Annoying creationists [Archive] - Page 15

kleinman

11th April 2007, 09:30 AM

[...]Whoops, you can’t describe how ribose could be created in the primordial RNA world[...]I am going to assume that, given that this thread has gone on for 3492 posts, anything that I have to say will not make kleinmann suddenly renounce his denial of evolution. However, I couldn't pass up an opportunity to pass up how utterly incorrect this statement is. I will not try to summarize the vast corpus on pre-biotic chemistry because it has already been done for me by Leslie Orgel in a masterful review (http://www.crbmb.com/cgi/reprint/39/2/99) published in 2004. Suffice it to say, if kleimann deigns to read it, it should answer many of his questions of how many of the simple biological molecules could have been formed from the formation of sugars by the condensation of formaldehyde in the formose reaction to the formation of nitrogenous bases by the condensation of hydrogen cyanide with itself and various other simpler nitrogenous compounds to a proposal of a simpler system than RNA (i.e, threose nucleic acid [TNA]) as a stepping stone from the formose reaction and the various HCN condensations to RNA. This review is meant to be a supplement to the oft mentioned Miller-Urey experiment because the main focus on these forums seems to on the creation of amino acid, but here we also have another explanation of the formation of nucleotides.
There are no end to evolutionists’ ridiculous speculations. If you believe the formose reaction will produce ribose, produce the experiment that does this. If you take the time to study the physical properties of ribose, you will find out this is an unstable molecule. Even if you could design an experiment in which you could produce ribose non-enzymatically (which you can’t), the ribose produced would be unstable and have a half life of only a few years and also be a racemic mixture.
The Wikipedia description of fitness landscape gives a precise description of why multiple selection pressures slows evolution.Even though I explicity wrote two fitness functions in Java-like code that demonstrate precisely the opposite? What you're saying here is a blunder equivalent to "the more integers you add, the bigger the result."
Are you talking about those code fragments you posted earlier? That’s a good example of an evolutionist idea of a proof. Put those code fragments into ev and see what kind of numbers you generate.
I'm really trying to spoon feed you here. Help me help you. How can I mathematically represent calculations on strings in a way you'll understand?
Delphi, you have worked on the concept of mutation and selection and you still have difficulty understanding the mathematics of this phenomena. Since you have difficulty grasping what ev is showing and you have difficulty comprehending why triple therapy is used for the treatment of HIV, let’s try another important clinical medical example.

Multiple drug therapy is often used in an attempt to treat cancer. In addition, radiation therapy is also used. These multiple selection pressures are used to suppress the reproduction of these malignant cells. These multiple treatment modalities are used in an attempt to cause extinction of these cell lines as well as prevent the emergence of more malignant cell lines. This is another example of how multiple selection pressures are used to modify the fitness landscape and slow or stop evolution.

This is how mutation and selection works. Multiple selection pressures do not speed up evolution, they interfere with each other and prevent evolution. This is what the mathematics shows, this is what the real world shows.
Hey! I said that over 4 months ago: I know, but Dr. Kleinman doesn't seem to get it. Why, I'm not sure, but I think it's A) He's not educated in computer models and simulations, and B) a bronze age holy book has disabled half of his gray matter.
Well, if you read this thread carefully, A) you would find reference to my PhD thesis which is a computer simulation of a biological system, the results of which have been published. I have also published another computer simulation which pertained to the solution of a non-linear partial differential equation. I have also been paid for commercial work using and writing computer simulations and have taught at the university level both undergraduate and graduate level thermodynamics and heat transfer. Included in this teaching was the instruction of the writing and use of computer simulations. B) Are you sure it is not you who has had half of his gray matter disabled by a rust age theory.
If there are, for example, 10 processes that enable evolution, and a computer simulation models 8 of them, then it's not valid to draw a conclusion like "evolution is too slow" unless the other two are also modeled. Ev does not model gene duplication, and the concensus is it's a critical process in "speeding up" evolution compared to evolution without duplication.
Mr Scott, it does not matter what the mechanism of mutation is, it is the multiple selection conditions which interfere with evolution. This is the mathematical and real fact you have yet to come to grips with. No mechanism of mutation will change this fact.
It's as if Kleinman is saying that, because a 4-cylinder car is shown to not be able to reach a destination in time, it's proven an 8-cylinder car couldn't. Real world evolution runs on many more cylinders than Ev models, and we are still discovering more as science continues to penetrate the beautiful, open-ended clockwork of evolution.
Your 8-cylinder car has 5 flat tires (spare tire included), no fuel and your destination is beyond the ends of the observable universe. Multiple selection processes interfere with evolution. The more selection conditions you have the slower the evolution. The fundamental mechanism of mutation and selection which you allege drives the theory of evolution does not work this way. This is shown mathematically and by real examples of the phenomena. No mutation mechanism will change this basic mathematics.
This is the fatal error in Dr. Kleinman's reasoning. He has not refuted it, so it's necessary to repeat it.
Denial does not constitute a valid scientific argument. If you deny the results of ev, put whatever mutation mechanism you want in the model and see whether it will overcome the effect of multiple selection conditions. This I will continue to repeat. This is one of the fatal errors in the theory of evolution. Another fatal error is you have no selection process that can evolve a gene from the beginning.
Ev represents a best case scenario for the theory of evolution. All creatures are affected equally and there is no extinction.How is that a best case scenario for evolution? That looks to me like an equilibrium scenario -- all creatures affected equally over space and time. That isn't how evolution works.
What ev does is maintain a stable unchanging set of selection pressures with no possibility of extinction. Even under these simple, stable conditions the evolution process is profoundly slow. Changing the selection conditions will slow evolution further.
How did you make that connection? The Wikipedia description of fitness landscape gives a precise description of why multiple selection pressures slows evolution.Can you post again what part of the wiki entry you think states this? Feel free to include some sentence diagrams to show this.
Certainly, I’ll repost the entry.
Fitness landscapes are often conceived of as ranges of mountains. There exist local peaks (points from which all paths are downhill, i.e. to lower fitness) and valleys (regions from which most paths lead uphill). A fitness landscape with many local peaks surrounded by deep valleys is called rugged.
and
Apart from the field of evolutionary biology, the concept of a fitness landscape has also gained importance in evolutionary optimization (http://en.wikipedia.org/wiki/Evolutionary_algorithm) methods such as genetic algorithms (http://en.wikipedia.org/wiki/Genetic_algorithm) or evolutionary strategies. In evolutionary optimization, one tries to solve real-world problems (e.g., engineering (http://en.wikipedia.org/wiki/Engineering) or logistics (http://en.wikipedia.org/wiki/Logistics) problems) by imitating the dynamics of biological evolution. For example, a delivery truck with a number of destination addresses can take a large variety of different routes, but only very few will result in a short driving time. In order to use evolutionary optimization, one has to define for every possible solution (http://en.wikipedia.org/wiki/Solution_point) s to the problem of interest (i.e., every possible route in the case of the delivery truck) how 'good' it is. This is done by introducing a scalar (http://en.wikipedia.org/wiki/Scalar_%28mathematics%29)-valued function (http://en.wikipedia.org/wiki/Function_%28mathematics%29) f(s) (scalar valued means that f(s) is a simple number, such as 0.3, while s can be a more complicated object, for example a list of destination addresses in the case of the delivery truck), which is called the fitness function (http://en.wikipedia.org/wiki/Fitness_function) or fitness landscape. A high f(s) implies that s is a good solution. In the case of the delivery truck, f(s) could be the number of deliveries per hour on route s. The best, or at least a very good, solution is then found in the following way. Initially, a population of random solutions is created. Then, the solutions are mutated and selected for those with higher fitness, until a satisfying solution has been found.
Evolutionary optimization techniques are particularly useful in situations in which it is easy to determine the quality of a single solution, but hard to go through all possible solutions one by one (it is easy to determine the driving time for a particular route of the delivery truck, but it is almost impossible to check all possible routes once the number of destinations grows to more than a handful).
Joobz, pay attention in particular to the last paragraph of the above quote from Wikipedia. Ev is an evolutionary optimization scheme. Convergence of ev occurs when three selection conditions are satisfied. The three selection conditions are 1) binding sites are located where they should be, 2) no spurious binding in the gene region and 3) no spurious binding sites in the non-gene region of the genome. It is the requirement that all three selection conditions be satisfied simultaneously that causes evolution to be profoundly slow. If you require that only a single selection condition be satisfied at a give time, ev converges very rapidly. Ev is showing exactly what that last paragraph of the post from Wikipedia is saying. Multiple selection conditions profoundly slow down the evolutionary process. This is also seen in reality.

fishbob

11th April 2007, 09:45 AM

joobz

11th April 2007, 10:19 AM

Certainly, I’ll repost the entry.

Evolutionary optimization techniques are particularly useful in situations in which it is easy to determine the quality of a single solution, but hard to go through all possible solutions one by one (it is easy to determine the driving time for a particular route of the delivery truck, but it is almost impossible to check all possible routes once the number of destinations grows to more than a handful).

[....cut for brevity...]

Joobz, pay attention in particular to the last paragraph of the above quote from Wikipedia. Ev is an evolutionary optimization scheme. Convergence of ev occurs when three selection conditions are satisfied. The three selection conditions are 1) binding sites are located where they should be, 2) no spurious binding in the gene region and 3) no spurious binding sites in the non-gene region of the genome. It is the requirement that all three selection conditions be satisfied simultaneously that causes evolution to be profoundly slow. If you require that only a single selection condition be satisfied at a give time, ev converges very rapidly. Ev is showing exactly what that last paragraph of the post from Wikipedia is saying. Multiple selection conditions profoundly slow down the evolutionary process. This is also seen in reality.
I believe your reading comprehension is lacking. A good thing to try is to stop thinking of ways to lie and pay attention to what is written.

The Ev. Opt technique is useful when understand each baby step, but can't figure out a priori the total response, which is the sum of the baby steps.

We know and can model how a simple water molecule moves in isolation. But time it takes to run a simulation of 1ml of water is extrememly long. Does this mean that 1 ml of water doesn't exist?

kleinman

11th April 2007, 10:19 AM

This is how mutation and selection works. Multiple selection pressures do not speed up evolution, they interfere with each other and prevent evolution. This is what the mathematics shows, this is what the real world shows.Half truth - typical.
Multiple selection pressures can interfere to diminish or intensify.
This is what the real world really shows.
Simple enough fishbob, I have given multiple examples both mathematical and real which demonstrate my hypothesis. Where is your mathematics or examples which show that multiple selection pressures intensify (whatever that means) evolution? You don’t even make half a case - typical.

Ichneumonwasp

11th April 2007, 10:43 AM

What ev does is maintain a stable unchanging set of selection pressures with no possibility of extinction.

Yes, equilibrium.

Even under these simple, stable conditions the evolution process is profoundly slow.

Yes, equilibrium conditions. Slow change, the theory predicts this.

Changing the selection conditions will slow evolution further.

How's that? Based on what data? We have great data with HIV and triple therapy (your own pet example). Multiple weak selection pressures with certain forms of triple therapy and no change in conditions (good compliance) -- resistance develops. Strong selection pressure with other forms of triple therapy and good compliance -- no resistance develops (over the short course). Strong selection pressure with that same form of triple therapy with poor compliance -- taking med, stopping, taking med again, stopping, taking med again, etc. -- resistance develops. Same thing with TB treatments -- the single best predictor of resistance development is por patient compliance -- changing selection conditions over time.

delphi_ote

11th April 2007, 10:53 AM

Multiple selection pressures do not speed up evolution, they interfere with each other and prevent evolution.
If you can point me to a way of mathematically representing fitness landscapes for you, I will show you that you're wrong. In some cases, selection pressures can reenforce one another (as in the example code I posted.) In some cases, they have no impact on each other. In some cases, they interefere with each other.

I'd be more than happy to show you what this looks like in a mathematical context, but you don't seem to understand what I type. If you'd care to point me to a way I can explain this to you, I'll do my best. If, on the other hand, you'd rather continue this discussion by flagrantly repeating this false statement, fine. Just please stop being so very proud of your ignorance.

kleinman

11th April 2007, 11:31 AM

Evolutionary optimization techniques are particularly useful in situations in which it is easy to determine the quality of a single solution, but hard to go through all possible solutions one by one (it is easy to determine the driving time for a particular route of the delivery truck, but it is almost impossible to check all possible routes once the number of destinations grows to more than a handful).
I believe your reading comprehension is lacking. A good thing to try is to stop thinking of ways to lie and pay attention to what is written.
A grammatically challenged alchemical engineer now thinks he can lecture on reading comprehension.
The Ev. Opt technique is useful when understand each baby step, but can't figure out a priori the total response, which is the sum of the baby steps.
Ev can’t figure it out, you can’t figure it out, no evolutionist can figure it out but you think it is scientifically true? Is this the kind of slop you teach in your alchemical engineering classes? Make sure you remain anonymous.
We know and can model how a simple water molecule moves in isolation. But time it takes to run a simulation of 1ml of water is extrememly long. Does this mean that 1 ml of water doesn't exist?
How does modeling of the dynamics of water molecules have anything to do with the acquisition of information by mutation and selection? You must have just finished a hearty meal at kjkent1’s table, red herring, string cheese and whine.

Joobz, your idea of a scientific proof is if you can’t do the computation it must be true. Well, your proof is complete. Abiogenesis is true because you can’t show how ribose is produced nonenzymatically and the theory of evolution is true because you can’t prove it mathematically. You are a credit to the field of alchemical engineering.
What ev does is maintain a stable unchanging set of selection pressures with no possibility of extinction.Yes, equilibrium.
You better check Wikipedia for the definition of equilibrium.
Even under these simple, stable conditions the evolution process is profoundly slow.Yes, equilibrium conditions. Slow change, the theory predicts this.
You don’t understand your own theory of evolution so why should I think you understand the meaning of equilibrium.
Changing the selection conditions will slow evolution further.How's that? Based on what data? We have great data with HIV and triple therapy (your own pet example). Multiple weak selection pressures with certain forms of triple therapy and no change in conditions (good compliance) -- resistance develops. Strong selection pressure with other forms of triple therapy and good compliance -- no resistance develops (over the short course). Strong selection pressure with that same form of triple therapy with poor compliance -- taking med, stopping, taking med again, stopping, taking med again, etc. -- resistance develops. Same thing with TB treatments -- the single best predictor of resistance development is por patient compliance -- changing selection conditions over time.
Choose any case you want in ev, allow information to accumulate than turn off selection and watch the information disappear. Your own example demonstrates this, drug resistant TB occurs more readily when you reduce the number of selective pressures. Why do you think multiple drugs are used to treat TB? Use a single drug and resistance to that drug rapidly appears. Take multiple drugs and maintain the multiple selective pressures and resistant strains are much slower to appear. It doesn’t take long for poor compliance (eliminating the multiple selection pressures) with treatment to yield resistant strains.

Ichneumonwasp, do you think you will get drug resistant strains of microbes if you don’t use any drugs at all?
Multiple selection pressures do not speed up evolution, they interfere with each other and prevent evolution.If you can point me to a way of mathematically representing fitness landscapes for you, I will show you that you're wrong. In some cases, selection pressures can reenforce one another (as in the example code I posted.) In some cases, they have no impact on each other. In some cases, they interefere with each other.
Ev is mathematically representing a fitness landscape. Have Paul put your code into ev and see whether you can speed up evolution. What is so nonsensical about your concept is that you think the mathematics will proceed more quickly the more complex you make the selection conditions. You are proposing the exact opposite of your Wikipedia link to fitness landscape. There are no fitness landscapes that become easier to optimize by adding more selection conditions to satisfy.
I'd be more than happy to show you what this looks like in a mathematical context, but you don't seem to understand what I type. If you'd care to point me to a way I can explain this to you, I'll do my best. If, on the other hand, you'd rather continue this discussion by flagrantly repeating this false statement, fine. Just please stop being so very proud of your ignorance.
Delphi, the only way you are going to represent any real fitness landscape is by functional notation. You can map the surface by generating data points with a computer model like ev. Somehow you are under the delusion that adding more selection conditions will make it easier to find an optimum on this surface. If you think this is true, define multiple selection conditions that converge rapidly and have Paul put them in ev and demonstrate your argument.

Until then, ev demonstrates that multiple selection conditions slow evolution, the examples of the treatment of HIV, cancer and now Ichneumonwasp example of the treatment of TB with multiple selection pressures slows evolution and your link to Wikipedia which describes fitness landscapes shows that multiple selection pressures slows evolution. Delphi, when are you going to give an example (either real or mathematical) which shows that multiple selection pressures speeds up evolution?

Ichneumonwasp

11th April 2007, 11:48 AM

Choose any case you want in ev, allow information to accumulate than turn off selection and watch the information disappear.

That's not the analogy. Exposure, remove, exposure, remove, exposure, remove, rinse, repeat.

Your own example demonstrates this, drug resistant TB occurs more readily when you reduce the number of selective pressures.

No, wrong. No drug exposure, no drug resistance. Resistance develops when people take the drug, then stop, then take the drug, then stop, then take the drug, then stop, rinse, repeat. This is not an example of reducing the number of selection pressures in some bland way. It is an example of multiple exposures and periods of remission for a given strong selection pressure(s). There is a big difference. You've not modelled this at all, so can make no comment about it. We know what happens without the selection pressure being placed -- no drug resistance. And with good patient compliance -- limited to no drug resistance. It is repeated exposures, followed by remission with a chance for the population to grow with new varieties, repeat exposure, etc. that results in drug resistance.

Come on, this phenomenon is very well known and well studied. Don't pretend that placing a selection pressure and removing it in any way mimics what I am talking about.

Take multiple drugs and maintain the multiple selective pressures and resistant strains are much slower to appear.

Nope, not always. You did check the link I provide above regarding the situation with HIV. It is, in fact, compliance with the drug regimen that causes drug resistance, even with multiple drugs in the regimen if the selection pressure of the multiple drugs is not high enough.

It doesn’t take long for poor compliance (eliminating the multiple selection pressures) with treatment to yield resistant strains.

If you take a drug and stop it (one instance of each), no resistance arises. That is the analogy you are providing with ev -- place selection pressure and then remove it. Resistance only arises when people take drugs in a sporadic fashion.

joobz

11th April 2007, 11:57 AM

Ev can’t figure it out, you can’t figure it out, no evolutionist can figure it out but you think it is scientifically true? Is this the kind of slop you teach in your alchemical engineering classes? Make sure you remain anonymous.
ahh your back to gibberish

Kleinman method:
Dismiss a clearly explained concept by quoting random words from said concept in a contemptable manner.

How does modeling of the dynamics of water molecules have anything to do with the acquisition of information by mutation and selection?
Simple. Molecular dynamics is a method of simulating a system by appling simple force rules over and over again. It looks at each interaction and adjusts the setting as a function of time. It is quite similar in function to ev. the exact mechanics differ, but the idea of optimization is the same.

kleinman

11th April 2007, 12:58 PM

Choose any case you want in ev, allow information to accumulate than turn off selection and watch the information disappear.That's not the analogy. Exposure, remove, exposure, remove, exposure, remove, rinse, repeat.
Ok, that’s an interesting challenge. Are you proposing exposure to single or multiple selection pressures? The example you give with developing drug resistant TB occurs when taking only one or two medications rather than the three or four that is recommended, this same affect is seen with HIV and poor compliance with treatment.

So how do you propose to demonstrate this effect? Paul, maybe you can help here and we can see what comes out in the wash.
Your own example demonstrates this, drug resistant TB occurs more readily when you reduce the number of selective pressures.No, wrong. No drug exposure, no drug resistance. Resistance develops when people take the drug, then stop, then take the drug, then stop, then take the drug, then stop, rinse, repeat. This is not an example of reducing the number of selection pressures in some bland way. It is an example of multiple exposures and periods of remission for a given strong selection pressure(s). There is a big difference. You've not modelled this at all, so can make no comment about it. We know what happens without the selection pressure being placed -- no drug resistance. And with good patient compliance -- limited to no drug resistance. It is repeated exposures, followed by remission with a chance for the population to grow with new varieties, repeat exposure, etc. that results in drug resistance.

Come on, this phenomenon is very well known and well studied. Don't pretend that placing a selection pressure and removing it in any way mimics what I am talking about.
If you look at what happens with compliance with multi-drug therapy is that patient’s often time won’t take particular drugs because of adverse reactions to those medications. In addition, taking multiple medications, multiple times a day often times leads to confusion on a patient’s part. They often forget to take medications. The mathematics dictates that drug resistance occurs quickly when taking only single medications. This is why public health departments have gotten involved in the treatment of TB. Patients must be witnessed taking their medications to insure they take all their medications.

The question here is whether turning on and off multiple selection pressures will speed up evolution. The mathematics shows that turning off all but one selection pressure will speed up evolution for that selection condition. Whether you can speed up evolution by turning on and off all selection conditions will not work in ev. This can be easily shown by turning selection on and off in the middle of a run. You also have the problem of how do you extend this concept to macroevolution. Turning off selection for a particular condition stops selection for beneficial mutations for that condition. This will slow evolution. The purpose of having selection is that increases the frequency of beneficial genetic sequences in the population. Any time you turn off selection you are losing this effect. But feel free to propose your idea to Paul and see whether your mathematics will work out.
Take multiple drugs and maintain the multiple selective pressures and resistant strains are much slower to appear.Nope, not always. You did check the link I provide above regarding the situation with HIV. It is, in fact, compliance with the drug regimen that causes drug resistance, even with multiple drugs in the regimen if the selection pressure of the multiple drugs is not high enough.
I missed your link. Post it again with appropriate quotes posted that you think makes your point.

Three weak selection pressures may not be adequate to cause extinction but they do slow the evolution of triple resistant strains. Give the drugs serially and you will get triple resistant strains much more quickly than if you give the drugs simultaneously.
It doesn’t take long for poor compliance (eliminating the multiple selection pressures) with treatment to yield resistant strains.If you take a drug and stop it (one instance of each), no resistance arises. That is the analogy you are providing with ev -- place selection pressure and then remove it. Resistance only arises when people take drugs in a sporadic fashion.
You are incorrect. What ev shows, with a single selection condition, that condition quickly evolves. When people take single drug therapy for HIV and TB, resistance to that drug rapidly appears. The problem of patient compliance with multi-drug treatment regimens is not getting them to take one drug; it is getting them to take all the medications consistently. Then you slow evolution of the drug resistant strains. If the selection pressure is strong enough, you can cause the microbe to go extinct (at least with respects to that person).
Ev can’t figure it out, you can’t figure it out, no evolutionist can figure it out but you think it is scientifically true? Is this the kind of slop you teach in your alchemical engineering classes? Make sure you remain anonymous.ahh your back to gibberish

Kleinman method:
Dismiss a clearly explained concept by quoting random words from said concept in a contemptable manner.
There you go Paul; joobz has clearly explained how to fix the profoundly slow rate of acquisition of information in ev. He hasn’t produced any data just some silly analogies.
How does modeling of the dynamics of water molecules have anything to do with the acquisition of information by mutation and selection?Simple. Molecular dynamics is a method of simulating a system by appling simple force rules over and over again. It looks at each interaction and adjusts the setting as a function of time. It is quite similar in function to ev. the exact mechanics differ, but the idea of optimization is the same.
The problem with this silly analogy is that ev does compute a rate of information acquisition that is profoundly slow. The reason it is slow is the multiple selection conditions. This effect becomes apparent before you reach a genome length of 100,000. The simulation of the molecular dynamics of a gram of water requires tracking 3E+22 particles each with at least 6 degrees of freedom for each particle. That is why this computation is so slow. Your scientific analogies are as incoherent as your grammar.

Dr Richard

11th April 2007, 01:09 PM

...is almost as interesting as joobz's avatar...

From the abstract: Fitness landscape of HIV-1 protease quasispecies (http://jvi.asm.org/cgi/content/abstract/JVI.01594-06v1)

"Here we show, at a high resolution (1%), the HIV-1 protease gene quasispecies landscape from three infected naïve individuals. A huge range of genetic configurations was found--67%, 71%, and 80% of the nucleotide clones, respectively, from the three individuals were different, --and these created a dense net that linked different parts of the viral population. Similarly, a vast diversity of different protease activities was also found. Importantly, 65% of the analyzed enzymes had detectable protease activity, and 11% of the minority individual variants showed similar or better fitness than the master (most abundant) enzyme, suggesting that the viral complexity in this genomic region does not exclusively depend on the enzyme's catalytic efficiency. Several high-fitness minority variants had only one substitution when compared to the master sequence, supporting the possibility that the rugged HIV-1 protease quasispecies fitness landscape may be formed by a continuous network that can be traversed by single mutational steps, without passing through defective or less-adapted proteins"

And from the discussion:

Overall, the three quasispecies analyzed displayed a number of notable features. First, within each quasispecies there were a large number of fitness optima or peaks. Because fitness optima were frequent, (65% of all analyzed proteases displayed a detectable enzymatic activity and 11% showed similar or better fitness than the master, most abundant enzyme), the HIV-1 potease quasispecies complexity does not exclusively depend on the enzyme’s catalytic efficiency. Moreover, in one quasispecies population (Fig. 9B), the master sequence was not the fittest sequence but rather represented a middle or low adaptive peak. Selective pressures in another region of the HIV-1 genome might favor a less-fit protease variant (14, 25, 29,41). Second, the fitness landscape was rugged. Several single substitutions were lethal and led the master sequence to drop down the peak. However, at other positions, single substitutions sent the master sequence to a new local optimum or peak, suggesting that the master sequence may walk through the quasispecies fitness landscape by single mutational steps without being trapped at suboptimal alleles (34, 56, 61). Third, although the three analyzed quasispecies shared some traits, such as the presence of several fitness optima, every protease quasispecies formed distinctive individual fitness landscapes. This is particularly interesting because the three quasispecies had similar nucleotide diversity (Fig. 1), suggesting that different selective constraints may have been acting on different quasispecies. Even quasispecies N and O, which had similar
amino acid diversity (Table I), formed very different fitness landscapes. Quasispecies N seemed to be composed of variants formed by different combinations of a reduced number of substitutions that generated a high proportion (>70%) of fit proteases. In contrast, within the O quasispecies there were many different amino acid changes all over the viral protease, the majority of these variants (>60%) being defective enzymes (Fig. 2 and 6). This result, together with the higher ds/dn ratio found in the O quasispecies, strongly suggests an absence of positive selective forces shaping this protease quasispecies. Therefore, random genetic drift and selection pressures within the protease coding region or in other viral genomic regions could be acting all together to generate the protease quasispecies landscape (4, 50, 51).

Note that there are several important points in this paper relevant to this discussion:

1. The sheer number of HIV virions in a single patient: 10^9 PER DAY. Again, makes Kleinmans population of erm... 64 seem a tad conservative.
2. The existence of many, many varieties of HIV within a single individual, creating the landscape as mapped.
3. The fact that each fitness landscape is different in each individual, due to different selection pressures
4. The fact that each landscape as mapped is for the protease only.
5. The fact that small populations of less fit virions are kept "in reserve" in case a new selection pressure manifests.

In summary, this paper demonstrates that multiple different selection pressures in fact increase the genetic diversity of the population and therefore accelerate evolution.

Thank you Kleinman for coming up with the example of HIV - the evolution present within one infected person is sufficient to refute your theory by providing many, many selection pressures and a massive population. You can turn off your PC now...

P.S. the Wiki article on Fitness Landscapes also links to a paper on HIV fitness landscapes modelling >3 loci http://arxiv.org/PS_cache/q-bio/pdf/0603/0603034v2.pdf. I it is a bit more complex than Kleinman seems to think...

Ichneumonwasp

11th April 2007, 02:05 PM

The example you give with developing drug resistant TB occurs when taking only one or two medications rather than the three or four that is recommended, this same affect is seen with HIV and poor compliance with treatment.

No, that is wrong. Drug resistance with TB drugs and with HIV triple therapy occurs with multiple drugs used when compliance is poor. Not just with one or two. There are well documented effects with particular HIV regimens using three drugs where resistance occurred with good compliance when the regiment itself did not supply enough selection pressure and multiple drug regimens in which no resistance occurs in compliant groups but resistance does emerge from the poor compliance groups. There are even arguments that we not introduce the drugs into some third world countries because of concerns over compliance -- this will result in the development of drug resistance as has been already shown.

I thought you knew this literature.

Of course, resistance occurs more easily with single drugs, especially with poor compliance. But there are actually triple therapy HIV regimens in which good compliance is the deciding factor for resistance to emerge -- again, those regimens that do not provide the strongest selective pressures.

Potency of selective pressure, differences in exposure across populations, and differences of exposure over time are all important factors in teh emergence of drug resistance.

Are you proposing exposure to single or multiple selection pressures?

I'm not proposing anything (just pointing out that your evidence does not fit the situation), but if you want to model it you should do both. It will depend on the strength of the selection pressure as to which protocol will be most likely to produce drug resistance. For strong pressures -- your multiple selection pressures, it would be a protocol with poor compliance, so you would need to expose and relent repeatedly across generations.

If you look at what happens with compliance with multi-drug therapy is that patient’s often time won’t take particular drugs because of adverse reactions to those medications. In addition, taking multiple medications, multiple times a day often times leads to confusion on a patient’s part. They often forget to take medications. The mathematics dictates that drug resistance occurs quickly when taking only single medications. This is why public health departments have gotten involved in the treatment of TB. Patients must be witnessed taking their medications to insure they take all their medications.

Yes, I know, and totally beside the point. I'm not speaking of patient motivations, but the effects of non-compliance on drug resistance. Studies including non-compliance as an outcome measure keep a very close eye on their patients and check for compliance usually in multiple ways -- pill counts, patient reports, reports of other witnesses, drug levels, etc.

Whether you can speed up evolution by turning on and off all selection conditions will not work in ev. This can be easily shown by turning selection on and off in the middle of a run. You also have the problem of how do you extend this concept to macroevolution. Turning off selection for a particular condition stops selection for beneficial mutations for that condition. This will slow evolution. The purpose of having selection is that increases the frequency of beneficial genetic sequences in the population. Any time you turn off selection you are losing this effect. But feel free to propose your idea to Paul and see whether your mathematics will work out.

If that is true, then ev doesn't mimic the real world. Turning off selection loses information only if the selection pressure is kept off. When the selection pressure is re-instituted, the situtation that you see is this: big selection pressures limit reproduction (the definition of a profound selection pressure). The surviving offspring are those most likely to be slightly resistant to the selection pressure. When the selection pressure is removed, then the population is allowed to grow in size with new variations. Some of those variations have a chance of surviving the next big instance of the same selection pressure. Repeat selection pressure -- possible big kill off, or if resistance has already magically developed, then one clone grows in size -- if the population dramatically declines, only those with the potential good changes survive. Release selection pressure -- clones increase with new variations. Repeat selection pressure, etc. That is what we see with drug resistance, even with multiple agents in both HIV and TB.

Three weak selection pressures may not be adequate to cause extinction but they do slow the evolution of triple resistant strains. Give the drugs serially and you will get triple resistant strains much more quickly than if you give the drugs simultaneously.

Of course, but that is not the model we are working with here. With both TB and HIV we use multiple drug cocktails. With the particular cocktails that are not as strong selective pressures as the newer ones, drug resistance occurs more readily. Of course, multiple drugs hit the organisms more and decrease population size, which decreases variability, etc. But when the selection pressures are not particularly strong, resistance can develop with good compliance. It depends critically on the strength of the selection pressures being employed. That's what I've been on about all along.

What ev shows, with a single selection condition, that condition quickly evolves. When people take single drug therapy for HIV and TB, resistance to that drug rapidly appears.

That is not an reply to what I said. What I said was that if you apply a single pressure and remove it, then no resistance will occur. Of course reistance develops with single drug exposures kept in place over a long time. Quick exposure and removal will not do much, though.

The problem of patient compliance with multi-drug treatment regimens is not getting them to take one drug; it is getting them to take all the medications consistently.

Yes, that is what I have been saying. Several times now.

Then you slow evolution of the drug resistant strains. If the selection pressure is strong enough, you can cause the microbe to go extinct (at least with respects to that person).

No, that is not what happens. When patients take antimicrobials inconsistently resistance develops more readily with strong selection pressures. The situation is more complex than this, though, because weaker selection pressures can produce drug resistance (even with multiple drugs in the cocktail) in the face of (and seemingly depending on) good compliance.

Here is the link regarding resistance in HIV (http://jac.oxfordjournals.org/cgi/content/full/53/5/696)

It isn't all that long. The important issues are that while resistance clearly develops in single drug therapies, it may also develop in multi-drug therapies that are not as good at suppressing the viral load. There are many other studies demonstrating that poor compliance to the commonly used and much better triple therapy programs is a result of poor compliance. For one teaser that does not include the multi-drug users.........

The widely accepted premise that non-adherence breeds resistance is now being challenged, at least as it pertains to anti-HIV therapy. Recent data from cohorts of individuals with well-characterized measures of adherence suggest that resistance to both protease and nucleoside reverse transcriptase inhibitors occurs primarily in highly adherent patients.9 In separate studies, Walsh et al.19 and Howard et al.20 demonstrated linear and direct associations between adherence and the number of drug resistance mutations. Gallego et al.21 found protease inhibitor resistance was limited to those individuals reporting more than 90% adherence.

kleinman

11th April 2007, 03:10 PM

Several single substitutions were lethal and led the master sequence to drop down the peak. However, at other positions, single substitutions sent the master sequence to a new local optimum or peak, suggesting that the master sequence may walk through the quasispecies fitness landscape by single mutational steps without being trapped at suboptimal alleles (34, 56, 61).
This is an interesting post Dr Richard and I took a particular portion of the quote and reposted it above. The reason I took this particular portion of the quote is because it describes what must be done to navigate a fitness landscape.

When only single drug therapy is being used to treat HIV, the single selection process is determining the direction of the walk. If a second drug is used, selection caused by this second drug will affect the direction of the walk through the fitness landscape. Each additional drug used (selection pressure) interferes with the direction of the walk that would prevent the master sequence from walking through the quasisspecies fitness landscape by single mutational steps without being trapped at suboptimal alleles.

1. The sheer number of HIV virions in a single patient: 10^9 PER DAY. Again, makes Kleinmans population of erm... 64 seem a tad conservative.
You still don’t understand the mathematics of mutation and selection and how population affects the rate of evolution. Doubling the population does not double the probability that a particular mutation will hit at a particular loci. For small populations, you can approximate population as having an additive affect on this probability but as your populations get larger and larger, this effect is much less than additive. I have run a series with a population of 10^6 and the effect of increasing population is becoming very small. Paul is supposed to be running another population series and you will see this effect once again.
2. The existence of many, many varieties of HIV within a single individual, creating the landscape as mapped.
How did this individual get so many varieties of the HIV virus? Did this individual receive three antiretroviral medicines consistently or was he treated with monotherapy?
3. The fact that each fitness landscape is different in each individual, due to different selection pressures
Certainly, different antiretroviral medicines (selection pressures) should lead to different genetic sequences in the viruses. However, a given antiretroviral medication should lead to particular genetic sequence that confers resistance to that medication. I’ve heard infectious disease lectures on the topic and particular mutations and given loci confirm the particular drug resistance.
4. The fact that each landscape as mapped is for the protease only.
If drugs which target other enzymes are in virus are introduced, it only makes it more difficult for the virus to evolve.
5. The fact that small populations of less fit virions are kept "in reserve" in case a new selection pressure manifests.
Again, from the infectious disease lectures I have heard, the drug resistant strains of HIV are less fit than the wild strain of the virus. Drug resistant viruses can not reproduce as quickly as the wild virus. The least fit of the viruses that are still able to reproduce will be the ones with the most drug resistance.
In summary, this paper demonstrates that multiple different selection pressures in fact increase the genetic diversity of the population and therefore accelerate evolution.
Of course there is more diversity if there are more selection pressures. If there are no selection pressures, the virus (and it’s corresponding genome) that reproduces most rapidly will quickly take over the population. Each selection pressure added to that virus slows the reproduction of that genome and allows other variants genetic sequences to appear. If you have sufficient selection pressure, you stop the reproduction of the virus completely. So Dr Richard, are you arguing that monotherapy should be used to treat HIV? If not, why? You are arguing that multiple selection pressures accelerate the evolution of the virus so physicians should use few drugs, not more drugs.
Thank you Kleinman for coming up with the example of HIV - the evolution present within one infected person is sufficient to refute your theory by providing many, many selection pressures and a massive population. You can turn off your PC now...
Far from refuting my theory, your paper supports my theory; see the quote I took from your post. Again, I ask you, does this paper support the use of monotherapy or triple antiviral agents for the treatment of HIV? You have alleged that multiple selective pressures increase the variants of the virus. By your logic, monotherapy should be used.
P.S. the Wiki article on Fitness Landscapes also links to a paper on HIV fitness landscapes modelling >3 loci http://arxiv.org/PS_cache/q-bio/pdf/0603/0603034v2.pdf (http://arxiv.org/PS_cache/q-bio/pdf/0603/0603034v2.pdf). I it is a bit more complex than Kleinman seems to think...
And it should reference these types of papers, multiple selection pressures applied simultaneously slow evolution of resistant strains. Apply the selection pressures one at a time and the master sequence of the virus much more easily walks the fitness landscape to evolve a resistant strain. Of course you seem to be arguing that monotherapy is the way to treat HIV, that way you won’t be making the virus evolve as quickly.
Here is the link regarding resistance in HIV (http://jac.oxfordjournals.org/cgi/content/full/53/5/696)

It isn't all that long. The important issues are that while resistance clearly develops in single drug therapies, it may also develop in multi-drug therapies that are not as good at suppressing the viral load. There are many other studies demonstrating that poor compliance to the commonly used and much better triple therapy programs is a result of poor compliance. For one teaser that does not include the multi-drug users.........
This article was published in 2004 meaning the data are at least a couple years older. I have attended CME lectures on the topic within the last year and triple therapy with monitoring and sequencing of the virus for drug resistant strains is the standard of care. The reason this is done is so the virus can not easily walk the fitness landscape and evolve new resistant strains.

