Annoying creationists

[Dr Adequate]

So, you don’t think natural selection has anything to do with the efficient use of energy for reproduction? Then what is natural selection all about?

You have read the references to Dr Schneider’s mathematics of mutation and selection but you have yet to understand them. If you run some simple cases (increase genome length and keep all other parameters constant) with ev, you will find that it is very easy to satisfy the three selection conditions on very short genomes. As you lengthen the genome; the generations for convergence increases at a supralinear rate. HIV has a genome length short enough (~18k) that this length genome will converge the three selection conditions in a reasonable length of time (reasonable number of generations). As you increase the genome length in ev, the generations for convergence becomes huge; try the model yourself. If you reduce the number of selection conditions to one, ev shows that this single selection condition will evolve much more rapidly than trying to evolve all three selection conditions simultaneously. This is exactly what is revealed in the real situation when combination therapy is used to treat HIV vs monotherapy treatment of this disease. This phenomenon is also demonstrated with pesticides, herbicides and rodenticides; combination use of these selection pressures delays the evolution of resistance to these selection pressures. This is the results you get from a peer reviewed and published mathematical model of mutation and natural selection and we have numerous real examples of this behavior. You have no mathematics to support your theory of evolution by mutation and selection and you have no examples that show multiple selection pressures accelerates evolution. In addition, you have no selection pressure that can evolve a gene from the beginning.

Well, you are not an expert on the mathematics of mutation and selection either. If you continue to study Dr Schneider’s mathematics and read the threads on this topic you will begin to understand why your theory is mathematically impossible. Multiple selection pressures slow evolution and you don’t have selection pressures that evolve genes from the beginning.

There you go Ichneumonwasp, prepare yourself for a hearty meal of red herring, string cheese and whine.

We start the meal with a big glass of whine. I doubt that Dr Schneider would call his mathematics “theistic”.

Next, you get a big serving of red herring.

And now we get some string cheese; which of the 10^500 alternative universes are we talking about?

Ichneumonwasp, would you care for another serving of string cheese?

And don’t let any mathematical science get in the way of your evolutionary belief system.

You almost got the former correct. The former belief is that we are owned by our creator but not to toy with us throughout or existence.

And we finish this meal with another glass of whine. Kjkent1, don’t you realize that the leaf is slave to the wind?

Nothing new here.

 

[Dr Adequate]

Evolution occurs at speeds orders of magnitude greater you say it should be occurring.

I've only needed to use the word "qunitillions" twice in my life, and both times it was 'cos I'd calculated the order of magnitude by which kleinman was wrong.

 

[kleinman]

Annoying Creationists

So, you don’t think natural selection has anything to do with the efficient use of energy for reproduction? Then what is natural selection all about?

wow, you really don't understand science.

I have to admit that I don’t understand your laws of alchemical engineering.

Of course natural selection has all to do with efficient energy use. What I'm saying is that the first law has nothing to do with energy efficiency. The first law doesn't care how efficient a process is. It only says that you can't make energy out of nothing. You can only switch between forms of energy. What that energy is used for or what it does doesn't matter.

Which law of thermodynamics do you use to compute energy efficiencies?

We start the meal with a big glass of whine. I doubt that Dr Schneider would call his mathematics “theistic”.

Dr. Schneider admits that ev does not model all of the real-world means by which evolutionary change occurs. That is how he answered your conclusion that ev is too slow.

Dr Schneider has neither publicly nor privately answered why ev is so slow. He did embrace Paul’s concept of Rcapacity but said it would take more study to verify Paul’s idea. More study has shown that it is the multiple selection conditions which slows the evolution process in ev, not Paul’s Rcapacity theory.

You refuse to accept this argument without further proof, however, you won't do any experiments to prove it. That's not Schneider's problem -- it's your problem.

Insertions/deletions, inversions, translocations and any other mechanism of scrambling a genome are not going to change the underlying mathematics of mutation and selection. The more selection conditions, the more difficult it is to navigate the fitness landscape to find optimums for all the selection conditions. This is fundamental to the mathematics of mutation and selection. There is no reason to believe that frame shifts or random shifting of portions of a genome are going to accelerate evolution. There are many reasons to believe that these types of mutations are far more destructive to living things.

I am not going to do the programming to include other mutation mechanisms in ev. I won’t do this for two reasons. The first is that I don’t believe any of these mechanisms will alter the underlying reason why ev converges so slowly for large genomes and the second is that evolutionists don’t accept the results of ev now and try to attribute the model to me. Evolutionists need to convince themselves of the mathematics of mutation and selection. The only way that will happen is if evolutionists do the mathematics themselves.

You almost got the former correct. The former belief is that we are owned by our creator but not to toy with us throughout or existence.

You're deluded if you read the Christian Bible as anything other than an example of a diety who toys with his creations.

Do you think God was toying with us when He sent his Son to die for our sins?

Why don't you explain to us how God punishes all women throughout history for Eve's original sin, by making their physique such that they are forced to suffer excrutiating pain during childbirth? That's not just toying -- it's sadistic torture!

