Annoying creationists

[kleinman]

Annoying Creationists

Perhaps if I post this reference so kindly given by Delphi then you might understand why mutation and selection can not do what you assert.
http://en.wikipedia.org/wiki/Fitness_landscape

Apart from the field of evolutionary biology, the concept of a fitness landscape has also gained importance in evolutionary optimization methods such as genetic algorithms or evolutionary strategies. In evolutionary optimization, one tries to solve real-world problems (e.g., engineering or 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 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-valued function 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 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).

The concept of a scalar valued fitness function f(s) also corresponds to the concept of a potential or energy function in physics. The two concepts only differ in that physicists traditionally think in terms of minimizing the potential function, while biologists prefer the notion that fitness is being maximized. Therefore, multiplying a potential function by -1 turns it into a fitness function, and vice versa.

You are trying to assert that hundreds, perhaps thousands of genes can be transformed in order to evolve a lizard population into a bird population. There is no mathematical or empirical basis for this type of speculation. Mutation and selection can only transform a tiny number of genes subject to selection conditions. This is why three drug therapy combination works for the treatment of HIV despite the fact that HIV is a very rapidly reproducing virus with huge populations and high mutation rates. Despite this, effective three drug combination therapy profoundly slow the ability of this virus to find a trajectory on the fitness landscape to optimize fitness against three selection conditions. If you were to use the same three drugs sequentially, the population could easily evolve to these selection conditions in weeks.

When you try to extrapolate this mathematical behavior to a slowly reproducing lizard population with much small population size than HIV and much smaller mutation rates, you can not transform these huge lizard genomes into bird genomes. It is mathematically impossible. The mutation and selection sorting/optimization process simply does not work this way. The concept of common descent is mathematically and empirically irrational and the persistent evolutionist assertion that mutation and selection does to this contributes to the premature death of millions of people with diseases subject to mutation and selection. Here is another example of how the mutation and selection sorting/optimization process actually works. http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15766932

The 2362 strain of Bacillus sphaericus (Bs) Neide is a highly mosquitocidal bacterium used in commercial bacterial larvicides primarily to control mosquitoes of the genus Culex. Unfortunately, Bs is at high risk for selecting resistance in mosquito populations, because its binary toxin apparently only binds to a single receptor type on midgut microvilli. A potential key strategy for delaying resistance to insecticidal proteins is to use mixtures of toxins that act at different targets within the insect, especially mixtures that interact synergistically. We tested this hypothesis for delaying the phenotypic expression of resistance by exposing Culex quinquefasciatus Say larvae to Bs alone or in combination with Cyt1A from Bacillus thuringiensis subsp. israelensis. Two laboratory lines of Cx. quinquefasciatus, one sensitive to Bs and the other containing Bs resistance alleles, were subjected to intensive selection pressure for 20 generations with either Bs 2362 or a 3:1 mixture of Bs 2362+Cyt1A. At the end of the study, the sensitive line had evolved >1000-fold resistance when selected with Bs alone, whereas the parallel line selected with Bs+Cyt1A exhibited only low resistance toward this mixture (RR95, 1.4). Similar results were observed in the lines containing Bs resistance alleles. Both lines selected with Bs+Cyt1A exhibited substantial resistance to Bs in the absence of Cyt1A. Although selection with Bs+Cyt1A did not prevent the underlying evolution of resistance to Bs, these results suggest that a mixture of Bs with other endotoxins, particularly one like Bs+Cyt1A in which the components interact synergistically, will provide longer lasting and more effective mosquito control than Bs alone.

Examples like this demonstrate empirically what Dr Schneider’s model shows mathematically and what the Wikipedia reference to fitness landscape are describing with single versus multiple conditions and the ability of a population to find a trajectory on the fitness landscape and to find an optima. It is the number of selection conditions and the number of genes targeted which dominates the mathematical and empirical behavior of the mutation and selection sorting/optimization process.