This is what the mathematics of mutation and selection shows and this is what the clinical response to these types of therapies show. Multiple selection pressures when applied simultaneously slow evolution.
The widely accepted premise that non-adherence breeds resistance is now being challenged, at least as it pertains to anti-HIV therapy. Recent data from cohorts of individuals with well-characterized measures of adherence suggest that resistance to both protease and nucleoside reverse transcriptase inhibitors occurs primarily in highly adherent patients.9 In separate studies, Walsh et al.19 and Howard et al.20 demonstrated linear and direct associations between adherence and the number of drug resistance mutations. Gallego et al.21 found protease inhibitor resistance was limited to those individuals reporting more than 90% adherence.
This is why I asked you if you can obtain drug resistance without using the drug. You can’t. If you don’t have fatal selection pressures against the virus, given enough time you will evolve drug resistant strains to that medication. If you administer the drug as monotherapy, that resistance comes about more quickly. If administered in combination with other medications, that resistance comes about more slowly because the virus has a more complex walk in the fitness landscape in order to develop the drug resistance.

Standard of care uses three drugs with monitoring for signs of resistance to any of the drugs. As soon as resistance to any one of the drugs is detected an attempt is made to substitute to a new drug.

Here’s a question for you and Dr Richard. If the person has a strain of HIV that is resistant to a particular drug and that drug is withdrawn, what happens to that population of the virus when that drug is withdrawn?

Ichneumonwasp

11th April 2007, 03:29 PM

kjkent1

11th April 2007, 04:01 PM

OK, I think I get it now. You completely misregard any information with which you cannot deal and pretend that you are answering a challenge by posting competely unrelated material.There is no fact (in my opinion) that you could possibly present which would cause kleinman to reject his belief system.

That's why it's called a "belief" system: facts are irrelevant.

joobz

11th April 2007, 04:35 PM

OK, I think I get it now. You completely misregard any information with which you cannot deal and pretend that you are answering a challenge by posting competely unrelated material.

Welcome to the Kleinman method:
Dismiss a clearly explained concept by quoting random words from said concept in a contemptable manner.

articulett

11th April 2007, 05:25 PM

Welcome to the Kleinman method:
Dismiss a clearly explained concept by quoting random words from said concept in a contemptable manner.

ignorance and arrogance are directly proportional to one's level of faith.

Q.E.D.

delphi_ote

11th April 2007, 06:00 PM

Delphi, when are you going to give an example (either real or mathematical) which shows that multiple selection pressures speeds up evolution?
As soon as you give me some notation you'll actually understand, as I already presented an example of this and it went right over your head.

mijopaalmc

11th April 2007, 06:55 PM

There are no end to evolutionists’ ridiculous speculations. If you believe the formose reaction will produce ribose, produce the experiment that does this. If you take the time to study the physical properties of ribose, you will find out this is an unstable molecule. Even if you could design an experiment in which you could produce ribose non-enzymatically (which you can’t), the ribose produced would be unstable and have a half life of only a few years and also be a racemic mixture.

So are you saying that you think the RNA-World Hypothesis is the only prebiotic hypothesis you accept?

You ignored, as usual, the proposal of threose nucleic acid (TNA) as a precusor to RNA. It is also possible that the pre-biotic world was a peptide world, given that there are many small molecules (e.g., carbonyl sulfide (http://www.sciencemag.org/cgi/content/abstract/306/5694/283)) that can catalyze abiotic peptide bond formation. Having read a good portion of this thread, I see little use in continuing to argue with you, as you have already decided that "evolutionists" are deluded in thinking that abiogenesis has a naturalist explanation and no amount of evidence on a topic concerning evolution and abiogenesis will convince you otherwise. I therefore bow out of this discussion as I can see that not only is the point I am making is tangential to the topic at hand, which other are doing a much better job of explaining, but also that it is a waste of my time to discuss something with someone who will deny any validity in the evidence I present.

kleinman

11th April 2007, 09:38 PM

This article was published in 2004 meaning the data are at least a couple years older. I have attended CME lectures on the topic within the last year and triple therapy with monitoring and sequencing of the virus for drug resistant strains is the standard of care. The reason this is done is so the virus can not easily walk the fitness landscape and evolve new resistant strains.

This is what the mathematics of mutation and selection shows and this is what the clinical response to these types of therapies show. Multiple selection pressures when applied simultaneously slow evolution.How nice that you keep up. Now answer the issues reaised, please. You've not even attempted to do so. The standard of care is not the issue. The issue revolves around the mechanisms of drug resistance and the creation of resistant strains in patients who are not compliant.
And the issue you are in complete denial of is that multiple selection pressures slow the evolutionary process. This is why multiple drug therapy is used with HIV and TB. You can still get drug resistant microbes with multiple drug therapy but the process is slowed.
If administered in combination with other medications, that resistance comes about more slowly because the virus has a more complex walk in the fitness landscape in order to develop the drug resistance.

Standard of care uses three drugs with monitoring for signs of resistance to any of the drugs. As soon as resistance to any one of the drugs is detected an attempt is made to substitute to a new drug. OK, I think I get it now. You completely misregard any information with which you cannot deal and pretend that you are answering a challenge by posting competely unrelated material.
Ichneumonwasp, apparently you are unaware that this thread is about the mathematics of mutation and selection. In particular this discussion is a centered around the ev computer model of mutation and selection. This model shows that multiple selection process slow evolution. The real examples of the treatment of HIV and your very nice example of the treatment of TB are demonstrations of this phenomenon. Until you come to grips with this mathematical fact, you will have difficulty understanding how and why these treatment strategies are used.
My first impulse was correct. You guys have fun playing this silly game for the forseeable future. I have better things to do with my time.
If you want to learn the mathematics of mutation and selection, spend some time studying the ev computer model. Then you will be able to properly understand why multiple drug therapies are use to treat HIV, TB, and cancer. These multiple selection pressures suppress the evolution of resistant strains of any particular drug. Of course these examples of how mutation and selection actually work shows that your theory of evolution is bunk. You can not achieve macroevolution because multiple selection pressures profoundly slow the evolutionary process.
Delphi, when are you going to give an example (either real or mathematical) which shows that multiple selection pressures speeds up evolution?As soon as you give me some notation you'll actually understand, as I already presented an example of this and it went right over your head.
You can use algebra and English; let me help you with the expression:
Let x = number of selection pressures.
If x > 1 then the number of examples where evolution proceeds more rapidly than when x = 1 is f.
There are no end to evolutionists’ ridiculous speculations. If you believe the formose reaction will produce ribose, produce the experiment that does this. If you take the time to study the physical properties of ribose, you will find out this is an unstable molecule. Even if you could design an experiment in which you could produce ribose non-enzymatically (which you can’t), the ribose produced would be unstable and have a half life of only a few years and also be a racemic mixture.So are you saying that you think the RNA-World Hypothesis is the only prebiotic hypothesis you accept?
As I said, there is no end to evolutionists’ ridiculous speculations.
You ignored, as usual, the proposal of threose nucleic acid (TNA) as a precusor to RNA. It is also possible that the pre-biotic world was a peptide world, given that there are many small molecules (e.g., carbonyl sulfide) that can catalyze abiotic peptide bond formation. Having read a good portion of this thread, I see little use in continuing to argue with you, as you have already decided that "evolutionists" are deluded in thinking that abiogenesis has a naturalist explanation and no amount of evidence on a topic concerning evolution and abiogenesis will convince you otherwise. I therefore bow out of this discussion as I can see that not only is the point I am making is tangential to the topic at hand, which other are doing a much better job of explaining, but also that it is a waste of my time to discuss something with someone who will deny any validity in the evidence I present.
Oh, I see, you like to call your ridiculous speculations “proposals”.

Mijopaalmc, since you are new to this thread and are already preparing to depart, perhaps you would tell us what the selection process that would evolve a gene from the beginning? Once you do that, would you tell us what the components of the DNA replicase system were doing before DNA could be replicated? In particular, could you tell us what helicase and gyrase were doing before there was DNA? There just doesn’t seem to be any evolutionists who can fill these gaps in your gap theory.

delphi_ote

11th April 2007, 10:12 PM

kleinman

11th April 2007, 11:37 PM

Let x = number of selection pressures.
If x > 1 then the number of examples where evolution proceeds more rapidly than when x = 1 is f. I cannot express a fitness function conveniently in algebra. You won't understand what I type. We need some way mathematically talking about functions of the type:
http://www.randi.org/latexrender/latex.php?$f(x)=y
http://www.randi.org/latexrender/latex.php?y\in{\mathbb R}
And x is a sequence of characters.
I understand functional notation. I also have some training and experience is solving multidimensional nonlinear functional equations. This is why when you presented the link to Wikipedia fitness landscapes, I immediately recognized the relationship and significance to the results from ev.

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

It is very easy to find an optimum if x is one dimensional. Finding this solution mathematically consists of computing points on the surface and using Newton-Raphson, secant method, interval halving or a variety of other methods for finding roots to this type of equation. However, mutation and selection does not look for this optimum systematically. What mutation and selection does is give random changes to a genome. If the change is beneficial that creature is more fit and is a better reproducer, if detrimental it is less fit and not as good a reproducer.

As you increase the number of dimensions to x (the number of selection pressures), this search for the optimum become more difficult. If done mathematically, it requires the evaluation of more points on the surface in order to find an appropriate search direction. If done by mutation and selection, the numbers of possible search directions confound the process. A random search is the slowest way of finding an optimum on the surface. This is why I continue to ask you for an example of a multiple selection pressure situation which would find an optimum more quickly than a fewer selection pressure situation. This condition does not make sense mathematically and is not what ev shows and I believe that Dr Schneider properly modeled mutation and selection. And it does not make sense when observing real world behavior of mutation and selection.

Multiple selection conditions confound the search for an optimum on the fitness surface. This is why the theory of evolution is mathematically impossible.

BPScooter

12th April 2007, 03:03 AM

Although it has been claimed to be mathematically impossible, I continue to consider that life on Earth can be understood through Darwinian ideas and arguments.

joobz

12th April 2007, 05:26 AM

I understand functional notation.
Of course you do. I've never doubted you were a smart man. That is why I consider you a dishonest liar. You are aware of the truth, but willfully ignore it.

I also have some training and experience is solving multidimensional nonlinear functional equations. This is why when you presented the link to Wikipedia fitness landscapes, I immediately recognized the relationship and significance to the results from ev.

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

It is very easy to find an optimum if x is one dimensional. Finding this solution mathematically consists of computing points on the surface and using Newton-Raphson, secant method, interval halving or a variety of other methods for finding roots to this type of equation. However, mutation and selection does not look for this optimum systematically. What mutation and selection does is give random changes to a genome. If the change is beneficial that creature is more fit and is a better reproducer, if detrimental it is less fit and not as good a reproducer.

As you increase the number of dimensions to x (the number of selection pressures), this search for the optimum become more difficult. If done mathematically, it requires the evaluation of more points on the surface in order to find an appropriate search direction. If done by mutation and selection, the numbers of possible search directions confound the process. A random search is the slowest way of finding an optimum on the surface. This is why I continue to ask you for an example of a multiple selection pressure situation which would find an optimum more quickly than a fewer selection pressure situation. This condition does not make sense mathematically and is not what ev shows and I believe that Dr Schneider properly modeled mutation and selection. And it does not make sense when observing real world behavior of mutation and selection.

Multiple selection conditions confound the search for an optimum on the fitness surface. This is why the theory of evolution is mathematically impossible.
Very very good. you just described why poor adaptation to severe (multiple or single) pressure(s) results in extinctions.

Do you consider pooring bleach in a culture plate a single pressure or multiple? Do we ever expect to see an evolutionary adaptation to handle molar concentrations of sodium hypochlorite?

Now, how does this fit with your magic 3 pressures?
Why do the three pressures you select have only 1 fitness optimum?
Why is only random point mutation the only form of genetic variation?
Why does a simulation = takes too long mean evolution isn't possible?

Paul C. Anagnostopoulos

12th April 2007, 06:30 AM

Now, how does this fit with your magic 3 pressures?
As I mentioned above, if Kleinman got the magic number 3 from Ev, it's easy to refute. I can trivially change Ev so it only has 2 pressures.

~~ Paul

Mr. Scott

12th April 2007, 08:16 AM

Well, if you read this thread carefully, A) you would find reference to my PhD thesis which is a computer simulation of a biological system, the results of which have been published. I have also published another computer simulation which pertained to the solution of a non-linear partial differential equation. I have also been paid for commercial work using and writing computer simulations and have taught at the university level both undergraduate and graduate level thermodynamics and heat transfer. Included in this teaching was the instruction of the writing and use of computer simulations.

How strange. You argue here as if you didn't understand computer simulations.

B) Are you sure it is not you who has had half of his gray matter disabled by a rust age theory

What is this rust age era you keep referring to?

Mr Scott, it does not matter what the mechanism of mutation is, it is the multiple selection conditions which interfere with evolution. This is the mathematical and real fact you have yet to come to grips with. No mechanism of mutation will change this fact.

How do you know the mechanism of mutation does not matter, particularly mechanisms not modeled by Ev?

Question for Paul: Has Ev been peer reviewed and verified as an accurate simulation in regards to its prediction of the absolute rate of real world evolution?

Question for Dr. Kleinman: Do you believe the Earth is closer to a few thousand years old or a few billion years old?

kleinman

12th April 2007, 09:20 AM

Although it has been claimed to be mathematically impossible, I continue to consider that life on Earth can be understood through Darwinian ideas and arguments.
You can do this but don’t claim it as science and don’t teach it to naïve children and tell them it is scientific fact.
I understand functional notation.Of course you do. I've never doubted you were a smart man. That is why I consider you a dishonest liar. You are aware of the truth, but willfully ignore it.
Why don’t you put some mathematics to your alchemical engineering and prove your case? Or why don’t you give us some real examples of where multiple selection pressures speed up evolution? You think if you wave your hands really fast you prove your case. I give you mathematics and real examples to support my case. The only thing you are proving is that you are a mathematically challenged alchemical engineer.
…As you increase the number of dimensions to x (the number of selection pressures), this search for the optimum become more difficult. If done mathematically, it requires the evaluation of more points on the surface in order to find an appropriate search direction. If done by mutation and selection, the numbers of possible search directions confound the process. A random search is the slowest way of finding an optimum on the surface. This is why I continue to ask you for an example of a multiple selection pressure situation which would find an optimum more quickly than a fewer selection pressure situation. This condition does not make sense mathematically and is not what ev shows and I believe that Dr Schneider properly modeled mutation and selection. And it does not make sense when observing real world behavior of mutation and selection.

Multiple selection conditions confound the search for an optimum on the fitness surface. This is why the theory of evolution is mathematically impossible.Very very good. you just described why poor adaptation to severe (multiple or single) pressure(s) results in extinctions.
Here once again you are proving that you are a mathematically challenged alchemical engineer. Ev does not model poor adaptation to severe selection pressure(s). Do you think that the mathematics changes with the severity of the selection pressures? I’ll answer this one for you. The mathematics does not change. The only thing that changes is the rate of information acquisition. This rate of information acquisition goes from profoundly slow to impossibly slow with multiple selection pressures.
Do you consider pooring bleach in a culture plate a single pressure or multiple? Do we ever expect to see an evolutionary adaptation to handle molar concentrations of sodium hypochlorite?
I wonder if you ever considered what happens chemically when you use chemically active chlorine or iodine as a disinfectant. This is an example of large number of multiple selection pressures. Chlorine and iodine combine chemically to large number of sites on a wide variety of biological molecules including proteins, DNA and other crucial molecules necessary to support life. These chemical additions of these large chemically active groups change the conformation of huge number of biological molecules simultaneously which is why these chemicals are effective disinfectants.
Now, how does this fit with your magic 3 pressures?
There is no magic to three selection pressures; it is just slower converging than one or two selection pressures. If you did some cases with ev, you would understand this. Apparently alchemical engineers don’t run the numbers.
Why do the three pressures you select have only 1 fitness optimum?
I never said this and ev does not demonstrate this, there are more than one perfect creature in ev.
Why is only random point mutation the only form of genetic variation?
The mechanism of mutation does not affect the fundamental mathematics that multiple selection conditions slow the evolution process. If you think that other mutation mechanisms change this fundamental mathematical principle, put that mechanism in ev an produce some data and show this.
Why does a simulation = takes too long mean evolution isn't possible?
It is why the simulation takes so long that shows why evolution isn’t possible. Dr Schneider’s simulation of random point mutations and natural selection properly captures the affect of multiple selection conditions. We now have multiple real examples of this phenomenon and Delphi’s Wikipedia description of fitness landscape also explains this phenomenon. So, we have the ev simulation which shows how profoundly slow multiple selection condition are and real examples of this behavior which show why macroevolution is not possible.
Now, how does this fit with your magic 3 pressures?As I mentioned above, if Kleinman got the magic number 3 from Ev, it's easy to refute. I can trivially change Ev so it only has 2 pressures.
You keep grabbing at this straw Paul but it won’t rescue your theory. It is easy to show with your computer model that 1 selection pressure converges much more rapidly than 2 selection pressures. Your own computer model shows this. Read Delphi’s link to the Wikipedia description of fitness landscape and understand why your computer model behaves like it does and shows why the theory of evolution is mathematically impossible. We all know how much you like landscapes.
Well, if you read this thread carefully, A) you would find reference to my PhD thesis which is a computer simulation of a biological system, the results of which have been published. I have also published another computer simulation which pertained to the solution of a non-linear partial differential equation. I have also been paid for commercial work using and writing computer simulations and have taught at the university level both undergraduate and graduate level thermodynamics and heat transfer. Included in this teaching was the instruction of the writing and use of computer simulations.How strange. You argue here as if you didn't understand computer simulations.
You argue here as if you hadn’t run any cases with ev.
B) Are you sure it is not you who has had half of his gray matter disabled by a rust age theory What is this rust age era you keep referring to?
You mean you don’t know when the theory of evolution got its major impetus?
Mr Scott, it does not matter what the mechanism of mutation is, it is the multiple selection conditions which interfere with evolution. This is the mathematical and real fact you have yet to come to grips with. No mechanism of mutation will change this fact.How do you know the mechanism of mutation does not matter, particularly mechanisms not modeled by Ev?
The search on the fitness landscape is done by random changes. It does not matter what kind of random changes there are. What drives the mathematics is the number of selection conditions.
Question for Paul: Has Ev been peer reviewed and verified as an accurate simulation in regards to its prediction of the absolute rate of real world evolution?
Yes Paul, let’s hear the answer to that question.
Question for Dr. Kleinman: Do you believe the Earth is closer to a few thousand years old or a few billion years old?
I have not done a scientific investigation into this question. For the sake of this debate, I have let evolutionists set the age of the earth.

joobz

12th April 2007, 10:39 AM

kleinman

12th April 2007, 12:08 PM

Why don’t you put some mathematics to your alchemical engineering and prove your case?Again, you speak gibberish. Running an ev simulation isn't running the "mathematics". I have run several simulations already and they are consistant with what has been presented here by several individuals.
Oh yes, we have seen all the data you haven’t posted and all the chemistry you can’t explain that proves your point.
Or why don’t you give us some real examples of where multiple selection pressures speed up evolution?Delphi gave a rather nice demontration of multiple selection pressures having a faster convergence than a single pressure. Why should I bother giving you another one?
Are you talking about Delphi’s code fragment that he hasn’t run in any simulation? I can see why that would impress you. It fits right in with your debating skills, which is not posting data and not explaining the chemistry of your theory.
You think if you wave your hands really fast you prove your case. I give you mathematics and real examples to support my case. The only thing you are proving is that you are a mathematically challenged alchemical engineer.Sure, If you say so.
You also demonstrate it so.
Here once again you are proving that you are a mathematically challenged alchemical engineer. Ev does not model poor adaptation to severe selection pressure(s). Do you think that the mathematics changes with the severity of the selection pressures?again, this question is gibberish. Are you saying that
weak and strong single stresses don't change the rate of evolutionary response?
Of course the rates change if you have weak or strong stresses but that doesn’t change the underlying mathematics. Do you think changing the mass changes the underlying mathematics of F=ma?
I’ll answer this one for you. The mathematics does not change. The only thing that changes is the rate of information acquisition. This rate of information acquisition goes from profoundly slow to impossibly slow with multiple selection pressures.
How accuate of values. Profoundly slow. hmm...This is a quantitative agrument? You accuse me of hand waving???
There already is plenty of quantitative data posted on this thread and the Evolutionisdead forum. I’ll repost the data again if you have trouble finding it. You know what posting of data is? That is what you don’t do in order to prove your case.
I wonder if you ever considered what happens chemically when you use chemically active chlorine or iodine as a disinfectant. This is an example of large number of multiple selection pressures. Chlorine and iodine combine chemically to large number of sites on a wide variety of biological molecules including proteins, DNA and other crucial molecules necessary to support life. These chemical additions of these large chemically active groups change the conformation of huge number of biological molecules simultaneously which is why these chemicals are effective disinfectants.EXCELLENT!!!! you've recognized my example for what it is. According to you, magnitude doesn't matter. yet, high concentrations will kill, yet mild forms of this kind of stress generate stress risistant strains. According to you, we could never generate a strain resistant to stresses like freezing, oxidative injury, ethanol levels becuase each of these represent "Multiple selection pressures".
What you are having a hard time recognizing is that mutation and natural selection is a profoundly slow process when you have multiple selection pressures acting simultaneously. Do you think that polar bears adapted to the freezing weather my mutation and selection? Wrong! They adapted by recombination and natural selection. Recombination is the rapid way for living things to adapt. Mutation and selection is profoundly slow when you have multiple selection pressures.
So, perhaps you can explain, then, how this group was able to evolve a yeast strain that was resistant to not only higher ethanol levels, but freezing and oxidative injury?
Cakar, ZP et. al. "Evolutionary engineering of multiple-stress resistant Saccharomyces cerevisiae."FEMS Yeast Res. 2005 Apr;5(6-7):569-78
Your link doesn’t work.
You claim I have no math to back me up, but Reality seems to have abandoned you.
Your idea of a proof now is a non-functioning link.

Paul C. Anagnostopoulos

12th April 2007, 12:41 PM

Paul C. Anagnostopoulos

12th April 2007, 12:44 PM

You keep grabbing at this straw Paul but it won’t rescue your theory. It is easy to show with your computer model that 1 selection pressure converges much more rapidly than 2 selection pressures.
I'm not trying to rescue any theory. I'm simply pointing out that there is nothing magic about three or more pressures.

EXCELLENT!!!! you've recognized my example for what it is. According to you, magnitude doesn't matter. yet, high concentrations will kill, yet mild forms of this kind of stress generate stress risistant strains. According to you, we could never generate a strain resistant to stresses like freezing, oxidative injury, ethanol levels becuase each of these represent "Multiple selection pressures".
Are you suggesting that Kleinman may have to move the goalpost yet again?

joobz

12th April 2007, 12:46 PM

Are you talking about Delphi’s code fragment that he hasn’t run in any simulation? I can see why that would impress you. It fits right in with your debating skills, which is not posting data and not explaining the chemistry of your theory.
Your inability to understand his post isn't problem, it's your's.

Do you understand how the 1 selection pressure is much more difficult to obtain than the three given?

Of course the rates change if you have weak or strong stresses but that doesn’t change the underlying mathematics. Do you think changing the mass changes the underlying mathematics of F=ma?
gibberish again. Does F=ma hold out for infetessimally small values of m or infinity large values of a?

simple changes in magnitudes of kenimatic viscosity can change flow from turbulent to laminar. Will you claim that the simplications used to describe laminar flow hold in the turbulent regime?

I agee that if we have a perfect model for all of evolution, that model wouldn't change. But we are not there yet. We have currently simplifications of that model and when values used are outside the realm of that model, it is no longer valid.

What you are having a hard time recognizing is that mutation and natural selection is a profoundly slow process when you have multiple selection pressures acting simultaneously. Do you think that polar bears adapted to the freezing weather my mutation and selection? Wrong! They adapted by recombination and natural selection. Recombination is the rapid way for living things to adapt. Mutation and selection is profoundly slow when you have multiple selection pressures.

Nice escape hatch. evolution is only allowed to occur by point mutation because you say so? All evidence of other mechanisms (that are known to be important) don't count?

There's a reason why your "solid well thought out" argument and mathematical evidence resides only in forum posts.

Your link doesn’t work.

Your idea of a proof now is a non-functioning link.
that was a copy/paste from pubmed.
I gave you the reference. look it up.

kjkent1

12th April 2007, 02:41 PM

Nice escape hatch. evolution is only allowed to occur by point mutation because you say so? All evidence of other mechanisms (that are known to be important) don't count.

There's a reason why your "solid well thought out" argument and mathematical evidence resides only in forum posts. This is the reoccuring theme with kleinman. He seems certain that only point mutation is real and all other mutations are illusory (or derivative). Ev doesn't model a translocation or large repeat, so, there's no way to measure what effect these mutations would have on the number of generations necessary for convergence of Rseq to Rfreq.

kleinman also seems unwilling to accept that the measurement of Rseq approaching Rfreq is an "average," not a genetic requirement. Ev simply measures genetic information gain, based on Rseq approaching Rfreq. It doesn't measure functionality, because the creatures have no function. We have no way to know what changes any particular mutation or genetic sequence imparts on its host.

For all we know, were we actually able to get some real world creature to start replicating according to the ev sequences, the results might show huge morphological changes well before Rseq approaches Rfreq.

kleinman's entire argument devolves to: evolution is impossible because ev's point mutation can't evolve a different genetic sequence within the same number of generations that would be required in the real world for a similar genetic sequence, without increasing the number of mutations per generation beyond the threshold where cancer and death prior to reproduction is most likely outcome.

Problem with this is that cancer is generally a somatic cell phenomenon. In a germ cell, a large number of mutations in any generation may stop reproduction, or, have a neutral effect, or produce a substantial change in the organism.

Ev can't model any of the above. Even if we turn up the number of mutations to a ridiculous level, many random point mutations are not the same as one large translocation, repeat, fusion, deletion, etc.

Ev shows information gain, which prior to ev, was the creationist bellwether for what's wrong with evolution. Having lost that position, the current argument is: too many combinations to reach a particular sequence in X number of trials makes evolution impossible.

The law of large numbers rejects this claim, because in order for a probability calculation to be valid in the first place, all outcomes leading to a probability p, must occur given a sufficient number of trials. There's no rule as to when a particular outcome must occur. No matter how unlikely an outcome may seem in advance, it could appear on any trial.

And, with evolution, no particular outcome is required. We're here because we're here because we're here -- not because we are an outcome which is required to occur. Homo sapien could have just as easily evolved to be 3 inches tall and look like a broccoli spear -- rather than a Shakespeare -- if you catch my genetic drift.

Sadly, the creationist mentality is that all outcomes are predetermined. Which is a remarkable paradox, considering that kleinman argues improbability makes evolution impossible. Because, if all outcomes are predetermined, then there is no such thing as improbability to make evolution impossible.

And, so on and so forth.

Paul C. Anagnostopoulos

12th April 2007, 03:09 PM

joobz

12th April 2007, 03:10 PM

For your convienience, here's the publication I mentioned.

Mr. Scott

12th April 2007, 03:14 PM

[the] ev computer model, a peer reviewed and published model of random point mutations and natural selection which shows this mechanism of evolution is so profoundly slow when using realistic genome lengths and mutation rates that nothing can evolve by this mechanism

I can guarantee you it [ev] makes no prediction about the rate of real world evolution, except possibly by accident.

Kleinman, you're busted. The Ev model is not peer-reviewed as a model of the speed of evolution. Further repetition of your claim, that it is, constitutes willful intent to deceive. It fascinates me that deception is proven to be an integral strategy in creationists' playbooks (e.g. Dover trial testimony). It just doesn't seem very Christian.

kleinman

12th April 2007, 03:32 PM

Question for Paul: Has Ev been peer reviewed and verified as an accurate simulation in regards to its prediction of the absolute rate of real world evolution?I can guarantee you it makes no prediction about the rate of real world evolution, except possibly by accident.
Hey Paul, did Dr Schneider make an accident when he published this in his peer reviewed publication about ev?
Second, the probability of finding 16 sites averaging 4 bits each in random sequences is 2^(-4x16)@5x10^-20 yet the sites evolved from random sequences in only ~10^3 generations, at an average rate of ~1 bit per 11 generations. Because the mutation rate of HIV is only 10 times slower, it could evolve a 4 bit site in 100 generations, about 9 months [35 (http://www-lecb.ncifcrf.gov/~toms/paper/ev/latex/node7.html#Perelson.Ho1996)], but it could be much faster because the enormous titer (10^10 new virions/day/person [17 (http://www-lecb.ncifcrf.gov/~toms/paper/ev/latex/node7.html#Loeb.Mullins1999)]) provides a larger pool for successful changes. Likewise, at this rate, roughly an entire human genome of ~4x10^9 bits (assuming an average of 1 bit/base, which is clearly an overestimate) could evolve in a billion years, even without the advantages of large environmentally diverse worldwide populations, sexual recombination and interspecies genetic transfer. However, since this rate is unlikely to be maintained for eukaryotes, these factors are undoubtedly important in accounting for human evolution.
Mr Scott, Dr Schneider and the peer reviewers at the Oxford University Press Journal, Nucleic Acids Research used the rate of information acquisition from ev to estimate the evolution of a human genome. This rate of information acquisition was based on a genome length of 256 bases and a mutation rate 100 times higher than seen in the HIV virus (not 10 times higher as Dr Schneider published in his article) with a population of 64 creatures. Just use a realistic mutation rate of 10^-6 in Dr Schneider’s case and his calculation returns 4 trillion years to evolve a human genome. Use a realistic genome length and his estimate becomes billions of times larger. Now Mr Scott, Paul whines that huge populations will make this estimate decline. It does perhaps 2 or 3 orders of magnitude. If you are lucky (and you evolutionists are not lucky) that gets the estimate down to maybe a few quadrillion years to accumulate the information to evolve a human genome.

Paul, I’m wondering how far you are going to back pedal on ev? Have you turn the seat around on your bicycle yet?
You keep grabbing at this straw Paul but it won’t rescue your theory. It is easy to show with your computer model that 1 selection pressure converges much more rapidly than 2 selection pressures. I'm not trying to rescue any theory. I'm simply pointing out that there is nothing magic about three or more pressures.
So 2 selection pressures are sufficient to slow down evolution profoundly?
EXCELLENT!!!! you've recognized my example for what it is. According to you, magnitude doesn't matter. yet, high concentrations will kill, yet mild forms of this kind of stress generate stress risistant strains. According to you, we could never generate a strain resistant to stresses like freezing, oxidative injury, ethanol levels becuase each of these represent "Multiple selection pressures".Are you suggesting that Kleinman may have to move the goalpost yet again?
Paul, you are the expert at moving goalposts. Let’s summarize what you have said about ev, ev started out representing reality, then it became a model of a small part of the evolutionary landscape, then it became a stylized model of mutation and selection and now you can guarantee it makes no prediction about the rate of real world evolution, except possibly by accident. You are the one slipping and sliding all over the evolutionary landscape. My goalposts have never moved, those goalposts are that ev shows that the theory of evolution is mathematically impossible and the reason is that competing selection conditions slow the evolutionary process. Ev shows this, the real world shows this, Delphi’s link to Wikipedia and the description of the fitness landscape shows this.

Paul, why don’t you take up joobz’s suggestion that less severe selection conditions cause evolution to go more quickly. I don’t know what joobz thinks of Dr Schneider’s selection since these conditions can not cause extinction. Or take up Ichneumonwasp’s suggestion to turn selection on and off and see whether that speeds up evolution in ev. I tried to tell Ichneumonwasp that turning selection off causes the loss of information in ev but I don’t think Ichneumonwasp was listening.

The distorted and unscientific view that evolutionists hold of how mutation and selection works impedes the understanding of how this phenomenon works. Evolutionists block the advancement of science.

joobz

12th April 2007, 03:38 PM

Evolutionists block the advancement of science.
Priceless. :D :D

kleinman

12th April 2007, 03:53 PM

Evolutionists block the advancement of science.Priceless.
However, joobz does a marvelous job of advancing the pseudoscience of alchemical engineering.

Mr. Scott

12th April 2007, 04:11 PM

Dr. Kleinman, have you been paid to undermine evolution, or has it all been volunteer work?

kjkent1

12th April 2007, 04:20 PM

A bit of chit-chat on Rfrequency and Rsequence:

http://www.lecb.ncifcrf.gov/~toms/paper/schneider1986/latex/node26.html

And some more:

http://www.bioinfo.de/isb/gcb01/poster/kim_et_al.html

And some real world discussion:

http://www.inb.uni-luebeck.de/research/bsad/

~~ PaulThat was informative. Apparently, I am incorrect on an important issue (and, so is Kleinman, who, when discussing the behavior of zero mistake weights, asserted that he didn't know whether Rseq approaching Rfreq was anything other than a coincidence, and then proceeded to argue as if it wasn't required).

According to Dr. Martinez's website:

"The binding sites for a given protein on the genome are characterized by the positional information Rfreq and the sequence information Rseq. We have investigated the relation between Rfreq and Rseq on the basis of maximum entropy analysis. By modelling co-evolution between the genome and the DNA-binding protein, we obtained the key result that the equality Rfreq = Rseq holds approximately for all biological systems which are genetically autonomous, i.e. which encode all their DNA-binding proteins within their own genome."

Note: there is no cite provided for the science paper which confirms the above quote. However, as the author of the quote is also apparently the author of a large number of peer-reviewed papers on the subject matter, I'm assuming the quote is accurate.

Paul, correct me if I'm misunderstanding, but if the above quote is true, then convergence of Rseq to Rfreq seems to be a fundamental property of DNA. (y/n)

If yes, then it's pretty damn important, because it suggests that ev needs a more realistic selection algorithm (which is what I've been arguing all along).

If no, then just ignore my post. LOL!

kleinman

12th April 2007, 04:46 PM

Dr. Kleinman, have you been paid to undermine evolution, or has it all been volunteer work?
If you paid closer attention to this thread, you would know the answer to this question. Does it matter what the answer is anyway. The appropriate question to ask is what does the mathematics of ev show and does it model reality. The answer to this question is that ev does properly model the mathematics of mutation and selection and that ev shows that multiple selection pressures interfere with the evolutionary process. Does this model reality? The answer is yes, there are numerous examples of this phenomenon. Does this find show that the theory of evolution is impossible? The answer to this question is again yes, because unless you hold to the view that macroevolution occurs by serial single selection processes, you can not accumulate information rapidly enough to achieve the large genetic transformations that the theory of evolution calls for.

Mutation and selection simply does not work the way evolutionists allege. When mutation and selection is properly understood, this principle can be used to fight disease in a systematic and coordinated manner. Multiple selection conditions slow the evolutionary process because these multiple conditions confound the walk on the fitness landscape. Single selection conditions allow for more rapid evolution of resistant strains of microbes. Ev shows this mathematically, and the therapy employed for the treatment of HIV, TB and other diseases shows this in reality.

So this is a good news/bad new story. The good news is that understanding mutation and selection has clinical medical benefit (as well as pest management and crop management), the bad news (for evolutionists) is that it proves your theory wrong.

Ev is a valuable computer model, now if Paul could only understand what his model shows.
If yes, then it's pretty damn important, because it suggests that ev needs a more realistic selection algorithm (which is what I've been arguing all along).

If no, then just ignore my post. LOL!
There are no selection processes that overcome the affect of multiple selection conditions slowing evolution. There are no selection processes at all that evolve a gene from the beginning.

joobz

12th April 2007, 04:51 PM

However, joobz does a marvelous job of advancing the pseudoscience of alchemical engineering.
You sound like a man standing on a beach screaming at the ocean for being too dry.

interesting to observe, but obviously out of touch with reality.

But I'll wait patiently for you too address the multiple points i've made.
Do you still hold to your "maths" claim?

kleinman

12th April 2007, 05:12 PM

However, joobz does a marvelous job of advancing the pseudoscience of alchemical engineering. You sound like a man standing on a beach screaming at the ocean for being too dry.

interesting to observe, but obviously out of touch with reality.
And you sound like a man with no mathematical training trying to argue about the mathematics of mutation and selection. This is not very interesting to observe but it seems to be the only effective debating tactic evolutionists have, that is boring me to death.
But I'll wait patiently for you too address the multiple points i've made.
Do you still hold to your "maths" claim?
What points are you talking about? Is it the one where you can’t explain how to produce ribose nonenzymatically yet you argue abiogenesis is true? Or is the one where you argue that less than fatal selection conditions acting simultaneously speed up the evolutionary process even though ev shows the exact opposite and you haven’t posted any data to support your hypothesis? Or is it the nonfunctional link that you provide? If you think your link counters my argument, post a quote from the link that you think supports your hypothesis.

