Annoying creationists

[rocketdodger]

Probability chimps and humas share a common ancestor, going just by the seven ERV insertions, is about 99.99999999999999999999999999999999999999999999999 999999999999999999% (65 nines after the decimal place) It's true! :D


Interesting. That is the exact probability that Kleinman is in fact not a doctor of anything and doesn't know what he is talking about. This is too much to be a coincidence...

[Paul C. Anagnostopoulos]

Well, if I get emotional like you, the same could be said about you rejecting everything, of course. You are not clear on how the entire universe works, yet you extrapolate, via an intelligently designed computer program, that there can't be an intelligent designer(s).
I must have missed the part where I used Ev as an argument against intelligent design per se. All I actually did was use it to show that information can evolve from randomness given sufficient structure. If you want to make the argument that the only way sufficient structure can exist is if it's put in place by an intelligent agent, I'm all ears. It sounds like it should be a logical argument, not an empirical one. The argument "Well, it's just too cute that an intelligent agent is arguing against intelligent design" doesn't cut it.


Can you outline where the ability to 'answer questions' makes something right or wrong? I must have missed that in logic class.
I will be most happy to address this issue as soon as you give me a list of other attributes of proposed empirical truths that could possibly be used to determine their veracity.

~~ Paul

[T'ai Chi]

All I actually did was use it to show that information can evolve from randomness given sufficient structure.


Well, then you did it the hard way. Randomness implies a probability distribution, which is itself a structure. There's nothing about 'evolve' in that, it is just an inherent property.

You showed something, yes, but a simulated something. I'm interested in biology too. Can you please show a complete detailed real evolutionary pathway in any biological thing?


I will be most happy to address this issue as soon as you give me a list of other attributes of proposed empirical truths that could possibly be used to determine their veracity.


Or you could just answer it since you obviously agree with 'X answers questions = X is right'.

[Paul C. Anagnostopoulos]

Well, then you did it the hard way. Randomness implies a probability distribution, which is itself a structure. There's nothing about 'evolve' in that, it is just an inherent property.
I was referring to Shannon information, of course. Not much of it in randomness.


You showed something, yes, but a simulated something. I'm interested in biology too. Can you please show a complete detailed real evolutionary pathway in any biological thing?
You're not listening. I never said that Ev demonstrates that the entire theory of evolution is correct. Nor did I say that it models any real evolutionary pathway. Quite large your strawman is, Master T'ai.


Or you could just answer it since you obviously agree with 'X answers questions = X is right'.
What a silly dodge. It's not sufficient to answer questions; the answers must also be correct. But back to my point:

I will be most happy to address this issue as soon as you give me a list of other attributes of proposed empirical truths that could possibly be used to determine their veracity. Surely you can name a few?

~~ Paul

[joobz]

Well, then you did it the hard way. Randomness implies a probability distribution, which is itself a structure. There's nothing about 'evolve' in that, it is just an inherent property.

You showed something, yes, but a simulated something. I'm interested in biology too. Can you please show a complete detailed real evolutionary pathway in any biological thing?

Or you could just answer it since you obviously agree with 'X answers questions = X is right'.

So, you seem intent on believing that there is an intelligent designer.
Ok, I'm more than willing to hear your evidence. Do you have anything supporting evidence for your designer that doesn't require a circular argument?

[T'ai Chi]

I was referring to Shannon information, of course. Not much of it in randomness.


What do you disagree with in http://www.ideacenter.org/contentmgr/showdetails.php/id/1236

Of course, you're not generating real random numbers anyway, but pseudo-random.

Either way, you get some numbers, you get some information. It doesn't really surprise me that information could increase, decrease, or stay the same as something changes over time as the numbers change. To me that is a trivial property of numbers. I could see even some random thing change a low level of information to a higher or smaller one given no selection at all.

But my beliefs aside, I'm more concerned if you have any actual real life biology to show, some detailed pathway, for example, of anything. I can show that the Empire State building can fit into the diagonal of a n-dimensional unit hypercube using math for Pete's sake :), so a simulation doesn't really impress me.

Then that whole 'life orginating' thing. Remember, you are the one claiming there must be a naturalisitc explanation.


You're not listening. I never said that Ev demonstrates that the entire theory of evolution is correct. Nor did I say that it models any real evolutionary pathway.


If I can't listen, then you can't read. Schneider's own page has a faq question on this very point. You know, the whole nagging 'I have some math, but not really rigorous biological demonstration of what is a biological concept that my math claims to show'. Not knocking math, but a simulation is a simulation. You're saying some Pascal can adequetely model all the variables in the universe or the Earth or something?


Surely you can name a few?


Well, I asked the first question about your belief. You claimed that 'X answers questions = X is right'. What is the rationale, if one exists, behind this belief system of yours? I guess magic 8 balls count for you.

[Kotatsu]

Not knocking math, but a simulation is a simulation.

Pst! Kleinman! I hope you're taking notes!

[Belz...]

Belz, those weak selection pressures slow the evolution of the strong selection pressure.

How ? Since you admit they are weaker, why would they matter all that much ?

You still haven't answered my point about the meteor, and I suspect you won't.

No Belz, you are chock-full of confusion of how mutation and selection works.

Somehow, I think so less and less.

Weak selection pressures don’t accelerate the evolution of a strong selection pressure

Who ever said they did ?

Rockdodger understands that the resistance to penicillin will evolve in vitro more quickly because of fewer weak selection pressures on the bacterial population.

You just keep redefining those terms, don't you ?

Each selection pressure imposes a trajectory on the fitness landscape interfering with the trajectories for the other selection pressures.

Uh-huh. But you must admit that the weaker ones less so.

[Belz...]

Well, I asked the first question about your belief. You claimed that 'X answers questions = X is right'. What is the rationale, if one exists, behind this belief system of yours? I guess magic 8 balls count for you.

"Gee, I hope nobody notices that I'm battling a strawman, here!"

"Uh oh! Somebody noticed. Maybe if I keep fighting it they'll forget it's a strawman!"

[delphi_ote]

Ah, but is this actually true? Is Windows less complex than e. coli? I guess you'd have to define complexity in some precise way, which I suspect you won't do. In fact, I predict you'll ignore this post altogether, because I'm discussing something substantive, and you usually flee to another thread as soon as anyone actually gets down to brass tacks.
:whistling

[kleinman]

Here’s one of Adequate’s posts where he admits to the truth of his understanding of the mathematics of mutation and selection.


So Adequate, none of your mathematical skills are relevant to the mathematics of mutation and selection? You can’t recognize a sorting/optimization problem? You can’t recognize an iterative problem when you see one? You are either incompetent in your field or a whackjob. But I don’t mind wasting a little of my time on you, it will be instructive to others who are interested in learning how the mutation and selection process actually works, both mathematically and empirically.

I need neither to whine nor lie about Adequate’s wacky graph. Adequate has already admitted that he knows nothing about the mathematics of mutation and selection and that he has no empirical evidence of his silly gif. Yeah! A new example of your reading comprehension diffiuculties.

Do you honestly believe that anyone would interpret that conversation as Dr. A saying he didn't understand evolution or that he isn't qualified to comment on evolution? Or that I am not qualified to see your argument as nonsense?
Sure I do, especially when it is posted in a thread entitled “Evolution: the Facts.”

It’s interesting to note that you also admit that evolution isn’t your field either. Here, let’s let the readers read yours and Adequate’s discussion.
http://forums.randi.org/showpost.php?p=3071566&postcount=241 (http://forums.randi.org/showpost.php?p=3071566&postcount=241)
If there was a "sticky" thread on drug delivery, biomaterials or polymer chemistry, I'd be there instantly. But evolution isn't my field.And I, sir, am a mathematician, and I may be the greatest expert in the UK on certain aspects of non-associative algebras, and on absolutely nothing else ... oh, certain aspects of neoclassical economics ... uses of geometry in design ... OK, there are lots of things I'm an expert on ... none of which are relevant to our great struggle between truth and bullcrap.

But when I put together an article summarising the present state of scientific knowledge for popular consumption, emphasising the skeptical point of view, the only requirements placed on me are that I should be honest, diligent, consciencious, and clear.

