier to your explanation.

I think I'll just go ahead and program a simulation that "mathematically" proves you wrong, then. It's easy since I can program it to do whatever I want.

The difference is that I have a peer...

Yeah, yeah.

That’s strange; my grammar checker doesn’t have a problem with this sentence.

Serves you right for trusting a machine to do a thinking person's work.

Perhaps the problem is that you have no mathematical basis for your theory of evolution by mutation and selection and you have no empirical evidence to support your viewpoint.

Non sequitur.

What you don’t realize is that your theory of evolution is in a jam.

You should've made comedian, not biologist. Oh, wait...

[Belz...]

Adequate, you better hurry out there and tell these scientists they have got it all wrong, that combination selection pressures accelerate evolution

You're really amazing, Klein. On the one hand, you say that ALL scientists in the world are wrong because evolution through mutation and selection is mathematically impossible -- and yet they believe it --; and at the same time you claim that they KNOW that multiple pressures slow evolution to a stop.

Which is it ?

[joobz]

You're really amazing, Klein. On the one hand, you say that ALL scientists in the world are wrong because evolution through mutation and selection is mathematically impossible -- and yet they believe it --; and at the same time you claim that they KNOW that multiple pressures slow evolution to a stop.

Which is it ?

It's what ever he wants it to be.
He intentionally ignores points that are not part of his idea. As a result, he still has failed to properly address the 7 assumptions that he made which are invalid.
1.)We don't know the mutation rate for all species for all time.
2.) Mutation rate isn't constant
3.) We don't know the number of selection pressures for all species for all time.
4.) Number of selection pressures isn't constant
5.) Point mutations aren't the only mutation/adaptation mechanism
6.) Ill defined concept of what a selection pressure is
7.) slow most definitely doesn't equal stop.

[Dr Adequate]

We all know your view point Adequate, you expressed this way when you described your graph.

Perhaps you should explain this do these scientists who published this citation.
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=10669360&dopt=AbstractPlus (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=10669360&dopt=AbstractPlus)

Adequate, you better hurry out there and tell these scientists they have got it all wrong, that combination selection pressures accelerate evolution. Because I presume that they know this already, 'cos it's obvious.

This is why all the results you've been trying to quote involve scientists applying simultaneous demographic pressures to a population.

Scientists aren't nuts.

http://forums.randi.org/images/smilies/doglaugh.gif
You all have a good weekend and I will be back next week if for no other reason than to annoy Adequate, my favorite annoyee. Translation: kleinman will continue to entertain me with his clownish antics.

Yes, kleinman. I know.

[Belz...]

I will be back next week if for no other reason than to annoy Adequate, my favorite annoyee

Troll.

[Dr Adequate]

Troll. Cat toy.

How long do you think it's going to take him to work out that y(x) and x/y(x) can both be monotonic strictly increasing functions of x?

We could have a sweepstake or something.

[Belz...]

The answer is: never. So why bother ?

[joobz]

The answer is: never. So why bother ?
This has become my view. Unless he comes up with new crazy things to say, it's all been done already. As such, he's simply spamming the thread with nonsensical, insulting idiocy, which is at least against 2 forum rules.

[Dr Adequate]

Well, perhaps we could just check the thread once a week, let's say Fridays, to see if he's thought of a new lie. I know he doesn't usually manage one new lie a week, but it's always worth seeing when he does.

[Paul C. Anagnostopoulos]

That's not a bad idea. We can let him chat Monday through Thursday, then respond over the weekend. Very efficient.

~~ Paul

[BPScooter]

I support the idea of reading on weekdays and posting on weekends. There's some comfort in that, for me personally.

Forgive the cut and paste, I haven't yet mastered links, this comes from Alex Boese's "Museum of Hoaxes" blog. I think this is the link:

http://www.museumofhoaxes.com/hoax/P7/

and here is the text of the article I found relevant:

The Difficulty of Debunking
The Washington Post has a depressing article about the difficulty of myth-busting. Experiments by Norbert Schwarz at the University of Michigan reveal that a few days after telling people a rumor is false, many of those people will have misremembered what they were told and think the rumor is true. The crux of the problem is that:
Denials inherently require repeating the bad information, which may be one reason they can paradoxically reinforce it.

Other psychologists have found that hearing the same thing again and again from the same source can actually trick the brain into thinking information is more credible, as if the information came from many sources:
People are not good at keeping track of which information came from credible sources and which came from less trustworthy ones, or even remembering that some information came from the same untrustworthy source over and over again. Even if a person recognizes which sources are credible and which are not, repeated assertions and denials can have the effect of making the information more accessible in memory and thereby making it feel true.

So what can myth-busters do? Unfortunately, not much. The only recommended tactic is to debunk rumors by not referring to the original rumor at all, and instead offering a completely different new assertion. For instance:
Rather than say, as Sen. Mary Landrieu (D-La.) recently did during a marathon congressional debate, that "Saddam Hussein did not attack the United States; Osama bin Laden did," Mayo said it would be better to say something like, "Osama bin Laden was the only person responsible for the Sept. 11 attacks" -- and not mention Hussein at all.

It's going to make it pretty hard to operate a myth-busting website if one of the rules is that I can't mention the myth I'm debunking. (Thanks, Joe!)
Posted By: Alex | Date: Tue Sep 04, 2007 | Permalink | Comments (8)
Category: Psychology

[Paul C. Anagnostopoulos]

Denials inherently require repeating the bad information, which may be one reason they can paradoxically reinforce it.
Okay, then, from now on we simply reply:

Wrong!


~~ Paul

[kjkent1]

Ok, let’s try to make this more precise. Do you hold to the view “one gene-one polypeptide”?Apparently, this question isn't relevant, as you continue below without referring to it further.

An evolved genetic system is set of enzymatic processes which are at a local optimum on the fitness landscape.And, how do you scientifically measure this evolved state?An example of such a genetic system is the Krebs cycle. A microevolutionary change to such a system occurs when a single selection pressure is targeted to a single gene in the system whereas a macroevolutionary change to such a system occurs when a single selection pressure is targeted to multiple genes in the system or multiple selection pressures are targeted to multiple genes in the system.It seems that you've left out a possibility: multiple selection conditions targeted to a single gene. Does this constitute micro or macro evolutionary change?
Now it is clear that according to this definition, microevolutionary processes occur regularly as seen with antimicrobial and cancer resistance.Is it "clear?"
Microevolutionary processes on the other hand are much more difficult to accomplish. Depending on the life forms, evolution by mutation and selection processes targeted against more than a single gene are seen only on very rapidly reproducing, huge populations with very short genomes. Demonstrating this type of macroevolutionary process on smaller populations of more complex life forms with much lower reproductive rates and much longer genomes is not observed, at least I haven’t seen any examples presented here.Fusion of 1st and 2nd chromosome in pre-humans leading to a split between humans and chimpanzees. Pretty "clear" demonstration of macroevolution, if you ask me -- or just about any well-respected scientist on planet Earth.
This is the mathematical and empirical barrier to the massive transformation required to metamorphose reptiles into birds or humans and chimpanzees from a primate precursor.The only barrier of which I'm aware, is the one you have created in your mind, Alan.
By the way, a friend of mine showed me a report that now says that humans and chimpanzee genomes are only 95% similar. Do you want to do the arithmetic for what is 5% of 3 billion? You have to account for these 150 million base differences in only 500,000 generations.A few repeats, retroviral insertions, additions, deletions fusions, etc., and it's done. You're making a much bigger deal out of this than really exists.

I hope the above definitions give a sense of the differences between macro and microevolution. What is clear from the mathematics of ev and the empirical evidence is that the greater the number of selection conditions the more difficult it is for the population to evolve to these multiple selection conditions.Life doesn't evolve to a selection condition. A mutation occurs, and its outcome is entirely unpredictable. The benefit or detriment is immediate. Then selection optimizes the mutation to the existing environment over time.

Anyway, this will be my last post until next Friday -- I'm going to follow suit with Dr. A, Paul, etc., and give you the entire week to rail at the gods unimpeded. So, have a great week.

[jimbob]

If there are no replicators, i.e. the population has been wiped out then that organism's evolution has stopped.

Isn't that the ideal goal of multiple antibiotic therapies, kill enough of the bacterial population so that it is wiped out, either by the antibiotics or the reamaining population by the immune system?

If this doesn't happen, then evolution will continue,

But I think I have detected several people saying this already.

May I make a plea.

Multiple nested quotes bore me. If you want to do this, it might be an idea to use the spoiler function, then it is easier to see the new parts of a post, and it might get read.

[kleinman]

A quick review of the comments made over the past weekend shows that you advocates for the theory of evolution are still having difficulty understanding the mathematics of mutation and selection. So let’s consider them in detail.
Paul, are you going to put this logic in ev and show us how this solves the problem of combination selection pressures profoundly slowing evolution? BTW, it’s September.No, I was just addressing your comment that recombination without error cannot increase information.
Paul, I can appreciate your approach. Not including this mechanism of mutation in the ev model allows you to speculate about the rate at which this mechanism would accumulate information. In addition, you don’t have to describe the selection pressure that would propagate such a mutation. You don’t reveal much about the mutation and selection process with this type of speculation but you do demonstrate the lack of a mathematical foundation for your theory.
derisive language noted.
Oh no joobz, pointing at the Madagascar rainforests and plate tectonics is a profound mathematical argument against the mathematics of ev and the hundreds of citations I have posted which substantiates this mathematics.
Now Belz, you need to remember what the title of the thread is.Yes, and you're a prime example of it.
You should know by now that I love to annoy evolutionists with ev, the peer reviewed and published model of random point mutation and natural selection and the massive amount of empirical data which supports the results form this model. Now only if you could annoy me with some mathematics of mutation and selection and/or some empirical examples which show that combination selection pressures accelerate evolution. Oh wait, joobz has proven that Madagascar rainforests and plate tectonics accelerates evolution.
Belz, you need to go back and read about Mendelian inheritance.Unless there exists a lot of variation in the first place, there can't be much variation due to inheritance, can there ? Where does this variation come from, Klein ?
Certainly there is variation in populations. However, when you take this variation to explain the evolution of birds from reptiles that you lose contact with the mathematical and empirical evidence of how mutation and selection works.
If you know of other selection pressures in knkent1’s example, feel free to tell us what they were.Since this isn't a response to my question, I'll take it that you don't have a clue what selection pressures were at work.
I guess you don’t know what they were either. That’s the problem with kjkent1’s example, it has not been repeated nor done in with any control.
You can only wish that the theory of evolution was made of straw.Are you an automatic post-generator ? You saw the word "straw" and made up a reply without actually making it relevant. What you said was a strawman, Klein. It's a shame that you never adress other people's points. I never said multiple pressures accelerated evolution. You did, via your strawman.
Oh no Belz, I’m just responding to the often used strawman argument employed by evolutionists when they can’t address the mathematical and empirical facts that refute their theory.
your theory is left only with moth holes.You should stop thinking that you're really clever and actually say something of substance, for a change.
Would it make you feel better if I called them “gaps” rather than “moth holes”?
Well Belz, if you think that the fox terrier evolve from the wolf by mutation and selection, why don’t you tell us which genes mutated and the loci of these mutations because the examples which I present define the genes being mutated and often times describe the exact loci where the mutations occur.Argument from ignorance. Well hidden, but that's what that is. _I_ was the one asking you a question, Klein. You have no interest in having an honest debate. Now all you're doing is playing the mirror/rebound argument game.
Belz, you are confusing mutation and selection with recombination and selection. The former is a profoundly slow process of change and the latter can give rapid changes in the phenotype of a population.
You keep making vague arguments assuming they are true while I argue from mathematical precision with precisely defined genes, mutations and loci.Really ?

Then perhaps you can answer your own question and tell me which genes differ between a fox terrier and a wolf ?
You are not asking the correct question, you should ask which alleles differ between a fox terrier and a wolf. Here is a citation which explains this.
http://www.nature.com/hdy/journal/v85/n6/full/6888050a.html (http://www.nature.com/hdy/journal/v85/n6/full/6888050a.html)
We have examined in Mexican wolves and related canids the amount of genetic variation for a class II gene in the major histocompatibility complex (MHC), thought to be part of the most important genetic basis for pathogen resistance in vertebrates. In Mexican wolves, descended from only seven founders over three lineages, there were five different alleles. These were in three phylogenetic groups, only one of which was shared between lineages. Using single stand conformation polymorphism (SSCP), we found that in samples of animals from the two polymorphic lineages, the observed heterozygosity was 0.74 and the genotypes were not different statistically from Hardy-Weinberg proportions. The Ghost Ranch lineage of Mexican wolves was monomorphic for the locus, consistent with the lower level of variation found previously for microsatellite loci and predicted from pedigree analysis. Samples of grey wolves, red wolves, and coyotes had 16 additional alleles. One Mexican wolf allele was also found in grey wolves and another allele was shared between grey and red wolves. Most of the nucleotide variation resulted in amino acid variation and there were five different amino acids found at two different positions. Only two of the 21 variable amino acid positions had solely synonymous nucleotide variation. The average heterozygosity for eight individual amino acid positions in the Mexican wolves was greater than 0.4. The estimated rate of nonsynonymous substitution was 2.5 times higher than that for synonymous substitution for the putative antigen binding site positions, indicative of positive selection acting on these positions. Examination of the known dog sequences for this locus showed that one of the Mexican wolf alleles was found in dogs and that the allele found in both grey and red wolves is also found in dogs.
What recombination and selection does is change the frequency of particular alleles in a population.
If you examine dog breeding carefully, you will find that the process is driven by recombination and selection, not mutation and selection but don’t let that stop you from proving to us that dog breeding is a mutation and selection process.Again, please explain how recombination can lead to variation if that variation is not created by mutation in the first place. Please.
Again, I refer you back to the Wikipedia reference on Mendelian genetics. When you combine Mendelian genetics with recombination, you can change the frequency of particular alleles in a population, thus changing the phenotype. This is an extremely rapid process. On rare occasions, you can obtain a new allele by mutation which is beneficial but this is a profoundly slow process as demonstrated by ev and the hundreds of examples which I have posted and will continue to post more examples.
Nope, genetically they are homologous.Then you also believe that tigers and lions are the same species ?
Tigers and lions can be bred and can give fertile offspring. Here is a site which discusses this issue. http://www.lairweb.org.nz/tiger/ligers2.html (http://www.lairweb.org.nz/tiger/ligers2.html)
I have never heard anyone use the term “race” when speaking of dogs, but hey, use any term you like.You know, if you weren't so damn ignorant, it would help a lot. Sorry to burst your bubble, but in French we say "race" because we don't have a direct word for "breed", and I didn't want to repeat "breed" three times in the same sentence. I thought you wouldn't mind, but I forgot that any word that doesn't suit you is a good reason to derail the argument.
If you wouldn’t were so ignorant of the mathematics of mutation and selection and understood the empirical examples which I am presenting, we wouldn’t having this discussion on race.
The theory of evolution is for you to prove Klein, if we were debating physics, you'd say that Newtonian physics is for me to prove. You're the one with an unorthodox idea. You prove YOUR theory.
Really, I’m using an evolutionist written mathematical model and hundreds of empirical examples that shows that combined selection pressures profoundly slow the evolutionary process. When are you going to present a single real example that shows otherwise? Your theory of evolution is mathematically impossible because mutation and selection only works with a tiny number of selection conditions simultaneously. You have no way to transform the thousands of genes necessary to metamorphose reptiles into birds. You don’t have the selection pressures, you don’t have the time if necessary to accomplish the transformation and you don’t have the path across the fitness landscape.
I am just pointing out to you the huge mathematical barrier to your explanation.I think I'll just go ahead and program a simulation that "mathematically" proves you wrong, then. It's easy since I can program it to do whatever I want.
That’s fine; Adequate posted his graph that shows that multiple selection pressures accelerate evolution. His problem and yours will be to demonstrate real examples of your mathematics. On the other hand, I can post hundreds of examples of Dr Schneider’s ev model which show that combination selection pressures profoundly slow the evolutionary process. That’s how mutation and selection works in reality.
That’s strange; my grammar checker doesn’t have a problem with this sentence.Serves you right for trusting a machine to do a thinking person's work.
I see, you don’t use any machines to help you in your work. I can see you are Y1K compliant.
Perhaps the problem is that you have no mathematical basis for your theory of evolution by mutation and selection and you have no empirical evidence to support your viewpoint.Non sequitur.
Sure it follows, you don’t have a mathematical basis for your theory and no examples which show that combined selection pressures accelerate evolution. Therefore you discard the result which ev shows and the hundreds of empirical examples which substantiates this result.
What you don’t realize is that your theory of evolution is in a jam.You should've made comedian, not biologist. Oh, wait...
I am waiting, when are you going to cherry pick some real examples which show that combination selection pressures accelerate evolution by mutation and selection.
Adequate, you better hurry out there and tell these scientists they have got it all wrong, that combination selection pressures accelerate evolution You're really amazing, Klein. On the one hand, you say that ALL scientists in the world are wrong because evolution through mutation and selection is mathematically impossible -- and yet they believe it --; and at the same time you claim that they KNOW that multiple pressures slow evolution to a stop.

Which is it ?
You should run some examples with ev a get a sense how great the effect the number of selection pressures has on the rate of convergence. Then you would understand the meaning of the citations I have and will continue to post.
Adequate, you better hurry out there and tell these scientists they have got it all wrong, that combination selection pressures accelerate evolution.Because I presume that they know this already, 'cos it's obvious.
Well, I’ll give you some more examples where it is not so obvious to them.
The answer is: never. So why bother ?
That’s the correct answer to this question; when will a real example of multiple selection pressures accelerating evolution be posted?
That's not a bad idea. We can let him chat Monday through Thursday, then respond over the weekend. Very efficient.
That’s ok with me, I’ll post real examples of mutation and selection Monday through Thursday which substantiates what ev shows and you can post, what can you post over the weekend?
The Difficulty of Debunking
So BPScooter, are you going to post a real example which shows that combined selection pressures accelerate evolution and debunk my hypothesis. I’ll continue to post citations which show that combined selection pressures profoundly slow the evolutionary process and you can post…
Denials inherently require repeating the bad information, which may be one reason they can paradoxically reinforce it.Okay, then, from now on we simply reply:

Wrong!
I’m with you on that one Paul, we have heard the same bad information on the theory of evolution for decades so now, not only is the theory of evolution mathematically impossible, it is wrong!
If there are no replicators, i.e. the population has been wiped out then that organism's evolution has stopped.

Isn't that the ideal goal of multiple antibiotic therapies, kill enough of the bacterial population so that it is wiped out, either by the antibiotics or the reamaining population by the immune system?
That’s correct, however there are no selection pressures that can be put on viruses which actually kill the viruses once they are in the host. The replicators can only be inhibited from reproducing. This is essentially what is being modeled with ev. Again, what this demonstrates is that combined selection pressures profoundly slow the ability of the population ability to adapt to these selection pressures simultaneously.
If this doesn't happen, then evolution will continue,

But I think I have detected several people saying this already.
It continues when there is no extinction but the process is profoundly slow, far to slow to explain how reptiles evolved to birds. There are no know selection pressures that would drive this transformation and even if there were, you simply do not have enough generations to accomplish all the genetic changes required.
May I make a plea.

Multiple nested quotes bore me. If you want to do this, it might be an idea to use the spoiler function, then it is easier to see the new parts of a post, and it might get read.
I’m responding to multiple different bloggers. I nest the quotes in order for readers to follow the line of discussion. The screen editor for this site modifies the BBS code on some posts.

Anyway, I’ve decided to post some citations which show that combination selection pressures profoundly slow evolution on more complex life forms, not just microbes. These following examples are from agriculture.

http://www.blackwell-synergy.com/doi/abs/10.1046/j.1365-3180.2003.00355.x (http://www.blackwell-synergy.com/doi/abs/10.1046/j.1365-3180.2003.00355.x)
A simulation study was conducted to examine the effect of pattern of herbicide use on development of resistance to two herbicides with different modes of action in finite weed populations. The effects of the size of the treatment area (analogous to initial weed population), germination fraction and degree of self-pollination in the weed were investigated. The results indicate that the probability of developing resistance to one or both herbicides decreases as the size of the area/initial population decreases. For treatment areas of 100 ha or less with an initial weed seedbank of 100 seeds m2 and initial frequencies of the resistance genes of 106, development of resistance to both herbicides (double-resistance) is uncommon within 50 years for all types of weeds if both herbicides are used in all years (used in combination). If herbicides are used in alternate years (rotated) double-resistance almost always occurs in 100 ha areas but is uncommon in areas of 1 ha or less. The results suggest that adoption of practices that limit movement of weeds in conjunction with using herbicides in combination rather than in rotation can substantially delay development of herbicide resistance.[/quote]

http://cals.arizona.edu/pubs/crops/az1101/az1101_13.html (http://cals.arizona.edu/pubs/crops/az1101/az1101_13.html)
[quote="Preemergence Herbicide Combinations for Onion Weed Control Study"]DCPA (Dacthal®) at 9.0 lb AI/A, the commercial standard herbicide, slightly reduced the number of plants and shortened the plant height compared to the untreated check. Preemergence (PREE) herbicide treatments that caused injury as height reduction similar to Dacthal included pendimethalin (Prowl®), propachlor (Ramrod®), metolachlor (Dual®), dimethenamid (Frontier®), ethofumesate (Nortron®), and benefin (Balan®). Visual observations did not indicate significant stand reduction or crop injury compared to plant counts. Treatments that caused minimal visible crop injury (<10%) were Ramrod, Balan and lower rates of Frontier and Nortron. Moderate to acceptable injury (15%) was observed on onions treated by Prowl, Dual, Frontier, and Nortron. Treatments that significantly reduced crop stand were Prefar at 6.0 lb AI/A, lactofen (Cobra®), thiazopyr (Visor®), and some combinations of the three herbicides. Combination treatments that caused marginally acceptable injury included Prowl plus Dual, Nortron plus Prowl, Prefar plus Nortron, Nortron plus Frontier, Ramrod plus Frontier, Ramrod plus Nortron, and Ramrod plus Balan. Early weed control ratings showed that Prowl at 0.5 and 0.75 lb AI/A, Nortron, Cobra, Visor applied alone gave acceptable control (>85%) of London rocket (Sisymbrium irio), sowthistle (Sonchus oleraceus), and sweetclover (Melilotus officinalis). Prowl at 0.75 lb AI/A and Cobra gave season-long control of all weeds. Early weed control ratings of combination herbicide treatments demonstrated that Prowl or Nortron combined with other herbicides gave acceptable weed control. Prowl at 0.50 lb AI/A plus Ramrod, Nortron, or Dual at the lower rates slightly improved weed control compared to each of the herbicides applied alone.
Once again, combined selection pressures slow the evolutionary process profoundly.

[kleinman]

Here are a couple more examples of combination selection pressures profoundly slowing on more complex life forms than microbes.
http://www.sciencemag.org/cgi/content/abstract/180/4087/741 (http://www.sciencemag.org/cgi/content/abstract/180/4087/741)
Strains of wild rats that are resistant to the anticoagulant action of coumarins and derivatives of indandione have been discovered in a number of geographic areas. These rats have now been shown to be more susceptible than normal rats are to the anticoagulant action of the vitamin K antagonist, 2-chloro-3-phytyl-1,4-naphthoquinone. This compound, either alone or in combination with warfarin, would appear to be an effective rodenticide in areas where resistance to the indirect anticoagulants is a problem.

http://www.msstate.edu/entomology/v7n2/art02.html (http://www.msstate.edu/entomology/v7n2/art02.html)
The EPA has also considered pesticide resistance when making determinations of whether unreasonable adverse effects would occur if registered uses of a pesticide are maintained. This determination is a component of the Agency's Special Review process. One example where pesticide resistance played an active role in assessing the benefits during the special review process were for the ethylene bisdithiocarbamates (EBDCs) fungicides. These fungicides include mancozeb, maneb, metiram, and nabam. Two other EBDC fungicides, amobam and zineb, were voluntarily cancelled several years ago. EBDCs are major agricultural fungicides controlling several important fungal pathogens on over 40 fruit and vegetable crops. There are no reports of pest resistance under field conditions after more than 40 years of use. Upon review of the benefits for EBDCs, the Agency concluded that EBDCs are an important tool in fungicide resistance management. For example, EBDCs in combination with benomyl, function in resistance management by controlling apple scab ( Venturia inaequalis ), sooty blotch ( Gloeodes pomigena ) and fly speck ( Shizothyrium pomi ) on apples. EBDCs in combination with copper function in resistance management by controlling bacterial spot ( Xanthomonas vesicatoria ) resistance on peppers and tomatoes. The importance of EBDCs for pesticide resistance management was considered both qualitatively (decrease in fruit quality) and quantitatively (decrease in fruit yields) by the EPA in estimating the fungicide's benefits. The uses of EBDCs were maintained on numerous commodities, in part, because of the benefits of EBDCs in fungicide resistance management ( 1 ).
Once again, the mathematical behavior of ev is verified. The concept of evolution by mutation and selection is simply an optimization problem in which the number of selection conditions has a profound effect on the rate of optimization. This is how mutation and selection actually works, not as speculated by the advocates of the theory of evolution.

[Belz...]

You should know by now that I love to annoy evolutionists

Yes, and that makes you a troll.

with ev, the peer reviewed and published model of random point mutation and natural selection and the massive amount of empirical data which supports the results form this model.

Yeah, yeah, and the fact that there are other sources of mutation but then you don't give a hoot about those. Why am I even talking to you ?

Now only if you could annoy me with some mathematics of mutation and selection and/or some empirical examples which show that combination selection pressures accelerate evolution.

I don't think you can add 2 and 2, Klein.

Certainly there is variation in populations. However, when you take this variation to explain the evolution of birds from reptiles that you lose contact with the mathematical and empirical evidence of how mutation and selection works.

Nice dodge. How do you account for the variation within a species, and how do you account for the various species ?

Oh no Belz, I’m just responding to the often used strawman argument employed by evolutionists when they can’t address the mathematical and empirical facts that refute their theory.

Again you should talk to those stupid scientists, not me.

You are not asking the correct question, you should ask which alleles differ between a fox terrier and a wolf. Here is a citation which explains this.

It doesn't explain the physical differences. Would you mind actually answering the question ?

What recombination and selection does is change the frequency of particular alleles in a population.

HOW are those variations there in the FIRST place ?

Tigers and lions can be bred and can give fertile offspring. Here is a site which discusses this issue.

You AGAIN refuse to answer my question. ARE tigers and lions the SAME species, YES or NO ?

If you wouldn’t were so ignorant of the mathematics of mutation and selection and understood the empirical examples which I am presenting, we wouldn’t having this discussion on race.

Do you deny that the French word for "breed" is "race" and that this is the source of your confusion ?

Your theory of evolution is mathematically impossible because mutation and selection only works with a tiny number of selection conditions simultaneously.

Sure, Klein. Anything you say.

You have no way to transform the thousands of genes necessary to metamorphose reptiles into birds.

And "recombination" does all that ?

That’s fine; Adequate posted his graph that shows that multiple selection pressures accelerate evolution. His problem and yours will be to demonstrate real examples of your mathematics.

Well, since that's your problem either we should be at a standstill.

I see, you don’t use any machines to help you in your work. I can see you are Y1K compliant.

Unfortunately machines can't interpret results.

Sure it follows, you don’t have a mathematical basis for your theory and no examples which show that combined selection pressures accelerate evolution. Therefore you discard the result which ev shows and the hundreds of empirical examples which substantiates this result.

Again, non sequitur. The logical way to deal with the premise is to abandon the theory. You're seeing what you want to see, Klein.

I am waiting, when are you going to cherry pick some real examples which show that combination selection pressures accelerate evolution by mutation and selection.

I won't. It's been done before, and you refuse to see what's right in front of you.

That’s the correct answer to this question; when will a real example of multiple selection pressures accelerating evolution be posted?

Are you a high-school kid, Klein ? Because that's exactly the kind of argument I expect from someone that age.

[kleinman]

You should know by now that I love to annoy evolutionistsYes, and that makes you a troll.
Certainly I post controversial and contrary messages against the theory of evolution but I back up my messages with mathematical and empirical evidence. On the other hand, you and the other supporters of the theory of evolution have failed to contradict my hypothesis either mathematically or empirically, well except joobz posts on the Madagascar rainforest and plate tectonics.
with ev, the peer reviewed and published model of random point mutation and natural selection and the massive amount of empirical data which supports the results form this model.Yeah, yeah, and the fact that there are other sources of mutation but then you don't give a hoot about those. Why am I even talking to you ?
The hundreds of real examples of evolution by mutation and selection that I have cited are not limited to random point mutations yet they show the same behavior that ev demonstrates mathematically, that is combined selection pressures profoundly slow the evolutionary process. If you don’t want to understand how mutation and selection actually works, you shouldn’t be talking with me.
Now only if you could annoy me with some mathematics of mutation and selection and/or some empirical examples which show that combination selection pressures accelerate evolution.I don't think you can add 2 and 2, Klein.
Sure I can, two different ways, with paper and pencil and with a computer, you on the other hand have no way to show that multiple selection pressures accelerate evolution because that is not how the mathematics works and there is no empirical data to show this.
Certainly there is variation in populations. However, when you take this variation to explain the evolution of birds from reptiles that you lose contact with the mathematical and empirical evidence of how mutation and selection works.Nice dodge. How do you account for the variation within a species, and how do you account for the various species ?
You have two ways to obtain variation, mutations and recombination. The former in combination with selection is profoundly slow; the latter in combination with selection is far more rapid. Recombination with selection can markedly alter the phenotype of a population in a rapid manner but can not transform one species to another. Mutation with selection can transform one species to another in theory but the theory is not mathematically possible. Mutation with selection is far too slow a process and no selection pressures exist which would allow for such transformations.
Oh no Belz, I’m just responding to the often used strawman argument employed by evolutionists when they can’t address the mathematical and empirical facts that refute their theory.Again you should talk to those stupid scientists, not me.
I’m posting the data from numerous scientists who are very good at measuring the affects of mutation and selection. I don’t think they are stupid at all. Likewise, I don’t think Dr Schneider is stupid. I think he properly modeled the mathematics of random point mutation and natural selection.
You are not asking the correct question, you should ask which alleles differ between a fox terrier and a wolf. Here is a citation which explains this.It doesn't explain the physical differences. Would you mind actually answering the question ?
Belz, in case you didn’t know, creatures which reproduce by meiosis and recombination have homologous chromosomal pairs. The alleles which are inherited by the offspring determine the genotype which in turn gives the phenotype. You have two sets of genes, one from each parent passed to the offspring with numerous different possible alleles for each gene. It is these different alleles which ultimately determine the phenotype. It only takes a few generations of interbreeding with mutts for the characteristics of a “pure bred” dog to disappear.
What recombination and selection does is change the frequency of particular alleles in a population.HOW are those variations there in the FIRST place ?
Hey Belz, I’m a creationist, I’m here proving the mathematical impossibility of your theory. On rare occasions, you can get new alleles by mutation and selection, which is being demonstrated in the citations I have been posting. This is a profoundly slow process when you have combined selection pressures. Ev also demonstrates how slow the process of mutation and selection is when you have multiple simultaneous selection pressures.
Tigers and lions can be bred and can give fertile offspring. Here is a site which discusses this issue.You AGAIN refuse to answer my question. ARE tigers and lions the SAME species, YES or NO ?
They can breed and give fertile offspring, what do you think? I’ll give you a more specific answer if you can explain what your question has to do with the mathematics of mutation and selection. I’m not interested in going off on some vague discussion of what a species is.
If you wouldn’t were so ignorant of the mathematics of mutation and selection and understood the empirical examples which I am presenting, we wouldn’t having this discussion on race.Do you deny that the French word for "breed" is "race" and that this is the source of your confusion ?
I don’t speak French and this issue has nothing to do with the mathematics of mutation and selection.
Your theory of evolution is mathematically impossible because mutation and selection only works with a tiny number of selection conditions simultaneously.Sure, Klein. Anything you say.
And what the mathematics of ev says and what the hundreds of empirical examples of mutation and selection which I have cited says, all show that multiple simultaneous selection pressures profoundly slow the evolutionary process.
You have no way to transform the thousands of genes necessary to metamorphose reptiles into birds.And "recombination" does all that ?
Oh, recombination and selection can create Chihuahuas and Great Danes in a relatively small number of generations but you are not going to get cats that way.
That’s fine; Adequate posted his graph that shows that multiple selection pressures accelerate evolution. His problem and yours will be to demonstrate real examples of your mathematics.Well, since that's your problem either we should be at a standstill.
I’m far from being at a standstill; I have numerous new citations which show that combination selection pressures profoundly slow the evolutionary process. You now have to extrapolate and speculate your way to the huge changes that are required to transform reptiles to birds with a mechanism that is profoundly slow. In addition, we know why the mechanism is profoundly slow.
I see, you don’t use any machines to help you in your work. I can see you are Y1K compliant.Unfortunately machines can't interpret results.
Right! My interpretation of the mathematics of mutation and selection is reflected by hundreds of real examples which have been repeated by scientists world wide, on the other hand, your interpretation of the mathematics of mutation and selection (do you have any mathematics of mutation and selection?) has no real examples.
Sure it follows, you don’t have a mathematical basis for your theory and no examples which show that combined selection pressures accelerate evolution. Therefore you discard the result which ev shows and the hundreds of empirical examples which substantiates this result.Again, non sequitur. The logical way to deal with the premise is to abandon the theory. You're seeing what you want to see, Klein.
Belz, the mathematics and empirical evidence is there if you want to see it.
I am waiting, when are you going to cherry pick some real examples which show that combination selection pressures accelerate evolution by mutation and selection.I won't. It's been done before, and you refuse to see what's right in front of you.
If it has been done before, it should be easy for you to post the evidence, so why not just post the evidence?
That’s the correct answer to this question; when will a real example of multiple selection pressures accelerating evolution be posted?Are you a high-school kid, Klein ? Because that's exactly the kind of argument I expect from someone that age.
Belz, it only takes a high-school kid with knowledge of basic calculus who understands how to do a minimization/maximization problem in order to understand why multiple selection pressures profoundly slow the evolutionary process. Let use joobz’s example that he cited to show you how to understand why multiple selection pressures has a profound slowing effect on the mutation/selection process.
http://www.pnas.org/cgi/content/full/104/34/13711 (http://www.pnas.org/cgi/content/full/104/34/13711)
http://www.pnas.org/content/vol104/issue34/images/medium/zpq0310771490005.gif
Fig. 5. A schematic view of fitness landscapes and evolution under fixed goal and MVG. (a) A typical trajectory under fixed goal evolution. The population tends to spend long periods on local maxima or plateaus. (b) A typical trajectory under MVG. Dashed arrows represent goal switches. An effectively continuous positive gradient on the alternating fitness landscapes leads to an area where global maxima exist in close proximity for both goals.
The top image shows the trajectory that the population takes on the fitness landscape to get to the global optimum for goal 1. The second and third images show the trajectory the population takes when the goals are switched back and forth from goals 1 and 2. The bottom image shows the trajectory the population takes to achieve both goals sequentially. Now if goals 1 and 2 are applied simultaneously, you have two different selection conditions pushing the population on two different trajectories. Selection condition 1 is trying to push the population to the global optimum 1 and selection condition 2 is trying to push the population to global optimum 2. A step that would be advantageous for one condition is disadvantageous for the other condition which confounds both selection conditions in their search for their new optimums. This is why combined selection pressures confound the evolutionary process. Here are some more real examples which demonstrate how mutation and selection actually works.
http://www.regional.org.au/au/roc/1990/roc199001.htm (http://www.regional.org.au/au/roc/1990/roc199001.htm)
Although there have been many cases of herbicide resistance throughout the world there has been little need for concerted control strategies because control of the resistant biotypes can usually be obtained by alternative herbicides. Management factors, especially the choice and combination of herbicides, have changed in response to the appearance of resistance. Triazine resistant weeds in the northern hemisphere exhibit little cross-resistance and have been controlled by alternative herbicides or a combination of triazine herbicide and a herbicide with a different mode of action. This has also been the case in Australia with the Avena

http://www.ext.vt.edu/pubs/agronomy/part12.pdf (http://www.ext.vt.edu/pubs/agronomy/part12.pdf)
Herbicide resistant weed species must be managed with a combination of herbicidal, cultural, and mechanical weed control techniques. Crop rotation, where appropriate, is critical to successful resistant weed management, as it may allow the use of a more competitive crop or a crop whose life cycle and associated management and harvest procedures disrupt the life cycle of the resistant species. Most critical to resistant weed management, however, is herbicide rotation. Whether in a continuous crop, or in a crop rotation, herbicide rotation must be employed to prevent the development of new herbicide resistant weed species or to manage existing weed species. Rotation of herbicides with differing modes of action and with high efficacy on the target species will prevent a resistant biotype from developing to the point that it constrains production. Combination of herbicides within an application or within a growing season is also effective for resistant weed management, where combinations of differing modes of actions will control an existing resistant biotype as well as prevent the development of new resistant species. As stated, the use of herbicides with high specificity in terms of mode of action increases the likelihood of the development of resistance. Herbicide rotations or combinations involving two herbicides with modes of action with this degree of specificity should be avoided if possible due to the possibility of the development of resistance to both compounds (multiple resistance).