With respects to holding to my “maths” claim, with your devastating lack of data in your posts, your lack of a chemical explanation for abiogenesis and your nonfunctional link, how could I continue to hold to my “maths” claim?

Paul C. Anagnostopoulos

12th April 2007, 06:08 PM

kjkent1

12th April 2007, 06:09 PM

There are no selection processes that overcome the affect of multiple selection conditions slowing evolution.Let's see your math, Alan. The constant whine is really boring.

Paul C. Anagnostopoulos

12th April 2007, 06:12 PM

Paul, correct me if I'm misunderstanding, but if the above quote is true, then convergence of Rseq to Rfreq seems to be a fundamental property of DNA. (y/n)
I believe so, yes. In fact, it is a fundamental property of any information system that "evolves" a sequence in which certain subsequences are distinguished from all other subsequences by some sort of pattern matching.

If yes, then it's pretty damn important, because it suggests that ev needs a more realistic selection algorithm (which is what I've been arguing all along).
Why do you say this?

~~ Paul

Paul C. Anagnostopoulos

12th April 2007, 06:16 PM

There are no selection processes that overcome the affect of multiple selection conditions slowing evolution.
As Mercutio and others have tried to tell you, this statement assumes that there is a predetermined goal toward which evolution is heading. Only then does the concept of the "speed of evolution" make any sense. Ev has a predetermined goal. Real life does not.

~~ Paul

Dr Adequate

12th April 2007, 06:36 PM

I understand functional notation. I also have some training and experience is solving multidimensional nonlinear functional equations. This is why when you presented the link to Wikipedia fitness landscapes, I immediately recognized the relationship and significance to the results from ev. But you did not. You mangled the article into complete gibberish. You didn't understand the first thing about it. You cited an article saying that evolutionary algorithms were "particularly successful" as proof that they weren't; you claimed they would have difficulty coping with the Travelling Salesman Problem if it only had three routes, when they are routinely applied to billions and trillions of routes; your stupid mistake was pointed out by a mathematician with experience of using evolutionary algorithms ... and now ...

And now you produce this windy boasting about how you "immediately recognized the significance" of the article --- as proof of your mathematical acumen?

Whom do you hope to fool?

---

P.S: I suspect the whimpering little coward has me on ignore. If anyone would like to quote this post, feel free.

Dr Adequate

12th April 2007, 06:43 PM

And you sound like a man with no mathematical training trying to argue about the mathematics of mutation and selection. This is not very interesting to observe but it seems to be the only effective debating tactic evolutionists have, that is boring me to death. The standard example of chutzpah is the man who, having murdered both his parents, asks for clemency from the court on the grounds that he is an orphan; but I think we have a new contender.

joobz

12th April 2007, 06:54 PM

But you did not. You mangled the article into complete gibberish. You didn't understand the first thing about it. You cited an article saying that evolutionary algorithms were "particularly successful" as proof that they weren't; you claimed they would have difficulty coping with the Travelling Salesman Problem if it only had three routes, when they are routinely applied to billions and trillions of routes; your stupid mistake was pointed out by a mathematician with experience of using evolutionary algorithms ... and now ...

And now you produce this windy boasting about how you "immediately recognized the significance" of the article --- as proof of your mathematical acumen?

Whom do you hope to fool?

---

P.S: I suspect the whimpering little coward has me on ignore. If anyone would like to quote this post, feel free.
I do not believe he has you on ignore, but i'll quote this regardless.

I enjoy the fact that he keeps feeling the need to remind us of his "mathematical competence" of his "engineering competence" and his "thermodynamic competence". It's almost as though he thinks we don't believe his abilities? :rolleyes:

kleinman

12th April 2007, 06:54 PM

Hey Paul, did Dr Schneider make an accident when he published this in his peer reviewed publication about ev?As he said, if Ev's rate is realistic, then certain consequences follow. Note that the final sentence you quoted suggests the rate is not realistic.
That’s a bit of an understatement. So what is Ev’s realistic rate of information acquisition?
Paul, I’m wondering how far you are going to back pedal on ev? Have you turn the seat around on your bicycle yet?I must have missed the part where I said that Ev represents a realistic simulation of the complete evolutionary landscape.
It’s not what you haven’t said about ev that causes you problems in this debate, it is what you have said. I think Dr Schneider has the same problem but even more extreme than you have. If Dr Schneider ever discusses his program publicly again, how is he going to address his numerous claims that ev simulates reality? I happen to think it does and it shows why the theory of evolution is mathematically impossible. I believe Dr Schneider did his computation properly, you programmed the online version properly but you completely misinterpreted your limited investigation of the behavior of the model.
So 2 selection pressures are sufficient to slow down evolution profoundly?No, I didn't say that. What I said was there is nothing magic about three or more pressures, even in your bizarre world of competing selection pressures.
Reality happens to be bizarre for evolutionists because you live in a world of misinterpretations. Your own computer model shows that Dr Schneider’s 2 (or 3) selection pressures profoundly slow the evolutionary process. This is an obvious finding when you consider what happens with any type of data sorting or optimization problem. Well, in your world of misinterpretation this is going to seem bizarre.
Paul, you are the expert at moving goalposts. Let’s summarize what you have said about ev, ev started out representing reality, then it became a model of a small part of the evolutionary landscape, then it became a stylized model of mutation and selection and now you can guarantee it makes no prediction about the rate of real world evolution, except possibly by accident.Oh, it does represent reality, exactly as much as required to show that information can evolve in a world with basic evolutionary processes. My other three statements are entirely compatible with one another.
And here again are the goalposts Paul, the rate which information evolves by mutation and selection is profoundly slow as shown by your ev model, too slow to support the theory of evolution. And why is this rate of at which information evolves so slow? It is because the multiple selection processes interfere with the acquisition of information.
There are no selection processes that overcome the affect of multiple selection conditions slowing evolution.Let's see your math, Alan. The constant whine is really boring.
Hey, didn’t I tell you about the evolutionist written, peer reviewed and published model of random point mutation and natural selection. It was written by a really smart guy at the National Cancer Institute and the online version of the model was written by a moderator on this forum. Do you want to hear more about the model?

I was really hoping my constant whine was annoying you. Just think of my whine as like the screeching of chalk on a chalk board. Microsoft needs to put that sound effect in Powerpoint, if for nothing else to keep evolutionists awake in their biology lectures.
There are no selection processes that overcome the affect of multiple selection conditions slowing evolution.As Mercutio and others have tried to tell you, this statement assumes that there is a predetermined goal toward which evolution is heading. Only then does the concept of the "speed of evolution" make any sense. Ev has a predetermined goal. Real life does not.
Now I understand your logic, if you have a predetermined goal, evolution goes profoundly slow, if you have no goal at all, it goes faster. Wow! How could anyone doubt this kind of logic?

You kids have a good weekend; try not to get subjected to too many selection pressures.

Dr Adequate

12th April 2007, 06:56 PM

Now I understand your logic... You think? Would you care to wager a little money on that proposition?

joobz

12th April 2007, 07:51 PM

You kids have a good weekend;
Thank you.

When you get back, remember to answer the following questions.
Why doesn't magnitude matter in modeling?
How come only point mutations matter?
Why does running a simulation = doing maths?
What is magical about 3 selection pressures?
Which selection pressure posed by Delphi would take less time?
Why do the yeast strains in the paper I posted develop resistance to the multiple selection pressures when you claim it would take too long to occur?

Dr Adequate

12th April 2007, 10:15 PM

Kleinman, you're busted. The Ev model is not peer-reviewed as a model of the speed of evolution. Further repetition of your claim, that it is, constitutes willful intent to deceive. It fascinates me that deception is proven to be an integral strategy in creationists' playbooks (e.g. Dover trial testimony). It just doesn't seem very Christian. He who begins by loving Christianity more than Truth, will proceed by loving his sect or church better than Christianity, and end in loving himself better than all. - Samuel Taylor Coleridge

delphi_ote

12th April 2007, 11:16 PM

Your f(x)=y, where x is a vector in your multidimensional functional equation describing a fitness landscape. In this case, the vector x defines points on the surface of the fitness landscape and the selection pressures, x1, x2, x3,… to the number of selection pressures define a direction for the walk on the fitness landscape. y is the fitness of the creature to reproduce. The optimum solution to this equation represents a value y which gives optimum reproduction.
No no no no no no no no! Slow down. We're already way off the tracks.

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

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

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

P.S. If anyone reading this has evolutionary algorithms and kernel methods experience, do you think there's a hint of an idea in that next to last paragraph? If so, PM me!

Paul C. Anagnostopoulos

13th April 2007, 05:24 AM

Now I understand your logic, if you have a predetermined goal, evolution goes profoundly slow, if you have no goal at all, it goes faster. Wow! How could anyone doubt this kind of logic?
I would doubt it, since that's not what I said. I said that if there is no goal, then the concept of the speed of evolution makes no sense.

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

~~ Paul

Mercutio

13th April 2007, 10:23 AM

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

Oh, my. Did he say that?

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

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

Mr. Scott

13th April 2007, 01:02 PM

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

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

linky (http://www.tuscaloosanews.com/article/20070413/ZNYT04/704130370/1001/NEWS06)

That's 1) Sulfomanides; 2) Beta-latcams; (3) Tetracyclines; (4) Fluoroquinolones.

...or, two successful adaptations past Kleinman Impossibility.

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

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

In other words, he's busted again.

kjkent1

13th April 2007, 04:10 PM

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

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

~~ PaulKleinman will simply state: "There is no selection method which will allow thirty-five million mutations to arise in the five million years since chimps and humans diverged" (or whatever the number is).Then he will ask you to define the selection method which could accomplish the divergence, because ev proves that it's impossible via point mutation.

And, while I find his use of the word "impossible" to be disingenuous as applied to the laws of probability and ev, I do think that it's reasonable to ask ourselves how we got from there to here within such a short period of time.

Maybe someone here already knows the specific answer to the question. If so, then an answer now, will avoid having to read another kleinman repeat protestation (probably not, but one can always hope).

delphi_ote

13th April 2007, 04:57 PM

Ichneumonwasp

14th April 2007, 05:21 AM

Kleinman will simply state: "There is no selection method which will allow thirty-five million mutations to arise in the five million years since chimps and humans diverged" (or whatever the number is).Then he will ask you to define the selection method which could accomplish the divergence, because ev proves that it's impossible via point mutation.

And, while I find his use of the word "impossible" to be disingenuous as applied to the laws of probability and ev, I do think that it's reasonable to ask ourselves how we got from there to here within such a short period of time.

Maybe someone here already knows the specific answer to the question. If so, then an answer now, will avoid having to read another kleinman repeat protestation (probably not, but one can always hope).

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

I think we are at the point where we understand the differences enough to essentially recreate the common ancestor (and split an infinitive), though I don't think we could claim to be perfectly accurate in such a model as of yet.

Any modelling of the changes necessary would need to include transfer of info through viral vectors, recombinations of chromosomes (which we know happened), probable gene duplications with modification, point mutations, probable feedback loops of new protein forms on promoter regions, differences in the timing of differential protein formations (during development -- change a downstream promoter slightly and the resulting gene product may be produced in greater quantity and at earlier times), and a variety of other factors in an incredibly complex system. We cannot hope to answer such a question easily by simply looking at different genomes since a full account of differences requires explanation of the gene product interactions. The god of the gaps has many more years of life left in him.

My guess is that a few key differences in gene expression during development result in most of the changes between us and other apes. Personally I wonder what would happen if the human FOXP2 gene were expressed in a chimp. Ethically no one will ever do the experiment, but I bet that gene has more properties than we currently think, depending on the protein milieu in which it is expressed, of course. And if chimps could talk? Might be interesting.

Paul C. Anagnostopoulos

14th April 2007, 07:19 AM

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

And, while I find his use of the word "impossible" to be disingenuous as applied to the laws of probability and ev, I do think that it's reasonable to ask ourselves how we got from there to here within such a short period of time.
Note that only about 50,000 of those differences affect protein sequences. That's 25,000 in each species. If we assume about 300,000 generations since humans and chimps diverged, that's about one protein change every 12 generations.

~~ Paul

Ichneumonwasp

14th April 2007, 08:08 AM

I have been thinking through the issue of debating this further and have decided to continue despite my earlier reservations (based on time commitment).

There are many issues at play here, so I will try to dissect them as best I can.

First, as to the issue of drug resistance in HIV and TB, there is a wealth of information --both from the past and current triple therapy regimens. A recent news report (http://www.innovations-report.com/html/reports/medicine_health/report-38840.html) covering a two year old study that examined compliance and the development of drug resistance indicates that compliance is the key issue in developing drug resistance and that drug resistance occurs in patients who are not properly compliant:

"Those who took 80 percent of their medication were likely to develop resistance most quickly. This probably means that they are taking enough medication to create a selective pressure," Dr. Harrigan said. "Which means that resistant virus mutations still have an opportunity to replicate instead of reducing the viral load to levels so low it can’t replicate at all."

The two key issues cited are those that I have harped on for the past two weeks – compliance issues that result in variable selection pressures (as opposed to constant pressure) and the strength of those pressures. This also speaks to the silly twisting of my arguments that Kleinman persists in perpetrating. Of course, if selection pressures are placed and permanently removed, information is lost. It is the irregular selection condition of poor compliance that provides a pressure but also allows sufficient reproduction that is important to the evolutionary process, especially as it relates to drug resistance.

When selection pressures are strong enough to decrease viral replication to the point where variability shrinks nearly to zero, then productive changes that will allow the virus to escape the selection pressures shrink nearly to zero. We all know that potent selection pressures slow the evolutionary process for the organism selected. That, in fact, is the definition of potency in a selection pressure (and why I have been harping on potency). The more potent a pressure is, by definition, the fewer offspring will emerge in the next generation. Fewer offspring means fewer experiments in variability, which means a slower rate of change. Triple therapy provides a profoundly (potently) selective pressure on HIV, as witnessed by significant reductions in viral load (I trust that I needn’t reference this phenomenon). But current triple therapy is effective only if compliance is nearly perfect (95+%) – if the selection pressures are kept in place and viral reproduction is kept to a bare minimum. When compliance is reduced to 80%, then enough viral replication occurs that new strains emerge and resistance develops. This level of compliance provides the same three selection pressures but still allows enough viral reproduction so that natural variability can produce resistant strains. So, by definition of selective pressures, 80% compliance with a triple therapy protocol constitutes three selection pressures that are less potent than triple therapy with 95+% compliance. The important factor is not the number of selection pressures but the potency of the selection pressures. The same phenomenon occurs with less potent HIV triple therapy regimens in which compliance was maintained at 95+% as I argued in a previous post and provided documentation for the emergence of resistant strains. Those particular triple therapy regimens are no longer used because the three selection pressures they employed are not potent enough to prevent the development of resistance. In fact, 95+% compliance on those regimens was the best predictor of resistance development. Once again, it is not the precise number of selection pressures that slows the process. It is the ability of those pressures to decrease reproduction/replication to a level where variability in the next generation is reduced.

Kleinman has repeatedly argued that three pressures act synergistically to reduce replication, and therefore variability, in HIV treatment. But this is not the case for all triple therapy regimens. As shown above, it is not the number of selection pressures that is critical. Three pressures will always slow the process more than one or two pressures – at the very least pressures must be additive, if not synergistic. But, three pressures will not necessarily stop the process or slow it to a point where “evolution becomes impossible”. The data from early trials with less potent triple therapies and relatively poor compliance with current triple therapy protocols demonstrate this fact unequivocally. It’s simply a numbers game. If enough progeny emerge in subsequent generations, then variability will, most likely, produce an organism that escapes the selection pressure(s), regardless of the number of those pressures. If the pressures are overwhelming, the species becomes extinct. If the pressures are so potent that variability is reduced to a minimum, then change will be slow or non-existent. If the number of progeny and variability are high enough, then new organisms evolve to escape the pressures.

With HIV triple therapy, if resistance to one drug emerges, the others can typically keep the viral load so low that variability cannot overcome the effects of the other drugs. It is not the case that three changes at once demolish the function of the target protein(s) – they proposed synergistic model. It is not possible that this is the explanation or multi-drug resistance in HIV would be impossible through whatever mechanism. But we do see multi-drug resistance in HIV, cited as evidence earlier (on more than one occasion and by more than one poster). Rather, no direct advantage necessarily accrues to the newly emerged strain resistant to one drug – it is still hit by the other two and viral loads remain low. If viral loads remain low enough, the process will be excruciatingly slow. If, however, viral loads increase due to poor compliance, then resistance to all three drugs becomes an option – and this is precisely what we see.

How does this relate to the ev model? I’m not sure that we need really ask the question simply because ev was never designed to model the entire evolutionary landscape. From my limited knowledge of it, ev was designed specifically to answer one question – can random mutation and natural selection increase information? Ev demonstrates that this simple process can do so without invoking the more profound process of gene duplication with subsequent modification. That argument is, therefore, laid to rest.

Kleinman insists that ev is an accurate portrait of the entire evolutionary landscape, but I don’t see how it is from the discussion I have seen. The population sizes are far too small to represent nature. This isn’t the fault of ev, though, because it wasn’t designed to answer the questions currently placed upon it. Recall that the single most important factor in the development of resistant strains of HIV is compliance. Poor compliance means more viral replication. The population size is absolutely critical to discussions of this sort. Reduce the population size enough and change slows dramatically. Adding three selection pressures necessarily reduces population size more than a single pressure of equal potency. So, necessarily, three selection pressures, holding potency of the selection pressures constant, will impact the speed of evolutionary change more than a single pressure. If those three pressures are modeled in a small enough population it will appear to stop the process cold in its tracks. There is likely some population threshold over which variability will almost always allow escape from multiple selection pressures, but I cannot pretend to know what such a threshold is – it would vary depending on circumstances and the organisms involved anyway.

Take an example run, in which the “genome” size is relatively large and three selection pressures are applied to an initial population size of 1000. If those criteria produce a “perfect creature” only after millions of generations, then why not the converse – millions of initial “creatures” may produce a “perfect creature” in approximately 1000 generations? How do we know this isn’t possible? Increasing initial population sizes to 10,000 or so will not help to elucidate the phenomenon because the variability is probably still too low. We simply cannot propose a linear relationship between increasing population size and numbers of generations to “perfect creature” over such a small range of population sizes. We would need to run simulations on these huge population sizes to tell, or do the commutative math and figure that a large population size is likely to produce an escape creature in short order. That is certainly what we see in nature and definitely what we see with HIV and TB. Maintain a low population size and triple therapy significantly slows the development of resistance. Allow population size to increase and resistance develops, even in the presence of the same three selection pressures (80% compliance condition). The above discussion, of course, neglects the significant problems with a “perfect creature” in this process, but I hope highlights the key issues.

I don't know if any of this discussion helps or is merely rehash of earlier debates in this thread (I suspect the latter), but here it is anyway. Since this is already too long, I will leave the rest until later.

Ichneumonwasp

14th April 2007, 08:23 AM

Note that only about 50,000 of those differences affect protein sequences. That's 25,000 in each species. If we assume about 300,000 generations since humans and chimps diverged, that's about one protein change every 12 generations.

~~ Paul

Interesting. To bolster that, do we have any estimates of the rate of protein change per generation in different species under different selection conditions? Fruit flys, for instance?

Nevermind. Here (http://www.pnas.org/cgi/content/full/102/1/140) is an interesting discussion of proposed rates that does not completely answer the question but does provide a good framework for thinking about it.

Mr. Scott

14th April 2007, 08:46 AM

Dr. Kleinman has repeatedly claimed that three is the threshold of mutations against selection pressures for microevolution, at which point the life form can no longer survive, as exemplified by the HIV virus. He's also asserted that the threshold between 2 and 3 adaptations is the threshold between micro and macro evolution, and that macroevolution is mathematically impossible.

He realy said these things?! What a riot!

My view on this issue is that once you get beyond a single point mutation you are already starting to enter the realm of macroevolution. Once you get to four point mutations I think you have gotten full into the realm of big evolutionary changes.

Macroevolution big change microevolution small change

Only in science fiction do we find super creatures arising from organisms subject to mutagens. In reality mutagens which cause divergence from the organism's genetic optimum kill the organism.

CDC CLASSIFIES GONORRHEA SUPERBUG (http://news.yahoo.com/s/ap/20070412/ap_on_he_me/resistant_gonorrhea)

kjkent1

14th April 2007, 06:32 PM

Note that only about 50,000 of those differences affect protein sequences. That's 25,000 in each species. If we assume about 300,000 generations since humans and chimps diverged, that's about one protein change every 12 generations.

~~ Paul"Well, bust my buttons! Why didn't you say that in the first place? That's a horse of a different color!" -- Doorman at the Gates of the Emerald City, The Wizard of Oz (1939).

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

delphi_ote

15th April 2007, 02:26 AM

Triple therapy provides a profoundly (potently) selective pressure on HIV, as witnessed by significant reductions in viral load (I trust that I needn’t reference this phenomenon). But current triple therapy is effective only if compliance is nearly perfect (95+%) – if the selection pressures are kept in place and viral reproduction is kept to a bare minimum. When compliance is reduced to 80%, then enough viral replication occurs that new strains emerge and resistance develops. This level of compliance provides the same three selection pressures but still allows enough viral reproduction so that natural variability can produce resistant strains. So, by definition of selective pressures, 80% compliance with a triple therapy protocol constitutes three selection pressures that are less potent than triple therapy with 95+% compliance. The important factor is not the number of selection pressures but the potency of the selection pressures.
I was hoping to do this mathematically, but you've done it brilliantly with an empirical result. I couldn't hope to get this point across more clearly than you just did. Your post utterly demolishes kleinman's multiple selection pressures mistake hypothesis. He needs to read this until he understands it, and the rest of us need to keep him focused on it until he does.

Very well researched, very well thought out, and very clearly explained.
:th:

Ichneumonwasp

15th April 2007, 03:29 PM

Why thank you.

I've been thinking about this issue and would appreciate your and Paul's (and kjkent1 and Joobz and anyone else's) input, but it seems to me that there are two issues that confound this entire debate. There is the issue of bioinformatics, which ev was designed to deal with -- my understanding is that the thrust of the simulations was to show how random mutation and selection can increase information. And there is the issue of survival of the fittest as occurs in real life. It isn't precisely clear to me that we should speak of HIV escaping triple therapy pressures as containing an increase in information. There is certainly a change in information, and it may represent an increase in total info, but I don't see why it must. For that virus all that is required is a change in the particular sites where the drugs work. If the replication system continues to function, either by assuming some new configuration of binding or simply assuming different protein folding such that the drugs can no longer attack it the way they were designed doesn't particularly matter.

I don't have a very good sense of how ev models survival of the fittest exactly because I don't think it was really designed to do so. There seems to be a surrogate measure -- perfect creature -- that contains of measure of bioinformational gain (which, again, is what the program was designed to investigate). In short, from my limited understanding of the workings of the program, it cannot be used the way that Kleinman is trying to use it. I'm only approaching it from the real world biological side of things, though, so any insights you guys could offer would be very appreciated.

cyborg

15th April 2007, 04:09 PM

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

Sensible people concluded this some 90 pages ago.

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

delphi_ote

15th April 2007, 05:13 PM

Sensible people concluded this some 90 pages ago.

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

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

joobz

15th April 2007, 06:22 PM

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

If anything would convince kleinman he's mistaken, it would be this incontrivertible evidence. I agree. Ichneumanwasp's post was very well done. However, I think Mr. Scott's addition is equally damning evidence against the multistressor argument. Coupled with the yeast example I found, there is no magic behind the number of stressors experienced, rather the strength the cummulative effect of stresses is of greatest importance.

While only one example is needed to refute Kleinman's multi-stressor hypothesis, we now have three seperate examples where species can adapt to multiple stressors; ichneumonwasp's HIV example, Mr. Scott's Gohnorrhea example and the example of enigneering yeast strains to exhibit resistance against specific stresses. Please Kleinman, what is your new theory? The magic three stressor hypothesis is dead.

delphi_ote

15th April 2007, 06:26 PM

I agree. Ichneumanwasp's post was very well done. However, I think Mr. Scott's addition is equally damning evidence against the multistressor argument. Coupled with the yeast example I found, there is no magic behind the number of stressors experienced, rather the strength the cummulative effect of stresses is of greatest importance.
Definitely. There's just something magical about it being kleinman's own example. :D

joobz

15th April 2007, 06:39 PM

Definitely. There's just something magical about it being kleinman's own example. :D
Agreed. But I get a kick out of the fact that three examples are like a jokes-for-nerds premise:
"A virus, a bacteria and a fungus walk into a bar...."

Paul C. Anagnostopoulos

15th April 2007, 07:20 PM

I don't have a very good sense of how ev models survival of the fittest exactly because I don't think it was really designed to do so. There seems to be a surrogate measure -- perfect creature -- that contains of measure of bioinformational gain (which, again, is what the program was designed to investigate).
Each creature is scored for number of mistake points (missing binding sites, spurious bindings within gene, spurious bindings outside gene). Then the creatures are sorted by mistake points. The creatures are compared in pairs: the best and worst, next best and next worst, etc. If the better one has fewer mistakes, it survives and replicates, killing the worse one. If there is a tie, it is broken according to a tie breaking parameter; the default is to keep both creatures.

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

"A virus, a bacteria and a fungus walk into a bar...."
An absolutely gorgeous protozoan is sitting at the bar having a drink ...

~~ Paul

Paul C. Anagnostopoulos

15th April 2007, 07:26 PM

So, if we accept your assumptions, for argument's sake, then what sort of numbers would you input into ev to show kleinman that the sort of changes he says are impossible, are actually very reasonable?
I don't think Ev's model is rich enough to demonstrate something like the divergence of chimp and humans.

~~ Paul

Foster Zygote

15th April 2007, 09:23 PM

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

kjkent1

15th April 2007, 10:58 PM

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

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

articulett

15th April 2007, 10:59 PM

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Ichneumonwasp

16th April 2007, 04:36 AM

I apologize for thinking you are a creationist

Was that directed at me?

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

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

Ichneumonwasp

16th April 2007, 04:45 AM

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

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

~~ Paul

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

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

Paul C. Anagnostopoulos

16th April 2007, 05:36 AM

Good, thanks. So, the model is well constructed for the determination of information gain and not very helpful for real world natural selection. Like I said several times before, I am very sure all this has been covered earlier and I just do not want to read this entire thread, but how in the world could something like this continue for so long when the model itself cannot answer the issues that Kleinman proposes?
Hey, it's a thread on the James Randi forum. It has a life of it's own. Kleinman's goalpost used to be in a different place: He was simply claiming that Ev demonstrates that not enough time has passed to evolve transcription factor binding sites on huge genomes using only point mutation. Unfortunately, we agreed, so his goalpost has evolved since then.

This looks to me like the strawman of strawmen; Behe on steroids; Dembski on PCP; Philip Johnson set loose in a boy's refectory with a bottle of Crisco and no nightwatchman.
Sig material! But as a moderator, I must refrain. :D

~~ Paul

Ichneumonwasp

16th April 2007, 05:44 AM

articulett

16th April 2007, 06:08 AM

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

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

Ev did its job. Let it rest.

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

articulett

16th April 2007, 06:21 AM

Was that directed at me?

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

Ichneumonwasp

16th April 2007, 06:22 AM

Thanks.

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

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

joobz

16th April 2007, 06:49 AM

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

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

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

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

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

kleinman

16th April 2007, 12:19 PM

You kids have a good weekend;Thank you.
When you get back, remember to answer the following questions.
Why doesn't magnitude matter in modeling?[/quote]
If you ask an interesting pertinent question, I will always try to answer your questions. Of course magnitude matters in modeling. This is why Dr Schneider’s failure to consider larger size genomes led to inappropriate extrapolations about the rate of information gain by mutation and selection. There are other practical issues that matter about magnitude that must be considered with modeling such as round off error.
How come only point mutations matter?[/quote]
I haven’t said that only point mutations matter. What I have said is that other mechanisms of mutations will not alter the fundamental mathematics that multiple selection conditions slow the evolutionary process. It doesn’t matter what form of mutation occurs in the mutation/selection cycle. It is the multiple selection conditions which slow the evolutionary process. What type of mutation mechanism do you propose to put into ev which would alter this mathematics?
Why does running a simulation = doing maths?[/quote]
Dr Schneider did the “maths”. Running a simulation (doing a parametric study) describes the behavior of the “maths”. Dr Schneider did the “maths” properly; he failed to describe the behavior of the “maths” appropriately by using a single set of parameters in the model to draw his conclusions. Are you sure you are an engineer? When you do a simulation, do you do a single case and draw your conclusions based on that single case?
What is magical about 3 selection pressures?[/quote]
The only thing “magical” about 3 selection pressures is that it causes evolution to proceed more slowly than 1 or 2 selection pressures.
Which selection pressure posed by Delphi would take less time?[/quote]
Ask Delphi this question then ask him to put his code fragments into ev to produce the data to prove it.
Why do the yeast strains in the paper I posted develop resistance to the multiple selection pressures when you claim it would take too long to occur?
After reading the paper, I know why you didn’t post any quotes from the paper because it supports my argument that multiple selection pressures slow evolution when applied simultaneously. Here is a quote from the paper:
For batch selection, the overnight cultures of chemically mutagenized S. cerevisiae (named as 101) at lateexponential phase were exposed to each of the four
stress conditions separately, as described in Fig. 1.
I added the bold facing. This situation is exactly analogous to using monotherapy to treat HIV or TB. You can rapidly obtain drug resistant strains to single drugs applied in series. These authors used the same strategy to obtain multiple-stress resistant Saccharomyces. You evolutionists continue to give evidence that makes my point.
Your f(x)=y, where x is a vector in your multidimensional functional equation describing a fitness landscape. In this case, the vector x defines points on the surface of the fitness landscape and the selection pressures, x1, x2, x3,… to the number of selection pressures define a direction for the walk on the fitness landscape. y is the fitness of the creature to reproduce. The optimum solution to this equation represents a value y which gives optimum reproduction.No no no no no no no no! Slow down. We're already way off the tracks.
I’ve always told you evolutionists that I would be patient with you. I’ll go whatever pace you need to go in order to understand the mathematics of mutation and selection.
Fitness only has meaning with respect to a specific genotype. To make this computation even close to reality, x must be a variable length string of characters from an alphabet (like a DNA sequence.) Multiple independent selection pressures could be represented as multiple functions on the genotype, which could then combined to form the organism's overall fitness. The total fitness represents that genotype's ability to produce offspring in a particular enviornment.
You don’t understand the meaning of a functional equation. A functional equation is the implicit notation that a variable is dependent upon one or more independent variables. So, f(x)=y is simply saying that y depends on the value of x (x1, x2, …). If y is the genotype’s ability to produce offspring in a particular environment (selection conditions, the x1, x2, …) then to optimize y, mutations to the genotype which increase y subject to x selection conditions will satisfy that walk on the fitness landscape to the optimum. In words, an organism’s fitness is dependent on the selection conditions.
Unless we're talking about a very trivial fitness function on trivial genomes, describing the surface of a fitness landscape is very difficult. Visualizing it in any meaningful way is almost impossible, as the "distance" between points is proportional to the probability of mutations between two genotypes.
Certainly the fitness landscape is very complex. This is why I contend there is no way to transform a gene from some initial function to some totally different function. That gene must take a path on the fitness landscape such that it is always selected for in order to make the transformation. Your concept of gene duplication to give the raw material to make new genes requires there to be some path on this complex fitness landscape which allows the transformation to be made. Three selection pressures make the transformation of genes on HIV very slow and this situation does not create new genes with new functions.
Unless you are willing to be patient and read carefully without making assumptions, this thread is going to keep repeating itself.
The only thing I am repeating is the mathematics that ev shows and the real examples of this mathematics. The reason I repeat it is that is how mutation and selection works.
Now I understand your logic, if you have a predetermined goal, evolution goes profoundly slow, if you have no goal at all, it goes faster. Wow! How could anyone doubt this kind of logic?I would doubt it, since that's not what I said. I said that if there is no goal, then the concept of the speed of evolution makes no sense.
So let’s look at what you said again.
As Mercutio and others have tried to tell you, this statement assumes that there is a predetermined goal toward which evolution is heading. Only then does the concept of the "speed of evolution" make any sense. Ev has a predetermined goal. Real life does not.
It certainly looks like you said that that real life does not have a predetermined goal toward which evolution is heading.
To be clear: It makes sense to look at an evolved function and ask how long it took, and through which steps it evolved. What doesn't make sense is to look forward and ask how long it will take for something interesting to happen, when that something is not predefined.
I understand why you take this view. Your own model shows that when you use it to look forward and ask how long it will take; it shows your belief system to be mathematically impossible. Paul, your prejudices are showing.

Paul, what you have done is to adopted Cyborg’s cruft theory of evolution.
Kleinman, it may surprise and disappoint you to hear it, but there was no particular reason evolution had to end up creating you. As predetermined goals go, there's nothing special about humans. Could be that the "predetermined goal" was banana slugs, and we are just one of millions of misses. Sure, you may feel that you are a "perfect creature"; e coli feel the same way about themselves, and if it came to a vote they'd win.
So tell us Mercutio, did all these living things come about by mutation and selection or mutation and no “predetermined goal”. If you take this second view, do you want to explain it to us mathematically?
In your world, does evolution require every creature to have a separate, predetermined pathway "from the beginning"?
Well, it appears in your world it appears that mutation and selection can not have a predetermined pathway, otherwise your theory is mathematically impossible. This is why you evolutionists have transformed the field of biology into a mushy soft collection of unrealistic extrapolations deficient of any mathematical foundation.
There are a number of news reports today about the verification of a gonorrhea "super bug" resistant to all but one of its useful classes of antibiotics. Seems it has aquired resistance to all four (4) previous classes, as explained in the following quote: Over the years, gonorrhea has become resistant to a number of antibiotic classes starting with sulfa, then penicillin and the tetracyclines before fluoroquinolones.
Of course this has happened; single selection pressures (monotherapy) can quickly evolve drug resistant strains. If you do a little more investigation you will find MRSA, pseudomonas and a variety of other microbes are displaying the same behavior that ev models. Joobz’s paper shows this same phenomenon to other types of selection stresses.
Dr. Kleinman's mathematics must therefore be incorrect, since the real world is not consistent with his prediction.
Don’t be silly Mr Scott; your example supports my contention. Single selection conditions can quickly evolve, the more selection conditions imposed, the slower the evolutionary process proceeds. Multiple selection conditions slow evolution.
The gonorrhea super bug Neisseria gonorrhoeae is now on its fifth antibiotic class -- the only one we now have to treat it. Now, Dr. Kleinman has repeatedly claimed that three is the threshold of mutations against selection pressures for microevolution, at which point the life form can no longer survive, as exemplified by the HIV virus. He's also asserted that the threshold between 2 and 3 adaptations is the threshold between micro and macro evolution, and that macroevolution is mathematically impossible.He realy said these things?! What a riot!
What really is a riot is that you said this:
There are plenty of examples of A-life evolving. I think Ev rankles the IDers because it is a model of actual life, and also because Schneider is fairly good at advertising it.
And then you said this:
To be clear: It makes sense to look at an evolved function and ask how long it took, and through which steps it evolved. What doesn't make sense is to look forward and ask how long it will take for something interesting to happen, when that something is not predefined.
So how long does it take to evolve binding sites on an e coli size genome?
Triple therapy provides a profoundly (potently) selective pressure on HIV, as witnessed by significant reductions in viral load (I trust that I needn’t reference this phenomenon). But current triple therapy is effective only if compliance is nearly perfect (95+%) – if the selection pressures are kept in place and viral reproduction is kept to a bare minimum. When compliance is reduced to 80%, then enough viral replication occurs that new strains emerge and resistance develops. This level of compliance provides the same three selection pressures but still allows enough viral reproduction so that natural variability can produce resistant strains. So, by definition of selective pressures, 80% compliance with a triple therapy protocol constitutes three selection pressures that are less potent than triple therapy with 95+% compliance. The important factor is not the number of selection pressures but the potency of the selection pressures.I was hoping to do this mathematically, but you've done it brilliantly with an empirical result. I couldn't hope to get this point across more clearly than you just did. Your post utterly demolishes kleinman's multiple selection pressures mistake hypothesis. He needs to read this until he understands it, and the rest of us need to keep him focused on it until he does.
The only thing that Ichneumonwasp has shown here is that reducing the selection pressure speeds up the evolutionary process. This is what ev shows and this is what I have contended for pages on this thread. Ichneumonwasp is making my point.
In short, from my limited understanding of the workings of the program, it cannot be used the way that Kleinman is trying to use it.Sensible people concluded this some 90 pages ago.
Why cyborg, it is nice to have you back. Do you know that Paul has adopted your cruft theory of evolution?
Kleinman is, however, an Energizer bunny, he just keeps on going on, and on, and on, and on, and...
That’s because you are such an encouragement to me.
I don't think anyone linked drug compliance to the selection pressure's potency yet. This adroit argument demolishes kleinman's hypothesis in a straightforward way. There's nothing subtle about it. Putting the same population under the same number of selection pressures while varying the potency can increase or decrease the rate of adaptation. Clearly adaptation is independent of the number of selection pressures.
Certainly changing the potency of selection pressures changes the rate of adaptation but you are wrong when you say adaptation is independent of the number of selection pressures. Your own Wikipedia link to fitness landscape should make that clear to you.
If anything would convince kleinman he's mistaken, it would be this incontrivertible evidence.
The incontrovertible evidence you and your fellow evolutionists have been posting supports what ev is showing and what I am contending.
So, if we accept your assumptions, for argument's sake, then what sort of numbers would you input into ev to show kleinman that the sort of changes he says are impossible, are actually very reasonable?I don't think Ev's model is rich enough to demonstrate something like the divergence of chimp and humans.
However, ev is rich enough to demonstrate what multiple selection pressures do to the rate of evolution. Multiple selection pressures profoundly slow the rate of evolution.
Wow! It's like I wandered back into this thread just as the Death Star was blowing up.
Now don’t get hit by any pieces of the theory of evolution as it is vaporized by ev.
I don't think Ev's model is rich enough to demonstrate something like the divergence of chimp and humans.I understand completely, but that won't stop kleinman from jumping all over your comments. I'm sure that the upcoming dialog will be fascinating.
I was really hoping it will be annoying rather than fascinating.
Each creature is scored for number of mistake points (missing binding sites, spurious bindings within gene, spurious bindings outside gene). Then the creatures are sorted by mistake points. The creatures are compared in pairs: the best and worst, next best and next worst, etc. If the better one has fewer mistakes, it survives and replicates, killing the worse one. If there is a tie, it is broken according to a tie breaking parameter; the default is to keep both creatures.