As someone who has delivered children, I am sure females are the stronger sex. This judgment of God is nothing compared to what God’s wrath can and will do. God does not let sin go un-judged and when God goes to execute judgment, there will be no rock to hide under. If you are smart, you will turn to God and beg forgiveness and God has made a way to do this.

Quite a God you've invented, Alan...quite a God.

This is not a God that I have invented, I’m just debunking the mutation and selection god that evolutionists think is the way we got here.

Kjkent1, don’t you realize that the leaf is slave to the wind?

Slavery is the causing of one person to labor on behalf of another by means of actual or threatened physical force or legal coercion (U.S. v. Kozminiski).

Your definition of slavery is too narrow little gator. The leaf goes where the wind tells it to go.

The leaf doesn't labor on behalf of the wind. The rat is forced to undergo experiments by the researcher. And, God forces Man to labor on His behalf at the threat of eternal damnation.

The wind can blow the leaf into the fire.

You have read the references to Dr Schneider’s mathematics of mutation and selection but you have yet to understand them. If you run some simple cases (increase genome length and keep all other parameters constant) with ev, you will find that it is very easy to satisfy the three selection conditions on very short genomes. As you lengthen the genome; the generations for convergence increases at a supralinear rate. HIV has a genome length short enough (~18k) that this length genome will converge the three selection conditions in a reasonable length of time (reasonable number of generations). As you increase the genome length in ev, the generations for convergence becomes huge; try the model yourself. If you reduce the number of selection conditions to one, ev shows that this single selection condition will evolve much more rapidly than trying to evolve all three selection conditions simultaneously. This is exactly what is revealed in the real situation when combination therapy is used to treat HIV vs monotherapy treatment of this disease. This phenomenon is also demonstrated with pesticides, herbicides and rodenticides; combination use of these selection pressures delays the evolution of resistance to these selection pressures. This is the results you get from a peer reviewed and published mathematical model of mutation and natural selection and we have numerous real examples of this behavior. You have no mathematics to support your theory of evolution by mutation and selection and you have no examples that show multiple selection pressures accelerates evolution. In addition, you have no selection pressure that can evolve a gene from the beginning.

So, when Kjkent1 ran his simulations using genome lengths of 256 to roughly 4K with 3 selection pressures and arrived at generation estimates ranging from 13,000 to 600K to 700K, you will accept that as realistic?

I have not duplicated kjkent1’s series but his numbers are similar to cases which I have run.

And you say that as genome size increases there is a non-linear effect on generation time such that generation times for convergence markedly increase? And you say that HIV with a genome length of 18K (roughly 4.5 times greater than the biggest genome that Kent ran) should be expected to converge in a realistic time frame?

The generation for convergence is approximately proportional to the genome length to the 2nd power for this range in ev.

Since the generation time for HIV-1 is either 1.2 or 2 days, depending on what source you use, and the generation time for convergence increases in a non-linear fashion according to your account when 3 pressures are applied, how is it that a genome sized roughly 18K in the real world achieves resistance to three drugs within the lifetime of a human being and within a few years (approximatelyly 600-700 generations)? Your mathematics should invalidate that finding, Dr. Kleinman, but reality begs to differ. In other words, aside from the fact that you have now conceded that resistance can occur in HIV and HIV triple therapy is not a good real world model for your "mathematical impossibility" for evolution, reality shows that the mathematics of evolution that you are proposing is simply wrong.

Where your analogy breaks down is with the HIV generation time. Ev only has one reproduction per generation per creature; HIV has many more reproductions than that in a single day.

Ev shows that an 18k genome can evolve 3 selection pressures simultaneously in a fairly short period of time. Huge populations lower the generations for convergence a couple of orders of magnitude, so ev is making a reasonable park estimate for what is happening with HIV. However, when you increase genome length in ev, the generations for convergence becomes huge. Dr Schneider said this on his frequently asked question page for ev http://www-lmmb.ncifcrf.gov/~toms/paper/ev/faq-for-ev.html :

If you had a reasonable sized genome would you find that there won't be an information gain? No. Don't be lazy, go try it yourself! But notice that it will take a lot more computation, and the runs may take some years unless you write a version that uses parallel processors.

Either throw out the model, throw out the surrogate measure of converging Rsequence --> Rfrequency, or admit that you have wasted all our time.

Why should we throw out the best model for mutation and selection that we have? If you had read this thread, you would know that there has been discussion on the convergence criteria used for our estimates. Paul believes that the “perfect creature” convergence is more appropriate than the Rsequence à Rfrequency condition. In many cases the generations for both are very similar.

This discussion has been far from a waste of time. I believe that the true behavior of mutation and selection has been revealed which has important clinical medical implications, not to mention I get the opportunity to annoy evolutionists.

Evolution occurs at speeds orders of magnitude greater you say it should be occurring.

It does if you believe that HIV only reproduces one time per day.

 

[joobz]

I have to admit that I don’t understand your laws of alchemical engineering.

