Annoying creationists

[Mr. Scott]

The topic of this thread is the mathematics of mutation and selection and the empirical evidence which supports this mathematics.

This is another lie. The topic of this thread (check the title) is "annoying creationists" which means, people who are creationist and are annoying. He did not start the thread, so he has no right to police the topic. Don't let Kleinman take control of the conversation.

 

[kleinman]

Annoying Creationists

You still point to that study, kleinman, and says that disproves evolution. You say the math there disproves it. Can you point me to what page and what paragraph specifically disproves evolution? I'm not seeing it.

Sure, I’ll help you with this Mister Earl. Let’s start with what Dr Schneider wrote in his publication.
http://nar.oxfordjournals.org/cgi/content/full/28/14/2794

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. Another use of the program may include understanding the sources and effects of skewed genomic composition (4,7,30,31). However, this could be caused by mutation rates, and/or it could be the result of some kind(s) of evolutionary pressure that we don’t understand, so how one implements the skew may well affect or bias the results.

Not only did Dr Schneider publish how to use ev to study how evolution works, Dr Schneider personally invited me to do this with his model in extensive discussions I had with him several years ago.

I did what Dr Schneider invited me to do; I did a systematic study of his computer model. The way you study a complex computer simulation like this is to do a parametric study. This is done by systematically varying the parameters in the model and tests how it affects the results. The results are posted earlier and throughout this thread. By far, the most dominant parameter in this sorting algorithm is the number of selection conditions.

However, once you study the mathematics of the mutation and selection sorting/optimization process, you will learn that the dominant parameter is the number of selection condition. These sorting algorithms (both mathematical and empirical) only are able to sort mutations quickly with single selection conditions targeted at single genes. As soon as you have multiple simultaneous selection pressures targeting different genes, the sorting process is profoundly slowed.

The paper itself admits that all conditions faced by biological critters in evolution weren't used in the simulation. This isn't important?

It is only of very minor importance. Dr Schneider modeled all the essential variables to get a reasonable simulation of the mutation and selection sorting/optimization process. The gaps in the model are filled by empirical evidence. HIV, Malaria and other microbes to recombination and other mechanisms of genome alteration but that does not change the basic fact that combination selection conditions profoundly impair these populations to evolve to these simultaneous selection conditions. These other factors are dominated by the number of selection conditions imposed on the population. This is the empirical fact of life of the mutation and selection sorting/optimization process. The mutation and selection sorting/optimization process can only sort quickly for a single selection condition targeted at a single gene. As soon as you introduce more selection conditions targeted at other genes, the evolutionary process is confounded.

Mutation and selection can not sort for large numbers of sorting conditions simultaneously.

Where is this stated in the paper?

It is not in his paper since Dr Schneider presented only a single case from his model with an unrealistically small genome. Dr Schneider knows that his model would take huge numbers of generations to evolve his selection conditions on any realistic length genome. This he has posted on his web site. I have posted this quote earlier, if you want I’ll post it again.

This is why combination therapy is used for the treatment of HIV, TB, HBV, HCV, cancer and numerous other conditions subject to mutation and selection. The use of monotherapy has led to MRSA, multi-drug resistant TB and gonorrhea and numerous other life forms subjected to this type of treatment.

That's evolution for you. Kill off the weak, and the strong breed and raise strong critters.

First of all, there are no therapies which kill viruses (other than immunization), you can only impair the reproduction of the virus. You are correct though otherwise and when you apply mathematical precision to this process, it shows how profoundly slow the mutation and selection sorting/optimization process is for all but a single selection condition targeting a single gene. As soon as you complicate the sorting process with additional selection conditions, the process is quickly drawn to a standstill.

This is why the theory of evolution is mathematically and empirically impossible.

I don't see a mathematical proof anywhere in that paper stating this. Is this your own interpretation? If not, what page can I find that proof on?

Oh, it’s there, do the studies that Dr Schneider suggested in his paper and you will see how all these parameters affect the evolutionary process.

It is not the drug companies which are failing millions; it is the illogical and irrational evolutionist view of how the mutation and selection sorting/optimization process works which is failing millions. Drug companies and medical researchers confronted with the deadly consequences of diseases subject to the principles on mutation and selection are forced into investigating and using combination therapies to stop the evolutionary process. If evolutionists had properly elucidated how mutation and selection actually works, this would have been done 50 years ago. Instead, evolutionists have successfully stifled the understanding of this process. Evolutionist have interfered with the advancement of science.

Call me picky but I thought combination therapy was used to good effect on TB more than 50 years ago. I recall no-one objecting because it ran counter to the notion of evolution. Indeed I cannot see why three hammers to the head at the same time rather one would run counter to evolution. The purpose of the medication is to ensure the virus is not fit enough to survive.

Of course there was understanding about this process 50 years ago. I posted a Nobel laureate speech which addressed this issue 50 years ago. It should have been clear 50 years ago that targeted monotherapy should never be used on a rapidly reproducing population. Instead it takes 5 years of monotherapy on HIV to relearn the lesson and they make the man who relearns this Time Magazine Man of the Year. How many more times do we have to relearn this lesson? If evolutionists have their way, this will go on forever.

 

[kjkent1]

What legal beagle does understand is that selection pressures do exactly as he describes above. Selection pressures impair populations from reproducing either by killing members of the population or preventing members from passing on their genetic information to the next generation. This is the fundamental basis for the mutation and selection process and is the core of the theory of evolution. What legal beagle does not understand is that if populations are forced to attain multiple mutations simultaneously is that they can not make that “immediate leap to the same evolutionary point that would have been arrived at, had the various therapies been sequentially applied”. It is mathematically and empirically much, much more difficult for populations to evolve to simultaneous selection pressures. See the citation below from an interview with David Ho, the originator of combination therapy for HIV.