So fitness is simply inversely proportional to the number of mistake points.Good, thanks. So, the model is well constructed for the determination of information gain and not very helpful for real world natural selection. Like I said several times before, I am very sure all this has been covered earlier and I just do not want to read this entire thread, but how in the world could something like this continue for so long when the model itself cannot answer the issues that Kleinman proposes?
You might ask whether Paul is speaking for himself or for the author of the computer model because the author of the model said the following:
Dr Schneider said the following in response to a critique of ev written by Royal Truman. This quote is taken from Dr Schneider’s web site at:
http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/truman/
A good simulation does not attempt to simulate everything; only the essential components are modeled. For the issue at hand, the form of the genetic code is not relevant; information measured by Shannon's method is more general than that.
And Dr Schneider said the following:
http://www.lecb.ncifcrf.gov/~toms/paper/ev/blog-ev.html (http://www.lecb.ncifcrf.gov/~toms/paper/ev/blog-ev.html)
The following are Dr Schneider’s responses to a critique of his paper Evolution of biological information by Dr Stephen E Jones.
Stephen E. Jones[/COLOR] (http://members.iinet.net.au/~sejones/)"]"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 (http://www.lecb.ncifcrf.gov/~toms/paper/schneider1986)
Stephen E. Jones[/COLOR] (http://members.iinet.net.au/~sejones/)"]It only becomes *real* biological information and random mutation and natural selection, when the simulation is tested in the *real* world, using *real* DNA, proteins, with *real* mutations and a *real* environment does the selecting. It is significant that Schneider does not propose this, presumably because he knows it wouldn't work.You are very bad at reading my mind, I have considered doing this experiment. Given the right conditions, it WILL WORK. Do you have th gumption to do the experiment yourself? That's the way real science works! FURTHERMORE, if you read the literature, you will recognize that related experiments have been repeatedly done for 20 years. Look up SELEX.
Stephen E. Jones[/COLOR] (http://members.iinet.net.au/~sejones/)"]In the rest of the paper he uses the single word "selection". I take this as a tacit admission that his model is not a simulation of *real* biological natural selection. No. A rose is a rose by any other name. Selection is selection whether it be natural (generally meaning the environment of earth), breeding (by humans usually, though perhaps some ants select their fungi), SELEX or in a computer simulation. Of COURSE it is a simulation of natural selection! The paper would not be relevant to biology and would not have been published in a major scientific journal if it were not!
Stephen E. Jones[/COLOR] (http://members.iinet.net.au/~sejones/)"]Schneider lets slip that there is another unrealistic element in his (and indeed all) computer simulations in that it (they) "does not correlate with time": So? Run the program slower if you want. Make one generation per 20 minutes to match rapid bacterial growth. THIS WILL NOT CHANGE THE FINIAL RESULT!
Stephen E. Jones[/COLOR] (http://members.iinet.net.au/~sejones/)"]Well, when Schneider's simulation is actually tested with *real* "life" (e.g. a bacterium), and under *real* mutation and natural selection it gains information, then, and only then, would "creationists" be favourably impressed. But if they are like me, they would already be impressed (but unfavourably) that Schneider does not mention in his paper that his simulation should now be so tested in the *real* "biological" world. 1. The simulation was of phenomena in the "real" world.
2. Dr. Jones is invited yet again to do an experiment.
The following is a response Dr Schneider made to a statement made by David Berlinski (http://www.discovery.org/scripts/viewDB/index.php?command=view&id=51&isFellow=true).
Where attempts to replicate Darwinian evolution on the computer have been successful, they have not used classical Darwinian principles, and where they have used such principles, they have not been successful. The ev program disproves this statement since it uses classical Darwinian principles and was successful.
The previous statements are clear that Dr Schneider believes that ev simulates the real world. Paul believed this until he saw the true behavior of ev.
Good, thanks. So, the model is well constructed for the determination of information gain and not very helpful for real world natural selection. Like I said several times before, I am very sure all this has been covered earlier and I just do not want to read this entire thread, but how in the world could something like this continue for so long when the model itself cannot answer the issues that Kleinman proposes?Hey, it's a thread on the James Randi forum. It has a life of it's own. Kleinman's goalpost used to be in a different place: He was simply claiming that Ev demonstrates that not enough time has passed to evolve transcription factor binding sites on huge genomes using only point mutation. Unfortunately, we agreed, so his goalpost has evolved since then.
The only thing that has moved in this discussion is your (d)evaluation of ev. We still have the same goalposts. Ev shows that the theory of evolution is mathematically impossible and we now have the explanation of why it is mathematically impossible. Multiple selection conditions profoundly slow the evolutionary process.
This looks to me like the strawman of strawmen; Behe on steroids; Dembski on PCP; Philip Johnson set loose in a boy's refectory with a bottle of Crisco and no nightwatchman.Sig material! But as a moderator, I must refrain.
Just because you are a moderator on this forum doesn’t mean you don’t reveal your prejudices and biases. In fact they reveal how sloppy you are as a mathematician and scientist. If the mathematics interferes with you belief system, you simply claim they don’t apply. You defend this by saying that without direction, evolution proceeds more quickly. Put that feature in ev and show us the mathematical proof of you theory.
I have half a mind to insist that Kleinman publish this idea. Immediately. How can he keep such all-important ideas away from the reading pulic? But, please, tell me where it will be published. I want to witness the public burning with my own eyes.

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

Ev did its job. Let it rest.
Ev is an excellent model of mutation and selection and how multiple selection conditions affects evolution. Just because Paul has gone into denial mode about what ev represents, we still have the author’s own statements about the model. If you studied ev a bit, you would comprehend my arguments.
1.) Why doesn't magnitude matter in modeling?
2.) Why do only point mutations matter?
3.) Why does running a simulation = doing maths?
4.) What is magical about 3 selection pressures?
5.) Which selection pressure posed by Delphi would take less time?
6.) Why do the yeast strains in the paper I posted develop resistance to the multiple selection pressures when you claim it would take too long to occur?
Already answered at the beginning of this post.
7.) How does the HIV adapt to three selection pressures?
Much more quickly with monotherapy than with triple drug therapy.
8.) Why is there evidence of a Gonorrhea Superbug?
Gonorrhea has been treated with monotherapy for years.
And some additional questions posed by ichneumanwasp:
7.) Why are you generalizing a model intended only to demonstrate information gain through mutation and selection?
Shouldn’t this be 9.)? I did this at Dr Schneider’s suggestion. He did this in email communications with me and he suggested this publicly in his publication on ev. The only thing I am generalizing from his model is that multiple selection conditions profoundly slow the evolutionary process. This is a general mathematical principle for mutation and selection no matter what the mechanism of mutation is. There are numerous real examples of the phenomenon including the ones you are raising here.
8.) How does this differ from any other post hoc analysis in science -- a type of analysis that is considered useful for future directions in research but extremely dangerous in drawing new conslusions?
Ev demonstrates a fundamental principle of mutation and selection. It shows why a Gonorrhea Superbug can arise so quickly. It also explains why so many other resistant strains of microbes arise because of the use of monotherapy. What is so dangerous about showing the theory of evolution to be mathematically impossible? It is simply a dumb theory that has failed to explain properly how mutation and selection works.
9.) On what grounds do you think that ev closely models all realities concerning evolution when even its creators do not?
Read Dr Schneider’s quotes that I have posted above and you will understand that the creator of the model believes his model simulates reality. I agree with him, he has properly modeled mutation and selection.
10.)How can you claim only a fourfold increase in change with increasing population size when you cannot model population sizes on the order of billions to many more as are seen in nature?
I have run simulations with a 10,000 fold increase in the population and it shows that the decrease in the generations for convergence occurs at less than an additive rate with increasing population. It is easy to understand why this occurs when you understand that doubling population less than doubles the probability of an appropriate mutation occurring at a particular locus. Paul is supposed to be running a population series now but does not seem to be posting any data. I have run and posted several population series and they all show the same mathematical behavior I’ve described here. Once I get a computer with more memory, I will run population cases with >10^6 creatures but the trends are already established.
11.) Related to the above, in a model with 90% kill off in a population of 60 or so, the remaining population from the selection pressure would be around 6. But a 90% kill off in a population of 1 billion would result in a population size of 100 million. A 99% kill-off results in a population size of 10 million. Are you suggesting that these differences in population size, in which every member generates new mutations, is incapable of producing viable offspring that can escape the selection pressures? I could certainly see only a fourfold increase in changes if you were talking about the difference between a population size of 60 and one of 6000. The difference in population size is not enough to expect new varieties that could escape these pressure, but a population of 10 million?
The selection pressures are independent of population sizes. Dr Richard has already said that with HIV, you are producing 10^9 viruses/day yet triple therapy still slows evolution. Complex creatures don’t reproduce at this rate and have much smaller populations. The fundamental mathematics of mutation and selection makes it impossible for any macroevolutionary process to occur.
12.) If you are modelling kill-off rates higher than 99%, then how does this differ from extinction models? How does this relate to natural conditions?
Increasing the kill off rate only slows the mathematics of mutation and selection further, you reduce population and that is the only parameter that accelerates evolution (for a given set of selection conditions).
If math or theory are in conflict with reality, which must we change to correct the error?
The mathematics of ev is consistent with reality. We have at least five real examples of what ev is demonstrating mathematically, including your example.

joobz

16th April 2007, 12:56 PM

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

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

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

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

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

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

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

I refuse to allow you to move this goalpost.

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

kjkent1

16th April 2007, 01:08 PM

Kleinman:

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

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

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

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

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

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

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

I have yet to see you provide any contrary proof.

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

kleinman

16th April 2007, 02:14 PM

I should have known you'd move the goal post again. So we now play the game of "a stress is what I call a stress".
Who are you quoting? Are you whining because I pointed out in your paper that they were applying selective pressures one at a time?
I wonder if you ever considered what happens chemically when you use chemically active chlorine or iodine as a disinfectant. This is an example of large number of multiple selection pressures. Chlorine and iodine combine chemically to large number of sites on a wide variety of biological molecules including proteins, DNA and other crucial molecules necessary to support life. These chemical additions of these large chemically active groups change the conformation of huge number of biological molecules simultaneously which is why these chemicals are effective disinfectants.Now, in that paper, they included an ethanol stress, an oxidative stress (in the form of hydrogen peroxide), a heat stress and a freeze-thaw stress. Each of these gross scale stresses actually represents a variety of independantly functioning stresses. By your own admission, the hydrogen peroxide (Which functions identically similarly to the chlorine or iodine) is a multi stress event in and of itself.
So let’s consider each of the selective pressures. Do you consider an ethanol stress as a large number of multiple selection pressures? Consider how these authors applied this stress. The used slowly increasing levels of ethanol alone without the other selective pressures applied at the same time. Once they had strains of their yeast that could tolerate an elevated level of ethanol, the then applied the next selection pressure.

Now consider their use of hydrogen peroxide, you are probably not aware of the enzyme superoxide dimutatase. By slowly increasing the concentration of hydrogen peroxide they are selecting strains that are better producers of this enzyme. You are not evolving this enzyme de novo; you are simply producing strains of the yeast that are good producers of this enzyme. The heat stress and freeze-thaw stress are multiple selection stressors but consider that these authors limited these stresses in order to produce viable yeast. Why don’t you write to these authors and ask them what would happen if they applied all for of their stressor conditions at the same time rather than one at a time.
I refuse to allow you to move this goalpost.
I neither need to nor want to move the goalposts. I’m just waiting for you evolutionists to get to the ball park.
Your theory has been refuted. Your math holds no logic. You are floundering in your foolishness.
You have refuted nothing; all you have shown is that with careful application of single selection pressures you can breed yeasts with particular properties to survive in particular environments. Now if you show that all their selection pressures can be applied simultaneously and you are able to breed this yeast as quickly as with single selection pressures then you would have a point.
None of the evidence, real world or mathematical, proves that all selective pressures are of equal force and effect. Nor does the evidence prove that multiple selective pressures are of additive power, extending without limit.
I’ve never said that all selective pressures are of equal force and effect. What I have said is that when you have multiple selective pressures, the multiple pressures slow the evolutionary process. You have played with the weighting factors for the different mistakes in ev and see that it changes the generations for convergence but none of the weight factors have such an extreme effect as when setting the value to 0. If you think changing the weights on the selection conditions in ev will allow larger genomes to converge, do some examples for us.

I also don’t believe that selection pressures are additive. Two selection pressures that alone might otherwise have minimal impact on the reproduction of a creature, when combined have a marked affect on the ability of the organism to reproduce. Triple antiviral agents for the treatment of HIV are an example of this. One agent has minimal effect on the reproduction virus while three agents together profoundly affect reproduction of the virus. The effect of the three agents is more than three times the affect of any single agent.
How do you know that the curve of selective pressures doesn't level off in its effect?
The curve for selective pressures is easily bracketed. At one extreme you have very mild selective pressures that have virtual no effect on the reproduction of the creature while at the other extreme, you have selective pressures that cause extinction. All other selective pressures fall with the range of these two selective pressures.
How do you know that "all" selective pressures interfere with each other?
That is the mathematical principle that is demonstrated by ev and is well described by Delphi’s reference to Wikipedia and the fitness landscape. You are requiring multiple stress conditions to be overcome simultaneously. This is mathematically and physiologically more difficult than overcoming a single selection condition at a time.
How do you know that some selective pressures don't negate or aid each other?
You may be able to come up with peculiar selective pressures that might do something like you suggest but in general this is not what the mathematics suggests.
You keep insisting on adherence to sound science -- maybe you should follow your own policy. Right now, you can modify the relative weight of the selective pressures in ev, and the results will alter the number of generations necessary for Rseq -> Rfreq. Missed bindings, spurious bindings inside, and spurious bindings outside display different selective pressures.

So, we know for a fact that all selective pressures are not equal.
Nothing affects convergence in ev like shutting off two of the three selection pressures. If you think you can markedly change the generations for convergence by simply varying the weights without setting any to zero, do some examples on a 32k or 64k genome and show us.
And as we can't test some other pressure, not found in ev, we can't conclude that selective pressures restrict evolution without limits. I submit that the effect of many selective pressures will center around a mean, and likely are normally distributed. My own experiments with ev show the appearance of this behavior even with only three pressures.
What ev is showing is that each additional selection pressure slows the evolution process. This is a general mathematical principle that does not matter what the selection pressure is. Read Wikipedia on fitness landscape. They say the same thing I am saying but using different terminology.
I have yet to see you provide any contrary proof.
Well, we have the mathematics of ev and we have numerous examples of how multiple selective pressure slow the evolution of resistant strains of microbes. Too bad you can’t see this proof. I’ll look for more examples of this and I’m sure you evolutionists will come up with more examples, like joobz example of developing multiple stress resistant yeasts by applying single pressures at a time.
PS. You don't annoy me. You're far too predictable to do that.
I’ll have to work on that.

joobz

16th April 2007, 02:48 PM

kleinman

16th April 2007, 03:43 PM

Now consider their use of hydrogen peroxide, you are probably not aware of the enzyme superoxide dimutatase. By slowly increasing the concentration of hydrogen peroxide they are selecting strains that are better producers of this enzyme.you can't help but be wrong can you?

Superoxide dismutase (SOD), whether you are talking about copper/zinc SOD or manganese SOD, catalyzes the conversion of Superoxide INTO hydrogen peroxide. It doesn't catalyze the degradation of H2O2. Catalase is the enzyme that degrades hydrogen peroxide. As well as (to lesser extents) the family of glutathione peroxidases.
I stand corrected here master of alchemical engineering. It is the family of peroxidases that decompose the peroxides. But the point is that the paper you provided describes the application of H2O2 as a single selection pressures in slowly increasing concentration to select yeasts which produce enzymes that decompose this oxidizer. That is unless you are arguing that the numerous proteins and other molecules which are damaged by H2O2 are all evolving to new forms that are not affected by H2O2.
SOD blocks injury as result of direct oxidation from superoxide, (such as the peroxidation of lipids), but not from hydrogen peroxide. Hydrogen peroxide can still generate hydroxyl radicals through fenton chemistry.

So, yes, hydrogen peroxide IS a multiple stressor. As is ethanol: Ethanol results in changes in membrane fluidity, alterations in membrane potential, and the generation of acetaldehyde.
So you are arguing that all the molecules which would be harmed by H2O2 and ethanol are all evolving to new forms which are resistant to the damage these chemicals would do. I think you and Delphi both need to lay off the ethanol.

Ichneumonwasp

16th April 2007, 04:32 PM

kleinman

16th April 2007, 06:19 PM

Ev is an excellent model of mutation and selection and how multiple selection conditions affects evolution.How does Ev model HIV triple therapy? Ev selects based on "mistakes" gained through a mutation process. Are you suggesting that HIV is selected by triple therapy solely by the development of mistakes in its genome? Ev is an excellent model of mutation and selection related to the development of information. It does not model HIV selection with triple therapy.
What ev models is the evolution of binding sites based on three selection conditions (Paul might call this two selection conditions). One selection condition is that a binding site must occur where it is expected to occur otherwise this is considered a mistake. A second selection condition is that a binding site must not be identified in the region of the gene associated with the binding site otherwise that is considered a mistake and the third selection condition is that a binding site must not be identified outside the binding site region of the genome otherwise that is considered a mistake. Paul calls the last two selection conditions the identification of spurious binding sites and will sometimes call these two selection conditions a single selection condition. What happens as you lengthen the genome length parameter in the model, it becomes more and more difficult to satisfy all three selection conditions and evolve the binding sites in the model. If you set any two of the three selection conditions to zero, the remaining selection condition will rapidly evolve satisfying that selection condition no matter how long the genome. The analogy of the ev model and the use of triple therapy for the treatment of HIV is that you are forcing the HIV virus to satisfy three selection pressures imposed by the triple drug therapy. This delays the evolution of resistant strains of the virus. It is this mathematics which ev simulates and which the use of triple selection conditions on the HIV virus demonstrates in reality. If you attempt to use monotherapy on the HIV virus, it quickly can evolve to that single selection condition. This is demonstrated mathematically in ev by setting two of the three selection conditions to zero.
HIV triple therapy works by inhibiting viral replication, not by selecting out mistakes. Selection pressures in the real world either limit reproduction or kill. Ev models, from what I can tell, killing. There are clear Darwinian pressures in place, but what constitutes a "defect" is arbitrarily designed. A "mistake" in nature depends upon context, not upon a pre-defined decision of an investigator.
Ev selecting out of mistakes is analogous to preventing replication of the virus. The selection rule in ev only allows the genomes with the fewest mistakes to reproduce. This is done for programming simplicity. If instead of modeling the evolution of binding sites on a random genome, the genetic sequence of HIV could be introduced into the model and random mutations to this genome could be allowed to this sequence based on using different selection conditions imposed by antiviral drugs and then you would get an almost exact simulation of the evolution of HIV virus subject to the selection conditions imposed by antiviral medications rather than the analogous situation of the evolution of binding sites. However the mathematical behavior of these two simulations would be very similar.
As to Dr. Schneider's comments, he is correct from what I can tell in what you have provided, but those comments are not applicable to this issue. His point was that his model employed Darwinian selection pressure. It does. It doesn't mimic what occurs in all situations, though, and certainly does not mimic the mechanism by which HIV triple therapy works. His model was designed for a particular purpose -- modelling mutation and selection as it relates to information gain.
I believe that Dr Schneider modeled the mathematics of mutation and selection correctly. The evolution of resistant strains of HIV would require some modification of Dr Schneider’s selection rules but otherwise, the mathematics is identical. Of course, you evolutionists can try to argue that frame shift mutations, inversions and other forms of mutations would speed up this process but I doubt it. Random point mutations drives this process.
But, there is a much larger issue. Suppose everything that Dr. Schneider said is wrong. Suppose that it is dead wrong. What then? You mean we should actually look at how the model works and how it actually relates to HIV and our use of triple therapy? We should not make bare appeals to authority? We should care about evidence and reasoning? Fancy that.
I happen to think that Dr Schneider modeled the mathematical mechanism of mutation and selection properly. So do the peer reviewers at Nucleic Acids Research. Where Dr Schneider slipped up in his analysis was using a 256 base genome with an extremely high, unrealistic mutation rate in the model to compute a rate of information acquisition by this mechanism. I did tell Dr Schneider that once the real behavior of his model was known that evolutionists would discredit the model. This response of the evolutionist community has been unanimous so far, including his own programmer, Paul.

I think Dr Schneider’s model points to an important principle (besides showing that the theory of evolution is mathematically impossible) of the way microbial infections are treated in general. In general, monotherapy for the treatment of infections is the rule and note how many multiple resistant microbes are appearing. The present view is that doctors are using too many antibiotics and that fewer antibiotics should be used. It may be that serious infection should always be treated with double or triple antimicrobials to prevent the emergence of resistant strains.
The only thing that Ichneumonwasp has shown here is that reducing the selection pressure speeds up the evolutionary process. This is what ev shows and this is what I have contended for pages on this thread. Ichneumonwasp is making my point.If I am making your point how is it that you couldn't realize that fact for the past two weeks? Please tell me what we have been discussing, because I am still making exactly the same point that I have been making all along -- that it is the potency of selection pressures that makes a difference in the real world and not the number of selection pressures (of course multiple selection pressures add together at the very least if potency is kept stable).

That or you have no idea what my point is now or has been in the past.
When you talk about noncompliance with treatment of HIV, you are talking about the missing of doses of one or more medications. Lifting the selection pressures has several benefits for the virus. The first is that the virus can reproduce more rapidly. The second is that if one or more drugs are consistently left out of the treatment plan by the noncompliant patient, it is much easier for the virus to evolve resistance to the remaining drug. Either way, less than therapeutic dosages of medication or the reduction of the number of drugs used accelerates the evolution of resistant strains of the virus.
To say that increasing selection pressure (potency not number) slows evolution is like saying 1+1=2. That is the friggin' definition of selection pressure, as I have argued for two weeks.
Of course increasing selection pressure potency slows evolution, in the extreme case it causes extinction. What you are still having difficulty understanding is that multiple selection pressures no matter what their potency slows evolution for each of the selection conditions.
So, let's go back over the argument again. The evidence offered demonstrates that it is not the number of pressures that is critical (you have repeatedly argued that it is the number and not the potency that is critical). With the exact same number of selection pressures, different triple therapy protocols and/or different medication schedules (80% vs 95+%) produce different results. When the potency of the selection pressure is reduced more virions are produced and variability is able to increase -- consequently, resistance develops more easily.
It is not quite that simple. Increasing the number of selection pressures will always slow the evolutionary process. This is a mathematical fact shown by ev. This is demonstrated by Delphi’s Wikipedia reference to fitness landscape. And this is shown in reality by the use of multiple antimicrobials which delays the evolution of resistant strains of these microbes. Where the mathematics gets more complex is when you have less potent selection pressures which in combination can still cause extinction. This is what is being approached with use of triple antiviral medications for the treatment of HIV. Alone, none of the drugs have the potency to completely stop the virus but in combination, the reproduction and evolution of the virus is almost completely stopped as long as compliance with treatment is maintained.
You cannot argue (successfully) that there is a synergistic effect such that the three selection pressures "kill" the reverse transcriptase. Multidrug resistance develops, and the reverse transcriptase works in the resistant strains. You cannot argue that three pressures are critical because there are three pressures in all three situations (actually many more, but that is beside the point, since we can play your way and you still lose) -- triple therapy with profound selection pressure and 95+% compliance (currently used triple therapies), triple therapy with 80% compliance and consequently lessened pressure (resistance develops), older triple therapies with less profound selection pressure with 95+% compliance (resistance develops).
If you recall, I have never said that these therapies kill the virus or the reverse transcriptase. What these therapies do is slow the reproduction of the virus. This by definition is what fitness is. Unless and until a single selection pressure is developed against the virus that completely stops reproduction of the virus, the only treatment available will be multiple drugs with less than complete prevention of the reproduction of the virus.
So, what is your solution to this impasse?
There is no impasse here. There is only your lack of understanding of the mathematics of mutation and selection. The key point that you don’t understand is that multiple selection pressures slow the evolutionary process. This is what ev shows, this is explained in Wikipedia in the description of the fitness landscape and is shown by the use of multiple drug regimens for the treatment of antimicrobial infection. Compliance with these therapies causes some confusion in the behavior of mutation and selection but the underlying mathematics is clear.
What ev is showing is that each additional selection pressure slows the evolution process.We can continue repeating the same arguments over and over. Everyone knows that the evolutionary process is slowed by the addition of selection pressures, if the new selection pressures produce independent effects. The additional pressures will be either additive or synergistic. But the important point is not the number but the total potency of the selection pressure. If all selection pressures are weak even a large number of them will not produce much of an effect -- take HIV triple therapy at a compliance of 20-30%. Resistance may develop, but it is harder to produce resistant strains at that level of compliance. At 80% compliance -- more selection pressure -- resistance develops more easily with triple therapy. That level provides enough pressure and enough room for viral replication so that resistence may develop in HIV. At 95+% compliance, the selection pressures are so profound that not enough viral replication can occur, so variability is reduced, so resistance does not develop. At lower compliance levels not enough selection pressure is created to drive the process as easily. Resistance is still possible, but it develops more slowly. So, no, it is not a simple arithmetical relationiship. More of parabola really, with little tails on the ends and a nice path running down the middle. Ni.
Potency of selection pressures does complicate the mathematics but I think you are starting to understand the point. Selection pressures don’t obey the simple addition. Selection pressures are highly non-linear. The only thing you can say in general about selection pressures is that increasing the number of selection pressures slows reproduction and confounds the evolution process.
It's all three selection pressures, according to your definitions, but different potencies.
Again, potencies of selection pressures affect the mathematics and real situations of evolution but the additional selection pressures always slow evolution. That is if kjkent1 doesn’t show us a case where two selection pressures acting simultaneously speed up evolution.

joobz

16th April 2007, 06:35 PM

Ichneumonwasp

16th April 2007, 07:22 PM

OK, let's see. You say:

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

To which I say:

Everyone knows that the evolutionary process is slowed by the addition of selection pressures, if the new selection pressures produce independent effects.

To which you say:

What you are still having difficulty understanding is that multiple selection pressures no matter what their potency slows evolution for each of the selection conditions.

Um, what?

No difficulty here. I have repeatedly said that adding new selection pressures, holding potency constant will increase the total selection pressure. So stop wasting my time, your time, and anyone else's time repeating the same strawman error over and over again.

Increasing the number of selection pressures will always slow the evolutionary process.

Actually no, we don't know that. We do not know if a particular pressure in one context would act as an independent pressure in the context of several other pressures. There may be one pressure that is so strong in reducing reproduction that additions will have no effect. There may be a mild pressure, such as heat in reducing sperm production that will have no real pressure in the real world because it is only applied to a select group that is busy being eaten by tigers. Additional selection pressures do not always slow the process.

And this is shown in reality by the use of multiple antimicrobials which delays the evolution of resistant strains of these microbes.

That is exactly what is not shown by the data on resistance. The development of resistance depends critically on the strength of the selection pressures. Three HIV drugs that are not terrible potent with nearly perfect compliance results in resistance. There is no denying that reality. Current, more potent triple therapies, with nearly perfect compliance slows the development of resistance. Current, more potent triple therapies, with 80% compliance speeds the development of resistance. Current, more potent therapies, with compliance below 80% slows the development of resistance.

Deal with that issue and that issue alone before proceeding further.

kleinman

16th April 2007, 07:24 PM

I stand corrected here master of alchemical engineering. It is the family of peroxidases that decompose the peroxides. But the point is that the paper you provided describes the application of H2O2 as a single selection pressures in slowly increasing concentration to select yeasts which produce enzymes that decompose this oxidizer. That is unless you are arguing that the numerous proteins and other molecules which are damaged by H2O2 are all evolving to new forms that are not affected by H2O2.Your factual errors have become quite numerous. You've claimed mastery of thermodynamics, but couldn't argue what thermo really is. Remember the, "Natural selection, which is a restatement of the 2nd law" silliness. You've claimed mastery of mathematics, claiming that magnitude doesn't matter. You've even used F=ma as an example, where we know it breaks down in instances of extreme velocity.
You've reiterated the importance of point selection as the only relavent method of mutation and that all others are of equal weight. Yet, the paper by Deem et. al., presented by Articulett the critical importance of gene transfer argues directly against this point. You claimed that 3 pressures halted evolution, and we have three examples where this isn't true. You claimed that SOD was the primary degrading enzyme of hydrogen peroxide, and this is, again, woefully wrong.
I wonder if you carefully read your own link. If you had you would have seen the following quote.
Permanent but gradually increasing oxidative-stress challenge was achieved by increasing the H2O2 concentration in the feed medium in daily (2.4 generations) 20-mM steps from 0 to 100 mM. Additionally, transient oxidative stress was applied by pulsing increasing volumes of H2O2 up to a final broth concentration of 1 M once a day for 68 generations. Transient temperature challenges were achieved by (i) two temperature
shocks of 52 C for 3 and 6 min with an intermediate steady-state growth physiology and (ii) temperature oscillations between 25 and 35 C which were achieved by programming a sinusoidal function in the temperature controller with a cycle time (2p) of 1 h. These oscillations were continued for 8 days or about 19 generations.
Now I’ll make this simple enough so even an alchemical engineer will understand it. I highlighted the number of generations so you could see it joobz. This paper has nothing to do with mutation and selection. These authors are simply selecting for populations that already have the capability to withstand H2O2, ethanol, increased temperatures and freeze/thaw cycles. You are not mutating and selecting the dozens, perhaps hundreds of genes and their associated proteins that are damaged by these types of stresses in less than 100 generations. For someone who has a PhD in engineering, your basic mathematical skills are nothing short of disappointing. Your mathematical skills make your grammatical skills look good.

joobz

16th April 2007, 07:41 PM

Now I’ll make this simple enough so even an alchemical engineer will understand it. I highlighted the number of generations so you could see it joobz. This paper has nothing to do with mutation and selection. These authors are simply selecting for populations that already have the capability to withstand H2O2, ethanol, increased temperatures and freeze/thaw cycles. You are not mutating and selecting the dozens, perhaps hundreds of genes and their associated proteins that are damaged by these types of stresses in less than 100 generations. For someone who has a PhD in engineering, your basic mathematical skills are nothing short of disappointing. Your mathematical skills make your grammatical skills look good.

Where is this magical 100 generations you mention? Why do you devine these numbers and call them Math? where/when does natural selection end and evolution begin? Is this the same line as macro/micro evolution?

Each of your posts become less and less logical.

kleinman

16th April 2007, 08:10 PM

What you are still having difficulty understanding is that multiple selection pressures no matter what their potency slows evolution for each of the selection conditions.Um, what?

No difficulty here. I have repeatedly said that adding new selection pressures, holding potency constant will increase the total selection pressure. So stop wasting my time, your time, and anyone else's time repeating the same strawman error over and over again.
And once again, you demonstrate you do not understand the mathematics of mutation and selection. The effects of multiple selection pressures are not additive. The only thing made out of straw here is your theory of evolution and it is being blown away by the ev computer model and the numerous real examples which confirm the mathematical behavior of this model.
Increasing the number of selection pressures will always slow the evolutionary process.Actually no, we don't know that. We do not know if a particular pressure in one context would act as an independent pressure in the context of several other pressures. There may be one pressure that is so strong in reducing reproduction that additions will have no effect. There may be a mild pressure, such as heat in reducing sperm production that will have no real pressure in the real world because it is only applied to a select group that is busy being eaten by tigers. Additional selection pressures do not always slow the process.
If the physical stress does not affect reproduction, it is not a selection pressure. If the physical stress does affect reproduction and then you add a different physical stress which affects reproduction, the combined affect of the two stresses will slow evolution more than additively. This is what the mathematics of ev shows, this is what Delphi’s link to Wikipedia and the description of fitness landscape shows.
And this is shown in reality by the use of multiple antimicrobials which delays the evolution of resistant strains of these microbes.That is exactly what is not shown by the data on resistance. The development of resistance depends critically on the strength of the selection pressures. Three HIV drugs that are not terrible potent with nearly perfect compliance results in resistance. There is no denying that reality. Current, more potent triple therapies, with nearly perfect compliance slows the development of resistance. Current, more potent triple therapies, with 80% compliance speeds the development of resistance. Current, more potent therapies, with compliance below 80% slows the development of resistance.
Three HIV drugs may not be terribly potent selection pressures when used individually but when used in combination they are far more potent than any single drug. Clearly, a single 100% potent drug that could stop reproduction of the virus completely would be the ideal case but no such drug exists. By combining less potent drugs, the evolution of resistant strains of the virus can be delayed and give people suffering with HIV a longer period of relief.
Deal with that issue and that issue alone before proceeding further.
Don’t worry; I will continue to deal with this issue because it is the core principle of the mathematics of mutation and selection. Multiple selection pressures slow the evolutionary process.
Now I’ll make this simple enough so even an alchemical engineer will understand it. I highlighted the number of generations so you could see it joobz. This paper has nothing to do with mutation and selection. These authors are simply selecting for populations that already have the capability to withstand H2O2, ethanol, increased temperatures and freeze/thaw cycles. You are not mutating and selecting the dozens, perhaps hundreds of genes and their associated proteins that are damaged by these types of stresses in less than 100 generations. For someone who has a PhD in engineering, your basic mathematical skills are nothing short of disappointing. Your mathematical skills make your grammatical skills look good.Where is this magical 100 generations you mention?
It is less than 100 generations. Either reread post #3602 or your link to the Evolutionary engineering of multiple-stress resistant Saccharomyces cerevisiae paper carefully and you will see how many generations they ran the selection process.

Ichneumonwasp

16th April 2007, 08:27 PM

Schneibster

16th April 2007, 08:38 PM

joobz

16th April 2007, 08:59 PM

It is less than 100 generations. Either reread post #3602 or your link to the Evolutionary engineering of multiple-stress resistant Saccharomyces cerevisiae paper carefully and you will see how many generations they ran the selection process.
Your intentional misdirections were originally frustrating, since I was assuming you intelligent. Now that you've demonstrated otherwise, I'll explain my response more clearly.

Now I’ll make this simple enough so even an alchemical engineer will understand it. I highlighted the number of generations so you could see it joobz. This paper has nothing to do with mutation and selection. These authors are simply selecting for populations that already have the capability to withstand H2O2, ethanol, increased temperatures and freeze/thaw cycles. You are not mutating and selecting the dozens, perhaps hundreds of genes and their associated proteins that are damaged by these types of stresses in less than 100 generations.
You're making the assumption that mutations must occur after the stress and that the natural selection that arises as a result of these post-stress mutations is evolution. You claim that this process must take at least 100+ generations and that anything less than this isn't an evolutionary event. I ask, why is 100 generations your goal post? Why not 1000, why not 50? What is your claim for this? have you run studies varing the mutation rate? you have invented numbers out of thin air without any meaning. This is far from a mathematical argument It is simply argument from ignorance.

Your assumption of mutations occuring only after stress is wrong. What about mutations that occured well before this stress? Does every mutation, gene exchange, have to result in immediate effect? Is it not a feature of evolution that some mutations just result in seemingly benign genetic diversity that doesn't mean much until the right stress comes along? You have set meaningless guidelines that life doesn't care about. Natural selection is the seive that selects for the mutations. It doesn't get rid of all mutations but the good ones. It just gets rid of the really really bad ones. When conditions change that resets what is considered really really bad, then a new set of phenotypes will be selected for. Sure, both mutation and natural seleciton must occur, but you don't get to dictate when these events happen. Life is allowed (and has been selected) to generate a cache of mutations that may provide future flexibility.

this is what I was saying when I stated:

Where is this magical 100 generations you mention? Why do you devine these numbers and call them Math? where/when does natural selection end and evolution begin? Is this the same line as macro/micro evolution?