Which law of thermodynamics do you use to compute energy efficiencies?

good question. To calculate efficiency you must first ask
What are you defining as "efficiency".

 

[Ichneumonwasp]

I didn't say that HIV reproduces once per day; I said it's generation time is once/day -- which is one of the models surrogate measures. You have repeatedly said that population size is of little or no importance, so all that is left is generation time to discuss.

If instead you will accept the generally agreed upon estimate of 10^9 viral particles per generation (in an untreated patient, as Dr. Richard earlier provided) that are produced in a day or so and accept the staggering number of possible muations that can occur, then in a genome length of 18K we have rapid development of resistance even in the presence of three selection pressures.

It doesn't take long for evolution to work. In a couple of years resistance develops in the real world when numerous offspring are produced, correct?

So, how is it that evolution becomes mathematically impossible? I'm still missing that little bit of logic. With generation times of roughly 15 minutes for many bacteria, we can witness nearly 100 generations/day. The number of individuals developed with exponential growth is astounding. So, if the issue is really the number of individuals as you seem to be implying now with HIV, then why didn't you say so. Reality still is reality. Resistance develops in short order where you have said that it shouldn't.

 

[Ichneumonwasp]

Or are you saying that HIV cannot be properly modelled by ev?

 

[Dr Adequate]

Ah, a new lie.

However, when you increase genome length in ev, the generations for convergence becomes huge. Dr Schneider said this on his frequently asked question page for ev

If you had a reasonable sized genome would you find that there won't be an information gain? No. Don't be lazy, go try it yourself! But notice that it will take a lot more computation, and the runs may take some years unless you write a version that uses parallel processors.

I notice that Dr Schneider says no such thing. Really, if you want to deceive people about what he said, quoting him is rather stupid, don't you think?

This discussion has been far from a waste of time.

I agree. It's always fun watching creationists make stupid mistakes about basic scientific and mathematical concepts, especially when they're as puffed up with self-conceit as you are.

I believe that the true behavior of mutation and selection has been revealed which has important clinical medical implications ...

It has indeed been revealed --- by real scientists, not by some fatuous creationist jerk babbling nonsense about socks and cheese.

Among the important medical implications of the true behavior of mutation and selection is the fact that in the real world, viruses and bacteria can evolve to cope with multiple selective pressures.

 

[kleinman]

Annoying Creationists

Which law of thermodynamics do you use to compute energy efficiencies?

good question. To calculate efficiency you must first ask
What are you defining as "efficiency".

When you are talking about fitness in the theory of evolution, you are talking about reproduction and it takes energy to reproduce. Those creatures which use more of the available energy to reproduce are more fit. Natural selection works to make best use of the available energy to reproduce.

I didn't say that HIV reproduces once per day; I said it's generation time is once/day -- which is one of the models surrogate measures. You have repeatedly said that population size is of little or no importance, so all that is left is generation time to discuss.

Population size is not sufficient to overcome the effect of increasing genome size when considering macroevolution. However when you compare the results from ev to reality, you need to compare apples with apples. Ev only models one reproduction per generation per creature.

If instead you will accept the generally agreed upon estimate of 10^9 viral particles per generation (in an untreated patient, as Dr. Richard earlier provided) that are produced in a day or so and accept the staggering number of possible muations that can occur, then in a genome length of 18K we have rapid development of resistance even in the presence of three selection pressures.

And ev shows an analogous result. In addition, ev shows that a single selection pressure evolves far more rapidly that all three selection pressures in combination. The same is seen with monotherapy of HIV.

It doesn't take long for evolution to work. In a couple of years resistance develops in the real world when numerous offspring are produced, correct?

Don’t forget, HIV is an extremely short genome when compared to even the smallest genome in a free living creature. Mutation and selection works with small genomes with limited selection pressures and huge populations and the resultant changes in the genes and their associated proteins are limited to changes in the conformation of proteins, not to the evolution of totally new genes. The problem for you evolutionists is that creatures with large genomes and small populations don’t have sufficient generations to accomplish any significant macroevolutionary changes.

So, how is it that evolution becomes mathematically impossible? I'm still missing that little bit of logic. With generation times of roughly 15 minutes for many bacteria, we can witness nearly 100 generations/day. The number of individuals developed with exponential growth is astounding. So, if the issue is really the number of individuals as you seem to be implying now with HIV, then why didn't you say so. Reality still is reality. Resistance develops in short order where you have said that it shouldn't.

It is macroevolution which is mathematically impossible. Aside from the issue that you don’t have any selection conditions that would evolve a gene from the beginning, mutation and selection is a very slow process when compared to recombination and selection.

Bacteria can not and does not sustain the reproductive rates you suggest for more than a few hours. Bacteria can accomplish microevolutionary changes in relatively short periods of time as seen with the development of drug resistance but the same phenomena as seen with HIV is seen with bacteria. That is, multiple drug therapy slows the evolution of drug resistant strains of the bacteria.