What the kleinman does not understand is that in nature, the variability of selective pressures in the environment routinely provides evolutionary opportunities, which are not present in the controlled experiments which kleinman routinely cites.

Were this not true, every disease would be cured and every creature rendered extinct.

Try to imagine a world where every organism is constantly bombarded by multiple high-levels of toxicity. Does this scenario appear anywhere in nature? Even in volcanic heat vents, bacteria have managed to find a niche and survive. Could this occur if the vents were always spewing out hot lava and methane? Doubtful. But, the vents are intermittent, sometimes quiet for decades -- even centuries. They may continue to leak toxic gases, but not always melted stone.

Kleinman's theory is based on a ridiculous premise of that all nature is entirely composed of environments which are absolutely fixed and subject to extreme selective pressures from multiple sources. He cites short-term experiments with heavy and constant multiple selective pressures and makes the ridiculous claim that this somehow mirrors the natural world.

Fortunately, the real world is not so unforgiving. Predictably, in the environments that are more forgiving there is more variety of life. And where the environments are incredibly harsh, there is less. Death Valley has less life than the Amazon Basin. Makes perfect sense.

Now were the REVERSE true, then kleinman might be on to something which would falsify evolution. But, as it is, the only thing that kleinman is falsifying is his diploma credentials.

 

[Mr. Scott]

Dr. Kleinman, have you ever used a strategy of drug therapy on any of your patients that was based on your own view of adaptive resistance, instead of a more accepted strategy because you believed the more accepted strategy was based on Darwinian evolution or conflicted with creationist, religious, or biblical concepts?

 

[Mister Earl]

Oh, it’s there, do the studies that Dr Schneider suggested in his paper and you will see how all these parameters affect the evolutionary process.

I've got a biological simulation program running at home. It started out with a two-dimentional stick and evolved it, through mutation and selection, into giant stick pyramids. I skewed the fitness requirement to give higher values for organism height. After I would up with those simulated organisms, I changed the fitness requirements towards mobility and lifespan. I gave them the ability to consume each other, and to generate slightly mutated offspring if a specific organism had eaten enough competitors. It'll be an interesting result when I get home, I fully expect to see fully ambulatory, cannibalistic, digital Ents. Anyway, I am familiar with the parameters set, I've tinkered with these programs myself, but not in any professional capacity. Call it a passing interest.

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. Another use of the program may include understanding the sources and effects of skewed genomic composition (4,7,30,31). However, this could be caused by mutation rates, and/or it could be the result of some kind(s) of evolutionary pressure that we don’t understand, so how one implements the skew may well affect or bias the results.

I note he states that the program is capable of a large number of additional parameters, but I'm not seeing where these were used during the study listed on that page. Under methodology he pretty much makes it clear he didn't use a great majority of parameters that would be important to have when simulating biological evolution. You note that you studied the program as well.

I did what Dr Schneider invited me to do; I did a systematic study of his computer model. The way you study a complex computer simulation like this is to do a parametric study. This is done by systematically varying the parameters in the model and tests how it affects the results. The results are posted earlier and throughout this thread. By far, the most dominant parameter in this sorting algorithm is the number of selection conditions.

When you did this study, did you keep your notes? Which parameters were used, and what results did you get? Do you have a data dump handy? Did you keep any records? If I wanted to replicate your tests, could I go off of your notes and get an identical result? Could I get a copy of this program somewhere? (I'll check the site when I get home from work, trying to wrap things up currently.)

It is not in his paper since Dr Schneider presented only a single case from his model with an unrealistically small genome. Dr Schneider knows that his model would take huge numbers of generations to evolve his selection conditions on any realistic length genome. This he has posted on his web site. I have posted this quote earlier, if you want I’ll post it again.

I agree with you here. If you want a more detailed model, you want an accurate representation as possible. You'd want to include every parameter you could, with a large gene pool and population (unless you wanted to test the lack of either as a stressor, of course)

First of all, there are no therapies which kill viruses (other than immunization), you can only impair the reproduction of the virus. You are correct though otherwise and when you apply mathematical precision to this process, it shows how profoundly slow the mutation and selection sorting/optimization process is for all but a single selection condition targeting a single gene. As soon as you complicate the sorting process with additional selection conditions, the process is quickly drawn to a standstill.

You don't think that combination therapy could lead to a strain of viruses that are resistant to all of the drugs used? If I could dig up documentation showing this has occured in the past, would you take this as an indication that evolution might possibly exist? I don't know of any off the top of my head, but I'll look if you like, for your benefit and mine.

Of course there was understanding about this process 50 years ago. I posted a Nobel laureate speech which addressed this issue 50 years ago. It should have been clear 50 years ago that targeted monotherapy should never be used on a rapidly reproducing population. Instead it takes 5 years of monotherapy on HIV to relearn the lesson and they make the man who relearns this Time Magazine Man of the Year. How many more times do we have to relearn this lesson? If evolutionists have their way, this will go on forever.

Do you have any documentation or references stating, specifically, that the reason "Monotherapy" is used is due to the proscribing doctor believing in evolution? Do you have any documented studies showing a mono/combo therapy and evolution/creation correlation? I don't see how you're linking them together, here.

 

[Nogbad]

Do you have any documentation or references stating, specifically, that the reason "Monotherapy" is used is due to the proscribing doctor believing in evolution? Do you have any documented studies showing a mono/combo therapy and evolution/creation correlation? I don't see how you're linking them together, here.