Each of your posts become less and less logical.

I just assumed you'd understand. I realized I made a bad assumption. You haven't demonstrated any ability to understand anything.

kleinman

16th April 2007, 09:13 PM

And once again, you demonstrate you do not understand the mathematics of mutation and selection. The effects of multiple selection pressures are not additive. The only thing made out of straw here is your theory of evolution and it is being blown away by the ev computer model and the numerous real examples which confirm the mathematical behavior of this model.Thank you mister strawman for the latest in the strawman arsenal.
You evolutionists really need some new plays in your playbook. That strawman argument is not going to work here. We have an evolutionist written, peer reviewed model of random point mutation and natural selection that supports my argument.
How does my saying that multiple selection pressures, as I have said more than once, are at the very least additive (given the right situation) and possibly synergistic come to mean that I somehow said that multiple selection pressures are additive and only additive?
This paragraph again shows that you don’t understand the mathematics of mutation and selection. Multiple selection pressures do not affect the generations to evolve additively. Multiple selection pressures slow evolution far more than additively. The sorting process is much slower and more difficult when you have multiple selection pressures. Selection pressures do not function synergistically. You can think of this as a database sorting problem. The more sorting conditions you have, the slower the sort goes.
Answer that and we will move along. No more lies. I will not stand for them. I am going to call you on every single lie that you tell me from now on in this thread. Answer this one. Admit your lie and we can move along.
Is that all you mathematically challenged evolutionists can do when you when you can’t understand the mathematics of your own theory? If you think that multiple selection pressures are additive, produce the mathematics that shows this because we already have a mathematical model written by an evolutionist, peer reviewed and published in the Oxford University Press Journal Nucleic Acids Research that shows you are wrong. You evolutionists have lived with your dumb ass theory so long that you can’t distinguish between the truth and a lie.

What is sad about this is that an important principle for the treatment of infectious diseases is being revealed here by the ev computer model and your evolutionary prejudices stand in the way of understanding this principle.
Good luck, Ichneumonwasp. kleinman's criterion is not whether he convinces anyone else; it's whether he can convince himself. Such people generally get locked up in asylums unless their brand of irrationality is religion. Hopefully we can fix that soon.
You evolutionists are the ones denying the results from your own mathematical model. The only irrationality in this discussion is the failure of you evolutionist to accept the results from ev but I am patient. I will keep repeating these mathematical facts until all but the most fanatical evolutionists understand them. Of course, is there any other type of evolutionist but the fanatical type?
Now I’ll make this simple enough so even an alchemical engineer will understand it. I highlighted the number of generations so you could see it joobz. This paper has nothing to do with mutation and selection. These authors are simply selecting for populations that already have the capability to withstand H2O2, ethanol, increased temperatures and freeze/thaw cycles. You are not mutating and selecting the dozens, perhaps hundreds of genes and their associated proteins that are damaged by these types of stresses in less than 100 generations.You're making the assumption that mutations must occur after the stress and that the natural selection that arises as a result of these post-stress mutations is evolution. You claim that this process must take at least 100+ generations and that anything less than this isn't an evolutionary event. I ask, why is 100 generations your goal post? Why not 1000, why not 50? What is your claim for this? have you run studies varing the mutation rate? you have invented numbers out of thin air without any meaning. This is far from a mathematical argument It is simply argument from ignorance.
Make it simple for yourself. Post a quote from your reference and show how many generations they ran their selection process. And then you will have proved that you are mathematically incompetent to describe the mutation and selection process.

Ichneumonwasp

16th April 2007, 10:04 PM

articulett

16th April 2007, 10:33 PM

Good luck, Ichneumonwasp. kleinman's criterion is not whether he convinces anyone else; it's whether he can convince himself. Such people generally get locked up in asylums unless their brand of irrationality is religion. Hopefully we can fix that soon.

I think that locking them in their own tax free conglomerations might be more cost effective. I'd be all for faith-based spending if it meant keeping the faith based away from me.

Mr. Scott

17th April 2007, 02:29 AM

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

Thank you, Dr. Kleinman.

joobz

17th April 2007, 04:05 AM

Make it simple for yourself. Post a quote from your reference and show how many generations they ran their selection process. And then you will have proved that you are mathematically incompetent to describe the mutation and selection process.
Is this argumentum non sequitorum? Stating random bizarre gibberish that doesn't address my comments isn't a defense. It is a transparent attempt at avoiding the questions.

Where is this magical 100 generations you mention? Why do you devine these numbers and call them Math? where/when does natural selection end and evolution begin? Is this the same line as macro/micro evolution?

IF Mr. Scott's assumptions are correct, and you have been paid to argue against evolution, I think that that was some money horribly spent. I've seen more rational views from Hammegk than I've ever seen from you.

Ichneumonwasp

17th April 2007, 04:47 AM

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

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

Why are you doing that, Dr. Alan Kleinman?

delphi_ote

17th April 2007, 09:53 AM

The only thing that Ichneumonwasp has shown here is that reducing the selection pressure speeds up the evolutionary process. This is what ev shows and this is what I have contended for pages on this thread. Ichneumonwasp is making my point.
Dr. Alan Kleinman, that is not what you have contended for pages. You contended that the number of selection pressures slowed evolution. I even asked you directly if that was your hypothesis, and you stated that it was.

Please stop being dishonest, Dr. Alan Kleinman.

delphi_ote

17th April 2007, 09:55 AM

joobz

17th April 2007, 10:59 AM

In case nobody has pointed this out previously, Dr. Alan Kleinman (http://www.pandasthumb.org/archives/2006/11/when_ignorance.html) has previously had problems with ev. He got taught a lesson by the folks at Panda's Thumb.
So, Dr. Alan Kleinamn, not only have you demonstrated your terrible understanding of fundemental scientific principles...but you show utter dishonesty in correcting these errors.

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

Dr. Alan Kleinman, Can you explain why you are wrong so often?

kjkent1

17th April 2007, 11:37 AM

Kleinman and Paul:

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

I realize that Kleinman is looking for 32-64K genomes, but I just don't have the time to do anything more than identify a trend.

I see two things in the table data:

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

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

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

Table source data is attached at: http://www.geocities.com/kjkent1/evo1.pdf

Mr. Scott

17th April 2007, 12:29 PM

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

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

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

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

Paul C. Anagnostopoulos

17th April 2007, 12:43 PM

2) There are some VERY weird coincidences where various mistake weights converge, or produce a perfect creature, at "exactly" the same number of generations. As I have suggested previously in this thread, I am suspect of the reliability of ev's random number generation, as the number of generations increases.
I'll see if I can reproduce this, but, if you're right, it's a problem for the Java developers.

~~ Paul

Paul C. Anagnostopoulos

17th April 2007, 01:47 PM

kjkent1

17th April 2007, 02:01 PM

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

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

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

Ichneumonwasp

17th April 2007, 03:04 PM

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

Paul C. Anagnostopoulos

17th April 2007, 05:41 PM

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

~~ Paul

Ichneumonwasp

17th April 2007, 06:55 PM

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

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

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

Paul C. Anagnostopoulos

17th April 2007, 08:02 PM

Variance in generation counts? Is there a way to adjust variance in the population aside from increasing the mutation rate?
Yes, there is great variance in the generation count depending on the random seed. I'm not sure what your second question means.

One of the big problems I have with the way Kleinman approaches this mess is his problem with mutation rates. Sure it doesn't match mutation rates elsewhere, but if there is no other means of providing variance within a population, then mutation rate in the model serves the purpose of providing the variation that would natural occur through replication errors.
I've run a long series of experiments varying only the mutation rate, and the generation count seems to vary linearly with it.

Or, are replication errors somehow built into the model? Or are they categorized as mutations?
The only kind of mutation is point mutations applied to each creature immediately after the best half of the creatures are reproduced.

~~ Paul

articulett

17th April 2007, 09:41 PM

Dr Adequate

17th April 2007, 10:40 PM

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

Shall i remind you, Dr. Alan Kleinman, what you have stated that is wrong? You forgot Lie #5.

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

kleinman

17th April 2007, 10:59 PM

This paragraph again shows that you don’t understand the mathematics of mutation and selection. Multiple selection pressures do not affect the generations to evolve additively. Multiple selection pressures slow evolution far more than additively. The sorting process is much slower and more difficult when you have multiple selection pressures. Selection pressures do not function synergistically. You can think of this as a database sorting problem. The more sorting conditions you have, the slower the sort goes.You really are not capable of understanding this, are you? I am discussing with you a real world example that you brought into the discussion. I didn't invent it. You introduced it. You have repeatedly mischaracterized my position. I pointed out your mischaracterizations.
I am not mischaracterizing your position; you just continue to miss the most important point. That point is that multiple selection conditions applied simultaneously slows evolution. This is clearly seen with the use of multiple drug therapy for the treatment of HIV. If you use monotherapy, resistance to that single drug quickly occurs. Now this doesn’t mean that triple therapy eliminates the possibility of resistance, it just slows the process. Drugs with different intensity of selection pressures will affect the rate at which drug resistance can emerge but the underlying mathematics remains the same. For example, a very potent drug which only requires a single base substitution to make that drug ineffective will make the prediction of the behavior of treatment somewhat difficult without collecting a large amount of clinical data or by doing a simulation with a model like ev that is reworked to specifically look at HIV and drug resistance.
You can be a man and admit your mistakes or you can continue to act like this. It is your decision.
If you read the entire thread, you would see that I do admit my mistakes. The case of HIV demonstrating that multiple drug therapy (selection pressures) slows the evolution of resistant strains is not one of my mistakes. Now be a scientist and mathematician and understand why what I am saying here is not a mistake.
You can discuss the ev model all you wish with the others. As I have repeated to you now, I think, seven times, we (you and I) are discussing HIV triple therapy. There is no sense in relying on ev to explain your position. We are discussing this real world issue. The interaction with ev occurs later.
You are having a difficult time understanding why multiple drug therapy is used to treat HIV, TB and should have been used to treat Gonorrhea, MRSA, pseudomonas and a variety of other multiple drug resistant microbes. If you understood the mathematics of mutation and selection that is demonstrated by ev and nicely described in Delphi’s Wikipedia reference to fitness landscape, you would better understand this argument. Dr Schneider’s model does accurately simulate an important real world phenomenon, which is multiple selection pressures slow evolution. His mathematics is not trivial but it is understandable.
Are you ready to apologize and move ahead with the discussion, leaving all the name calling and obfuscation behind?
I owe no apology here and stop being a cry baby.
Dr. Alan Kleinman, when I asked if you were paid for undermining evolution, you dodged the question on the basis that one should have been able to know the answer from reading some other of the 3,510 postings here. It took you more typing to refuse to answer than you would have if you had answered. I'll make it easy for you. If you have been paid, will be paid, or expect to be paid for undermining or attempting to undermine evolution, just answer with a "y" else with a "n".
I am under no obligation to answer every stupid question raised by you evolutionists. However, in an attempt to stop your incessant whining, I will answer your stupid question. I have not been paid; I will not be paid and do not expect to be paid for revealing the truth about your dumb ass theory of evolution. One reason I do this thread is because I enjoy annoying thin skinned, whining, crybaby evolutionists by using their own mathematical model to prove your theory is hogwash. This is not my primary reason though for doing this thread. That reason is none of your business.
Thank you, Dr. Kleinman.
Anytime Mr Scott (unless it is a stupid question).
The only thing that Ichneumonwasp has shown here is that reducing the selection pressure speeds up the evolutionary process. This is what ev shows and this is what I have contended for pages on this thread. Ichneumonwasp is making my point.Dr. Alan Kleinman, that is not what you have contended for pages. You contended that the number of selection pressures slowed evolution. I even asked you directly if that was your hypothesis, and you stated that it was.
Excuse me. When someone is in noncompliance with their HIV treatment, they are reducing the number of selection pressures as well as the intensity of the selection pressures. Were you not the one who said that if the intensity of the selection pressure was sufficient, it causes extinction? What happens when you reduce the intensity of this selection pressure?
Yes, Dr. Alan Kleinman, I would like to know as well. Have you been paid for this?
Are these the best questions that you thin skinned, crybaby evolutionists can come up with?
While you are at it, could you also address the issue of continually referring to the mathematical modelling of "evolution" as it relates to the real world in your very specific example of HIV triple therapy. Since the very question at hand is whether or not the mathematical model is effective for examining this question, why do you continue to dodge questions about HIV triple therapy and drug resistance in the real world? Do you fear that resistance developing in HIV strains indicates that this model does not relate to all real world examples of evolutionary change? Is that the problem, Dr. Kleinman?
Apparently you took dumbbell mathematics in your premed courses so it is taking time to bring you up to speed on the mathematics of mutation and selection. We can start with the principle that multiple selection conditions slow the evolutionary process. You can ask why and you could ask that I demonstrate this to you with the ev model and I could answer that I have already done this but since you are not up to speed on this mathematics, I will repeat it again for you if you are interested.
Why are you doing that, Dr. Alan Kleinman?
It is enough for you to know that I enjoy annoying people who believe in a dumb ass theory and try to pass it off as science. Since you are a physician, you might appreciate the diagnostic criteria for evolutionism; they have denialophila, hyperextraplopia, speculitis and amathematica sciencea.
Please stop being dishonest, Dr. Alan Kleinman.
You are the one being dishonest. You understand what Wikipedia is describing about the fitness landscape. This is exactly what ev is simulating. You started to acknowledge this but for some reason you backed off. It wouldn’t having anything to do with it might ruin your career in the evolutionist dominated field of biology?
In case nobody has pointed this out previously, Dr. Alan Kleinman has previously had problems with ev. He got taught a lesson by the folks at Panda's Thumb.
Delphi, you really need to lay off the sterno. Why don’t you post a quote from this link where I was taught a lesson about ev? You are really scraping the bottom of the barrel looking for some way to respond to what ev is showing.
Per Kleinman's request, I have some data from ev. The attached table is based on running ev with all defaults, except that I limited the population to eight (8) creatures, and I changed the mistake weights and genome length as indicated in the table.
You haven’t label your selection pressures.
1) Three selection pressures converge faster than either/both one and/or two, in some, but not all cases. This suggests that if the trends below hold, then kleinman's theory that multiple selective pressures slow evolution in all cases is falsified.
You have demonstrated nothing of the kind. All your cases have three selection pressures. The only thing you have shown is that varying the weights for the selection pressures varies the generations for convergence.
2) There are some VERY weird coincidences where various mistake weights converge, or produce a perfect creature, at "exactly" the same number of generations. As I have suggested previously in this thread, I am suspect of the reliability of ev's random number generation, as the number of generations increases.
Paul might address this issue however I believe Paul and Dr Schneider have compared evjava and evpascal and get identical results using either languages’ random number generator.
Note: as usual, I am not using zero (0) mistake weights, because to do so is to permit perfect creatures to be reported even though Rseq has not approached Rfreq. This is result of ev creating mistakes in the mutation function, and then completely ignoring those mistakes in the selection function. The result is a creature which ev reports as "perfect," but which, in fact, is described by random information. This state violates the fundamental premise of ev: that Rseq ~ Rfreq in all independent living organism -- Therefore, the state is invalid.
You are using an excuse so as not to set two of the three selection conditions to zero because this demonstrates the crucial behavior of the mathematics of mutation and selection. Since you haven’t, I will do it for your G=4096 case.
Generations to perfect creature
Missed binding sites weight=1\166
Spurious binding sites gene=1\572
Spurious binding sites outside gene=1\493
Your best case for three selection conditions was 17,781 generations
What happens if we set only one selection condition weight to 0?
Generations to perfect creature
Missed binding sites weight=1, Spurious binding sites in gene=1\33,942*
Missed binding sites weight=1, Spurious binding sites outside gene=1\643,480*
Spurious binding sites in gene=1, Spurious binding sites outside gene=1\476
* note Rseq->Rfreq in at least two of the three cases where one of the selection conditions was set to 0.
For completeness, I include the case when all three selection condition weights are set equal to one and the generations for convergence=491,071
Clearly, the case in red above has only two selection conditions and takes more generations for convergence to perfect creature than the case for three selection conditions. The question is this an effect of the stochastic properties of the model or that two selection conditions can take more generations to converge than three selection conditions which would refute my hypothesis. So what happens for G=2048?
Generations to perfect creature
Missed binding sites weight=1, Spurious binding sites in gene=1\11,439*
Missed binding sites weight=1, Spurious binding sites outside gene=1\34,768*
Spurious binding sites in gene=1, Spurious binding sites outside gene=1\360
* note Rseq->Rfreq in at least two of the three cases where one of the selection conditions was set to 0.
The generations for convergence for weights of 1 for all three cases for G=2048 is 107,168
How about for G=1024?
Generations to perfect creature
Missed binding sites weight=1, Spurious binding sites in gene=1\5,794*
Missed binding sites weight=1, Spurious binding sites outside gene=1\29,228*
Spurious binding sites in gene=1, Spurious binding sites outside gene=1\102
* note Rseq->Rfreq in at least two of the three cases where one of the selection conditions was set to 0.
The generations for convergence for weights of 1 for all three cases for G=1024 is 43,354
How about for G=512?
Generations to perfect creature
Missed binding sites weight=1, Spurious binding sites in gene=1\2,792*
Missed binding sites weight=1, Spurious binding sites outside gene=1\10,113*
Spurious binding sites in gene=1, Spurious binding sites outside gene=1\36
* note Rseq->Rfreq in at least two of the three cases where one of the selection conditions was set to 0.
The generations for convergence for weights of 1 for all three cases for G=512 is 8,916
Again, a case where two selection conditions take more generations to converge than three selection conditions.
The generations for convergence for weights of 1 for all three cases for G=1024 is 43,354
How about for G=256?
Generations to perfect creature
Missed binding sites weight=1, Spurious binding sites in gene=1\1,441*
Missed binding sites weight=1, Spurious binding sites outside gene=1\1,194*
Spurious binding sites in gene=1, Spurious binding sites outside gene=1\78
* note Rseq->Rfreq in at least two of the three cases where one of the selection conditions was set to 0.
The generations for convergence for weights of 1 for all three cases for G=256 is 2,424
So kjkent1’s argument that you need all three selection conditions for Rseq->Rfreq is refuted. Kjkent1, your argument is a red herring anyway since selection is not based on Rseq->Rfreq. This is only an secondary result. Missed binding sites and one of the spurious binding site conditions gives his condition. However, in two of the five series, two selection conditions take more generations to evolve to the perfect creature than do three selection conditions. Is this an artifact of the stochastic calculation or does this refute my argument? I also have not posted the data when two of the three selection conditions are set to 0. These cases take far fewer generations to converge than either the two or three selection condition cases. I will post this data and expand kjkent1’s series beyond the G=4096 case in order to establish the trends.
Don’t be silly Mr Scott; your example supports my contention. Single selection conditions can quickly evolve, the more selection conditions imposed, the slower the evolutionary process proceeds. Multiple selection conditions slow evolution.Alan Kleinman, you are the one being silly. You've said point blank that more than one mutation in response to selection pressure enters the realm of macro-evolution, and that 3-4 was definitely macroevolution, and that macroevolution was mathematically impossible. When you made these statements, you did not offer the caveat that these adaptations must be simultaneous. Indeed, such mutations are usually sequential* even when simultaneous pressures are present. They can and will happen when the intensity of one or more selective pressures is sufficient to supply pressure but not so great as to cause extinction, like the sweet spot in which evolution runs at maximum speed when antibiotic compliance is weak.
There may be a “sweet spot” in which evolution runs at maximum speed and I think you may be correct with this assertion, but you need to demonstrate this mathematically and that it accelerates evolution sufficiently to make your theory possible. You have a really big problem though; you have never described the selection process that would evolve a gene from the beginning. And now you have to describe two selection processes that would evolve two genes from the beginning and that there is some optimum pressure that would allow these two conditions to evolve simultaneously.
*Parallel mutations can be combined when cells exchange genetic material. even cells of different species can "share notes" on selective pressure adaptations. I have a photo of cells caught in the act in my library I will look up. Even pandas and people can combine adptatations to varying selective pressures via sexual congress, thus speeding evolution far beyond what Ev currently models.
What??????? How do different species “share notes” via sexual congress?
It really is silly of you, Dr. Kleinman, to suggest that point mutations as modeled by the Ev simulation, and point mutations alone, suggest an upper limit on the rate of evolution. No such assertion can be justified and is as far away from "mathematic proof" as can be. The genetic and geographical records prove that evolution is indeed fast enough to account for the diversity of life on Earth. The process is just too complex to model with today's computers, Dr. Kleinman. Please stop spreading your hoax the Ev disproves evolution. Quite the contrary is true. You embarass even the creationist community.
As I have said from the earliest posts on this thread, if you think you have some other mechanism of mutation or any other mechanism that would accelerate evolution, put that feature into ev and show how it works mathematically. Otherwise all you have is a collection of dumb ass words that you say explains your dumb ass theory. The theory of evolution started without a mathematical basis and your dumb ass words do not substitute for a mathematical explanation. As it stands, ev shows that the theory of evolution is mathematically impossible.
I think it's just a marvelous coincidence. I verified the generation counts in Kjkent's table, row 8, columns 1 and 2. Then I reran those two cases with a different random number seed (10) and got two different generation counts.
There may be more to than a coincidence, row 6, columns 1, 3 and 4 have the same generations for convergence and row 9, columns 1 and 2 have the same generations for convergence.
kleinman should offer to do that task, in as much as the curret results seem to send his theory of "multiple selective pressures profoundly slows evolution" into the circular file.
The next series I am going to run will do a more thorough investigation of 1, 2 and 3 selection conditions since I have already shown that you don’t need all three selection conditions for Rseq->Rfreq and that 2 selection conditions sometimes take more generations to converge than 3 selection conditions. Whether this effect is due to the noise introduced into the data by the stochastic nature of the calculation or whether 2 selection conditions can actually converge more quickly than three selection needs to be established. I believe the former is the cause of this affect but more data is needed to establish the trend.

You have hit upon something peculiar in the behavior of ev. I think running more cases alone may not explain why you get identical generations for convergence despite different weights on the selection conditions. My first guess would be that one of the three selection conditions is controlling the generations for convergence. The problem with that view is your G=2560 has 3 cases with generations for convergence of 200,079 and there is no weight factor that is common to all three cases. It may require tracking which mistakes each generation are driving the selection process.
And since we know, and have provided examples, that in nature multiple selection pressures, at the right level of pressure, actually increase the chance for resistance to develop.
Certainly as Mr Scott has suggested there may be a “sweet spot” where evolution can be accelerated. You have suggested that this curve may be parabolic. However, this rate of evolution will never be as rapid as when a single selection pressure is applied. You have two ways of establishing the rates of evolution. You can collect data in real situations such as the treatment of HIV or you can look at mathematical models to establish this behavior. You are trying to take a single data point on the fitness landscape for HIV to support your argument. I believe the general behavior of ev with 1, 2 and 3 selection conditions and the use of multiple antimicrobials to treat difficult infections and the failure and consequences of using monotherapy to treat MRSA, Gonorrhea, pseudomonas and other multiply resistant microbes will have far more weight in this debate.

The establishment of the true behavior of mutation and selection goes beyond proving whether the theory of evolution is true or not. The proper understanding of this mechanism of mutation and selection impacts the treatment of infectious diseases.
Variance in generation counts? Is there a way to adjust variance in the population aside from increasing the mutation rate?
Ichneumonwasp, you are behind the curve on the way ev works. Each of the parameters in ev has unique effects on the generations for convergence. Increasing populations decreases the generations of convergence at a decreasing rate as you increase population, increasing mutation rate decreases the generations for convergence to a point where the generations for convergence starts to increase. The major factor which increases the generations for convergence is the genome length which increases at an increasing rate as you lengthen the genome. There has been a lot of data posted on this thread and the Evolutionisdead forum which shows this.
One of the big problems I have with the way Kleinman approaches this mess is his problem with mutation rates. Sure it doesn't match mutation rates elsewhere, but if there is no other means of providing variance within a population, then mutation rate in the model serves the purpose of providing the variation that would natural occur through replication errors.
The way I have approached this mess is by doing a systematic parametric study of the behavior of ev. I have done hundreds of cases investigating how mutation rates, population, genome length, binding site width affect convergence of this model. This data has all been posted but evolutionists are all over the map discussing other issues including whether I am being paid to destroy the theory of evolution.
Or, are replication errors somehow built into the model? Or are they categorized as mutations?
Paul, do you want to explain to Ichneumonwasp how your model works? Never mind, I see on your next post that you do explain these points.
Dr. Alan Kleinman, when I asked if you were paid for undermining evolution, you dodged the question on the basis that one should have been able to know the answer from reading some other of the 3,510 postings here. It took you more typing to refuse to answer than you would have if you had answered. I'll make it easy for you. If you have been paid, will be paid, or expect to be paid for undermining or attempting to undermine evolution, just answer with a "y" else with a "n".

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

delphi_ote

17th April 2007, 11:18 PM

kleinman

17th April 2007, 11:43 PM

Excuse me. When someone is in noncompliance with their HIV treatment, they are reducing the number of selection pressures as well as the intensity of the selection pressures.They're taking the same number of drugs in both cases. You defined the number of drugs taken as the number of selection pressures.
Really, how many drugs are people taking when they are noncompliant with their treatment?
Were you not the one who said that if the intensity of the selection pressure was sufficient, it causes extinction? What happens when you reduce the intensity of this selection pressure?Dr. Alan Kleinman, it is dishonest to pretend the opposite of your contention is what you were arguing for all along.
What I have been arguing is that increasing the number of selection pressures slows evolution. I have not argued how the intensity of selection pressures affects evolution. This is an argument that has been raised by kjkent1, Mr Scott and Ichneumonwasp. I suspect that the intensity of selection pressures has a non-linear affect on the rate of evolution. The number of selection pressures and the intensity of selection pressures are independent variables in this system. Once the general effect of multiple selection pressures is established then the effects of intensity of selection pressures can be investigated. From the data I have already obtained from ev, I believe the number of selection pressures is more important than the intensity of the selection pressures unless the intensity of the selection pressure is sufficient to cause extinction.

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

delphi_ote

17th April 2007, 11:58 PM

Really, how many drugs are people taking when they are noncompliant with their treatment?
All of their meds, but less than the required dosage.
From the data I have already obtained from ev, I believe the number of selection pressures is more important than the intensity of the selection pressures unless the intensity of the selection pressure is sufficient to cause extinction.
But you were proven wrong on this in the HIV compliance study, Dr. Alan Kleinman. Argue all you like, but you're going to have a very hard time when reality disagrees with you.
I neither need nor want to lie in this debate.
Then stop doing it. While you're at it, stop waffling back and forth on your positions whenever you find it convenient.

Dr Adequate

18th April 2007, 12:25 AM

I neither need nor want to lie in this debate. Ironically, you've lied so often about whether you tell lies that this is numbered as Lie #0 in my catalogue of your habitual lies.

kleinman

18th April 2007, 12:38 AM

Really, how many drugs are people taking when they are noncompliant with their treatment?All of their meds, but less than the required dosage.
You don’t know this a priori. Sometimes patients will not take a particular medicine because they don’t like the side affect it gives. The form of the noncompliance must be clearly defined.
From the data I have already obtained from ev, I believe the number of selection pressures is more important than the intensity of the selection pressures unless the intensity of the selection pressure is sufficient to cause extinction.But you were proven wrong on this in the HIV compliance study, Dr. Alan Kleinman. Argue all you like, but you're going to have a very hard time when reality disagrees with you.
You are jumping to a conclusion here. Ichneumonwasp has not shown that despite compliance with multi-drug therapy that drug resistance occurs as quickly as if monotherapy were used.
I neither need nor want to lie in this debate.Then stop doing it. While you're at it, stop waffling back and forth on your positions whenever you find it convenient.
I’m not lying you silly jack ass. You’ve been whining for pages that I’ve been moving the goalposts when my argument from the very beginning has been that ev shows your theory to be mathematically impossible. Your own Wikipedia link to fitness landscape shows why ev’s convergence is so slow.

You started to describe this problem properly when you said the following:
Unless we're talking about a real population. High enough selection pressure will slow the rate of evolution because the population will die off.

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

In the end, the number of selection pressures don't matter. It's the shape of the resulting fitness landscape that matters. We can only really talk about fitness landscape in a concrete way in terms of simulations like ev.
There are two things you got wrong in this quote. The first is that high selection pressures will slow evolution in real populations and simulations because the population will die off and the second is that the number of selection pressures does matter. This is explained in your own Wikipedia link to fitness landscapes.

kjkent1

18th April 2007, 12:40 AM

Dr Adequate

18th April 2007, 02:12 AM

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

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

Adequate has no excuse; he just has nothing to offer on the topic. I exposed the halfwitted nonsense that is Lie #5. I exposed Lie #1 and Lie #2, if it comes to that.

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

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

He has even run out of jpeg and gifs.

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

http://img81.imageshack.us/img81/2959/nobelxw9.jpg

Ichneumonwasp

18th April 2007, 04:59 AM

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

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

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

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

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

Paul C. Anagnostopoulos

18th April 2007, 05:49 AM

What I have been arguing is that increasing the number of selection pressures slows evolution.
Well, except when you were arguing that it stopped evolution.

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

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

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

So, make up your mind. Or is zero selection pressures a "special case," that you get to proclaim as unviable, because it doesn't fit with your personal belief system?
Alan Kleinman should stop referring to a "perfect creature" in his arguments, since we all agree that is a misleading term when one or more mistake counts are set to zero. Then he would have to explain exactly what is happening when one or more mistake counts are set to zero and a creature evolves with zero mistakes.

~~ Paul

Ichneumonwasp

18th April 2007, 06:31 AM

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

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

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

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

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

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

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

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

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

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

Ichneumonwasp

18th April 2007, 06:55 AM

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

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

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

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

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

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

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

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

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

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

Ichneumonwasp

18th April 2007, 06:56 AM

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

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

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

~~ Paul

Thanks Paul.

Mr. Scott

18th April 2007, 07:02 AM

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

If you google search for the keywords "Interspecies bacterial conjugation" (http://www.google.com/search?hl=en&q=Interspecies+bacterial+conjugation+&btnG=Search) you will see some nice articles about it.

One I'm reading now is Interspecies Bacterial Conjugation by Plasmids from Marine Environments (http://mbe.oxfordjournals.org/cgi/reprint/15/4/385.pdf)

Here’s the nomenclature: Horizontal and Vertical gene exchange. It's reasonable to surmise that evolution proceeded quite slowly vertically (for a billion years or so) until microbial conjugation commenced, at which point horizontal genetic promulgation was added to vertical promulgation. In this process, many, many beneficial mutations that occur in parallel will combine for the benefit of subsequent generations. It's no wonder that, in higher animals, such horizontal transmission of DNA is almost universal. Evolution probably could not have proceeded at its post-sexual pace without it.

I presume Ev does not include anything like horizontal transmission of DNA. Am I right, Paul? That would seem to me to impale Alan Kleinman's basic assertion with yet another fatal wound.

From Transgenic plants (http://www.escience.ws/b572/L20/L20.htm):

http://forums.randi.org/imagehosting/673646261ea21597a.jpg

Mr. Scott

18th April 2007, 07:23 AM

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

I just wanted to eliminate the possibility that you were paid to undermine evolution.

Based on that and the other cues in the above statement, I'm concluding that it's a vendetta. I suspect evolutionists harmed your career -- perhaps forcing you into retirement.

Your enjoyment at annoying evolutionists is a sign you are angry, and anger always has pain at its source. When I sense someone's pain, I back off.

When one has been wronged, if one must indulge in revenge, one should focus on the individual/s who wronged him, and not blast away at all individuals of the same demographic. The evolutionists you want to annoy did nothing to harm Dr. Alan Kleinman, and don't deserve to be targets of your rage. Revenge doesn't seem to be a very Christian behaviour -- especially against individuals who didn't harm you.

Is this really how you want to live your retirement? In an unending, scattershot quest for revenge?

joobz

18th April 2007, 07:48 AM

If you google search for the keywords "Interspecies bacterial conjugation" (http://www.google.com/search?hl=en&q=Interspecies+bacterial+conjugation+&btnG=Search) you will see some nice articles about it.

One I'm reading now is Interspecies Bacterial Conjugation by Plasmids from Marine Environments (http://mbe.oxfordjournals.org/cgi/reprint/15/4/385.pdf)

Here’s the nomenclature: Horizontal and Vertical gene exchange. It's reasonable to surmise that evolution proceeded quite slowly vertically (for a billion years or so) until microbial conjugation commenced, at which point horizontal genetic promulgation was added to vertical promulgation. In this process, many, many beneficial mutations that occur in parallel will combine for the benefit of subsequent generations. It's no wonder that, in higher animals, such horizontal transmission of DNA is almost universal. Evolution probably could not have proceeded at its post-sexual pace without it.

I presume Ev does not include anything like horizontal transmission of DNA. Am I right, Paul? That would seem to me to impale Alan Kleinman's basic assertion with yet another fatal wound.

From Transgenic plants (http://www.escience.ws/b572/L20/L20.htm):

http://forums.randi.org/imagehosting/673646261ea21597a.jpg

Not only can cells exchange DNA, They also exchange organelles. This to me is completely amazing.

Yup, life is rather cool. I wished Kleinman could see the wonder that is really there. The wonder that is reality. Instead of creating a wall of lies to hide himself in.

Dr. Kleinman, I noticed you haven't answered anything I and posted? Is it an admission of errors? Do you now see how we have at least 3 examples of multiple stress evolution?

kleinman

18th April 2007, 10:27 AM

You are using an excuse so as not to set two of the three selection conditions to zero because this demonstrates the crucial behavior of the mathematics of mutation and selection.Kleinman, I don't need an advantage to beat you in an argument.

You are currently arguing that my data is false because I exclude zero mistake weights. Okay, well what about the case where all mistake weights are set to zero. Ev reports a perfect creature in the first generation, every time, and regardless of the genome length.
On this issue, you have neither advantage nor argument. Without selection you have no evolution. You are also under a misconception if you think that changing the weight factors is equivalent to changing the intensity of a selection pressure. In order for you to learn why changing the weight factors does not represent changing the intensity of a selection pressure, take any one of your cases where you have a weight factor of 100 for all three selection conditions and run an identical case with all the weight factors set to 1. Then compare the generations for convergence. After you do this, answer the following question. Should increasing selection pressures by 100 fold affect the rate of evolution? Once you answer this question, consider this. Why does ev give these generations for convergence despite increasing the weight factors by 100 fold?