Evolutionists have extrapolated microevolutionary processes to macroevolution such as the evolution of birds from reptiles. You simply do not have the number of generations, populations and selection pressures to do this by mutation and selection. The number of genetic changes to morph these huge genomes from the one form to the other is mathematically impossible.

Ev shows how mutation and selection works. Mutation and selection can accomplish microevolutionary changes but the process is slowed as the genome length increases and as the number of selection pressures increases.

Or are you saying that HIV cannot be properly modelled by ev?

If you had read this thread, you would have seen that I suggested that ev be modified to more exactly model the evolution of drug resistance with HIV, I suggested this more than once. This would be a proper use of the concept of mutation and selection unlike the unscientific and mathematically deficient extrapolation of the concept that evolutionists propose.

Try to model the transformation of a reptile genome to a bird genome. You simply don’t have the selection pressures, population sizes and time to accomplish such transformations on these large genomes by mutation and selection.

 

[Ichneumonwasp]

Ev only models one reproduction per generation per creature.

Now wait a second, I entered this discussion because you pushed quite fervently the idea that ev modelled real world evolutionary processes and HIV triple therapy was the perfect example of this real world modelling showing that three selection pressures so thoroughly slowed the process that evolution was not possible. You gave ground finally on the fact that HIV triple therapy does not stop evolution but allows resistance to develop and now it is quite apparent that ev could never model the effects of triple therapy on HIV in the first place. So do you now deny the validity of HIV triple therapy as a real world example for ev?

Why have you been wasting my time with all of the misrepresentations?

In addition, ev shows that a single selection pressure evolves far more rapidly that all three selection pressures in combination. The same is seen with monotherapy of HIV.

Why do you keep repeating this since I haven't questioned it? It isn't actually correct, though, since a single pressure can result in extinction.

Don’t forget, HIV is an extremely short genome when compared to even the smallest genome in a free living creature.

Which matters how? In the early stages of life all genomes would have been short, and they would have had extremely short generation times producing multiple copies each -- especially if origins included peptides which RNA used as a template. With bacteria we already see other forms of lateral information transfer, which allowed one species to "solve" an evolutionary problem and pass it to the next guy, a process that dramatically sped the evolutionary process. In such a scenario, how do we even know how many real selection pressures acted at any one time in the early biosphere?

The problem for you evolutionists is that creatures with large genomes and small populations don’t have sufficient generations to accomplish any significant macroevolutionary changes.

What? Since when did asexual reproduction and only mutation become the norm for evolutionary change in large genomes with small populations?

You do realize that most of the mutations that cause changes in animals occur in genes that regulate development. Small changes in early development result in huge potential changes in adults.

Bacteria can not and does not sustain the reproductive rates you suggest for more than a few hours.

They do if they are under multiple strong selection pressures killing them off left and right. Isn't that the point here?

Bacteria can accomplish microevolutionary changes in relatively short periods of time as seen with the development of drug resistance but the same phenomena as seen with HIV is seen with bacteria. That is, multiple drug therapy slows the evolution of drug resistant strains of the bacteria.

So now that you cannot support the idea of HIV triple therapy being a realistic real world example this turns into a microevolution vs. macroevolution debate?

If you had read this thread, you would have seen that I suggested that ev be modified to more exactly model the evolution of drug resistance with HIV, I suggested this more than once.

OK, then you admit that ev was not a good model for HIV triple therapy and yet the entire thrust of your argument when I joined this thread was that HIV triple therapy was the perfect model of three selection pressures stopping evolution just like ev shows.

In other words, you lied to me, Dr. Kleinman. You knowingly and deliberately misrepresented what you now claim to know as the truth. You lied to all of us, Dr. Kleinman. And now you are left with no real world example of your precious three selection pressures.

 

[joobz]

When you are talking about fitness in the theory of evolution, you are talking about reproduction and it takes energy to reproduce. Those creatures which use more of the available energy to reproduce are more fit. Natural selection works to make best use of the available energy to reproduce.

Exactly. It is the efficiency of reproduction. See, you need an additional rule or two on top of the laws to explain the mechanism behind evolution. Therefore, natural selection isn't a simple "restatement of the 1st law."

 

[kjkent1]

Try to model the transformation of a reptile genome to a bird genome. You simply don’t have the selection pressures, population sizes and time to accomplish such transformations on these large genomes by mutation and selection.

This is false. Unnamed's alternative selection algorithm substantially increases the evolutionary performance of ev, such that it is fast enough to satisfy the necessary generational constraints -- even using only random point mutations. Add to that the other potential mutation classes and evolution is more than fast enough to produce whatever real-world changes are required to produce the variety of speciation that has occurred since life arose on Earth.

 

[cyborg]

Ah, a new lie.

I notice that Dr Schneider says no such thing. Really, if you want to deceive people about what he said, quoting him is rather stupid, don't you think?

kleinman doesn't get the difference between computational time and model time?

BWAHAHHAHAHA, I knew there was a reason I still read this thread. What a dumbass.