If you don't think that you can do that, then you shouldn't write about anything at all, even when arguing with whackjobs. If you can, then your articles may be of interest to thousands of people.

In which case, why waste your time on nutters?

Your call.
Now the question is joobz, do you really have any expertise, knowledge or training in chemistry? It is doubtful when you produce speculation like this.
Envision a system of millions of forming and destructive chemical reactions. Now, envision that intermediates of there reactions associate through non-covalent means and that this complex becomes protected against the destructive reactive pathway, perhaps by a reversible precipitation. These new complexes result in a localized increased of new chemical species. These chemical species then progress in a new series of reaction... that is what I mean through cooperative means. I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?
It’s hard to determine which is dumber, your silly speculations of how abiogenesis occurs or this:
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
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.
http://forums.randi.org/images/smilies/doglaugh.gif
Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?
Adequate’s silly gif and his contradictory claims what his silly gif shows. You and Adequate have produced the dumb and dumber arguments of the theory of theory of evolution in nice detail. Joobz, do you really have a PhD in chemical engineering?
The conversation was really why we spend time goofing on you. It is more related to the fact that your arguments are so mundane that they don't require a significant level of expertise in the field and that they don't really deserve any more time. Except that it's fun watching you say silly stupid things, such as the quoted comment above.
Oh, I see, you were just goofing with your cooperative chemistry argument.
http://forums.randi.org/images/smilies/doglaugh.gif
1) You claim that nobody besides you understands the underlying mathematics of mutation and selection. The only evidence you have for this is apparently the fact that you repeat it over and over. You have not given us a single derivation, solid understanding, or even proper use of an equation or concept this entire thread.
Oh no rocketdodger, I am sure that you don’t understand the mathematics of mutation and selection, you admit it.
http://forums.randi.org/showpost.php?p=3007230&postcount=5718 (http://forums.randi.org/showpost.php?p=3007230&postcount=5718)
I am eager to participate in this discussion but I don't know the mathematical details of the topic, only general ideas. Paul, is there a good introductory source (assuming I am fluent in mathematics) where I can learn what this equation you guys are talking about represents? All this Rseq~ and Rfreq~ stuff is lost on me.
The evidence is apparent by the results of the ev computer simulation and hundreds of real examples of mutation and selection which show that combination selection pressures profoundly slow the evolutionary process. The reason you are unable to see this evidence is your bias which puts you into denial.
2) You claim that additional sorting conditions "slow down" sorting/optimization problems. You have not presented any formal arguments showing us why this would be true. On the contrary, you have done nothing but make personal attacks against Adequate when he demonstrates otherwise.
I have produced hundreds of empirical examples which show that additional selection conditions slow down the evolutionary process and you have agreed to that which means you have some common sense. Adequate’s silly graph shows nothing. Adequate admits there are no experiments available to show any validity to his silly graph but rocketdodger, why don’t you help out Adequate and produce the experiment.

And rocketdodger, when was the last time an evolutionist produced a formal mathematical proof of how mutation and selection actually works. We have numerous mathematical models (including Dr Schneider’s ev model) which show that combination selection pressures profoundly slow the evolutionary process and a vast amount of empirical data which substantiates this mathematical fact and you have Adequate’s silly graph and no empirical data to support this silly graph.
3) You claim that mutation and selection is simply a sorting/optimization problem. You have not presented any formal arguments to show that this is true.
Oh, I see, my “informal” arguments using a peer reviewed and published model of mutation and selection and hundreds or real example which substantiates this results isn’t formal enough for you. Rocketdodger, if you do a google search with these key word, yo will come up with thousands of references like this:
http://www.springerlink.com/content/ahe70qmqg2f5ukxl/ (http://www.springerlink.com/content/ahe70qmqg2f5ukxl/)
In this paper we discuss some questions of applying evolutionary algorithms to multiobjective optimization problems with continuous variables. A main question of transforming evolutionary algorithms for scalar optimization into those for multiobjective optimization concerns the modification of the selection step. In an earlier article we have analyzed special properties of selection rules called efficiency preservation and negative efficiency preservation.

Here, we discuss the use of these properties by applying an accordingly modified selection rule to some test problems. The number of efficient alternatives of a population for different test problems provides a better understanding of the change of data during the evolutionary process. Also effects of the number of objective functions are treated. We also analyze the influence of the number of objectives and the relevance of these results in the context of the 1/5 rule, a mutation control concept for scalar evolutionary algorithms which cannot easily be transformed into the multiobjective case.
Evolution by mutation and selection is analogous to optimization theory.
If you understood the mechanisms behind mutation and selection, Kleinman, then you would be able to present formal arguments to back up your claims.

Since you do not, we can assume you either do not in fact understand those mechanisms or that you realize any formal arguments developed from those mechanisms would refute your theory.

Instead, you rely on the behavior of bombarding us with random citations featuring arbitrarily highlighted sentences in the hopes that it makes you look smarter than a cumquat -- it has not had this effect.
Rocketdodger, I thought all my citations proved your argument, how could they also be random?
There it is folks; the theory of evolution must be true because Mr Scott has shown that feathers can grow on birds. That must be the kind of common sense that rocketdodger is talking about. Kotatsu, I admit that feathers do grow on birds, I will not ignore thisThe usual dodge via ridicule and strawman argument. I see you ignored my mention that bird DNA includes the genetic mechanism for making teeth.

The key to understanding the creationist mind is to tune in to where they dodge or outright ignore points they can't refute. Kleinman is a textbook example of this psychological syndrome confirmation bias. He offers skeptics a tremendous benefit in stimulating conversation supporting evolution and studying the psychology of creationists.
The usual evolutionist dodge, changing the subject. The central principle of the theory of evolution, “mutation and selection” doesn’t work the way they allege either mathematically or empirically so change the subject and argue that there are some similarities between genes and therefore they must have evolved from each other.

The key to understanding the evolutionist mind is the propensity for them to make irrational extrapolations and speculations and then deny the mathematical and empirical evidence that contradicts the central principle of their theory.
I must admit that I have fallen behind on my Marvel comics reading as well since mutation and selection doesn’t work that way. Kotatsu, since it mathematically impossible for mutation and selection to do such a transformation, how do dinosaurs transform into birds? Wait a minute, this has happened. Big Bird turned into Barney on Sesame Street.I assume these are references to American popular culture, but they are quite meaningless to me. Sorry.