 

[X]

Forgive me if I haven't read every post, but it seems to me that Klienman keeps repeating nonsense about how his math is superior to ours, coupled with random quotes from various sources (several of which seem to support evilution) instead of actuall responding to questions.

Come to think of it, does he even have an argument besides "You evolutionists just don't get it."?

 

[Shalamar]

Forgive me if I haven't read every post, but it seems to me that Klienman keeps repeating nonsense about how his math is superior to ours, coupled with random quotes from various sources (several of which seem to support evilution) instead of actuall responding to questions.

Come to think of it, does he even have an argument besides "You evolutionists just don't get it."?

Nope. He doesn't get it. At least he's stopped calling people names because they trust in science. Mr. Kleinman doesn't like science. Makes people think!

 

[coops]

So is this your definition of micro-evolution Kleinman?

Do you state that micro-evolution is when a single gene evolves in response to a single selection pressure?

Are you also then stating that anything other than this is macro-evolution and hence impossible?

Would you agree with the following statement ' 'it is impossible for more than a single gene to simultaneously evolve in any organism as this would constitute macro-evolution.'

Yet another bump for Kleinman.

Kleinman, if you have no intention of ever answering my questions please just let me know. Just a simple 'Coops, i have no interest in discussing specifics with you.' and i'll stop bugging you to explain yourself.

Or better yet, you could answer my question.

Up to you really.


PS - perhaps someone could re-post my message. maybe Kleinman has put me on ignore by accident and can't see my question. Thats the only logical reason that i can think of for his continued refusal to answer.

Thanks

 

[coops]

double post

 

[kleinman]

Annoying Creationists

I don’t have anyone on ignore and it is not my mathematical model. It is Dr Schneider (head of computational molecular biology at the National Cancer Institute) peer reviewed and published mathematical model of random point mutations and natural selection. The online version of the model was written by Paul C. Anagnostopoulos, a moderator on this forum. What Dr Schneider’s mathematical model demonstrates is the fundamental behavior of the mutation and selection sorting/optimization process. What Dr Schneider’s model shows is that the number of selection conditions dominates the rate at which selection conditions can be satisfied. Dr Schneider’s model which has three selection conditions is profoundly slow at evolving all three conditions on all but the tiniest genomes. On the other hand, setting any two of the three selection conditions in Dr Schneider’s model to zero, the remaining selection condition evolves in a trivially small number of generations. This mathematical behavior is reflected in the real behavior of mutation and selection as demonstrated by the hundreds of real examples I have posted and will continue to post. The mutation and selection sorting/optimization process can only rapidly evolve a tiny number of selection conditions simultaneously. This is the mathematical and empirical fact of life you evolutionists just can not fathom. This is why the theory of evolution is mathematically impossible. Because you evolutionists dominate the field of biology with your mathematically irrational and illogical concept of the mutation and selection sorting/optimization process; you mislead virtually everyone who must deal with real problems of mutation and selection. It is this obfuscation of the mutation and selection sorting/optimization process that contributes to the death of millions of people suffering from disease subject to mutation and selection. Rather than properly teaching the basic science and mathematics of the mutation and selection sorting/optimization process, you mislead naïve school children and virtually everyone else with your irrational and illogical speculations and assertions. The mutation and selection sorting/optimization process does not work the way you assert. It is mathematically and empirically impossible.

 

[coops]

I don’t have anyone on ignore ....

If you don't have me on ignore could you please answer my question Kleinman?

I've already posted it enough times today I don't think it necessary to add it to the post as well.

If you can't or won't answer my simple question in a direct manner could you at least explain WHY you can't or won't?