If Paul was attempting to model the intensity of selection pressures by his weight factors scheme, he missed modeling reality in this case. It is going to take a little more sophisticated mathematics and programming to capture the effects of varying the intensity of selection pressures.
You can't have your cake and eat it, too, bubba! If mistake weights of zero are valid, then ev proves that a completely random genome can produce a viable life form without selection in the first generation.
Don’t be silly.
And, that is the EXACT definition of your "gene from the beginning."
A “gene from the beginning” is the initial formation and appearance of a gene. There is no selection process than can select for something that doesn’t exist. Natural selection can only act on existing genes.
So, make up your mind. Or is zero selection pressures a "special case," that you get to proclaim as unviable, because it doesn't fit with your personal belief system?
A zero selection weight in ev is equivalent to removing that selective pressure. However, varying nonzero selection weights is not equivalent to varying the intensity of the selection pressure. This has nothing to do with my personal beliefs, these are mathematical facts that we are dealing with.
I am happy for Adequate because he seems to have found a purpose in life.Yes. That's more fun than it sounds, by the way, you should try it some time.
Why I have a purpose in life Adequate, it is to annoy you. It’s not much of a challenge but you do what you are called to do. It’s nice that you have found a jpeg to spice up your otherwise dull and boring posts.
I haven't read the rest, but this caught my eye passing through quickly:
That’s obvious. If you had read this thread thoroughly and the thread on the Evolutionisdead forum and Dr Schneider’s web site on ev with its associate publications you might have some idea on the mathematics of mutation and selection.
Why do you continue to lie and misrepresent my arguments, Dr. Alan Kleinman? Please answer why you continue to do this?
I am not misrepresenting your argument. You are confusing the number of selection pressures and the intensity of selection pressures. These are independent variables in the mathematics of mutation and selection. If you had some understanding of the mathematics of mutation and selection, this would be readily apparent to you.
What I have been arguing is that increasing the number of selection pressures slows evolution.Well, except when you were arguing that it stopped evolution.
Why Paul, multiple selection pressures can and does stop evolution. It is called extinction.
I’m not lying you silly jack ass. You’ve been whining for pages that I’ve been moving the goalposts when my argument from the very beginning has been that ev shows your theory to be mathematically impossible.That's the claim, not the goalpost.
Ev sure does a good job supporting my claim. I really like your programming skills. Hey, maybe you would tell us if changing the weights on the selection conditions in ev is equivalent to changing the intensity of selection pressures.
Alan Kleinman should stop referring to a "perfect creature" in his arguments, since we all agree that is a misleading term when one or more mistake counts are set to zero. Then he would have to explain exactly what is happening when one or more mistake counts are set to zero and a creature evolves with zero mistakes.
I can’t help that you use confusing terminology. What you mean by a “perfect creature” is a genome which has evolved satisfying all three selection conditions in your model. Setting weight factors to zero is simply turning off selection for that condition. Setting all three weight factors to zero is mathematically equivalent to turning off selection in the model
I am not mischaracterizing your position; you just continue to miss the most important point. That point is that multiple selection conditions applied simultaneously slows evolution. This is clearly seen with the use of multiple drug therapy for the treatment of HIV. If you use monotherapy, resistance to that single drug quickly occurs.So, there you go again, Dr. Kleinman, mischaracterizing my position. Since I have not only stated repeatedly that increasing selection pressure slows evolution and have, in fact, provided repeat posting of the relevant passages from previous posts to show you that I have said exactly that, why do you persist, Dr. Kleinman, in arguing that I am saying the opposite? Why do persist in this behavior, Dr. Kleinman?
The reason why I persist in this behavior is that I am engaged in a discussion with someone who does not have any understanding of the mathematics of mutation and selection. In order to try to explain something to you of this mathematics, I will persist in telling you that there is a difference between the number of selection pressures and the intensity of selection pressures. These are different independent variables in the mathematics of mutation and selection. Once you acknowledge this, then we can start talking about what ev demonstrates based on the number of selection pressures. The effect of the intensity of selection pressures is going to be more difficult to discuss since ev does not have the capability to vary the intensity of selection pressures at this time.
Certainly as Mr Scott has suggested there may be a “sweet spot” where evolution can be accelerated. You have suggested that this curve may be parabolic. However, this rate of evolution will never be as rapid as when a single selection pressure is applied. You have two ways of establishing the rates of evolution. You can collect data in real situations such as the treatment of HIV or you can look at mathematical models to establish this behavior. You are trying to take a single data point on the fitness landscape for HIV to support your argument.So, now you agree that multiple selection pressures do not stop evolution? OK< then the argument is at an end.
Of course multiple selection pressures can stop evolution, it is called extinction. It is dependent on the intensity of the selection pressures as well as the type of selection pressures. This is a highly nonlinear mathematical relationship which if you want to understand this is going to require some study on your part.
What??????? How do different species “share notes” via sexual congress?If you google search for the keywords "Interspecies bacterial conjugation" you will see some nice articles about it.
I understand this mechanism of gene transfer but you said:
Even pandas and people can combine adptatations to varying selective pressures via sexual congress, thus speeding evolution far beyond what Ev currently models.
I think you have extrapolated the concept of interspecies gene transfers a bit beyond reality.
I am under no obligation to answer every stupid question raised by you evolutionists. However, in an attempt to stop your incessant whining, I will answer your stupid question. I have not been paid; I will not be paid and do not expect to be paid for revealing the truth about your dumb ass theory of evolution. One reason I do this thread is because I enjoy annoying thin skinned, whining, crybaby evolutionists by using their own mathematical model to prove your theory is hogwash. This is not my primary reason though for doing this thread. That reason is none of your business.I just wanted to eliminate the possibility that you were paid to undermine evolution.

Based on that and the other cues in the above statement, I'm concluding that it's a vendetta. I suspect evolutionists harmed your career -- perhaps forcing you into retirement.
You have transcended stupidity and are now delusional. How do you know that I am doing this because I enjoy showing mathematically challenged, pseudo-intellectuals that their dumb theory is mathematically impossible using their own computer model? But that isn’t the reason either. Well, you can psychoanalyze me by my writings on this topic if that amuses you, but I do thank you for your example of the Gonorrhea super bug, it is a perfect example of why monotherapy (single selection pressure) gives rapid evolution of resistant strains of this bacteria.
Dr. Kleinman, I noticed you haven't answered anything I and posted? Is it an admission of errors? Do you now see how we have at least 3 examples of multiple stress evolution?
I did answer you. Your publication on the selection of yeasts resistant to multiple stressors is an example of the selection of beneficial alleles in a population to particular stresses. This is and example of breeding, not an example of mutation and selection. In fact, your case is an example of the loss of genetic information in the gene pool.

Paul C. Anagnostopoulos

18th April 2007, 11:08 AM

Ichneumonwasp

18th April 2007, 11:12 AM

I am not misrepresenting your argument.

Yes, you are. You have repeatedly stated that I do not understand that three selection pressures can slow evolution. That is a bald-faced misrepresentation of my position and my direct statements. Do you deny this?

You are confusing the number of selection pressures and the intensity of selection pressures.

No, there is no confusion here. I am forcefully stating that the number of selection pressures (three in your example) is not sufficient to stop evolution in all instances as you have argued previously. It is the intensity of the selection pressures that determines how the evolutionary process is impacted.

So, again, yes, you have misrepresented my argument. Why do continue to do this Dr. Kleinman?

These are independent variables in the mathematics of mutation and selection.

Really? So you agree with what I have been telling you now for three weeks? Did this only just dawn on you or have you simply been playing a game?

If you had some understanding of the mathematics of mutation and selection, this would be readily apparent to you.

Well, well, since I have been arguing for three weeks that these are independent variables and you now seem to see that they are independent variables (actually they are not completely independent), how does it now follow that I do not understand the mathematics of mutation and selection? To repeat Inigo Montoya again, you keep using these words. I do not think they mean what you think they mean. But it is quite amusing to see you repeat them over and over.

The reason why I persist in this behavior is that I am engaged in a discussion with someone who does not have any understanding of the mathematics of mutation and selection

And yet, you only just proved above that I do. Golly, fancy that. Keep repeating it like a mantra. It is so very amusing. I need the amusement, so please continue.

In order to try to explain something to you of this mathematics, I will persist in telling you that there is a difference between the number of selection pressures and the intensity of selection pressures.

Golly, jeepers, really? Because you've never made the distinction until this post. I have been the one making that distinction. Glad to see you've finally joied the party.

The effect of the intensity of selection pressures is going to be more difficult to discuss since ev does not have the capability to vary the intensity of selection pressures at this time.

Oh, really? Oh, yeah, we discussed this three friggin' weeks ago, when I brought it up.

Of course multiple selection pressures can stop evolution, it is called extinction.

That is not the issue we were discussing earlier and you know it. You stated that multiple selection pressures always profoundly slow evolution so that it can stop the process. We all know that extinction can and does occur.

It is dependent on the intensity of the selection pressures as well as the type of selection pressures.

Well, I'm certainly glad that I finally got through to you on that issue, since you've repeated it three times in this post but never would acknowledge the point earlier. Do you really think you are the one introducing this idea into this thread?

OK, now that we have all that gibberish out of the way, will you now address the issues at hand? You specifically stated that three selection pressures acting simultaneously so profoundly slows evolution that the process essentially stops. Yet, the early trials of HIV triple therapy with less potent agents produced resistant strains of HIV at 95+% compliance. How do you reconcile your earlier stance and this data? Do you admit that HIV triple therapy is not a good model for you to use as a real world example?

Paul C. Anagnostopoulos

18th April 2007, 11:17 AM

On this issue, you have neither advantage nor argument. Without selection you have no evolution. You are also under a misconception if you think that changing the weight factors is equivalent to changing the intensity of a selection pressure. In order for you to learn why changing the weight factors does not represent changing the intensity of a selection pressure, take any one of your cases where you have a weight factor of 100 for all three selection conditions and run an identical case with all the weight factors set to 1. Then compare the generations for convergence. After you do this, answer the following question. Should increasing selection pressures by 100 fold affect the rate of evolution? Once you answer this question, consider this. Why does ev give these generations for convergence despite increasing the weight factors by 100 fold?
Uniformly increasing the mistake counts does not increase "selection pressure." Changing them nonuniformly, however, does change the relative selection pressures.

Don’t be silly.
Kjkent is not being silly. He is simply playing on your simplistic interpretation of the term "perfect creature." A perfect creature arises instantaneously if all mistake counts are set to zero.

A zero selection weight in ev is equivalent to removing that selective pressure. However, varying nonzero selection weights is not equivalent to varying the intensity of the selection pressure. This has nothing to do with my personal beliefs, these are mathematical facts that we are dealing with.
Varying nonzero mistake counts varies the relative selection pressures.

Your entire thesis about multiple selection pressures is based on setting some of Ev's mistake counts to zero. Unfortunately, when you do that, you are not evolving the same final creature as when all three mistake counts are nonzero. Thus, it is meaningless to compare the time required to evolve the final creatures.

~~ Paul

Paul C. Anagnostopoulos

18th April 2007, 11:22 AM

Why Paul, multiple selection pressures can and does stop evolution. It is called extinction.
Ah, now stopping = extinction. Well, since Ev does not model extinction, you can't use it to draw any conclusions about the real world.

I can’t help that you use confusing terminology. What you mean by a “perfect creature” is a genome which has evolved satisfying all three selection conditions in your model. Setting weight factors to zero is simply turning off selection for that condition. Setting all three weight factors to zero is mathematically equivalent to turning off selection in the model
Yes, that is what "perfect creature" means until I change Ev's GUI. When I change it, I will trash your entire thesis. Your thesis is based on a graphical user interface.

Until then, could you explain to us what functions have evolved in three perfect creatures: one where all mistake counts are positive; one where some mistake counts are zero; and one where all mistake counts are zero.

~~ Paul

joobz

18th April 2007, 12:37 PM

I did answer you. Your publication on the selection of yeasts resistant to multiple stressors is an example of the selection of beneficial alleles in a population to particular stresses. This is and example of breeding, not an example of mutation and selection. In fact, your case is an example of the loss of genetic information in the gene pool.
A dodge. You've been played out, Dr. Kleinman. You have been clearly outed as a dishonest fool. Perhaps such games work in your circle, but thankfully those in science don't accept such follishness.

Have fun.

Mr. Scott

18th April 2007, 01:45 PM

I think you have extrapolated the concept of interspecies gene transfers a bit beyond reality.

Oh, I meant that Pandas interchange genes with other Pandas horizontally, like people with people, through intraspecies sexual congress. Did not intend anyone to infer I meant between pandas and people.

Still, the exclusion of horizontal genetic interchange is a major problem with your central thesis, Dr. Kleinman.

I intended it as a subtle reference to an infamous book. Sorry for the confusing wording.

On the other hand, I read that a zoo panda bit a zoo patron a few months ago. Can we count out the possibility that bacteria that may have picked up a panda gene might then subsequently transfer it to a human? Is there a mathematical proof that this is impossible?

Religious propaganda in public schools: 'Of Pandas and People' (http://www.textbookleague.org/53panda.htm)

http://forums.randi.org/imagehosting/6736462673691e152.jpg

joobz

18th April 2007, 02:13 PM

I think you have extrapolated the concept of interspecies gene transfers a bit beyond reality.

Oh, I meant that Pandas interchange genes with other Pandas horizontally, like people with people, through intraspecies sexual congress. Did not intend anyone to infer I meant between pandas and people.

Mr. Scott, I think you are making the mistake in assuming Dr. Alan Kleinman was actually making an "honest mistake" of your meaning. He knows full well what the argument is and knows full well what everyone is saying. Dr. Kleinman knows he can't argue on a honest/real level. So he must make intentional missunderstandings of our argument and turn them into strawmen. It is the only thing he has left.

Remember the Dr. Alan Kleinman method:
Dismiss a clearly explained concept by quoting random words from said concept in a contemptable manner.

Mr. Scott

18th April 2007, 02:39 PM

How do you know that I am doing this because I enjoy showing mathematically challenged, pseudo-intellectuals that their dumb theory is mathematically impossible using their own computer model?

Because you said it?

One reason I do this thread is because I enjoy annoying thin skinned, whining, crybaby evolutionists

You aren't succeeding in annoying us. I've exchanged numerous private messages with other posters here, and the consensus is we are enjoying this immensely.

If you can supply mathematical proof that evolution is impossible, that might annoy us. You haven't done that, but I know how hard you've tried.

kjkent1

18th April 2007, 03:22 PM

Kent is not being silly. He is simply playing on your simplistic interpretation of the term "perfect creature." A perfect creature arises instantaneously if all mistake counts are set to zero.Thank you. This is becoming farcical. kleinman is doing precisely what I suggested: he is arguing that the zero mistake weights show that evolution profoundly increases in speed when two mistake weights are set to zero. But, as soon as three mistake weights are set to zero, and every creature is rendered instantly perfect, that particular example is invalid -- because if it's not, then abiogenesis is conclusively proved, and kleinman's theory is utterly destroyed.

There's big trouble in kleinmantown tonight! The annoying creationist must either concede that ev proves a gene from the beginning is guaranteed where no selective pressure exists, or that evolution is not necessarily slowed by multiple selection pressures.

Or, if he wants to be illogical, he can declare both or neither. But, that wouldn't be very scientific, now would it?

hehehehehehehehehe...

delphi_ote

18th April 2007, 06:06 PM

Paul C. Anagnostopoulos

18th April 2007, 06:22 PM

Not worth the bother, Delphi. It's been repeat theatre for months.

~~ Paul

Dr Adequate

18th April 2007, 06:33 PM

Why I have a purpose in life Adequate, it is to annoy you. That's a particularly pitiable form of monomania. I feel rather sorry for you.

I can't give you any annoyance, but you do make me giggle now and then. And Lie #5 made me hoot with laughter the first time you told it.

---

What's your religion again? I've not come across a sect which teaches that the purpose of life is to annoy me. Most of them aim for something a bit more, y'know, sublime.

delphi_ote

18th April 2007, 06:48 PM

Not worth the bother, Delphi. It's been repeat theatre for months.
Alright. I guess I'll start organizing my sock drawer, then.

kleinman

18th April 2007, 06:55 PM

I presume Ev does not include anything like horizontal transmission of DNA. Am I right, Paul? That would seem to me to impale Alan Kleinman's basic assertion with yet another fatal wound.You are right. And it's not even on the to-do list!
Another evolutionist with no idea what ev is about. Well Paul, Mr Scott has solved you mathematical conundrum with horizontal transmission of DNA. I’m sure you evolutionists can find panda genes in humans. You must make sure the evolutionary landscape is complete and don’t forget panspermia.
I am not misrepresenting your argument.Yes, you are. You have repeatedly stated that I do not understand that three selection pressures can slow evolution. That is a bald-faced misrepresentation of my position and my direct statements. Do you deny this?
Oh, ok, sorry I misrepresented your position. Do you think that multiple selection pressures applied simultaneously can accelerate evolution and if so do you have any mathematical or real examples of this.
On this issue, you have neither advantage nor argument. Without selection you have no evolution. You are also under a misconception if you think that changing the weight factors is equivalent to changing the intensity of a selection pressure. In order for you to learn why changing the weight factors does not represent changing the intensity of a selection pressure, take any one of your cases where you have a weight factor of 100 for all three selection conditions and run an identical case with all the weight factors set to 1. Then compare the generations for convergence. After you do this, answer the following question. Should increasing selection pressures by 100 fold affect the rate of evolution? Once you answer this question, consider this. Why does ev give these generations for convergence despite increasing the weight factors by 100 fold?Uniformly increasing the mistake counts does not increase "selection pressure." Changing them nonuniformly, however, does change the relative selection pressures.
Your scheme for changing the weights is far from being realistic. If you increase the weights uniformly, you get the same generations for convergence for each case. If you want to model selection pressures realistically, your selection pressures need to be tied to the dead of creatures. A hundred fold increase in the selection intensity would cause far more deaths.
Don’t be silly.Kjkent is not being silly. He is simply playing on your simplistic interpretation of the term "perfect creature." A perfect creature arises instantaneously if all mistake counts are set to zero.
That fits perfectly with his string cheese theory of evolution.
A zero selection weight in ev is equivalent to removing that selective pressure. However, varying nonzero selection weights is not equivalent to varying the intensity of the selection pressure. This has nothing to do with my personal beliefs, these are mathematical facts that we are dealing with.Varying nonzero mistake counts varies the relative selection pressures.
The way you model the variance in selection pressure by varying the weights neglects a very important realistic effect. If the selection pressure represents the concentration of an antimicrobial agent, increasing that value 100 fold probably would markedly impair the microbes’ ability to reproduce. Selection intensity is a highly nonlinear variable. If the intensity is high enough, it causes extinction. You have not included this effect in the model.
Your entire thesis about multiple selection pressures is based on setting some of Ev's mistake counts to zero. Unfortunately, when you do that, you are not evolving the same final creature as when all three mistake counts are nonzero. Thus, it is meaningless to compare the time required to evolve the final creatures.
Of course you don’t evolve the same final creature when you change the selection pressures. What is meaningful is that it takes huge numbers of more generations to evolve the three selection conditions in ev than evolving any single selection condition. It is much more difficult to find an optimum on the fitness landscape when you are trying to satisfy three selection conditions than when you are trying to satisfy a single selection condition.
Why Paul, multiple selection pressures can and does stop evolution. It is called extinction.Ah, now stopping = extinction. Well, since Ev does not model extinction, you can't use it to draw any conclusions about the real world.
Extinction also = death, extermination, destruction, annihilation, and disappearance. If you include this in ev, it only makes evolution more difficult, especially when you increase the weights on your selection conditions by 100 fold. Dr Schneider had no problem drawing conclusions about the real world despites the model’s lack of an extinction algorithm. Have you told Dr Schneider he shouldn’t have drawn any conclusions about the real world?
I can’t help that you use confusing terminology. What you mean by a “perfect creature” is a genome which has evolved satisfying all three selection conditions in your model. Setting weight factors to zero is simply turning off selection for that condition. Setting all three weight factors to zero is mathematically equivalent to turning off selection in the model.Yes, that is what "perfect creature" means until I change Ev's GUI. When I change it, I will trash your entire thesis. Your thesis is based on a graphical user interface.
That’s ridiculous Paul, what are you going to do, change the code in ev so that you can’t set a selection pressure weight equal to zero? You do that, I like it when you have to hide the real behavior of your model in a lame attempt to make your case.
Until then, could you explain to us what functions have evolved in three perfect creatures: one where all mistake counts are positive; one where some mistake counts are zero; and one where all mistake counts are zero.
That’s easy to explain, you have three selection conditions, one condition where it is a mistake if a binding site is not located where it should, the second condition is that it’s a mistake if a binding site is located in the gene region of the genome and the third condition is that is a mistake if a binding site is located outside of the gene region. Interestingly, it does not take all three selection conditions to evolve your binding sites. Setting any one of the selection conditions to zero simply stops selection for that condition. Setting all three of the weight factors to zero is equivalent to turning selection off in the model. What is the function of the genome when you set one or two of the selections to zero? That function is simply to satisfy the selection conditions imposed on your creatures.
I did answer you. Your publication on the selection of yeasts resistant to multiple stressors is an example of the selection of beneficial alleles in a population to particular stresses. This is and example of breeding, not an example of mutation and selection. In fact, your case is an example of the loss of genetic information in the gene pool.A dodge. You've been played out, Dr. Kleinman. You have been clearly outed as a dishonest fool. Perhaps such games work in your circle, but thankfully those in science don't accept such follishness.
If you read more than the title of your paper, you would realize what I have said about your article is not a dodge, but what can you expect from an alchemical engineer who believes in abiogenesis and can’t explain how ribose arose in his primordial world.
I think you have extrapolated the concept of interspecies gene transfers a bit beyond reality.Oh, I meant that Pandas interchange genes with other Pandas horizontally, like people with people, through intraspecies sexual congress. Did not intend anyone to infer I meant between pandas and people.
Are we back on the topic of recombination again? Well if you understood that recombination without error can not increase the information in the gene pool and recombination and natural selection can cause the loss of information in the gene pool by the loss of alleles. Let’s see if Paul and Dr Schneider will include recombination in ev and whether it increases the information in the gene pool.
I admire your willpower, guys. I can't even keep up with the malarkey. Parsing together the meaning of this inconsistent word salad he's puked all over our forum is too exhausting. Is there even a substantive discussion anymore? Can someone attempt to translate? Or should I just give up and go do something more productive with my life?
Delphi, why don’t you start with your Wikipedia link to fitness landscape? Once you understand your own link, the rest of this discussion will fall into place for you.
Not worth the bother, Delphi. It's been repeat theatre for months.
Maybe you and Delphi should take more power naps. Maybe the mathematics of mutation and selection will come to you in your dreams. It certainly isn’t coming to you while you are awake.

Dr Adequate

18th April 2007, 07:03 PM

Delphi, why don’t you start with your Wikipedia link to fitness landscape? Once you understand your own link, the rest of this discussion will fall into place for you. What makes Lie #5 particularly funny is your windy, pompous, self-important attempts to patronise the people who can see through your pathetic, half-baked delusions.

articulett

18th April 2007, 07:35 PM

I admire your willpower, guys. I can't even keep up with the malarkey. Parsing together the meaning of this inconsistent word salad he's puked all over our forum is too exhausting. Is there even a substantive discussion anymore? Can someone attempt to translate? Or should I just give up and go do something more productive with my life?

Well, as near as I can figure, Kleinman's point boils down to, "My god is true...la, la, la, I can't hear you...nyah, nyah". (But maybe I'm missing the nuances.)

delphi_ote

18th April 2007, 07:50 PM

Can someone bump the jukebox, please? I know I requested "Fitness Landscape", but I'd like to hear a new tune now.

Is a function that maps a genotype to the real numbers that hard to understand? Don't they teach domain and range in elementary school? Fitness landscape. A landscape of fitness values. It defines itself.

I'd like to propose the following function:

$kleinman:\mathbb{R} \rightarrow (\mathbb{C} - \mathbb{R})

(What do you get when you take the real numbers away from the complex numbers?)

Dr Adequate

18th April 2007, 07:51 PM

Why Lie #5 Is Funny

I thought I'd just explain this briefly for the non-mathematicians here, so we can all join in the laugh.

The wikipedia article fitness landscape gives an example of an optimization problem which can be solved by an evolutionary algorithm. The problem is:

"A delivery truck with a number of destination addresses can take a large variety of different routes, but only very few will result in a short driving time."

This is a brief statement of what mathematicians call the Travelling Salesman Problem: we are given a number of towns (we'll call the number n) and the distances between them. The travelling salesman wishes to visit every town on the list and return to his starting point while minimising the distance travelled.

Now the number of possible routes is the factorial of n (written n!) where by definition n! = 1 x 2 x 3 x ... x (n - 1) x n. This grows rapidly with n. For example, 20! = 2432902008176640000

This means that if we want to find a good route, looking at all the possible routes is not practical. As the wiki article says:

"It is almost impossible to check all possible routes once the number of destinations grows to more than a handful."

Checking every route would be equivalent, in biology, to a creator creating life-forms by trying every possible genome and seeing which ones work. This would be wasteful and time-consuming, and so would checking every route in the Travelling Salesman problem (in computer science, such a method is known as a "brute force algorithm").

So instead of using brute force, computer scientists use an evolutionary algorithm: we simulate the process of evolution so that the "genomes" are potential routes, the "fitness" is the shortness of the route, and the "mutations" are supplied by the computer's random number generator.

As the wiki article says, evolutionary algorithms are "particularly effective" at optimising this and similar problems when the number of routes is too large for a brute force algorithm to be effective.

---

Now, let's look at the mess kleinman's made of this.

In the first place, he thinks, for some crazy reason, that the various alternative routes correspond to selection pressures, when in fact they correspond to potential genomes.

But this blunder, though gross, pales into insignificance next to his belief that a mere three potential routes would pose a problem for an evolutionary algorithm.

That's the stupidest statement I've ever heard anyone make about computer science. Evolutionary algorithms are, as the wikipedia article says, "particularly effective" at solving the problem in cases where brute force algorithms are impractical --- i.e. in cases where there are trillions, quadrillions, or quintillions of routes.

I don't know where kleinman got his delusions on this subject from, since they have no connection with the text of the article he keeps whining about. Perhaps he hears voices in his head. If so, they're as dumb as he is.

Add to this his endless pompous bragging about how he "immediately grasped the significance" of the wiki article, and we have a recipe for Krazy Kreationist Komedy with Kleinman the Klown.

joobz

18th April 2007, 08:20 PM

Why Lie #5 Is Funny

Nicely worded. Thank you.

Couple this with his continual Assertions of his masterful mathematical skills and yet fully missing the nice code that Delphi wrote that showed how 3 selection pressures can be faster than 1 pressure.... :D

kleinman

18th April 2007, 08:24 PM

But maybe I'm missing the nuances.
You are missing much more than the nuances.
Can someone bump the jukebox, please? I know I requested "Fitness Landscape", but I'd like to hear a new tune now.
You want to hear a new tune, Dr Schneider has moved on. What’s the problem? Are you having a little problem with the mathematics of mutation and selection?
Is a function that maps a genotype to the real numbers that hard to understand? Don't they teach domain and range in elementary school? Fitness landscape. A landscape of fitness values. It defines itself.
The basic concept is not that hard to understand if you realize that the mapping can only be done implicitly. You don’t have an explicit algebraic relationship and it is hard for some people to realize that you can solve equations that you can’t write down. It is the mapping of the fitness landscape that is difficult to do especially when you have multiple selection conditions. What Paul seems to think is that an optimum on the fitness landscape can be found more quickly by a series of random directionless steps then if a systematic search is done of the landscape. Evolution works by a series of random directionless steps. That is the slowest way of finding an optimum.
I'd like to propose the following function:
http://www.randi.org/latexrender/latex.php?$kleinman:\mathbb{R} \rightarrow (\mathbb{C} - \mathbb{R})
Delphi, you deserve your own equation as well:

Delphi + EtOH -> Wikipedia & fitness landscape -> organize sock drawer

Have you ever noticed that it takes longer to organize your sock drawer the more different color socks you have? It’s very easy to organize your socks if they are all the same color.

Dr Adequate

18th April 2007, 08:37 PM

What Paul seems to think is that an optimum on the fitness landscape can be found more quickly by a series of random directionless steps then if a systematic search is done of the landscape. Evolution works by a series of random directionless steps. S - E - L - E - C - T - I - O - N, retard.

That is the slowest way of finding an optimum. No, the slowest method is the "systematic search" you suggest. If you tried applying that to the Travelling Salesman Problem with a mere 20 towns, your wait for an answer would be terminated by the heat death of the universe. To quote from the wikipedia article on fitness landscapes:

"It is almost impossible to check all possible routes once the number of destinations grows to more than a handful."

This is why computer scientists use evolutionary algorithms instead, which, as the wiki article says, are "particularly effective".

You've got a real gift for being wrong, haven't you?

Dr Adequate

18th April 2007, 08:51 PM

Delphi, you deserve your own equation as well:

Delphi + EtOH -> Wikipedia & fitness landscape -> organize sock drawer You don't know what an equation is?

Sheesh.

Anyway, please return to your pompous, vaccuous bragging about your mathematical abilities.

kjkent1

18th April 2007, 09:21 PM

delphi_ote

18th April 2007, 11:00 PM

$\mathbb{R}
$\mathbb{R}^c
I must re-think my theory. He doesn't always map the real to the imaginary.

Dr Adequate

19th April 2007, 02:01 AM

Okay, I think it's time to update the kleinman FAQ.

This FAQ will demonstrate two things.

First, that the stuff kleinman recites is nothing more than the retarded droolings of a monomaniac with a grudge against reality.

Second, that his grotesque blunders have been pointed out to him so clearly that he knows that the stuff he's reciting is rubbish; and that therefore he is not merely contemptible for his stupidity and his vanity, as are all creationists; but also for his deep habitual dishonesty.

To prove the second point, the FAQ will consist of posts which have already been made and which prove the first of these points.

Enjoy.

* How kleinman screwed up with ev

The mistake Kleinman has made, or one of them, is to take a realistic value for p (the probability of a point mutation for a given base) but not for n (the population). This gives a totally unrealistic value for the probability that a given substition will occur in the gene pool per generation, which is given by:

q = 1 - (1 - p/3)n

If, for example, we take a realistic value for p of 10-8, then for a measly million organisms, q is 0.3%. For a lousy billion, it's 96.4%.

If we use a more realistic order of magnitude for the bacteria, say something like the 1014 present in a single human gut, then my calculator isn't accurate enough to tell us the difference between q and 1.

Schneider is forced by practical constraints to take n to be small, and has compensated for this by using an unrealistic value for p to give himself a realistic value for q. This is eminently sensible, since it is the amount of variation within the gene pool, rather than the variation between individuals per generation, that determines the rate of evolution.

Kleinman, on the other hand, has chosen his numbers so that the value for q is wildly unrealistic; this is why his estimate of the time the process would take is also wildly unrealistic.

* Kleinman's interpretation of data from ev:

G=1000, mutation rate = 1 mutation per 1000 bases per generation, gamma = 16, binding site width = 6:
Population \ generation for convergence
2 \ failed to converge
4 , 66547
8 , 15916
16 , 17257
32 , 16416
64 , 9082
128 , 9378
256 , 4078
512 , 3685
1024 , 2793
2048 , 2080
4096 , 2565
6000 , 1541
8192 , 1798
16384 , 1001
32768 , 743
65536 , 633
131072 , 483
262144 , 702
524288 , 642
1048576 , 438
ev demonstrates decreasing rates of convergence with increasing population.

* Multiple selection pressures:

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

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

linky (http://www.tuscaloosanews.com/article/20070413/ZNYT04/704130370/1001/NEWS06)

That's 1) Sulfomanides; 2) Beta-latcams; (3) Tetracyclines; (4) Fluoroquinolones.

...or, two successful adaptations past Kleinman Impossibility.

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

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

In other words, he's busted again.

* New genes:

Evolution of novel genes (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11682312)

The origin of new genes (http://www3.uta.edu/faculty/betran/naturereviews.pdf)

Novel genes derived from noncoding DNA in Drosophila melanogaster (http://www.pnas.org/cgi/reprint/103/26/9935.pdf)

* The de novo origin of genomes: RNA species from a bucket of chemicals:

Evidence for de novo production of self-replicating and environmentally adapted RNA structures by bacteriophage Qbeta replicase. (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=432262&tools=bot)

Template-free generation of RNA species that replicate with bacteriophage T7 RNA polymerase. (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=451910)

Template-free RNA synthesis by Q beta replicase (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2422560&dopt=Abstract)

De novo DNA synthesis by yeast DNA polymerase I associated with primase activity. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6395659&dopt=Abstract)

De Novo synthesis of DNA-like molecules by polynucleotide phosphorylase in vitro (http://www.springerlink.com/content/g6af4blfqjxekm4k/)

De Novo Initiation of RNA Synthesis by the RNA-Dependent RNA Polymerase (NS5B) of Hepatitis C Virus (http://jvi.asm.org/cgi/content/abstract/74/2/851)

Template-free generation of RNA species that replicate with bacteriophage T7 RNA polymerase (http://edoc.mpg.de/262342)

De novo RNA synthesis by a recombinant classical swine fever virus RNA-dependent RNA polymerase (http://content.febsjournal.org/cgi/content/abstract/270/24/4952)

De novo RNA synthesis catalyzed by HCV RNA-dependent RNA polymerase (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10679285&dopt=Abstract)

Template-free, polymerase-free DNA polymerization (http://www.rsc.org/publishing/journals/CC/article.asp?doi=b501132a)

Template-Free Primer-Independent DNA Synthesis by Bacterial DNA Polymerases I Using the DnaB Protein from Escherichia coli (http://www.springerlink.com/content/h24132172v62l7j8/)

* Kleinman's inability to understand evolutionary algorithms:

Why Lie #5 Is Funny

I thought I'd just explain this briefly for the non-mathematicians here, so we can all join in the laugh.

The wikipedia article fitness landscape gives an example of an optimization problem which can be solved by an evolutionary algorithm. The problem is:

"A delivery truck with a number of destination addresses can take a large variety of different routes, but only very few will result in a short driving time."

This is a brief statement of what mathematicians call the Travelling Salesman Problem: we are given a number of towns (we'll call the number n) and the distances between them. The travelling salesman wishes to visit every town on the list and return to his starting point while minimising the distance travelled.

Now the number of possible routes is the factorial of n (written n!) where by definition n! = 1 x 2 x 3 x ... x (n - 1) x n. This grows rapidly with n. For example, 20! = 2432902008176640000

This means that if we want to find a good route, looking at all the possible routes is not practical. As the wiki article says:

"It is almost impossible to check all possible routes once the number of destinations grows to more than a handful."

Checking every route would be equivalent, in biology, to a creator creating life-forms by trying every possible genome and seeing which ones work. This would be wasteful and time-consuming, and so would checking every route in the Travelling Salesman problem (in computer science, such a method is known as a "brute force algorithm").

So instead of using brute force, computer scientists use an evolutionary algorithm: we simulate the process of evolution so that the "genomes" are potential routes, the "fitness" is the shortness of the route, and the "mutations" are supplied by the computer's random number generator.

As the wiki article says, evolutionary algorithms are "particularly effective" at optimising this and similar problems when the number of routes is too large for a brute force algorithm to be effective.

---

Now, let's look at the mess kleinman's made of this.

In the first place, he thinks, for some crazy reason, that the various alternative routes correspond to selection pressures, when in fact they correspond to potential genomes.

But this blunder, though gross, pales into insignificance next to his belief that a mere three potential routes would pose a problem for an evolutionary algorithm.

That's the stupidest statement I've ever heard anyone make about computer science. Evolutionary algorithms are, as the wikipedia article says, "particularly effective" at solving the problem in cases where brute force algorithms are impractical --- i.e. in cases where there are trillions, quadrillions, or quintillions of routes.

I don't know where kleinman got his delusions on this subject from, since they have no connection with the text of the article he keeps whining about. Perhaps he hears voices in his head. If so, they're as dumb as he is.

Add to this his endless pompous bragging about how he "immediately grasped the significance" of the wiki article, and we have a recipe for Krazy Kreationist Komedy with Kleinman the Klown.

* Kleinman on the definition of "macroevolution" (thanks to Dr Richard and Mr Scott):

If you had read this thread you would already have known that I accept that microevolutionary processes occur. I have always acknowledged this.
I am working with the evolutionist definition, which is there is no difference between micro and macroevolution
With respects to macroevolution, we can work with your definition that there is no distinction between micro and macroevolution
I happen to like the terms micro and macroevolution to distinguish between evolutionary events which occur and those which don’t occur
let’s work from the assumption that macroevolution is simply the sum of a series of microevolutionary steps
The goal post for microevolution is the transformation of a gene from some initial function to a new and completely different function and the evolution of a gene from the beginning. There is/are no selection process(es) that can accomplish this.
The goal post for evolution is the transformation of a gene from some initial function to a new and completely different function and the evolution of a gene from the beginning. There is/are no selection process(es) that can accomplish this.
I posed the cases of the evolution of a gene from the beginning and the transformation of a gene from one form to an entirely new form as examples of macroevolution
I’m accepting for the sake of discussion that there is no distinction between micro and macroevolution
I have not presented the definition for macroevolution
Paul holds the position that a series of microevolutionary changes can lead to a macroevolutionary change. This is why I set up the goal post of the evolution of a gene from the beginning and the transformation of a gene from one form to another
My view on this issue is that once you get beyond a single point mutation you are already starting to enter the realm of macroevolution.
The goal post for macroevolution is the transformation of a gene from some initial function to a new and completely different function and the evolution of a gene from the beginning. There is/are no selection process(es) that can accomplish this

* Department of "did he really say that?":

Kleinman on natural selection:

I am interested if you can explain why a beneficial mutation can be selected for.

Kleinman on "macroevolution":

My view on this issue is that once you get beyond a single point mutation you are already starting to enter the realm of macroevolution.

Kleinman thinks he has a clue:

We do have clues. Most mutations are harmful, ask anyone with a genetic disease.

The purpose of Kleinman's life, according to Kleinman:

I have a purpose in life Adequate, it is to annoy you.

BPScooter

19th April 2007, 02:27 AM

I simply have to speak here, for the sake of future suffering readers that may not speak English as the natal tongue, and to help my own understanding:

"ev" is a computer program designed to probe certain areas in possible design space, with constraints and possibilities set up in advance, right?

*really smart people made this program to get some insight about certain esoterica regarding information and its development and transfer, right?

*an equally smart person has seized upon aspects of this to further an alternate theory: evolution is "mathematicallly impossible" and in the doing so refute "dumbass" theories, and quiet "silly" "whining" people with the contention that they are ignorant of the "math".

In terms of rhetoric, I think Kleinman is missing a great opportunity to convince, and seeking opportunities to offend. I admit, the term "liar" has been applied to him. This tends to raise the ante.

Perhaps all of you will be happy to know that I have been reading Dawkins' Blind Watchmaker for the first time and giggled at the quaint references to BASIC and Pascal in it.

:-) cheers to you all, keep it decent if you can.

Dr Adequate

19th April 2007, 05:42 AM

I simply have to speak here, for the sake of future suffering readers that may not speak English as the natal tongue, and to help my own understanding:

"ev" is a computer program designed to probe certain areas in possible design space, with constraints and possibilities set up in advance, right?

*really smart people made this program to get some insight about certain esoterica regarding information and its development and transfer, right?

*an equally smart person ... Ah, let me stop you there.

Kleinman has expended thousands and thousands of words reciting a handful of very, very stupid lies over and over again to a tiny audience of people all of whom know that he's lying, and whose main reason for participating this thread is to laugh at his buffoonish antics. Which aspect of that strikes you as smart?