However, to answer your question, the transition between dinosaurs and birds was accomplished by the same mechanisms as all other evolution: mutations of various sorts and selection of various sorts.
No Kotatsu, these are not comments on American popular culture, they are comments on evolutionist popular culture because mutation and selection simply does not work the way you allege, the mathematics and empirical evidence of mutation and selection contradict your scientifically and mathematically baseless speculations and extrapolations.
That mechanism is random mutations and natural selection. This sorting process is profoundly slowed when more than a single gene is being transformed at a time.I realise this is an inconsequential tangent, and most likely will not be satisfactorily addressed, but do you hold that its is entirely impossible for a sperm to contain mutations in every single gene compared to the genome of the father? If so, what mechanism in the cell prevents this from happening at least occasionally by sheer coincidence? I know there are several control mechanisms, but as mutations can happen in even very conservative regions, there must be occasions when these control mechanisms are somehow not enough.
So, the now we have the theory of evolution by “sheer coincidence”, Kotatsu, you take speculation to new levels.
In addition, we are still waiting for you tell us what that selection pressure is that would transform reptiles or dinosaurs into birds. So not only do you lack any selection pressure that would do this, you can only transform a single gene at a time with the mutation and selection process.I have already provided you with a list precisely of that, which you have so far chosen to misinterpret and mock. In the vain hope that this time you might actually read it and try to understand it, I refer you to that list again. It can easily be found by clicking on my screen name and select the option "Find more posts by Kotatsu".
Oh, that’s right, you said a reptile chased in into a tree and it would be beneficial for that reptile to grow wings. You evolutionists really practice some weird thinking.
Kotatsu, the underlying mathematics of mutation and selection and the empirical evidence which supports this mathematics refutes the conclusions you try to draw from you phylogenetics pictures. Mutation and selection is a profoundly slow process for more than the transformation of a single gene and you don’t have the selection pressures which would accomplish the huge transformations you allege for common descent.Then perhaps you would be so kind to explain to me exactly what it is we see in a phylogenetic tree? Why do the data sets almost invariably form nested hierarchies and show that the ingroup taxa, at least, appear to be the result of common descent modified step by step over time? Chose any tree you like, and explain this to me. I am a systematicist and an aspiring taxonomist, and surely you would not be so cruel as to not explain this to me, would you? Just imagine if you are correct --- which, by the way, you are not --- would you deprive me of the exact knowledge which you allegedly possess --- but which, for some reason, you have hitherto smugly chosen to keep to yourself --- that would convince me that the arguments and data needed to convert to your view are within my own field?
What you are seeing are connections which are mathematically and empirically impossible. These are extrapolations and speculations that are contradicted by the way mutation and selection actually works.
And, while you are at it, could you perhaps finally answer Belz' question about what that Archaeopteryx actually is? This has been bugging me for some time. As you can so summarily dismiss the fossils we claim are forms transitional between dinosaurs and birds, I am sure you have a better explanation of what they really are than an "evolutionary [R]orschach test".
There are many unusual species which evolutionists like you speculate and extrapolate that appear by evolution. However, you are in denial about how mutation and selection actually works. Combination selection pressures confound the evolutionary process. A population can most easily evolve against a single selection pressure directed at a single gene. As soon as multiple selection pressures come into play, these multiple selection pressures confound the evolutionary process. That is what the mathematical evidence shows and that is what the empirical evidence shows.
There it is folks; the theory of evolution must be true because Mr Scott has shown that feathers can grow on birds. That must be the kind of common sense that rocketdodger is talking about. Kotatsu, I admit that feathers do grow on birds, I will not ignore this.That is not the important thing that MrScott showed us, Kleinman. The important thing was that it takes only one mutation to change scales into feathers. Does this fact mean nothing to you, more than yet another way to behave in what I can only assume is a deliberately buffoonish way? To me, it means that your arguments are lessened enormously with regard to the dinosaur-bird evolution. If one mutation is all it takes, then I would think it odd if no dinosaurs ever evolved feathers. And once you have feathers --- remember that the dinosaurs thought ancestral to birds were largely arboreal --- all the other morphological differences between dinosaurs and birds seem inconsequential, for the groundwork --- making feathers out of scales --- have already been laid, and the rest are just consequences of this.
Mr Scott has not shown that scales transform into feathers, all Mr Scott has shown is that feather can grow on birds in unusual locations when there is a mutation. Kotatsu, have you ever heard of teratomas?
So, maybe we had an alien visitor 4.5 million years ago, and it did a little genetic engineering. Now, this begs the question of where the alien came from -- which is why evolution is a much more plausible conclusion.Can you imagine how awesome it would be if we found conclusive evidence for such a thing?
There goes the theme music for Twilight Zone again.
Delphi, when are you going to tell us how a temperature change transforms a reptile population into a bird population? Or is this just another of your arrogant and incoherent ideas.Do you have an entire planet I can use as a laboratory and a few hundred million years to wait around? I can't promise the exact results you want, but I could give it a try.
You will need more than that to prove the nonsense that you call the theory of evolution. Mutation and selection doesn’t work that way.
How long will you deny how mutation and selection actually works?How do they "actually works", kleinman?
Delphi, you should know the answer to that question. It works the way the Wikipedia reference to fitness landscape describes, the reference you made to this discussion.
Delphi, explain to us how any gene can evolve de novo by mutation and selection.This has been explained to you again and again...
You have never explained how a gene can evolve de novo; you have only speculated that gene duplication can some how make new genes. How does the original gene come to be?
Happy birthday to the thread!
What’s the matter Myriad, run out of things to say about the mathematics of mutation and selection? Have you tried to giggle, oops jiggle the weight factors in ev?
Remember when Kleinman didn't understand how your quick simple code could demonstrate that multiple selection pressures could indeed be faster than 1 huge one.

Good times, good times.Ah, yes. Those were the good old days. I was so young and naive, in the prime of my life. You were a dashing businessman full of bravado. We were ready to take on the world! Er... wait. Maybe I'm thinking of something else.

But yes, those were the halcyon days when I imagined that, perhaps, Kleinman might actually read and think about the things we typed. Despite all the very intelligent posts the community has made to help nudge him toward the truth, he still clings to roughly the same set of nonsense he did when we all entered this thread. These things have been demonstrated without ambiguity over and over again for a year, and he still gets it wrong.
I remember those days as well; joobz told us about cooperative chemistry yet can’t even describe how ribose could form nonenzymatically, you told us that reptiles turn into birds by a simple temperature change, ah, those were the good old days.
Not knocking math, but a simulation is a simulation.Pst! Kleinman! I hope you're taking notes!
Of course I am Kotatsu, here is a note from your lecture: Reptile chased into tree->reptile grows wings.
Ah, but is this actually true? Is Windows less complex than e. coli? I guess you'd have to define complexity in some precise way, which I suspect you won't do. In fact, I predict you'll ignore this post altogether, because I'm discussing something substantive, and you usually flee to another thread as soon as anyone actually gets down to brass tacks.
Does that mean you are going to make another human skateboard movie?

Since you evolutionists still don’t understand that evolution by mutation and selection is simply a sorting/optimization problem where the number of selection conditions (sorting/optimization conditions) profoundly slows the process, I’ll present you with more examples of how this process actually works.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=127494 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=127494)
Our results show that some antibiotic treatments can select for mutator bacteria present at low frequencies among all wild-type populations. Actually, by selecting for a resistance allele, the antibiotic selective pressure also selected for a mutator allele as the mechanism that generated the resistance. Moreover, mutators could also facilitate the modification of the active sites of detoxification enzymes to shift the resistance from resistance to a low dose to resistance to a high dose (17) and extend their resistance spectra (12). It could also rapidly accumulate compensatory mutations that limit the cost to the bacteria associated with the resistance alleles (1). Mutator bacteria can be considered risk markers for antibiotic therapy. If corroborated by epidemiological data, our results would suggest that, in the case of a first therapeutic failure and if time allows, a diagnostic assay for the presence of mutators should determine the next therapeutic step. If a drug is available for which mutational events can very rarely generate antibiotic resistance, such as AMP at a high concentration used against the bacteria in the present study, then it is the first choice for use against the mutators. Otherwise, the use of a combination therapy seems to be the best alternative. As the selection of mutator bacteria is favored by several bacterial and environmental factors (18), some conditions (e.g., a large bacterial population) allow the selection of such strains more than others. In these cases, if possible, therapies should be initiated directly with a protocol that limits the risk of selection of mutators. For example, the use of antibiotics that inhibit a single enzyme should probably be set aside, even when used in combination therapies, as we did in the present work.
http://www.ajtmh.org/cgi/content/full/71/2_suppl/179 (http://www.ajtmh.org/cgi/content/full/71/2_suppl/179)

Increasing resistance of Plasmodium falciparum malaria to antimalarial drugs is posing a major threat to the global effort to "Roll Back Malaria". Chloroquine and sulfadoxine-pyrimethamine (SP) are being rendered increasingly ineffective, resulting in increasing morbidity, mortality, and economic and social costs. One strategy advocated for delaying the development of resistance to the remaining armory of effective drugs is the wide-scale deployment of artemisinin-based combination therapy. However, the cost of these combinations are higher than most of the currently used monotherapies and alternative non-artemisinin-based combinations. In addition, uncertainty about the actual impact in real-life settings has made them a controversial choice for first-line treatment. The difficulties in measuring the burden of drug resistance and predicting the impact of strategies aimed at its reduction are outlined, and a mathematical model is introduced that is being designed to address these issues and to clarify policy options.
and

Resistance to antimalarial drugs is resulting in avoidable morbidity, mortality, and financial losses. Urgent measures are needed now to reduce the current and future burden of disease. There is little justification for the continued use of ineffective drugs because effective drugs are currently available. The decisions of which drug regimen to change to, and how to implement the change in a way that maximizes potential benefit, are more difficult, but delaying a decision to switch because of these difficulties can only result in increased morbidity and mortality. Furthermore, delaying a switch to ACTs potentially puts at risk one of the key advantages of this strategy, which is to delay the emergence of resistance. The longer the decision is delayed, the more entrenched will become the unregulated use of the artemisinins and partner drugs as monotherapies. Partly because of the uncertainties, there is still significant reluctance to take action amongst potential funders and some national governments, both of whose commitment is essential for the success of any change in policy.