 

[kleinman]

The answer to your question is that the mutation and selection sorting/optimization process is dominated mathematically and empirically by the number of selection (optimization) conditions and genes targeted by these selection conditions. If you have a single selection pressure targeting a single gene, this sorting/optimization process can be done fairly quickly as seen when monotherapy was tried with HIV and the fairly rapid evolution of resistance to bacteria when single drug therapy is used with these microbes. As soon as you add a second selection pressure, the mutation and selection sorting/optimization process is profoundly slowed. Each additional selection pressure slows the evolutionary process much, much, much more. That is how the mutation and selection sorting/optimization process works mathematically and that is how it works empirically. You can not transform entire genomes by the mutation and selection sorting/optimization process. It is mathematically and empirically irrational to think that you can. Here are more empirical examples of how the mutation and selection sorting/optimization process actually works.
http://www3.interscience.wiley.com/cgi-bin/abstract/112607405/ABSTRACT?CRETRY=1&SRETRY=0

The following possible methods of minimising the risks of resistance are considered: (a) adjustment of the dosage and frequency of spraying so that resistance genes are effectively recessive; (b) detection and eradication of new foci of resistance before they have a chance to spread; (c) spraying a mosaic of unrelated insecticides with the intention that immigrants from one sector of the mosaic to another will dilute the frequency of resistance genes; (d) re-introduction of susceptibility genes into the progeny of wild females by the release of heterozygous males with resistance genes translocated on to their Y chromosome so that they are protected from insecticidal killing but will pass susceptibility to their female progeny; (e) replacement of a resistant by a susceptible population by means of a negatively heterotic system such as bidirectional cytoplasmic incompatibility. A plausible case can be made for each of these methods based on theoretical models and appropriate assumptions. However, an assessment of whether any of them will really beof any value depends on the answers to certain questions in the field. Therefore field projects have been initiated on Anopheles culicifacies in Sri Lanka and Pakistan, Culex quinquefasciatus in Tanzania and Anopheles arabiensis in Sudan. The results so far are summarized.

http://www.dcp2.org/pubs/DCP/55/Section/8167

Some interventions, such as the use of drug combinations, reduce the likelihood that resistance will emerge, whereas other interventions, such as improvements in drug prescribing and patient compliance with dosing, reduce the likelihood that a resistant pathogen will survive and proliferate.

and

The appropriate choice of drug treatment is an important step in delaying the evolution of drug resistance. Drug combinations that include drugs with different targets were first used in the treatment of tuberculosis and have now become routine practice in the treatment of cancer and HIV/AIDS. Combinations of artemisinin and its derivatives with other antimalarials, notably mefloquine, have accelerated recoveries, increased cure rates, and reduced transmissibility. In the refugee camps on the western border of Thailand, where most of the recent studies with artemisinin combinations have been conducted, the use of combinations delayed the development of resistance and reduced the incidence of disease (Nosten and others 2000). The rationale behind drug combinations is that, if resistance results from spontaneous genetic mutations, the chance that a parasite will emerge that is simultaneously resistant to two drugs with unrelated modes of action (that is, drug targets) is the mathematical product of the individual parasite mutation frequencies multiplied by the total number of parasites exposed to the drugs (White 1998, 1999). Combinations, therefore, reduce enormously the probability that a resistant mutant will arise. Sequential deployment of the drugs is much less effective, because it does not exploit the multiplicative reduction in selection risk.

and

In the context of antibiotics, combinations have typically been used to broaden the spectrum of antimicrobial coverage rather than to reduce the likelihood of the emergence of resistance. With the development of new penicillins and cephalosporins with broader spectra of activity a decade ago, most serious infections have been treated with monotherapy. The use of combination therapy to preserve new classes of antibiotics from the emergence of resistance at a societal level may be rational, but it has not been implemented because of cost concerns and the potential for enhanced toxicity associated with the use of more agents than necessary to effect a cure in an individual patient.

There are no empirical examples of the mutation and selection sorting/optimization process which shows that it works any other way. Combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process. The failure of evolutionists to understand and teach the basic science and mathematics of this process properly contributes to the premature death of millions of people suffering from diseases subject to mutation and selection. The simple answer to your question is that you can not evolve entire genomes by the mutation and selection sorting/optimization process. You do not have the selection conditions and if you did, you can barely evolve a population of HIV to three selection conditions despite its huge population, rapid reproductive rate and high mutation rate. You evolutionists need to learn the basic science and mathematics of the mutation and selection sorting/optimization process. Study Dr Schneider’s peer reviewed and published mathematical model of the process, then you will realize why your theory is mathematically and empirically irrational and illogical.