 

[kleinman]

Annoying Creationists

Ev only models one reproduction per generation per creature.

Now wait a second, I entered this discussion because you pushed quite fervently the idea that ev modelled real world evolutionary processes and HIV triple therapy was the perfect example of this real world modelling showing that three selection pressures so thoroughly slowed the process that evolution was not possible. You gave ground finally on the fact that HIV triple therapy does not stop evolution but allows resistance to develop and now it is quite apparent that ev could never model the effects of triple therapy on HIV in the first place. So do you now deny the validity of HIV triple therapy as a real world example for ev?

If you had read this thread, you would find that I have repeatedly said the ev represents a plausible model of mutation and selection. It is Dr Schneider and Paul (until he found out what ev really shows) who have said that ev models reality. What Dr Schneider has done is captured important mathematical principles of mutation and selection. Those principles that he has captured is that multiple selection pressures slow the evolutionary process, increasing the genome length slows the evolutionary process and increasing population accelerates the evolutionary process but not at markedly high rates. All these factors are well illustrated by the use of combination therapy to treat HIV. These same principles are demonstrated with the use of combination therapy to treat TB and the consequences of monotherapy for the treatment of MRSA, Gonorrhea, pseudomonas and other microbes. If these examples are not enough to demonstrate the validity of the ev model, consider the examples of combination pesticides, herbicides and rodenticides which were presented earlier. All these examples show that multiple selection pressures slow the evolution of resistant strains of life forms to these selection pressures. Ev shows how the important elements of mutation and selection work and they don’t have the capability of doing what you evolutionists allege. The theory of evolution is mathematically impossible.

Why have you been wasting my time with all of the misrepresentations?

Whining does not change the results from ev and the numerous real examples of how mutation and selection works.

In addition, ev shows that a single selection pressure evolves far more rapidly that all three selection pressures in combination. The same is seen with monotherapy of HIV.

Why do you keep repeating this since I haven't questioned it? It isn't actually correct, though, since a single pressure can result in extinction

I keep repeating this because this is the reason the theory of evolution is mathematically impossible. Unless you are going to contend that reptiles evolved into birds by a single selection pressures applied sequentially, there is no mathematical possibility for these genomes to morph from one to another in the time available and the small populations.

Don’t forget, HIV is an extremely short genome when compared to even the smallest genome in a free living creature.

Which matters how? In the early stages of life all genomes would have been short, and they would have had extremely short generation times producing multiple copies each -- especially if origins included peptides which RNA used as a template. With bacteria we already see other forms of lateral information transfer, which allowed one species to "solve" an evolutionary problem and pass it to the next guy, a process that dramatically sped the evolutionary process. In such a scenario, how do we even know how many real selection pressures acted at any one time in the early biosphere?

If you had read this thread, you would know that this topic has already been addressed. The smallest genome for any free living organism is about 500k base pairs. There are symbionts with shorter genomes but these life forms are dependent upon a host for essential metabolic processes. HIV is totally dependent on a host to reproduce. There is no evidence or reason to believe that there were life forms in your primordial world with short genomes. The theory of evolution is dependent on speculation and unscientific extrapolation. Do you want us to believe that the tens of thousands of different genes that we see in life forms all developed on life forms with tiny genomes and then assembled to make the modern life forms we see today? The insulin gene is about 12k base pairs, what size genome did this gene appear?

The problem for you evolutionists is that creatures with large genomes and small populations don’t have sufficient generations to accomplish any significant macroevolutionary changes.

What? Since when did asexual reproduction and only mutation become the norm for evolutionary change in large genomes with small populations?

Since you haven’t read this thread, I will remind you that recombination without error can not and does not increase the information in the gene pool. Recombination with natural selection can cause the loss of information from the gene pool by the loss of alleles.

You do realize that most of the mutations that cause changes in animals occur in genes that regulate development. Small changes in early development result in huge potential changes in adults.

Why don’t you give us some examples of this? All the examples I can think of are very destructive to the creature that have these mutations. I guess you can call this huge potential changes in adults. I’d also like to here the explanation how these mutations occur simultaneously in both males and females.

Bacteria can not and does not sustain the reproductive rates you suggest for more than a few hours.

They do if they are under multiple strong selection pressures killing them off left and right. Isn't that the point here?

If the bacteria are being killed off left and right then you don’t have huge populations and that is one of the few parameters that accelerates evolution. Don’t forget, selection pressures suppress the fitness of living things to reproduce. What makes you think bacteria will reproduce every 15 minutes when subjected to selection pressures. Some bacteria produce spores when subject to selection pressures and the generation times can extend out to years.

Bacteria can accomplish microevolutionary changes in relatively short periods of time as seen with the development of drug resistance but the same phenomena as seen with HIV is seen with bacteria. That is, multiple drug therapy slows the evolution of drug resistant strains of the bacteria.

So now that you cannot support the idea of HIV triple therapy being a realistic real world example this turns into a microevolution vs. macroevolution debate?