I was a bit baffled by that too. I thought the primary consideration was to not over-use various medications because they are not exactly without their downside either. With regards HIV I thought the main problem was finding a medication that actually pinned the little blighter down for more than 5 minutes not some esoteric concern with evolutionary theory.

 

[kleinman]

Annoying Creationists

What legal beagle does understand is that selection pressures do exactly as he describes above. Selection pressures impair populations from reproducing either by killing members of the population or preventing members from passing on their genetic information to the next generation. This is the fundamental basis for the mutation and selection process and is the core of the theory of evolution. What legal beagle does not understand is that if populations are forced to attain multiple mutations simultaneously is that they can not make that “immediate leap to the same evolutionary point that would have been arrived at, had the various therapies been sequentially applied”. It is mathematically and empirically much, much more difficult for populations to evolve to simultaneous selection pressures. See the citation below from an interview with David Ho, the originator of combination therapy for HIV.

What the kleinman does not understand is that in nature, the variability of selective pressures in the environment routinely provides evolutionary opportunities, which are not present in the controlled experiments which kleinman routinely cites.

Now don’t hold back legal beagle, tell us what all these evolutionary opportunities are.

Oh, it’s there, do the studies that Dr Schneider suggested in his paper and you will see how all these parameters affect the evolutionary process.

I've got a biological simulation program running at home. It started out with a two-dimentional stick and evolved it, through mutation and selection, into giant stick pyramids. I skewed the fitness requirement to give higher values for organism height. After I would up with those simulated organisms, I changed the fitness requirements towards mobility and lifespan. I gave them the ability to consume each other, and to generate slightly mutated offspring if a specific organism had eaten enough competitors. It'll be an interesting result when I get home, I fully expect to see fully ambulatory, cannibalistic, digital Ents. Anyway, I am familiar with the parameters set, I've tinkered with these programs myself, but not in any professional capacity. Call it a passing interest.

What you will find is that these sorting algorithms only work quickly with trivial sorting conditions. When you start looking at real populations, they can also only sort on very simple sorting conditions.

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. Another use of the program may include understanding the sources and effects of skewed genomic composition (4,7,30,31). However, this could be caused by mutation rates, and/or it could be the result of some kind(s) of evolutionary pressure that we don’t understand, so how one implements the skew may well affect or bias the results.

I note he states that the program is capable of a large number of additional parameters, but I'm not seeing where these were used during the study listed on that page. Under methodology he pretty much makes it clear he didn't use a great majority of parameters that would be important to have when simulating biological evolution. You note that you studied the program as well.

This is where Dr Schneider blundered in his analysis. He used only a single trivial case to describe his complex model. When you do a thorough analysis of his model it shows something completely different than the conclusions that Dr Schneider drew using his single case from his model.

I did what Dr Schneider invited me to do; I did a systematic study of his computer model. The way you study a complex computer simulation like this is to do a parametric study. This is done by systematically varying the parameters in the model and tests how it affects the results. The results are posted earlier and throughout this thread. By far, the most dominant parameter in this sorting algorithm is the number of selection conditions.

When you did this study, did you keep your notes? Which parameters were used, and what results did you get? Do you have a data dump handy? Did you keep any records? If I wanted to replicate your tests, could I go off of your notes and get an identical result? Could I get a copy of this program somewhere? (I'll check the site when I get home from work, trying to wrap things up currently.)

I started this study over 1 ½ years ago when I was discussing this model with Dr Schneider and Paul Anagnostopoulos (a moderator on this forum and co-worker with Dr Schneider). I studied the model for about two months while discussing these issues privately with Dr Schneider and Paul. I decided I wanted to discuss what his model was showing publicly but Dr Schneider decided not to, however Paul was willing to discuss the model of the Evolutionisdead forum. Paul then invited me to discuss the model on this forum and I took up his offer. The online version of ev was written by Paul and you can find it through the following link.
http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/
About a quarter of the way down the page there is a hot region you can click on to start the program that looks like this.
Click Here to Start the Evj Model

I have kept extensive notes and most of my data has been posted here or on the Evolutionisdead Forum. (Unfortunately the thread has been dropped from the forum but I have copies of most of the information posted.) Early on this discussion I contacted the editors of Nucleic Acid Research and wanted to write a letter to the editor describing what I had found but they said they do not take letters to the editor.

It is not in his paper since Dr Schneider presented only a single case from his model with an unrealistically small genome. Dr Schneider knows that his model would take huge numbers of generations to evolve his selection conditions on any realistic length genome. This he has posted on his web site. I have posted this quote earlier, if you want I’ll post it again.

I agree with you here. If you want a more detailed model, you want an accurate representation as possible. You'd want to include every parameter you could, with a large gene pool and population (unless you wanted to test the lack of either as a stressor, of course)

Dr Schneider had almost all the features in his model that are seen in the online version. In fact Dr Schneider has done studies with his model but has not published the results. I believe he hasn’t published the results because he didn’t understand why his model requires huge numbers of generations to evolve when you use anything other than a trivially small genome length. The answer to this is quite simple. His three selection conditions give far to complex a fitness landscape for anything other than a trivially small genome. If you set two of the three selection conditions to zero, you can quickly evolve the remaining selection condition. 4^G is a huge search space for anything other than a restricted sorting condition that only targets a small part of that 4^G search space. As soon as you expand your sorting conditions to multiple parts of the genome, the sorting algorithm is stalled for large genomes.

First of all, there are no therapies which kill viruses (other than immunization), you can only impair the reproduction of the virus. You are correct though otherwise and when you apply mathematical precision to this process, it shows how profoundly slow the mutation and selection sorting/optimization process is for all but a single selection condition targeting a single gene. As soon as you complicate the sorting process with additional selection conditions, the process is quickly drawn to a standstill.