[joobz]

Ah, kleinman, your back. And here I thought you were done humiliating yourself. But I see now you are going for the "most stupid ideas in a single post" award.


Now the question is joobz, do you really have any expertise, knowledge or training in chemistry? It is doubtful when you produce speculation like this.


Perhaps you'd like to explain why that is wrong. I'd love to hear a real critique.
Let me show you how it is done.
Your theory of evolution being impossible is wrong becuase the following assumptions you make are wrong:
1.)slow doesn't equal stop
2.)you do not know the rate of mutation or adaptation emergence
3,)This rate isn't constant
4.)selection pressures do not remain temporally constant
5.)the number of pressures are unknown
You must explain why these points are invalid.
Remember, however, we have evidence that evolution occurs in the presence of multiple selection conditions (thank you for that, BTW). Unless, of course, you believe that creatures in nature don't have multiple pressures on them.

[kleinman]

Now the question is joobz, do you really have any expertise, knowledge or training in chemistry? It is doubtful when you produce speculation like this.
Perhaps you'd like to explain why that is wrong. I'd love to hear a real critique.
Let me show you how it is done.
Your theory of evolution being impossible is wrong becuase the following assumptions you make are wrong:
1.)slow doesn't equal stop
2.)you do not know the rate of mutation or adaptation emergence
3,)This rate isn't constant
4.)selection pressures do not remain temporally constant
5.)the number of pressures are unknown
You must explain why these points are invalid.
Remember, however, we have evidence that evolution occurs in the presence of multiple selection conditions (thank you for that, BTW).
Joobz, PhD in speculational engineering again posts his speculations. What I post is the mathematical results from Dr Schneider’s peer reviewed and published model of random point mutations and natural selection which show that combination selection pressures profoundly slow the evolutionary process. In addition, I post empirical examples which substantiate this mathematical finding, something which you can not do with your speculations. Since you admit that evolution is not your field, I’ll fill you in on the mathematics of the mutation and selection sorting problem. The dominant parameter in this problem by far is the number of selection (sorting) conditions. All other parameters have much smaller effect on the rate of evolution. It is for this reason that the theory of evolution is mathematically impossible. The only concept more ridiculous than the theory of evolution is your theory of abiogenesis by cooperative chemistry.

So let’s post another example of how mutation and selection actually works.
http://hbvadvocate.org/news/NewsUpdates_pdf/2.2_Conference_Reports/EASL_2002_Agenda/Section4/zoulim.pdf (http://hbvadvocate.org/news/NewsUpdates_pdf/2.2_Conference_Reports/EASL_2002_Agenda/Section4/zoulim.pdf)
The most important issue, when starting antiviral therapy, is to prevent drug resistance. As a rationale, the use of inhibitors with different mechanism of action and different resistance profiles should be favoured in clinical trials to obtain an additive or synergistic antiviral effect to limit the risk of emergence of drug resistant strains (3). One study showed a potential beneficial effect of the association of famciclovir and lamivudine by accelerating the kinetics of viral clearance compared to lamivudine monotherapy (36).
and
HBV resistance to lamivudine is a frequent and significant therapeutical problem. With the results of clinical trials and independent studies, clinicians have now a better knowledge of the incidence of drug resistance and its clinical consequence. There are still many clinical questions to be answered regarding the predictive factors of lamivudine resistance development and of the severity associated with viral resistance. New drugs are being evaluated in experimental models and clinical trials. Among them, Adefovir dipivoxil is the more advanced in clinical development and represents a very promising inhibitor that has been assessed in phase III trials and should be registered soon. It has an interesting antiviral profile with i) a potent activity against lamivudine resistant strains which is useful as a rescue treatment of lamivudine resistance, ii) and the absence of selection of drug resistant strains up to 3 years of therapy. As new progress has been made, we have now not only the capacity to control lamivudine resistance but also many tools to detect and prevent treatment failure. In this view, it will be important to determine the best strategy to prevent drug resistance using combinations of nucleoside analogues such as lamivudine, adefovir, and others, with immunostimulatory approaches based on pegylated interferon alfa, new therapeutic vaccines or others.

[rocketdodger]

Now the question is joobz, do you really have any expertise, knowledge or training in chemistry? It is doubtful when you produce speculation like this

I told you already, Kleinman, that the process joobz talks about is in fact not speculation, it is a common phenomenon in chemistry. If you knew anything about organic chemistry, in particular chemical synthesis, you would be familiar with it. Yet more proof that you are a group of bible study children who figured out how to use google.


Oh no rocketdodger, I am sure that you don’t understand the mathematics of mutation and selection, you admit it.

And like I said before, I was asking about the equations and variable names in the context of the ev program. I understand the mathematics very well -- much better than you, in fact, , as evidenced by my ability to actually formalize my arguments. Contrast this with your posts, which are nothing more than pasted results from google searches.


The evidence is apparent by the results of the ev computer simulation and hundreds of real examples of mutation and selection which show that combination selection pressures profoundly slow the evolutionary process. The reason you are unable to see this evidence is your bias which puts you into denial.

There is evidence, of something, but you have completely failed to show us that it is in fact evidence of your theory, as opposed to anything else. The people you normally deal with might accept any argument put in text and given to them, but we don't operate that way here.

I have produced hundreds of empirical examples which show that additional selection conditions slow down the evolutionary process and you have agreed to that which means you have some common sense.

Kleinman: "Apples are red."
Me: "Some are, yes, but some are green."
Kleinman: "So you agree that apples are red."
Me: "No, apples can be red."
Kleinman: "Everyone, rocketdodger agrees that apples are red."
Me: *sigh*


Adequate’s silly graph shows nothing. Adequate admits there are no experiments available to show any validity to his silly graph but rocketdodger, why don’t you help out Adequate and produce the experiment.

Adequate's graph shows the same conclusion you would come to if you actually tried to formalize the nonsense flowing out of your mouth (or fingers, as it were). Quite simply, it shows that according to the model you yourself are using the time it takes for complete fixation under 50 pressures at once is less than the time it takes for complete fixation if you apply the 50 pressures in sequence, one at a time. This is impossible for you to understand, of course, because doing so involves more than googling and pasting.


We have numerous mathematical models (including Dr Schneider’s ev model) which show that combination selection pressures profoundly slow the evolutionary process and a vast amount of empirical data which substantiates this mathematical fact and you have Adequate’s silly graph and no empirical data to support this silly graph.

1) You don't even understand Schneider's ev model, because if you did you would be able to say more than "Schneider's ev model shows this and that."

2) Its a good thing you don't, because it will produce the same graph that Adequate is using.

Oh, I see, my “informal” arguments using a peer reviewed and published model of mutation and selection and hundreds or real example which substantiates this results isn’t formal enough for you.

Those arguments aren't even informal -- they aren't arguments at all. You have not provided a single coherent argument for why all of the studies you throw at us support your theory. Posting a pasted abstract and saying "look, see!" does not constitute an argument. Well, unless you are a bible school kiddie.

In fact, the only thing you have provided a valid argument for is why in many cases multiple selective pressures don't profoundly slow evolution.

Evolution by mutation and selection is analogous to optimization theory.

Lol. Do you even know what that statement means? No, you do not. If evolution by mutation and selection is analagous to optimization theory, can you tell us why? No, you cannot.

If you did and could, then you would suddenly see that all of your assumptions and claims are wrong -- something you will never be able to realize until you at least try to formalize your arguments, even if just a little.


Rocketdodger, I thought all my citations proved your argument, how could they also be random?

As in "what crap can I google and paste on to the thread today?"

Admit it, you haven't read in full even a single study that you have cited. You don't even know what the sentences you highlight mean.