 

[coops]

So is this your definition of micro-evolution Kleinman?

Do you state that micro-evolution is when a single gene evolves in response to a single selection pressure?

Are you also then stating that anything other than this is macro-evolution and hence impossible?

Would you agree with the following statement ' 'it is impossible for more than a single gene to simultaneously evolve in any organism as this would constitute macro-evolution.'

Kleinman, does this earlier post of mine accurately summarise your views on what is and is not possible within evolution?

I'm not sure if its intentional or not, but your previous post didn't specifically answer my question.

If my summary of your position is wrong in any way could you please let me know the specifics of where i have misinterpreted you?

Thanks

 

[kleinman]

Annoying Creationists

The answer to your question is that the mutation and selection sorting/optimization process is dominated mathematically and empirically by the number of selection (optimization) conditions and genes targeted by these selection conditions. If you have a single selection pressure targeting a single gene, this sorting/optimization process can be done fairly quickly as seen when monotherapy was tried with HIV and the fairly rapid evolution of resistance to bacteria when single drug therapy is used with these microbes. As soon as you add a second selection pressure, the mutation and selection sorting/optimization process is profoundly slowed. Each additional selection pressure slows the evolutionary process much, much, much more. That is how the mutation and selection sorting/optimization process works mathematically and that is how it works empirically. You can not transform entire genomes by the mutation and selection sorting/optimization process. It is mathematically and empirically irrational to think that you can. Here are more empirical examples of how the mutation and selection sorting/optimization process actually works.
http://www3.interscience.wiley.com/cgi-bin/abstract/112607405/ABSTRACT?CRETRY=1&SRETRY=0

The following possible methods of minimising the risks of resistance are considered: (a) adjustment of the dosage and frequency of spraying so that resistance genes are effectively recessive; (b) detection and eradication of new foci of resistance before they have a chance to spread; (c) spraying a mosaic of unrelated insecticides with the intention that immigrants from one sector of the mosaic to another will dilute the frequency of resistance genes; (d) re-introduction of susceptibility genes into the progeny of wild females by the release of heterozygous males with resistance genes translocated on to their Y chromosome so that they are protected from insecticidal killing but will pass susceptibility to their female progeny; (e) replacement of a resistant by a susceptible population by means of a negatively heterotic system such as bidirectional cytoplasmic incompatibility. A plausible case can be made for each of these methods based on theoretical models and appropriate assumptions. However, an assessment of whether any of them will really beof any value depends on the answers to certain questions in the field. Therefore field projects have been initiated on Anopheles culicifacies in Sri Lanka and Pakistan, Culex quinquefasciatus in Tanzania and Anopheles arabiensis in Sudan. The results so far are summarized.

http://www.dcp2.org/pubs/DCP/55/Section/8167

Some interventions, such as the use of drug combinations, reduce the likelihood that resistance will emerge, whereas other interventions, such as improvements in drug prescribing and patient compliance with dosing, reduce the likelihood that a resistant pathogen will survive and proliferate.

and

The appropriate choice of drug treatment is an important step in delaying the evolution of drug resistance. Drug combinations that include drugs with different targets were first used in the treatment of tuberculosis and have now become routine practice in the treatment of cancer and HIV/AIDS. Combinations of artemisinin and its derivatives with other antimalarials, notably mefloquine, have accelerated recoveries, increased cure rates, and reduced transmissibility. In the refugee camps on the western border of Thailand, where most of the recent studies with artemisinin combinations have been conducted, the use of combinations delayed the development of resistance and reduced the incidence of disease (Nosten and others 2000). The rationale behind drug combinations is that, if resistance results from spontaneous genetic mutations, the chance that a parasite will emerge that is simultaneously resistant to two drugs with unrelated modes of action (that is, drug targets) is the mathematical product of the individual parasite mutation frequencies multiplied by the total number of parasites exposed to the drugs (White 1998, 1999). Combinations, therefore, reduce enormously the probability that a resistant mutant will arise. Sequential deployment of the drugs is much less effective, because it does not exploit the multiplicative reduction in selection risk.