You don't think that combination therapy could lead to a strain of viruses that are resistant to all of the drugs used? If I could dig up documentation showing this has occured in the past, would you take this as an indication that evolution might possibly exist? I don't know of any off the top of my head, but I'll look if you like, for your benefit and mine.

Certainly you can have viruses resistant to all drugs used. The way to do this is to use sequential monotherapy. That is in fact what was done for the first five years of treatment of HIV. That introduced a huge number of resistant strains of viruses into the gene pool. This makes it much more difficult to find effective three drug combinations for treating HIV. We’ve done the same thing treating many bacterial infections with monotherapy. We now have MRSA, multi-drug resistant TB and gonorrhea and so on. The way the mutation and selection sorting/optimization process actually works, this approach to treating infections is the ideal way to accelerate the evolutionary process. Use single (drugs) selection pressures, then when the microbes adapt to that drug use the next drug. Combination therapy confounds this process.

Of course there was understanding about this process 50 years ago. I posted a Nobel laureate speech which addressed this issue 50 years ago. It should have been clear 50 years ago that targeted monotherapy should never be used on a rapidly reproducing population. Instead it takes 5 years of monotherapy on HIV to relearn the lesson and they make the man who relearns this Time Magazine Man of the Year. How many more times do we have to relearn this lesson? If evolutionists have their way, this will go on forever.

Do you have any documentation or references stating, specifically, that the reason "Monotherapy" is used is due to the proscribing doctor believing in evolution? Do you have any documented studies showing a mono/combo therapy and evolution/creation correlation? I don't see how you're linking them together, here.

When I was in medical training we were specifically told not to use combination therapy to treat infections unless you could not identify the causative agent and you wanted to broaden the spectrum of treatment. This was not done because it was specifically an evolutionist viewpoint but because it could kill normal body flora, it cost more, increased risks of adverse reactions and so on. However, the unintended consequence of decades of sequential monotherapy is strains of microbes resistant to many antimicrobials. These are real examples of how evolution by mutation and selection works and illustrates what Dr Schneider’s ev model shows. I have had evolutionists argue on this thread that emergence of resistance is not evolution by mutation and selection. Once you realize that mutation and selection is simply a sorting algorithm strongly dependent on the complexity of the sorting conditions, it become clear why this happens. Evolution by mutation and selection only occurs quickly when you have single selection conditions targeting a single gene. As soon as you target more than a single gene, it is much, much more difficult for a population to sort for beneficial and detrimental mutations to these multiple selection conditions. Unless you want to argue that the transformation of a reptile population to a bird population occurred one gene at a time sequentially, evolutionbymutationandselectiondidn’tdoit.

No Thursday afternoon post would be complete with more empirical examples of how the mutation and selection sorting/optimization process actually works. So here is a couple more.
http://breastcancer.evidencewatch.com/

Several critical trials, including FASG (French Adjuvant Study Group) 05 and NCIC (National Cancer Institute of Canada) MA.5 demonstrated the that optimal dosing of epirubicin in combination chemotherapy regimens achieves superior long-term 10-year survival in node-positive breast cancer patients at high relapse risk, and that for node-negative patients ECMF (optimal-dose epirubicin at 100 mg/m2 followed by CMF), compared to the classical CMF regimen, produced significantly better RFS (relapse free survival) and OS (overall survival), irrespective of nodal status. These positive findings in node-negative disease had been also earlier found by the Danish Breast Cancer Group (Moridsen et al. (1999 ASCO Annual Meeting): Adjuvant anthracycline in breast cancer. Improved outcome in premenopausal patients following substitution of methotrexate in the CMF combination with epirubicin) who compared CEF (cyclophosphamide, epirubicin, and fluorouracil) to CMF, finding that 93% of the node-negative patients who received CEF (with 60 mg/m2 epirubicin) had 6 year survival compared with 83% of those who received CMF. (See also the review of S Gluck, Oncologist (2005): Adjuvant Chemotherapy for Early Breast Cancer: Optimal Use of Epirubicin) which noted that extended follow-up has confirmed that higher-dose combination chemotherapy regimens containing epirubicin improve therapeutic efficacy for both node-positive and node-negative early breast cancer patients).

http://www2.umdnj.edu/pharmweb/Annual%20Report/Annual%20Report05.pdf

Clinical development of anticancer treatments usually requires the combination of more than one drug for improved efficacy (either additive or synergistic), with each agent having different target.

Now you all have a good weekend and watch out for those annoying creationists, they post mathematical and empirical data of how the mutation and selection sorting/optimization process actually works.

 

[Mr. Scott]

I've got a biological simulation program running at home. It started out with a two-dimentional stick and evolved it, through mutation and selection, into giant stick pyramids.

That reminds me of this wonderful computer simulation of evolution I found on YouTube, which evolves a clock from random clock parts:

 

[joobz]

I assume you are talking about Dr Schneider’s ev model. As a starting point in a parametric study of ev, I suggest begin by investigating how genome length affect the generations. Increase the genome length by factors of two and see what happens to the number of generations to achieve a “perfect creature”. A “perfect creature” is one which satisfies all three selection conditions in the model.

What I did when I did my parametric study was to set up a spreadsheet to keep track of all the cases and parameters used to generate the data.

I see you are still have trouble understanding the nature of multiple selection pressures and what it means in terms of supporting the theory of evolution. That's ok, you think the theory evil and so are therefore are obviously confused as to what evil/good means. Afterall, your faith supports slavery and therefore doesn't allow a person to accurately interpret morality. This isn't your fault. You're simply a product of dumb evil lies. The dumbest one is that evolution has an morality. It's no more evil than the theory of gravity.