[Belz...]

Certainly I post controversial and contrary messages against the theory of evolution but I back up my messages with mathematical and empirical evidence.

The hundreds of real examples of evolution by mutation and selection that I have cited are not limited to random point mutations yet they show the same behavior that ev demonstrates mathematically, that is combined selection pressures profoundly slow the evolutionary process.

No, you don't. You put forth cherry-picked examples and simply IGNORE the opposite examples. You give no reason why we should ignore those examples except that, for some reason, they have only one selection pressure -- which proves that you are wrong about evolution because you admit that there are examples of evolution occuring because of a small number of pressures --, or because they use some other mechanism -- which proves that evolution works.

You don't have a case and you know it. You've been cornered and you're using various dishonest means of debate in order to maintain your ridiculous position.

Recombination with selection can markedly alter the phenotype of a population in a rapid manner but can not transform one species to another.

You're not answering my question: how can recombination create NEW information ? Where does this variation ORIGINATE from ?

You AGAIN refuse to answer my question. ARE tigers and lions the SAME species, YES or NO ?

They can breed and give fertile offspring, what do you think?

That's neither a yes nor a no.

I don’t speak French and this issue has nothing to do with the mathematics of mutation and selection.

Nice dodge. You're the one who brought it up.

Belz, it only takes a high-school kid with knowledge of basic calculus who understands how to do a minimization/maximization problem in order to understand why multiple selection pressures profoundly slow the evolutionary process.

Again, then: why haven't those stupid scientists caught up to that ?

Hey Belz, I’m a creationist

Obviously.

[kleinman]

Certainly I post controversial and contrary messages against the theory of evolution but I back up my messages with mathematical and empirical evidence.No, you don't. You put forth cherry-picked examples and simply IGNORE the opposite examples. You give no reason why we should ignore those examples except that, for some reason, they have only one selection pressure -- which proves that you are wrong about evolution because you admit that there are examples of evolution occuring because of a small number of pressures --, or because they use some other mechanism -- which proves that evolution works.

You don't have a case and you know it. You've been cornered and you're using various dishonest means of debate in order to maintain your ridiculous position.
Belz, my hypothesis is quite simple. I contend that the reason ev converges so slowly for any realistic length genome is the combination of three selection pressures being applied simultaneously. I then looked in the scientific literature of actual examples of mutation and selection and behold, there is a vast number of citations which shows this is exactly how mutation and selection works. If I am cherry picking examples, I have a vast orchard to choose from. If you think I am ignoring examples which show the opposite, post your examples and contradict my hypothesis. Evolution does work but only on a microevolutionary basis. There is no mathematical or empirical mechanism to combine these microevolutionary events into macroevolutionary changes such as transforming reptiles into birds. There are simply too many genes which must be transformed and no selection pressures or sufficient number of generations to accomplish the huge number of changes required.
Recombination with selection can markedly alter the phenotype of a population in a rapid manner but can not transform one species to another.You're not answering my question: how can recombination create NEW information ? Where does this variation ORIGINATE from ?
Belz, recombination without error can not create new information (new alleles) in the gene pool, recombination with selection can cause the loss of information (alleles) from the gene pool.
They can breed and give fertile offspring, what do you think?That's neither a yes nor a no.
I will give you a direct answer yes or no answer to this question if you can explain how the definition of species relates to the mathematics of mutation and selection. Otherwise, you are just trying to get this thread off topic.
I don’t speak French and this issue has nothing to do with the mathematics of mutation and selection.Nice dodge. You're the one who brought it up.
I don’t think so Belz; you are the one who brought up race.
Belz, it only takes a high-school kid with knowledge of basic calculus who understands how to do a minimization/maximization problem in order to understand why multiple selection pressures profoundly slow the evolutionary process.Again, then: why haven't those stupid scientists caught up to that ?
Belz, I don’t think the problem is stupidity. I think the problem is that there are many people committed to the theory of evolution for other than mathematical/scientific reasons.
Hey Belz, I’m a creationistObviously.
And I can prove your world view is mathematically impossible and back it up with a vast amount of cherry picked empirical data. Here’s another cherry for you.
http://www.aragriculture.org/weeds/herbicide_resistance.pdf (http://www.aragriculture.org/weeds/herbicide_resistance.pdf)
The fact that a combination of herbicides has been required to provide adequate season long weed control has helped to prevent herbicide resistance weeds from becoming a problem in cotton. Although horseweed is a problem in all conservation tillage areas and does impact cotton farmers, other confirmed and suspected resistant weeds are more common in soybeans, wheat and rice where single herbicides have been used to control a particular species over several years. Hopefully, the lessons learned from Roundup Ready® soybeans will help prevent resistance from becoming a problem after the introduction of Roundup Ready Flex® cotton.
I guess this actually is a boll of cotton.

[Belz...]

Belz, recombination without error can not create new information (new alleles) in the gene pool

Excellent!! Then you admit that mutation is the only way to ADD information to the gene pool ? Then let me ask you this: if mutation is the only way, and evolution through mutation/selection is impossible, how do you explain evolution ?

I will give you a direct answer yes or no answer to this question if you can explain how the definition of species relates to the mathematics of mutation and selection.

I'll take that as a "I don't have a clue, because I have no idea what 'species' means."

I don’t think so Belz; you are the one who brought up race.

No, you are. I said the word, you brought up the issue.

Belz, I don’t think the problem is stupidity. I think the problem is that there are many people committed to the theory of evolution for other than mathematical/scientific reasons.

You know, Klein, you really should stop trying other people's minds. You're very, very bad at it.

And I can prove your world view is mathematically impossible and back it up with a vast amount of cherry picked empirical data.

Thanks for admitting your dishonest methods.

[kleinman]

Belz, recombination without error can not create new information (new alleles) in the gene pool Excellent!! Then you admit that mutation is the only way to ADD information to the gene pool ? Then let me ask you this: if mutation is the only way, and evolution through mutation/selection is impossible, how do you explain evolution ?
Belz, you need to be a little more accurate when you try to paraphrase me. What I have said it the theory of evolution by mutation and selection is mathematically impossible, not that evolution by mutation is mathematically impossible. There are many real problems of mutation and selection which society must deal with. The evolutionist view how mutation and selection actually works is wrong Mutation and selection can not and does not do what evolutionists claim.
I will give you a direct answer yes or no answer to this question if you can explain how the definition of species relates to the mathematics of mutation and selection.I'll take that as a "I don't have a clue, because I have no idea what 'species' means."
You know, Belz, you really should stop trying other people's minds. You're very, very bad at it.
I don’t think so Belz; you are the one who brought up race.No, you are. I said the word, you brought up the issue.
So, let’s read what you said again.
http://forums.randi.org/showpost.php?p=2938247&postcount=5519 (http://forums.randi.org/showpost.php?p=2938247&postcount=5519)
Subjective opinion. Many races of dogs won't or can't breed with other races.
So Belz, are you claiming that lions and tigers are different races of cats?
Belz, I don’t think the problem is stupidity. I think the problem is that there are many people committed to the theory of evolution for other than mathematical/scientific reasons.
You know, Klein, you really should stop trying other people's minds. You're very, very bad at it.
I'll take that as a "I don't have a clue, because I have no idea what 'the mathematics of mutation and selection' means."
And I can prove your world view is mathematically impossible and back it up with a vast amount of cherry picked empirical data.Thanks for admitting your dishonest methods.
Hey, my last citation posted was a hand picked cotton boll of empirical data. Now don’t complain just because the field of the theory of evolution is barren of any fruit which shows that combination selection pressures accelerate evolution.

[Paul C. Anagnostopoulos]

Subjective opinion. Many races of dogs won't or can't breed with other races.

So Belz, are you claiming that lions and tigers are different races of cats?
'Race X won't breed with race Y' does not imply that 'Z won't breed with W implies that Z and W are different races.'

~~ Paul

[Belz...]

Belz, you need to be a little more accurate when you try to paraphrase me. What I have said it the theory of evolution by mutation and selection is mathematically impossible, not that evolution by mutation is mathematically impossible.

Yes, that is PRECISELY what I said. Don't you read other people's posts ?

You know, Belz, you really should stop trying other people's minds. You're very, very bad at it.

Apparently, Klein, French is not the only language you don't speak.

So, let’s read what you said again.

So Belz, are you claiming that lions and tigers are different races of cats?

You know, there is no low to which you won't stoop to avoid answering that question.

I'll take that as a "I don't have a clue, because I have no idea what 'the mathematics of mutation and selection' means."

Klein, you must have been the laughing stock at school debates.

Clearly, Klein, you have no ability to read what other people write, you have no understanding of the English language, you have no clue how to debate, your grasp of mathematics and logic is abysmal, you know next to nothing about evolution and your antiquated religious bias is clouding your judgment. Add your trollish behaviour to that, and that makes you an utter clod when it comes to arguing on a forum.

Good luck with your delusions.

[kleinman]

Subjective opinion. Many races of dogs won't or can't breed with other races.So Belz, are you claiming that lions and tigers are different races of cats?'Race X won't breed with race Y' does not imply that 'Z won't breed with W implies that Z and W are different races.'
There you go Paul, now you are off to the races. Now who is going to win the race to be the last to understand the mathematics of mutation and selection?
Belz, you need to be a little more accurate when you try to paraphrase me. What I have said it the theory of evolution by mutation and selection is mathematically impossible, not that evolution by mutation is mathematically impossible.Yes, that is PRECISELY what I said. Don't you read other people's posts ?
Sure I do, and if they have a good idea, I like to co-opt it.
You know, Belz, you really should stop trying other people's minds. You're very, very bad at it.Apparently, Klein, French is not the only language you don't speak.
I am fluent in several computer languages though and what those languages are saying is that the theory of evolution is mathematically impossible.
So, let’s read what you said again.

So Belz, are you claiming that lions and tigers are different races of cats?You know, there is no low to which you won't stoop to avoid answering that question.
Now you are just lion Belz!
I'll take that as a "I don't have a clue, because I have no idea what 'the mathematics of mutation and selection' means."Klein, you must have been the laughing stock at school debates.
Not at all Belz, this is my first debate. Perhaps you could give us some hints?
Clearly, Klein, you have no ability to read what other people write, you have no understanding of the English language, you have no clue how to debate, your grasp of mathematics and logic is abysmal, you know next to nothing about evolution and your antiquated religious bias is clouding your judgment. Add your trollish behaviour to that, and that makes you an utter clod when it comes to arguing on a forum.
Sure I do, joobz wants to talk about Madagascar rainforests and plate tectonics, kjkent1 thinks that the number of selection pressures are irrelevant to the rate of evolution, Adequate thinks that the more selection pressures you have the greater the rate of evolution and you want to know if lions and tigers are different races.

Now, since you don’t like my cotton pickin’ citation I thought I should give you a cherry pickin’ citation.
http://web1.msue.msu.edu/epubs/pestpubs/E154/4-Fungicides.pdf (http://web1.msue.msu.edu/epubs/pestpubs/E154/4-Fungicides.pdf)
Vangard (6) (cyprodinil) is a systemic fungicide registered on grapes, apples, peaches, tart cherries, plums. Do not apply Vangard to sweet cherries. Vangard should not be applied past bloom in stone This fungicide has protectant as well as post-infection activity and becomes rainfast 2 hours after application. Under heavy disease pressure, other registered fungicides should be used in combination or rotation Vangard. Vangard is a reduced-risk fungicide.
There you go Belz, now you can really accuse me of cherry pickin’ my citations to show that combination selection pressures slow the evolutionary process.

[Belz...]

Sure I do, and if they have a good idea, I like to co-opt it.

I think you meant "cop-out".

I am fluent in several computer languages though and what those languages are saying is that the theory of evolution is mathematically impossible.

That's funny, since computer languages aren't designed to communicate with people, and since languages don't "say" anything in the first place.

Now you are just lion Belz!

No low to which you won't stoop.

Not at all Belz, this is my first debate.

Well, may I suggest that calling people names, misrepresenting their argument, lying, making up stuff and trying to sound clever rather than actually adressing responses is NOT the way to go ?

Sure I do

Sure you do what ? Considering how many things I enumerated, can I assume you stopped at the first item ? That would explain a great many things about your ability to debate, here.


Anyway, since you haven't adressed any of my points -- ever --, I'll leave you to your ridiculous divine revelations and instead focus on real science and real theories. Have fun dwelling on your make-belief.

Goodbye.

[kleinman]

Sure I do, and if they have a good idea, I like to co-opt it.I think you meant "cop-out".
No Belz, you want me to cop-out because this is a debate you can’t win. I have co-opted Dr Schneider’s computer model that he thought proved how the theory of evolution works but now it is shown how mutation and selection actually works. Dr Schneider’s model is not the only simulation which shows that combination selection pressures slow the evolutionary process. There are many mathematical models which show the same thing, another example is posted below.
I am fluent in several computer languages though and what those languages are saying is that the theory of evolution is mathematically impossible.That's funny, since computer languages aren't designed to communicate with people, and since languages don't "say" anything in the first place.
Oh really, so what does computer code do?
Now you are just lion Belz!No low to which you won't stoop.
It’s a race to the bottom.
Not at all Belz, this is my first debate.Well, may I suggest that calling people names, misrepresenting their argument, lying, making up stuff and trying to sound clever rather than actually adressing responses is NOT the way to go ?
Now Belz, what names have I called you? You have accused me of not having the ability to read what other people write when you have already admitted you have not read this thread, you have accused me of having a grasp of mathematics and logic which is abysmal when you don’t even try to read and understand what ev is showing. You accuse me of knowing nothing about evolution when you can’t tell the difference between mutation and selection and recombination and selection. And you accuse me of not addressing your responses when I have asked a single question which no one on this thread will address, that is to show a single real example which demonstrates that multiple simultaneous selection pressures accelerate evolution. Instead I get arguments from people who want to discuss anything but that. I can understand this debating approach since if mutation and selection actually works the way I have hypothesized and which the mathematical and empirical evidence supports then the theory of evolution becomes impossible (of course which it is).
Sure I doSure you do what ? Considering how many things I enumerated, can I assume you stopped at the first item ? That would explain a great many things about your ability to debate, here.
If the best question you can ask is whether lions and tigers are the same species then the mathematics of mutation and selection is a topic you should avoid.
Anyway, since you haven't adressed any of my points -- ever --, I'll leave you to your ridiculous divine revelations and instead focus on real science and real theories. Have fun dwelling on your make-belief.

Goodbye.
Belz, you don’t need divine revelation to understand how evolution by mutation and selection actually works, there is mathematics and empirical evidence which explains how it works. It is your make-belief that this process can transform reptiles into birds. It is mathematically and empirically impossible. So how does evolution by mutation and selection actually work? It works like ev shows, simultaneous selection pressures profoundly slow the process. Here is another mathematical model which demonstrates the exact same thing.
http://www.blackwell-synergy.com/doi/pdf/10.1046/j.1365-3156.2001.00800.x (http://www.blackwell-synergy.com/doi/pdf/10.1046/j.1365-3156.2001.00800.x)
If drugs are used in combination, then the frequency of parasites resistant to both drugs will be very low. For example, if 0.1% are resistant to drug A and 0.005% are resistant to drug B, then parasites resistant to both will initially be present at a frequency of 0.1 * 0.05% = 0.00005% (assuming that the same gene cannot encode resistance to both drugs). Thus using drugs in combination from the outset may greatly increase the useful therapeutic lifespan of the drug, because lowering the starting frequency delays the point at which a significant amount of resistance emerges.
And
One important general point from the models is that use of combination therapy in their initial deployment is invariably better than introducing one drug alone, followed by introduction of the second-line drug once the first becomes ineffective (see, for example, Curtis & Otoo 1986; Smith 1990; Bonhoeffer et al. 1997; for malaria, helminths and bacteria, respectively).
Single selection pressures evolve much more rapidly than multiple selection pressures, that is what the mathematics shows and that is what the empirical evidence shows. Now if you want to enter the world of make-believe, and then imagine reptiles evolving into birds, you have to make-believe that selection pressures exist to transform those huge number of genes and that somehow all those selection pressures cooperate in the process. The only problem with that make-believe world is that the mathematical and empirical evidence directly contradicts this fantasy.

I’ll continue to post more empirical examples of how mutation and selection actually works and other mathematical models which show that combination selection pressures slow the evolutionary process. You evolutionists feel free to post your examples which contradicts these mathematical and empirical facts.

[Belz...]

No Belz, you want me to cop-out because this is a debate you can’t win.

Can't win against unfalsifiable theories, indeed.

Goodbye, Klein.

[kleinman]

No Belz, you want me to cop-out because this is a debate you can’t win.Can't win against unfalsifiable theories, indeed.

Goodbye, Klein.
Too bad the theory of evolution isn’t one of those unfalsifiable theories because it can be falsified both mathematically and empirically. The way the theory of evolution by mutation and selection is falsified is by the way mutation and selection actually works. The way mutation and selection actually works is that multiple selection pressures profoundly slow the evolutionary process. This affect is seen with insecticide resistance as shown below.
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=15667718&dopt=AbstractPlus (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=15667718&dopt=AbstractPlus)
When the larvae of Anopheles stephensi, a malaria vector, were selected with deltamethrin for 40 successive generations, there was a 60-fold increase in larval resistance to deltamethrin but no increase in the resistance of the adult mosquitoes. This result, and the observation that deltamethrin selection of adults for 40 generations resulted in only a six-fold increase in adult resistance to deltamethrin, indicated some stage specificity. When F(24) deltamethrin-resistant larvae were selected with 1:5 deltamethrin-piperonyl butoxide (deltamethrin-PBO), instead of deltamethrin alone, for 16 generations, the level of resistance to deltamethrin in the F(40) larvae was reduced by 6%-21%. Similarly, selection with deltamethrin-PBO of adults of the parental strain for 20 generations reduced the speed of the development of resistance to deltamethrin, compared with that seen using selection with deltamethrin alone. Deltamethrin selection appears to select initially a monooxygenase-based mechanism. When the monooxygenase-based mechanism is blocked, by treatment with PBO, selection of a kdr-type mechanism is accelerated, as is evident from increased cross-resistance to 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT) in the adults selected with deltamethrin-PBO. The implications of these results are discussed in terms of the management of the larval and adult stages of An. stephensi .
See Belz, you have to go into denial of these mathematical and empirical facts because your unfalsifiable theory has been falsified.

[Lucifuge Rofocale]

I’ll continue to post more empirical examples of how mutation and selection actually works and other mathematical models which show that combination selection pressures slow the evolutionary process. You evolutionists feel free to post your examples which contradicts these mathematical and empirical facts.

Let's suppose for a moment that CSP slow EP and that Ptedoractyls didn't exist. How does it falsify Evolution instead of making it just slower?

[kleinman]

I’ll continue to post more empirical examples of how mutation and selection actually works and other mathematical models which show that combination selection pressures slow the evolutionary process. You evolutionists feel free to post your examples which contradict these mathematical and empirical facts.Let's suppose for a moment that CSP slow EP and that Ptedoractyls didn't exist. How does it falsify Evolution instead of making it just slower?
Are you implying that Pterodactyls transformed into birds? Lucifuge, what I don’t think you appreciate is how slow the mutation/selection process is with CSP. This is why it takes things like viruses and bacteria with huge populations and rapid generation times in order to evolve when subjected to only 3 or 4 combined pressures. Life forms like reptiles which have much smaller populations and much longer generation times simply don’t have sufficient generations to accomplish the huge transformations needed to metamorphose reptiles into birds, so many genes, so little time and no selection pressures that would accomplish such an exaggerated transformation.

[Lucifuge Rofocale]

Thats all right, now please answer my question:How does it falsify Evolution instead of making it just slower? What is the "little time"? (Hint - remember that you have to account for the begin of the reproductory age in your calculations, not the entire lifespan of the selectioned specia. Also you have to account for punctuated evolution. Take into account the selfish gene theory and don't treat a complete DNA as a unit)

[kleinman]

Thats all right, now please answer my question:How does it falsify Evolution instead of making it just slower? What is the "little time"? (Hint - remember that you have to account for the begin of the reproductory age in your calculations, not the entire lifespan of the selectioned specia. Also you have to account for punctuated evolution. Take into account the selfish gene theory and don't treat a complete DNA as a unit)
It is clear that you haven’t read this thread because your questions have been answered previously, but I will repeat part of the exchange which involved Meadmaker, Paul and myself.
So Paul’s estimate for the number of generations to evolve 96 loci in the ev model for a population of 1 million, G=100,000 and mutation rate=1/genome/generation is 210,000,000 generations. If you assume the generation time for this population is one generation per day, you get a mere 575,000 years. Meadmaker, do you want to do the calculation to estimate the number of years required to evolve those 96 loci for a population that reproduces once a year?I'm thinking about 210,000,000 years. Did transcription factors evolve in organisms with a 1-year reproduction cycle? No Paul, transcription factors did not evolve in organisms with a 1-year reproduction cycle and they did not evolve on organisms with a genome length of 256 bases because such creatures only exist in your imagination and of course in Dr Schneider’s computer simulation.
With respects to Stephen Gould’s hypothesis of punctuated equilibrium, this has also been discussed on this thread but I will repeat the key problems of the hypothesis here. The mathematical problems are that Gould hypothesizes that punctuated equilibrium occurs with small subpopulations in short periods of time (as few as 10,000 years in his writings). Both large numbers of generations and large populations are needed for mutation and selection to evolve to anything other than a single selection pressure. If Gould’s hypothesis has any validity it is with recombination and natural selection not mutation and natural selection.

Now answer my question, are you implying that Pterodactyls transformed into birds?

[Lucifuge Rofocale]

No I didn't. I already said that I will assume that Pterodactyls didn't exists, remember?

Please don't ask me to read all the thread....it has 140 pages by now.

About Gould, is he is right then there is time for evolution to transform reptyls into birds?

And.... what's wrong with 210 MY? What's the error margin of your calculus, giving that there are other evolution mechanisms than CSP?

[kleinman]

About Gould, is he is right then there is time for evolution to transform reptyls into birds?
No, Gould’s hypothesis of punctuated equilibrium is wrong. Gould limits two of the most important parameters in he mathematics of mutation and selection, time and population size (the most important parameter in the mutation and selection is the number of selection conditions). Punctuated equilibrium fails as an explanation for the lack of transitional fossils in the fossil record.
And.... what's wrong with 210 MY? What's the error margin of your calculus, giving that there are other evolution mechanisms than CSP?
That’s 210 MY to evolve only 96 loci. Mutation and selection is a profoundly slow way of adding information to the gene pool. With respects to the margin of error because other mechanisms of mutation, I’ll answer with a citation.
For those of you who contend that insertions and deletions will overcome the effect of combination therapy, here is a citation which shows that HIV evolution despite recombination and now insertions and deletions is still slowed by combination therapy.
http://jvi.asm.org/cgi/content/full/81/9/4713 (http://jvi.asm.org/cgi/content/full/81/9/4713)
Deletions, insertions, and amino acid substitutions in the ß3-ß4 hairpin loop-coding region of human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) have been associated with resistance to nucleoside RT inhibitors when appearing in combination with other mutations in the RT-coding region. In this work, we have measured the in vivo fitness of HIV-1 variants containing a deletion of 3 nucleotides affecting codon 69 (69) of the viral RT as well as the replication capacity (RC) ex vivo of a series of recombinant HIV-1 variants carrying an RT bearing the 69 deletion or the T69A mutation in a multidrug-resistant (MDR) sequence background, including the Q151M complex and substitutions M184V, K103N, Y181C, and G190A. Patient-derived viral clones having RTs with 69 together with S163I showed increased RCs under drug pressure. These data were consistent with the viral population dynamics observed in a long-term-treated HIV-1-infected patient. In the absence of drugs, viral clones containing T69A replicated more efficiently than those having 69, but only when patient-derived sequences corresponding to RT residues 248 to 527 were present. These effects could be attributed to a functional interaction between the C-terminal domain of the p66 subunit (RNase H domain) and the DNA polymerase domain of the RT. Finally, recombinant HIV-1 clones bearing RTs with MDR-associated mutations, including deletions at codon 69, showed increased susceptibilities to protease inhibitors in phenotypic assays. These effects correlated with impaired Gag cleavage and could be attributed to delayed maturation and decreased production of active protease in those variants.
And
Antiretroviral therapy including nucleoside and nonnucleoside reverse transcriptase (RT) inhibitors, protease (PR) inhibitors, and entry inhibitors as part of combination drug regimens has contributed to a decrease in mortality and morbidity among human immunodeficiency virus type 1 (HIV-1)-infected patients (26, 31). However, drug-resistant HIV-1 variants, which are a major factor contributing to treatment failure (11, 37), often emerge during the course of antiretroviral treatment as a result of impotent regimens, suboptimal adherence, pharmacological hurdles, or ineffectively treated compartments. Long-term HIV chemotherapy with repetitive treatment failure and frequent antiretroviral drug changes is often associated with the accumulation of drug resistance mutations that confer increased phenotypic resistance and lead to the clinically undesirable selection of multidrug-resistant (MDR) HIV-1 strains.

Resistance to multiple nucleoside RT inhibitors has been associated with an amino acid substitution at the nucleoside binding site of the enzyme (e.g., Q151M) and with insertions or deletions in the ß3-ß4 hairpin loop in the finger subdomain (amino acid residues 56 to 77) of HIV-1 RT. The acquisition of resistance through the Q151M pathway was first observed in virus isolated from patients receiving zidovudine and didanosine (40). Viral clones harboring this amino acid substitution displayed moderate resistance to zidovudine and zalcitabine and low-level resistance to other nucleoside analogues (17, 40). Further acquisition of additional mutations, such as A62V, V75I, F77L, and F116Y, rendered viruses that were highly resistant to zidovudine, didanosine, zalcitabine, and stavudine. Another group of MDR viruses are those having insertions or deletions in HIV-1 RT (reviewed in reference 25). Viruses with a dipeptide insertion (usually Ser-Ser, Ser-Gly, or Ser-Ala) between RT codons 69 and 70 and additional mutations, such as M41L, A62V, K70R, and T215Y, display high-level resistance to zidovudine and moderate levels of resistance to other nucleoside analogues (3, 6, 7, 19, 23, 39, 41, 43, 46). Similarly, deletions around positions 67 to 70 of the RT are associated with resistance to RT inhibitors, in some cases through complex interactions with other mutations in the RT-coding region (14, 15, 42, 45). However, deletions are less frequently observed than insertions, accounting for approximately 0.2% of the HIV-infected patients treated with nucleoside RT inhibitors (24), and are usually accompanied by other drug resistance mutations. The mechanisms and evolutionary pathways by which these deletions develop are not known.
So not only does HIV do recombination, it also does mutations with insertions and selections yet the evolution of the virus is slowed with combination therapy.
Lucifuge, do you want to hazard a guess on how much of the genome is affected by an insertion or deletion?

[Lucifuge Rofocale]

No, Gould’s hypothesis of punctuated equilibrium is wrong. Gould limits two of the most important parameters in he mathematics of mutation and selection, time and population size (the most important parameter in the mutation and selection is the number of selection conditions). Punctuated equilibrium fails as an explanation for the lack of transitional fossils in the fossil record.

Sorry for not being clear enought. The question was : About Gould, is he is right then there is time for evolution to transform reptyls into birds?. Would you please answer that?


That’s 210 MY to evolve only 96 loci. Mutation and selection is a profoundly slow way of adding information to the gene pool. With respects to the margin of error because other mechanisms of mutation, I’ll answer with a citation.


Thanks for the citation.
I understand that you are using the studies on virus populations subject to a very limted set of CSP to derive conclusions for organisms with more complex DNA subject to to a very wider set of CSP? Am I right?


Lucifuge, do you want to hazard a guess on how much of the genome is affected by an insertion or deletion?
I wouldn't dare.

[kleinman]

No, Gould’s hypothesis of punctuated equilibrium is wrong. Gould limits two of the most important parameters in he mathematics of mutation and selection, time and population size (the most important parameter in the mutation and selection is the number of selection conditions). Punctuated equilibrium fails as an explanation for the lack of transitional fossils in the fossil record.Sorry for not being clear enought. The question was : About Gould, is he is right then there is time for evolution to transform reptyls into birds?. Would you please answer that?
Gould formulated the hypothesis of punctuated equilibrium in an attempt to explain the lack of transitional forms in the fossil record. Gould must have assumed that it was possible to evolve reptiles into birds very rapidly otherwise why would he formulate the hypothesis? The problem with Gould’s hypothesis is he denies two important parameters for the mutation and selection process, time and large populations. The mathematics just does not hold up for Gould’s hypothesis.
That’s 210 MY to evolve only 96 loci. Mutation and selection is a profoundly slow way of adding information to the gene pool. With respects to the margin of error because other mechanisms of mutation, I’ll answer with a citation.
Thanks for the citation. I understand that you are using the studies on virus populations subject to a very limted set of CSP to derive conclusions for organisms with more complex DNA subject to to a very wider set of CSP? Am I right?
No, you are not right. Not only have I posted citations from the field of virology, but I have also posted citations from the fields of bacteriology, parasitology, oncology, agriculture, entomology, ecology as well as mathematics, all which show that CSP profoundly slow the evolutionary process.
Lucifuge, do you want to hazard a guess on how much of the genome is affected by an insertion or deletion?I wouldn't dare.
Come on, show a little initiative. What would happen if the insertion or deletion was in the middle of a gene?

[Lucifuge Rofocale]

Gould formulated the hypothesis of punctuated equilibrium in an attempt to explain the lack of transitional forms in the fossil record. Gould must have assumed that it was possible to evolve reptiles into birds very rapidly otherwise why would he formulate the hypothesis? The problem with Gould’s hypothesis is he denies two important parameters for the mutation and selection process, time and large populations. The mathematics just does not hold up for Gould’s hypothesis.

Sorry, I can't simply formulate my question in a different way, so I'll repeat it again just in case you missed it. Please note that I corrected a typo (in bold):

About Gould, if he is right then there is time for evolution to transform reptyls into birds?.

No, you are not right. Not only have I posted citations from the field of virology, but I have also posted citations from the fields of bacteriology, parasitology, oncology, agriculture, entomology, ecology as well as mathematics, all which show that CSP profoundly slow the evolutionary process.

I'd love to see something about the problem at hand, maybe in a complex organism like a dino. Or maybe you can try with this little fish http://news.bbc.co.uk/olmedia/975000/images/_979950_fish300.jpg http://news.bbc.co.uk/2/hi/science/nature/979950.stm

Come on, show a little initiative. What would happen if the insertion or deletion was in the middle of a gene?


I guess the protein involved would remain the same, change or not be produced at all.

[Paul C. Anagnostopoulos]

There you go Paul, now you are off to the races. Now who is going to win the race to be the last to understand the mathematics of mutation and selection?
All righty then.

~~ Paul

[kleinman]

Gould formulated the hypothesis of punctuated equilibrium in an attempt to explain the lack of transitional forms in the fossil record. Gould must have assumed that it was possible to evolve reptiles into birds very rapidly otherwise why would he formulate the hypothesis? The problem with Gould’s hypothesis is he denies two important parameters for the mutation and selection process, time and large populations. The mathematics just does not hold up for Gould’s hypothesis.Sorry, I can't simply formulate my question in a different way, so I'll repeat it again just in case you missed it. Please note that I corrected a typo (in bold):

About Gould, if he is right then there is time for evolution to transform reptyls into birds?.
Gould was not right either about his hypothesis for punctuated equilibrium or that there was time for evolution to transform reptiles into birds.
No, you are not right. Not only have I posted citations from the field of virology, but I have also posted citations from the fields of bacteriology, parasitology, oncology, agriculture, entomology, ecology as well as mathematics, all which show that CSP profoundly slow the evolutionary process. I'd love to see something about the problem at hand, maybe in a complex organism like a dino. Or maybe you can try with this little fish.
Lucifuge, there is something you don’t understand about the fundamental mathematics of mutation and selection. Each selection pressure has a trajectory on the fitness landscape to its new local optimum. When you have a single selection pressure, there is only a single trajectory or perhaps a single set of trajectories to that new local optimum. When you have multiple selection pressures, you have multiple trajectories (or sets of trajectories) to each of the new local optimums. The problem for evolving these conditions simultaneously is that a particular step on a given trajectory to a new local optimum that increases the fitness for a particular gene may be reducing the fitness for other genes. The actual trajectory that the population takes in the attempt to satisfy all the selection conditions becomes far more difficult for the population to traverse. This is what the mathematics shows and this is what the empirical evidence shows. In addition, ev shows that as the genome length increases, evolving the same set of binding sites becomes much more difficult than on a unrealistically short genome. Longer genome creatures have a more difficult time adapting to multiple selection pressures than shorter genome life forms such as viruses and bacteria.
Come on, show a little initiative. What would happen if the insertion or deletion was in the middle of a gene?I guess the protein involved would remain the same, change or not be produced at all.
Consider the following three possibilities; you have an insertion/deletion in 1) the binding site of the gene, 2) in the gene itself or 3) in the stop codon for the gene. What do you think would happen in each of these three circumstances?

While you are consider this, here are some more citations which show that combination selection pressures profoundly slow the evolutionary process.
http://nzsm.spis.co.nz/article904.htm (http://nzsm.spis.co.nz/article904.htm)
Prevention of herbicide resistance must be the aim of any weed management programme. There is a compelling need to educate growers to rotate herbicides with different modes of action and thus reduce the selection pressures for particular resistance mechanisms. Prophylactic or "insurance" spraying must be replaced by a truly integrated approach with herbicides being used less often, and only in combination with other methods.

http://www.weeds.iastate.edu/mgmt/qtr98-4/resistanceupdate.htm (http://www.weeds.iastate.edu/mgmt/qtr98-4/resistanceupdate.htm)
Any time a herbicide is used in a field it is placing selection pressure on the weed population and increasing the frequency of resistant weed biotypes. The only way to eliminate the risk of resistance is to stop using the herbicide, which obviously isn’t a desirable option. Therefore, we must look for ways of managing the risk of resistance. The key to managing resistance is to evaluate the selection pressure of individual herbicides relative to other weed management strategies. Basically, the greater the reliance on a specific herbicide or herbicides with similar sites of action, the greater the selection pressure on the weed population, and the sooner resistance will appear in a weed population.

For most growers, managing resistance will primarily involve herbicide selection. The two main considerations for herbicide selection are rotation of herbicides and the use of alternative modes of action. Repeated use of herbicides with the same site of action places continual selection pressure on weed populations. The simplest and most effective method of managing herbicide resistance is to rotate herbicide sites of action annually.

The use of herbicides with multiple sites of action, applied either as tank mixes, premix formulations, or sequential applications, may provide some benefit in managing resistance. A second herbicide will only reduce selection pressure if it is effective on the same weed species as the first product. For example, Bicep contains two herbicides with two different sites of action, Dual and atrazine. This combination should be effective at reducing selection pressure on pigweed since both Dual and atrazine are active on this species. This combination would be less likely at reducing the potential for Dual resistance in foxtail since the rate of atrazine found in Bicep provides little control of foxtail. Thus, when using multiple sites of action, it is critical to evaluate how much overlap in activity among the herbicides being used is present. In most situations there will be several species in which only one of the herbicides is placing selection pressure on the population, and therefore selecting for resistant biotypes.
You all have a good weekend; perhaps you will surprise us with a citation that shows that multiple selection pressures accelerate evolution. We’ll see next week.