Since you evolutionists still don’t understand that evolution by mutation and selection is simply a sorting/optimization problem where the number of selection conditions (sorting/optimization conditions) profoundly slows the process

You are right, none of us understand this. Please tell us why mutation and selection is simply a sorting/optimization problem.

[kjkent1]

Joobz, PhD in speculational engineering again posts his speculations. What I post is the mathematical results from Dr Schneider’s peer reviewed and published model of random point mutations and natural selection which show that combination selection pressures profoundly slow the evolutionary process. In addition, I post empirical examples which substantiate this mathematical finding, something which you can not do with your speculations. Since you admit that evolution is not your field, I’ll fill you in on the mathematics of the mutation and selection sorting problem. The dominant parameter in this problem by far is the number of selection (sorting) conditions. All other parameters have much smaller effect on the rate of evolution. It is for this reason that the theory of evolution is mathematically impossible. The only concept more ridiculous than the theory of evolution is your theory of abiogenesis by cooperative chemistry.
All of your citations and quotes definitively show that an organism population subjected to one overwhelmingly strong selection pressure will evolve quickly. Thus, you now must produce proof that this condition appears so rarely in natural environments, that evolution would not have sufficient generational time to occur.

The geological and fossil records demonstrate that evolution has occurred within the generational time available.

Do you have any contradictory evidence to either discredit the observed record or to demonstrate that organism populations in natural environments are never subjected to a single overwhelming selective pressure?

If you do not have such evidence, then your hypothesis is inconclusive at best, and at worst, your own evidence demonstrates the potential for rapid evolutionary change under a single overwhelming selective pressure.

Your constant posting of the same litany of evidence, which undermines your own hypothesis, is incredibly OCD.

[rocketdodger]

Since you admit that evolution is not your field, I’ll fill you in on the mathematics of the mutation and selection sorting problem.

Is it your field, Kleinman? We have been very revealing with our qualifications, despite the fact that we know you will use such information against us. Would you care to return the favor? Please tell us:

a) Your educational background, including any degrees you have gotten and any research you have taken part in.

b) Your current job and position, as stated on your business card.

[joobz]

Is it your field, Kleinman? We have been very revealing with our qualifications, despite the fact that we know you will use such information against us. Would you care to return the favor? Please tell us:

a) Your educational background, including any degrees you have gotten and any research you have taken part in.

b) Your current job and position, as stated on your business card.
Hi Rocketdodger. Kleinman is simply trying to goad me and live up to his Annoying claim. I do not value his opinion, so what he says is really immaterial. I just hope for new funny things to read. As of yet, he has only repeated his same nonsense.



As for his credentials. He's stated that he is Dr. Alan Kleinman. A physician with a PhD in engineering (I do not remember which field). He even posted a link to his thesis as proof of his degree. I could critique his PhD for irregularities in his publication track that raise interesting questions. But, I see no reason to doubt him or this. As it is irrelevant. His terrible arguments and woefully terrible understanding of science is much more telling.

[rocketdodger]

But, I see no reason to doubt him or this.

I do. His inability to
1) even read our posts before addressing them
2) understand our posts when he does read them
3) understand his own posts

suggests to me that he is full of it.

As it is irrelevant.

True. I would still like to know if I am dealing with a fool that slid through his university's graduate program or (as I contend) a group of bible study children.

[T'ai Chi]

Pst! Kleinman! I hope you're taking notes!

Well, Kleinman is entitled to critique a model he feels is not reflective of reality, or for whatever other reason. Especially if the people who made the model are trying to convince others it is reflective of reality.

[kleinman]

Now the question is joobz, do you really have any expertise, knowledge or training in chemistry? It is doubtful when you produce speculation like thisI told you already, Kleinman, that the process joobz talks about is in fact not speculation, it is a common phenomenon in chemistry. If you knew anything about organic chemistry, in particular chemical synthesis, you would be familiar with it. Yet more proof that you are a group of bible study children who figured out how to use google.
Joobz admits his chemistry is pure speculation and you admit you have no understanding of the mathematics of mutation and selection. Not only do I understand how to use google, I understand something about the mathematics of mutation and selection and it is easily recognized as a sorting/optimization problem. The rate of convergence of these types of problems is profoundly affected by the number of sorting/optimization (selection) conditions. If you understood that much about the mathematics of mutation and selection, all the citations posted would become understandable to you.
Oh no rocketdodger, I am sure that you don’t understand the mathematics of mutation and selection, you admit it.And like I said before, I was asking about the equations and variable names in the context of the ev program. I understand the mathematics very well -- much better than you, in fact, , as evidenced by my ability to actually formalize my arguments. Contrast this with your posts, which are nothing more than pasted results from google searches.
Dr Schneider has posted extensively about his ev model including a glossary of his variables used in his calculations.

Why shouldn’t I cite evidence of how mutation and selection actually works? There is an abundance of this evidence available. Why don’t you use google and find a citation which shows that n+1 selection pressures evolve more rapidly than n selection pressures?
The evidence is apparent by the results of the ev computer simulation and hundreds of real examples of mutation and selection which show that combination selection pressures profoundly slow the evolutionary process. The reason you are unable to see this evidence is your bias which puts you into denial.There is evidence, of something, but you have completely failed to show us that it is in fact evidence of your theory, as opposed to anything else. The people you normally deal with might accept any argument put in text and given to them, but we don't operate that way here.
The crux of this debate is whether fewer selection pressures evolve more rapidly than more selection pressures. If the former position which is the one I take is true, then the question is what happens to the evolutionary process as you increase the number of selection pressures. Both the mathematics and empirical evidence show that your position and the theory of evolution is mathematically impossible.
I have produced hundreds of empirical examples which show that additional selection conditions slow down the evolutionary process and you have agreed to that which means you have some common sense.Kleinman: "Apples are red."
Me: "Some are, yes, but some are green."
Kleinman: "So you agree that apples are red."
Me: "No, apples can be red."
Kleinman: "Everyone, rocketdodger agrees that apples are red."
Me: *sigh*
Your analogy is not quite correct rocketdodger.
Kleinman: Only single selection pressures targeted to single genes evolve rapidly.
Rocketdodger: That proves that evolution occurs rapidly.
Kleinman: Combination selection pressures profoundly slow the evolutionary process.
Rocketdodger: Weak selection pressures occur with strong selection pressures so single selection pressures don’t exist.
Kleinman: Weak selection pressures only act to slow the evolution of strong selection pressures and either weak or strong selection pressures interfere with the evolutionary process. Two or more strong selection pressures profoundly affect the population’s ability to evolve to these strong selection pressures simultaneously.
Rocketdodger: No they don’t n+1 selection pressures evolve more quickly than n selection pressures.
Kleinman: Well rocketdodger, here are mathematical examples and hundreds of empirical examples which show how mutation and selection actually works.
Rocketdodger: The mathematics can’t be true because it doesn’t agree with my belief system and the citations can’t be true because you found them with google.
Adequate’s silly graph shows nothing. Adequate admits there are no experiments available to show any validity to his silly graph but rocketdodger, why don’t you help out Adequate and produce the experiment.Adequate's graph shows the same conclusion you would come to if you actually tried to formalize the nonsense flowing out of your mouth (or fingers, as it were). Quite simply, it shows that according to the model you yourself are using the time it takes for complete fixation under 50 pressures at once is less than the time it takes for complete fixation if you apply the 50 pressures in sequence, one at a time. This is impossible for you to understand, of course, because doing so involves more than googling and pasting.
Adequate admits that he has no real examples of his mathematics and that he doesn’t know anything about the mathematics of mutation and selection. If Adequate could, he would be googling and pasting but there are no real examples of his ridiculous proposal because mutation and selection simply don’t work that way. There are no sorting/optimization/iteration problems that work that way which converge more quickly the more sorting/optimization/iteration conditions imposed on the problem. Mutation and selection does not work the way Adequate is speculating. There is plenty of mathematical and empirical evidence which show that both you and Adequate are wrong about the way mutation and selection actually works.
We have numerous mathematical models (including Dr Schneider’s ev model) which show that combination selection pressures profoundly slow the evolutionary process and a vast amount of empirical data which substantiates this mathematical fact and you have Adequate’s silly graph and no empirical data to support this silly graph.1) You don't even understand Schneider's ev model, because if you did you would be able to say more than "Schneider's ev model shows this and that."