Now, if you would look at the concept of multiple selection pressures without the evil blinders of your faith, you would see that variable evironments help accelerate the evolutionary process. Since nature is variable (as proofed by the existence of weather), we know evolution is possible. Your theory helps support this point, Thank you!


As such, we know that anyone who would use creationist ideas to support medical advances would be endangering multitudes of people and therefore be commiting true evil.

So, Have you, Dr. Kleinman, ever used your creationist theories to determine the course of action for treatment of patients?

 

[Shalamar]

Kleinman seems enamored of ev. Can ev be run to have random, and variable selection pressures?

And no, He still doesn't have any math. He simply fails to understand, which is why he is continuing with the personal attacks.

 

[kjkent1]

Kleinman seems enamored of ev. Can ev be run to have random, and variable selection pressures?

And no, He still doesn't have any math. He simply fails to understand, which is why he is continuing with the personal attacks.

Kleinman isn't enamored by ev. Kleinman attempted to challenge ev's author, Dr. Thomas Schneider, on the same issues that Kleinman argues here. Schneider publicly rebuked Kleinman by posting the reasons why Kleinman's argument fails on Schneider's blog site at the NIH, and Kleinman has been using this "Annoying Creationist" forum to try to discredit Schneider, ever since -- principally because Paul Agnostolopolous, who wrote the java version of Schneider's ev program has remained in this dialog as Schneider's surrogate (only God knows why Paul does so, but, I give him credit for being so charitable).

Thus, this entire thread is all about kleinman getting his ego bruised.

As for whether ev can be run with variable selective pressures: no. More to the point is the question of whether or not the three ev mistake weight variables which kleinman contends represent selection pressures, actually serve this function.

One previous poster, a physicist going by the alias "sol invictus" suggested that the mistake weights are not selective pressures at all, and therefore that kleinman's entire premise is completely crackpot.

In my humble opinion, the mistake weights cannot really be selective pressures, because the selection algorithm doesn't select on them individually -- it adds them up and then selects on their aggregate total value.

But, kleinman thinks that he's found the holy grail of creationism in ev, and that because experiments with heavy selective pressures tends to slow resistance formation in target pathogens, that this somehow means that evolution itself is impossible in nature.

Kleinman believes every "kind" (biblical creature) is created by divine will and evolution at the level of speciation is impossible, because ev genomes evolve to produce zero mistakes, as defined by the algorithm, very slowly, and he thinks that his referenced experiments back up that position.

In other words, the fossil, geologic and radiometric records are all wrong, ancient retroviral insertions do not provide an audit trail of evolutionary change, the fusion of the great ape 2p and 2q chromosomes into the 2nd human chromosome is a fraud, etc...

The weirdest part of this entire exercise is that kleinman really is a dual doctorate academic, licensed as both a mechanical engineer and a medical physician, who should have learned something about critical thinking during his lifetime.

I suppose that given 6 billion people on Earth, there must be at least one person with the intelligence to accumulate and understand all of the relevant evidence and yet still draw all the wrong conclusions. And, that person inhabits this forum on randi.org.

And now you know...the rest of the story.

 

[Shalamar]

Ok. That makes a lot of sense. It is.. bizzare that he fights against the author of the program, while trying to say that the program disproves evolution.

 

[Belz...]

The topic of this thread is the mathematics of mutation and selection and the empirical evidence which supports this mathematics.

Translation: "I don't have any"

It is not the drug companies which are failing millions; it is the illogical and irrational evolutionist view of how the mutation and selection sorting/optimization process works which is failing millions.

If you are correct and the "citations" you provide show what you say they show, then we are already using what you claim works... how is that failing millions ?

Let me repeat what Kent said:

What the kleinman does not understand is that in nature, the variability of selective pressures in the environment routinely provides evolutionary opportunities, which are not present in the controlled experiments which kleinman routinely cites.

 

[Belz...]

What you will find is that these sorting algorithms only work quickly with trivial sorting conditions. When you start looking at real populations, they can also only sort on very simple sorting conditions.

In NATURE, Kleinman. In NATURE.

And more from Kent:

In my humble opinion, the mistake weights cannot really be selective pressures, because the selection algorithm doesn't select on them individually -- it adds them up and then selects on their aggregate total value.

 

[Mister Earl]

Once you realize that mutation and selection is simply a sorting algorithm strongly dependent on the complexity of the sorting conditions, it become clear why this happens. Evolution by mutation and selection only occurs quickly when you have single selection conditions targeting a single gene. As soon as you target more than a single gene, it is much, much more difficult for a population to sort for beneficial and detrimental mutations to these multiple selection conditions.

Makes sense to me, Kleinman. Wouldn't the result, over a longer span of time of course, wind up with diverging but similar species? Also, it your last notes you talk in great detail about how evolution works and doesn't work. I thought initially that you were saying evolution didn't exist. What is your stance, here, exactly!

 

[rocketdodger]

What you will find is that these sorting algorithms only work quickly with trivial sorting conditions. When you start looking at real populations, they can also only sort on very simple sorting conditions.

Once you realize that mutation and selection is simply a sorting algorithm strongly dependent on the complexity of the sorting conditions, it become clear why this happens. Evolution by mutation and selection only occurs quickly when you have single selection conditions targeting a single gene. As soon as you target more than a single gene, it is much, much more difficult for a population to sort for beneficial and detrimental mutations to these multiple selection conditions.

The usual lies from Kleinman.