[Lucifuge Rofocale]

Well. I guess I should make my question again:
About Gould, if he is right then there is time for evolution to transform reptyls into birds?.
Lucifuge, there is something you don’t understand about the fundamental mathematics of mutation and selection. Each selection pressure has a trajectory on the fitness landscape to its new local optimum. When you have a single selection pressure, there is only a single trajectory or perhaps a single set of trajectories to that new local optimum. When you have multiple selection pressures, you have multiple trajectories (or sets of trajectories) to each of the new local optimums. The problem for evolving these conditions simultaneously is that a particular step on a given trajectory to a new local optimum that increases the fitness for a particular gene may be reducing the fitness for other genes. The actual trajectory that the population takes in the attempt to satisfy all the selection conditions becomes far more difficult for the population to traverse. This is what the mathematics shows and this is what the empirical evidence shows. In addition, ev shows that as the genome length increases, evolving the same set of binding sites becomes much more difficult than on a unrealistically short genome. Longer genome creatures have a more difficult time adapting to multiple selection pressures than shorter genome life forms such as viruses and bacteria.

I guess that the ones that don't understand it are those damn fishes in http://news.bbc.co.uk/2/hi/science/nature/979950.stm . After seeing that, I'd like you to reconsideer the part of your post I bolded.

Consider the following three possibilities; you have an insertion/deletion in 1) the binding site of the gene, 2) in the gene itself or 3) in the stop codon for the gene. What do you think would happen in each of these three circumstances?

Any of the three posibilities I mentioned before.

While you are consider this, here are some more citations which show that combination selection pressures profoundly slow the evolutionary process.

Which is what those fishes still don't understand!

You all have a good weekend; perhaps you will surprise us with a citation that shows that multiple selection pressures accelerate evolution. We’ll see next week.


I wouldn't dare either. Have a nice weekend too.

[joobz]

ah, another week of the same old intentional dodging of questions and posting of information that does not support Kleinman's evolution is impossible hypothesis.

Let's restate the reasons why Kleinman's argument is utterly rediculous.
1.) Slow doesn't equal stop.
2.) Point mutation isn't the only method of adaptation
3.) Mutation rate is variable
4.) Number of selection pressures are never remain constant
5.) Evolutionary evidence is well documented and substantiated by molecular biology
6.) a model built on assumptions that are not universal does not have univeral applicability
7.) Not a single source Kleinman has mentioned ever said "stopped evolution" only delayed emergence.

[kjkent1]

http://news.bbc.co.uk/2/hi/science/nature/979950.stm
Well, it seems that someone else has provided another empirical example (in addition to flavobacterium K172) to support my contention that the number of selection pressures is irrelevant to macroevolutionary change.

And yet, Dr. Kleinman, you continue to assert that the mathematics do not permit this sort of evolutionary change to occur.

So, there seems to be but two possibilities: (1) the mathematics, as exemplified by Schneider's ev program, do not model the entire gamut of evolutionary processes, because we observe rapid macroevolutionary change, or (2) God creates macroevolutionary change by application of His magical powers.

Alan, you're entitled to your thesism -- but as a scientist, you cannot accept #2, until you have eliminated every other possibility. And, you still have a long way to go!

[Dr Adequate]

So, it's Friday, it's troll-feeding day.

Kleinman hasn't actually told any new lies, so far as I can see, but he's resurrected the lie about Stephen Jay Gould.

Kleinman does not, of course, explain what lie he wishes to tell about Stephen Jay Gould, because kleinman is a coward and a fool.

So there are no new lies here.

See y'all next Friday.

[Dr Adequate]

A quick review of the comments made over the past weekend shows that you advocates for the theory of evolution are still having difficulty understanding the mathematics of mutation and selection. So let’s consider them in detail.

Paul, I can appreciate your approach. Not including this mechanism of mutation in the ev model allows you to speculate about the rate at which this mechanism would accumulate information. In addition, you don’t have to describe the selection pressure that would propagate such a mutation. You don’t reveal much about the mutation and selection process with this type of speculation but you do demonstrate the lack of a mathematical foundation for your theory.

Oh no joobz, pointing at the Madagascar rainforests and plate tectonics is a profound mathematical argument against the mathematics of ev and the hundreds of citations I have posted which substantiates this mathematics.

You should know by now that I love to annoy evolutionists with ev, the peer reviewed and published model of random point mutation and natural selection and the massive amount of empirical data which supports the results form this model. Now only if you could annoy me with some mathematics of mutation and selection and/or some empirical examples which show that combination selection pressures accelerate evolution. Oh wait, joobz has proven that Madagascar rainforests and plate tectonics accelerates evolution.

Certainly there is variation in populations. However, when you take this variation to explain the evolution of birds from reptiles that you lose contact with the mathematical and empirical evidence of how mutation and selection works.

I guess you don’t know what they were either. That’s the problem with kjkent1’s example, it has not been repeated nor done in with any control.

Oh no Belz, I’m just responding to the often used strawman argument employed by evolutionists when they can’t address the mathematical and empirical facts that refute their theory.

Would it make you feel better if I called them “gaps” rather than “moth holes”?

Belz, you are confusing mutation and selection with recombination and selection. The former is a profoundly slow process of change and the latter can give rapid changes in the phenotype of a population.

You are not asking the correct question, you should ask which alleles differ between a fox terrier and a wolf. Here is a citation which explains this.
http://www.nature.com/hdy/journal/v85/n6/full/6888050a.html (http://www.nature.com/hdy/journal/v85/n6/full/6888050a.html)

What recombination and selection does is change the frequency of particular alleles in a population.

Again, I refer you back to the Wikipedia reference on Mendelian genetics. When you combine Mendelian genetics with recombination, you can change the frequency of particular alleles in a population, thus changing the phenotype. This is an extremely rapid process. On rare occasions, you can obtain a new allele by mutation which is beneficial but this is a profoundly slow process as demonstrated by ev and the hundreds of examples which I have posted and will continue to post more examples.

Tigers and lions can be bred and can give fertile offspring. Here is a site which discusses this issue. http://www.lairweb.org.nz/tiger/ligers2.html (http://www.lairweb.org.nz/tiger/ligers2.html)

If you wouldn’t were so ignorant of the mathematics of mutation and selection and understood the empirical examples which I am presenting, we wouldn’t having this discussion on race.

Really, I’m using an evolutionist written mathematical model and hundreds of empirical examples that shows that combined selection pressures profoundly slow the evolutionary process. When are you going to present a single real example that shows otherwise? Your theory of evolution is mathematically impossible because mutation and selection only works with a tiny number of selection conditions simultaneously. You have no way to transform the thousands of genes necessary to metamorphose reptiles into birds. You don’t have the selection pressures, you don’t have the time if necessary to accomplish the transformation and you don’t have the path across the fitness landscape.

That’s fine; Adequate posted his graph that shows that multiple selection pressures accelerate evolution. His problem and yours will be to demonstrate real examples of your mathematics. On the other hand, I can post hundreds of examples of Dr Schneider’s ev model which show that combination selection pressures profoundly slow the evolutionary process. That’s how mutation and selection works in reality.

I see, you don’t use any machines to help you in your work. I can see you are Y1K compliant.

Sure it follows, you don’t have a mathematical basis for your theory and no examples which show that combined selection pressures accelerate evolution. Therefore you discard the result which ev shows and the hundreds of empirical examples which substantiates this result.

I am waiting, when are you going to cherry pick some real examples which show that combination selection pressures accelerate evolution by mutation and selection.

You should run some examples with ev a get a sense how great the effect the number of selection pressures has on the rate of convergence. Then you would understand the meaning of the citations I have and will continue to post.

Well, I’ll give you some more examples where it is not so obvious to them.

That’s the correct answer to this question; when will a real example of multiple selection pressures accelerating evolution be posted?

That’s ok with me, I’ll post real examples of mutation and selection Monday through Thursday which substantiates what ev shows and you can post, what can you post over the weekend?

So BPScooter, are you going to post a real example which shows that combined selection pressures accelerate evolution and debunk my hypothesis. I’ll continue to post citations which show that combined selection pressures profoundly slow the evolutionary process and you can post…

I’m with you on that one Paul, we have heard the same bad information on the theory of evolution for decades so now, not only is the theory of evolution mathematically impossible, it is wrong!

That’s correct, however there are no selection pressures that can be put on viruses which actually kill the viruses once they are in the host. The replicators can only be inhibited from reproducing. This is essentially what is being modeled with ev. Again, what this demonstrates is that combined selection pressures profoundly slow the ability of the population ability to adapt to these selection pressures simultaneously.

It continues when there is no extinction but the process is profoundly slow, far to slow to explain how reptiles evolved to birds. There are no know selection pressures that would drive this transformation and even if there were, you simply do not have enough generations to accomplish all the genetic changes required.

I’m responding to multiple different bloggers. I nest the quotes in order for readers to follow the line of discussion. The screen editor for this site modifies the BBS code on some posts.

Anyway, I’ve decided to post some citations which show that combination selection pressures profoundly slow evolution on more complex life forms, not just microbes. These following examples are from agriculture.

http://www.blackwell-synergy.com/doi/abs/10.1046/j.1365-3180.2003.00355.x (http://www.blackwell-synergy.com/doi/abs/10.1046/j.1365-3180.2003.00355.x)
A simulation study was conducted to examine the effect of pattern of herbicide use on development of resistance to two herbicides with different modes of action in finite weed populations. The effects of the size of the treatment area (analogous to initial weed population), germination fraction and degree of self-pollination in the weed were investigated. The results indicate that the probability of developing resistance to one or both herbicides decreases as the size of the area/initial population decreases. For treatment areas of 100 ha or less with an initial weed seedbank of 100 seeds m2 and initial frequencies of the resistance genes of 106, development of resistance to both herbicides (double-resistance) is uncommon within 50 years for all types of weeds if both herbicides are used in all years (used in combination). If herbicides are used in alternate years (rotated) double-resistance almost always occurs in 100 ha areas but is uncommon in areas of 1 ha or less. The results suggest that adoption of practices that limit movement of weeds in conjunction with using herbicides in combination rather than in rotation can substantially delay development of herbicide resistance.[/quote]

http://cals.arizona.edu/pubs/crops/az1101/az1101_13.html (http://cals.arizona.edu/pubs/crops/az1101/az1101_13.html)

Once again, combined selection pressures slow the evolutionary process profoundly.

Here are a couple more examples of combination selection pressures profoundly slowing on more complex life forms than microbes.
http://www.sciencemag.org/cgi/content/abstract/180/4087/741 (http://www.sciencemag.org/cgi/content/abstract/180/4087/741)


http://www.msstate.edu/entomology/v7n2/art02.html (http://www.msstate.edu/entomology/v7n2/art02.html)

Once again, the mathematical behavior of ev is verified. The concept of evolution by mutation and selection is simply an optimization problem in which the number of selection conditions has a profound effect on the rate of optimization. This is how mutation and selection actually works, not as speculated by the advocates of the theory of evolution.


Certainly I post controversial and contrary messages against the theory of evolution but I back up my messages with mathematical and empirical evidence. On the other hand, you and the other supporters of the theory of evolution have failed to contradict my hypothesis either mathematically or empirically, well except joobz posts on the Madagascar rainforest and plate tectonics.

The hundreds of real examples of evolution by mutation and selection that I have cited are not limited to random point mutations yet they show the same behavior that ev demonstrates mathematically, that is combined selection pressures profoundly slow the evolutionary process. If you don’t want to understand how mutation and selection actually works, you shouldn’t be talking with me.

Sure I can, two different ways, with paper and pencil and with a computer, you on the other hand have no way to show that multiple selection pressures accelerate evolution because that is not how the mathematics works and there is no empirical data to show this.

You have two ways to obtain variation, mutations and recombination. The former in combination with selection is profoundly slow; the latter in combination with selection is far more rapid. Recombination with selection can markedly alter the phenotype of a population in a rapid manner but can not transform one species to another. Mutation with selection can transform one species to another in theory but the theory is not mathematically possible. Mutation with selection is far too slow a process and no selection pressures exist which would allow for such transformations.

I’m posting the data from numerous scientists who are very good at measuring the affects of mutation and selection. I don’t think they are stupid at all. Likewise, I don’t think Dr Schneider is stupid. I think he properly modeled the mathematics of random point mutation and natural selection.

Belz, in case you didn’t know, creatures which reproduce by meiosis and recombination have homologous chromosomal pairs. The alleles which are inherited by the offspring determine the genotype which in turn gives the phenotype. You have two sets of genes, one from each parent passed to the offspring with numerous different possible alleles for each gene. It is these different alleles which ultimately determine the phenotype. It only takes a few generations of interbreeding with mutts for the characteristics of a “pure bred” dog to disappear.

Hey Belz, I’m a creationist, I’m here proving the mathematical impossibility of your theory. On rare occasions, you can get new alleles by mutation and selection, which is being demonstrated in the citations I have been posting. This is a profoundly slow process when you have combined selection pressures. Ev also demonstrates how slow the process of mutation and selection is when you have multiple simultaneous selection pressures.

They can breed and give fertile offspring, what do you think? I’ll give you a more specific answer if you can explain what your question has to do with the mathematics of mutation and selection. I’m not interested in going off on some vague discussion of what a species is.

I don’t speak French and this issue has nothing to do with the mathematics of mutation and selection.

And what the mathematics of ev says and what the hundreds of empirical examples of mutation and selection which I have cited says, all show that multiple simultaneous selection pressures profoundly slow the evolutionary process.

Oh, recombination and selection can create Chihuahuas and Great Danes in a relatively small number of generations but you are not going to get cats that way.

I’m far from being at a standstill; I have numerous new citations which show that combination selection pressures profoundly slow the evolutionary process. You now have to extrapolate and speculate your way to the huge changes that are required to transform reptiles to birds with a mechanism that is profoundly slow. In addition, we know why the mechanism is profoundly slow.

Right! My interpretation of the mathematics of mutation and selection is reflected by hundreds of real examples which have been repeated by scientists world wide, on the other hand, your interpretation of the mathematics of mutation and selection (do you have any mathematics of mutation and selection?) has no real examples.

Belz, the mathematics and empirical evidence is there if you want to see it.

If it has been done before, it should be easy for you to post the evidence, so why not just post the evidence?

Belz, it only takes a high-school kid with knowledge of basic calculus who understands how to do a minimization/maximization problem in order to understand why multiple selection pressures profoundly slow the evolutionary process. Let use joobz’s example that he cited to show you how to understand why multiple selection pressures has a profound slowing effect on the mutation/selection process.
http://www.pnas.org/cgi/content/full/104/34/13711 (http://www.pnas.org/cgi/content/full/104/34/13711)
http://www.pnas.org/content/vol104/issue34/images/medium/zpq0310771490005.gif

The top image shows the trajectory that the population takes on the fitness landscape to get to the global optimum for goal 1. The second and third images show the trajectory the population takes when the goals are switched back and forth from goals 1 and 2. The bottom image shows the trajectory the population takes to achieve both goals sequentially. Now if goals 1 and 2 are applied simultaneously, you have two different selection conditions pushing the population on two different trajectories. Selection condition 1 is trying to push the population to the global optimum 1 and selection condition 2 is trying to push the population to global optimum 2. A step that would be advantageous for one condition is disadvantageous for the other condition which confounds both selection conditions in their search for their new optimums. This is why combined selection pressures confound the evolutionary process. Here are some more real examples which demonstrate how mutation and selection actually works.
http://www.regional.org.au/au/roc/1990/roc199001.htm (http://www.regional.org.au/au/roc/1990/roc199001.htm)


http://www.ext.vt.edu/pubs/agronomy/part12.pdf (http://www.ext.vt.edu/pubs/agronomy/part12.pdf)



Belz, my hypothesis is quite simple. I contend that the reason ev converges so slowly for any realistic length genome is the combination of three selection pressures being applied simultaneously. I then looked in the scientific literature of actual examples of mutation and selection and behold, there is a vast number of citations which shows this is exactly how mutation and selection works. If I am cherry picking examples, I have a vast orchard to choose from. If you think I am ignoring examples which show the opposite, post your examples and contradict my hypothesis. Evolution does work but only on a microevolutionary basis. There is no mathematical or empirical mechanism to combine these microevolutionary events into macroevolutionary changes such as transforming reptiles into birds. There are simply too many genes which must be transformed and no selection pressures or sufficient number of generations to accomplish the huge number of changes required.

Belz, recombination without error can not create new information (new alleles) in the gene pool, recombination with selection can cause the loss of information (alleles) from the gene pool.

I will give you a direct answer yes or no answer to this question if you can explain how the definition of species relates to the mathematics of mutation and selection. Otherwise, you are just trying to get this thread off topic.

I don’t think so Belz; you are the one who brought up race.

Belz, I don’t think the problem is stupidity. I think the problem is that there are many people committed to the theory of evolution for other than mathematical/scientific reasons.

And I can prove your world view is mathematically impossible and back it up with a vast amount of cherry picked empirical data. Here’s another cherry for you.
http://www.aragriculture.org/weeds/herbicide_resistance.pdf (http://www.aragriculture.org/weeds/herbicide_resistance.pdf)

I guess this actually is a boll of cotton.


Belz, you need to be a little more accurate when you try to paraphrase me. What I have said it the theory of evolution by mutation and selection is mathematically impossible, not that evolution by mutation is mathematically impossible. There are many real problems of mutation and selection which society must deal with. The evolutionist view how mutation and selection actually works is wrong Mutation and selection can not and does not do what evolutionists claim.

You know, Belz, you really should stop trying other people's minds. You're very, very bad at it.

So, let’s read what you said again.
http://forums.randi.org/showpost.php?p=2938247&postcount=5519 (http://forums.randi.org/showpost.php?p=2938247&postcount=5519)

So Belz, are you claiming that lions and tigers are different races of cats?

I'll take that as a "I don't have a clue, because I have no idea what 'the mathematics of mutation and selection' means."

Hey, my last citation posted was a hand picked cotton boll of empirical data. Now don’t complain just because the field of the theory of evolution is barren of any fruit which shows that combination selection pressures accelerate evolution.


There you go Paul, now you are off to the races. Now who is going to win the race to be the last to understand the mathematics of mutation and selection?

Sure I do, and if they have a good idea, I like to co-opt it.

I am fluent in several computer languages though and what those languages are saying is that the theory of evolution is mathematically impossible.

Now you are just lion Belz!

Not at all Belz, this is my first debate. Perhaps you could give us some hints?

Sure I do, joobz wants to talk about Madagascar rainforests and plate tectonics, kjkent1 thinks that the number of selection pressures are irrelevant to the rate of evolution, Adequate thinks that the more selection pressures you have the greater the rate of evolution and you want to know if lions and tigers are different races.

Now, since you don’t like my cotton pickin’ citation I thought I should give you a cherry pickin’ citation.
http://web1.msue.msu.edu/epubs/pestpubs/E154/4-Fungicides.pdf (http://web1.msue.msu.edu/epubs/pestpubs/E154/4-Fungicides.pdf)

There you go Belz, now you can really accuse me of cherry pickin’ my citations to show that combination selection pressures slow the evolutionary process.


No Belz, you want me to cop-out because this is a debate you can’t win. I have co-opted Dr Schneider’s computer model that he thought proved how the theory of evolution works but now it is shown how mutation and selection actually works. Dr Schneider’s model is not the only simulation which shows that combination selection pressures slow the evolutionary process. There are many mathematical models which show the same thing, another example is posted below.

Oh really, so what does computer code do?

It’s a race to the bottom.

Now Belz, what names have I called you? You have accused me of not having the ability to read what other people write when you have already admitted you have not read this thread, you have accused me of having a grasp of mathematics and logic which is abysmal when you don’t even try to read and understand what ev is showing. You accuse me of knowing nothing about evolution when you can’t tell the difference between mutation and selection and recombination and selection. And you accuse me of not addressing your responses when I have asked a single question which no one on this thread will address, that is to show a single real example which demonstrates that multiple simultaneous selection pressures accelerate evolution. Instead I get arguments from people who want to discuss anything but that. I can understand this debating approach since if mutation and selection actually works the way I have hypothesized and which the mathematical and empirical evidence supports then the theory of evolution becomes impossible (of course which it is).

If the best question you can ask is whether lions and tigers are the same species then the mathematics of mutation and selection is a topic you should avoid.

Belz, you don’t need divine revelation to understand how evolution by mutation and selection actually works, there is mathematics and empirical evidence which explains how it works. It is your make-belief that this process can transform reptiles into birds. It is mathematically and empirically impossible. So how does evolution by mutation and selection actually work? It works like ev shows, simultaneous selection pressures profoundly slow the process. Here is another mathematical model which demonstrates the exact same thing.
http://www.blackwell-synergy.com/doi/pdf/10.1046/j.1365-3156.2001.00800.x (http://www.blackwell-synergy.com/doi/pdf/10.1046/j.1365-3156.2001.00800.x)

And

Single selection pressures evolve much more rapidly than multiple selection pressures, that is what the mathematics shows and that is what the empirical evidence shows. Now if you want to enter the world of make-believe, and then imagine reptiles evolving into birds, you have to make-believe that selection pressures exist to transform those huge number of genes and that somehow all those selection pressures cooperate in the process. The only problem with that make-believe world is that the mathematical and empirical evidence directly contradicts this fantasy.

I’ll continue to post more empirical examples of how mutation and selection actually works and other mathematical models which show that combination selection pressures slow the evolutionary process. You evolutionists feel free to post your examples which contradicts these mathematical and empirical facts.


Are you implying that Pterodactyls transformed into birds? Lucifuge, what I don’t think you appreciate is how slow the mutation/selection process is with CSP. This is why it takes things like viruses and bacteria with huge populations and rapid generation times in order to evolve when subjected to only 3 or 4 combined pressures. Life forms like reptiles which have much smaller populations and much longer generation times simply don’t have sufficient generations to accomplish the huge transformations needed to metamorphose reptiles into birds, so many genes, so little time and no selection pressures that would accomplish such an exaggerated transformation.


It is clear that you haven’t read this thread because your questions have been answered previously, but I will repeat part of the exchange which involved Meadmaker, Paul and myself.

With respects to Stephen Gould’s hypothesis of punctuated equilibrium, this has also been discussed on this thread but I will repeat the key problems of the hypothesis here. The mathematical problems are that Gould hypothesizes that punctuated equilibrium occurs with small subpopulations in short periods of time (as few as 10,000 years in his writings). Both large numbers of generations and large populations are needed for mutation and selection to evolve to anything other than a single selection pressure. If Gould’s hypothesis has any validity it is with recombination and natural selection not mutation and natural selection.

Now answer my question, are you implying that Pterodactyls transformed into birds?


No, Gould’s hypothesis of punctuated equilibrium is wrong. Gould limits two of the most important parameters in he mathematics of mutation and selection, time and population size (the most important parameter in the mutation and selection is the number of selection conditions). Punctuated equilibrium fails as an explanation for the lack of transitional fossils in the fossil record.

That’s 210 MY to evolve only 96 loci. Mutation and selection is a profoundly slow way of adding information to the gene pool. With respects to the margin of error because other mechanisms of mutation, I’ll answer with a citation.
For those of you who contend that insertions and deletions will overcome the effect of combination therapy, here is a citation which shows that HIV evolution despite recombination and now insertions and deletions is still slowed by combination therapy.
http://jvi.asm.org/cgi/content/full/81/9/4713 (http://jvi.asm.org/cgi/content/full/81/9/4713)

And

So not only does HIV do recombination, it also does mutations with insertions and selections yet the evolution of the virus is slowed with combination therapy.
Lucifuge, do you want to hazard a guess on how much of the genome is affected by an insertion or deletion?


Gould formulated the hypothesis of punctuated equilibrium in an attempt to explain the lack of transitional forms in the fossil record. Gould must have assumed that it was possible to evolve reptiles into birds very rapidly otherwise why would he formulate the hypothesis? The problem with Gould’s hypothesis is he denies two important parameters for the mutation and selection process, time and large populations. The mathematics just does not hold up for Gould’s hypothesis.

No, you are not right. Not only have I posted citations from the field of virology, but I have also posted citations from the fields of bacteriology, parasitology, oncology, agriculture, entomology, ecology as well as mathematics, all which show that CSP profoundly slow the evolutionary process.

Come on, show a little initiative. What would happen if the insertion or deletion was in the middle of a gene?


Gould was not right either about his hypothesis for punctuated equilibrium or that there was time for evolution to transform reptiles into birds.

Lucifuge, there is something you don’t understand about the fundamental mathematics of mutation and selection. Each selection pressure has a trajectory on the fitness landscape to its new local optimum. When you have a single selection pressure, there is only a single trajectory or perhaps a single set of trajectories to that new local optimum. When you have multiple selection pressures, you have multiple trajectories (or sets of trajectories) to each of the new local optimums. The problem for evolving these conditions simultaneously is that a particular step on a given trajectory to a new local optimum that increases the fitness for a particular gene may be reducing the fitness for other genes. The actual trajectory that the population takes in the attempt to satisfy all the selection conditions becomes far more difficult for the population to traverse. This is what the mathematics shows and this is what the empirical evidence shows. In addition, ev shows that as the genome length increases, evolving the same set of binding sites becomes much more difficult than on a unrealistically short genome. Longer genome creatures have a more difficult time adapting to multiple selection pressures than shorter genome life forms such as viruses and bacteria.

Consider the following three possibilities; you have an insertion/deletion in 1) the binding site of the gene, 2) in the gene itself or 3) in the stop codon for the gene. What do you think would happen in each of these three circumstances?

While you are consider this, here are some more citations which show that combination selection pressures profoundly slow the evolutionary process.
http://nzsm.spis.co.nz/article904.htm (http://nzsm.spis.co.nz/article904.htm)


http://www.weeds.iastate.edu/mgmt/qtr98-4/resistanceupdate.htm (http://www.weeds.iastate.edu/mgmt/qtr98-4/resistanceupdate.htm)

You all have a good weekend; perhaps you will surprise us with a citation that shows that multiple selection pressures accelerate evolution. We’ll see next week. You remember how we debunked all your halfwitted lies and proved that the gibberish you recite is stupid crap?

Perhaps you've forgotten, so perhaps I should remind you: we debunked all your halfwitted lies and proved that the gibberish you recite is stupid crap.

You remember that?

See you next Friday, when I'll have a look at this thread and see if you've invented a new lie. Which I doubt. My expectation is that you'll recite the same ol' halfwitted lies and recite the same ol' crap.

[Dr Adequate]

Oh yes, the word count. If we exclude the stuff kleinman uses to pad out his crap, he's written about 4500 words of crap this week. That's a lot of crap.

It's lucky that his time isn't in the least valuable, and that he can devote his life to writing crap.

[Dr Adequate]

Oh, while we're doing kleinman facts, he's used the word "empirical" 23 times this week to describe the crazy nonsense fantasy world in his head.

On the other hand, he has stopped raving about cheese. It seems that now he's at least pretending to be sane.

Is anyone deceived?

[Belz...]

Sorry for not being clear enought. The question was : About Gould, is he is right then there is time for evolution to transform reptyls into birds?. Would you please answer that?



Thanks for the citation.
I understand that you are using the studies on virus populations subject to a very limted set of CSP to derive conclusions for organisms with more complex DNA subject to to a very wider set of CSP? Am I right?


I wouldn't dare.

There, there, Lucifuge...

Belz... here.

Perhaps you've missed Klein's entire point:

"That’s 210 MY to evolve only 96 loci. Mutation and selection is a profoundly slow way of adding information to the gene pool. "

See ? Mutation and selection is a PROFOUNDLY slow way of adding information. Therefore, no amount of time is enough. Don't you just LOVE those vague answers ?

[Kotatsu]

No Paul, transcription factors did not evolve in organisms with a 1-year reproduction cycle and they did not evolve on organisms with a genome length of 256 bases because such creatures only exist in your imagination and of course in Dr Schneider’s computer simulation.

I must have missed this the first time around. I would like some clarification: is it organisms with 1-year reproduction cycles, animals with 256 bases long genomes, or both that only exist in Paul's imagination and in Dr Schneider's computer simulation?

[Mercutio]

If I say it loud and often
My opponents' will will soften—
That it’s wholly without merit does not matter in the least;
In a battle of attrition
Repetition, repetition,
Is the surest way to guarantee their numbers are decreased.

All this time of yours I’m wasting
With my cutting and my pasting
Is a strategy intelligently (perfectly!) designed;
In a war ‘twixt God and Science
I have chosen my reliance
On a plan to leave each one of you bored quite out of your mind!

If you’re leaving out of boredom
I will simply spout some more dumb
And insulting little falsehoods which have long-since been destroyed;
Though I choose to bear false witness,
Fighting reproductive fitness
Is a noble undertaking—I’m sure God won’t be annoyed.

See, it really doesn’t matter
If I’m batty as a hatter--
When I libel evolution, then I'm lying for the Lord;
So it’s Onward, Christian Soldiers
And get used to being told yours
Is a theory that’s impossible, it’s totally impossible,
Mathematically impossible, demonstrably impossible,
Empirically impossible and logically impossible
In every way impossible…repeated, till you’re bored.

[Lucifuge Rofocale]

But he has lots of studies about HIV and others.....:D
As you have noted, K's entire argument depends on one simple little answer, wich I'll need to get from his own hands.


There, there, Lucifuge...

Belz... here.

Perhaps you've missed Klein's entire point:

"That’s 210 MY to evolve only 96 loci. Mutation and selection is a profoundly slow way of adding information to the gene pool. "

See ? Mutation and selection is a PROFOUNDLY slow way of adding information. Therefore, no amount of time is enough. Don't you just LOVE those vague answers ?

[Belz...]

If I say it loud and often
My opponents' will will soften—
That it’s wholly without merit does not matter in the least;
In a battle of attrition
Repetition, repetition,
Is the surest way to guarantee their numbers are decreased.

All this time of yours I’m wasting
With my cutting and my pasting
Is a strategy intelligently (perfectly!) designed;
In a war ‘twixt God and Science
I have chosen my reliance
On a plan to leave each one of you bored quite out of your mind!

If you’re leaving out of boredom
I will simply spout some more dumb
And insulting little falsehoods which have long-since been destroyed;
Though I choose to bear false witness,
Fighting reproductive fitness
Is a noble undertaking—I’m sure God won’t be annoyed.

See, it really doesn’t matter
If I’m batty as a hatter--
When I libel evolution, then I'm lying for the Lord;
So it’s Onward, Christian Soldiers
And get used to being told yours
Is a theory that’s impossible, it’s totally impossible,
Mathematically impossible, demonstrably impossible,
Empirically impossible and logically impossible
In every way impossible…repeated, till you’re bored.

Astonishing as usual, Mercutio. Well said.

[BPScooter]

Awesome, Mercutio. You rang my bells of Poe and Service and Carroll at the same time. You ever considered doing more of this? Something like Shropshire Lad rhyming I bet you'd be great with :-)

[disclaimer, this was not a kitten]

[kleinman]

There you go Paul, now you are off to the races. Now who is going to win the race to be the last to understand the mathematics of mutation and selection?All righty then.
Paul, why don’t you tell us some more about your Rcapacity concept? All wrongy then.
what the empirical evidence shows.I guess that the ones that don't understand it are those damn fishes in http://news.bbc.co.uk/2/hi/science/nature/979950.stm (http://news.bbc.co.uk/2/hi/science/nature/979950.stm) . After seeing that, I'd like you to reconsideer the part of your post I bolded.
Now Lucifuge, perhaps you haven’t noticed that in the citations which I have posted which support my contention that multiple selection pressures profoundly slow the evolution process, the selection pressures are explicitly defined and the target gene or genes are identified. Unless you can do this with your citation, all you are telling is a fish story which lays an egg.
Consider the following three possibilities; you have an insertion/deletion in 1) the binding site of the gene, 2) in the gene itself or 3) in the stop codon for the gene. What do you think would happen in each of these three circumstances?Any of the three posibilities I mentioned before.
Never mind.
While you are consider this, here are some more citations which show that combination selection pressures profoundly slow the evolutionary process.Which is what those fishes still don't understand!
The selection pressures and the target genes for those selection pressures that you telling in your fish story.
1.) Slow doesn't equal stop.
It’s nice to know that you acknowledge that combination selection pressures slow evolution. It is now for you to learn that combination selection pressures slow evolution so much that the theory of evolution does not beat the clock.
2.) Point mutation isn't the only method of adaptation
Joobz, you should know that HIV is not limited to point mutations, you pointed out that HIV does recombination yet this virus still demonstrates what ev shows. I have also posted a citation which shows that HIV does insertions and deletions yet this virus still demonstrates that combination selection pressures still profoundly slow the evolutionary process.
3.) Mutation rate is variable
That doesn’t change the fact that multiple selection pressures profoundly slow evolution. Perhaps you can give us a real example which demonstrates your contention. Oops, you did, it's the Madagascar rainforest! You just forgot to tell us what the selection pressures are and the target genes for those pressures are.
4.) Number of selection pressures are never remain constant
That’s true, if you have a single selection pressure; that condition can evolve quite rapidly. Do you want to tell us what those single selection pressures were that evolved reptiles into birds?
5.) Evolutionary evidence is well documented and substantiated by molecular biology
Microevolutionary evidence is well documented, you just like to extrapolate that evidence beyond reason and what the mathematics shows.
6.) a model built on assumptions that are not universal does not have univeral applicability
Dr Schneider seems to think that he has modeled the essentials of mutation and selection and there are several other models already cited on this thread which demonstrate the same mathematical behavior which Dr Schneider’s model demonstrates, that is combined selection pressures profoundly slow the evolutionary process. In addition it has already been demonstrated with HIV and numerous other examples of mutation and selection that this is how the phenomenon works. Joobz, when are you going to produce either mathematical contradictory evidence or empirical contradictory evidence that combined selection pressures profoundly slow the evolutionary process? Instead you post this same old shopping list without mathematical or empirical evidence to back up your speculations.
7.) Not a single source Kleinman has mentioned ever said "stopped evolution" only delayed emergence.
Joobz, you don’t read your own citations so why should I expect you to read the citations which I have posted. Here are a few recent examples of citations which say precisely what joobz says they don’t mention.

https://www.the-jci.org/article.php?id=30890 (https://www.the-jci.org/article.php?id=30890) Sequential ABL kinase inhibitor therapy selects for compound drug-resistant BCR-ABL mutations with altered oncogenic potency where these authors say the following “Our findings demonstrate the potential hazards of sequential kinase inhibitor therapy and suggest a role for a combination of ABL kinase inhibitors, perhaps including VX-680, to prevent the outgrowth of cells harboring drug-resistant BCR-ABL mutations.”
Of course joobz will have trouble understanding the meaning of “preventing evolution” and “stopping evolution”

http://www.annals.org/cgi/content/full/128/11/951 (http://www.annals.org/cgi/content/full/128/11/951) Resisting Resistance: Maximizing the Durability of Antiretroviral Therapy where these authors say “Second, to maximize genetic barriers to resistance, drugs that require the virus to undergo multiple mutations to achieve resistance should be combined with the most efficacious agents in other therapeutic classes”
Of course joobz will have trouble understanding the meaning of “maximizing genetic barriers to evolution” and “stopping evolution”

http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=cmed6.section.10764 (http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=cmed6.section.10764) Combination Chemotherapy where these authors say “In fact, essentially all curative chemotherapy involves combinations of 2 and usually 3 or more agents”
Of course joobz will have trouble understanding the meaning of “curative chemotherapy” and “stopping evolution”

http://www.priory.com/cmol/TBMultid.htm (http://www.priory.com/cmol/TBMultid.htm) Multi-Drug Resistant Tuberculosis where this author says “By combining the two drugs, streptomycin and PAS in the regimen the emergence of drug resistant bacteria was largely prevented and cure became the norm.”
Of course joobz will have trouble understanding the meaning of “largely prevented and cure became the norm” and “stopping evolution”

Now joobz, we have heard your story of how cooperative chemical reactions leads to abiogenesis, perhaps you could tell us your story of how cooperative selection pressures lead to the evolution of birds from reptiles.
http://news.bbc.co.uk/2/hi/science/nature/979950.stm (http://news.bbc.co.uk/2/hi/science/nature/979950.stm)Well, it seems that someone else has provided another empirical example (in addition to flavobacterium K172) to support my contention that the number of selection pressures is irrelevant to macroevolutionary change.
Lucifuge likes to post the same kind of mush as you do, no defined selection pressures and no target genes, just fish stories.
You remember how we debunked all your halfwitted lies and proved that the gibberish you recite is stupid crap?
Yes, we all remember how you did it. Let’s review your tale.
Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
And this?
More optimisation takes more time. This is what my model shows.
http://forums.randi.org/images/smilies/doglaugh.gif
No Paul, transcription factors did not evolve in organisms with a 1-year reproduction cycle and they did not evolve on organisms with a genome length of 256 bases because such creatures only exist in your imagination and of course in Dr Schneider’s computer simulation.I must have missed this the first time around. I would like some clarification: is it organisms with 1-year reproduction cycles, animals with 256 bases long genomes, or both that only exist in Paul's imagination and in Dr Schneider's computer simulation?
Paul will have to answer for what exists in his imagination. As for creatures with 256 base genomes, they only exist in Dr Schneider’s computer model. The smallest genome for any free living organism known is about 500,000 bases long.
If I say it loud and often
My opponents' will will soften—
That it’s wholly without merit does not matter in the least;
In a battle of attrition
Repetition, repetition,
Is the surest way to guarantee their numbers are decreased.