2) Its a good thing you don't, because it will produce the same graph that Adequate is using.
Let’s see, I’ve been discussing ev online on this thread with Paul (the author of the online version of ev) for more than a year now and also engaged in public debate on this model for several months more on the Evolutionisdead forum. I have done parametric studies of the ev model running hundreds of cases with the model. If that is not enough, I have had private discussions with Dr Schneider for several months about his ev model before I started this public discussion. So rocketdodger, if you can generate Adequate’s silly graph with ev, have at it. Rocketdodger, have you even run a single case with ev?
Oh, I see, my “informal” arguments using a peer reviewed and published model of mutation and selection and hundreds or real example which substantiates this results isn’t formal enough for you.Those arguments aren't even informal -- they aren't arguments at all. You have not provided a single coherent argument for why all of the studies you throw at us support your theory. Posting a pasted abstract and saying "look, see!" does not constitute an argument. Well, unless you are a bible school kiddie.

In fact, the only thing you have provided a valid argument for is why in many cases multiple selective pressures don't profoundly slow evolution.
So what are you worried about, if I am wrong, this will all just blow away but if I’m correct, the theory of evolution by mutation and selection is blown away. And rocketdodger, in case you haven’t noticed, I have the mathematical and empirical evidence to support my argument.
Evolution by mutation and selection is analogous to optimization theory.Lol. Do you even know what that statement means? No, you do not. If evolution by mutation and selection is analagous to optimization theory, can you tell us why? No, you cannot.

If you did and could, then you would suddenly see that all of your assumptions and claims are wrong -- something you will never be able to realize until you at least try to formalize your arguments, even if just a little.
Sure I can tell you why mutation and selection is analogous to optimization theory, I have been telling you why. Mutation and selection is all about finding a fitness optimum, take a look at the figures I have posted which show the fitness landscape. The difference is that when doing an optimization problem, you try to find the optimum by a systematic search while with the mutation and selection process, the search is done by random mutations. This is a much slower process than used in systematic search algorithms.
Rocketdodger, I thought all my citations proved your argument, how could they also be random?As in "what crap can I google and paste on to the thread today?"

Admit it, you haven't read in full even a single study that you have cited. You don't even know what the sentences you highlight mean.
Take any of the citations I have posted and prove that they show something other than what I contend. You are just jealous, you have no citations which support the ridiculous contention that n+1 selection conditions evolve more rapidly than n selection conditions.
Since you evolutionists still don’t understand that evolution by mutation and selection is simply a sorting/optimization problem where the number of selection conditions (sorting/optimization conditions) profoundly slows the processYou are right, none of us understand this. Please tell us why mutation and selection is simply a sorting/optimization problem.
Again? Ok, for you rocketdodger, I’ll do it. Mutation and selection is a sorting process for beneficial and detrimental mutations with the optimization condition, the fitness of the population to reproduce. Check out the mathematics and empirical evidence of this rocketdodger, that’s what you will find out how the mutation and selection process actually works.
Since you admit that evolution is not your field, I’ll fill you in on the mathematics of the mutation and selection sorting problem.Is it your field, Kleinman? We have been very revealing with our qualifications, despite the fact that we know you will use such information against us. Would you care to return the favor? Please tell us:

a) Your educational background, including any degrees you have gotten and any research you have taken part in.

b) Your current job and position, as stated on your business card.
All the information is already posted on this thread.
Hi Rocketdodger. Kleinman is simply trying to goad me and live up to his Annoying claim. I do not value his opinion, so what he says is really immaterial. I just hope for new funny things to read. As of yet, he has only repeated his same nonsense.

As for his credentials. He's stated that he is Dr. Alan Kleinman. A physician with a PhD in engineering (I do not remember which field). He even posted a link to his thesis as proof of his degree. I could critique his PhD for irregularities in his publication track that raise interesting questions. But, I see no reason to doubt him or this. As it is irrelevant. His terrible arguments and woefully terrible understanding of science is much more telling.
There you go rocketdodger. Don’t forget I have a BS in advanced biological sciences as well. Joobz, why don’t you try to find some irregularities in my PhD thesis or any of my publications? Go for it joobz, PhD in alchemical engineering.
Joobz, PhD in speculational engineering again posts his speculations. What I post is the mathematical results from Dr Schneider’s peer reviewed and published model of random point mutations and natural selection which show that combination selection pressures profoundly slow the evolutionary process. In addition, I post empirical examples which substantiate this mathematical finding, something which you can not do with your speculations. Since you admit that evolution is not your field, I’ll fill you in on the mathematics of the mutation and selection sorting problem. The dominant parameter in this problem by far is the number of selection (sorting) conditions. All other parameters have much smaller effect on the rate of evolution. It is for this reason that the theory of evolution is mathematically impossible. The only concept more ridiculous than the theory of evolution is your theory of abiogenesis by cooperative chemistry.All of your citations and quotes definitively show that an organism population subjected to one overwhelmingly strong selection pressure will evolve quickly. Thus, you now must produce proof that this condition appears so rarely in natural environments, that evolution would not have sufficient generational time to occur.
Hey kjkent1, if you can prove that reptiles evolved into birds one strong selection pressure at a time, go for it.
The geological and fossil records demonstrate that evolution has occurred within the generational time available.
It didn’t happen by mutation and selection, it is mathematically and empirically impossible. You better go back to the drawing board and formulate a new interpretation of the fossil record.
Do you have any contradictory evidence to either discredit the observed record or to demonstrate that organism populations in natural environments are never subjected to a single overwhelming selective pressure?
We have plenty of evidence, both mathematical and empirical which show that mutation and selection does not work the way you allege. Since mutation and selection is the fundamental mechanism used to justify the theory of evolution, this mathematical and empirical evidence pulls the rug out from the theory of evolution.
Your constant posting of the same litany of evidence, which undermines your own hypothesis, is incredibly OCD.
It must be the pleasure I get in annoying evolutionists.

[Paul C. Anagnostopoulos]

Either way, you get some numbers, you get some information. It doesn't really surprise me ...
Good.


But my beliefs aside, I'm more concerned if you have any actual real life biology to show, some detailed pathway, for example, of anything.
What are you asking for? A complete explanation of the evolution of something? Probably hopeless. If that causes you to reject evolution, then you have to reject all of science.


You're saying some Pascal can adequetely model all the variables in the universe or the Earth or something?
Of course not. I *********** repeat: I never said that Ev demonstrates that the entire theory of evolution is correct.


Well, I asked the first question about your belief. You claimed that 'X answers questions = X is right'. What is the rationale, if one exists, behind this belief system of yours?
That wasn't my claim. Let's review:

Be sure to not leave out any steps. Since you are the one claiming a scientific path for this, should be easy to provide all the steps, and not make any scientistic jumps that require your faith to fill.

You are, for consistency, rejecting all of the science, since not every question has been answered in its entirety, right?

And, to an even greater degree, you are rejecting the goddidit hypothesis, since not a single question has been answered by it, right?

Can you outline where the ability to 'answer questions' makes something right or wrong? I must have missed that in logic class.
You appear to be rejecting evolution because we do not have all the steps, that is, we have not answered all the questions. You are not rejecting it because you don't like the answers we have so far, but because we do not have all of them. If that is the case, then the godddidit hypothesis is in even deeper trouble.

That is all I was saying.

~~ Paul

[joobz]

Joobz admits his chemistry is pure speculation and you admit you have no understanding of the mathematics of mutation and selection. Where did I say that I didn't understand the mathematics?

Joobz, why don’t you try to find some irregularities in my PhD thesis or any of my publications?

Well, if you must know. I was refering to the fact that you only had two publications from your thesis and those two publications had two seperate advisors on them. This wouldn't be a big deal if you were an experimentalist, but you were a modeling guy. most modelling PhDs I know will have ~5-7 pubs from their thesis. Couple this with the fact that you were first author on only one of them, and it doesn't really seem like you did much in your PhD.