For anyone new to this thread, you should know that both Dr. Adequate and I have independently written programs that rigorously prove, mathematically, that this claim of Kleinman's about sorting algorithms is FALSE.

We have also shown him, mathematically, why ev cannot be used to generate the conclusions he has arrived at regarding sorting algorithms.

Finally, we have asked him to show, mathematically, why his claim is true. He has been unable to even begin anything resembling a mathematical argument nor post a link to one that someone else thought up.

Hence, anything Kleinman says about sorting algorithms can be safely ignored.

I also strongly advise anyone reading Kleinman's posts to find the source of the quotations he uses of others on this thread, rather than taking his posts at face value, as he is known for misinformation.

 

[Belz...]

No, no, no, Dodger!! Those weren't REAL scottsmen sorting algirithms.

 

[kjkent1]

This was just posted in another thread. It should cause considerable discomfort for the kleinman and his theory of impossible evolution and abiogenesis (of course, he'll never admit it):

http://www.sciencedaily.com/releases/2008/01/080102142555.htm

Searching PubMed using the keywords: "Lambowitz fungus RNA" generates several hits on this subject. Apparently the author has been working in this line of evolutionary research for quite a while.

 

[kleinman]

Annoying Creationists

Did the light come on for any of you evolutionists on how the mutation and selection sorting/optimization process actually works this past weekend? Let’s find out.

I've got a biological simulation program running at home. It started out with a two-dimentional stick and evolved it, through mutation and selection, into giant stick pyramids.

That reminds me of this wonderful computer simulation of evolution I found on YouTube, which evolves a clock from random clock parts:

You evolutionists love to make the irrational and illogical extrapolation of these simple sorting problems to the massive and complex sorting required to transform reptiles into birds. Not only are the sorting conditions for these massive and complex transformation non-existent, even if they did exist, you do not have enough generations to accomplish such massive transformations. The mutation and selection sorting/optimization process only works for tiny numbers of selection conditions targeted to small portion of the genome. That’s what your simulations above are describing.

Kleinman seems enamored of ev. Can ev be run to have random, and variable selection pressures?

And no, He still doesn't have any math. He simply fails to understand, which is why he is continuing with the personal attacks.

Kleinman isn't enamored by ev. Kleinman attempted to challenge ev's author, Dr. Thomas Schneider, on the same issues that Kleinman argues here. Schneider publicly rebuked Kleinman by posting the reasons why Kleinman's argument fails on Schneider's blog site at the NIH, and Kleinman has been using this "Annoying Creationist" forum to try to discredit Schneider, ever since -- principally because Paul Agnostolopolous, who wrote the java version of Schneider's ev program has remained in this dialog as Schneider's surrogate (only God knows why Paul does so, but, I give him credit for being so charitable).

Didn’t you know that Dr Schneider has challenged creationists to debate the validity of ev?
http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/williams/

Here's a challenge for the creationists: Stop complaining and do a scientific test of your own ideas. Rewrite Ev so that the total number of mistakes of all organisms is computed. Divide the number of mistakes of each organism by this total to get relative mistake scores. Then alter the sorting algorithm to sort probabilistically based on these relative mistake scores. One way to implement this would be to sum the mistakes of two organisms that are being compared and divide each organism's mistakes by that pair wise total. Then pick a random number between 0 and 1 and compare it to that total. Use this to determine whether or not the organisms switch places in the sort. (Note you will have to deal with the special case of zero.) In other words, make the selective process be probabilistic so that there is nothing at all like truncation.

What do you predict will happen?
Will the evolution still occur?
Will Rsequence still approach Rfrequency?
This gauntlet was thrown on the ground on 2005 May 15.

Notice that, since creatioinists stop complaining when defeated, the most extremely difficult part of the challenge above is "do a scientific test of your own ideas"!

and

2006 Nov 28: Solution to the Challenge.

No creationist responded to this by doing the hard work. However a few moments of thought shows that the programming is not necessary. When one adds the mistakes of two organisms and divides by the total the sorting order is preserved. Therefore the results will be the same: Rsequence will still evolve to match Rfrequency.

Dr Schneider, I have taken up the gauntlet and have shown that your computer simulation of random point mutations and natural selection shows that the theory of evolution is mathematically impossible. I will now show you where your error in understanding the mutation and selection sorting/optimization process occurs. This error is demonstrated on your following page.
http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/AND-multiplication-error.html

The multiplication rule. It is well known from elementary probability theory that if two events are independent, then we may multiply the probabilities of each event to determine the probability of having both events occur. Suppose that there are two events A and B, with the probability of occurrence for A being PA and the probability of occurrence for B being PB. Further assume that the events neither influence each other nor do they both have a common source of influence. Then the probability that both events occur is PA x PB. That is, when the events A and B are independent, the probability that event A AND event B both occur is found by multiplying the probabilities of the individual events.

Example: A single die is a cube having 6 numbered faces, numbered by dots. The probability of getting a single dot from an unbiased die is 1 out of 6 or 1/6. The probability of getting two dice each to have one dot (snake eyes) is 1/6 multiplied by 1/6 or 1/36 = 0.028. Consider now a case where the two dice are glued together so that on one side there is a snake eyes. We toss the two and only read them if they don't end up on the end as a stack one on top of the other. Since there are 4 sides, the probability of 'snake eyes' is 1/4 = 0.25. The non-independence dramatically increased the probability of the event nine fold.

So far so good Dr Schneider.