All this time of yours I’m wasting
With my cutting and my pasting
Is a strategy intelligently (perfectly!) designed;
In a war ‘twixt God and Science
I have chosen my reliance
On a plan to leave each one of you bored quite out of your mind!

If you’re leaving out of boredom
I will simply spout some more dumb
And insulting little falsehoods which have long-since been destroyed;
Though I choose to bear false witness,
Fighting reproductive fitness
Is a noble undertaking—I’m sure God won’t be annoyed.

See, it really doesn’t matter
If I’m batty as a hatter--
When I libel evolution, then I'm lying for the Lord;
So it’s Onward, Christian Soldiers
And get used to being told yours
Is a theory that’s impossible, it’s totally impossible,
Mathematically impossible, demonstrably impossible,
Empirically impossible and logically impossible
In every way impossible…repeated, till you’re bored.
Moving goalposts was the complaint but whines of repetition now the refrain,
No new plays in your book, neither strategy gets you in the game.
No mathematics to demonstrate your theory or empirical examples to make us weary.
Extrapolation, speculation is your proof, nothing from reality to make us scoot.
Mutation/selection, how does it work? Nothing like you evolutionists assert.

So how does mutation and selection actually work mathematically? Here is another mathematical study which shows how.
http://aac.asm.org/cgi/content/abstract/41/2/363 (http://aac.asm.org/cgi/content/abstract/41/2/363)
We present and analyze a series of mathematical models for the emergence of resistance during antibiotic treatment of an infected host. The models consider the population dynamics of antibiotic- sensitive and -resistant bacteria during the course of treatment and addresses the following problems: (i) the probability of obtaining a resistant mutant during the course of treatment as a function of antibiotic exposure; (ii) the conditions under which high, infrequent doses of an antibiotic are predicted to succeed in preventing the emergence of resistance; (iii) the conditions for the success of multiple drug treatment in suppressing the emergence of resistance and the relationship between antibiotic synergism and suppression of resistance; and (iv) the conditions under which nonadherence to the prescribed treatment regimen is predicted to result in treatment failure due to resistance. We analyze the predictions of the model for interpreting and extrapolating existing experimental studies of treatment efficacy and for optimizing treatment protocols to prevent the emergence of resistance.
Joobz, “suppressing resistance” and “prevent the emergence of resistance” is “stopping evolution”, of course if you want to post an example which shows that multiple selection pressures accelerate evolution, that would make this an interesting discussion but it appears that I must bore you all with a totally one sided discussion of how mutation and selection actually works.

[kjkent1]

http://news.bbc.co.uk/2/hi/science/nature/979950.stmWell, it seems that someone else has provided another empirical example (in addition to flavobacterium K172) to support my contention that the number of selection pressures is irrelevant to macroevolutionary change.Lucifuge likes to post the same kind of mush as you do, no defined selection pressures and no target genes, just fish stories.I see. So, it's mushy science when an obviously newly evolved species is discovered, because it doesn't fit your attempt to falsify the theory of evolution by negation -- while you simultaneously favor the entirely non-scientific conclusion that magic rules the universe?

Evolution has no ultimate goal, so search alogrithms are utterly useless to predict a future organism's likely appearance, form and/or function.

Why don't you describe a search algorithm which has no goal.

Note: ev's "goal" is that Rseq ~ Rfreq, which is a known quality for all "tested" independently living organisms. But, this goal does not constrain the ultimate characteristics of the organism. It only suggests that either (1) the appearance of a mutation that tends to diverge Rseq and Rfreq is a temporary condition which is moderated over time by subsequent random point mutations and selections against missing and spurious bindings, or (2) that the appearance of a mutation that tends to diverge Rseq and Rfreq is more harmful to the survival probability of the organism, vis-a-vis the appearance of a mutation that tends to converge or maintain the organism's Rseq ~ Rfreq state.

Alan, it's time for you to actually consider the other possibilities, rather than fixate on your incomplete and obviously incorrect theory.

[kleinman]

Lucifuge likes to post the same kind of mush as you do, no defined selection pressures and no target genes, just fish stories.I see. So, it's mushy science when an obviously newly evolved species is discovered, because it doesn't fit your attempt to falsify the theory of evolution by negation -- while you simultaneously favor the entirely non-scientific conclusion that magic rules the universe?
No, it’s mushy science when you try to extrapolate these microevolutionary changes to the evolution of birds from reptiles. It is mathematically and empirically impossible. Mutation and selection simply does not work that way. It doesn’t take magic to explain mutation and selection, mathematics and empirical data does it quite nicely.
Evolution has no ultimate goal, so search alogrithms are utterly useless to predict a future organism's likely appearance, form and/or function.
Wrong kjkent1; evolution has predictable goals as the mathematics and empirical data of mutation and selection shows. Particular drug treatments of infectious diseases lead to predictable mutations at particular loci. This effect is used to identify if resistance to a particular drug has evolved. This same phenomenon is seen in the use of herbicides, insecticides and cancer treatments. Mutations at particular loci identify if resistance to a particular selection pressure has occurred. The mathematics of mutation and selection show the same behavior as the empirical data show. Mutation and selection does have specific, precise and repeatable goals.
Why don't you describe a search algorithm which has no goal.
You are the supporter of the theory of evolution and contend that mutation and selection has no goal. Describe your own algorithms. While you are doing that you can explain why when using particular drugs for treating HIV, the same mutations appear over and over in response to particular drugs when you argue there is no goal for evolution.
Note: ev's "goal" is that Rseq ~ Rfreq, which is a known quality for all "tested" independently living organisms. But, this goal does not constrain the ultimate characteristics of the organism. It only suggests that either (1) the appearance of a mutation that tends to diverge Rseq and Rfreq is a temporary condition which is moderated over time by subsequent random point mutations and selections against missing and spurious bindings, or (2) that the appearance of a mutation that tends to diverge Rseq and Rfreq is more harmful to the survival probability of the organism, vis-a-vis the appearance of a mutation that tends to converge or maintain the organism's Rseq ~ Rfreq state.
You are wrong about this kjkent1, Rseq ~ Rfreq is neither the goal nor the selection condition for ev.
Alan, it's time for you to actually consider the other possibilities, rather than fixate on your incomplete and obviously incorrect theory.
Now what possibility do you want me to consider, your string cheese theory, Adequate’s ridiculous assertion that simultaneous combination selection pressures accelerate evolution, or perhaps joobz’s Madagascar rainforest theory? Kjkent1, the mathematics and empirical data of mutation and selection is understandable. The mathematic of mutation and selection is simply an optimization problem and as seen in all optimization problems, the more optimization conditions that must be satisfied simultaneously, the slower the mathematics proceeds. The empirical data of mutation and selection demonstrates this effect. This is how mutation and selection actually works. Why would I want to abandon my mathematical and scientific training and embrace the mathematically and empirically irrational theory of evolution?

Here’s another citation which demonstrates how mutation and selection actually works.
http://www.msstate.edu/entomology/v8n2/news.html (http://www.msstate.edu/entomology/v8n2/news.html)
At this point, the discovery of glyphosate resistant ryegrass is not a disaster, but rather a single confirmed case over hundreds of thousands of farms. Glyphosate is effective on a wide spectrum of weeds and is considered relatively safe because it breaks down rapidly and is largely inactivated on contact with soil. Thus, glyphosate must be retained as an effective herbicide. Integrated weed management, a combination of weed control techniques, is promoted to avoid the further emergence of herbicide resistance.
Combination selection pressures slow evolution, which is how mutation and selection actually works kjkent1, both mathematically and empirically.

[Belz...]

Moving goalposts was the complaint but whines of repetition now the refrain,
No new plays in your book, neither strategy gets you in the game.
No mathematics to demonstrate your theory or empirical examples to make us weary.
Extrapolation, speculation is your proof, nothing from reality to make us scoot.
Mutation/selection, how does it work? Nothing like you evolutionists assert.

I hope that wasn't supposed to be poetic. Or to rhyme...

[kjkent1]

No, it’s mushy science when you try to extrapolate these microevolutionary changes to the evolution of birds from reptiles. It is mathematically and empirically impossible. Mutation and selection simply does not work that way. It doesn’t take magic to explain mutation and selection, mathematics and empirical data does it quite nicely.The mathematics and empirical evidence merely show that Rseq ~ Rfreq in all independently living life forms. That's nothing close to a proof of the impossibility of evolution. It doesn't explain the fossil record or the observed examples of macroevolution that exist (and, of which homo sapiens is an example).

Wrong kjkent1; evolution has predictable goals as the mathematics and empirical data of mutation and selection shows. Particular drug treatments of infectious diseases lead to predictable mutations at particular loci. This effect is used to identify if resistance to a particular drug has evolved. This same phenomenon is seen in the use of herbicides, insecticides and cancer treatments. Mutations at particular loci identify if resistance to a particular selection pressure has occurred. The mathematics of mutation and selection show the same behavior as the empirical data show. Mutation and selection does have specific, precise and repeatable goals.Nothing in the above paragraph describes a "goal" of evolution. Moreover, your stating that mutation are "predictable" appears as a straightforward assertion that you contend selection drives mutation, and that mutation is non-random. If that's what you really believe, then you should just come right out and say so, because it explains everything about your position.

So, let me ask you straight out: do you reject the existence of randomness in this universe?

Because if you do, then this thread is about to head in an entirely new direction.

You are the supporter of the theory of evolution and contend that mutation and selection has no goal. Describe your own algorithms. While you are doing that you can explain why when using particular drugs for treating HIV, the same mutations appear over and over in response to particular drugs when you argue there is no goal for evolution.If evolution has no goal, then there can be no search algorithm, because a search requires a goal or it's not a search. So, there's really nothing for me to describe. You contend that a goal exists, so it's up to you to prove that goal's existence, so as to validate any search algorithm that you may support.

You are wrong about this kjkent1, Rseq ~ Rfreq is neither the goal nor the selection condition for ev.I"m wrong because you say so, or because you can prove it. The express goal of ev, and the only goal stated by Schneider is that Rseq -> Rfreq over the course of the algorithm's progress.

Now what possibility do you want me to consider, your string cheese theory, Adequate’s ridiculous assertion that simultaneous combination selection pressures accelerate evolution, or perhaps joobz’s Madagascar rainforest theory? Kjkent1, the mathematics and empirical data of mutation and selection is understandable. The mathematic of mutation and selection is simply an optimization problem and as seen in all optimization problems, the more optimization conditions that must be satisfied simultaneously, the slower the mathematics proceeds. The empirical data of mutation and selection demonstrates this effect. This is how mutation and selection actually works. Why would I want to abandon my mathematical and scientific training and embrace the mathematically and empirically irrational theory of evolution?You've already abandoned your scientific training in order to subscribe to a belief that magic rules the universe -- so, agreeing to abandon it for some other reason should be easy.

If you really were a scientist, then you would be actively engaged in trying to figure out how the creator creates. Because we have all these species and fossils hanging out and no scientific explanation for them other than evolution -- which by the way, explains them perfectly, once you understand what evolution actually is.

Apparently, you don't really understand, because you are asserting that selection drives mutation -- a conclusion for which no proof whatsoever exists.

Here’s another citation which demonstrates how mutation and selection actually works.
http://www.msstate.edu/entomology/v8n2/news.html (http://www.msstate.edu/entomology/v8n2/news.html)

Combination selection pressures slow evolution, which is how mutation and selection actually works kjkent1, both mathematically and empirically.Combination selection pressures kill organisms and reduce the opportunity for random mutation. However, random mutation can be increased by increasing the random background radiation in the environment, independent of any selection pressure. This, by itself, ruins your conclusion.

[Paul C. Anagnostopoulos]

Paul, why don’t you tell us some more about your Rcapacity concept? All wrongy then.
Happy to. The "gene" in Ev recognizes binding sites by matching a particular pattern that evolves in the binding sites but nowhere else. This pattern is illustrated by the sequence logo, and the number of bits required in the pattern is approximately Rfrequency.

If the number of bits that can be encoded in the binding sites, Rcapacity, is significantly less than Rfrequency, then it is extremely difficult for the pattern to evolve. It is rather like trying to index a vector with an index variable that has fewer than $\log_2 \mathit{vectorsize}$ bits.

What this has to do with your original remark I cannot imagine.

So Belz, are you claiming that lions and tigers are different races of cats?



Paul will have to answer for what exists in his imagination. As for creatures with 256 base genomes, they only exist in Dr Schneider’s computer model. The smallest genome for any free living organism known is about 500,000 bases long.
And you're claiming that this was the case when the first transcription factors evolved, right?


You are the supporter of the theory of evolution and contend that mutation and selection has no goal. Describe your own algorithms. While you are doing that you can explain why when using particular drugs for treating HIV, the same mutations appear over and over in response to particular drugs when you argue there is no goal for evolution.
I'll do that if you'll first explain why water keeps flowing to the lowest elevations. Surely water has a goal.

~~ Paul

[kleinman]

Moving goalposts was the complaint but whines of repetition now the refrain,
No new plays in your book, neither strategy gets you in the game.
No mathematics to demonstrate your theory or empirical examples to make us weary.
Extrapolation, speculation is your proof, nothing from reality to make us scoot.
Mutation/selection, how does it work? Nothing like you evolutionists assert.I hope that wasn't supposed to be poetic. Or to rhyme...
Why Belz, there is more poetry and rhyme in that little post than there is mathematics or empirical evidence in your theory of evolution. This following citation explains a little of the problem that you have with mutation and selection as an explanation for how life came to be.

http://www.cbc.yale.edu/old/cce/papers/ALife/node1.html (http://www.cbc.yale.edu/old/cce/papers/ALife/node1.html)
The process of adaptation can only proceed to the extent as favourable mutations occur. This is usually not a major concern to biologists, because they study the endproducts of evolution, and their very existence is powerful evidence that the favourable mutations have occured at a sufficient rate. However, the computer scientists, who want to solve engineering problems with evolutionary algorithms, start with inferior designs and want to improve them. For them the time it takes to actually obtain the improvement is money. In studying how quickly an improvement can be obtained it was discovered that the mutation/selection process is not universally effective. This is not an entirely new insight (see for instance Eden (1967), Bossert (1967), Simon (1965) or Bremermann (1966)), and it is also easy to see why this is the case. There is no way to improve the performance of a conventional computer program by randomly exchanging letters in the source code. However, Darwinian "evolution" of computer programs is indeed possible, as shown by the Tierra program of Thom Ray (1992) and the genetic programming methods (Koza, 1992). Hence, the Darwinian solution of optimization problems is possible if and only if the problem is "coded" in a way that makes the mutation-selection procedure an effective one. This fact is known as the "representation problem:" how to code a problem such that random variation and selection can lead to a solution? The representation problem is about the likelihood to obtain an improvement by mutation and/or recombination.

For biology the "representation problem" has some unsettling implications. If, as evolutionary biology asserts, all adaptations are the result of mutation and selection, organisms have to be evolvable. But how and why did an evolvable genetic representation of the phenotype originate in the first place? Is there an evolution of genetic representations of the phenotype? What are the evolutionary forces that shape genetic representations? The thesis of this essay is that the concept of genetic representations of the phenotype and its evolution forms a link among seemingly unrelated problems of evolutionary biology: the role of epistasis in adaptation, genetic canalization, developmental constraints, developmental and morphological integration, the evolution of complex adaptations, the biological basis of homology and perhaps the origin of body plans. Further it will be suggested that computer science and biology experience a phase of substantive convergence of interests, which makes computerscience the strongest allie in the attac on many of the still unsolved problems in evolutionary biology.
This convergence this author talks about is only theoretical. The reason this convergence does not enter reality is several fold. The first is that even the most complex computer code contains only a tiny fraction of the information found in the DNA of a living organism. And second, selection or optimization conditions do not exist that would give the massive transformation of the genome of a reptile to a bird, therefore if the transformation is to occur by huge numbers of tiny steps you are then confronted with the reality of how combined selection pressures interfere with the multiple trajectories each of these selection pressures impose on the population as it tries to navigate the fitness landscape.

Evolutionists assume that the mutation/selection process must work because life is here but when the mathematical and empirical properties of mutation and selection are examined, this circular reasoning of evolutionists breaks down and shows your theory to be mathematically and empirically impossible. You can get what appears to be a mathematical example of how mutation and selection works when you apply mutation and selection to a trivially small genome but when the search space (genome size) and number of selection pressures (optimization conditions) increases, this mathematical analogy collapses. This is what Dr Schneider showed in his publication of ev in Nucleic Acids Research but note that he has never published any other results from his model. Dr Schneider knows that his model would take years to converge for any realistic size genome if it would converge at all. Not much poetry or rhyme here just hard mathematical and empirical facts that show the theory of evolution to be impossible.
No, it’s mushy science when you try to extrapolate these microevolutionary changes to the evolution of birds from reptiles. It is mathematically and empirically impossible. Mutation and selection simply does not work that way. It doesn’t take magic to explain mutation and selection, mathematics and empirical data does it quite nicely.The mathematics and empirical evidence merely show that Rseq ~ Rfreq in all independently living life forms. That's nothing close to a proof of the impossibility of evolution. It doesn't explain the fossil record or the observed examples of macroevolution that exist (and, of which homo sapiens is an example).
Ev only shows the Rseq ~ Rfreq condition for unrealistically small genomes. The more important result from ev is that each of the individual selection conditions can evolve rapidly, even with tiny populations and on longer genomes than Rseq ~ Rfreq can be achieved. It is this mathematical fact which is demonstrated in the empirical data of mutation and selection. This mathematical fact is demonstrated in other mathematical models of mutation and selection.
Wrong kjkent1; evolution has predictable goals as the mathematics and empirical data of mutation and selection shows. Particular drug treatments of infectious diseases lead to predictable mutations at particular loci. This effect is used to identify if resistance to a particular drug has evolved. This same phenomenon is seen in the use of herbicides, insecticides and cancer treatments. Mutations at particular loci identify if resistance to a particular selection pressure has occurred. The mathematics of mutation and selection show the same behavior as the empirical data show. Mutation and selection does have specific, precise and repeatable goals.Nothing in the above paragraph describes a "goal" of evolution. Moreover, your stating that mutation are "predictable" appears as a straightforward assertion that you contend selection drives mutation, and that mutation is non-random. If that's what you really believe, then you should just come right out and say so, because it explains everything about your position.
Kjkent1, the goal is the fitness of the population to reproduce. This goal leads to repeatable examples of mutation and selection where the same mutations appear in different populations subject to the same selection pressures. This property is used for example in the treatment of people suffering from HIV. When particular mutations are identified in the population of viruses, then resistance to a particular drug is likely.
So, let me ask you straight out: do you reject the existence of randomness in this universe?
I don’t look at the issue in this way. There are many real problems which can not be solved using deterministic methods, so stochastic methods are used. Dr Schneider’s ev computer model is an example of this. The question you should ask is how well does the model fit reality? It all comes down to which mathematical tools give a reasonable representation of a phenomenon.
Because if you do, then this thread is about to head in an entirely new direction.
I haven’t moved the goalposts since my original post on the Evolutionisdead forum. Very few of the people debating on this forum want to talk about the mathematics of mutation and selection. The mathematics of mutation and selection is a losing issue for the theory of evolution but it does explain how mutation and selection actually works.
You are the supporter of the theory of evolution and contend that mutation and selection has no goal. Describe your own algorithms. While you are doing that you can explain why when using particular drugs for treating HIV, the same mutations appear over and over in response to particular drugs when you argue there is no goal for evolution.If evolution has no goal, then there can be no search algorithm, because a search requires a goal or it's not a search. So, there's really nothing for me to describe. You contend that a goal exists, so it's up to you to prove that goal's existence, so as to validate any search algorithm that you may support.
I have demonstrated that evolution has a goal, which is the fitness of the population to reproduce. The consequence of this goal leads to particular mutations appearing at particular loci with increasing frequency when particular selection pressures are applied to the population. This occurs with viral disease treatment, bacterial disease treatment, parasitic disease treatment, weed selection with herbicides, cancer treatment…
You are wrong about this kjkent1, Rseq ~ Rfreq is neither the goal nor the selection condition for ev.I"m wrong because you say so, or because you can prove it. The express goal of ev, and the only goal stated by Schneider is that Rseq -> Rfreq over the course of the algorithm's progress.
Not only do I say this, Paul says this as well.
Now what possibility do you want me to consider, your string cheese theory, Adequate’s ridiculous assertion that simultaneous combination selection pressures accelerate evolution, or perhaps joobz’s Madagascar rainforest theory? Kjkent1, the mathematics and empirical data of mutation and selection is understandable. The mathematic of mutation and selection is simply an optimization problem and as seen in all optimization problems, the more optimization conditions that must be satisfied simultaneously, the slower the mathematics proceeds. The empirical data of mutation and selection demonstrates this effect. This is how mutation and selection actually works. Why would I want to abandon my mathematical and scientific training and embrace the mathematically and empirically irrational theory of evolution?You've already abandoned your scientific training in order to subscribe to a belief that magic rules the universe -- so, agreeing to abandon it for some other reason should be easy.
When was the last time you had to deal with a real problem of mutation and selection? I haven’t and wouldn’t abandon my mathematical or scientific training to describe this problem. The mathematics of mutation and selection and the empirical data obtained from real examples of mutation and selection is telling you something that you are refusing to listen to, there is no magic here kjkent1, only hard mathematical and empirical facts. What these facts are saying is that combination selection pressures profoundly slow the evolutionary process.
If you really were a scientist, then you would be actively engaged in trying to figure out how the creator creates. Because we have all these species and fossils hanging out and no scientific explanation for them other than evolution -- which by the way, explains them perfectly, once you understand what evolution actually is.
There are plenty of scientists who are offering explanations you are looking for. I’m working on the mathematics of mutation and selection front and so far the score is hundreds of citations supporting my hypothesis that multiple selection pressures profoundly slow the evolutionary process to zero citations showing that multiple selection pressures accelerates evolution.
Apparently, you don't really understand, because you are asserting that selection drives mutation -- a conclusion for which no proof whatsoever exists.
You don’t have it quite correct. What particular selection pressures do is lead to the increase in frequency of particular mutations appearing in the populations. This fact is used to identify resistance of microbes to particular drugs.
Combination selection pressures slow evolution, which is how mutation and selection actually works kjkent1, both mathematically and empirically. Combination selection pressures kill organisms and reduce the opportunity for random mutation. However, random mutation can be increased by increasing the random background radiation in the environment, independent of any selection pressure. This, by itself, ruins your conclusion.
What you still don’t understand is that you don’t need huge populations to evolve resistance to single selection pressures. Ev demonstrates this and HIV when initial treated with monotherapy demonstrates this. It is the number of selection conditions which dominates the mathematics of mutation and selection, not the mutation rate, not the type of mutation and not recombination. Study ev a get yourself an education in the mathematics of mutation and selection.
Paul, why don’t you tell us some more about your Rcapacity concept? All wrongy then.Happy to. The "gene" in Ev recognizes binding sites by matching a particular pattern that evolves in the binding sites but nowhere else. This pattern is illustrated by the sequence logo, and the number of bits required in the pattern is approximately Rfrequency.

If the number of bits that can be encoded in the binding sites, Rcapacity, is significantly less than Rfrequency, then it is extremely difficult for the pattern to evolve. It is rather like trying to index a vector with an index variable that has fewer than http://www.randi.org/latexrender/latex.php?$\log_2 \mathit{vectorsize}$ bits.

What this has to do with your original remark I cannot imagine.
Happy to, ev very rapidly recognizes the binding sites when this selection condition is applied alone, likewise binding site sequences can very rapidly be removed from the non-binding site region or the gene region when those conditions are applied singly. It is only when you try to apply all three selection conditions simultaneously that ev has difficulty evolving binding sites on all but the shortest genomes. If you watch what is happening with the model when you have too long of a genome, the number of mistakes initially drop fairly rapidly until a local optimum is reached where the number of mistakes plateau, ev than has difficultly finding a trajectory that satisfies all three selection conditions to the global optimum. Joobz posted a citation which demonstrates what ev is doing under these circumstances.
http://www.pnas.org/cgi/content/full/104/34/13711 (http://www.pnas.org/cgi/content/full/104/34/13711)
http://www.pnas.org/content/vol104/issue34/images/medium/zpq0310771490005.gif
Fig. 5. A schematic view of fitness landscapes and evolution under fixed goal and MVG. (a) A typical trajectory under fixed goal evolution. The population tends to spend long periods on local maxima or plateaus. (b) A typical trajectory under MVG. Dashed arrows represent goal switches. An effectively continuous positive gradient on the alternating fitness landscapes leads to an area where global maxima exist in close proximity for both goals.
The top image shows the trajectory that the population takes on the fitness landscape to get to the global optimum for goal 1. The second and third images show the trajectory the population takes when the goals are switched back and forth from goals 1 and 2. The bottom image shows the trajectory the population takes to achieve both goals sequentially. Now if goals 1 and 2 are applied simultaneously, you have two different selection conditions pushing the population on two different trajectories. Selection condition 1 is trying to push the population to the global optimum 1 and selection condition 2 is trying to push the population to global optimum 2. A step that would be advantageous for one condition is disadvantageous for the other condition which confounds both selection conditions in their search for their new optimums. This is why combined selection pressures confound the evolutionary process. This is the same reason ev becomes very slow converging for longer genomes. Paul, ev is getting stuck at a local optimum.
Paul will have to answer for what exists in his imagination. As for creatures with 256 base genomes, they only exist in Dr Schneider’s computer model. The smallest genome for any free living organism known is about 500,000 bases long.And you're claiming that this was the case when the first transcription factors evolved, right?
Paul, no transcription factors evolved, what ev demonstrates is how slow three selection conditions evolve simultaneously on all but the tiniest genomes.
You are the supporter of the theory of evolution and contend that mutation and selection has no goal. Describe your own algorithms. While you are doing that you can explain why when using particular drugs for treating HIV, the same mutations appear over and over in response to particular drugs when you argue there is no goal for evolution.I'll do that if you'll first explain why water keeps flowing to the lowest elevations. Surely water has a goal
It’s gravity Paul. Now if you want to make an analogy to evolution, put sun light on water, it evaporates some of the water and the elevation of those evaporated water molecules increases. Now you put energy, mutation and selection into molecules and what can you accomplish? Not nearly what you evolutionists assert. Your own mathematics shows how little can be accomplished with mutation and selection and the empirical data substantiates this.

[kleinman]

It seems you evolutionists are still having difficulty understanding the mathematics of mutation and selection. Dr Schneider’s model shows what happens to the rate of convergence when multiple selection pressures are applied to a system evolving by mutation and selection.
These scientists from the Oxford University show with their model the same phenomenon.
http://www.pnas.org/cgi/content/abstract/94/22/12106 (http://www.pnas.org/cgi/content/abstract/94/22/12106)
The spread of bacteria resistant to antimicrobial agents calls for population-wide treatment strategies to delay or reverse the trend toward antibiotic resistance. Here we propose new criteria for the evaluation of the population-wide effects of treatment protocols for directly transmitted bacterial infections and discuss different usage patterns for single and multiple antibiotic therapy. A mathematical model suggests that the long-term benefit of single drug treatment from introduction of the antibiotic until a high frequency of resistance precludes its use is almost independent of the pattern of antibiotic use. When more than one antibiotic is employed, sequential use of different antibiotics in the population ("cycling") is always inferior to treatment strategies where, at any given time, equal fractions of the population receive different antibiotics. However, treatment of all patients with a combination of antibiotics is in most cases the optimal treatment strategy.
This scientist from Liverpool School of Tropical Medicine understands the mathematics of mutation and selection.
http://www.blackwell-synergy.com/doi/pdf/10.1046/j.1365-3156.2001.00800.x (http://www.blackwell-synergy.com/doi/pdf/10.1046/j.1365-3156.2001.00800.x)
If drugs are used in combination, then the frequency of parasites resistant to both drugs will be very low. For example, if 0.1% are resistant to drug A and 0.005% are resistant to drug B, then parasites resistant to both will initially be present at a frequency of 0.1 * 0.05% = 0.00005% (assuming that the same gene cannot encode resistance to both drugs). Thus using drugs in combination from the outset may greatly increase the useful therapeutic lifespan of the drug, because lowering the starting frequency delays the point at which a significant amount of resistance emerges.
And
One important general point from the models is that use of combination therapy in their initial deployment is invariably better than introducing one drug alone, followed by introduction of the second-line drug once the first becomes ineffective (see, for example, Curtis & Otoo 1986; Smith 1990; Bonhoeffer et al. 1997; for malaria, helminths and bacteria, respectively).
The following reference written by a scientist from Japan who is modeling evolution of life discovered the problem with multiple selection pressures.
http://www-karc.nict.go.jp/BA/staff/hsuzuki/papers/1999_AL.pdf (http://www-karc.nict.go.jp/BA/staff/hsuzuki/papers/1999_AL.pdf)
Abstract A novel machine language genetic programming system that uses one-dimensional core memories is proposed and simulated. The core is compared to a biochemical reaction space, and in imitation of biological molecules, four types of data words (Membrane, Pure data, Operator, and Instruction) are prepared in the core. A program is
represented by a sequence of Instructions. During execution of the core, Instructions are transcribed into corresponding Operators, and Operators modify, create, or transfer Pure data. The core is hierarchically partitioned into sections by the Membrane data, and the data transfer between sections
by special channel Operators constitutes a tree data-flow structure among sections in the core. In the experiment, genetic algorithms are used to modify program information. A simple machine learning problem is prepared for the environment data set of the creatures (programs), and the fitness value of a creature is calculated from the Pure data excreted by the creature. Breeding of programs that can
output the predefined answer is successfully carried out. Several future plans to extend this system are also discussed.
And
After several experiments that used GAs to evolve a population of programs (operator matrices), I found that this system could evolve particular kinds of programs
efficiently, and yet it suffers from a serious drawback as a computational system. As is well known, for a system to be able to execute any kind of computation, or for a computational system to be equivalent to the universal Turing machine, it must be able to execute some kind of judging operations. In the data-flow architecture, this operation is typically achieved by a specific type of operator (a comparator) that compares two operand data and outputs a control datum. In the present system, however, this operation cannot work well because the template matching typically selects many operands at once and a comparator cannot choose an appropriate pair of operands for the judgment (Figure 2). The multiple selection of operands, which was at first devised to improve the performance of the system, destroys the computational capability of the system.
This is what the mathematics of mutation and selection is about. It is an optimization problem done in response to selection conditions. Single selection conditions, fairly easy to adapt (optimize) to, multiple selection conditions, much more difficult to adapt (optimize) to. This is why it is mathematically impossible for reptiles to evolve to birds (far too many optimization conditions). Even if you could describe the selection conditions which would cause such a transformation (which you can’t), there are far too many genes which have to be optimized for such a process to be mathematically possible. The only way to accelerate the evolutionary process significantly is to apply sequential selection pressures. Here is an example of how it is done in the laboratory.
https://archive.ugent.be/retrieve/3141/PhD+Thesis.pdf (https://archive.ugent.be/retrieve/3141/PhD+Thesis.pdf)
The random nature of in vitro evolution offers several advantages compared to the rational protein design approach. Most importantly, little prior information is required regarding the structure and function of the protein under selection. In fact, sequencing of the selected clones can broaden the understanding of wild type protein structure and function by highlighting new important residues and structural elements or by giving insight in the mutational tolerance of a protein (Spiller et al., 1999; Stoop et al., 2000; Rossenu et al., 2003). Furthermore, the method is relatively fast and allows for large functional progression if multiple selection and randomization rounds are performed. Its power is reflected in the possibility to combine different optimized traits in a single protein (Cherry et al., 1999; Coco et al., 2001), the isolation of multiple synergistic mutations (Cherry et al., 1999), novel folds (Lo Surdo et al., 2004), additional properties absent in the parent population (Campbell et al., 1997) and the selection of mutations that were unlikely to be predicted in advance (Moore & Arnold, 1996; Crameri et al., 1997).

[axon]

This is why it is mathematically impossible for reptiles to evolve to birds (far too many optimization conditions).
This made me laugh out loud, I'm going to use this as my quote of the week.

[axon]

I gather from browsing the thread you don't think that evolution is responsible for the diversity of life on Earth?

[kleinman]

This is why it is mathematically impossible for reptiles to evolve to birds (far too many optimization conditions).This made me laugh out loud, I'm going to use this as my quote of the week.
So let’s see how many of your axons are still having synapses, post an example of multiple selection pressures accelerating evolution.
I gather from browsing the thread you don't think that evolution is responsible for the diversity of life on Earth?
You evolutionists like to speculate and extrapolate the diversity you can obtain from mutations and recombination far beyond the limit which the mathematics and empirical data shows, so why not give us a single example of multiple selection pressures accelerating evolution. When you discover that you can’t find a single real example of this phenomenon, you start to understand why there are too many optimization (selection) conditions required to transform reptiles into birds. Neither mutation and selection nor recombination and selection can accomplish what you evolutionist allege, neither phenomenon works that way mathematically or empirically. Let’s see if your axon is connected to a cell body and you can provide some mathematical or empirical evidence to contradict what I have shown to make this an interesting discussion or are you just another evolutionist who can post smilies.

[axon]

So let’s see how many of your axons are still having synapses, post an example of multiple selection pressures accelerating evolution.
How do you define and measure "accelerating evolution"? And in the real world how do you count the number of selection pressures on an organism???

[kjkent1]

So let’s see how many of your axons are still having synapses, post an example of multiple selection pressures accelerating evolution.

You evolutionists like to speculate and extrapolate the diversity you can obtain from mutations and recombination far beyond the limit which the mathematics and empirical data shows, so why not give us a single example of multiple selection pressures accelerating evolution. When you discover that you can’t find a single real example of this phenomenon, you start to understand why there are too many optimization (selection) conditions required to transform reptiles into birds. Neither mutation and selection nor recombination and selection can accomplish what you evolutionist allege, neither phenomenon works that way mathematically or empirically. Let’s see if your axon is connected to a cell body and you can provide some mathematical or empirical evidence to contradict what I have shown to make this an interesting discussion or are you just another evolutionist who can post smilies.

Alan, the reason why everyone laughs is because of the ridiculousness of your assertions.

You set up a straw man that the only means of proving evolution is for your opponents to provide evidence of multiple selection pressures accelerating evolution.

However, none of your opponents find that such evidence is relevant to prove evolution, so there's no reason for anyone to provide it.

And, since you refuse to entertain any other evidence, there's nothing for any of us to do -- except roll our respective eyes and laugh.

Suppose that you have an environment with many selective pressures but one in particular, is of overwhelming character. Example: Antelopes need to run fast in order to survive attacks by predators. Whatever other pressures may exist, none is as profoundly important as running fast.

You treat all of the selective pressures found in nature as if they all have identical weight. This is like homeopathy. No credible scientist would seriously consider a claim that homeopathic remedies work. Similarly, no credible scientist would seriously consider selection for missing or spurious bindings as a direct means of an antelope avoiding an attack by a cheetah.

The presence of the cheetah requires that its prey either evolve in a hurry to run fast or die out. In many cases in evolutionary history, extinction has been the result of such overwhelming selective pressure. However, the antelope survives, and the only real world possibility for this fact is because it gained a mutation or mutations in the face of its predator which permitted that survival.

Of course, you can always argue that God created the cheetah and the antelope. But, that's not very scientific.

You are fixated on a ridiculous point. Multiple selective pressures are no impediment to evolution, except where selection is so intense that it leads to extinction. The fact that multiple selection pressures of great weight, such as those present in your cited examples, may slow evolution in some instances, does not prevent the occurrance of a mutation, which is, by definition random and unpredictable, in othe instances where there is one overwhelming selective pressure at work.