and

In the context of antibiotics, combinations have typically been used to broaden the spectrum of antimicrobial coverage rather than to reduce the likelihood of the emergence of resistance. With the development of new penicillins and cephalosporins with broader spectra of activity a decade ago, most serious infections have been treated with monotherapy. The use of combination therapy to preserve new classes of antibiotics from the emergence of resistance at a societal level may be rational, but it has not been implemented because of cost concerns and the potential for enhanced toxicity associated with the use of more agents than necessary to effect a cure in an individual patient.

There are no empirical examples of the mutation and selection sorting/optimization process which shows that it works any other way. Combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process. The failure of evolutionists to understand and teach the basic science and mathematics of this process properly contributes to the premature death of millions of people suffering from diseases subject to mutation and selection. The simple answer to your question is that you can not evolve entire genomes by the mutation and selection sorting/optimization process. You do not have the selection conditions and if you did, you can barely evolve a population of HIV to three selection conditions despite its huge population, rapid reproductive rate and high mutation rate. You evolutionists need to learn the basic science and mathematics of the mutation and selection sorting/optimization process. Study Dr Schneider’s peer reviewed and published mathematical model of the process, then you will realize why your theory is mathematically and empirically irrational and illogical.

 

[coops]

The answer to your question is >deleted as duplicate post<.

Can you give a yes or no answer to my question Kleinman?

I gave a summary of my understanding of your position. Can you respond by simply stating either -
a) yes, your summary is correct.
b) no, your summary is incorrect.

If the answer is b then please feel free to correct my statement accordingly.

Your above duplicate post really doesnt make it clear to me where you specifically draw the line between micro-evolution and macro-evolution.

 

[rocketdodger]

I really think this man is insane.

 

[Belz...]

Evolutionists have a hard time understanding

Creationists have a hard time breathing, let alone thinking.

If you evolutionists didn’t have so much difficulty with the mathematics of the mutation and selection sorting/optimization process, you would realize that microevolution never becomes macroevolution.

That's not even logical.

Hey, Klein. When did you decide to stop answering posts and instead focus on spamming this thread ?

 

[Mr. Scott]

Dr. Kleinman, why do you believe the time it takes for a computer program to sort one generation of genomes in Ev corresponds with the time it takes nature to "sort" genomes in a generation by natural selection?

 

[CurtC]

I really think this man is insane.

I just popped into this thread for the first time in a long time, and I'm not convinced it's a real person. It's like a spambot.

 

[CurtC]

I really think this man is insane.

I just popped into this thread for the first time in a long time, and I'm not convinced it's a real person. It's like a spambot.

 

[Nogbad]

I don't think the Doc is a spambot but I am considering the posibility he has written a programme so he can type mutation and selection sorting/optimization by depressing just two keys.

 

[Belz...]

Actually, he's probably got entire paragraphs pre-programmed into macros...

 

[m_huber]

So this man, who denies that fossils are valid evidence of evolution, who believes that entering an invalid set of numbers into a computer program modeling the interior of a human body debunks evolution, who thinks that microevolution and macroevolution are separate enough entities to claim that only one happens, but not the other, who answers no specific refutations of his arguments, who chooses to laugh at anyone who disagrees with him (ignoring any opportunity to learn from them), this man is a medical doctor?

 

[joobz]

Remember kleinman said that the evolution of nylon eating bacteria isn't proof of evolution because

17.) nylon-eating bacteria-a polymerase evolves into a polymerase, what’s your point?

Yes, his argument is that it doesn't count because an enzyme evolves into another enzyme.