[rocketdodger]

Joobz admits his chemistry ... all the citations posted would become understandable to you.

Your response had nothing to do with my post. Congratulations on yet another failure.

Dr Schneider has posted extensively about his ev model including a glossary of his variables used in his calculations.

What does this have to do with whether or not you understand it?

Why shouldn’t I cite evidence of how mutation and selection actually works? There is an abundance of this evidence available.

And a complete lack of understanding regarding that evidence on your part, which is why you consistently dodge questions by simply posting more citations.


Why don’t you use google and find a citation which shows that n+1 selection pressures evolve more rapidly than n selection pressures?

I don't need google, I simply used all the citations you provided us:

Bacteria -- n pressures, slow mutation.
Bacteria + penicillin -- n + 1 pressures, rapid mutation.

Of course you will deny this somehow...

Your analogy is not quite correct rocketdodger.

The odds of you actually having any degrees, given your displayed maturity level, are extremely slim.


There are no sorting/optimization/iteration problems that work that way which converge more quickly the more sorting/optimization/iteration conditions imposed on the problem.


I agree, there are not. But this has very little to do with evolution, and if you actually tried to explain why you think evolution is merely a sorting/optimization problem you would soon see this. But like I said.. you cannot explain why, because you do not know why. All you know is the nonsense you put together from random google results.


Mutation and selection does not work the way Adequate is speculating. There is plenty of mathematical and empirical evidence which show that both you and Adequate are wrong about the way mutation and selection actually works.

Actually, there isn't. If you could pull your head out of where it is, and actually think about what Adequate is saying, you would realize that not a single one of the studies you have cited has any information about the issue Adequate brings up. Of course, you would rather google and paste more nonsense than stop to think.

Let’s see, I’ve been discussing ev online on this thread with Paul (the author of the online version of ev) for more than a year now and also engaged in public debate on this model for several months more on the Evolutionisdead forum.

Wrong. Despite the actual attempts by others at a legitimate discussion, you have done nothing but regurgitate nonsense over and over. Please provide me with one single example of a response you have made that actually addresses the issue brought up in the post that elicited the response.


I have done parametric studies of the ev model running hundreds of cases with the model.


Proof?


If that is not enough,


It is not, even if it was true.


I have had private discussions with Dr Schneider for several months about his ev model before I started this public discussion.


If you did, which I doubt, they would follow the template you have provided us in this thread. That makes you more of a heckler than a "correspondent" I am sorry to say. I wonder what Schenider himself would have to say about this claim of yours...


So rocketdodger, if you can generate Adequate’s silly graph with ev, have at it. Rocketdodger, have you even run a single case with ev?

Working on it.


Sure I can tell you why mutation and selection is analogous to optimization theory, I have been telling you why.

Listening...


Mutation and selection is all about finding a fitness optimum, take a look at the figures I have posted which show the fitness landscape. The difference is that when doing an optimization problem, you try to find the optimum by a systematic search while with the mutation and selection process, the search is done by random mutations. This is a much slower process than used in systematic search algorithms.

...Thats it? Like I said, what you learned from a google search. Why is mutation and selection "all about" finding a fitness optimum? What is a fitness optimum? What is a fitness landscape? How are they created? What can change them?

Take any of the citations I have posted and prove that they show something other than what I contend.

I did. I showed you that all of your citations demonstrate that mutation can happen very rapidly when there is a single strong selective pressure and multiple weak selective pressures. You even admitted this.


You are just jealous, you have no citations which support the ridiculous contention that n+1 selection conditions evolve more rapidly than n selection conditions.

Except if the n pressures are all weak, and the n + 1th pressure is relatively strong... in which case you agree. Of course you don't realize this ...

Again? Ok, for you rocketdodger, I’ll do it. Mutation and selection is a sorting process for beneficial and detrimental mutations with the optimization condition, the fitness of the population to reproduce.

Ahhh.. now we are making progress. Actually, the condition is the relative fitness of individuals who carry the mutation to reproduce, which is somewhat different.

Now, how is the sorting accomplished, and why do you think adding more conditions makes the sorting process slower?

[kleinman]

But my beliefs aside, I'm more concerned if you have any actual real life biology to show, some detailed pathway, for example, of anything.What are you asking for? A complete explanation of the evolution of something? Probably hopeless. If that causes you to reject evolution, then you have to reject all of science.
Paul, your own model shows mathematically how mutation and selection works, which is that multiple selection pressures profoundly slow the evolutionary process. So now your argument for the theory of evolution is that a complete explanation of the evolution of something is hopeless. This is proof based on ignorance. There is plenty of data both mathematical and empirical which show how mutation and selection works. You don’t have to throw out any science, just throw out the mythology of the theory of evolution.
You're saying some Pascal can adequetely model all the variables in the universe or the Earth or something?Of course not. I *********** repeat: I never said that Ev demonstrates that the entire theory of evolution is correct.
That right Paul, what ev demonstrates is that combination selection pressures profoundly slow the evolutionary process. That’s why ev converges so slowly for all but the tiniest genome lengths and that same behavior is seen in real examples of mutation and selection. I really like Dr Schneider and your model. Did you notice that Dr Schneider is still supporting his model? So do I. It properly models the essential mathematical features of the mutation and selection process.
You appear to be rejecting evolution because we do not have all the steps, that is, we have not answered all the questions. You are not rejecting it because you don't like the answers we have so far, but because we do not have all of them. If that is the case, then the godddidit hypothesis is in even deeper trouble.
What steps Paul? Ev shows that multiple selection pressures evolve profoundly slowly. The only way you get rapid evolution is one gene at a time and that is not evolution to some new function. You have no selection pressures that can evolve a gene de novo and evolution against multiple selection pressures is a profoundly slow process. The mathematical and empirical evidence of mutation and selection shows that evolutiondidn’tdoit.
Joobz admits his chemistry is pure speculation and you admit you have no understanding of the mathematics of mutation and selection.Where did I say that I didn't understand the mathematics?
You prove you don’t understand mathematics with your next statement.
Joobz, why don’t you try to find some irregularities in my PhD thesis or any of my publications?Well, if you must know. I was refering to the fact that you only had two publications from your thesis and those two publications had two seperate advisors on them. This wouldn't be a big deal if you were an experimentalist, but you were a modeling guy. most modelling PhDs I know will have ~5-7 pubs from their thesis. Couple this with the fact that you were first author on only one of them, and it doesn't really seem like you did much in your PhD.
I have published publicly on two topics and you don’t understand the mathematics of either. The first was the solution to an nonlinear inverse partial differential equation which I doubt you even know what it is let alone understand the mathematics and the second was on the thermodynamics of nonlinear phase change which again, I doubt you understand the mathematics of this problem. What is interesting about my PhD thesis is that I was looking at why thermography was not proving to be useful in diagnosing breast cancer. If you study the mathematics I worked on, you will understand why thermography is useless for this. I seem to be good at proving the negative. The mathematics of mutation and selection proves why the theory of evolution isn’t true. Most of my scientific writing I have been paid for and was not for public consumption. I couldn’t do what you people in academics like to do, publish the same material over and over to get tenure. Oh, my advisor didn’t change on my PhD thesis or publication on that topic. Joobz, you are just incompetent in mathematics and can’t tell the difference between the publications. Joobz, you can’t find the irregularities in something which you don’t understand. You don’t understand the mathematics of my publications and you don’t understand the mathematics of mutation and selection. That you prove to us by example.