[kleinman]

So let’s see how many of your axons are still having synapses, post an example of multiple selection pressures accelerating evolution.How do you define and measure "accelerating evolution"? And in the real world how do you count the number of selection pressures on an organism???
It’s simple axon; it is the number of mutation/selection cycles needed to adapt to the selection pressures. If you read this thread carefully, you will find out that it is much easier for a population to adapt to a single selection pressure. What that means is that it takes fewer mutation/selection cycles to evolve to that pressure. However if you have two selection (optimization) conditions, it takes far more mutation/selection cycles to evolve to those two selection conditions simultaneously than if the population is subjected to the same selection conditions sequentially. Combined concurrent selection pressures profoundly slow the evolutionary process, that is how mutation and selection works.
You evolutionists like to speculate and extrapolate the diversity you can obtain from mutations and recombination far beyond the limit which the mathematics and empirical data shows, so why not give us a single example of multiple selection pressures accelerating evolution. When you discover that you can’t find a single real example of this phenomenon, you start to understand why there are too many optimization (selection) conditions required to transform reptiles into birds. Neither mutation and selection nor recombination and selection can accomplish what you evolutionist allege, neither phenomenon works that way mathematically or empirically. Let’s see if your axon is connected to a cell body and you can provide some mathematical or empirical evidence to contradict what I have shown to make this an interesting discussion or are you just another evolutionist who can post smilies.Alan, the reason why everyone laughs is because of the ridiculousness of your assertions.
I think your sting cheese theory of evolution defines the ridiculousness of assertions. At least my assertions have a mathematical and empirical foundation.
You set up a straw man that the only means of proving evolution is for your opponents to provide evidence of multiple selection pressures accelerating evolution.
The only thing made of straw in this discussion is the theory of evolution and it is being blown away by the mathematical and empirical facts of how mutation and selection actually works. What’s the score now, hundreds of citations which show that combined selection pressures profoundly slow evolution to zero citations which show that combined selection pressures accelerate evolution, and you try to make points with the your old straw man argument. You definitely need a new playbook as well as some mathematics and empirical evidence to support your dead theory.
However, none of your opponents find that such evidence is relevant to prove evolution, so there's no reason for anyone to provide it.
Now there’s a sound scientific approach for your theory, deny the mathematical and empirical evidence. You really know how to prove your theory.
And, since you refuse to entertain any other evidence, there's nothing for any of us to do -- except roll our respective eyes and laugh.
What other evidence of mutation and selection have you provided, your nylon digesting bacteria which you can’t define the selection pressures, joobz’s Madagascar rain forest, Lucifuge Rofocale’s fish story which lays an egg or perhaps your string cheese theory of evolution? I have and will continue to post precise mathematical and empirical citations of how mutation and selection actually works and that is combined selection pressures profoundly slow evolution while you whine “irrelevant” and “straw man” and we’ll all wait for you to post mathematical or empirical evidence which shows otherwise.
Suppose that you have an environment with many selective pressures but one in particular, is of overwhelming character. Example: Antelopes need to run fast in order to survive attacks by predators. Whatever other pressures may exist, none is as profoundly important as running fast.
Ok, let’s listen to your supposition.
You treat all of the selective pressures found in nature as if they all have identical weight. This is like homeopathy. No credible scientist would seriously consider a claim that homeopathic remedies work. Similarly, no credible scientist would seriously consider selection for missing or spurious bindings as a direct means of an antelope avoiding an attack by a cheetah.
Really, I treat all selection pressures as if they have equal weight? When did I do this? Anyway, let’s read on.
The presence of the cheetah requires that its prey either evolve in a hurry to run fast or die out. In many cases in evolutionary history, extinction has been the result of such overwhelming selective pressure. However, the antelope survives, and the only real world possibility for this fact is because it gained a mutation or mutations in the face of its predator which permitted that survival.
Kjkent1, if you think that faster antelopes are going to evolve by mutation and selection due to cheetahs chasing them, you really haven’t learn much in these discussions of evolution. What will happen with these antelopes is that their population will evolve by recombination and selection. The survivors with longer legs and stronger muscles will breed with other survivors with longer legs and stronger muscles giving offspring with even better running capabilities and endurance. Mutation and selection is far too slow a process to help antelopes evolve to this kind of selection pressure.
Of course, you can always argue that God created the cheetah and the antelope. But, that's not very scientific.
Hey kjkent1, it is your theory which is mathematically and empirically impossible, you are the one who has abandoned the scientific method.
You are fixated on a ridiculous point. Multiple selective pressures are no impediment to evolution, except where selection is so intense that it leads to extinction. The fact that multiple selection pressures of great weight, such as those present in your cited examples, may slow evolution in some instances, does not prevent the occurrance of a mutation, which is, by definition random and unpredictable, in othe instances where there is one overwhelming selective pressure at work.
That ridiculous point that you are talking about is the core principle of the theory of evolution by mutation and selection. You can’t describe selection pressures that would accomplish the huge transformations required by your theory and every example of combined selection pressures show that it profoundly slows the evolution process when it doesn’t cause extinction. This is why combination therapy is used to treat HIV, TB, Malaria, cancer… What is ridiculous is that you evolutionists are in denial of this mathematical and empirical fact. Somewhere in your unscientific imaginations you see combined selection pressures somehow cooperating to transform reptiles into birds. The only problem with this fantasy trip is that you have no mathematical or empirical evidence to back this up. You do have plenty of speculation, extrapolation and denial to back up your theory.

[jimbob]

As a sometime lurker in this thread, could you clear up a question for me?

Kleinman, Are you saying that evolution stops if there are multiple selection pressures even when these are not sufficient to render the population extinct?

[kleinman]

Kleinman, Are you saying that evolution stops if there are multiple selection pressures even when these are not sufficient to render the population extinct?
No, what I am saying is that when you have multiple selection pressures, the mutation/selection process becomes so profoundly slow that you can’t achieve the massive genetic transformations required for macroevolution. Consider what happens to HIV when the virus is subjected to three selection pressures simultaneously versus these selection pressures being applied sequentially. In the former instance it takes years for the virus to evolve resistance, in the later case it occurs in weeks. This type of behavior is demonstrated mathematically with ev and numerous other models of mutation and selection in which the population can not go extinct yet the population is subjected to multiple selection pressures simultaneously.

These combined selection pressures interfere with the population’s ability to locate a new fitness optimum on the fitness landscape. Each selection pressure is pushing the population’s trajectory on the fitness landscape in its own best direction interfering with finding any local optimum for any of the selection conditions. This effect is demonstrated very nicely with joobz example:
http://www.pnas.org/cgi/content/full/104/34/13711 (http://www.pnas.org/cgi/content/full/104/34/13711)
http://www.pnas.org/content/vol104/issue34/images/medium/zpq0310771490005.gif
Fig. 5. A schematic view of fitness landscapes and evolution under fixed goal and MVG. (a) A typical trajectory under fixed goal evolution. The population tends to spend long periods on local maxima or plateaus. (b) A typical trajectory under MVG. Dashed arrows represent goal switches. An effectively continuous positive gradient on the alternating fitness landscapes leads to an area where global maxima exist in close proximity for both goals.
The top image shows the trajectory that the population takes on the fitness landscape to get to the global optimum for goal 1. The second and third images show the trajectory the population takes when the goals are switched back and forth from goals 1 and 2. The bottom image shows the trajectory the population takes to achieve both goals sequentially. Now if goals 1 and 2 are applied simultaneously, you have two different selection conditions pushing the population on two different trajectories. Selection condition 1 is trying to push the population to the global optimum 1 and selection condition 2 is trying to push the population to global optimum 2. A step that would be advantageous for one condition is disadvantageous for the other condition which confounds both selection conditions in their search for their new optimums. This is why combined selection pressures confound the evolutionary process and makes the mutation selection process mathematically impossible to accomplish macroevolutionary changes even when the selection pressures do not cause extinction.

[oponol]

Kleinman it appears to me that you are talking about the difficultly of reaching global optima, but species aren't at global optima they are stuck at local optima as we would expect

[kleinman]

Kleinman it appears to me that you are talking about the difficultly of reaching global optima, but species aren't at global optima they are stuck at local optima as we would expect.
Not at all, take the example of treatment of HIV. Monotherapy of this virus allow for a very rapid evolution of the virus population to a new local optimum. Combination therapy interferes with virus population achieving that local optimum or the local optima for the other selection pressures. Each selection pressure is trying to drive the population on a trajectory to its own local optimum on the fitness landscape to satisfy that selection condition. That’s what I am illustrating using the figure in my previous post.

[oponol]

Not at all, take the example of treatment of HIV. Monotherapy of this virus allow for a very rapid evolution of the virus population to a new local optimum. Combination therapy interferes with virus population achieving that local optimum or the local optima for the other selection pressures. Each selection pressure is trying to drive the population on a trajectory to its own local optimum on the fitness landscape to satisfy that selection condition. That’s what I am illustrating using the figure in my previous post.

I can see what you mean, and that tug of war situation is true in some situations, but not in others. I believe the paper presents an ideal case where two seperate goals aid convergance on a solution rather than inhibit it.

[kjkent1]

It’s simple axon; it is the number of mutation/selection cycles needed to adapt to the selection pressures. If you read this thread carefully, you will find out that it is much easier for a population to adapt to a single selection pressure. What that means is that it takes fewer mutation/selection cycles to evolve to that pressure. However if you have two selection (optimization) conditions, it takes far more mutation/selection cycles to evolve to those two selection conditions simultaneously than if the population is subjected to the same selection conditions sequentially. Combined concurrent selection pressures profoundly slow the evolutionary process, that is how mutation and selection works.What you are failing to mention is that the mathematical model on which your entire conclusion relies, does not model anything other than point mutation and selection against missing and spurious bindings -- and that the model's author, Dr. Schneider, has expressly explained that this deficiency limits the model's ability to account for the other process which are required to explain evolution.
I think your sting cheese theory of evolution defines the ridiculousness of assertions. At least my assertions have a mathematical and empirical foundation.I don't appreciate this particular misrepresentation. String theory as applies to evolution, is the work of Dr. Leonard Susskind, Felix Boch Professor of Physics at Stanford University. If you find the theory ridiculous, you should discuss your concerns with Lenny.
The only thing made of straw in this discussion is the theory of evolution and it is being blown away by the mathematical and empirical facts of how mutation and selection actually works. What’s the score now, hundreds of citations which show that combined selection pressures profoundly slow evolution to zero citations which show that combined selection pressures accelerate evolution, and you try to make points with the your old straw man argument. You definitely need a new playbook as well as some mathematics and empirical evidence to support your dead theory.The score is evolution is a fact, and you don't know what you're talking about, because precisely none of your examples demonstrate anything other than that extremely toxic conditions can kill a target population before it has an opportunity to mutate.
However, your examples routinely do evolve resistance, regardless of the amount of toxins imposed upon them, and this falsifies your conclusion directly.
Now there’s a sound scientific approach for your theory, deny the mathematical and empirical evidence. You really know how to prove your theory.I'll repeat it so you don't miss it: you haven't produced any evidence to support your position, so there's nothing to deny.
What other evidence of mutation and selection have you provided, your nylon digesting bacteria which you can’t define the selection pressures, joobz’s Madagascar rain forest, Lucifuge Rofocale’s fish story which lays an egg or perhaps your string cheese theory of evolution? I have and will continue to post precise mathematical and empirical citations of how mutation and selection actually works and that is combined selection pressures profoundly slow evolution while you whine “irrelevant” and “straw man” and we’ll all wait for you to post mathematical or empirical evidence which shows otherwise.So, you admit that you have been presented with examples that you cannot explain, and which you choose to denigrate via an argument by incredulity, rather than by logical argumentation.
Really, I treat all selection pressures as if they have equal weight? When did I do this? Anyway, let’s read on.Yes, you do, because if you didn't, you would be unable to maintain that multiple selection pressures always slow and ultimately stop evolution. Obviously, were one selection pressure so overwhelming that it rendered all others in the instant environment meaningless by comparison, that would permit rapid evolution which you claim is impossible. Therefore you MUST treat all selection pressures as equal -- or at least signficant with respect to a target organism.

Kjkent1, if you think that faster antelopes are going to evolve by mutation and selection due to cheetahs chasing them, you really haven’t learn much in these discussions of evolution. What will happen with these antelopes is that their population will evolve by recombination and selection. The survivors with longer legs and stronger muscles will breed with other survivors with longer legs and stronger muscles giving offspring with even better running capabilities and endurance. Mutation and selection is far too slow a process to help antelopes evolve to this kind of selection pressure.You mean that because you say so, that antelopes cannot mutate to run faster, they can only recombine. Not because you have any actual evidence to support your conclusion.
Once again, you choose to ignore any evidence which is not compatible with your conclusion. You insert recombination as the only possible selective force, not because you have any supporting evidence, but only because you require this to be true in order to support your conclusion. This is the height of arrogance, and non-science.

Hey kjkent1, it is your theory which is mathematically and empirically impossible, you are the one who has abandoned the scientific method.Because you say so, not because you have a shred of proof.Hubris to the extreme! When you go to the store, if they don't have milk, do you probably declare it non-existent throughout the known universe. ROFLMAO!

That ridiculous point that you are talking about is the core principle of the theory of evolution by mutation and selection. You can’t describe selection pressures that would accomplish the huge transformations required by your theory and every example of combined selection pressures show that it profoundly slows the evolution process when it doesn’t cause extinction. This is why combination therapy is used to treat HIV, TB, Malaria, cancer… What is ridiculous is that you evolutionists are in denial of this mathematical and empirical fact. Somewhere in your unscientific imaginations you see combined selection pressures somehow cooperating to transform reptiles into birds. The only problem with this fantasy trip is that you have no mathematical or empirical evidence to back this up. You do have plenty of speculation, extrapolation and denial to back up your theory.Sorry, but selection pressures are not required to cause mutations. Mutations occur on their own. And, if a mutation is beneficial to an organism in the instant environment, it sticks, and then random point mutation and selection for missing and spurious bindings causes the resulting genome to converge Rseq ~ Rfreq over time -- until the next major mutation event occurs.

[kleinman]

Not at all, take the example of treatment of HIV. Monotherapy of this virus allow for a very rapid evolution of the virus population to a new local optimum. Combination therapy interferes with virus population achieving that local optimum or the local optima for the other selection pressures. Each selection pressure is trying to drive the population on a trajectory to its own local optimum on the fitness landscape to satisfy that selection condition. That’s what I am illustrating using the figure in my previous post.I can see what you mean, and that tug of war situation is true in some situations, but not in others. I believe the paper presents an ideal case where two seperate goals aid convergance on a solution rather than inhibit it.
Simple enough oponol, give us an example where two separate goals aid convergence on a solution. You can make that a mathematical example or an empirical example. So far no evolutionist has been able to produce such an example. On the other hand, I have posted hundreds of citations which show that combination selection pressures profoundly slow evolution from numerous scientific fields including both mathematical and empirical examples.
It’s simple axon; it is the number of mutation/selection cycles needed to adapt to the selection pressures. If you read this thread carefully, you will find out that it is much easier for a population to adapt to a single selection pressure. What that means is that it takes fewer mutation/selection cycles to evolve to that pressure. However if you have two selection (optimization) conditions, it takes far more mutation/selection cycles to evolve to those two selection conditions simultaneously than if the population is subjected to the same selection conditions sequentially. Combined concurrent selection pressures profoundly slow the evolutionary process, that is how mutation and selection works.What you are failing to mention is that the mathematical model on which your entire conclusion relies, does not model anything other than point mutation and selection against missing and spurious bindings -- and that the model's author, Dr. Schneider, has expressly explained that this deficiency limits the model's ability to account for the other process which are required to explain evolution.
What you fail to mention is that the empirical examples I have posted are not limited to random point mutations yet they still exhibit the same behavior which ev demonstrates. In addition, I have posted citations of other mathematical models which also demonstrate the same behavior. Why don’t you other mechanisms of mutations to ev and show us that it changes the finding that combination selection pressures slow evolution?
I think your sting cheese theory of evolution defines the ridiculousness of assertions. At least my assertions have a mathematical and empirical foundation.I don't appreciate this particular misrepresentation. String theory as applies to evolution, is the work of Dr. Leonard Susskind, Felix Boch Professor of Physics at Stanford University. If you find the theory ridiculous, you should discuss your concerns with Lenny.
Too bad string theory doesn’t explain how mutation and selection actually works while ev does.
The only thing made of straw in this discussion is the theory of evolution and it is being blown away by the mathematical and empirical facts of how mutation and selection actually works. What’s the score now, hundreds of citations which show that combined selection pressures profoundly slow evolution to zero citations which show that combined selection pressures accelerate evolution, and you try to make points with the your old straw man argument. You definitely need a new playbook as well as some mathematics and empirical evidence to support your dead theory.The score is evolution is a fact, and you don't know what you're talking about, because precisely none of your examples demonstrate anything other than that extremely toxic conditions can kill a target population before it has an opportunity to mutate.
However, your examples routinely do evolve resistance, regardless of the amount of toxins imposed upon them, and this falsifies your conclusion directly.
Microevolution is fact; the evolutionist extrapolation of microevolution to the evolution of birds from reptiles is fiction. In case you weren’t aware of this fact, HIV is not killed by any of the treatments available at this time. This example demonstrates precisely how mutation and selection works and that is that combination selection pressures profoundly slow evolution. That the fact how mutation and selection actually works and how you can achieve microevolution.
Now there’s a sound scientific approach for your theory, deny the mathematical and empirical evidence. You really know how to prove your theory.I'll repeat it so you don't miss it: you haven't produced any evidence to support your position, so there's nothing to deny.
I know, your string cheese theory explains everything about evolution. According to you there are 10^500 alternative universes. Hundreds of real examples of mutation and selection which show that combination selection pressures profoundly slow evolution have no validity in whatever universe you happen to be in right now.
What other evidence of mutation and selection have you provided, your nylon digesting bacteria which you can’t define the selection pressures, joobz’s Madagascar rain forest, Lucifuge Rofocale’s fish story which lays an egg or perhaps your string cheese theory of evolution? I have and will continue to post precise mathematical and empirical citations of how mutation and selection actually works and that is combined selection pressures profoundly slow evolution while you whine “irrelevant” and “straw man” and we’ll all wait for you to post mathematical or empirical evidence which shows otherwise.So, you admit that you have been presented with examples that you cannot explain, and which you choose to denigrate via an argument by incredulity, rather than by logical argumentation.
Examples which you can’t identify the selection pressures or the target genes to those selection pressures. The theory of evolution only looks reasonable when you apply these types of vague analysis. When you apply mathematical precision to the theory of evolution, it is a flop.
Really, I treat all selection pressures as if they have equal weight? When did I do this? Anyway, let’s read on.Yes, you do, because if you didn't, you would be unable to maintain that multiple selection pressures always slow and ultimately stop evolution. Obviously, were one selection pressure so overwhelming that it rendered all others in the instant environment meaningless by comparison, that would permit rapid evolution which you claim is impossible. Therefore you MUST treat all selection pressures as equal -- or at least signficant with respect to a target organism.
I don’t treat selection pressures one way or the other. All I have done on this thread and the Evolutionisdead forum is reported the results of ev and posted citations which demonstrate these results. Are you implying that I have control over the magnitude of selection pressures in all these citations I have posted? Anyway, if you think that the intensity of selection pressures makes a difference in the finding that multiple selection pressures profoundly slow evolution, give us an example of you hypothesis.
Kjkent1, if you think that faster antelopes are going to evolve by mutation and selection due to cheetahs chasing them, you really haven’t learn much in these discussions of evolution. What will happen with these antelopes is that their population will evolve by recombination and selection. The survivors with longer legs and stronger muscles will breed with other survivors with longer legs and stronger muscles giving offspring with even better running capabilities and endurance. Mutation and selection is far too slow a process to help antelopes evolve to this kind of selection pressure.You mean that because you say so, that antelopes cannot mutate to run faster, they can only recombine. Not because you have any actual evidence to support your conclusion.
Once again, you choose to ignore any evidence which is not compatible with your conclusion. You insert recombination as the only possible selective force, not because you have any supporting evidence, but only because you require this to be true in order to support your conclusion. This is the height of arrogance, and non-science.
There is plenty of evidence that recombination and natural selection is a much faster process than mutation and selection. If you think mutation and selection is a rapid mechanism for adaptation for you antelope example, tell us what the selection pressures are and the target genes to those pressures and explain why the antelopes don’t grow wings?
Hey kjkent1, it is your theory which is mathematically and empirically impossible, you are the one who has abandoned the scientific method.Because you say so, not because you have a shred of proof.Hubris to the extreme! When you go to the store, if they don't have milk, do you probably declare it non-existent throughout the known universe. ROFLMAO!
Not because I say so, it is the huge number of mathematical and empirical examples which I have posted, all which show that combination selection pressures profoundly slow evolution. This is why combination therapy is used to treat HIV, TB, Malaria, cancer,… Of course you evolutionists know of the existence of secret selection pressures which cooperate to evolve reptiles into birds.
That ridiculous point that you are talking about is the core principle of the theory of evolution by mutation and selection. You can’t describe selection pressures that would accomplish the huge transformations required by your theory and every example of combined selection pressures show that it profoundly slows the evolution process when it doesn’t cause extinction. This is why combination therapy is used to treat HIV, TB, Malaria, cancer… What is ridiculous is that you evolutionists are in denial of this mathematical and empirical fact. Somewhere in your unscientific imaginations you see combined selection pressures somehow cooperating to transform reptiles into birds. The only problem with this fantasy trip is that you have no mathematical or empirical evidence to back this up. You do have plenty of speculation, extrapolation and denial to back up your theory.Sorry, but selection pressures are not required to cause mutations. Mutations occur on their own. And, if a mutation is beneficial to an organism in the instant environment, it sticks, and then random point mutation and selection for missing and spurious bindings causes the resulting genome to converge Rseq ~ Rfreq over time -- until the next major mutation event occurs.
Without selection pressures, you can not increase the frequency of a particular mutation in the gene pool. That’s the point of this debate kjkent1, how rapidly can you increase the frequency of beneficial mutations in the gene pool. It turns out that when there are combination selection pressures, it is a profoundly slow process.

[axon]

It’s simple axon; it is the number of mutation/selection cycles needed to adapt to the selection pressures. If you read this thread carefully, you will find out that it is much easier for a population to adapt to a single selection pressure. What that means is that it takes fewer mutation/selection cycles to evolve to that pressure. However if you have two selection (optimization) conditions, it takes far more mutation/selection cycles to evolve to those two selection conditions simultaneously than if the population is subjected to the same selection conditions sequentially. Combined concurrent selection pressures profoundly slow the evolutionary process, that is how mutation and selection works.
Ah I think I see where the problem is. How in the real world to you quantize "selection pressures" into discrete independent packages? (Or if not independent how do you measure thier interdependence?). I would suggest that you can't. Also what is optimization? How do you know when something is optimized?

Another point (which may have already been covered) is how do you assign realistic weights to the contribution of different types of "mutation" to optimization, e.g point mutation, intron insertion, genome fusing etc.

[cyborg]

Another point (which may have already been covered) is how do you assign realistic weights to the contribution of different types of "mutation" to optimization, e.g point mutation, intron insertion, genome fusing etc.

Well, kleinman's method is to fiddle the numbers until he gets the outcome he is looking for.

Which when we reject as valid he of course takes as proof that we are evil heathen bastards.

[axon]

Just out of interest kleinman, as you don't think birds evolved from reptiles, have you ever considered how birds came to be here?

[cyborg]

have you ever considered about how birds came to be here?

He'll refer you to a copy of the Bible for that answer.

[Paul C. Anagnostopoulos]

Paul, no transcription factors evolved, what ev demonstrates is how slow three selection conditions evolve simultaneously on all but the tiniest genomes.
And you're claiming that there never were small genomes, right?


It’s gravity Paul. Now if you want to make an analogy to evolution, put sun light on water, it evaporates some of the water and the elevation of those evaporated water molecules increases. Now you put energy, mutation and selection into molecules and what can you accomplish? Not nearly what you evolutionists assert. Your own mathematics shows how little can be accomplished with mutation and selection and the empirical data substantiates this.
This is a load of gibberish. Does gravity have a goal?

~~ Paul

[kleinman]

It’s simple axon; it is the number of mutation/selection cycles needed to adapt to the selection pressures. If you read this thread carefully, you will find out that it is much easier for a population to adapt to a single selection pressure. What that means is that it takes fewer mutation/selection cycles to evolve to that pressure. However if you have two selection (optimization) conditions, it takes far more mutation/selection cycles to evolve to those two selection conditions simultaneously than if the population is subjected to the same selection conditions sequentially. Combined concurrent selection pressures profoundly slow the evolutionary process, that is how mutation and selection works.Ah I think I see where the problem is. How in the real world to you quantize "selection pressures" into discrete independent packages? (Or if not independent how do you measure thier interdependence?). I would suggest that you can't. Also what is optimization? How do you know when something is optimized?
Axon, you need to enter 21st century science. We use selection pressures targeted to specific genes all the time. The targets for these selection pressures are not only identified, the specific mutations required for adaptation to these selection pressures are often identified. You may better know these selection pressures by names such as antibiotic, antiviral agents, pesticides, herbicides,… These selection pressures are “quantized” by the number of mutations required to evolve resistance, the intensity the selection pressure impairs the fitness of the population to reproduce and other factors. Some selection pressures target more than a single gene for example disinfectants such as bleach or iodine binds to numerous different biological molecules denaturing large numbers of enzymes simultaneously. These types of selection pressures are extremely difficult for populations to adapt to and resistance to these types of materials are virtually non-existent.

How do you know when something is optimized? There are two ways of knowing this. In the mathematical sense an optimum is located when the slope of the curve goes to zero. From an empirical sense, a local optimum is attained when a population becomes resistant to a selection pressure.

Axon, now that you have an explanation of these principles, do you want to give us an example where multiple selection pressures accelerate evolution?
Another point (which may have already been covered) is how do you assign realistic weights to the contribution of different types of "mutation" to optimization, e.g point mutation, intron insertion, genome fusing etc.
It appears these different types of mutation and recombination do not overcome the affect that multiple selection pressures profoundly slow the evolutionary process. The evolution of HIV demonstrates this. HIV does a wide variety of mutations such as point mutations, insertion/deletions, as well as recombination and despite this; combination selection pressures profoundly slow the evolution of this short genome population with very rapid generation times and huge populations. Note that Dr Schneider’s ev model does not allow for extinction yet evolution by the mutation/selection process becomes profoundly slow on all but the tiniest genomes when all three selection conditions are applied. However, if you only use one of the three selection pressures in the model, the simulation can quickly optimize that single selection condition, even with tiny populations. It is not the weights of the selection pressures or the types of mutations which drives the mathematics of mutation and selection; it is the number of selection conditions which dominates this phenomenon.
Another point (which may have already been covered) is how do you assign realistic weights to the contribution of different types of "mutation" to optimization, e.g point mutation, intron insertion, genome fusing etc.Well, kleinman's method is to fiddle the numbers until he gets the outcome he is looking for.
Fiddle the numbers any way you want and cherry pick your citations and give us anything that contradicts my hypothesis that multiple selection pressures profoundly slows the evolutionary process by mutation and selection. So far cyborg, the only thing you have provided us is “cruft”.
Just out of interest kleinman, as you don't think birds evolved from reptiles, have you ever considered how birds came to be here?
Yes I have but it is outside the topic of discussion here. Right now we are talking about the mathematics of mutation and selection and the empirical data which demonstrates this mathematics. So far, the mathematics and empirical data shows that birds can not evolve from reptiles by mutation and selection, it is mathematically impossible because the process is far too slow. The reason why this process is so slow is that combination selection pressures profoundly slow the evolutionary process.
Paul, no transcription factors evolved, what ev demonstrates is how slow three selection conditions evolve simultaneously on all but the tiniest genomes.And you're claiming that there never were small genomes, right?
Whenever you are ready to post your evidence, we are ready to listen but so far you have posted zilch. It seems that zilch is the word to describe the evidence that evolutionists have for their argument that mutation/selection created life. All the mathematical (including your own computer simulation) and empirical evidence says something entirely different about the mutation/selection process. It is profoundly slow for all but single selection conditions, but feel free to deny these mathematical and empirical facts of how mutation and selection actually works.
It’s gravity Paul. Now if you want to make an analogy to evolution, put sun light on water, it evaporates some of the water and the elevation of those evaporated water molecules increases. Now you put energy, mutation and selection into molecules and what can you accomplish? Not nearly what you evolutionists assert. Your own mathematics shows how little can be accomplished with mutation and selection and the empirical data substantiates this.is is a load of gibberish. Does gravity have a goal?
Paul, gravity is a force and there are consequences to this force. It is a causative factor that leads to effects just as a selection pressure is a causative factor that leads to effects. When you properly model these causative factors for a system, you can predict the effects. Your own computer simulation has done this for mutation and selection and it shows how profoundly slow this process is due to the combined selection pressures.

Now if you want an example of gibberish, read your own description of Rcapacity. What you fail to recognize is that despite the length of the genome such that Rf > 2 * site width, the model does start to converge but reaches a local optimum before the selection conditions can converge.

Since you deny the results of your own model, let’s see if an empirical example will convince you of how mutation and selection actually works.
http://cottoninfo.ucdavis.edu/IMAGES/CCRVol72.pdf (http://cottoninfo.ucdavis.edu/IMAGES/CCRVol72.pdf)
Final Insect Management Considerations—2004: Non-pyrethroid and combinations. Useful during Situation II when an adult invasion is not overwhelming but gradual. Both Centric and Assail (chloronicotinyls or neonicotinoids) have shown promise in reducing adult populations prior to cutout. There is some concern about the efficacy of products that require translaminar action after leaves have begun to “harden off” In addition, these products may have already been used once and the concern for serious insecticide resistance management looms. Other choices are limited but include Lorsban combined with endosulfan (Thiodan/Thionex).
and
Pyrethroid combinations. These are useful options when a large migrating adult population (Situation III) occurs, especially near defoliation. While knockdown is good, residual control is limited. When combined with an organophosphate, a synergism occurs that enhances control. This approach can be applied right at defoliation using DEF or using other defoliants when products such as Orthene or other organo-phosphate insecticides are included.
Aphids and Whitefly. Making decisions when both pests are present requires evaluation of the most threatening insect. Combination treatments will likely be needed. Keep in mind that use of pyrethroid combinations for whitefly control will likely flare aphids, if present. If whitefly adults were of primary concern, Lorsban/Thiodan would also help re-duce aphid
How about another example from the field of oncology since your co-worker Dr Schneider works at the National Cancer Institute.
http://www.dissectmedicine.com/resistance (http://www.dissectmedicine.com/resistance)
"Long-term endocrine therapy with either aromatase inhibitors (AIs) or tamoxifen may lead to endocrine resistance and disease progression. Recent years have seen advances in our understanding of the complex biological mechanisms associated with resistance. Growth factor signaling pathways appear to be upregulated in hormone-resistant tumours and interact with oestrogen-receptor (ER) signaling, which remains functional even after long-term endocrine deprivation. Signaling through the human epidermal and insulin-like growth-factor receptor (HER and IGFR, respectively) pathways may promote ligand-independent ER gene transcription and stimulate growth factor signaling. Therapeutic agents that inhibit these signal transduction pathways, when combined with AIs, may offer breast cancer patients new hope for more robust, longer-term remissions. Preliminary data from phase II studies of combination therapies are encouraging. There is a large programme of ongoing randomised, controlled trials, the results of which should pave the way for integrating combination therapies into clinical practice. To identify which patients will respond best to particular combinations of treatments, biomarkers and gene expression profiles are being investigated as predictors of sensitivity or resistance. In time, breast cancer treatment will become truly individualised because physicians will be able to match patients with a variety of disease phenotypes to optimal combination therapies." British Journal of Cancer (2006) 95, 661-666.
Paul, that’s how mutation and selection actually works, your own program shows it and the empirical evidence shows it, combination selection pressures profoundly slows evolution.

[axon]

These selection pressures are “quantized” by the number of mutations required to evolve resistance, the intensity the selection pressure impairs the fitness of the population to reproduce and other factors.
But resistance is not an all or nothing property. Take antibiotics, there could be a million mutations that will confer resistance; they would involve such things are increasing the speed of breaking down the antibiotic, decreasing the rate of uptake, mutations that enable the bacteria to live in environments that do not have antibiotics etc. It seems difficult to pin down a selection pressure that only acts on one mutation site/enzyme/metabolic pathway, as opposed to the whole organism.
Some selection pressures target more than a single gene for example disinfectants such as bleach or iodine binds to numerous different biological molecules denaturing large numbers of enzymes simultaneously. These types of selection pressures are extremely difficult for populations to adapt to and resistance to these types of materials are virtually non-existent.
Rubbish. How about the selection pressure of a lion eating a gazelle? The selection pressure targets all the enzymes at once, and somehow some gazelles manage to survive the "being eaten by lion selection pressure". You seem to be suggesting that their cannot be evolution if it involves a selection pressure (which is an diffuse concept anyway) acting on multiple "sites of mutation" targets.
How do you know when something is optimized? There are two ways of knowing this. In the mathematical sense an optimum is located when the slope of the curve goes to zero. From an empirical sense, a local optimum is attained when a population becomes resistant to a selection pressure.
I get mathematical optimization, (I'm actually doing some in the background right now!), but in life the environmental conditions are constantly changing. Thus, if you lived in a completely static universe you could (somehow) evolve and reach an optimum for those conditions. But in real life as you are optimizing to selection pressures the selection pressures them selves are changing.

Axon, now that you have an explanation of these principles, do you want to give us an example where multiple selection pressures accelerate evolution?
Not yet. You've said on several occasions that it is mathematically impossible for reptiles to evolve into birds. I'm interested how you quantify mathematically a reptile, and a bird. In other words what (of the top of your head) animals could mathematically evolve from another?

[axon]

Yes I have but it is outside the topic of discussion here.
Well other than evolution the other 2 usual sources for variety of life on Earth people believe are god and panspermia. Which of these is it (or a new third option)? Whatever your answer I more than willing to continue discussing selection pressures and what not.

[kleinman]

These selection pressures are “quantized” by the number of mutations required to evolve resistance, the intensity the selection pressure impairs the fitness of the population to reproduce and other factors.But resistance is not an all or nothing property. Take antibiotics, there could be a million mutations that will confer resistance; they would involve such things are increasing the speed of breaking down the antibiotic, decreasing the rate of uptake, mutations that enable the bacteria to live in environments that do not have antibiotics etc. It seems difficult to pin down a selection pressure that only acts on one mutation site/enzyme/metabolic pathway, as opposed to the whole organism.
Axon, take a look at the literature for the evolution for HIV for example (I have posted many citations on this topic on this thread). Particular drugs lead to particular mutations at particular loci which in turn are used to identify if the population is resistant to that drug. This phenomenon is used to identify evolution of resistance to selection pressures in other cases as well including but not limited to bacteriology, parasitology, oncology, entomology, agriculture… Selection pressures lead to predictable increases in frequency of particular mutations in populations being subjected to these selection pressures.
Some selection pressures target more than a single gene for example disinfectants such as bleach or iodine binds to numerous different biological molecules denaturing large numbers of enzymes simultaneously. These types of selection pressures are extremely difficult for populations to adapt to and resistance to these types of materials are virtually non-existent.Rubbish. How about the selection pressure of a lion eating a gazelle? The selection pressure targets all the enzymes at once, and somehow some gazelles manage to survive the "being eaten by lion selection pressure". You seem to be suggesting that their cannot be evolution if it involves a selection pressure (which is an diffuse concept anyway) acting on multiple "sites of mutation" targets.
Really, do you want to give us an example of a life form that can survive in high concentrations of chlorine or iodine? This is why these substances are used as disinfectants.