In terms of rhetoric, I think Kleinman is missing a great opportunity to convince ... No, not really. Demosthenes himself couldn't make kleinman's crap convincing. It's not the schizophrenic raving about cheese and alchemy, nor the stupid made-up words, nor the screaming, twitching temper-tantrums that really let him down. It's the fact that everything he says is bollocks.

Rhetoric is, as it were, the final polish we give to our thoughts to make them shine --- but one cannot polish a turd.

Ichneumonwasp

19th April 2007, 06:04 AM

Oh, ok, sorry I misrepresented your position.

That I can respect. Thank you.

Do you think that multiple selection pressures applied simultaneously can accelerate evolution and if so do you have any mathematical or real examples of this.

Accelerate evolution? That depends on how we define evolution. Mathematical or real examples -- depends on how you take my explanation below concerning the involved principles.

Multiple selection pressures (holding potency of each pressure constant) will decrease variability more than one selection pressure of the same potency. This follows from the definition of "selection pressure". If we define evolution in terms of the number of variants (which represent a form of change over time), then evolution will be slowed in this instance. Actually, at this stage, any definition of evolution means that the process is slowed -- again, at this stage.

However, there is another sense of the word "evolution", referring to the accumulation of changes over time.

So, for instance, if there were no selection pressures, variability in organisms would reach maximum. But we couldn't sepeak of information in the same way that we do now. We would see a blinding array of different organisms, but any changes could occur and disappear with no consequence one way or the other. By applying selection pressures, we would slow this process of change (one meaning of evolution). Multiple selection pressures (holding potency constant) would slow this process even more.

Since information would basically be inconequential, however, we would not see what our world holds. Selection pressures obviously determine what sorts of changes survive and leave behind more copies of themselves (by definition, again). Multiple selection pressures applied simultaneously impact the process more. While they would slow the process of increasing variability and slow the evolutionary process (at that stage), they actually would be more profound at spurring cumulative changes over time.

For HIV, a single selection pressure would be likely to result in resistance to a single drug (or drug class). Multiple relatively weak (weak compared to current practices) pressures would spur resistance to multiple drugs. So, while multiple selection pressures (holding potency constant) will slow the process of change (defined as increasing variability) in the initial stages, they will ultimately result in greater change if the organisms survive.

Like most philosohpical debates, in other words, the issue revolves about the particular definitions of the words used.

Paul C. Anagnostopoulos

19th April 2007, 06:54 AM

Your scheme for changing the weights is far from being realistic. If you increase the weights uniformly, you get the same generations for convergence for each case. If you want to model selection pressures realistically, your selection pressures need to be tied to the dead of creatures. A hundred fold increase in the selection intensity would cause far more deaths.
The mistake counts were not added to provide uniform selection pressure increase, but to allow the relative selection pressures to vary. You were not involved in the discussion with Cristi Pavel that resulted in this feature.

That fits perfectly with his string cheese theory of evolution.
You're really avoiding this issue, aren't you?

The way you model the variance in selection pressure by varying the weights neglects a very important realistic effect. If the selection pressure represents the concentration of an antimicrobial agent, increasing that value 100 fold probably would markedly impair the microbes’ ability to reproduce. Selection intensity is a highly nonlinear variable. If the intensity is high enough, it causes extinction. You have not included this effect in the model.
Correct.

Of course you don’t evolve the same final creature when you change the selection pressures. What is meaningful is that it takes huge numbers of more generations to evolve the three selection conditions in ev than evolving any single selection condition. It is much more difficult to find an optimum on the fitness landscape when you are trying to satisfy three selection conditions than when you are trying to satisfy a single selection condition.
No argument there, at least as far as Ev is concerned. But you're not extrapolating this to all possible selection pressures in the real world, are you?

That’s ridiculous Paul, what are you going to do, change the code in ev so that you can’t set a selection pressure weight equal to zero? You do that, I like it when you have to hide the real behavior of your model in a lame attempt to make your case.
As long as you stop making any claims about evolving "perfect creatures" when one or more mistake counts are zero, I'm happy to drop this subject. When mistake counts are zero, the creature is not "perfect" in the original meaning of the term.

That’s easy to explain, you have three selection conditions, one condition where it is a mistake if a binding site is not located where it should, the second condition is that it’s a mistake if a binding site is located in the gene region of the genome and the third condition is that is a mistake if a binding site is located outside of the gene region. Interestingly, it does not take all three selection conditions to evolve your binding sites. Setting any one of the selection conditions to zero simply stops selection for that condition. Setting all three of the weight factors to zero is equivalent to turning selection off in the model. What is the function of the genome when you set one or two of the selections to zero? That function is simply to satisfy the selection conditions imposed on your creatures.
Excellent, so we agree that the creatures have different evolved functions, depending on the mistake counts. It is therefore quite dangerous to compare the number of generations to evolve these different functions. A vague generalization about Ev requiring more generations when all mistake counts are nonzero is fine. Extrapolation to the real world is not.

~~ Paul

kleinman

19th April 2007, 09:29 AM

Alright. I guess I'll start organizing my sock drawer, then.Concur. I will get out the Roundup and the sprayer and take care of the weeds which appeared by magic in my yard during the past few months.
Another example of a single selective pressure, watch out that you don’t select for resistant weeds, it’s much easier with a single selective pressure.
I must re-think my theory. He doesn't always map the real to the imaginary.
Just how many socks do you have in your drawer?
I simply have to speak here, for the sake of future suffering readers that may not speak English as the natal tongue, and to help my own understanding:
We plan on having this thread translated into Vulcan.
"ev" is a computer program designed to probe certain areas in possible design space, with constraints and possibilities set up in advance, right?
Yes, these are the areas of the design space Dr Schneider intended to investigate:
Variations of the program could be used to investigate how population size, genome length, number of sites, size of recognition regions, mutation rate, selective pressure, overlapping sites and other factors affect the evolution.
*really smart people made this program to get some insight about certain esoterica regarding information and its development and transfer, right?
I don’t know what you mean by esoterica.
Dr Schneider said the following about his model:
Actual biological materials were used to determine the original hypothesis. Read the literature: Schneider1986 (http://www.lecb.ncifcrf.gov/~toms/paper/schneider1986)
And he said this about ev.
The simulation was of phenomena in the "real" world.
*an equally smart person has seized upon aspects of this to further an alternate theory: evolution is "mathematicallly impossible" and in the doing so refute "dumbass" theories, and quiet "silly" "whining" people with the contention that they are ignorant of the "math".
Oh yes, I seized upon genome length, mutation rate, population size and selection pressure, all esoteric features in the ev model that Dr Schneider thought should be investigated. And each of these esoteric features show your theory to be mathematically impossible.
In terms of rhetoric, I think Kleinman is missing a great opportunity to convince, and seeking opportunities to offend. I admit, the term "liar" has been applied to him. This tends to raise the ante.
What you don’t understand BPScooter is that the simple act of challenging the theory of evolution is an offense to evolutionists. Evolutionists use a similar strategy that lawyers use in court. If you have the law on your side, argue the law, if you have the facts on your side, argue the facts, if you have neither, attack your opponent. The evolutionist variant of this principle is if you have the mathematics, argue the mathematics, if you have the facts, argue the facts and since evolutionists have neither, they call me a liar. This shows how weak the evolutionist case is.
Perhaps all of you will be happy to know that I have been reading Dawkins' Blind Watchmaker for the first time and giggled at the quaint references to BASIC and Pascal in it.
Maybe Dawkins needs Turbo Basic.
:-) cheers to you all, keep it decent if you can.
And Adequate, if you can’t keep it decent, at least don’t be dull and boring.
Do you think that multiple selection pressures applied simultaneously can accelerate evolution and if so do you have any mathematical or real examples of this.Accelerate evolution? That depends on how we define evolution. Mathematical or real examples -- depends on how you take my explanation below concerning the involved principles.
In ev, this is very easy to define, it is the reduction in the number of generations necessary to evolve to selective conditions. In real examples, the examples are analogous. Consider the case of treating HIV again. Monotherapy leads to the emergence of resistant strains more quickly (fewer generations) than combination therapy.
Multiple selection pressures (holding potency of each pressure constant) will decrease variability more than one selection pressure of the same potency. This follows from the definition of "selection pressure". If we define evolution in terms of the number of variants (which represent a form of change over time), then evolution will be slowed in this instance. Actually, at this stage, any definition of evolution means that the process is slowed -- again, at this stage.
That’s interesting that you would describe the affect of selection pressure this way. Alleles that would allow a creature to survive and reproduce when there is no selective pressure could be a disadvantage when a particular selective pressure is applied. Are you saying that selective pressure reduces information in the gene pool?
However, there is another sense of the word "evolution", referring to the accumulation of changes over time.
This is why you need to familiarize yourself with ev. Dr Schneider has attempted to put stringent mathematical definitions to the concept of mutation and selection. Until you have some understanding of how he did this, you will not have systematic way of discussing how each of the variables affects the evolutionary process. Putting this mathematical framework on the debate gives a way of testing the hypotheses.
So, for instance, if there were no selection pressures, variability in organisms would reach maximum. But we couldn't sepeak of information in the same way that we do now. We would see a blinding array of different organisms, but any changes could occur and disappear with no consequence one way or the other. By applying selection pressures, we would slow this process of change (one meaning of evolution). Multiple selection pressures (holding potency constant) would slow this process even more.
Selection pressures always act. The variability (divergence of genes) is always going to be limited. If a gene diverges to the point that the gene no longer functions, there will be a selection pressure against that creature. This is why I have problems with Delphi’s concept of gene duplication as a mechanism for creating new genes. The transformation of the gene to a new function must take a path on the fitness landscape that never causes selection against that creature.
Since information would basically be inconequential, however, we would not see what our world holds. Selection pressures obviously determine what sorts of changes survive and leave behind more copies of themselves (by definition, again). Multiple selection pressures applied simultaneously impact the process more. While they would slow the process of increasing variability and slow the evolutionary process (at that stage), they actually would be more profound at spurring cumulative changes over time.
The problem you have is that the mathematics of ev shows that the number of generations required to accumulate these changes (by random point mutations) is huge. The number of generations required is far too large to support the concept of macroevolution.
For HIV, a single selection pressure would be likely to result in resistance to a single drug (or drug class). Multiple relatively weak (weak compared to current practices) pressures would spur resistance to multiple drugs. So, while multiple selection pressures (holding potency constant) will slow the process of change (defined as increasing variability) in the initial stages, they will ultimately result in greater change if the organisms survive.
In the early stage of treatment, even with weak selective pressures, the evolutionary process is slowed until an appropriate resistant allele can evolve and that allele gets selected for and becomes dominant in the population.
Like most philosohpical debates, in other words, the issue revolves about the particular definitions of the words used.
This is why I like debating ev. The definitions are mathematical and the assumptions used at arriving at these definitions can be easily scrutinized. If you are going to continue on in this discussion, you had better familiarize yourself with ev. This thread is about the mathematics of mutation and selection.
Your scheme for changing the weights is far from being realistic. If you increase the weights uniformly, you get the same generations for convergence for each case. If you want to model selection pressures realistically, your selection pressures need to be tied to the dead of creatures. A hundred fold increase in the selection intensity would cause far more deaths.The mistake counts were not added to provide uniform selection pressure increase, but to allow the relative selection pressures to vary. You were not involved in the discussion with Cristi Pavel that resulted in this feature.
Modeling relative selection pressures more realistically will take much more than the strategy that you have employed. Even with your simple strategy, the relative selective pressures change as you lengthen the genome. With large genomes, the non-binding site region becomes the dominant source of spurious binding mistakes. This is why as you lengthen the genome, even with a mutation rate fixed to a number of bases, that the number of generations for convergence increases.
The way you model the variance in selection pressure by varying the weights neglects a very important realistic effect. If the selection pressure represents the concentration of an antimicrobial agent, increasing that value 100 fold probably would markedly impair the microbes’ ability to reproduce. Selection intensity is a highly nonlinear variable. If the intensity is high enough, it causes extinction. You have not included this effect in the model.Correct.
Do you want to venture a guess whether including this effect would speed or slow the evolutionary process? I’ll stick my neck out and guess that this will slow evolution by reducing populations.
Of course you don’t evolve the same final creature when you change the selection pressures. What is meaningful is that it takes huge numbers of more generations to evolve the three selection conditions in ev than evolving any single selection condition. It is much more difficult to find an optimum on the fitness landscape when you are trying to satisfy three selection conditions than when you are trying to satisfy a single selection condition.No argument there, at least as far as Ev is concerned. But you're not extrapolating this to all possible selection pressures in the real world, are you?
Yes I am extrapolating this result to all possible selection pressures. Increasing the number of selection pressures is simply increasing the number of sorting conditions. It doesn’t matter what the selection conditions are. Delphi’s Wikipedia link to fitness landscape discusses the same issue. This is a basic mathematical principle of optimization. When Delphi went to sort his sock drawer; the more colors of socks he has the slower the sort proceeds. If all his socks are of a single color, any two socks he grabs randomly out of the drawer gives a match.
That’s ridiculous Paul, what are you going to do, change the code in ev so that you can’t set a selection pressure weight equal to zero? You do that, I like it when you have to hide the real behavior of your model in a lame attempt to make your case.As long as you stop making any claims about evolving "perfect creatures" when one or more mistake counts are zero, I'm happy to drop this subject. When mistake counts are zero, the creature is not "perfect" in the original meaning of the term.
It is your terminology which is causing confusion. What you call a “perfect creature” is nothing more than a genome with a sequence of bases that satisfies all three of your selection condition. Reducing the number of selection conditions by setting selection weights to zero gives a genome with a sequence of bases that satisfies the remaining selection conditions when you click the check box – Pause on perfect creature. You can’t use your confusing terminology to obscure what is occurring mathematically.
That’s easy to explain, you have three selection conditions, one condition where it is a mistake if a binding site is not located where it should, the second condition is that it’s a mistake if a binding site is located in the gene region of the genome and the third condition is that is a mistake if a binding site is located outside of the gene region. Interestingly, it does not take all three selection conditions to evolve your binding sites. Setting any one of the selection conditions to zero simply stops selection for that condition. Setting all three of the weight factors to zero is equivalent to turning selection off in the model. What is the function of the genome when you set one or two of the selections to zero? That function is simply to satisfy the selection conditions imposed on your creatures.Excellent, so we agree that the creatures have different evolved functions, depending on the mistake counts. It is therefore quite dangerous to compare the number of generations to evolve these different functions. A vague generalization about Ev requiring more generations when all mistake counts are nonzero is fine. Extrapolation to the real world is not.
I don’t agree that you have creatures that have evolved different functions. The creatures have evolved to satisfy each of the selection conditions. In the case of three selection conditions your “perfect creature” has evolved a genome to satisfy all three selection condition. When you set some of the selection conditions to zero, you evolve a genome to satisfy the remaining selection conditions. Do you think when HIV develops resistance to a particular drug it matters whether this occurs during monotherapy or combination therapy?

What is dangerous is your extrapolation of these microevolutionary events to macroevolution. Your extrapolation is not an extrapolation to the real world.

Mr. Scott

19th April 2007, 09:39 AM

Dr. Alan Kleinman is wrong about how the three selection pressures affect the rate of evolution. What matters is the combined intensity of selection pressures, not their count, as explained in the article Patients whose therapy fails having used at least three classes of drugs (http://www.bhiva.org/guidelines/2005/HIV/resistance.html).

using a number of such drugs together might have a cumulative benefit which outweighs the potential toxicity

Here's how it works:

1) A virus colony like HIV can be stopped if an anti-viral drug is used at sufficient intensity to stop all virus individuals before any of them have time to adapt.

2) Dosages of anti-viral drugs must nevertheless be low enough to avoid harming the patient, so it may not be wise to administer the concentration required to stop the entire colony before resistance develops.

3) Administration of three different anti-virals may roughly triple the pressure against the virus while not tripling the level of toxicity to the patient.

4) The advantage of multi-drug therapy is therefore to change the ratio of efficacy to patient toxicity. It's not to increase the count of selection pressures.

5) Application of multi-drug therapy below compliance would likely result in multi-adaptation to all the drugs (macroevolution in Kleinspeak).

6) Dr. Kleinman's HIV example of triple-drug therapy as evidence that macroevolution can't happen, is therefore utterly bogus.

Cancer treatments likewise can involve a similar approach. The best chance of cancer recovery comes from using more than one approach against the cancer colony, typically 1) physical removal of the cells, 2) radiation, 3) chemotherapy. This works because each of the three remedies will have an additive effect at fighting the cancer but not at harming the patient. The operation will remove as little good tissue as practical, the radiation and chemo likewise. Their effects are additive against the cancer but not against the patient.

Multi-drug therapy works on the same principle. It has nothing at all to do with "three point mutations are impossible therefore evolution is impossible." It's a way to launch a toxic attack on a virus that is not toxic to the patient.

Kleinman, you're busted again.

kleinman

19th April 2007, 09:57 AM

Paul C. Anagnostopoulos

19th April 2007, 10:23 AM

Paul C. Anagnostopoulos

19th April 2007, 10:26 AM

Ichneumonwasp

19th April 2007, 11:56 AM

There's no sense in rehashing the rest of your replies, but......

This is why I like debating ev. The definitions are mathematical and the assumptions used at arriving at these definitions can be easily scrutinized. If you are going to continue on in this discussion, you had better familiarize yourself with ev. This thread is about the mathematics of mutation and selection.

The very issue of this thread is whether or not ev serves as a proper model for what you think it does. You cannot assume that ev properly models the mathematics of evolution (as it exists in the real world). You provided as support for this idea (that ev does model evolutionary change properly) HIV triple therapy as directly analogous to ev's functions. In your assessment of ev you have claimed that ev proves that evolution is so slow when three selection pressures are used that it could never have accounted for the bounty that surrounds us. However, if HIV triple therapy is analogous to the function of ev, as you have proposed, then your theory is wrong. Resistance develops in the presence of HIV triple therapy when the potency of this therapy is taken into account -- specifically when the potency is not as strong as the currently used treatments. And this resistance develops relatively quickly on an evolutionary time scale.

I am forced to conclude either: (1) ev does not adequately model three selection pressures as they relate to the development of resistance or (2) ev does not adequately model the development of resistance in a realistic time frame, which may simply be an issue of population size (which ev cannot handle).

Whatever the explanation, ev does not trump reality. Reality wins this debate. You can like ev as a model all you want, but where it fails, it fails. It served its purpose to demonstrate, with the use of Darwinian pressures, an increase in information. It wasn't designed to be used in the way that you are using it; and your own personal hand-picked example -- HIV triple therapy -- reveals that it does not correctly model reality.

Paul C. Anagnostopoulos

19th April 2007, 12:12 PM

I am forced to conclude either: (1) ev does not adequately model three selection pressures as they relate to the development of resistance or (2) ev does not adequately model the development of resistance in a realistic time frame, which may simply be an issue of population size (which ev cannot handle).
I'll go with (1). If Ev's simplistic multi-pressure model happens to mimic real-world evolution of drug resistance, either that is a stunning coincidence or real-world resistance is trivial. Wait, or both.

~~ Paul

Paul C. Anagnostopoulos

19th April 2007, 12:16 PM

Ichneumonwasp

19th April 2007, 12:25 PM

I'll go with (1). If Ev's simplistic multi-pressure model happens to mimic real-world evolution of drug resistance, either that is a stunning coincidence or real-world resistance is trivial. Wait, or both.

~~ Paul

That would be the most likely, I think, too.

Either Kleinman must give up his model or give up his example. Either way it looks bad. Give up the example and he doesn't have a real world link for the model, and it becomes a nice abstraction of uncertain provenance (at least as far as the full range of evolutionary pressure/history/etc., which is what you have said all along).

Ichneumonwasp

19th April 2007, 12:28 PM

Hang on a mo. Did I miss something? Has Kleinman presented the mathematics of multiple selection pressures?

~~ Paul

He continues to claim that he has modelled the mathematics. I haven't seen any data.

kleinman

19th April 2007, 03:43 PM

Modeling relative selection pressures more realistically will take much more than the strategy that you have employed. Even with your simple strategy, the relative selective pressures change as you lengthen the genome. With large genomes, the non-binding site region becomes the dominant source of spurious binding mistakes. This is why as you lengthen the genome, even with a mutation rate fixed to a number of bases, that the number of generations for convergence increases.I agree, a realistic model of selection pressures is way more complex. Thus I would not draw any conclusions about selection pressures in the real world. The feature was added for the same reason as the tie-breaking feature: at the insistence of a creationist.
You left off an important adjective in your response. My conclusion about the effects of multiple selection pressure is not based on relative selective pressures. It is based on turning selection pressures on and off in ev. This finding is substantiated by Delphi’s Wikipedia reference to fitness landscape. By the way Delphi, how is your sock drawer coming?

And why does it take the insistence of creationists for you evolutionists to do a thorough mathematical scientific proof of your claims?
Do you want to venture a guess whether including this effect would speed or slow the evolutionary process? I’ll stick my neck out and guess that this will slow evolution by reducing populations.Well, extinction would certainly slow the evolution of the extinct species, yes.
That’s the way to stick your neck out little turtle. I’m not so sure that it would be difficult to develop an algorithm that could be used in ev that would model relative selective pressures. Even without this feature, being able to turn on and off individual selective pressures reveals what happens to the mathematics of mutation and selection when you have multiple selective pressures.
Yes I am extrapolating this result to all possible selection pressures. Increasing the number of selection pressures is simply increasing the number of sorting conditions. It doesn’t matter what the selection conditions are. Delphi’s Wikipedia link to fitness landscape discusses the same issue. This is a basic mathematical principle of optimization. When Delphi went to sort his sock drawer; the more colors of socks he has the slower the sort proceeds. If all his socks are of a single color, any two socks he grabs randomly out of the drawer gives a match.So you're claiming that there is no possible way we could have two orthogonal selection pressures to which an organism adapts in parallel?
You need to reread again what I have said again. I’m not sure what you mean by orthogonal selection pressures but additional selection pressure slow the evolution of each of the individual selection condition when compared to evolution based on an individual selection pressure alone.
Also, I can sort any number of sock colors at the same speed: I look at each sock and drop it in the correct pile. Perhaps you really mean to discuss selection speed?
You are making my point. You first sort your socks by color and then put them in pairs. If all the socks are a single color, you don’t have to do the work of the sort, you simply put them in pairs. With a single selection condition, a mutation is determined to be beneficial or detrimental and the ability to reproduce is known. If you have multiple selection conditions, a mutation may be beneficial for one selection condition and detrimental for another selection condition. The total selection process becomes much more complex. Ev shows how difficult this mathematics becomes for satisfying multiple selection conditions when compared to satisfying a single selection condition.
It is your terminology which is causing confusion. What you call a “perfect creature” is nothing more than a genome with a sequence of bases that satisfies all three of your selection condition. Reducing the number of selection conditions by setting selection weights to zero gives a genome with a sequence of bases that satisfies the remaining selection conditions when you click the check box – Pause on perfect creature. You can’t use your confusing terminology to obscure what is occurring mathematically.Yes, my terminology is causing confusion. Therefore, you should not employ my terminology in making your point. We all agree that different numbers of selection pressures will cause Ev to arrive at a zero-mistake creature in different numbers of generations. But to refer to all those various creatures as "perfect creatures" obscures the issue.
If you think of a “perfect creature” as one which has satisfied all the selection conditions placed on it then this terminology is understandable. You just don’t like when I co-opt anything of yours.
I don’t agree that you have creatures that have evolved different functions. The creatures have evolved to satisfy each of the selection conditions. In the case of three selection conditions your “perfect creature” has evolved a genome to satisfy all three selection condition. When you set some of the selection conditions to zero, you evolve a genome to satisfy the remaining selection conditions.And thus, those two creatures have evolved different functions. One distinguishes binding sites from all other sites. The other does not.
So what! Define any three selection conditions and evolving the conditions one at a time will occur much more quickly than trying to evolve all three selection conditions simultaneously.
Mr Scott, you are confusing several principles. Those principles you are confusing are selection pressures, intensity of selection pressures and extinction. The mathematics is clear; increasing the number of selection pressures slows evolution. The number of selection pressures and the intensity of selection pressures determine whether extinction occurs. When you treat patients with HIV and use selection pressures that are insufficient to cause extinction of the virus, you will get resistant strains of the virus to those selection pressures. The fewer the number of selection pressures, the more rapidly the resistant strains appear.And the intensity of those selection pressures doesn't matter? Three mild pressures will always result in "slower evolution" than two brutal pressures?
Of course the intensity of selection pressures can determine extinction but the point is that selection pressure and selection intensity are independent variables in the mathematics of mutation and selection. In ev, it is not the intensity of the selection pressures that makes evolution so slow, it is the number of selection pressures which makes evolution so slow. Varying the intensity of the selection pressures is not going to reverse the huge number of generations required to evolve the three selection conditions in ev. The dominant variables in the mutation selection mechanism of evolution are genome length and the number of selection pressures. This is what ev shows. Other variables including population and mutation rate have much less profound effect on the mathematical behavior of the model.
This is why I like debating ev. The definitions are mathematical and the assumptions used at arriving at these definitions can be easily scrutinized. If you are going to continue on in this discussion, you had better familiarize yourself with ev. This thread is about the mathematics of mutation and selection.The very issue of this thread is whether or not ev serves as a proper model for what you think it does. You cannot assume that ev properly models the mathematics of evolution (as it exists in the real world). You provided as support for this idea (that ev does model evolutionary change properly) HIV triple therapy as directly analogous to ev's functions. In your assessment of ev you have claimed that ev proves that evolution is so slow when three selection pressures are used that it could never have accounted for the bounty that surrounds us. However, if HIV triple therapy is analogous to the function of ev, as you have proposed, then your theory is wrong. Resistance develops in the presence of HIV triple therapy when the potency of this therapy is taken into account -- specifically when the potency is not as strong as the currently used treatments. And this resistance develops relatively quickly on an evolutionary time scale.
The basic approach evolutionists have to ev is that if it shows something that supports your theory it is a valid, if it shows something that contradicts your theory, the model is not valid. You evolutionists are filled with prejudices and biases. But let’s see what Dr Schneider has said about his model:
A good simulation does not attempt to simulate everything; only the essential components are modeled. For the issue at hand, the form of the genetic code is not relevant; information measured by Shannon's method is more general than that.
Dr Schneider’s model shows important essential relationships between genome length, selection conditions, mutation rates and population. If you take the time to study the model, you will find that genome length and the number of selection conditions are the dominant variables in the mathematics of mutation and selection.
I am forced to conclude either: (1) ev does not adequately model three selection pressures as they relate to the development of resistance or (2) ev does not adequately model the development of resistance in a realistic time frame, which may simply be an issue of population size (which ev cannot handle).I'll go with (1). If Ev's simplistic multi-pressure model happens to mimic real-world evolution of drug resistance, either that is a stunning coincidence or real-world resistance is trivial. Wait, or both.
Well Paul, you have your own model of the mathematics mutation and selection which reveals something about genome lengths and selection pressures and you dismiss it out of hand because it doesn’t agree with your world view. Dr Schneider thinks that ev models reality, you used to think this until you finally studied the behavior of the model. Well, I’m still with you Dr Schneider. Your evolutionists partners may deny the validity of your work but we creationists will stick with you. I will any way.
Mr Scott, you are confusing several principles. Those principles you are confusing are selection pressures, intensity of selection pressures and extinction. The mathematics is clear; increasing the number of selection pressures slows evolution.Hang on a mo. Did I miss something? Has Kleinman presented the mathematics of multiple selection pressures?
Paul, you must have missed something. Didn’t you read Delphi’s Wikipedia link to fitness landscape? Don’t you see what happens to the convergence of ev when you reduce the selection conditions to one? Multiple selection conditions slow evolution, your program shows this and Delphi’s link shows this very nicely.
I'll go with (1). If Ev's simplistic multi-pressure model happens to mimic real-world evolution of drug resistance, either that is a stunning coincidence or real-world resistance is trivial. Wait, or both.That would be the most likely, I think, too.
What makes you think the mathematics of real-world evolution of drug resistance is any different than from the mathematics of any other mutation and selection process?
Either Kleinman must give up his model or give up his example. Either way it looks bad. Give up the example and he doesn't have a real world link for the model, and it becomes a nice abstraction of uncertain provenance (at least as far as the full range of evolutionary pressure/history/etc., which is what you have said all along).
Ichneumonwasp, this is not my model of mutation and natural selection. This is the peer reviewed and published model of mutation and natural selection, written by Dr Tom Schneider, head of computational molecular biology and the National Cancer Institute. This model shows that three selection pressures simultaneously slow the evolution process for each of the conditions. While single selection conditions evolve much more rapidly. This is exactly what we see when combination therapy is used for treating HIV and TB and what results with monotherapy with the treatment of MRSA, Gonorrhea, pseudomonas and cancers as well. So it is not my model to give up and my examples work just fine, thank you.
Hang on a mo. Did I miss something? Has Kleinman presented the mathematics of multiple selection pressures?He continues to claim that he has modelled the mathematics. I haven't seen any data.
Dr Schneider modeled the mathematics. The reason you haven’t seen any data is you haven’t read this thread or the Evolutionisdead forum where this discussion started. Here is some new data for you.

The following data from ev is based on a mutation rate of 1 mutation/256 bases/generation, G was varied, and the weight factors were set to 0 or 1 for the following series of cases. All other parameters were left at default values. The top row in the table gives the weight factors for missed binding sites, spurious binding sites in the gene and spurious binding sites outside the gene.

G \111 \110 \101 \011 \100 \010 \001
8192 \20237 \881 \22324 \20 \1 \13 \19
16384 \49963 \424 \41260 \20 \1 \21 \28
32768 \140958\436 \284,000+\20 \1 \9 \20

There are a couple of interesting numbers in this table highlighted in red. These two cases with two selection conditions actually took more generations to evolve than the three selection condition case. However, the single selection condition cases are able to converge thousands of times more quickly than the three selection condition cases for any of the three selection conditions. It is amazing how quickly a single selection condition can evolve, even on a lengthier genome.

delphi_ote

19th April 2007, 04:26 PM

Has Kleinman presented the mathematics of multiple selection pressures?
Yes.
Delphi + EtOH -> Wikipedia & fitness landscape -> organize sock drawer

kleinman

19th April 2007, 04:42 PM

Has Kleinman presented the mathematics of multiple selection pressures?Yes.Delphi + EtOH -> Wikipedia & fitness landscape -> organize sock drawer
I hope my mathematics is not too obscure. Delphi, if you have any trouble organizing your sock drawer, Paul will help you. He’s very good at the mathematics of sorting socks.

delphi_ote

19th April 2007, 05:14 PM

Paul C. Anagnostopoulos

19th April 2007, 05:28 PM

You are making my point. You first sort your socks by color and then put them in pairs. If all the socks are a single color, you don’t have to do the work of the sort, you simply put them in pairs. With a single selection condition, a mutation is determined to be beneficial or detrimental and the ability to reproduce is known. If you have multiple selection conditions, a mutation may be beneficial for one selection condition and detrimental for another selection condition. The total selection process becomes much more complex. Ev shows how difficult this mathematics becomes for satisfying multiple selection conditions when compared to satisfying a single selection condition.
The sock drawer is a silly analogy. What if you have no a priori knowledge that all the socks are the same color? Then you always have to sort them and it takes the same amount of time regardless of the number of colors.

If you think of a “perfect creature” as one which has satisfied all the selection conditions placed on it then this terminology is understandable. You just don’t like when I co-opt anything of yours.
Okay, misuse the term. But then you have to address Kjkent's point that a "perfect creature" arises instantaneously with no selection pressures at all. Don't you see that you're just shooting yourself in the foot?

So what! Define any three selection conditions and evolving the conditions one at a time will occur much more quickly than trying to evolve all three selection conditions simultaneously.
You can't use Ev to demonstrate this. If you turn on one pressure until the mistake count is zero, then turn it off and turn on a second pressure, you won't end up with a creature that distinguishes binding sites from other sites. You'll end up with a creature that performs a different function.

~~ Paul

Paul C. Anagnostopoulos

19th April 2007, 05:33 PM

There are a couple of interesting numbers in this table highlighted in red. These two cases with two selection conditions actually took more generations to evolve than the three selection condition case. However, the single selection condition cases are able to converge thousands of times more quickly than the three selection condition cases for any of the three selection conditions. It is amazing how quickly a single selection condition can evolve, even on a lengthier genome.
Well then, at least you admit there is nothing special about three or more pressures. Note how even more amazing it is when there are zero selection conditions.

What you are doing here is extrapolating the rather degraded case of a single selection pressure in Ev to cover the entire real world of evolution. You are claiming there is not a single case of evolution accommodating two selection pressures more quickly than one pressure. You are making a claim about the entire landscape of biochemistry. You have some seriously enlarged gonads there, my friend.

~~ Paul

Dr Adequate

19th April 2007, 08:13 PM

He's still telling Lie #5?

Kleinman, what part of "particularly effective" are you too dumb to understand?

Dr Adequate

19th April 2007, 08:25 PM

And Adequate, if you can’t keep it decent, at least don’t be dull and boring. You are lecturing people on decency? Well, that's good for a chuckle.

If you find reality "dull and boring", I suggest that you crawl off and read the Bible. You'll like that, it has magic talking animals, and none of that nasty mathematics that you have such difficulty in understanding.

Now, is that your sole riposte to my expose of Lie #5, or do you have anything to say in your defense?

C'mon, I want to see you try to twist the words "particularly effective". What's the point of keeping a tame creationist if it won't do the Silly Dance for us?

Schneibster

19th April 2007, 08:57 PM

And Adequate, if you can’t keep it decent, at least don’t be dull and boring.Looks like another one for the "did he really say that" file.

Dr. Adequate, that was an excellent summation on the last page. Just in case anyone missed it, here's a linky-poo (http://forums.randi.org/showpost.php?p=2533858&postcount=3669).

kjkent1

19th April 2007, 08:59 PM

Okay, misuse the term. But then you have to address Kjkent's point that a "perfect creature" arises instantaneously with no selection pressures at all. Don't you see that you're just shooting yourself in the foot?I don't believe that the real Dr. Alan Kleinman is on the other end of this argument. It's got to be someone else, because no one with a Ph.D and MD could possibly be so ignorant.

You've defined a perfect creature as one substantially free of both missed or spurious bindings. If we turn the pressure off that selects for one of these features, then the resulting creature cannot possibly meet the original definition -- it's not the same creature.

For some reason, kleinman appears to believe that because ev reports a perfect creature, that the resulting creature must therefore necessarily be perfect.

That's great. Here, let's do this, then:

main()
{
printf("Evolution is true.");
}

Game over.

joobz

19th April 2007, 10:29 PM

Hang on a mo. Did I miss something? Has Kleinman presented the mathematics of multiple selection pressures?

~~ Paul
No, but Dr. Kleinman has presented many other facinating scientific "facts".

I can compose a list to add to Dr. Adequate's Kleinman FAQ if need be.

Dr Adequate

19th April 2007, 11:57 PM

No, but Dr. Kleinman has presented many other facinating scientific "facts".

I can compose a list to add to Dr. Adequate's Kleinman FAQ if need be.

You mean stuff like the "Kleinman Lectures On Probability Theory"?

You are confusing the probability of a particular event occurring which must have a value between 0 and 1 with probability that a particular event may occur by a series of mutually exclusive events which can have probabilities greater than 1 ...

The probability of throwing a 1 in either of two rolls of a die is 1/6 + 1/6 = 1/3.

Yeah, that's funny.

And then he wishes to tell us what he thinks is "mathematically impossible".

BPScooter

20th April 2007, 02:44 AM

OK, I bow out and really didn't contribute much. I felt a little creepy when the people I tend to trust were all-of-a-sudden called "dumbass." That's nearly like calling me a "dumbass," which takes me so far aback that I went back and a-back in this thread and realized I have no rationale for being reading this in the first place.

joobz

20th April 2007, 04:49 PM

You mean stuff like the "Kleinman Lectures On Probability Theory"?

I forgot about that. The great part was with with the notion that probability can exceed 1.

I was considering these gems:

Since natural selection is a restatement of the 1st law of thermodynamics, what selection pressure would lead to the formation of a self replicating ligase?

In case You were wondering 1st law, which states that heat and work are equivilent/interchangable (dE=dQ-dW) is identical to saying that the species best adapted for survival will survive.

Look at the word thermodynamics. The simplest examples in the study of thermodynamics are equilibrium cases, in general, thermodynamics studies as the word says dynamic or changing situations.
This one had me rolling. classical thermodynamics is a study of heat(thermo) and work (dynamics). the newer work in non-equilibrium thermo is a kinetic study, but requires additional arguments not handled by what kleinman is refering to.

This would be honest mistakes for anyone, but coupled with his assertion of his fine engineering and mathematics background and claims of having taught thermodyanmics, it is a quite funny.

articulett

20th April 2007, 05:49 PM

This is not my primary reason though for doing this thread. That reason is none of your business.

Umm....let me guess...to get some extra credit heaven bonus points?

Taffer

20th April 2007, 11:21 PM

Well, looks like I'm not needed. Kleinman hasn't changed his argument one bit. Oh well.