The multiplication rule does not apply to biological evolution. A common error in the non-scientific literature and poorly written papers is to assume that probabilities multiply for computing components of living things such as proteins. A typical argument notes that proteins are about 300 amino acids long and that there are 20 different kinds of amino acids. If such a string were to be generated using independent selection of the amino acids, then the probability of generating any particular string is 20-300, a very small number indeed. While this may be true for random strings, it does not directly apply to proteins found in living organisms. Why? Because individual mutations accumulate one-at-a-time and there is amplification (replication) between steps. That is, if one starts with a given amino acid string, the mutations in the genome (from which the string is derived) are sequential. A mutation occurs, perhaps changing the amino acid string. If the change is bad, which is true for the majority of changes, the organism dies and its genes are gone. (In diploids, recessive defects will be removed more slowly since they are only exposed when an organism becomes homozygous for the mutation.) If a rare lucky change occurs that has some advantage (or at best is neutral or only slightly deleterious) then the organism may survive to produce offspring. The possibility of appearance and acceptance (by natural selection processes) of mutations in the offspring therefore depends strongly on whether the previous generation survived and on the number of progeny. Genetic algorithm experiments, such as the Ev evolution program demonstrate clearly that the probability of generating what would be an extremely rare genetic string if the steps were independent, can be high. So the evolution of a 300 amino acid protein is reasonably easy to attain.

I added the highlighting. Here is where you go wrong Dr Schneider. The amplification which you talk about only occurs when you have single selection conditions targeting a small area of the genome. When you have multiple selection conditions, this amplification effect is defeated. This is demonstrated by your own ev simulation of random point mutations and natural selection. Ev does not demonstrate that the evolution of a 300 amino acid protein is reasonably easy to attain, it demonstrates the exact opposite.

Dr Schneider, you have erred in your interpretation of how the mutation and selection sorting/optimization process works. Your failure to correct this error is contributing to the premature death of millions of people suffering from diseases subject to the principles of mutation and selection. This includes people suffering from cancer, a disease which the governmental organization you work for, The National Cancer Institute is dedicated to find cures. You are using tax payer dollars to improperly teach how the mutation and selection sorting/optimization process works. You are working against the cure for cancer by your erroneous teaching and interpretation of the mutation and selection sorting/optimization process.

Kjkent1, haven’t you noticed that Dr Schneider has stopped discussing his model publicly, something which he had done previously for years. I don’t discredit Dr Schneider's computer simulation, I agree with his mathematics. However, I discredit his illogical interpretation of a single case from his model. Dr Schneider has two options, he can publicly admit what his mathematical model shows or he can remain silent. He has chosen the latter option despite the fact that he has publicly challenged creationists to debate his model.

Once you realize that mutation and selection is simply a sorting algorithm strongly dependent on the complexity of the sorting conditions, it become clear why this happens. Evolution by mutation and selection only occurs quickly when you have single selection conditions targeting a single gene. As soon as you target more than a single gene, it is much, much more difficult for a population to sort for beneficial and detrimental mutations to these multiple selection conditions.

Makes sense to me, Kleinman. Wouldn't the result, over a longer span of time of course, wind up with diverging but similar species? Also, it your last notes you talk in great detail about how evolution works and doesn't work. I thought initially that you were saying evolution didn't exist. What is your stance, here, exactly!

This should make sense to you since the mathematical and empirical data show exactly how the mutation and selection sorting/optimization process actually works.

I’m not sure what you mean by “diverging but similar species”. What selection does is reduce variation. Selection pressures eliminate pheno-deviants which do not have the properties to survive. Only in environments with reduced selection pressures can you get increasing diversity in the population.

I have never said that evolution does not occur. What I have said is the ev shows that the theory of evolution is mathematically impossible and the empirical evidence substantiates this mathematical finding. The concept of common descent is mathematically and empirically impossible. Common descent is the core belief of the theory of evolution and this belief is mathematically and empirically wrong, the mutation and selection sorting/optimization process simply can not do what evolutionists allege. In fact evolutionist teaching of this belief interferes with understanding of how this process actually works.

Once you realize that mutation and selection is simply a sorting algorithm strongly dependent on the complexity of the sorting conditions, it become clear why this happens. Evolution by mutation and selection only occurs quickly when you have single selection conditions targeting a single gene. As soon as you target more than a single gene, it is much, much more difficult for a population to sort for beneficial and detrimental mutations to these multiple selection conditions.

For anyone new to this thread, you should know that both Dr. Adequate and I have independently written programs that rigorously prove, mathematically, that this claim of Kleinman's about sorting algorithms is FALSE.

I like to post the rigorous proofs of these evolutionist mythematicians. Here is rocketdodger’s rigourous proof.

I found a combination of parameters last night that led to over 100 pressures being faster than a single one, but I forgot what it was

And Adequate made his rigorous with the following.

The red line shows generations to achieve fixation of n alleles acted on by n selection pressures, the n+1th selection pressure being introduced only after the nth allele is fixed.

The blue line shows generations to achieve fixation of n alleles acted on by n selection pressures simultaneously.

All other features and parameters of the two models are identical. The model is designed so that the relative advantage of n+1 new genes over n (when selection is acting) is the same for all n, i.e. each new allele carries the same advantage.

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.

And then Adequate goes on to say this:

More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.

Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?

And Adequate responded:

So far as I know, no-one has done the experiment.

and

and too bad you don’t have any empirical examples of your silly graph ...

As I have explained to you, I produced the model because I've not heard of this precise experiment being done.

The claim that the greater the number of selection pressures, the faster the evolutionary sorting process proceeds demonstrates the complete mathematical incompetence of the evolutionist mythematicians. The mutation and selection sorting/optimization process simply does not work that way. How many more millions of people need to die prematurely from diseases subject to the principles of mutation and selection before you evolutionists will learn this lesson?