You have no understanding what a selection pressure is when you state that a lion eating a gazelle targets all the genes at once. This is the type of vague mush that evolutionists must resort to in order to try and support their mushy theory. Ultimately, every selection pressure acts at the genetic level. Why don’t you tell us what mutations will increase in frequency in the population when a lion eats a gazelle?
How do you know when something is optimized? There are two ways of knowing this. In the mathematical sense an optimum is located when the slope of the curve goes to zero. From an empirical sense, a local optimum is attained when a population becomes resistant to a selection pressure.I get mathematical optimization, (I'm actually doing some in the background right now!), but in life the environmental conditions are constantly changing. Thus, if you lived in a completely static universe you could (somehow) evolve and reach an optimum for those conditions. But in real life as you are optimizing to selection pressures the selection pressures them selves are changing.
Again with the mush for your mushy theory, we have hard mathematical and empirical evidence how mutation and selection actually works. Evolution by mutation and selection is simply an optimization problem. These types of problems become profoundly slow to converge when you have more than a single optimization condition. If you continually change the optimization conditions nothing will ever reach a local optimum or evolve anything except under very controlled circumstances and that is not with combined selection pressures. But let’s see if you can get beyond your vague mush, give us a mathematical or empirical example which illustrates your contention how multiple selection pressures accelerate evolution and your lion/gazelle example doesn’t tell us what the selection pressure(s) is/are or what the target gene(s) is/are.
Axon, now that you have an explanation of these principles, do you want to give us an example where multiple selection pressures accelerate evolution?Not yet. You've said on several occasions that it is mathematically impossible for reptiles to evolve into birds. I'm interested how you quantify mathematically a reptile, and a bird. In other words what (of the top of your head) animals could mathematically evolve from another?
Axon, I realize this is a very long thread but this issue has been discussed previously. Let’s start with the huge variation between the size of bird and reptile genomes. Then you can start looking at individual genes which may have some similarity between the two life forms, and then you have to start accounting for these differences. Humans and chimpanzees supposedly descended from a common ancestor yet these two genomes have at least 150,000,000 base differences. You have only about 500,000 generations to account for these differences. The mathematics of mutation and selection shows that evolutionist accounting fails the audit.

We’ll be patient and wait for you to post an example of multiple selection pressures accelerating evolution, either mathematical or empirical but why do I think this wait will be eternal?
Yes I have but it is outside the topic of discussion here.Well other than evolution the other 2 usual sources for variety of life on Earth people believe are god and panspermia. Which of these is it (or a new third option)? Whatever your answer I more than willing to continue discussing selection pressures and what not.
Panspermia simply changes the site for creation or evolution. Either we were created or we spontaneously arose and evolve. In the later case, it is shown to be mathematical and empirically impossible.

[axon]

Axon, take a look at the literature for the evolution for HIV for example (I have posted many citations on this topic on this thread).
Could you do me a favour (as the thread is very long) and point me to a direct link or post with a citation that I can look up.

Really, do you want to give us an example of a life form that can survive in high concentrations of chlorine or iodine? This is why these substances are used as disinfectants.
You made the point that resistance to these substances hasn't evolved as they target many enzymes at once. The point I made is that predatory lions target many genes at once. Targetting many genes at once does not preclude evolution.

Why don’t you tell us what mutations will increase in frequency in the population when a lion eats a gazelle?[/SIZE][/FONT]
The mutations that aid gazelles in avoiding being eaten by lions will increase in frequency. And off the top of my head I don't have the genomes of gazelles from the last million years.
But let’s see if you can get beyond your vague mush, give us a mathematical or empirical example which illustrates your contention how multiple selection pressures accelerate evolution and your lion/gazelle example doesn’t tell us what the selection pressure(s) is/are or what the target gene(s) is/are.
Well, I have never contended that multiple selection pressures accelerate evolution. My point is that there is never a situation where there is a single selection pressure to compare with multiple selection pressures. But if you give me a link, I'll read up on it so we can discuss a specific example.

I realize this is a very long thread but this issue has been discussed previously. Let’s start with the huge variation between the size of bird and reptile genomes. Then you can start looking at individual genes which may have some similarity between the two life forms, and then you have to start accounting for these differences. Humans and chimpanzees supposedly descended from a common ancestor yet these two genomes have at least 150,000,000 base differences. You have only about 500,000 generations to account for these differences. The mathematics of mutation and selection shows that evolutionist accounting fails the audit
Well if the above numbers are correct, I'd say on average it'll be 300 base changes per generation. Doesn't seem like too many does it? I do know that I am genetically pretty different from my father, those could be the 300 bases!

Panspermia simply changes the site for creation or evolution. Either we were created or we spontaneously arose and evolve. In the later case, it is shown to be mathematical and empirically impossible.
Have you looked into the mathematical possibility of being created? :-)

[jimbob]

http://forums.randi.org/showthread.php?postid=2976447#post2976447

These combined selection pressures interfere with the population’s ability to locate a new fitness optimum on the fitness landscape. Each selection pressure is pushing the population’s trajectory on the fitness landscape in its own best direction interfering with finding any local optimum for any of the selection conditions. This effect is demonstrated very nicely with joobz example:

If it doesn't wipe out the entire population, then what you have here looks like a situation where speciation would occur.

[Paul C. Anagnostopoulos]

Whenever you are ready to post your evidence, we are ready to listen but so far you have posted zilch.
So you won't claim that there never were small genomes, yet you claim to have a proof that transcription factors can't evolve in genomes because they are too large.


Paul, gravity is a force and there are consequences to this force.
A consequence is not a goal.


Now if you want an example of gibberish, read your own description of Rcapacity. What you fail to recognize is that despite the length of the genome such that Rf > 2 * site width, the model does start to converge but reaches a local optimum before the selection conditions can converge.
Why does it reach that local optimum? It must be like trying to index a 1000-entry table with a 7-bit integer: It reaches a local optimum around entry number 128 and just can't get past there.

~~ Paul

[Paul C. Anagnostopoulos]

So Alan, how do you explain this data:

population 64
genome size 2048, Rfrequency = 7
sites 16
mutation 2/generation

weight/site width, Rcapacity, generations

8/9, 18, 15623
7/8, 16, 23063
6/7, 14, 30241
5/6, 12, 28625
4/5, 10, 30501
3/4, 8, 31814
2/3, 6, --- (still 16 mistakes after 120,000 generations)

Why the spike just as Rcapacity goes below Rfrequency?

~~ Paul

[oponol]

Simple enough oponol, give us an example where two separate goals aid convergence on a solution.You can make that a mathematical example or an empirical example.

The genome of each individual consists of a byte consisting of eight bits, least significant bit on the right. The phenotype is the integer value represented by that byte.

Goal A: selective pressure to reach 10001000 = 136

Problem is in many runs your population gets stuck at a local optimum like this:
01111111 = 127

Flipping any of those bits takes you further from goal A of 136 than you are already. In fact it would take the spontaneous flipping of the right 4 bits to get closer to the goal.

But if you have an additional goal B to reduce the number of 1s in the sequence, that provides pressure against going anywhere near a genome like 01111111 in the first place.

[kleinman]

Axon, take a look at the literature for the evolution for HIV for example (I have posted many citations on this topic on this thread).Could you do me a favour (as the thread is very long) and point me to a direct link or post with a citation that I can look up.
For those of you who complain that I repeat myself, I do this because axon has asked me to do so. Here are a few recent examples where it shows that combination therapy slows the evolution of HIV.
http://www.sciencemag.org/cgi/content/abstract/269/5224/696 (http://www.sciencemag.org/cgi/content/abstract/269/5224/696)
Combinations of antiretroviral drugs that prevent or delay the appearance of drug-resistant human immunodeficiency virus-type 1 (HIV-1) mutants are urgently required. Mutants resistant to 3'-azidothymidine (AZT, zidovudine) became phenotypically sensitive in vitro by mutation of residue 184 of viral reverse transcriptase to valine, which also induced resistance to (-)2'-deoxy-3'-thiacytidine (3TC). Furthermore, AZT-3TC coresistance was not observed during extensive in vitro selection with both drugs. In vivo AZT-3TC combination therapy resulted in a markedly greater decreased in serum HIV-1 RNA concentrations than treatment with AZT alone, even though valine-184 mutants rapidly emerged. Most samples assessed from the combination group remained AZT sensitive at 24 weeks of therapy, consistent with in vitro mutation studies.
http://www.annals.org/cgi/content/full/128/11/951 (http://www.annals.org/cgi/content/full/128/11/951)
First and foremost, it is critical to maximize the potency of therapy from the beginning. This can be done by choosing the most potent drugs possible, using them at their maximum tolerated doses, and using them in combination. The objective should be nothing short of maximal suppression of viral replication because the first attempt is likely to be the most successful.

Second, to maximize genetic barriers to resistance, drugs that require the virus to undergo multiple mutations to achieve resistance should be combined with the most efficacious agents in other therapeutic classes. Whenever possible, drugs should be from classes to which the patient is therapy-naive or should be as different from previously used drugs as possible.

Finally, these aggressive therapeutic regimens should be made as tolerable and user-friendly as possible (without compromising efficacy) to encourage long-term adherence and continued viral suppression.
http://www.aafp.org/afp/980600ap/maenza.html (http://www.aafp.org/afp/980600ap/maenza.html)
The primary goal of antiretroviral therapy for human immunodeficiency virus (HIV) infection is suppression of viral replication. Evidence indicates that the optimal way to achieve this goal is by initiating combination therapy with two or more antiretroviral agents. The agents now licensed in the United States for use in combination therapy include five nucleoside analog reverse transcriptase inhibitors (zidovudine, didanosine, zalcitabine, stavudine and lamivudine), two nonnucleoside reverse transcriptase inhibitors (delavirdine and nevirapine) and four protease inhibitors (saquinavir, ritonavir, indinavir and nelfinavir). Current recommendations suggest that antiretroviral therapy be considered in any patient with a viral load higher than 5,000 to 20,000 copies per mL, regardless of the CD4+ count. Selection of the combination regimen must take into account the patient's prior history of antiretroviral use, the side effects of these agents and drug­drug interactions that occur among these agents and with other drugs as well. Because of the potential for viral resistance, nonnucleoside reverse transcriptase inhibitors and protease inhibitors should only be used in combination therapy. Antiretroviral agents are rapidly being developed and approved, so physicians must make increasingly complex treatment decisions about medications with which they may be unfamiliar.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=24062 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=24062)
Exposure to 3TC of HIV-1 mutant strains containing non-nucleoside reverse transcriptase inhibitor (NNRTI)-specific mutations in their reverse transcriptase (RT) easily selected for double-mutant viruses that had acquired the characteristic 184-Ile mutation in their RT in addition to the NNRTI-specific mutations. Conversely, exposure of 3TC-resistant 184-Val mutant HIV-1 strains to nine different NNRTIs resulted in the rapid emergence of NNRTI-resistant virus strains at a time that was not more delayed than when wild-type HIV-1(IIIB) was exposed to the same compounds. The RTs of these resistant virus strains had acquired the NNRTI-characteristic mutations in addition to the preexisting 184-Val mutation. Surprisingly, when the 184-Ile mutant HIV-1 was exposed to a variety of NNRTIs, the 188-His mutation invariably occurred concomitantly with the 184-Ile mutation in the HIV-1 RT. Breakthrough of this double-mutant virus was markedly accelerated as compared with the mutant virus selected from the wild-type or 184-Val mutant HIV-1 strain. The double (184-Ile + 188-His) mutant virus showed a much more profound resistance profile against the NNRTIs than the 188-His HIV-1 mutant. In contrast with the sequential chemotherapy, concomitant combination treatment of HIV-1-infected cells with 3TC and a variety of NNRTIs resulted in a dramatic delay of virus breakthrough and resistance development.
And
Because the enormous virus replication dynamics and virus plasma load in vivo exceed by several orders of magnitude those present in cell culture experiments (18, 19), it is expected that the mutations that emerge during such an intensive virus replication may easily counteract any potentially decreased mutation rate resulting from the higher fidelity of the mutant RT. Moreover, if our observations on the accelerated breakthrough of 184-Ile mutant virus in the presence of NNRTIs can be extrapolated to man, it would seem contraindicated to successively use 3TC and NNRTIs. Such procedure (sequential therapy) may even precipitate virus breakthrough. Also, it has been shown that ratios of CCID50 to p24 are at least four times higher in culture fluids of peripheral blood mononuclear cell and MT-4 (5) or CEM cells (personal observations) infected by the 184-Val HIV-1 mutant than in cells infected with HIV-1/IIIB (wild type). One should therefore avoid giving the virus the opportunity to convert into a more infectious form upon treatment with 3TC as a single agent.
And
Because we found that 3TC is inhibitory to NNRTI-resistant HIV-1 strains, and, vice versa, NNRTIs efficiently inhibit 3TC-resistant viruses (10), the marked suppressive effect noted with the combination of 3TC and NNRTIs may be attributed to a complementary suppression of the NNRTI- and 3TC-specific resistance mutations by 3TC and NNRTIs, respectively. Instead of using 3TC and NNRTIs in sequential order, our studies indicate that 3TC should be simultaneously combined with the NNRTIs. This strategy should be aimed at delaying as long as possible the emergence of drug-resistant virus strains.
Let’s see what the scientists at the University of Chicago have to say about simultaneous versus sequential selection pressures.
http://www.medscape.com/viewarticle/521671_3 (http://www.medscape.com/viewarticle/521671_3)
A major goal of HAART is to suppress plasma HIV RNA below detectable levels by combining 3 or more antiretroviral agents from 1 or more classes. The use of agents from different classes lessens the development of resistance.[34] However, antiretroviral regimens containing drugs from more than 2 classes are not routinely recommended for patients who are treatment naive, because those in whom a 3-class regimen fails may become resistant to drugs in all 3 classes, leaving them with fewer options for subsequent therapy. A HAART regimen should have acceptable short- and long-term toxicity and must fit the patient's comorbidity profile and lifestyle.[35] Currently recommended initial HAART regimens specify the use of 2 NRTIs and either an NNRTI or a PI.[2]
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=7538547&dopt=AbstractPlus (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=7538547&dopt=AbstractPlus)
L-697,661 is a human immunodeficiency virus type 1 (HIV-1)-specific nonnucleoside reverse transcriptase (RT) inhibitor. Its tolerability and activity in combination with zidovudine were evaluated in a 48-week double-blind study. One hundred nineteen zidovudine-naive HIV-1-infected patients with CD4 cell counts of 200-500/mm3 received either combination therapy, L-697,661 alone, or zidovudine alone. Activity was assessed by CD4 cell count changes. Selection for L-697,661-resistant virus was monitored by susceptibility testing of RT expressed by circulating viral RNA. Therapy was generally well tolerated. All groups receiving zidovudine exhibited transient increases in CD4 cell counts, while the L-697,661 monotherapy group showed a significant decline and yielded RT > 100-fold resistant to L-697,661 and associated with substitutions at RT residue 181. The RT from patients receiving combination therapy was maximally 15-fold less susceptible to L-697,661. Hence, cotreatment with zidovudine prevents selection of HIV-1 variants that are highly resistant to L-697,661 in patients naive to both compounds.
Again, these examples demonstrate how mutation and selection actually works. Combined selection pressures slow the evolutionary process. Some day you dim bulbs of evolutionism may understand this mathematical and empirical fact.
You will find this evolutionary behavior reenacted on many stages. I have posted many citations concerning the evolution of the Malaria parasite which show that combination therapy again slows evolution, this effect is seen in oncology, bacteriology, agriculture (evolution of weeds subjected to herbicides), virology, pesticides (rodenticides, insecticides, fungicides) all delay the evolution of resistance when used in combinations, then there are the many mathematical models of mutation and selection cited including ev written by Dr Tom Schneider from the National Cancer Institute. All of these empirical and mathematical citations show that combination selection pressures slow the evolutionary process. If you understand that evolution by mutation and selection is simply an optimization or sorting problem of beneficial and detrimental mutation then the results from these citations is obvious when you have more than a single optimization or sorting condition. (PS, I have more citations which discuss the evolution of the HIV virus when subjected to combination therapy, I will post these citations again if you want.)
Really, do you want to give us an example of a life form that can survive in high concentrations of chlorine or iodine? This is why these substances are used as disinfectants.You made the point that resistance to these substances hasn't evolved as they target many enzymes at once. The point I made is that predatory lions target many genes at once. Targetting many genes at once does not preclude evolution.
The lion is not targeting every gene in the herd. It is only targeting the weakest (oldest, slowest, youngest, injured,…) member of the herd. It can be argued that lions removing sick, injured and old members of the population don’t change the fitness of the population to reproduce because the members they take wouldn’t reproduce anyway because of their condition. If you sprayed chlorine gas over the herd of gazelles, then you would be targeting every gene in the pool.
Why don’t you tell us what mutations will increase in frequency in the population when a lion eats a gazelle?The mutations that aid gazelles in avoiding being eaten by lions will increase in frequency. And off the top of my head I don't have the genomes of gazelles from the last million years.
Now you are making a claim that multiple genes are being transformed by your example and you don’t have any proof. This is typical of the speculations that evolutionist make about how mutation and selection actually works. The examples I have cited including the ones you asked me to post again are specific, repeated measurements by many different scientists in many different fields that show again and again that combination selection pressures profoundly slow the evolutionary process. This phenomenon can be understood mathematically if you understand how optimization, database sorting and iteration problems work. The more conditions in which you optimize by, sort by or iterate by, the slower the mathematical process works and it doesn’t take many of these conditions to make the problem converge extremely slowly. Evolution by mutation and selection is one of these types of problems.
But let’s see if you can get beyond your vague mush, give us a mathematical or empirical example which illustrates your contention how multiple selection pressures accelerate evolution and your lion/gazelle example doesn’t tell us what the selection pressure(s) is/are or what the target gene(s) is/are.Well, I have never contended that multiple selection pressures accelerate evolution. My point is that there is never a situation where there is a single selection pressure to compare with multiple selection pressures. But if you give me a link, I'll read up on it so we can discuss a specific example.
Start with the HIV examples I have posted above for empirical examples. If you want to try a mathematical example, the ev computer simulation is available online at http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/evj/evjava/index.html (http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/evj/evjava/index.html) and we are discussing the results from this model on this thread.
I realize this is a very long thread but this issue has been discussed previously. Let’s start with the huge variation between the size of bird and reptile genomes. Then you can start looking at individual genes which may have some similarity between the two life forms, and then you have to start accounting for these differences. Humans and chimpanzees supposedly descended from a common ancestor yet these two genomes have at least 150,000,000 base differences. You have only about 500,000 generations to account for these differences. The mathematics of mutation and selection shows that evolutionist accounting fails the audit Well if the above numbers are correct, I'd say on average it'll be 300 base changes per generation. Doesn't seem like too many does it? I do know that I am genetically pretty different from my father, those could be the 300 bases!
The variation of human genome is about 1%, the mutation rate for human genome reproduction is about 1 in 10^7 bases and there are about 3*10^9 base pairs in the human genome. Perhaps you would give us an estimate for how many of these mutations are beneficial, detrimental or neutral.
Panspermia simply changes the site for creation or evolution. Either we were created or we spontaneously arose and evolve. In the later case, it is shown to be mathematical and empirically impossible.Have you looked into the mathematical possibility of being created? :-)
I’m don’t have to, all I have to do is show that evolution by mutation and selection is mathematically impossible and actually it is pretty easy to do. ;-)
These combined selection pressures interfere with the population’s ability to locate a new fitness optimum on the fitness landscape. Each selection pressure is pushing the population’s trajectory on the fitness landscape in its own best direction interfering with finding any local optimum for any of the selection conditions. This effect is demonstrated very nicely with joobz example:If it doesn't wipe out the entire population, then what you have here looks like a situation where speciation would occur.
Not really, what you would actually have is something that would look like a successful combination treatment of a HIV patient, very low population viruses that do not have good reproductive fitness. You have to remember that selection pressures affect the fitness of a population to reproduce, so unless the population can adapt to the selection pressures, any surviving members of the population will have a difficult time reproducing.
Whenever you are ready to post your evidence, we are ready to listen but so far you have posted zilch.So you won't claim that there never were small genomes, yet you claim to have a proof that transcription factors can't evolve in genomes because they are too large.
Paul, you have no evidence that tiny replicators ever existed and your own model shows what happens on any genome that even approaches the size of any know free living organism. Your own model is my proof.
Paul, gravity is a force and there are consequences to this force.A consequence is not a goal.
Whether it is a consequence, result, effect, outcome, there is a cause and effect relationship, just like there is a cause and effect relationship for mutation and selection. Your own model has the objective of showing how mutation and selection can lead to the evolution of binding sites, it just misses the goal for all but the tiniest genomes.
Now if you want an example of gibberish, read your own description of Rcapacity. What you fail to recognize is that despite the length of the genome such that Rf > 2 * site width, the model does start to converge but reaches a local optimum before the selection conditions can converge.Why does it reach that local optimum? It must be like trying to index a 1000-entry table with a 7-bit integer: It reaches a local optimum around entry number 128 and just can't get past there.
You said it previously; there is more than one perfect creature in the model. The fitness landscape for ev is much more complex than you think. Your attempt at an analogy here doesn’t make sense. Any one of the three selection conditions can evolve easily despite the length of the genome.
So Alan, how do you explain this data:

population 64
genome size 2048, Rfrequency = 7
sites 16
mutation 2/generation

weight/site width, Rcapacity, generations

8/9, 18, 15623
7/8, 16, 23063
6/7, 14, 30241
5/6, 12, 28625
4/5, 10, 30501
3/4, 8, 31814
2/3, 6, --- (still 16 mistakes after 120,000 generations)

Why the spike just as Rcapacity goes below Rfrequency?
Weight width=2, site width=3, other parameters as you used above.
With single selection pressures, generations for zero mistakes
Missed binding sites, 1 generation
Spurious binding within gene, 1 generation
Spurious binding outside gene, 1 generation

Paul, the explanation is that you seriously underestimate the complexity of the fitness landscape when you have three selection conditions. There are many perfect creatures therefore many local optima. Ev is simply getting stuck at a local optimum that isn’t zero mistakes.
Simple enough oponol, give us an example where two separate goals aid convergence on a solution. You can make that a mathematical example or an empirical example.The genome of each individual consists of a byte consisting of eight bits, least significant bit on the right. The phenotype is the integer value represented by that byte.

Goal A: selective pressure to reach 10001000 = 136

Problem is in many runs your population gets stuck at a local optimum like this:
01111111 = 127

Flipping any of those bits takes you further from goal A of 136 than you are already. In fact it would take the spontaneous flipping of the right 4 bits to get closer to the goal.

But if you have an additional goal B to reduce the number of 1s in the sequence, that provides pressure against going anywhere near a genome like 01111111 in the first place.
If you apply goal A and B simultaneously, goal B will be pushing the trajectory toward 00000000. Goal B is only useful to push the sequence off an invalid goal A local optimum. This is similar to this example.
http://www.pnas.org/cgi/content/full/104/34/13711 (http://www.pnas.org/cgi/content/full/104/34/13711)
http://www.pnas.org/content/vol104/issue34/images/medium/zpq0310771490005.gif
Fig. 5. A schematic view of fitness landscapes and evolution under fixed goal and MVG. (a) A typical trajectory under fixed goal evolution. The population tends to spend long periods on local maxima or plateaus. (b) A typical trajectory under MVG. Dashed arrows represent goal switches. An effectively continuous positive gradient on the alternating fitness landscapes leads to an area where global maxima exist in close proximity for both goals.
Sequential selection pressures are how you accelerate evolution.

[axon]

The lion is not targeting every gene in the herd. It is only targeting the weakest (oldest, slowest, youngest, injured,…) member of the herd.
But the lion is targetting every gene in the individual.

Now you are making a claim that multiple genes are being transformed by your example and you don’t have any proof.
You want me to provide proof that the killing and eating of a gazelle from a population removes the genes in that gazelle from the population??? This is what is happening. The selection pressure of "lion attack" changes the frequency of all genes in the population,as the eaten gazelle has lost all its genes.
Or in more mathematical terms....
let n = number of individual genomes in a population.
let L = number of successful lion attacks

After every lion attack , new gazelle population = n - L.

The variation of human genome is about 1%, the mutation rate for human genome reproduction is about 1 in 10^7 bases and there are about 3*10^9 base pairs in the human genome.
But it's not just mutation rate which changes genomes. Changing the position of sequences changes the genome too. How do you deal with meiosis?

I’m don’t have to, all I have to do is show that evolution by mutation and selection is mathematically impossible and actually it is pretty easy to do. ;-)
Have you considered publishing your proof? Nature would certainly be interested, and if it is indeed a mathematical proof it would be near on impossible to dispute, and maybe also a Nobel prize for you!
[

[axon]

Oh and thanks for the links. I'll have a read of the HIV stuff (probably over the weekend, damn work intereferes with life)

[cyborg]

[/SIZE][/FONT]
The genome of each individual consists of a byte consisting of eight bits, least significant bit on the right. The phenotype is the integer value represented by that byte.

Goal A: selective pressure to reach 10001000 = 136

Problem is in many runs your population gets stuck at a local optimum like this:
01111111 = 127

Flipping any of those bits takes you further from goal A of 136 than you are already. In fact it would take the spontaneous flipping of the right 4 bits to get closer to the goal.

But if you have an additional goal B to reduce the number of 1s in the sequence, that provides pressure against going anywhere near a genome like 01111111 in the first place.

Simple and beautifully put - he will be annoyed.

kleinman will now probably call it your "string bit theory" or something equally matching his devastating wit.

[cyborg]

Have you considered publishing your proof?

A sheet of paper containing:

"Run Ev with these parameters. Evolution is impossible idiot evolutionarians."

May constitute proof to kleinman but no one else is much interested. Of course this just confirms to kleinman the conspiricy to keep the Bible down.

[Belz...]

Why Belz, there is more poetry and rhyme in that little post than there is mathematics or empirical evidence in your theory of evolution.

Some mathematician you make to think that 0 > 0.

[kleinman]

The lion is not targeting every gene in the herd. It is only targeting the weakest (oldest, slowest, youngest, injured,…) member of the herd.But the lion is targetting every gene in the individual.
Then every gene in that individual went extinct.
Now you are making a claim that multiple genes are being transformed by your example and you don’t have any proof.You want me to provide proof that the killing and eating of a gazelle from a population removes the genes in that gazelle from the population??? This is what is happening. The selection pressure of "lion attack" changes the frequency of all genes in the population,as the eaten gazelle has lost all its genes.
That’s correct those genes are now extinct. Now if this was an injured gazelle unable to reproduce, how does this affect the fitness of the population to reproduce?
Or in more mathematical terms....
let n = number of individual genomes in a population.
let L = number of successful lion attacks

After every lion attack , new gazelle population = n - L.
So now you conclude that every gene in this new gazelle population has evolved to a new species? How about if a gazelle dies of disease, is that new gazelle population a new species? How about if a gazelle dies while trying to ford a river, is that new gazelle population a new species?

Axon, your example does not describe evolution by mutation and selection. If the gazelle population is going to evolve to a lion attack it is going to be by recombination and selection by producing faster gazelles with more endurance in the run. Alleles will be selected that give these features. Mutation and selection is far to slow a process to help the gazelle population adapt to lion attacks.
The variation of human genome is about 1%, the mutation rate for human genome reproduction is about 1 in 10^7 bases and there are about 3*10^9 base pairs in the human genome.But it's not just mutation rate which changes genomes. Changing the position of sequences changes the genome too. How do you deal with meiosis?
Recombination without error can not increase information in the gene pool, recombination with selection can cause the loss of information (alleles) from the gene pool.
I don’t have to, all I have to do is show that evolution by mutation and selection is mathematically impossible and actually it is pretty easy to do. ;-)Have you considered publishing your proof? Nature would certainly be interested, and if it is indeed a mathematical proof it would be near on impossible to dispute, and maybe also a Nobel prize for you!
I am publishing my findings, right here on the James Randi Educational Foundation forum. It is not just proving the theory of evolution to be mathematically impossible, it is important to understand how mutation and selection actually works. There are many important problems we have to deal with that are governed by mutation and selection such as the evolution of resistance of diseases to the drugs we use (HIV, HBV, HCV, influenza, TB, Malaria, cancer…), resistance in agriculture to pesticides, herbicides and so on. All these examples show that combination selection pressures profoundly slow the evolution of resistance to these selection pressures. The only thing I have done here is put the mathematical and empirical pictures together and then the actual way that mutation and selection works becomes apparent.
Oh and thanks for the links. I'll have a read of the HIV stuff (probably over the weekend, damn work intereferes with life)
I have posted many other links about HIV which show that combination selection pressures profoundly slow the evolution of the virus. If you don’t want to search through the thread to find these links I’ll repost them as well. Then when you finish those links, I’ll repost all the citations which show that combination therapy markedly delays the evolution of resistance of Malaria, then I’ll repost all the citations from oncology that show that combination treatment of cancer markedly delays the evolution of resistance, then I’ll repost all the citations from agriculture that show that combination herbicides marked delay the evolution of resistant weeds, then TB, HBV, HCV, rodenticides,…
But if you have an additional goal B to reduce the number of 1s in the sequence, that provides pressure against going anywhere near a genome like 01111111 in the first place.Simple and beautifully put - he will be annoyed.
I’m not annoyed at all. If you have goal B which reduces the number of 1s in the sequence, not only does in provide pressure against going anywhere near a genome like 01111111 it will also provide pressure against going anywhere near a genome like 10001000, his intended goal for goal A. Goal B just keeps getting rid of those nasty ole’ 1s.
kleinman will now probably call it your "string bit theory" or something equally matching his devastating wit.
I like the “cruft byte theory” a bit better.
Have you considered publishing your proof?A sheet of paper containing:

"Run Ev with these parameters. Evolution is impossible idiot evolutionarians."
Now cyborg, I have never called evolutionarians “idiots” and it’s not with a sheet of paper, where are we now, 141 pages? Don’t forget, axon is considering some of the hundreds of citations which I have posted which shows empirically what ev is showing mathematically, something which most of you evolutionarians try to ignore.
May constitute proof to kleinman but no one else is much interested. Of course this just confirms to kleinman the conspiricy to keep the Bible down.
I know, this is such a boring thread, now if you could post an example where simultaneous selection pressures accelerate evolution, which would make it interesting. Or perhaps you will post an example of you cruft theory of evolution?

Here’s another example of multiple selection pressures profoundly slowing evolution.
http://www.phri.org/research/pdf/res_art_drlica22.pdf (http://www.phri.org/research/pdf/res_art_drlica22.pdf)
OBJECTIVE: To describe the mutant selection window, discuss supporting evidence and limitations, and suggest potential applications for clinical practice.

DATA SOURCES: A MEDLINE search (1990–December 2003) of the English-language literature was conducted using the key words antibiotic, antimicrobial, resistance, mutant, selection window, prevention, MPC, and MSW in various combinations. Original investigations and reviews evaluating the mutant selection window, including abstracts and proceedings, were considered for inclusion. Published articles were also cross-referenced, and experts were contacted to locate additional pertinent data.

STUDY SELECTION AND DATA EXTRACTION: All data sources identified were evaluated and all information deemed relevant was included.

DATA SYNTHESIS: Until recently, physicians have had few ways to preserve antimicrobials from resistance other than by prescribing the agents less often. The mutant selection window hypothesis may modify this paradigm by shifting the focus to dosing strategies that reduce the growth of resistant mutants. Conventional dosing strategies have been formulated on the likelihood of curing an individual patient. Unfortunately, doses that cure patients appear to enrich resistant subpopulations of bacteria, thus promoting resistance. Antimicrobial–pathogen combinations can be identified that minimize mutant selection and cure patients while possibly restricting the progression of resistance.

CONCLUSIONS: The mutant selection window hypothesis provides a framework for considering the contribution of dosing to resistance, and it offers ideas for restricting the enrichment of resistant mutants and antimicrobial resistance.
And
Use of MPC as a dosing guide is distinct from currently accepted practice since compounds are selected by virtue of their anti-mutant activity and likelihood of cure rather than solely on favorable patient outcome (cure) rate. The latter may be similar for many members of the same drug class despite differences in activity against mutants. Consideration of the selection window hypothesis suggests that combination therapy should be implemented much more often than is currently the practice.
How about another example from the field of oncology?
http://clincancerres.aacrjournals.org/cgi/content/full/10/16/5299?ck=nck (http://clincancerres.aacrjournals.org/cgi/content/full/10/16/5299?ck=nck)

Oncolytic virotherapy is the use of genetically engineered viruses that specifically target and destroy tumor cells via their cytolytic replication cycle. Viral-mediated tumor destruction is propagated through infection of nearby tumor cells by the newly released progeny. Each cycle should amplify the number of oncolytic viruses available for infection. Our understanding of the life cycles of cytolytic viruses has allowed manipulation of their genome to selectively kill tumor cells over normal tissue. Because the mechanism of tumor destruction is different, oncolytic virotherapy should work synergistically with current modes of treatment such as chemotherapy and radiation therapy. This article focuses on oncolytic adenoviruses that have been created and tested in preclinical and clinical trials in combination with chemotherapy, radiation therapy, and gene therapy.
And
Cancer remains one of the top causes of death in adults and children. Progress has been made in the overall survival of cancer patients after the emergence of better imaging and diagnostic techniques, improved understanding of the molecular processes that cause cancer, and additional knowledge of treatment using combined chemo- and radiotherapy. However, survival has not improved with current chemotherapy and radiation regimens in patients diagnosed with metastatic disease and certain tumors such as malignant neoplasms of the brain, pancreas, and liver. This is usually due to tumor cells developing genetic mechanisms that override apoptosis caused by chemotherapy and radiation damage to their DNA. This confers resistance to treatment through clonal expansion of genetically resistant tumor cells. Much effort has been directed toward finding alternate pathways that would complement therapeutic induction of apoptosis, overcome multidrug resistance, and ultimately improve overall cure rates. Although the dream of developing a single curative drug per cancer type drives the field, the reality is that combination therapy will be the most effective way of improving survival.
And
The theory, based on combination chemotherapy, is that attacking tumor cells through different mechanisms of action will prevent tumor cells from having time to develop resistance to treatment.
Why is combination therapy for cancer the reality? This is the reality because combination selection pressures profoundly slow the evolution of resistant cells.

[Belz...]

Have you considered publishing your proof? Nature would certainly be interested, and if it is indeed a mathematical proof it would be near on impossible to dispute, and maybe also a Nobel prize for you!


I agree. It would go a long way toward convincing me that Kleinman isn't just a loon.

[kleinman]

Have you considered publishing your proof? Nature would certainly be interested, and if it is indeed a mathematical proof it would be near on impossible to dispute, and maybe also a Nobel prize for you!I agree. It would go a long way toward convincing me that Kleinman isn't just a loon.
Now I understand, if you publish in the James Randi Educational Foundation forum you are a loon but if you publish in Nature that suddenly makes your hypothesis true. Belz, your logic on publication matches your logic on mutation and selection.

[axon]

That’s correct those genes are now extinct. Now if this was an injured gazelle unable to reproduce, how does this affect the fitness of the population to reproduce?
In a myriad of ways. The herd is now smaller, there is more food available, the "weakest gazelle in the group" is now a different gazelle with a different set of genes etc

So now you conclude that every gene in this new gazelle population has evolved to a new species? How about if a gazelle dies of disease, is that new gazelle population a new species? How about if a gazelle dies while trying to ford a river, is that new gazelle population a new species?
What are you talking about? Where have I concluded any of the above? My point is that when a lion kills a gazelle, it changes the frequency of alleles in the whole gazelle population.

Axon, your example does not describe evolution by mutation and selection. If the gazelle population is going to evolve to a lion attack it is going to be by recombination and selection by producing faster gazelles with more endurance in the run. Alleles will be selected that give these features. Mutation and selection is far to slow a process to help the gazelle population adapt to lion attacks.
This is your assertion. However I have yet to see a hypothesis that is better than mutation and selection, do enlighten me if you have one.

I am publishing my findings, right here on the James Randi Educational Foundation forum.
This is a joke, yes? You seem intelligent enough to understand the merits of publishing an article in a peer-reviewed journal and compared to writing comments a thread on the internet.

It seems that you don't believe macroevolution but do believe microevolution, as you say that mutation and selection are too slow to account for the diversity. Does this mean that you think macroevolution can occur given enough time?