You still don’t understand the mathematics of mutation and selection. What ev shows is that with a single selection pressure, the rate of evolution to this selection pressure is much less sensitive to genome length. When you have multiple selection pressures, the length of the genome has a much greater effect on the rate of evolution. You should run some cases with ev, it will give you an education on the mathematics of mutation and selection. You know it is a peer reviewed and published model of mutation and selection.

If you had read this thread, you would have seen that I suggested that ev be modified to more exactly model the evolution of drug resistance with HIV, I suggested this more than once.

OK, then you admit that ev was not a good model for HIV triple therapy and yet the entire thrust of your argument when I joined this thread was that HIV triple therapy was the perfect model of three selection pressures stopping evolution just like ev shows.

Oh, ev is not an exact model of HIV triple therapy but the model does show what happens with three selection conditions and what happens to the mathematics of mutation and selection as you lengthen the genome. This fundamental mathematical behavior of mutation and selection is applicable to what is seen with combination therapy for HIV, combination therapy for other microbes such as TB, the consequences of monotherapy for the treatment MRSA, Gonorrhea, pseudomonas and other microbes and the use of combination pesticides, herbicides and rodenticides. Ev properly models this mathematical behavior.

In other words, you lied to me, Dr. Kleinman. You knowingly and deliberately misrepresented what you now claim to know as the truth. You lied to all of us, Dr. Kleinman. And now you are left with no real world example of your precious three selection pressures.

I keep telling you evolutionists that I neither need to nor want to lie to you, I have the mathematics of a peer reviewed and published computer simulation of mutation and natural selection to make my point, that and numerous real examples of this mathematics. So if you think that multiple selection pressures do not slow the evolution of resistant strains of HIV, why don’t you advocate monotherapy for this disease? Perhaps you want to call for monotherapy for the treatment of TB? Perhaps you think that agriculture scientists are wrong when they say that combination herbicides slow the evolution of resistant strains of weeds? Do you want to argue the same for pesticides and rodenticides? I’ll be patient with you and show you how the mathematics of mutation and selection works. Once you understand this mathematics, you will understand why the theory of evolution is mathematically impossible.

When you are talking about fitness in the theory of evolution, you are talking about reproduction and it takes energy to reproduce. Those creatures which use more of the available energy to reproduce are more fit. Natural selection works to make best use of the available energy to reproduce.

Exactly. It is the efficiency of reproduction. See, you need an additional rule or two on top of the laws to explain the mechanism behind evolution. Therefore, natural selection isn't a simple "restatement of the 1st law."

Why don’t you tell us what the additional rule or two are?

Try to model the transformation of a reptile genome to a bird genome. You simply don’t have the selection pressures, population sizes and time to accomplish such transformations on these large genomes by mutation and selection.

This is false. Unnamed's alternative selection algorithm substantially increases the evolutionary performance of ev, such that it is fast enough to satisfy the necessary generational constraints -- even using only random point mutations. Add to that the other potential mutation classes and evolution is more than fast enough to produce whatever real-world changes are required to produce the variety of speciation that has occurred since life arose on Earth.

Oh really little gator? Does Unnamed’s alternative selection algorithm satisfy the necessary generational constraints? The last time I checked, Dr Schneider’s model was peer reviewed and published. Even Unnamed questions his own selection process in this exchange:

In addition, there is no selection process for a partially completed gene.

I don't think that's true, but if it were, then my change would be meaningless.

Kjkent1, how do you select for something that is not functioning such as a partially completed gene? There is no selection process that can select for something that does not exist.

kleinman doesn't get the difference between computational time and model time?

Don’t you mean generations computed in the model and real generation time? I’ll let Dr Schneider answer this one; this is from his ev blog page:

Schneider lets slip that there is another unrealistic element in his (and indeed all) computer simulations in that it (they) "does not correlate with time":

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

Hey Cyborg, don’t you want to explain your cruft theory of evolution to Ichneumonwasp?

 

[joobz]

Why don’t you tell us what the additional rule or two are?

I don't know...
How about starting with the maximization of available reproductive energy (RE); dRE=0.

assuming that this energy term can account for the entirety of successful reproductive outcomes for a single species in an ecosystem.

 

[kleinman]

Annoying Creationists

Why don’t you tell us what the additional rule or two are?

How about starting with the maximization of available reproductive energy (RE); dRE=0.

That’s what Delphi’s Wikipedia reference to fitness landscape is all about. Natural selection is seeking an optimum on that fitness landscape. That optimum occurs when the amount of energy available for reproduction is maximized, what you call dRE=0.

assuming that this energy term can account for the entirety of successful reproductive outcomes for a single species in an ecosystem.

What other variable accounts for reproductive fitness? Every activity of life requires energy. The more of the available energy that can be dedicated to reproduction, the more fit that creature is. This principle applies to recombination and natural selection as well as mutation and natural selection. Selection pressures put demands on the energy resources of a creature. Multiple selection pressures put increased demands on the creature’s energy resources, at the same time making adaptation to these multiple pressures by mutation and selection more difficult.