* Taffer wonders off to do something more productive.

Ichneumonwasp

21st April 2007, 09:29 AM

The basic approach evolutionists have to ev is that if it shows something that supports your theory it is a valid, if it shows something that contradicts your theory, the model is not valid. You evolutionists are filled with prejudices and biases. But let’s see what Dr Schneider has said about his model:

You may continue to conjure any straw man you wish, but here is, once again, the point:

You have a computer model (Dr. Schneider's model, so that you will stop harping on trivial minituae as though you are making a point). You claim this computer simulation models the reality of evolution in all its particulars. You have argued that the intersection of this simulation and reality is the behavior of HIV in the presence of triple therapy. You argued that three selection pressures in ev demonstrate that evolution cannot occur on a realistic time scale. You have been shown with the very example you cite as the intersection of reality and your computer model that what you think the model proves is incorrect. The model does not win in this situation. Reality does. And since the model was not intended to simulate this issue, I'm not the least surprised.

For the nth time, I am not claiming anything about ev except that it was designed to show one thing -- that information can increase in a very simple model of mutation and selection. That is all that the model was designed to do and that is what it does.

There is no conspiracy to quell the demons of ev. Your entire argument depends on ev modelling the reality of evolution in all its particulars (not just one aspect of reality -- information gain -- as it was designed to do). When it fails to model all of evolutionary reality, reality wins, not the model. The model only goes so far as it can explain anything in the real world. It's the same with all models. The only thing I have denied is the ability of ev to do what you said it does. It simply does not model what you propose. Your own, hand-picked, example -- the only real-world example you have offered -- demonstrates this fact.

Dr Schneider’s model shows important essential relationships between genome length, selection conditions, mutation rates and population. If you take the time to study the model, you will find that genome length and the number of selection conditions are the dominant variables in the mathematics of mutation and selection.

How nice. Need I remind you, again, that the model does what it was designed to do and not what you argue it does. Nothing else in this argument matters. You can argue till you're blue in the face and your fingers cramp at the keyboard that ev models important relationships between genome length, selection conditions, mutation rates, and population and we will all sit back and say "Well, yeah, that is how it is designed, so tell us something we don't know." What it doesn't model is the reality of triple therapy for HIV under all treatment conditions. If you have no real-world analogy, then the model is useless for that purpose. Dr. Schneider provided his real world analogy for what the model was created to do -- demonstrate the emergence of information under Darwinian conditions.

Well Paul, you have your own model of the mathematics mutation and selection which reveals something about genome lengths and selection pressures and you dismiss it out of hand because it doesn’t agree with your world view. Dr Schneider thinks that ev models reality, you used to think this until you finally studied the behavior of the model.

And that is utter BS and another prime example of your penchant for misrepresenting others' arguments. I have yet to see Paul once claim that ev does not model something of reality. He has maintained that ev did its job -- demonstrating an increase in information. That is what Dr. Schneider claims as well -- repeatedly from the quotes you have provided of him. I have yet to see anyone but you claim that ev models all aspects of the evolutionary landscape. You have specifically stated that it predicts the inability of evolution to occur on a realistic time scale if three selection pressures are applied. Your example for this in the real world -- HIV triple therapy -- when all the information about it is considered, actually shows the opposite. Unless you can show some real-world example of how this model that you think explains what occurs in the real world functions, then I'm afraid that your argument is dead in the water. Otherwise, all you have is a model that does nothing but sit in the corner.

What makes you think the mathematics of real-world evolution of drug resistance is any different than from the mathematics of any other mutation and selection process?

First, I never said it was. The "mathematics" of real-world evolution of drug resistance shows that three selection pressures does not stop the process and does not slow it to the point that evolution cannot happen on a realistic time scale. That is what the HIV triple therapy story tells us.

But, there is no question, whatsoever, that different mechanisms play into resistance with different organisms. I am not aware of any lateral transfer of information amongst viruses (there probably is some example of this, though), but there is clear lateral transmission of information in bacteria through plasmids. That is an entirely different mechanism from random mutation and selection and a process that dramatically speeds "evolution".

Ichneumonwasp, this is not my model of mutation and natural selection. This is the peer reviewed and published model of mutation and natural selection, written by Dr Tom Schneider, head of computational molecular biology and the National Cancer Institute.

Wow, really? Please leave the rhetoric at home. We all know the facts here.

This model shows that three selection pressures simultaneously slow the evolution process for each of the conditions.

The model was designed to show increases in information. It performs that task.

It shows that three selection pressures slow the evolutionary process. Well, so does reality. Yes, of course. But that has not been your argument until very recently. If your only argument is that three selection pressures (potency held constant) slow evolution, then we all agree. Yes, for one particular definition of "evolution" -- defined as increased variability in a population -- three pressures, potency held constant, slows evolution.

That, quite simply, has not been your argument through this incredibly long series of posts. You have argued that evolution is so profoundly slowed that it could never account for significant change in realistic time frames. Have you changed that argument?

While single selection conditions evolve much more rapidly. This is exactly what we see when combination therapy is used for treating HIV and TB and what results with monotherapy with the treatment of MRSA, Gonorrhea, pseudomonas and cancers as well. So it is not my model to give up and my examples work just fine, thank you.

We have never debated whether single selection conditions evolve more rapidly than three selection conditions. I don't even see the point in arguing that. Why do you bring this up? No one that I am aware of has contended the opposite position, so what is your point? Is this simply another attempt to misrepresent my position? Should I repeat all the other instances of your attempts to misrepresent my position, Dr. Alan Kleinman?

I am not accusing you of creating the model. I am accusing you of using the model for ends it was not designed. Such post-hoc analysis may be useful in science to suggest future research but is notoriously unreliable in arriving at conclusions.

Dr Schneider modeled the mathematics. The reason you haven’t seen any data is you haven’t read this thread or the Evolutionisdead forum where this discussion started. Here is some new data for you.

That isn't what I asked for. I said that you had not provided data for the mathematics of ev. As in an equation. I have seen plenty of data from individual runs. You continue to harp on the mathematics of ev. Show me the mathematics of it. Show me the equations and let's apply them to the real world and see how they work. If the mathematics of ev models all aspects of the evolutionary landscape then we may continue to discuss it as an accurate model of the evolutionary landscape. If it doesn't, then we scrap it for that purpose and admit that it did it's job -- it showed that information can increase under Darwinian conditions of mutation and natural selection.

Ichneumonwasp

21st April 2007, 10:01 AM

Mr Scott, you are confusing several principles. Those principles you are confusing are selection pressures, intensity of selection pressures and extinction. The mathematics is clear; increasing the number of selection pressures slows evolution.

I'm calling you out on this one, Dr. Kleinman. Mr. Scott did not confuse any of those issues in his post. In fact, what he did was distinguish the contributions of each. Then entire thrust of his post, Dr. Kleinman, was to show how it is you that confuses these issues. The mathematics of evolution in the real world (and, no, I am not claiming that he supplied an equation) is quite clear in Mr. Scott's post, Dr. Alan Kleinman -- the number of selection pressures is not the critical element. Rather, it is the intensity of selection pressure that serves as the critical element. As we have demonstrated to you repeatedly, the number of pressures may result in extinction, may result in profound slowing of the evolutionary process, or may result in the development of resistance. The critical determinant of the outcome is not the number of selection pressures, Dr. Kleinman, but the intensity of the total pressure.

Mr. Scott

21st April 2007, 03:30 PM

I'm calling you out on this one, Dr. Kleinman. Mr. Scott did not confuse any of those issues in his post. In fact, what he did was distinguish the contributions of each. Then entire thrust of his post, Dr. Kleinman, was to show how it is you that confuses these issues. The mathematics of evolution in the real world (and, no, I am not claiming that he supplied an equation) is quite clear in Mr. Scott's post, Dr. Alan Kleinman -- the number of selection pressures is not the critical element. Rather, it is the intensity of selection pressure that serves as the critical element. As we have demonstrated to you repeatedly, the number of pressures may result in extinction, may result in profound slowing of the evolutionary process, or may result in the development of resistance. The critical determinant of the outcome is not the number of selection pressures, Dr. Kleinman, but the intensity of the total pressure.

Indeed!

Refuting Dr. Alan Kleinman's own primary example of the impossibility of macroevolution (3-drug HIV treatments) is the article which soundly contradicts Dr. Kleinman's assertion. Please read it!

Based on the UK CHIC cohort study, it is estimated that nearly 40% of HIV-infected patients in the UK have experienced all main classes of antiretroviral drugs and of these 15% are known to have virologically failed all three classes [243].

linkola (http://www.bhiva.org/guidelines/2005/HIV/resistance.html#Patients)

So, 15% of these patients' HIV colonies have done something Kleinman asserts is mathematically impossible: macroevolved. :D

kleinman

23rd April 2007, 10:29 AM

I hope my mathematics is not too obscure. Delphi, if you have any trouble organizing your sock drawer, Paul will help you. He’s very good at the mathematics of sorting socks.Obscure? Heavens no! Your capacity for mathematical reasoning is abundantly clear. Please, show us more of these "equations." I'm sure they'll further elucidate your "insight" into this complicated subject.
Oh, Dr Schneider has documented his mathematical equations extensively which describes mutation and natural selection in his web site and his peer reviewed publications as well as posting his Pascal version of the ev computer simulation on his web site. You have pointed us to the very helpful Wikipedia reference to the mathematics of the fitness landscape. I’ll point you back to the hundreds of cases run with ev that show that as genome length is increased and realistic mutation rates are use in the model, the number of generations needed to evolve the binding sites becomes too large to support the theory of evolution. And if you look at the behavior of ev when you set two of the three selection conditions to zero, it becomes obvious why mutation and selection becomes an impossible mechanism for macroevolution. Multiple selection conditions cause the rate of convergence of the model to become profoundly slow.

This type of mathematical behavior is seen in numerous applications. Whether it is in database sorting, optimization problems or your example of sorting your sock drawer, the more conditions which you sort on, optimize on or evolve on, the slower the process goes. There are no mathematical examples where this process speeds up as the system becomes more complex. This simple conclusion can be drawn on this complicated subject.
You are making my point. You first sort your socks by color and then put them in pairs. If all the socks are a single color, you don’t have to do the work of the sort, you simply put them in pairs. With a single selection condition, a mutation is determined to be beneficial or detrimental and the ability to reproduce is known. If you have multiple selection conditions, a mutation may be beneficial for one selection condition and detrimental for another selection condition. The total selection process becomes much more complex. Ev shows how difficult this mathematics becomes for satisfying multiple selection conditions when compared to satisfying a single selection condition.The sock drawer is a silly analogy. What if you have no a priori knowledge that all the socks are the same color? Then you always have to sort them and it takes the same amount of time regardless of the number of colors.
Ok, let’s see how close we can make the sock analogy to mutation and selection. Let’s assume you have no a priori knowledge of the number of colors socks. You start by randomly choosing two socks out of the drawer. If they match, roll them together, if not, start a pile of each color. Continue this process until you finish taking all the socks from the drawer. If the socks are all of one color, your task is finished. If your socks are multiple colored, you have to take the now sorted piles of socks and roll them together. It takes more time and work to match and roll multiple different colors of socks than to match and roll a collection of single color socks. Delphi has come up with very nice, simple example, of why multiple selection conditions slow evolution.
If you think of a “perfect creature” as one which has satisfied all the selection conditions placed on it then this terminology is understandable. You just don’t like when I co-opt anything of yours.Okay, misuse the term. But then you have to address Kjkent's point that a "perfect creature" arises instantaneously with no selection pressures at all. Don't you see that you're just shooting yourself in the foot?
I’m not misusing your term “perfect creature”, I’m defining for readers of the thread exactly what this term means. This definition is perfectly consistent with Kjkent1’s point that a “perfect creature” arises instantaneously with no selection pressures at all. No selection pressure means there are no mistakes. I’m not shooting myself in the foot; I’m shooting your theory of evolution in the heart.
So what! Define any three selection conditions and evolving the conditions one at a time will occur much more quickly than trying to evolve all three selection conditions simultaneously.You can't use Ev to demonstrate this. If you turn on one pressure until the mistake count is zero, then turn it off and turn on a second pressure, you won't end up with a creature that distinguishes binding sites from other sites. You'll end up with a creature that performs a different function.
Why don’t you explain to us what the function of mutation and selection is?
There are a couple of interesting numbers in this table highlighted in red. These two cases with two selection conditions actually took more generations to evolve than the three selection condition case. However, the single selection condition cases are able to converge thousands of times more quickly than the three selection condition cases for any of the three selection conditions. It is amazing how quickly a single selection condition can evolve, even on a lengthier genome.Well then, at least you admit there is nothing special about three or more pressures. Note how even more amazing it is when there are zero selection conditions.
You are missing a point to argue. What you may have is a situation where the two selection case puts the model on a point in the fitness landscape that gives few easy paths to an optimum while adding a third selection condition enables the model to find a path to an optimum. You should not be amazed that zero selection conditions leads to zero mistakes, you have stopped performing mutation and selection under this circumstance.
What you are doing here is extrapolating the rather degraded case of a single selection pressure in Ev to cover the entire real world of evolution. You are claiming there is not a single case of evolution accommodating two selection pressures more quickly than one pressure. You are making a claim about the entire landscape of biochemistry. You have some seriously enlarged gonads there, my friend.
There are many other mathematical situations that exhibit similar behavior to what ev demonstrates. This effect of the “degraded” the behavior ev not only intuitively obvious but also is seen in many similar applications. Why don’t you give us an example of multiple selection conditions that evolve more quickly than a single selection condition? This is the extrapolation you are making.
You've defined a perfect creature as one substantially free of both missed or spurious bindings. If we turn the pressure off that selects for one of these features, then the resulting creature cannot possibly meet the original definition -- it's not the same creature.
Do you think semantics is not going to win this debate little gator? Why don’t you try some mathematics? Why don’t you try to tell us what the purpose of mutation and selection is?
OK, I bow out and really didn't contribute much. I felt a little creepy when the people I tend to trust were all-of-a-sudden called "dumbass." That's nearly like calling me a "dumbass," which takes me so far aback that I went back and a-back in this thread and realized I have no rationale for being reading this in the first place.
You haven’t read this thread very carefully, if you had you would have seen that I called the theory of evolution “dumbass”.
Since natural selection is a restatement of the 1st law of thermodynamics, what selection pressure would lead to the formation of a self replicating ligase?In case You were wondering 1st law, which states that heat and work are equivilent/interchangable (dE=dQ-dW) is identical to saying that the species best adapted for survival will survive.
If you apply the concept of the first law to natural selection, what you are saying is that the creature that can put more energy toward reproduction than other life activities will be the most successful creature by your theory of evolution. So how do you select for something that does not exist?
Well, looks like I'm not needed. Kleinman hasn't changed his argument one bit. Oh well.
In one breath, you evolutionists complain that I’m always moving the goalposts and in your next breath you complain I haven’t changed my argument one bit. Would you evolutionists make up your mind?
* Taffer wonders off to do something more productive.
Are you sure you mean “wonder” or did you mean to say “wander”? Wonder means to speculate.
The basic approach evolutionists have to ev is that if it shows something that supports your theory it is a valid, if it shows something that contradicts your theory, the model is not valid. You evolutionists are filled with prejudices and biases. But let’s see what Dr Schneider has said about his model:You may continue to conjure any straw man you wish, but here is, once again, the point:
Dr Schneider’s statements are not my conjectures. He is the author of this peer reviewed and published model of mutation and selection and he believes his model simulates reality. It appears he is going to be that last evolutionist to believe this.
You have a computer model (Dr. Schneider's model, so that you will stop harping on trivial minituae as though you are making a point). You claim this computer simulation models the reality of evolution in all its particulars. You have argued that the intersection of this simulation and reality is the behavior of HIV in the presence of triple therapy. You argued that three selection pressures in ev demonstrate that evolution cannot occur on a realistic time scale. You have been shown with the very example you cite as the intersection of reality and your computer model that what you think the model proves is incorrect. The model does not win in this situation. Reality does. And since the model was not intended to simulate this issue, I'm not the least surprised.
So you think that when ev shows that its multiple selection conditions slows evolution profoundly is “trivial minituae” and that the use of combination therapy for the treatment of HIV to slow the evolution of resistant strains of the virus is “trivial minituae”. I will take this “trivial minituae” any time over your contorted interpretation of reality as you attempt to fit these observations to your ridiculous theory.
For the nth time, I am not claiming anything about ev except that it was designed to show one thing -- that information can increase in a very simple model of mutation and selection. That is all that the model was designed to do and that is what it does.
You are in denial Ichneumonwasp. This is what Dr Schneider designed ev to do:
Variations of the program could be used to investigate how population size, genome length, number of sites, size of recognition regions, mutation rate, selective pressure, overlapping sites and other factors affect the evolution.
This sentence is from the peer reviewed and published paper Ev Evolution of Biological Information written by Dr Schneider and was published in Nucleic Acids Research.

It is abundantly clear that Dr Schneider designed his model for more than the one thing you have suggested. When you investigate the other features of his model, it shows the theory of evolution to be mathematically impossible. The number of generations required to evolve binding sites with realistic genome lengths and mutation rates becomes huge, too huge to support the theory of evolution. The reason the number of generations becomes huge is that multiple selection conditions slow the evolutionary process. The model also shows that increasing population does not markedly accelerate the evolutionary process as evolutionists like to claim.
There is no conspiracy to quell the demons of ev. Your entire argument depends on ev modelling the reality of evolution in all its particulars (not just one aspect of reality -- information gain -- as it was designed to do). When it fails to model all of evolutionary reality, reality wins, not the model. The model only goes so far as it can explain anything in the real world. It's the same with all models. The only thing I have denied is the ability of ev to do what you said it does. It simply does not model what you propose. Your own, hand-picked, example -- the only real-world example you have offered -- demonstrates this fact.
I like the way Dr Schneider argues this point:
A good simulation does not attempt to simulate everything; only the essential components are modeled. For the issue at hand, the form of the genetic code is not relevant; information measured by Shannon's method is more general than that.
With respects to my “hand-picked example”, there are numerous examples of the use of combination therapy to slow the evolution of resistant strains of microbes, HIV and TB happen to be the most obvious and there are numerous examples of the use of monotherapy and the evolution of multidrug resistant strains of microbes such as Gonorrhea, MRSA, pseudomonas being obvious examples. I suspect that a similar pattern would be seen with the use of herbicides and pesticides.
Dr Schneider’s model shows important essential relationships between genome length, selection conditions, mutation rates and population. If you take the time to study the model, you will find that genome length and the number of selection conditions are the dominant variables in the mathematics of mutation and selection.How nice. Need I remind you, again, that the model does what it was designed to do and not what you argue it does. Nothing else in this argument matters. You can argue till you're blue in the face and your fingers cramp at the keyboard that ev models important relationships between genome length, selection conditions, mutation rates, and population and we will all sit back and say "Well, yeah, that is how it is designed, so tell us something we don't know." What it doesn't model is the reality of triple therapy for HIV under all treatment conditions. If you have no real-world analogy, then the model is useless for that purpose. Dr. Schneider provided his real world analogy for what the model was created to do -- demonstrate the emergence of information under Darwinian conditions.
Again, let’s see what Dr Schneider intended for his model which was published in the peer reviewed journal, Nucleic Acids Research.
Variations of the program could be used to investigate how population size, genome length, number of sites, size of recognition regions, mutation rate, selective pressure, overlapping sites and other factors affect the evolution.
You are not going to win this debate by misinterpreting what Dr Schneider’s intentions are for his model. I happen to believe that Dr Schneider properly modeled mutation and selection. This is seen by the evolutionary consequences of the use of combination therapy for the treatment of infectious diseases.
Well Paul, you have your own model of the mathematics mutation and selection which reveals something about genome lengths and selection pressures and you dismiss it out of hand because it doesn’t agree with your world view. Dr Schneider thinks that ev models reality, you used to think this until you finally studied the behavior of the model.And that is utter BS and another prime example of your penchant for misrepresenting others' arguments. I have yet to see Paul once claim that ev does not model something of reality. He has maintained that ev did its job -- demonstrating an increase in information. That is what Dr. Schneider claims as well -- repeatedly from the quotes you have provided of him. I have yet to see anyone but you claim that ev models all aspects of the evolutionary landscape. You have specifically stated that it predicts the inability of evolution to occur on a realistic time scale if three selection pressures are applied. Your example for this in the real world -- HIV triple therapy -- when all the information about it is considered, actually shows the opposite. Unless you can show some real-world example of how this model that you think explains what occurs in the real world functions, then I'm afraid that your argument is dead in the water. Otherwise, all you have is a model that does nothing but sit in the corner.
Well, you can squirm around and try to find a way to reinterpret the many quotes of Dr Schneider but only an extremely prejudiced and biased reader will find your contorted interpretations acceptable.
What makes you think the mathematics of real-world evolution of drug resistance is any different than from the mathematics of any other mutation and selection process?First, I never said it was. The "mathematics" of real-world evolution of drug resistance shows that three selection pressures does not stop the process and does not slow it to the point that evolution cannot happen on a realistic time scale. That is what the HIV triple therapy story tells us.
However, the three selection pressure does slow evolution, that is what ev shows and that is what this example shows.
But, there is no question, whatsoever, that different mechanisms play into resistance with different organisms. I am not aware of any lateral transfer of information amongst viruses (there probably is some example of this, though), but there is clear lateral transmission of information in bacteria through plasmids. That is an entirely different mechanism from random mutation and selection and a process that dramatically speeds "evolution".
Lateral transfer of information can not and does not increase the information in the gene pool. Neither does recombination without error.
Ichneumonwasp, this is not my model of mutation and natural selection. This is the peer reviewed and published model of mutation and natural selection, written by Dr Tom Schneider, head of computational molecular biology and the National Cancer Institute.Wow, really? Please leave the rhetoric at home. We all know the facts here.
The fact is you alleged this was my model when you said the following:
Either Kleinman must give up his model or give up his example. Either way it looks bad. Give up the example and he doesn't have a real world link for the model, and it becomes a nice abstraction of uncertain provenance (at least as far as the full range of evolutionary pressure/history/etc., which is what you have said all along).
This is Dr Schneider’s model and it very nicely explains why combination therapy is useful in slowing the evolution of resistant strains when treating HIV.
This model shows that three selection pressures simultaneously slow the evolution process for each of the conditions.The model was designed to show increases in information. It performs that task.
Every time you say this, I will post Dr Schneider’s statement that appeared in his peer reviewed publication about his model. Hopefully you will get the hint and either abandon your useless argument and acknowledge what his model shows or at least come up with a more sensible argument.
Variations of the program could be used to investigate how population size, genome length, number of sites, size of recognition regions, mutation rate, selective pressure, overlapping sites and other factors affect the evolution.
It shows that three selection pressures slow the evolutionary process. Well, so does reality. Yes, of course. But that has not been your argument until very recently. If your only argument is that three selection pressures (potency held constant) slow evolution, then we all agree. Yes, for one particular definition of "evolution" -- defined as increased variability in a population -- three pressures, potency held constant, slows evolution.
If you read this thread carefully, you will see that I told Paul that the reason the generations for convergence were increasing so rapidly with increasing genome length was the effect of increased spurious binding in the nonbinding site region of the genome. It was only when I became aware that you could set weight factors to zero that I could show that multiple selection conditions was what was slowing evolution in ev.

If you think that varying the potency of selection pressures will somehow overcome the effect that multiple selection pressures slow evolution, you need to show this.
That, quite simply, has not been your argument through this incredibly long series of posts. You have argued that evolution is so profoundly slowed that it could never account for significant change in realistic time frames. Have you changed that argument?
Taffer seems to think that I haven’t changed my argument, you think I have. The only thing I have changed in my argument is to give an explanation why ev evolves so slowly with long genomes.
While single selection conditions evolve much more rapidly. This is exactly what we see when combination therapy is used for treating HIV and TB and what results with monotherapy with the treatment of MRSA, Gonorrhea, pseudomonas and cancers as well. So it is not my model to give up and my examples work just fine, thank you.We have never debated whether single selection conditions evolve more rapidly than three selection conditions. I don't even see the point in arguing that. Why do you bring this up? No one that I am aware of has contended the opposite position, so what is your point? Is this simply another attempt to misrepresent my position? Should I repeat all the other instances of your attempts to misrepresent my position, Dr. Alan Kleinman?
You are not the only evolutionist I am discussing these issues with. You sometime take quotes addressed to Paul, Mr Scott or others and assume I am addressing responses to you. Mr Scott raised the issue of super bug Gonorrhea; I have just incorporated it into the discussion. I am under no obligation to restrict my discussion with you to only what you want to talk about. If I did that, you have already attempted to reinterpret what Dr Schneider’s intent is for his model and there would be no discussion at all. You evolutionist just like to whine. You think you can frame a mathematical discussion this way but it doesn’t work.
I am not accusing you of creating the model. I am accusing you of using the model for ends it was not designed. Such post-hoc analysis may be useful in science to suggest future research but is notoriously unreliable in arriving at conclusions.
Well, here we go again:
Variations of the program could be used to investigate how population size, genome length, number of sites, size of recognition regions, mutation rate, selective pressure, overlapping sites and other factors affect the evolution.
Not only has Dr Schneider invited this type of analysis with his model publicly through his peer reviewed and published paper on his model, he also personally invited me to do this type of analysis in direct email communication with me. Ichneumonwasp, stop whining that the result of this type of analysis shows your theory is mathematically impossible. It does show how mutation and selection works and this is useful for understanding how to address the evolution of drug resistance when treating infectious diseases.
Dr Schneider modeled the mathematics. The reason you haven’t seen any data is you haven’t read this thread or the Evolutionisdead forum where this discussion started. Here is some new data for you.That isn't what I asked for. I said that you had not provided data for the mathematics of ev. As in an equation. I have seen plenty of data from individual runs. You continue to harp on the mathematics of ev. Show me the mathematics of it. Show me the equations and let's apply them to the real world and see how they work. If the mathematics of ev models all aspects of the evolutionary landscape then we may continue to discuss it as an accurate model of the evolutionary landscape. If it doesn't, then we scrap it for that purpose and admit that it did it's job -- it showed that information can increase under Darwinian conditions of mutation and natural selection.
There is no need for me to reiterate Dr Schneider’s derivations here. Read his publications and you can find the equations he used to derive his model. In addition, Dr Schneider modeled enough of the evolutionary landscape to describe the mathematics of mutation and selection. Again, Dr Schneider has well said:
A good simulation does not attempt to simulate everything; only the essential components are modeled. For the issue at hand, the form of the genetic code is not relevant; information measured by Shannon's method is more general than that.
Other mutation mechanisms will not change the mathematical fact that increasing the number of selection pressures slows the evolutionary process.

Why would an evolutionist want to scrap a peer reviewed and published model of random point mutation and natural selection?
Mr Scott, you are confusing several principles. Those principles you are confusing are selection pressures, intensity of selection pressures and extinction. The mathematics is clear; increasing the number of selection pressures slows evolution.I'm calling you out on this one, Dr. Kleinman. Mr. Scott did not confuse any of those issues in his post. In fact, what he did was distinguish the contributions of each. Then entire thrust of his post, Dr. Kleinman, was to show how it is you that confuses these issues. The mathematics of evolution in the real world (and, no, I am not claiming that he supplied an equation) is quite clear in Mr. Scott's post, Dr. Alan Kleinman -- the number of selection pressures is not the critical element. Rather, it is the intensity of selection pressure that serves as the critical element. As we have demonstrated to you repeatedly, the number of pressures may result in extinction, may result in profound slowing of the evolutionary process, or may result in the development of resistance. The critical determinant of the outcome is not the number of selection pressures, Dr. Kleinman, but the intensity of the total pressure.
You aren’t going to accusing me of misrepresenting what you have said, are you?

You have just focused the argument when you said that “the number of selection pressures in not the critical element”. Ev shows that the number of selection pressures is critical in slowing the evolutionary process. What are the critical parameters in the mutation and selection process of evolution? As it stands now, the mathematics of ev shows that genome length and the number of selection conditions are the dominant parameters in the mutation and selection process.
So, 15% of these patients' HIV colonies have done something Kleinman asserts is mathematically impossible: macroevolved.
Mr Scott, the James Randi Educational Forum pussy cat, this is not what I have asserted. What I have asserted is that multiple selection conditions slow the evolutionary process and the use of combination therapy for the treatment of HIV nicely demonstrates this. In addition, this is not a demonstration of macroevolution. What gene has evolved from the beginning? What new function has evolved for these already existing genes?

kjkent1

23rd April 2007, 12:34 PM

Do you think semantics is not going to win this debate little gator? Why don’t you try some mathematics?I'd tell you to screw off, but that would indicate that you'd succeeded in annoying me.

I'm one of the only persons on this thread who has actually done any experiments using ev to back my position. As for mathematics, you haven't produced any -- you just fall back on "Dr Schneider did the math already." Well, you've extrapolated ev to do everything but wash dishes at this point, so don't bother suggesting that I do anything, at least until you've actually done something yourself, other than cry the same unending river of nonsense.
Why don’t you try to tell us what the purpose of mutation and selection is?There's no purpose to mutation and selection. "Life is a process of matter that occurs under suitable conditions and evolves while those conditions persist." -- Phillip Wylie.

It has been scientifically established that all independent life forms have a genetic sequence wherein Rseq ~ Rfreq. So, if you mess with ev and produce a perfect creature that doesn't exhibit this state, or that doesn't continue to drift towards that state, then what you've produced is crapola. You may as well pour sand on the floor and call it a sand castle.

Ichneumonwasp

23rd April 2007, 12:56 PM

You aren’t going to accusing me of misrepresenting what you have said, are you?

As should be immediately obvious to anyone who can read I was accusing you of misrepresenting Mr. Scott's position, Dr. Alan Kleinman, since that is precisely what you did. Since you did not answer any of the charges, I assume that you agree to have misrepresented his position as well?

You have already admitted that you misrepresented my position, Dr. Alan Kleinman.

You seem to have a penchant for misrepresentation.

As it stands now, the mathematics of ev shows that genome length and the number of selection conditions are the dominant parameters in the mutation and selection process.

There is no reason to repeat the virtual lack of information in that long post, Dr. Kleinman. So, tell me now, since you have not done so in the past when I have asked, what is the equation that models the dominant parameters in the mutation and selection process? Tell me this mathematics that you continually claim so that we can all examine it and decide if it fits with the reality we see around us. Tell me this equation for evolution, Dr. Kleinman.

kleinman

23rd April 2007, 01:34 PM

Do you think semantics is not going to win this debate little gator? Why don’t you try some mathematics?I'd tell you to screw off, but that would indicate that you'd succeeded in annoying me.
Oh, go ahead and say it. We all know how annoyed all you evolutionists are that anyone would dare challenge your belief system.
I'm one of the only persons on this thread who has actually done any experiments using ev to back my position. As for mathematics, you haven't produced any -- you just fall back on "Dr Schneider did the math already." Well, you've extrapolated ev to do everything but wash dishes at this point, so don't bother suggesting that I do anything, at least until you've actually done something yourself, other than cry the same unending river of nonsense.
Really? Paul did you read this? Myriad, did you read this? kjkent1 is the only one who has actually done experiments using ev to back his position. You need to read this thread more carefully and the thread on the Evolutionisdead forum and then you wouldn’t make statements like this. But why should I expect an evolutionist to read anything carefully?
Why don’t you try to tell us what the purpose of mutation and selection is?There's no purpose to mutation and selection. "Life is a process of matter that occurs under suitable conditions and evolves while those conditions persist." -- Phillip Wylie.
So mutation and selection has no relationship to fitness and reproduction?
It has been scientifically established that all independent life forms have a genetic sequence wherein Rseq ~ Rfreq. So, if you mess with ev and produce a perfect creature that doesn't exhibit this state, or that doesn't continue to drift towards that state, then what you've produced is crapola. You may as well pour sand on the floor and call it a sand castle.
Is that what you’ve proven with ev? So ev showing that multiple selection conditions slows the evolutionary process has nothing to do with reality?
You aren’t going to accusing me of misrepresenting what you have said, are you?As should be immediately obvious to anyone who can read I was accusing you of misrepresenting Mr. Scott's position, Dr. Alan Kleinman, since that is precisely what you did. Since you did not answer any of the charges, I assume that you agree to have misrepresented his position as well?
Do you evolutionists ever quit whining?
You have already admitted that you misrepresented my position, Dr. Alan Kleinman.
So let’s see, what is your position now? You have finally come to the conclusion that multiple selection conditions slow evolution however you don’t think this is a dominant parameter in the mathematics. You’ve got it half right now.
As it stands now, the mathematics of ev shows that genome length and the number of selection conditions are the dominant parameters in the mutation and selection process.There is no reason to repeat the virtual lack of information in that long post, Dr. Kleinman. So, tell me now, since you have not done so in the past when I have asked, what is the equation that models the dominant parameters in the mutation and selection process? Tell me this mathematics that you continually claim so that we can all examine it and decide if it fits with the reality we see around us. Tell me this equation for evolution, Dr. Kleinman.
You evolutionists whine if I don’t respond to your posts and now you whine when I do respond to your posts. Dr Schneider has clearly explained how he intended to use ev to study the parameters in the mathematics of mutation and selection. When you do study these parameters, it is clear that genome length and the number of selection conditions dominate the mathematics.

Ichneumonwasp, since you seem to have difficulty in grasping the fact that multiple selection conditions slows and dominates the mathematics of evolution as demonstrated by the real cases of the treatment of infectious diseases with combination therapy, here some other examples of how multiple selection conditions slow evolution.

Here is an example from Wikipedia:
Tankmixing pesticides is the combination of two or more pesticides with different modes of action. This practice may improve individual pesticide application results in addition to the benefit of delaying the onset of or mitigating existing pest resistance.
You can find this quote at http://en.wikipedia.org/wiki/Pesticide (http://en.wikipedia.org/wiki/Pesticide)

How about for herbicides, does the use of multiple herbicides slow evolution?
Here is something from Iowa State:
The evolution of herbicide resistance within a weed population is based on selection pressure. The more frequently a herbicide is used, the more pressure placed on a weed population, and the sooner resistance will appear at a troublesome level in the population. Using alternative modes of action can reduce the potential for selecting resistant weeds by placing different selection pressures on weed populations. In a system relying only on glyphosate, a weed possessing a trait allowing it to survive glyphosate will rapidly increase in frequency. But if a second herbicide is used with glyphosate, this alternative herbicide may kill the weed with the glyphosate resistant trait and prevent it from increasing within the weed population. Theoretically this approach is sound and can reduce the potential for herbicide resistance.
You can find this quote at http://www.weeds.iastate.edu/mgmt/2004/combination.shtml (http://www.weeds.iastate.edu/mgmt/2004/combination.shtml)

How about rodenticides, does the use of multiple rodenticides slow evolution?
Here is something from German researchers:
Coumatetralyl (Racumin ) has been known since 1957 as a multiple dose anticoagulant and has been used successfully over many decades. In the seventies and especially the eighties, rats developed an increased resistance to anticoagulants in certain regions of Central Europe. Also, the addition of vitamin K to animal feed (especially to chicken feed) has reduced the efficacy against rats and mice in farm buildings. Combinations of anticoagulants with different types of vitamin D are generally described to increase the efficacy of action against rodents. It was found that especially the combination of coumatetralyl with cholecalciferol (vitamin D3) could overcome the above mentioned problems. Cholecalciferol causes hypercalcemia and, therefore, has a different mode of action compared to anticoagulants. The combination of these active ingredients leads to an obvious increase in efficacy against rodents, even under difficult conditions. The formulation with optimal rodenticidal efficacy contains 0.04 % coumatetralyl and 0.025 % cholecalciferol mixed in rolled oats.
You can find this paper at http://72.14.253.104/search?q=cache:rHo5amSD9IAJ:digitalcommons.unl.edu/cgi/viewcontent.cgi%3Farticle%3D1047%26context%3Dvpc16 +combination+rodenticide+resistance&hl=en&ct=clnk&cd=4&gl=us (http://72.14.253.104/search?q=cache:rHo5amSD9IAJ:digitalcommons.unl.edu/cgi/viewcontent.cgi%3Farticle%3D1047%26context%3Dvpc16 +combination+rodenticide+resistance&hl=en&ct=clnk&cd=4&gl=us)

Multiple selection pressures slow evolution in all types of life forms and all types of circumstances. This is what ev reveals and this is what is seen in reality. This is how the mathematics of mutation and selection works. Multiple selection conditions slow the evolutionary process. If the potency of the selection pressures is sufficient, you get extinction. If the potency of the selection pressures is not sufficient to cause extinction, the evolutionary process is slowed.

So Paul, you proposed that the appearance of oxygen is the selection pressure that led to the evolution of hemoglobin gene. Is that a weak or potent selection pressure? Did the genes which code for the enzymes of the Krebs cycle evolve at the same time? When did the insulin gene evolve? How about all the genes which code for structural proteins? Did all this evolution you proposed that occurred evolve simultaneously? Or did all the genes required for living creatures come about one at a time?

Mutation and natural selection can not and does not do what you evolutionists allege. Ev shows how mutation and natural selection works and it can not accomplish a macroevolutionary process. Your theory is mathematically impossible.