[kleinman]

That’s correct those genes are now extinct. Now if this was an injured gazelle unable to reproduce, how does this affect the fitness of the population to reproduce?In a myriad of ways. The herd is now smaller, there is more food available, the "weakest gazelle in the group" is now a different gazelle with a different set of genes etc
Now tell us how this accelerates evolution by mutation and selection. Tell us what the target genes are and how a lion killing the weakest gazelle in the population accelerates the evolution of those target genes. If you are going to argue that all the genes are targeted, give us some measurement that we can use to determine that all these genes are evolving.
So now you conclude that every gene in this new gazelle population has evolved to a new species? How about if a gazelle dies of disease, is that new gazelle population a new species? How about if a gazelle dies while trying to ford a river, is that new gazelle population a new species?What are you talking about? Where have I concluded any of the above? My point is that when a lion kills a gazelle, it changes the frequency of alleles in the whole gazelle population.
You are arguing from a view of recombination and selection not mutation and selection. This is a very common problem with evolutionists. You can not distinguish between recombination and selection and mutation and selection. In the former case alleles are selected for their fitness advantage while in the later, mutations are selected for their fitness advantage. Recombination and selection is a very rapid mechanism for changing the properties of a population in a relatively small number of generations (consider the amount of variations achieved with dogs in only about 10,000 generations). Mutation and selection is a far slower process especially when more than a single gene is targeted.
Axon, your example does not describe evolution by mutation and selection. If the gazelle population is going to evolve to a lion attack it is going to be by recombination and selection by producing faster gazelles with more endurance in the run. Alleles will be selected that give these features. Mutation and selection is far to slow a process to help the gazelle population adapt to lion attacks.This is your assertion. However I have yet to see a hypothesis that is better than mutation and selection, do enlighten me if you have one.
Then give us something that can be measured other than your assertion that every gene is targeted when a gazelle is eaten by a lion. Once you start reading the citations I have posted, you will start to understand how mutation and selection actually works empirically. If you want to understand how mutation and selection works mathematically, you can study the peer reviewed and published mathematical model ev. What these examples show is that combination selection pressures profoundly slow evolution. These examples of mutation and selection clearly identify the selection pressures, the target genes and often identify the specific mutations required to confer resistance to these selection pressures. Mutation and selection certainly works but you are not going to achieve the massive genetic transformations that evolutionists allege. Mutation and selection simply doesn’t work the way you allege. The empirical and mathematical evidence shows otherwise.
I am publishing my findings, right here on the James Randi Educational Foundation forum.This is a joke, yes? You seem intelligent enough to understand the merits of publishing an article in a peer-reviewed journal and compared to writing comments a thread on the internet.
I guess you call it a joke when an evolutionist asserts that every gene in a gazelle herd is targeted when a lion eats the weakest member of the herd. It is this kind of mush that evolutionists take as fact.

I use the results of Dr Schneider’s peer reviewed and published model of random point mutations and natural selection to show that combination selection pressures profoundly slow the evolutionary process and evolutionists discredit the simulation despite it has been peer reviewed and published in Nucleic Acids Research, an Oxford University Press journal. It doesn’t matter where it is published, if it contradicts the evolutionist belief system, evolutionists will discredit it no matter how many citations demonstrate the finding empirically or how many different mathematical models show the same result. If it is true, it doesn’t matter where it is published.
It seems that you don't believe macroevolution but do believe microevolution, as you say that mutation and selection are too slow to account for the diversity. Does this mean that you think macroevolution can occur given enough time?
Even if you have an eternity of time, macroevolution will not occur because you don’t have the selection pressures to accomplish the process. You don’t have selection pressures that can evolve a gene de novo and you don’t have the selection pressures that would achieve the massive genetic transformations require to metamorphose reptiles to birds unless you believe that a lion eating a gazelle will make a gazelle grow wings.

Here’s another example how mutation and selection actually works.
http://www.phri.org/research/pdf/res_art_drlica02.pdf (http://www.phri.org/research/pdf/res_art_drlica02.pdf)
The selection of antibiotic-resistant mutant bacteria is proposed to occur in a drug concentration range (the mutant selection window) that extends from the minimum inhibitory concentration (MIC) of susceptible cells to the MIC of the least susceptible, single-step bacterial mutants (the mutant prevention concentration [MPC]). MPCs were estimated for tobramycin, chloramphenicol, rifampicin, penicillin, vancomycin, and several fluoroquinolones by use of Escherichia coli and Staphylococcus aureus. Comparisons among reported serum drug levels indicate that new fluoroquinolones are the least likely to enrich populations of resistant mutant bacteria during monotherapy. These data partly explain the selective enrichment of populations of resistant mutant bacteria in medical practice. The mutant selection window range (MPC:MIC) was narrowed for fluoroquinolones by structure modification, pointing to a new direction in antibiotic refinement. The mutant selection window and the MPC were determined for combinations of rifampicin and tobramycin, using S. aureus, as a guide for combination therapy with compounds that alone cannot block enrichment of mutant bacterial populations.
And
The mutant selection window forms the conceptual basis of a pharmacodynamic approach to slow the development of resistance by keeping 2 or more mutational steps ahead of bacterial populations. By use of drug concentrations greater than the mutant MPC or by use of combination therapy to stay beyond the mutant selection window, the agents directly attack mutant bacteria. The data presented here should help guide further animal and clinical tests. To date, none has been reported. The standard empirical approach, which relates antimicrobial exposure to the susceptibility of cells and to clinical outcome, relies on host defenses to remove mutant bacteria. This approach allows anti-microbial concentrations to fall inside the mutant selection window; thus, it is expected to restrict enrichment only of mutant bacterial populations that confer low to moderate levels of resistance. However, as pharmacodynamic parameters such as Cmax/MIC are raised, a point will be reached at which drug concentrations exceed the MPC throughout therapy. At that point, the standard pharmacodynamic approach will converge with the mutant selection window strategy.
Axon, if selection pressures are directed at more than a single gene, the mutation and selection process is confounded making it much more difficult for the population to evolve to the multiple selection conditions. The sorting process for beneficial and detrimental mutation becomes much more difficult, profoundly slowing the evolutionary process by mutation and selection. That is how the mutation and selection process actually works.

[axon]

Even if you have an eternity of time, macroevolution will not occur because you don’t have the selection pressures to accomplish the process. You don’t have selection pressures that can evolve a gene de novo and you don’t have the selection pressures that would achieve the massive genetic transformations require to metamorphose reptiles to birds unless you believe that a lion eating a gazelle will make a gazelle grow wings.

Ok, I've read some of the early pages of the thread and I think I get where you are coming from. Bear in mind several things though, ev is not a complete model of evolution, as Schnieder himself says in the original paper. The criteria for disproving evolution is a little higher than running some numbers through ev. You're argument reads a little like creationists who proclaim that if there isn't a complete fossil record then evolution couldn't have happened (except here you'd like a complete mathematical description). However if you genuinely believe what you are posting I do find it strange that you don't publish the frankly remarkable and ground-breaking findings in a proper journal.

Also you don't think macroevolution can occur. But you do think microevolution can occur. How do you distinguish between the two? For example you don't think birds can evolve from reptiles. Can snakes evolve from lizards?

[kleinman]

Even if you have an eternity of time, macroevolution will not occur because you don’t have the selection pressures to accomplish the process. You don’t have selection pressures that can evolve a gene de novo and you don’t have the selection pressures that would achieve the massive genetic transformations require to metamorphose reptiles to birds unless you believe that a lion eating a gazelle will make a gazelle grow wings.Ok, I've read some of the early pages of the thread and I think I get where you are coming from. Bear in mind several things though, ev is not a complete model of evolution, as Schnieder himself says in the original paper. The criteria for disproving evolution is a little higher than running some numbers through ev. You're argument reads a little like creationists who proclaim that if there isn't a complete fossil record then evolution couldn't have happened (except here you'd like a complete mathematical description). However if you genuinely believe what you are posting I do find it strange that you don't publish the frankly remarkable and ground-breaking findings in a proper journal.
Apparently you haven’t read either this thread or Dr Schneider’s writings thoroughly. No computer simulation perfectly models reality. The question you need to answer is; does that model capture the essential features of reality to give predictive power to the model? Dr Schneider’s model shows that the reason it converges so slowly is the combination of three selection pressures. Is this behavior reflected in the empirical data? The answer to this question is yes many times over. It is not the type of mutation the drives the behavior of the mutation/selection process, it is the number of selection conditions that dominates both the mathematical behavior of mutation/selection models and the empirical behavior of this type of phenomenon. Once you start examining the real examples of mutation and selection that are readily available, you will start to understand how this process actually works. It is an extremely slow process that is limited to only a few selection pressures at most and that is with only the most rapidly reproducing, short genome populations such as viruses, bacteria and organisms that produce huge numbers of offspring such as parasites and plants. Even so, more than a single selection pressure has profound effect on these populations to evolve to these selection pressures.

What is so ground breaking about this discussion? The only thing I have done is pointed out something in the mathematical behavior of Dr Schneider’s computer model and then shown there are many real examples of this behavior. In addition, a search of the literature shows there are many other mathematical models which show the same thing, which is combination selection pressures slows profoundly slow evolution by the mutation and selection process.
Also you don't think macroevolution can occur. But you do think microevolution can occur. How do you distinguish between the two? For example you don't think birds can evolve from reptiles. Can snakes evolve from lizards?
Many perhaps most evolutionists don’t draw a distinction between micro and macroevolution. They argue that macroevolution is simply a collection of microevolutionary steps. Microevolution has clearly identifiable selection pressures and target genes to those selection pressures. Now that it is become clearer how mutation and selection actually works, how do you put these types of processes together to get your macroevolutionary change? What are those selection pressures that transform reptiles into birds or lizards into snakes, or humans and chimpanzees from a primate precursor? Evolutionists have grossly over extrapolated and speculated what mutation and selection can do. It can not evolve a gene de novo and it can not bring about massive transformations of genomes.

[axon]

don’t draw a distinction between micro and macroevolution. They argue that macroevolution is simply a collection of microevolutionary steps. Microevolution has clearly identifiable selection pressures and target genes to those selection pressures. Now that it is become clearer how mutation and selection actually works, how do you put these types of processes together to get your macroevolutionary change? What are those selection pressures that transform reptiles into birds or lizards into snakes, or humans and chimpanzees from a primate precursor? Evolutionists have grossly over extrapolated and speculated what mutation and selection can do. It can not evolve a gene de novo and it can not bring about massive transformations of genomes.[/SIZE][/FONT]
Well I think we'll have to agree to disagree. You're right that no model is a perfect model, but similarly some models are no good for modelling things they weren't designed for. Personally I think the mistake is coming from trying to quantize selection pressures as if they were discrete entities. And I think that you win in the extrapolation stakes by going from plugging numbers into ev to proclaiming the mathematical impossibility of birds evolving from reptiles. Still keep up the god work :-)

[jimbob]

Kleinman,
Back to your response about multiple optima (image below, hidden for brevity)
http://www.pnas.org/content/vol104/issue34/images/medium/zpq0310771490005.gif

If you consider the whole fitness landscape, this just says that there are several different optima, which are separated from each other by troughs, and so are not likely to travel from one to another.

I think this is part of your argument, is that correct?

However if members of the population are surviving, and reproducing they are obviously optimal enough to reproduce.

Surely the presence of these different simultaneous peaks is the reason for speciation?

Forget bacteria for a moment and consider a carnivorous cat-like animal. Some offspring, being slightly larger, are better at catching larger prey, whilst others, being lighter, and faster are better at catching faster prey. They move towards different optimal sizes and shapes, because the selection pressures help drive them apart.

One ends up as a proto-lion and another as a proto-cheetah.

The cheetah will type will not be able to evolve into a lion-like animal, whilst there are lions about, as it would not be able to compete with lions. If lions were wiped out, its descendents would still probably fail to fill the lion's niche, as a leopard descendant would have a head start for example. If there were no (other*) big cats/predators then a cheetah descendant could conceviably fill this niche.

Where do you disagree with this reasoning?

*I believe there is argument as to whether this should just refer to lions, tigers, leopards, and jaguars or also large felines too.

[kleinman]

Back to your response about multiple optima…

If you consider the whole fitness landscape, this just says that there are several different optima, which are separated from each other by troughs, and so are not likely to travel from one to another.

I think this is part of your argument, is that correct?
Yes
However if members of the population are surviving, and reproducing they are obviously optimal enough to reproduce.

Surely the presence of these different simultaneous peaks is the reason for speciation?
These peaks represent phenotypes that are most fit to reproduce for a given set of selection pressures. If the selection pressures are insufficient to drive the population to extinction, for this fitness landscape, that is there is diversity in the population such that some members of the populations can survive and reproduce in the trough regions of the fitness landscape, the selection pressures will move portions of the population to the particular peaks. It is only when you try to get members of the population to evolve resistance to both selection pressures simultaneously that you have trouble getting a trajectory which would accomplish this.

Consider this simple example. Take a population of bacteria that is sensitive to two different antibiotics. Place them in a sub-lethal concentration of one of the antibiotics and allow the population to adapt to that selection pressure. Then take that population and subject it to the second antibiotic and allow it to adapt to the second selection pressure. Now take a second population of bacteria sensitive to both antibiotics and place this population in a sub-lethal concentration of both antibiotics. This population may still be able to evolve resistance to both drugs but it is much slower than the case of the first population of bacteria subjected to the selection pressures sequentially. This is do to the fact the two simultaneous selection pressures interfere with each others trajectory to the fitness two fitness optima.

This is in fact what is observed with the treatment of HIV as well and explains why combination therapy maintains effectiveness far longer than sequential therapy.
Forget bacteria for a moment and consider a carnivorous cat-like animal. Some offspring, being slightly larger, are better at catching larger prey, whilst others, being lighter, and faster are better at catching faster prey. They move towards different optimal sizes and shapes, because the selection pressures help drive them apart.
Ok
One ends up as a proto-lion and another as a proto-cheetah.
Recombination and selection can cause large morphologic changes in populations but this is not mutation and selection. Recombination without error can not increase the information in the gene pool and recombination with selection can cause the loss of information (alleles) from the gene pool.
The cheetah will type will not be able to evolve into a lion-like animal, whilst there are lions about, as it would not be able to compete with lions. If lions were wiped out, its descendents would still probably fail to fill the lion's niche, as a leopard descendant would have a head start for example. If there were no (other*) big cats/predators then a cheetah descendant could conceviably fill this niche.
Recombination and selection can have rapidly occurring, large effects on populations but without error can not transform reptiles to birds or canines and felines from some precursor animal.
Where do you disagree with this reasoning?
Your reasoning is correct; it just is not an example of mutation and selection.
*I believe there is argument as to whether this should just refer to lions, tigers, leopards, and jaguars or also large felines too.
With recombination and selection you can get Chihuahuas and Great Danes, Belgian draft horses and miniature horses and you probably could breed miniature cats and cats that weigh hundreds of pounds but these are not examples of mutation and selection.

[jimbob]

re Post #5356 (http://forums.randi.org/showthread.php?postid=2983432#post2983432)

I was probably unclear.

I was taking it as implicit that the offspring would tend to resemble their parents, but with slight (random) differences, which we now know are caused by mutations.

I agree that error is needed. Random "errors" that are "useful" tend to survive, whilst those that are not will get weeded out.

If a trait (e.g. running speed) is controlled by many genes, and a slightly faster and lighter feline's descendents start to fill the cheetah's niche, then any random mutations that reduce speed will tend to be weeded out (with a strong selection pressure) whilst any mutations that increase speed will tend to be preserved.

I can't see quite what you are getting at. You have just stated an advantage of sexual reproduction as opposed to asexual reproduction. But my argument (without recombination) would also work with a population of asexually reproducing organisms too (it is just that I like big cats).

[kleinman]

If a trait (e.g. running speed) is controlled by many genes, and a slightly faster and lighter feline's descendents start to fill the cheetah's niche, then any random mutations that reduce speed will tend to be weeded out (with a strong selection pressure) whilst any mutations that increase speed will tend to be preserved.
Increasing running speed in a population by mutation and selection would be an extremely difficult if not an impossible process while recombination and selection can accomplish this type of transformation very quickly. This strategy is used in breeding race horses.
I can't see quite what you are getting at. You have just stated an advantage of sexual reproduction as opposed to asexual reproduction. But my argument (without recombination) would also work with a population of asexually reproducing organisms too (it is just that I like big cats).
Sexual reproduction, especially when breeding is non-random can lead to very rapid morphological changes in a population. However recombination without error can not achieve the transformations called for by the theory of evolution. The only possible mechanism for achieving these transformations is mutations (including recombination errors). When you examine the mathematical an empirical evidence of how mutation and selection works, you find that this is far too slow a process to accomplish what you allege because combination selection pressures profoundly slow the process. Consider the Malaria parasite. This parasite reproduces sexually and asexually in its life cycle yet two selection pressures profoundly affect the ability of this parasite to evolve against these selection pressures.
http://bmb.oxfordjournals.org/cgi/content/full/71/1/29 (http://bmb.oxfordjournals.org/cgi/content/full/71/1/29)
Sub-Saharan Africa is faced with a crisis of rising levels of resistance to antimalarial drugs and few available and affordable alternatives. Combination chemotherapy, using two or more drugs with different mechanisms and sites of action together, is proposed as a mechanism for slowing the process of development of resistance. In Thailand, this approach has resulted in a sustained increase in the cure rate. Whether such an effect would be seen in Africa is not known. This article reviews the rationale behind combination therapy, the drugs available and the available evidence from combination therapy trials in Africa. Treatment of uncomplicated malaria in pregnancy and infants is also discussed.
and
Combination chemotherapy, using two or more drugs together with different mechanisms and sites of action, is proposed as a mechanism for slowing the process of development of resistance.18 This is standard practice in the treatment of HIV and tuberculosis. The probability of mutations arising spontaneously to both drug A and drug B is equal to the probability of a mutation arising to drug A multiplied by the probability of a mutation arising to drug B. Artemisinins have been suggested as ideal drugs for use in combination therapies; this treatment is known as artemisinin combination therapy (ACT). Artemisinins have the broadest antimalarial activity against parasites, from the ring stage to early schizonts, and cause the fastest decline in parasite numbers of all the antimalarial drugs. In a typical adult malaria infection with 2% parasitaemia, the total number of parasites in the individual is approximately 10^12. Every 2 days artemisinins reduce this parasite load by a factor of 10^4. This compares with factors of 10^3 for CQ and SP, 10^2 for mefloquine and 10 for tetracycline.19 Where there is a slower kill rate, parasites persist in the blood for longer. Resistant mutations may then be selected in the presence of falling drug concentrations. Artemisinins have very short half-lives and as a monotherapy must be taken for at least 7 days. This is operationally impractical and is likely to lead to high treatment failure rates. As ACT, the artemisinin is taken for 3 days, significantly reducing the parasite numbers and leaving the remaining parasites to be killed by the second drug or the host immune system.
and
In Thailand, resistance to CQ and SP led to the introduction of mefloquine monotherapy in 1984 as treatment for uncomplicated malaria. Within 10 years treatment failure rates were >40%. The combination of mefloquine with artesunate (ART) was introduced in 1994 and resulted in a sustained high cure rate, a reversal of the in vitro mefloquine resistance and a sustained decline in the incidence of P. falciparum malaria in that area.20 Whether such an effect would be seen in Africa, where transmission intensity, acquired immunity and treatment practices are very different, is not known and is the subject of much debate. 21
Despite huge populations, both sexual and asexual reproduction, this parasite’s evolution against selection pressures is profoundly slowed with two selection pressures. This is an example where mutation and selection is required to adapt to the selection pressures. Recombination and natural selection can not accomplish what the Malaria parasite needs to adapt to these selection pressures. There are no alleles in the Malaria parasite gene pool that would confer resistance to these selection pressures, they have to evolve by mutation and selection and that process is profoundly slow when there are two selection pressures applied simultaneously. That is what I am getting at.

[kleinman]

Here are a couple more citations for you to consider as you learn how mutation and selection actually works. The first is an example where monotherapy and combination therapy are contrasted in the treatment of HIV.
http://www.journals.uchicago.edu/JID/journal/issues/v181n3/990850/990850.html (http://www.journals.uchicago.edu/JID/journal/issues/v181n3/990850/990850.html)
We examined the in vitro resistance profile of abacavir in combination passage with other nucleoside analogues, with zidovudine/lamivudine-resistant clinical isolates, and clinically as monotherapy or in combination with zidovudine. There is increasing evidence of subtle interactions between mutations' conferring resistance to different drugs, resulting either in cross-resistance or in some reversal of resistance, and background genotypes' influencing nucleoside RT inhibitor (NRTI) resistance [911, 26]. Our results suggest that similar interactions between key mutations and background genotypes will also be important to abacavir efficacy. Selection experiments in the presence of drug combinations may be of considerable value in predicting the in vivo potency of antiviral combinations. Virus passage experiments in vitro in the presence of drug combinations showed that zidovudine influenced the pattern of mutations selected by abacavir, such that only the K65R substitution was selected. The evolution of mixed viral infections in the presence of various ratios of abacavir and zidovudine suggested that this differential selection is likely to be at least partially due to this inhibitor combination's exerting opposing selective pressures at RT codon M184V. Consistent with these results, in vivo results (see below) indicate that the combination of abacavir with zidovudine appeared to slow the rate and perhaps also the pattern of development of mutations' conferring abacavir resistance. The effect of the addition of lamivudine on delaying the development of zidovudine resistance has been noted elsewhere [9, 27].
In the following example, the authors recognize that combination selection pressures slow the evolution of resistant pathogens and are developing a coherent strategy to make use of this phenomenon.
http://www.phri.org/research/pdf/res_art_drlica05.pdf (http://www.phri.org/research/pdf/res_art_drlica05.pdf)
Studies with fluoroquinolones have led to a general method for restricting the selection of antibiotic-resistant mutants. The strategy is based on the use of antibiotic concentrations that require cells to obtain 2 concurrent resistance mutations for growth. That concentration has been called the “mutant prevention concentration” (MPC) because no resistant colony is recovered even when 1*10^10cells are plated. Resistant mutants are selected exclusively within a concentration range (mutant selection window) that extends from the point where growth inhibition begins, approximated by the minimal inhibitory concentration, up to the MPC. The dimensions of the mutant selection window can be reduced in a variety of ways, including adjustment of antibiotic structure and dosage regimens. The window can be closed to prevent mutant selection through combination therapy with 2 antimicrobial agents if their normalized pharmacokinetic profiles superimpose at concentrations that inhibit growth. Application of these principles could drastically restrict the selection of drug-resistant pathogens.
As you consider these and the other examples which have been cited here on this thread, try to imagine what selection pressures acting on different gene targets would somehow evolve more quickly with simultaneous selection pressures. In honor of joobz’s speculations of how abiogenesis occurs, we will call them “cooperating” selection pressures.

It would make this a very interesting discussion if someone can post a mathematical or empirical example of “cooperating” selection pressures.

While you ponder this, you all have a good weekend and may all your selection pressures “cooperate” with you.

[Paul C. Anagnostopoulos]

Paul, you have no evidence that tiny replicators ever existed and your own model shows what happens on any genome that even approaches the size of any know free living organism. Your own model is my proof.
Then you don't know what a proof is.


Whether it is a consequence, result, effect, outcome, there is a cause and effect relationship, just like there is a cause and effect relationship for mutation and selection.
Yes, it could be all those things. What it isn't is a goal.

Weight width=2, site width=3, other parameters as you used above.
With single selection pressures, generations for zero mistakes
Missed binding sites, 1 generation
Spurious binding within gene, 1 generation
Spurious binding outside gene, 1 generation

Paul, the explanation is that you seriously underestimate the complexity of the fitness landscape when you have three selection conditions. There are many perfect creatures therefore many local optima. Ev is simply getting stuck at a local optimum that isn’t zero mistakes.
Of course, you completely ignored my question. Rcapacity is irrelevant when there is only one pressure.

So let me repeat: How do you explain the data in post #5619?


Any one of the three selection conditions can evolve easily despite the length of the genome.
Because Rcapacity is irrelevant for single conditions.

~~ Paul

[joobz]

It's thursday, so I'd figure I'd ask if Kleinman has managed to justify any of his assumptions:

1.) Mutation rate remains constant
2.) Mutation rate is known
3.) Number of selection pressures for all species for all time in all areas is known
4.) Number of selection pressures is constant
5.) Slection pressure magnitude is constant and equal for all pressures
6.) Point mutations are the only mutation/adaptation mechanism
7.) defining selection pressure is unimportant
8.) slow equals stop


or is he still spouting the same easily refutable nonsense?

[kleinman]

I have to postpone my weekend adjournment to respond to Paul’s post, if for no other reason but to annoy the originator of this thread.

Paul, you have no evidence that tiny replicators ever existed and your own model shows what happens on any genome that even approaches the size of any know free living organism. Your own model is my proof.Then you don't know what a proof is.
Well your model certainly isn’t a proof that the human genome evolved in a billion years. Ev certainly shows that its selection conditions can’t evolve on a realistic length genome for any know free living organism.
Whether it is a consequence, result, effect, outcome, there is a cause and effect relationship, just like there is a cause and effect relationship for mutation and selection.Yes, it could be all those things. What it isn't is a goal.
You wouldn’t be talking about your so called moving goal posts, would you now? Evolution by mutation and selection is a cause and effect relationship and when modeled properly you should be able to predict the behavior of this phenomenon. Now what ev is predicting is that combined selection pressures profoundly slow the evolutionary process or do you want to join with Adequate and contend that more selection conditions accelerates evolution.
Weight width=2, site width=3, other parameters as you used above.
With single selection pressures, generations for zero mistakes
Missed binding sites, 1 generation
Spurious binding within gene, 1 generation
Spurious binding outside gene, 1 generation

Paul, the explanation is that you seriously underestimate the complexity of the fitness landscape when you have three selection conditions. There are many perfect creatures therefore many local optima. Ev is simply getting stuck at a local optimum that isn’t zero mistakes.Of course, you completely ignored my question. Rcapacity is irrelevant when there is only one pressure.

So let me repeat: How do you explain the data in post #5619?
I haven’t ignored your question, you just can’t recognize when ev gets stuck at a local optimum. Since you can’t understand the words, let me draw you a picture.
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The reason the model stops converging is that it is stuck at a local optimum at point A. In order to get to the global optimum, point C, it must take a trajectory that takes it across a trough on the fitness landscape, trough B. Every time the population tries to traverse the trough B, the number of mistakes increase and the population is pushed back to the local optimum, point A. Ascii art, primitive but effective.
Any one of the three selection conditions can evolve easily despite the length of the genome.Because Rcapacity is irrelevant for single conditions.
Rcapacity has no relevance to reality. What ev demonstrates and is relevant to reality is that single selection conditions evolve far more rapidly than multiple simultaneous selection. Real examples of mutation and selection behave the same way.

Here’s an interesting argument why this works.
http://pcwww.liv.ac.uk/~mjames/2005%20Drug%20Resistance%20Updates%20(Hastings%20a nd%20Donnelly).pdf (http://pcwww.liv.ac.uk/~mjames/2005%20Drug%20Resistance%20Updates%20(Hastings%20a nd%20Donnelly).pdf)
The magnitude of natural selection determines the usefulness of antimalarial drug combination therapy (CT). A simple example, taken from Watkins et al. (2005) can illustrate the effect (Fig. 3). Suppose a resistant allele frequency is increasing in a parasite population at a rate of 10% per parasite generation (or about 60% increase per year assuming five parasite generations per year). Suppose also that adding a second drug approximately halves parasitological failure rate so, crudely, cutting the rate of increase to 5% per parasite generation (Watkins et al., 2005). Therefore, it would appear on first examination that adding this second drug to a failing first line treatment to make a CT is doomed to failure because the change has been made too late (Watkins et al., 2005). If, however, the selective disadvantage of the mutant allele in the absence of drug pressure is large and the 10% increase per parasite generation results from the difference between drug pressure favouring resistance at a rate 30% and natural selection eliminating it a rate of −20%, then net selection for resistance is 10% as before. However, adding a second drug will halve the drug pressure from 30 to 15%, giving an overall selection coefficient of 15% − 20% = −5%, indicating that resistance will start to decline at a rate of 5% per generation and CT may have a useful long-term future. Put simply, the addition of the second drug reduces the mutation’s advantage in treated humans (because it is less likely to survive CT than a single drug), making natural selection in untreated people the dominant force and resulting in the mutation being eliminated from the population. This is equivalent to pushing its fitness below the threshold set by natural selection in a manner analogous to a single gene system (Koella and Antia, 2003), and is even more plausible once the effects of recombination are added (Hastings, 1997). This is obviously a simplified argument, illustrated in Fig. 3, but demonstrates that far from being just an academic exercise, determining the presence and magnitude of costs associated with resistance can qualitatively alter the fate of new CT treatments.
Combination selection pressures, it profoundly slows evolution.

[Paul C. Anagnostopoulos]

The reason the model stops converging is that it is stuck at a local optimum at point A. In order to get to the global optimum, point C, it must take a trajectory that takes it across a trough on the fitness landscape, trough B. Every time the population tries to traverse the trough B, the number of mistakes increase and the population is pushed back to the local optimum, point A. Ascii art, primitive but effective.
Blah, blah, blah. Why is it that a perfect creature emerges just fine until Rfrequency becomes greater than Rcapacity?


Rcapacity has no relevance to reality.
I don't care. You said that Rcapacity doesn't explain the behavior of Ev, so I want to know how you explain the results shown in post #5619.


Well your model certainly isn’t a proof that the human genome evolved in a billion years. Ev certainly shows that its selection conditions can’t evolve on a realistic length genome for any know free living organism.
It shows no such thing. It only shows that in Ev it takes millions of generations.

~~ Paul

[jimbob]

If an organism is optimised enough to produce ib average at least one reproducing offspring per parent then it is adequately optimised. It doesn't matter if it is unlikely to reach an even better local optimum.

Competing pressures act to flatten the curve, but at any point there is still a local gradient, even if it is zero.

As thereis fossil evidence of evolutionary history, and some mutations (e.g. neotony) can have a large effect, I suggest that if the sums don't suggest this is possible in the time available, then the numbers or assumptions are wrong.

Kleinman, do you think that there is any evidence that birds evolved from dinosaurs?

If not what are the fossils doing?

[Belz...]

Now I understand, if you publish in the James Randi Educational Foundation forum you are a loon but if you publish in Nature that suddenly makes your hypothesis true. Belz, your logic on publication matches your logic on mutation and selection.

To what "logic" are you refering ? I'm merey asking you to prove your claim. How is that "logic" one way or another ?

And I see you don't put much value in peer-review. That will come as a huge surprise to people reading this thread.

[Belz...]

Gee, Klein. Here's a novel idea: why don't you get the designers of the simulations to tell us how they interpret those results ?

Let's see exactly how many people who know how the model works agree with you.

[cyborg]

Now I understand, if you publish in the James Randi Educational Foundation forum you are a loon but if you publish in Nature that suddenly makes your hypothesis true.

Wrong on both counts - as usual.

[Dr Adequate]

Did he think of any new lies?

[Paul C. Anagnostopoulos]

No new lies, but I'm wondering if we need a list of evasions. I want an explanation of the results in post #5619 other than "it's stuck at a local optimum," or whatever the antievolutionary explanation du jour happens to be.

~~ Paul

[Dr Adequate]

He seems to have added a delusion about the works of Kashtan et el supporting his gibberish. I can't see where he says why he thinks this --- perhaps he hasn't thought of a lie on that subject yet.

Apart from that, it's the same old boring lying trash, isn't it?

Ah well, I'll check in next week and see if the "halfwit" aspect of his character has so far overcome the "tedious bore" aspect as to cause him to make a new funny.

[oponol]

The genome of each individual consists of a byte consisting of eight bits, least significant bit on the right. The phenotype is the integer value represented by that byte.

Goal A: selective pressure to reach 10001000 = 136

Problem is in many runs your population gets stuck at a local optimum like this:
01111111 = 127

Flipping any of those bits takes you further from goal A of 136 than you are already. In fact it would take the spontaneous flipping of the right 4 bits to get closer to the goal.

But if you have an additional goal B to reduce the number of 1s in the sequence, that provides pressure against going anywhere near a genome like 01111111 in the first place.

If you apply goal A and B simultaneously, goal B will be pushing the trajectory toward 00000000. Goal B is only useful to push the sequence off an invalid goal A local optimum.

And by doing that it aids convergance on a solution. The local optimum hinders convergance. Simulataneously applying goal A and B effectively removes that hinderance and so aids convergance.

[jimbob]

Can someone tell me what invalid goal A local optimum is?

If the population is increasing, or stable, whilst at this local optimum, then by definition it is an adequate optimisation; even if it is not the "best*" optimisation.

Surely talking about multiple mutually exclusive, optimal solution families is one way of describing the process of speciation; could someone confirm this for me please?

*An example of a better optimisation in humanity would be an appendix that doesn't rupture. It would not affect the aesthetics of the human form, so any hypothetical designer can't have left it in for that reason. But it is far from optimal.

[kjkent1]

Can someone tell me what is?

If the population is increasing, or stable, whilst at this local optimum, then by definition it is an adequate optimisation; even if it is not the "best*" optimisation.

Surely talking about multiple mutually exclusive, optimal solution families is one way of describing the process of speciation; could someone confirm this for me please?

*An example of a better optimisation in humanity would be an appendix that doesn't rupture. It would not affect the aesthetics of the human form, so any hypothetical designer can't have left it in for that reason. But it is far from optimal.If all life forms were competing as selective pressures against each other and converge towards the fittest organism and multiple selective pressures ultimately halt evolution, then the result would have quickly been that only one organism would be left standing, and it would be a perfect fit for its environment.

Assuming this is where we are headed, and homo sapiens is the perfect creature, then I wish someone would explain the marvelous perfection found in the female human reproductive system. It hurts like hell, one week every month, bleeds uncontrollably, and when it has children, the head doesn't fit through the opening except while producing excrutiating pain.

Women need special doctors and frequently need their entire reproductive system removed. Prior to modern medicine a fairly large minority of women died during childbirth.

If this is kleinman's notion of perfect optimization, then we should reinstate torture as a routine in society, because clearly everyone can benefit from some seriously cruel and unusual punishment.

[kleinman]

The reason the model stops converging is that it is stuck at a local optimum at point A. In order to get to the global optimum, point C, it must take a trajectory that takes it across a trough on the fitness landscape, trough B. Every time the population tries to traverse the trough B, the number of mistakes increase and the population is pushed back to the local optimum, point A. Ascii art, primitive but effective.Blah, blah, blah. Why is it that a perfect creature emerges just fine until Rfrequency becomes greater than Rcapacity?
Paul, I marvel at your tenacity at clinging to illogical and irrational concepts. So let’s consider your Rcapacity concept and try to bring some logic back into the discussion.
Ev is evolving a code in the binding sites that matches the gene. This requires Rfrequency bits of information, more or less. If Rcapacity < Rfrequency, the code can't evolve at all, regardless of the amount of time it would require if it could.
And you define Rcapacity as:
G dominates gamma when comparing the effects of the two parameters on the generations for convergence.Agreed, provided Rfreq stays within reasonable limits (doesn't approach 2 * the binding site width, which is Rcapacity).
You then attempt to demonstrate your concept with the following series.
So Alan, how do you explain this data:

population 64
genome size 2048, Rfrequency = 7
sites 16
mutation 2/generation

weight/site width, Rcapacity, generations

8/9, 18, 15623
7/8, 16, 23063
6/7, 14, 30241
5/6, 12, 28625
4/5, 10, 30501
3/4, 8, 31814
2/3, 6, --- (still 16 mistakes after 120,000 generations)

Why the spike just as Rcapacity goes below Rfrequency?
So, When the weight width=2 and site width=3 in your above series, Rcapacity=6 and this case does not converge and your argument is that there is not Rfrequency bits of information for the case to evolve.

First, I will show you that there are sequences of bases for this case that would give a perfect creature. Start with the following case, similar to your non-convergent case above except G=512.

G=512, site width=3, weight width=2, mutations rate=2 per generation per genome, and the generations for convergence to perfect creature=15,083. The only difference between this case and your non-convergent case is the portion of the genome which consists of the nonbinding site region. If you duplicate that portion of the genome (the nonbinding site region) until you have a genome length of 2048, you would have a perfect creature that would satisfy the conditions of your non-convergent case, so there are perfect creatures that exist in the fitness landscape for your non-convergent case.

The only difference between the G=512 case which converges and your G=2048 case which does not converge is the length of the nonbinding site regions of both genomes. The G=2048 case can have more mistakes in the nonbinding site region than the G=512. What these extra mistakes in your G=2048 case do is interfere with the model finding a trajectory to a perfect creature optimum on the fitness landscape, which we know exist.

Now Paul, let me show you how to map out the fitness landscape for ev.

Each point on the fitness landscape is mapped by the following functional equation.

f(Gi) = mistakesi where i = 1 to 4^G

Note for your non-convergent case G=2048 and you have 4^2048 points on your fitness landscape. This is a huge domain to search to find sequences that satisfy all three selection conditions. Also note that it is trivially simple to find sequences that satisfy any one of the selection conditions from your non-convergent case as demonstrated by the following.