 

[Ichneumonwasp]

Some of the regulatory genes altered between chimp and human (we can only tell the differences between the two extant species and not the common ancestor, obviously) -- FOXP2 and the regulatory regions near the protocadherin gene. Different variants of the gene product for FOXP2 are, in part, responsible for human language use and likely also effect vocal structures. Differences in timing of protocadherin are responsible for other morphological changes in brain. Proteomic interactions are only at an embryonic stage of explanation. No real explanation for many of the bigger regulatory alterations will emerge until we have a better understanding of the impact that timed expression of different protein species produces. It is becoming clearer that mutations needn't even involve exons to produce dramatic effects -- witness the devestating results of Friederich's ataxia, a triplet repeat disease involving an intron. Witness also the altered protein folding that can result from "silent" mutations. Consider the enormous variety of gene product resulting form alternate splicing -- and the unbelievably complex interactons among these gene products, especially in relation to development.

You seem to have an extremely truncated understanding of genetics and proteomics if you think morphologic change is the result only of copy error in exons. You have heard of this little thing called "crossing over" that transpires in sexual reproduction -- you know that little process by which a promoter region can be placed near a region that was previously "pseudogene", or how a new promoter region may be created by this process? Ev doesn't model those processes. Ev doesn't account for the proteomic interactions that result in actual morphology. You cannot think of bare information in the genome and have any sense of what happens in the real world as a result of that genome functioning through the production of proteins and their various interactions.

Ev was designed to model information gain. It does that. That is what both Dr Schneider and Paul referred to when they stated that ev models reality. Neither said that ev models all of reality as it relates to evolution. You have quoted Dr. Schneider repeatedly in that regard. Paul says the same thing. the surrogate measure for enough information gain does not correlate with survival in the real world necessarily, so looking at generations to convergence is nice, but not an accurate model for all situations. HIV clearly cannot be modelled by ev.

The rest of your post is simply a repeat of the same lies. They can remain where they are.

 

[joobz]

That’s what Delphi’s Wikipedia reference to fitness landscape is all about. Natural selection is seeking an optimum on that fitness landscape. That optimum occurs when the amount of energy available for reproduction is maximized, what you call dRE=0.

That's wonderful. But then why did you claim that natural selection was a restatment of the 1st law?

Why did you claim that probability can be greater than 1?

Why do claim to have a mathematical basis, when you fail to present any math?

 

[kleinman]

Annoying Creationists

Some of the regulatory genes altered between chimp and human (we can only tell the differences between the two extant species and not the common ancestor, obviously) -- FOXP2 and the regulatory regions near the protocadherin gene. Different variants of the gene product for FOXP2 are, in part, responsible for human language use and likely also effect vocal structures. Differences in timing of protocadherin are responsible for other morphological changes in brain. Proteomic interactions are only at an embryonic stage of explanation. No real explanation for many of the bigger regulatory alterations will emerge until we have a better understanding of the impact that timed expression of different protein species produces. It is becoming clearer that mutations needn't even involve exons to produce dramatic effects -- witness the devestating results of Friederich's ataxia, a triplet repeat disease involving an intron. Witness also the altered protein folding that can result from "silent" mutations. Consider the enormous variety of gene product resulting form alternate splicing -- and the unbelievably complex interactons among these gene products, especially in relation to development.

Do you want to explain what the selective pressure were that led to the differences between the human and chimp genes and how these transformations were accomplished because mutation and selection is a profoundly slow mechanism as shown by ev.

You seem to have an extremely truncated understanding of genetics and proteomics if you think morphologic change is the result only of copy error in exons. You have heard of this little thing called "crossing over" that transpires in sexual reproduction -- you know that little process by which a promoter region can be placed near a region that was previously "pseudogene", or how a new promoter region may be created by this process? Ev doesn't model those processes. Ev doesn't account for the proteomic interactions that result in actual morphology. You cannot think of bare information in the genome and have any sense of what happens in the real world as a result of that genome functioning through the production of proteins and their various interactions.

It is not that my view is truncated; it is that your view of mutation and selection is grossly over-extrapolated. My view is supported by a peer reviewed and published mathematical model of mutation and natural selection and your view is a collection of observations that has no mathematical foundation. Crossing over does not create new information in the gene pool, you can change the way the information is expressed by crossing over. Are you going to argue that reptiles evolved to birds by crossing over? Do you think that humans and chimps evolved from the primate precursor by crossing over? Humans and chimps don’t even have the same number of chromosomes. You can not create new information in the gene pool without mutation and selection. There is no other mechanism for creating new genes and there is no selection pressure that can create a gene from the beginning. Recombination can alter the way genes are expressed but you can not create new genes this way. Recombination and natural selection can cause the loss of alleles (and thus reduce the diversity of a species). That is what “crossing over” gives to the theory of evolution. Feel free to put recombination with crossing over in ev. You will find you can’t create new genes this way.