This was just posted in another thread. It should cause considerable discomfort for the kleinman and his theory of impossible evolution and abiogenesis (of course, he'll never admit it):

This doesn’t make me uncomfortable at all. Let’s see what your citation has to say:

"It's thought that RNA, or a molecule like it, may have been among the first molecules of life, both carrying genetic code that can be transmitted from generation to generation and folding into structures so these molecules could work inside cells," said Purdue structural biologist Barbara Golden. "At some point, RNA evolved and became capable of making proteins. At that point, proteins started taking over roles that RNA played previously - acting as catalysts and building structures in cells."

and

By studying the three-dimensional version of the fungus protein bound to an RNA molecule, scientists from Purdue University and the University of Texas at Austin have been able to visualize how life progressed from an early self-replicating molecule that also performed chemical reactions to one in which proteins assumed some of the work.

"Now we can see how RNA progressed to share functions with proteins," said Alan Lambowitz, director of the University of Texas Institute for Cellular and Molecular Biology. "This was a critical missing step."

Dr Lambowitz forgot more than one critical step. For example how do you form ribose nonenzymatically in the primordial soup? And even if you could form ribose non-enzymatically, how do you form RNA bases in the primordial soup when ribose is an unstable molecule which quickly breaks down. It is these types of gross speculations which form the basis of the theory of evolution and abiogenesis. I wonder if Dr Lambowitz understands the mathematics of the mutation and selection sorting/optimization process? I doubt it.

Now kjkent1, you’ve claimed that there all kinds of “evolutionary opportunities” in the natural world. Tell us what the selection pressure is that formed this fungal protein discussed in your citation. I’ll help you with your explanation, it was a mushroom cloudy day that evolved this fungal protein, that is how the Wookie Weatherman explains evolution.

So now that we have had another tour of evolutionist mythematics, speculations and plain old irrational and illogical thinking, let’s give some more examples of how the mutation and selection sorting/optimization process actually works.
http://www.connect.org/press/nl2005-09-06.htm

The researchers also found that the chemotherapy agent campthothecin (CPT), a clinically important anticancer agent, reduced the activity of the Chk1 protein.

"These findings lend strong support to the idea that inactivation of Chk1 contributes to the antitumor activity of CPT by allowing cells bearing damaged DNA to progress through the cell cycle, leading to an unsuccessful and often lethal attempt to undergo cell division," Abraham says. "Combination therapy, which pairs a chemotherapy agent with an inhibitor of Chk1, may therefore be an effective strategy to increase the efficacy of certain anticancer drugs, and may well overcome clinical resistance to these drugs."

http://www.uku.fi/vaitokset/2007/isbn978-951-27-0612-9.pdf

The concept of using single agent therapy has been noted as being unsuccessful in achieving a complete cure and thus combination therapy with the existing conventional modalities probably offers the greatest potential.

http://sist-aab.cirad.fr/rubrique.php3?id_rubrique=237

A combination of two drugs shows promise in treating a rare and therapy-resistant type of melanoma that originates in the eye and spreads to other organs, according to a new study led by Duke University Comprehensive Cancer Center researchers.

and

ICAAC: Dapivirine safe and tolerable as potential vaginal microbicide; displays potential in combination with other agents

and

A combination of drugs widely used to treat infections caused by HIV appears to stop brain damage caused by the virus as well, according to a study published in the Oct. 9, 2007, issue of Neurology, the medical journal of the American Academy of Neurology

and

Mayo Clinic today reported promising interim results from a Phase II trial of a new combination therapy for patients with recurrent ovarian cancer that is resistant to platinum therapy.

and

Oncolytics Biotech to begin a clinical trial using intravenous administration of Reolysin in combination with cyclophosphamide, a chemotherapeutic agent as well as immune modulator, in patients with advanced cancers.

and

A small clinical trial in Uganda, conducted within a long-established Medecins Sans Frontieres treatment program for African sleeping sickness, has found that a new combination treatment using the drugs nifurtimox and eflornithine holds promise and deserv

and

Adding a single dose of two common anti-HIV drugs can prevent HIV-positive pregnant women from developing resistance to an entire class of drugs, potentially improving future treatment options. Providing tenofovir and emtricitabine with nevirapine during

and

Pairing a new thalidomide derivative with a steroid slows progress of multiple myeloma, an incurable bone marrow cancer, and prolongs the lives of patients who have relapsed from previous treatment, researchers report in the Nov. 22 New England Journal of

and

Relapsed chronic lymphocytic leukemia (CLL) patients who had a complete response to combination therapy that included the drug oblimersen survived significantly longer than patients treated with chemotherapy alone, a team led by researchers at the Univers

and

Results from two investigational Phase I trials of ZOLINZA (vorinostat) in combination with bortezomib provide preliminary anti-tumor activity in patients with relapsed and/or refractory multiple myeloma.

and

A combination of a "targeted" therapy and chemotherapy shrank metastatic brain tumors by at least 50 percent in one-fifth of patients with aggressive HER2-positive breast cancer, according to data presented by Dana-Farber Cancer Institute investigators at

and

As reported recently in the journal Hepatology, WIN-R, a multicenter study of over 5,000 patients with hepatitis C virus showed treatment with weight-based REBETOL® (ribavirin, USP) in combination with pegylated interferon alfa-2b achieved significantly h

The more complex the sorting conditions the much, much more slowly the mutation and selection sorting/optimization process proceeds. The theory of evolution by mutation and selection is mathematically and empirically impossible. That is what Dr Schneider’s ev computer simulation or random point mutations and natural selection shows and that is what the empirical data shows.

 

[Belz...]

Yes, Klein. Destroying a life tends to prevent it from passing on its genes.