Weight width=2, site width=3, other parameters as you used above.
With single selection pressures, generations for zero mistakes
Missed binding sites, 1 generation
Spurious binding within gene, 1 generation
Spurious binding outside gene, 1 generation

In a population of 64, random sequences of bases will give you sequences of bases which will satisfy any of the three selection conditions on at least one member of the population. The problem is getting all three selection conditions satisfied on one member of the population. Your non-convergent cases can not find a trajectory to the perfect creature from the initial point in the fitness landscape. In fact, selection can interfere with the model finding a rfect creature optimum. Let me demonstrate this to you graphically.

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A member of the population at point D will be selected over a member at point E because member D has fewer mistakes on the fitness landscape than does member E. This occurs despite that member D is on a trajectory to optimum A which is a lower optimum than member E which is on a trajectory to optimum C (the perfect creature optimum). Ev will always converge on a local optimum; it just may not be a perfect creature optimum. It isn’t Rcapacity that prevents convergence on a perfect creature optimum; it is the complexity of the fitness landscape and the existence of other local optimums that prevents ev from finding a trajectory to a perfect creature optimum every time.
Rcapacity has no relevance to reality.I don't care. You said that Rcapacity doesn't explain the behavior of Ev, so I want to know how you explain the results shown in post #5619.
Not only does Rcapacity have no relevance to reality, it does not explain why ev does not converge to a perfect creature under some circumstances as I have shown above.
Well your model certainly isn’t a proof that the human genome evolved in a billion years. Ev certainly shows that its selection conditions can’t evolve on a realistic length genome for any know free living organism.It shows no such thing. It only shows that in Ev it takes millions of generations.
Paul, that is over 200 million generations for a 100k genome and as you know, the search space increases at 4^G. What that shows mathematically is that satisfying multiple simultaneous selection conditions is profoundly slow, far too slow for the theory of evolution to be mathematically possible. And you know what Paul, that is what real examples of mutation and selection shows as well.
It's thursday, so I'd figure I'd ask if Kleinman has managed to justify any of his assumptions:

1.) Mutation rate remains constant
2.) Mutation rate is known
3.) Number of selection pressures for all species for all time in all areas is known
4.) Number of selection pressures is constant
5.) Slection pressure magnitude is constant and equal for all pressures
6.) Point mutations are the only mutation/adaptation mechanism
7.) defining selection pressure is unimportant
8.) slow equals stop


or is he still spouting the same easily refutable nonsense?
Well, joobz, the speculation master of cooperative chemistry for abiogenesis and cooperative selection pressures for evolution, has yet to post any examples of mutation and selection which supports his contentions. Wait, yes he has, when he posts real examples of mutation and selection they support my hypothesis. So he posts examples of the Madagascar rain forest and plate tectonics as examples of multiple selection pressures accelerating mutation and selection. Joobz, post some more examples, if they are real examples of mutation and selection, they support my hypothesis and if they are Madagascar rainforest and plate tectonic examples they are good for a laugh.
If an organism is optimised enough to produce ib average at least one reproducing offspring per parent then it is adequately optimised. It doesn't matter if it is unlikely to reach an even better local optimum.
So, are you arguing that reptiles hadn’t reached an optimum so they continued on evolving until they became birds?
Competing pressures act to flatten the curve, but at any point there is still a local gradient, even if it is zero.
If the gradient is zero, the population stabilizes at that point.
As thereis fossil evidence of evolutionary history, and some mutations (e.g. neotony) can have a large effect, I suggest that if the sums don't suggest this is possible in the time available, then the numbers or assumptions are wrong.
Sure evolution takes place on a microevolutionary basis. Recombination and selection can give striking changes in the morphology of a population such is demonstrated with dog breeding but you don’t get reptiles transforming into birds by mutation and selection, it is mathematically and empirically impossible. Mutation and selection simply can’t accomplish such changes. The selection pressures don’t exist and even if they did, the process of mutation and selection is far too slow.
Kleinman, do you think that there is any evidence that birds evolved from dinosaurs?
There is no mathematical or empirical evidence that mutation and selection can accomplish such a transformation. There are people who extrapolate fossil findings or look for similarities between genes between reptiles and birds and speculate these similarities mean that one was derived from the other but the mathematics of mutation and selection and the empirical evidence which supports this mathematics shows that these speculations and extrapolations are mathematically impossible.
If not what are the fossils doing?
There are plenty of non-evolutionist scientists who can discuss this issue with you. This thread is about the mathematics of mutation and selection and the empirical evidence which supports this mathematics. What this mathematics of mutation and selection shows is that your interpretation and subsequent speculations and extrapolations is contradicting these mathematical and empirical findings of the way mutation and selection actually works.
Now I understand, if you publish in the James Randi Educational Foundation forum you are a loon but if you publish in Nature that suddenly makes your hypothesis true. Belz, your logic on publication matches your logic on mutation and selection.To what "logic" are you refering ? I'm merey asking you to prove your claim. How is that "logic" one way or another ?
Your logic that something can not be true until it is published in a peer reviewed journal. I have and will continue to prove my claim that multiple selection pressures profoundly slow the evolutionary process. I have and will continue doing this using both mathematical and empirical examples. It doesn’t matter whether this is published in Nature or on the James Randi Educational Foundation forum.
And I see you don't put much value in peer-review. That will come as a huge surprise to people reading this thread.
I have nothing against the peer review process. In fact, I am using a peer reviewed and published model of mutation and selection to make my mathematical argument and I post hundreds of examples from peer reviewed journals. Why do you discredit all these examples, you don’t put much value in peer-review. That will come as a huge surprise to people reading this thread.
Gee, Klein. Here's a novel idea: why don't you get the designers of the simulations to tell us how they interpret those results ?

Let's see exactly how many people who know how the model works agree with you.
I discussed the model privately with Dr Schneider and Paul for several months before opening this discussion publicly. Paul (Dr Schneider’s programmer for the online version of ev) has agreed to discuss the model publicly and has back peddled extensively from the claims that Dr Schneider has made about the model. So far, Dr Schneider has refused to talk publicly about his model since this thread has started despite the fact he has said the following.
This gauntlet was thrown on the ground on 2005 May 15.

Notice that, since creatioinists stop complaining when defeated, the most extremely difficult part of the challenge above is "do a scientific test of your own ideas"!
Well, I studied and tested Dr Schneider’s model and it does demonstrate how mutation and selection works and the way his model shows how mutation and selection works shows that the theory of evolution is mathematically impossible. There are plenty of peer reviewed mathematical and empirical examples which substantiates this finding.
Now I understand, if you publish in the James Randi Educational Foundation forum you are a loon but if you publish in Nature that suddenly makes your hypothesis true.Wrong on both counts - as usual.
Hey cyborg, that’s Belz position, you have proved with your cruft theory of evolution that Belz’s position is wrong.
Did he think of any new lies?
Nothing like this whopper from my favorite annoyee and PhD in tantrumatics.
Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
http://forums.randi.org/images/smilies/doglaugh.gif
If you apply goal A and B simultaneously, goal B will be pushing the trajectory toward 00000000. Goal B is only useful to push the sequence off an invalid goal A local optimum. And by doing that it aids convergance on a solution. The local optimum hinders convergance. Simulataneously applying goal A and B effectively removes that hinderance and so aids convergance.
Why don’t you stop speculating? Set up the calculation and run the numbers and prove your point.
invalid goal A local optimum Can someone tell me what … is?
Oponal is trying to evolve a particular sequence on numbers. A particular selection condition does not give that sequence so he uses another selection condition to try to achieve that optimum that he is seeking.
If this is kleinman's notion of perfect optimization, then we should reinstate torture as a routine in society, because clearly everyone can benefit from some seriously cruel and unusual punishment.
I don’t think torture should be reinstituted; I am content to annoy evolutionists. Why don’t I annoy you with a couple more examples of combination selection pressures profoundly slowing evolution? The first example is again dedicated to Dr Schneider and the folks at the National Cancer Institute.

http://www.asco.org/portal/site/ASCO/menuitem.34d60f5624ba07fd506fe310ee37a01d/?vgnextoid=76f8201eb61a7010VgnVCM100000ed730ad1RCR D&vmview=abst_detail_view&confID=23&index=y&abstractID=102323 (http://www.asco.org/portal/site/ASCO/menuitem.34d60f5624ba07fd506fe310ee37a01d/?vgnextoid=76f8201eb61a7010VgnVCM100000ed730ad1RCR D&vmview=abst_detail_view&confID=23&index=y&abstractID=102323)
Synergistic effects of imatinib and interferonα (IFN) on CML cells were demonstrated in vitro. Imatinib selectively inhibits the proliferation of BCR-ABL+ cells, IFN has both antiproliferative and immunomodulatory properties and induces cytotoxic T lymphocytes (CTL). To define the tolerability and efficacy of combination therapy with imatinib and pegylated IFNα2a (Pegasys), a phase I/II study was conducted in 32 Ph+ chronic phase CML patients, recruited within 6-355 days from diagnosis. Pegasys was added on day 15 and then given once weekly, during 8 weeks. Cohorts comprised 300 or 400mg imatinib + 90 or 180μg Pegasys. A 5th cohort of pts received 400mg imatinib for 6 weeks, 300 mg from day 43 combined with 180μg Pegasys for 8 weeks (n=7). Efficacy: Within phase I 30/32 pts (94%) reached a complete hematologic remission, 19 (59%) a major cytogenetic response (Ph+<35%), 8 (25%) being complete. After a maintenance phase of median 309 days major response rate was 79% with 63% complete responders. Ratios BCR-ABL/ABL determined by quantitative RT-PCR reached a median level of 0.44% (range 0.002-35). Toxicity: Grade 3 non-hematologic adverse events were reported in 5 pts. Gr.3 leukopenia occurred in 9 pts, gr.3/4 neutropenia in 4 and 3 pts, respectively, gr.3 thrombopenia in 2 cases. Overall, gr.3/4 cytopenias was observed in 13/32 pts. Cytopenia was rare (1/7 cases) if Pegasys was commenced after 6 weeks imatinib monotherapy. Pts received 71% of the scheduled Pegasys and 95% of imatinib doses. Since imatinib downregulates myeloblastin expression, CTLs could not be detected in 2 pts. with complete cytogenetic remission. Conclusion: The combination treatment of imatinib and Pegasys is feasible and results in a high rate of hematologic and cytogenetic response. Predominant dose limiting toxicities are cytopenias, which are less frequent if Pegasys therapy is commenced after >=6 weeks imatinib monotherapy in order to allow restoration of normal hematopoiesis. Consecutive treatment with Pegasys and imatinib, or combination of imatinib, 400mg/day and Pegasys, 180μg/week starting after 6 weeks is suggested for further studies.
http://hivinsite.ucsf.edu/InSite?page=ar-01-04 (http://hivinsite.ucsf.edu/InSite?page=ar-01-04)
Many antiretroviral combinations containing stavudine have been found to be effective at suppressing HIV viral load and increasing CD4 cell counts. In general, 3-drug combinations have been found to have a more sustained effect than 2-drug combinations. Stavudine should not be administered concurrently with certain medications because of additive or overlapping potential adverse effects. For example, the combination of stavudine and didanosine should be avoided because of increased risk of peripheral neuropathy and hyperlactatemia, and should not be used in pregnant women because of reports of lactic acidosis with pancreatitis or hepatic steatosis.
Combination selection pressures profoundly slow the evolutionary process. This is a mathematical and empirical fact.

[Belz...]

I have nothing against the peer review process. In fact, I am using a peer reviewed and published model of mutation and selection to make my mathematical argument and I post hundreds of examples from peer reviewed journals. Why do you discredit all these examples, you don’t put much value in peer-review. That will come as a huge surprise to people reading this thread.

Is there any of your replies that doesn't involve tu quoques ?

Combination selection pressures profoundly slow the evolutionary process. This is a mathematical and empirical fact.

...that your are yet to demonstrate.

[Paul C. Anagnostopoulos]

So, When the weight width=2 and site width=3 in your above series, Rcapacity=6 and this case does not converge and your argument is that there is not Rfrequency bits of information for the case to evolve.
I said that it becomes suddenly much more difficult to evolve.


G=512, site width=3, weight width=2, mutations rate=2 per generation per genome, and the generations for convergence to perfect creature=15,083. The only difference between this case and your non-convergent case is the portion of the genome which consists of the nonbinding site region. If you duplicate that portion of the genome (the nonbinding site region) until you have a genome length of 2048, you would have a perfect creature that would satisfy the conditions of your non-convergent case, so there are perfect creatures that exist in the fitness landscape for your non-convergent case.
But the "nonbinding site region" would have holes in it where the binding sites are. What would you put in those holes as you performed this artificial duplication?


The only difference between the G=512 case which converges and your G=2048 case which does not converge is the length of the nonbinding site regions of both genomes. The G=2048 case can have more mistakes in the nonbinding site region than the G=512. What these extra mistakes in your G=2048 case do is interfere with the model finding a trajectory to a perfect creature optimum on the fitness landscape, which we know exist.
Yes, but compare the 2/3 case to all the ones above it: They all have G=2048. Why does the 2/3 case suddenly take so much more time to converge?

population 64
genome size 2048, Rfrequency = 7
sites 16
mutation 2/generation

weight/site width, Rcapacity, generations

8/9, 18, 15623
7/8, 16, 23063
6/7, 14, 30241
5/6, 12, 28625
4/5, 10, 30501
3/4, 8, 31814
2/3, 6, --- (still 16 mistakes after 120,000 generations)


~~ Paul

[kleinman]

I have nothing against the peer review process. In fact, I am using a peer reviewed and published model of mutation and selection to make my mathematical argument and I post hundreds of examples from peer reviewed journals. Why do you discredit all these examples, you don’t put much value in peer-review. That will come as a huge surprise to people reading this thread. Is there any of your replies that doesn't involve tu quoques ?
Belz, you are the one who is preaching that it must be peer reviewed in order for it to be true yet when I post hundreds of peer reviewed citations that shows that combination selection pressures profoundly slow evolution, you discredit them. Find a peer reviewed example or make your own case that mutation and selection somehow works some other way. So far you have done neither.
Combination selection pressures profoundly slow the evolutionary process. This is a mathematical and empirical fact....that your are yet to demonstrate.
If you keep looking, you will see it.
So, When the weight width=2 and site width=3 in your above series, Rcapacity=6 and this case does not converge and your argument is that there is not Rfrequency bits of information for the case to evolve.I said that it becomes suddenly much more difficult to evolve.
You’ve got it backwards Paul. The vast majority of cases with ev are difficult to evolve. Only when you get small enough cases is ev capable of evolving the selection conditions simultaneously.
G=512, site width=3, weight width=2, mutations rate=2 per generation per genome, and the generations for convergence to perfect creature=15,083. The only difference between this case and your non-convergent case is the portion of the genome which consists of the nonbinding site region. If you duplicate that portion of the genome (the nonbinding site region) until you have a genome length of 2048, you would have a perfect creature that would satisfy the conditions of your non-convergent case, so there are perfect creatures that exist in the fitness landscape for your non-convergent case.But the "nonbinding site region" would have holes in it where the binding sites are. What would you put in those holes as you performed this artificial duplication?
Paul, my point here is that there are sequences of bases on a G=2048 base genome that will satisfy all three selection conditions or are you saying that in the 4^2048 different possible combination of bases that there are none that will satisfy the 3 selection conditions in ev? The problem with ev in these examples that do not converge is that the model can not find a trajectory to these zero mistake sequences unless the starting point of the evolutionary process falls within a particular domain on the fitness landscape.
The only difference between the G=512 case which converges and your G=2048 case which does not converge is the length of the nonbinding site regions of both genomes. The G=2048 case can have more mistakes in the nonbinding site region than the G=512. What these extra mistakes in your G=2048 case do is interfere with the model finding a trajectory to a perfect creature optimum on the fitness landscape, which we know exist.Yes, but compare the 2/3 case to all the ones above it: They all have G=2048. Why does the 2/3 case suddenly take so much more time to converge?
I explained this in the previous post. If you want to understand specifically why the 2/3 case suddenly takes so many more generations to converge (if it will converge at all), you need to map out the fitness landscape and examine where your optimization process is starting. I suspect that with these short binding site cases on longer genomes that you are introducing many more mistake possibilities in the non-binding site region, but the ultimate reason the model won’t converge on these cases is that a trajectory can not be found on the fitness landscape from the random starting points. Any time you are trying to carry out an optimization on a very complex surface, the optimum found will be dependent on the start point on the optimization surface.

It would be interesting to actually map out the fitness landscape for some cases from ev but even Dr Schneider’s published case would require the computation of 4^256 points (number of mistakes on each of these genomes). It would help explain why the mutation and selection process is so profoundly slow with multiple selection pressures.

[Paul C. Anagnostopoulos]

Paul, my point here is that there are sequences of bases on a G=2048 base genome that will satisfy all three selection conditions or are you saying that in the 4^2048 different possible combination of bases that there are none that will satisfy the 3 selection conditions in ev?
No, I'm saying it suddenly becomes extraordinarily more difficult to evolve a perfect creature.


I explained this in the previous post. If you want to understand specifically why the 2/3 case suddenly takes so many more generations to converge (if it will converge at all), you need to map out the fitness landscape and examine where your optimization process is starting. I suspect that with these short binding site cases on longer genomes that you are introducing many more mistake possibilities in the non-binding site region, ...
Yes, and that is because the binding sites are too narrow to allow a unique-enough pattern for the gene to match. What else could "more mistake possibilities" mean?

The genome doesn't have to be particularly long. Look at this experiment:

population 64
genome size 256, Rfrequency = 5
sites 8
mutation 1/generation

weight/site width, Rcapacity, generations

5/6, 12, 587
4/5, 10, 1148
3/4, 8, 963
2/3, 6, 1982
1/2, 4, --- (still 8 mistakes after 100,000 generations)


... but the ultimate reason the model won’t converge on these cases is that a trajectory can not be found on the fitness landscape from the random starting points. Any time you are trying to carry out an optimization on a very complex surface, the optimum found will be dependent on the start point on the optimization surface.
Yes, but why does the trajectory suddenly become difficult to find? Does it have something to do with the ratio of the gene length to the genome size?

~~ Paul

[kleinman]

Paul, my point here is that there are sequences of bases on a G=2048 base genome that will satisfy all three selection conditions or are you saying that in the 4^2048 different possible combination of bases that there are none that will satisfy the 3 selection conditions in ev?No, I'm saying it suddenly becomes extraordinarily more difficult to evolve a perfect creature.
It is becoming extraordinarily difficult to find a perfect creature optimum but not at finding any local optimum.
I explained this in the previous post. If you want to understand specifically why the 2/3 case suddenly takes so many more generations to converge (if it will converge at all), you need to map out the fitness landscape and examine where your optimization process is starting. I suspect that with these short binding site cases on longer genomes that you are introducing many more mistake possibilities in the non-binding site region, ...Yes, and that is because the binding sites are too narrow to allow a unique-enough pattern for the gene to match. What else could "more mistake possibilities" mean?
What “more mistake possibilities” mean is a more complex fitness landscape or optimization surface is being generated. Finding a trajectory to a particular optimum (perfect creature optimum) becomes more difficult until it becomes virtually impossible because other non-perfect creature local optimum block the trajectories to the perfect creature local optimum.
... but the ultimate reason the model won’t converge on these cases is that a trajectory can not be found on the fitness landscape from the random starting points. Any time you are trying to carry out an optimization on a very complex surface, the optimum found will be dependent on the start point on the optimization surface.Yes, but why does the trajectory suddenly become difficult to find? Does it have something to do with the ratio of the gene length to the genome size?
Clearly the ratio of gene length to genome size affects the shape of the fitness landscape but again, I think you are looking at this problem backwards probably because Dr Schneider published only his single 256 base case. This small case falls into only a limited range of cases which will converge. The vast majority of cases won’t converge to a perfect creature or will take such a huge number of generations that it reveals the mathematical difficultly for the theory of evolution by mutation and selection.

[Belz...]

Belz, you are the one who is preaching that it must be peer reviewed in order for it to be true

Strawman.

yet when I post hundreds of peer reviewed citations that shows that combination selection pressures profoundly slow evolution, you discredit them.

Strawman again. When did I discredit them ? I said that you interpret things in your own twisted way and cherry-pick your examples. How does that discredit them ?

Find a peer reviewed example or make your own case that mutation and selection somehow works some other way. So far you have done neither.

Why don't you just get off of your lazy behind and make things change in the scientific community ? If this earth-shattering new idea of yours is true, you should have no problem causing a major paradigm change that will alter evolution for all time. So why don't you ?

If you keep looking, you will see it.

So far, no joy.

[kleinman]

Belz, you are the one who is preaching that it must be peer reviewed in order for it to be trueStrawman.
Well Belz, it’s the strawman that broke the evolution of camel’s back.
yet when I post hundreds of peer reviewed citations that shows that combination selection pressures profoundly slow evolution, you discredit them.Strawman again. When did I discredit them ? I said that you interpret things in your own twisted way and cherry-pick your examples. How does that discredit them ?
I also cotton picked a few choices. Hey Belz, what is it with this strawman thing? Are you from Oz? We’ll have to bail you out from your strawman mentality.
Find a peer reviewed example or make your own case that mutation and selection somehow works some other way. So far you have done neither.Why don't you just get off of your lazy behind and make things change in the scientific community ? If this earth-shattering new idea of yours is true, you should have no problem causing a major paradigm change that will alter evolution for all time. So why don't you ?
How do know that what is going on here has no affect on the scientific community?
If you keep looking, you will see it.So far, no joy.
Don’t you get any joy in understanding how mutation and selection actually works? There are many real problems that are affected by this phenomenon. Well, at least you are getting annoyed.

[Paul C. Anagnostopoulos]

What “more mistake possibilities” mean is a more complex fitness landscape or optimization surface is being generated. Finding a trajectory to a particular optimum (perfect creature optimum) becomes more difficult until it becomes virtually impossible because other non-perfect creature local optimum block the trajectories to the perfect creature local optimum.

Clearly the ratio of gene length to genome size affects the shape of the fitness landscape but again, I think you are looking at this problem backwards probably because Dr Schneider published only his single 256 base case. This small case falls into only a limited range of cases which will converge. The vast majority of cases won’t converge to a perfect creature or will take such a huge number of generations that it reveals the mathematical difficultly for the theory of evolution by mutation and selection.
Notice how you are suddenly no longer addressing my question. Why does finding the trajectory become precipitously more difficult just as Rcapacity is exceeded? I can make this happen regardless of the genome size and regardless of the ratio of gene length to genome size.

You are now appealing to the complexity of fitness landscapes to avoid the question.

~~ Paul

[kleinman]

What “more mistake possibilities” mean is a more complex fitness landscape or optimization surface is being generated. Finding a trajectory to a particular optimum (perfect creature optimum) becomes more difficult until it becomes virtually impossible because other non-perfect creature local optimum block the trajectories to the perfect creature local optimum.

Clearly the ratio of gene length to genome size affects the shape of the fitness landscape but again, I think you are looking at this problem backwards probably because Dr Schneider published only his single 256 base case. This small case falls into only a limited range of cases which will converge. The vast majority of cases won’t converge to a perfect creature or will take such a huge number of generations that it reveals the mathematical difficultly for the theory of evolution by mutation and selection.Notice how you are suddenly no longer addressing my question. Why does finding the trajectory become precipitously more difficult just as Rcapacity is exceeded? I can make this happen regardless of the genome size and regardless of the ratio of gene length to genome size.
Paul, you talk as if ev stops trying to find an optimum for the given selection conditions when your so called Rcapacity limit is exceeded. Ev does in fact find an optimum; it just isn’t a perfect creature optimum. This is why a have posted this figure several times to give you an idea of what the trajectory appears like for a search for an optimum. I’ll post it again and hopefully you will see the point I am trying to make.
http://www.pnas.org/cgi/content/full/104/34/13711 (http://www.pnas.org/cgi/content/full/104/34/13711)
http://www.pnas.org/content/vol104/issue34/images/medium/zpq0310771490005.gif
Fig. 5. A schematic view of fitness landscapes and evolution under fixed goal and MVG. (a) A typical trajectory under fixed goal evolution. The population tends to spend long periods on local maxima or plateaus. (b) A typical trajectory under MVG. Dashed arrows represent goal switches. An effectively continuous positive gradient on the alternating fitness landscapes leads to an area where global maxima exist in close proximity for both goals.
Note that this is a very simple fitness landscape in this example but note how the model lingers around local optima in the top figure. It is similar to the way ev behaves. Ev generates fitness landscapes that have huge numbers of points. If you want to get an accurate idea of why ev takes trajectories that don’t lead to perfect creature optima, you will have to generate the fitness landscape and watch which trajectory the model takes.
You are now appealing to the complexity of fitness landscapes to avoid the question.
It is a fact that ev generates fitness landscapes that have astronomically huge number of points. Despite this, a population of creatures on this fitness landscape will take a trajectory on this fitness landscape to some local optimum. It has nothing to do with the information content of a binding site. It has everything to do with the shape of the fitness landscape and the starting point from which you start your search for an optimum. This is why; even when the model converges on a non-perfect creature optimum, the convergence is stable. If you want a more precise description of why ev behaves like this, the only way I can think of approaching this is to generate the full fitness landscape and track the trajectory as ev converges on some local optimum. You should also track the number of mistakes for each selection condition as the model converges.

[joobz]

It's thursday, so I'd figure I'd ask if Kleinman has managed to justify any of his assumptions:

1.) Mutation rate remains constant
2.) Mutation rate is known
3.) Number of selection pressures for all species for all time in all areas is known
4.) Number of selection pressures is constant
5.) Slection pressure magnitude is constant and equal for all pressures
6.) Point mutations are the only mutation/adaptation mechanism
7.) defining selection pressure is unimportant
8.) slow equals stop


or is he still spouting the same easily refutable nonsense?

Well, joobz, the speculation master of cooperative chemistry for abiogenesis and cooperative selection pressures for evolution, has yet to post any examples of mutation and selection which supports his contentions. Wait, yes he has, when he posts real examples of mutation and selection they support my hypothesis. So he posts examples of the Madagascar rain forest and plate tectonics as examples of multiple selection pressures accelerating mutation and selection. Joobz, post some more examples, if they are real examples of mutation and selection, they support my hypothesis and if they are Madagascar rainforest and plate tectonic examples they are good for a laugh.

In other words, you are unable to justify your assumptions.

[kleinman]

Well, joobz, the speculation master of cooperative chemistry for abiogenesis and cooperative selection pressures for evolution, has yet to post any examples of mutation and selection which supports his contentions. Wait, yes he has, when he posts real examples of mutation and selection they support my hypothesis. So he posts examples of the Madagascar rain forest and plate tectonics as examples of multiple selection pressures accelerating mutation and selection. Joobz, post some more examples, if they are real examples of mutation and selection, they support my hypothesis and if they are Madagascar rainforest and plate tectonic examples they are good for a laugh.In other words, you are unable to justify your assumptions.
That’s right joobz; I haven’t been able to justify my assumptions except with a few hundred real examples of mutation and selection. You previously showed interest in the influenza virus. I came across a few examples of combination selection pressures slowing the evolution of the influenza virus. Here is a couple of citations from an area you previously showed interest in.
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=17591026&dopt=AbstractPlus (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=17591026&dopt=AbstractPlus)
BACKGROUND: The clinical management of H5N1 influenza virus infection in humans remains unclear. Combination chemotherapy with drugs that target different viral proteins might be more effective than monotherapy. METHODS: BALB/c mice were treated by oral gavage for 5 days with amantadine (1.5, 15 or 30 mg/kg/day) and oseltamivir (1 or 10 mg/kg/day) separately or in combination. Mice were challenged 24 h after initiation of treatment with 10 mouse 50% lethal doses of either amantadine-sensitive (having S31 in the M2 protein) or amantadine-resistant (having N31 in the M2 protein) recombinant A/Vietnam/1203/04 (H5N1) virus. RESULTS: Combination treatment with amantadine (15 or 30 mg/kg/day) and oseltamivir (10 mg/kg/day) provided greater protection (60% and 90%, respectively) against lethal infection with amantadine-sensitive H5N1 virus than did monotherapy. Moreover, spread of the virus to the brain was prevented by both combination regimens. The efficacy of the drug combinations against amantadine-resistant H5N1 virus was comparable to that of oseltamivir alone. Oseltamivir produced a dose-dependent effect against both recombinant H5N1 viruses (P < 0.05) but did not provide complete protection against lethal infection. Importantly, no mutations in the HA, NA and M2 proteins were detected when the two drugs were used in combination. CONCLUSIONS: Combination chemotherapy provided a survival advantage over single-agent treatment of mice inoculated with neurotropic H5N1 influenza virus. This strategy might be an option for the control of pandemic influenza viruses that are sensitive to amantadine. Combinations that include other drugs should be explored.

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=PubMed&Cmd=ShowDetailView&TermToSearch=16516984&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstractPlus (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=PubMed&Cmd=ShowDetailView&TermToSearch=16516984&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstractPlus)
Rapid development of resistant influenza variants after amantadine treatment is one of the main drawbacks of M2 blockers. On the other hand, the emergence of variants with low susceptibility to the neuraminidase (NA) inhibitors is limited. In the present study we examined whether combination therapy with two classes of anti-influenza drugs can affect the emergence of resistant variants in vitro. We observed that virus yields of human A/Nanchang/1/99 (H1N1), A/Panama/2007/99 (H3N2), and A/Hong Kong/156/97 (H5N1) viruses in MDCK cells were significantly reduced (P<0.005) when the cells were treated with the combination of amantadine and low doses of oseltamivir carboxylate (< or =1microM). After five sequential passages in MDCK cells, the M2 protein of viruses cultivated with amantadine alone mutated at positions V27A and S31N/I. Viruses cultivated with oseltamivir carboxylate (> or =0.001microM) possessed mutations in the hemagglutinin (HA) protein. These variants showed reduced efficiency of binding to sialic acid receptors and decreased sensitivity to NA inhibitor in plaque reduction assay. Importantly, no mutations in the HA, NA, and M2 proteins were detected when the drugs were used in combination. Our results suggest that combination chemotherapy with M2 blocker and NA inhibitor reduced the emergence of drug-resistant influenza variants in vitro. This strategy could be an option for the control of influenza virus infection, and combinations with other novel drugs should be explored.

[joobz]

That’s right joobz; I haven’t been able to justify my assumptions except with a few hundred real examples of mutation and selection.
Were were right up until that grey section there,
because NONE of your citations have said:
1.) Mutation rate remains constant
2.) Mutation rate is known
3.) Number of selection pressures for all species for all time in all areas is known
4.) Number of selection pressures is constant
5.) Slection pressure magnitude is constant and equal for all pressures
6.) Point mutations are the only mutation/adaptation mechanism
7.) defining selection pressure is unimportant
8.) slow equals stop

[kleinman]

That’s right joobz; I haven’t been able to justify my assumptions except with a few hundred real examples of mutation and selection.Were were right up until that grey section there, because NONE of your citations have said:
1.) Mutation rate remains constant
2.) Mutation rate is known
3.) Number of selection pressures for all species for all time in all areas is known
4.) Number of selection pressures is constant
5.) Slection pressure magnitude is constant and equal for all pressures
6.) Point mutations are the only mutation/adaptation mechanism
7.) defining selection pressure is unimportant
8.) slow equals stop
Of course none of the real examples of mutation and selection assume that the mutation rate remains constant, or is the mutation rate known, or are the number of selection pressures for all species for all time in all areas known or are selection pressures constant or selection pressure magnitude constant and equal for all selection pressures or point mutations are the only mutation/adaptation mechanism, of course defining selection pressures are important and so slow that evolution effectively stops is enough to prove my hypothesis.

Now if you were as good at coloring text in your citations as you try to be with my statements, you could do something like this:
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=PubMed&Cmd=ShowDetailView&TermToSearch=17066897&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstractPlus (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=PubMed&Cmd=ShowDetailView&TermToSearch=17066897&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstractPlus)
Mouse models have been widely used for evaluating potential influenza virus inhibitors. However, the viral strains traditionally used in these models are fairly old and do not represent currently circulating viruses in nature. We developed two new lethal infection models in mice using mouse-adapted influenza A/New Caledonia/20/99 (H1N1) and influenza B/Sichuan/379/99 viruses. Both virus infections were used to study oral treatment with oseltamivir and ribavirin, both alone and in combination. Oral treatments were given twice daily for 5 days starting 4 h before infection in initial studies. Against influenza A, oseltamivir was active at 10, 20, and 40 mg/kg/day, protected 80-100% of mice from death and reduced lung consolidation - ribavirin was similarly effective at 20, 40, and 80 mg/kg/day. When treatments were initiated after virus challenge, delaying treatment with oseltamivir even 1 day caused it to be ineffective. Ribavirin prevented mortality by 50-80% when treatments were delayed 1-4 days after infection. The combination of the two drugs (oseltamivir at 20 mg/kg/day and ribavirin at 40 mg/kg/day) was no better than ribavirin alone. In contrast to what we observed with influenza A virus infections, oseltamivir and ribavirin showed similar dose-related antiviral activities against influenza B virus infections. The compounds both significantly increased survival when treatments started up to 4 days after infection, but ribavirin was more active than oseltamivir (50-80% survival compared to 30-40% survival, respectively, when starting treatments on days 2-4 after infection). By varying the doses of each drug that were used in combination (oseltamivir at 1.25, 2.5 and 5 mg/kg/day; ribavirin at 5, 10 and 20 mg/kg/day) certain dosage combinations were superior to either compound used alone as assessed by decreased mortality, lung virus titre, lung score and lung weight parameters. These activities differed from published results with older, more established virus strains as oseltamivir was less effective and ribavirin was more active than previously reported.
Joobz, too bad you can’t color highlight any of your citations, but you have proven yourself to be the champion speculator on this thread with your cooperative chemistry hypothesis for abiogenesis and cooperative selection pressures for the theory of evolution.

What was that again joobz? Madagascar rainforests and plate tectonics accelerates the mutation/selection process??????
http://forums.randi.org/images/smilies/doglaugh.gif

[OnlyTellsTruths]

Oh no! You got math in my biology, and biology in your math! This isn't ever gonna clean up.

[kleinman]

Oh no! You got math in my biology, and biology in your math! This isn't ever gonna clean up.
Now, now OnlyTellsTruths, you already haven’t lived up to your name, it isn’t your biology and it isn’t my math. Anyway, nothing like a little bit of math to clean up the field of biology and a little bit of biology to make mathematics interesting. Hey OnlyTellsTruths, welcome to the discussion.

[joobz]

What was that again joobz?
I don't know what that was. (i assume you are refering to your post).
It definitely wasn't a justification of your assumptions.
1.) Mutation rate remains constant
2.) Mutation rate is known
3.) Number of selection pressures for all species for all time in all areas is known
4.) Number of selection pressures is constant
5.) Slection pressure magnitude is constant and equal for all pressures
6.) Point mutations are the only mutation/adaptation mechanism
7.) defining selection pressure is unimportant
8.) slow equals stop

[kleinman]

What was that again joobz?I don't know what that was. (i assume you are refering to your post).
It definitely wasn't a justification of your assumptions.
1.) Mutation rate remains constant
2.) Mutation rate is known
3.) Number of selection pressures for all species for all time in all areas is known
4.) Number of selection pressures is constant
5.) Slection pressure magnitude is constant and equal for all pressures
6.) Point mutations are the only mutation/adaptation mechanism
7.) defining selection pressure is unimportant
8.) slow equals stop
What, no color coding of my post? I’ve color coded your post just to prove that I read them. When are you going to post some more citations? I like the citations you use. Since you haven’t posted any new citations here’s another which show that combination selection pressures slow the evolution of resistance.
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=PubMed&Cmd=ShowDetailView&TermToSearch=17163384&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstractPlus (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=PubMed&Cmd=ShowDetailView&TermToSearch=17163384&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstractPlus)
The goals of antiviral treatment for influenza are to decrease symptoms and functional disability and, more important, to decrease associated complications, hospitalizations, and mortality. Four drugs have been approved for treatment of and prophylaxis against influenza in the United States, but they are underutilized. The M2 ion channel inhibitors amantadine and rimantadine are effective for prophylaxis, and they decrease the duration of symptoms if they are used for early treatment of influenza A. The rapid emergence of resistance during therapy and, recently, the circulation of resistant H3N2 viruses in the community ha