Ev was designed to model information gain. It does that. That is what both Dr Schneider and Paul referred to when they stated that ev models reality. Neither said that ev models all of reality as it relates to evolution. You have quoted Dr. Schneider repeatedly in that regard. Paul says the same thing. the surrogate measure for enough information gain does not correlate with survival in the real world necessarily, so looking at generations to convergence is nice, but not an accurate model for all situations. HIV clearly cannot be modelled by ev.

Well, the peer reviewers at Nucleic Acids Research don’t seem to agree with you. Paul has back pedaled markedly on his view of ev, Dr Schneider has been silent about ev since this thread has started, but what has he said about the reality of this model previously? How about this quote from his ev-faq page:

Why don't you do a real biological experiment instead of just a computer model?

The primary reason is that we don't have infinite resources and time. If you have the resources (a molecular biology lab), are interested in doing an experiment, and would like to discuss it please contact me.

And Dr Schneider also said the following in response to Stephen Jones:

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

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

So, Ichneumonwasp, you appear to be a Dr Schneider’s mind reader and should win the James Randi $1 million paranormal challenge.

The rest of your post is simply a repeat of the same lies. They can remain where they are.

You evolutionists wished what I say was a lie but the truth has much more power than a lie, which is why your theory of evolution is kaput, it is based on a lie. Your theory is mathematically impossible.

That’s what Delphi’s Wikipedia reference to fitness landscape is all about. Natural selection is seeking an optimum on that fitness landscape. That optimum occurs when the amount of energy available for reproduction is maximized, what you call dRE=0.

That's wonderful. But then why did you claim that natural selection was a restatment of the 1st law?

Because that is what it is.

Why did you claim that probability can be greater than 1?

I initially made the error that the effect of population was additive of the probability that a good mutation would occur at a particular locus. Myriad corrected my error and I acknowledged the correction. The effect of increasing population on the probability that a good mutation occurs at a particular locus is less than additive. This explains why huge populations don’t accelerate evolution like you evolutionists like to allege. This is shown by ev. I don’t mind at all talking about this. You are probably still making this same error. You evolutionists don’t accept correction.

Why do claim to have a mathematical basis, when you fail to present any math?

Certainly I have presented “math”, it is Dr Schneider’s peer reviewed and published mathematical model of mutation and selection, and it shows that your theory of evolution is mathematically impossible. Of course, you alchemical engineers think anything is possible, that’s your proof for abiogenesis.

 

[Dr Adequate]

Do you want to explain what the selective pressure were that led to the differences between the human and chimp genes and how these transformations were accomplished because mutation and selection is a profoundly slow mechanism as shown by ev.

It is not that my view is truncated; it is that your view of mutation and selection is grossly over-extrapolated. My view is supported by a peer reviewed and published mathematical model of mutation and natural selection and your view is a collection of observations that has no mathematical foundation. Crossing over does not create new information in the gene pool, you can change the way the information is expressed by crossing over. Are you going to argue that reptiles evolved to birds by crossing over? Do you think that humans and chimps evolved from the primate precursor by crossing over? Humans and chimps don’t even have the same number of chromosomes. You can not create new information in the gene pool without mutation and selection. There is no other mechanism for creating new genes and there is no selection pressure that can create a gene from the beginning. Recombination can alter the way genes are expressed but you can not create new genes this way. Recombination and natural selection can cause the loss of alleles (and thus reduce the diversity of a species). That is what “crossing over” gives to the theory of evolution. Feel free to put recombination with crossing over in ev. You will find you can’t create new genes this way.

Well, the peer reviewers at Nucleic Acids Research don’t seem to agree with you. Paul has back pedaled markedly on his view of ev, Dr Schneider has been silent about ev since this thread has started, but what has he said about the reality of this model previously? How about this quote from his ev-faq page:

And Dr Schneider also said the following in response to Stephen Jones:

So, Ichneumonwasp, you appear to be a Dr Schneider’s mind reader and should win the James Randi $1 million paranormal challenge.

You evolutionists wished what I say was a lie but the truth has much more power than a lie, which is why your theory of evolution is kaput, it is based on a lie. Your theory is mathematically impossible.

Because that is what it is.

I initially made the error that the effect of population was additive of the probability that a good mutation would occur at a particular locus. Myriad corrected my error and I acknowledged the correction. The effect of increasing population on the probability that a good mutation occurs at a particular locus is less than additive. This explains why huge populations don’t accelerate evolution like you evolutionists like to allege. This is shown by ev. I don’t mind at all talking about this. You are probably still making this same error. You evolutionists don’t accept correction.

Certainly I have presented “math”, it is Dr Schneider’s peer reviewed and published mathematical model of mutation and selection, and it shows that your theory of evolution is mathematically impossible. Of course, you alchemical engineers think anything is possible, that’s your proof for abiogenesis.

No new lies here.

For a confirmed fantasist, you're peculiarly lacking in imagination.

 

[Dr Adequate]

I keep telling you evolutionists that I neither need to nor want to lie to you

So why do you keep doing so?

Demonic possession, perhaps?