Since you evolutionists can’t figure out the mathematics of mutation and selection how about some more citations which show that combination selection pressures profoundly slow the evolutionary process. I know how much you evolutionists enjoy these citations.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=127054 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=127054)
It has been assumed that the risk that an organism will develop resistance to two agents is the product of the risks of developing resistance to each separately. For example the risk of resistance for a combination of rifampin, streptomycin, and isoniazid is10^−25/bacterium/generation. The risk of mutants emerging in a patient depends partly on this and the size of bacterial populations within compartments. Therefore, risk of resistance may be more accurately calculated using the formula P = 1 − (1 − r)n where P is the probability of drug resistance emerging, r is the mutation rate, and n is the number of bacilli in a lesion, usually calculated to be 10^8 per lesion (72). If single-drug therapy with a risk of mutation of 10^−6 is used, the risk of resistance emerging is 100%. If two drugs with a combined mutation rate of 10^−12 are used, then the risk is 0.01%; however, if the bacterial population in a lesion is 10^10 and the mutation rate is 10^−12, then there is a 1% risk of resistance emerging.
And
Drug-resistant tuberculosis poses a significant threat to human health, and it is important to understand how the resistance emerges if we are to reverse the upward trend. Treatment with internationally approved regimens results in a very high cure rate with few relapses and without the emergence of resistance. These regimens are effective in preventing the emergence of resistance because combination chemotherapy makes it highly unlikely that there will be a spontaneous mutant resistant to all of the components of chemotherapy. Patients with uncomplicated tuberculosis who receive inadequate treatment provide a selection advantage for resistant mutants because bacteria may be exposed to monotherapy, permitting the emergence of resistance to single agents and then to multiple agents as the protection of combination chemotherapy is eroded. That M. tuberculosis cells within the body are susceptible to different components of antituberculosis chemotherapy means that the risk of resistant mutants emerging is higher than would be expected if the whole population of bacterial cells could be counted together. Clinical complications such as empyema and extensive cavitation permit a large population to develop in a compartment into which drugs may not penetrate. This large bacterial pool increases the population for mutation, and with poor penetration there is an increased likelihood of resistance emerging. A similar situation may develop in patients with extensive disease or poor immunity (Fig. 1).
http://jvi.asm.org/cgi/content/full/75/19/9502 (http://jvi.asm.org/cgi/content/full/75/19/9502)
Highly active antiretroviral therapy (HAART) with reverse transcriptase inhibitors in combination with protease inhibitors has proven to suppress human immunodeficiency virus type 1 (HIV-1) replication to undetectable levels in patients (11, 12, 17). HIV-1 variants frequently evolve that escape HAART by developing resistance to the inhibitors used (4, 15, 19, 28, 40, 42). Of patients first treated with a single drug regimen and then going onto HAART, as many as 40% have a viral rebound within the first 3 years, and this number is likely to be higher outside of controlled studies (20, 35). Moreover, transmission of drug-resistant HIV has been observed and is likely to increase with more patients on combination therapy (25, 38). Thus, there is a need to fully understand the sequence of molecular changes to HIV concomitant with development of resistance to protease inhibitors. In turn, this knowledge should facilitate the development of new inhibitors with activities against drug-resistant isolates.
Rocketdodger, why don’t you fire up google this weekend and see if you can find a real empirical example which shows that n+1 selection pressures evolve more quickly than n selection pressures.

You all have a good weekend and maybe you evolutionists will figure out how mutation and selection actually works next week and I’ll be back next week with more citations to annoy you with the mathematical and empirical facts of this phenomenon.

[rocketdodger]

I can't find the link to Kleinman's thesis and background, anyone have it handy?

[delphi_ote]

:words:
When I'm right, I'm right (http://forums.randi.org/showthread.php?postid=3100515#post3100515).
:whistling

[joobz]

I have published publicly on two topics and you don’t understand the mathematics of either.
I didn't bother reading your publications and judging by the number of citations, nobody else bothered reading them either or found them very useful.

The first was the solution to an nonlinear inverse partial differential equation which I doubt you even know what it is let alone understand the mathematics and the second was on the thermodynamics of nonlinear phase change which again, I doubt you understand the mathematics of this problem.You sound very defensive. I think it funny that you invoke PDEs as though it'd make you sound smarter.

What is interesting about my PhD thesis is that I was looking at why thermography was not proving to be useful in diagnosing breast cancer. If you study the mathematics I worked on, you will understand why thermography is useless for this. I seem to be good at proving the negative. The mathematics of mutation and selection proves why the theory of evolution isn’t true. Most of my scientific writing I have been paid for and was not for public consumption. I couldn’t do what you people in academics like to do, publish the same material over and over to get tenure. Oh, my advisor didn’t change on my PhD thesis or publication on that topic.
So you are saying you only had 1 publication from your thesis? You are even more impressive.:rolleyes:

Joobz, you are just incompetent in mathematics and can’t tell the difference between the publications. Joobz, you can’t find the irregularities in something which you don’t understand. You don’t understand the mathematics of my publications and you don’t understand the mathematics of mutation and selection. That you prove to us by example.
I'm sorry, but attempting to goad me through insults and lies won't make your failings any less obvious or sad.

[kjkent1]

All of your citations and quotes definitively show that an organism population subjected to one overwhelmingly strong selection pressure will evolve quickly. Thus, you now must produce proof that this condition appears so rarely in natural environments, that evolution would not have sufficient generational time to occur.Hey kjkent1, if you can prove that reptiles evolved into birds one strong selection pressure at a time, go for it.At the risk of repeating myself: The geological and fossil records demonstrate that evolution has occurred within the generational time available.

It didn’t happen by mutation and selection, it is mathematically and empirically impossible. You better go back to the drawing board and formulate a new interpretation of the fossil record.How bizarre you are. You can say that it didn't happen by mutation and selection, but, once again, the geological and fossil record demonstrates that it did happen. And, if as you contend, the only way it could have happened was "one strong selection pressure at a time," then, to paraphrase Sherlock Holmes, "Eliminate all of the other possibilities, and whatever you are left with, no matter how improbable, must be the truth."

So, once more, then: Do you have any contradictory evidence to either discredit the observed record or to demonstrate that organism populations in natural environments are never subjected to a single overwhelming selective pressure?

No one is interested in your showing more examples of combination selection pressures -- especially as each of your examples is conditioned on the difference between the observed outcome of one strong pressure showing evolutionary change, vis-a-vis combination pressures showing evolutionary stability. That is, all of your examples prove evolution occurs, one strong pressure at a time. And, the fossil record confirms this.

The truth is incredibly simple Alan. Mutations occur and send life forms off into unpredictable directions. The aggregate of such changes is a morphological change in the organism.

Your problem, if I may, is that you are a determinist, not much different from Einstein. In your world of cause and effect, there is no room for random chance to interfere. Einstein lost this debate a century ago. God plays dice with the universe, and the result is that we are here to argue about it.

[Foster Zygote]

As you come up with this witless crap every coupla months or so, could I refer you to the last time I refuted this pile of crud?

http://fstdt.com/winace/pics/broken_record.jpg

By the way, are you hammegk's kid brother?

Is the B side of that single "Stochastic Means Random"?

[rocketdodger]

I finally read up on and ran the ev program. Unfortunately, I am unable to produce a graph like Dr. Adequate, probably because (although I didn't realize it at first) he used some other model/program.

Why can't I reproduce such a graph using ev? Because as it turns out, ev has nothing to do with selective pressures...at all... so Kleinman, how on Earth are you using ev to support your claim that "combination selection pressures profoundly slow evolution?"

You said "this is what the mathematics of mutation and selection show" but so far, other than ev, you have cited no mathematics (nor presented any yourself) at all.

[Kotatsu]

Well, Kleinman is entitled to critique a model he feels is not reflective of reality, or for whatever other reason. Especially if the people who made the model are trying to convince others it is reflective of reality.

You have misunderstood this thread. While more or less everyone else has understood that the model in question is just a model, which doesn't claim to model all of reality, and which certainly doesn't model all of reality, Kleinman is the person who has repeatedly claimed that it does, or, at least, that it is so accurate and so complete that results from the model, when in conflict with results from reality, counters and supersedes these, and should replace them. Kleinman's "critique" of the model is virtually non-existent, whereas the rest of us have long ago realised the limitations of the model, and act accordingly.

It is not the "evolutionarians" of this thread who are holding this model to be a sacred standard of our way to view the world. I assume you have not read any part of the thread prior to joining in, or you would have spotted this.

[Kotatsu]

No Kotatsu, these are not comments on American popular culture, they are comments on evolutionist popular culture because mutation and selection simply does not work the way you allege, the mathematics and empirical evidence of mutation and selection contradict your scientifically and mathematically baseless speculations and extrapolations.

Actually being biologist, as opposed to you, I must, if I am to believe you, ask what sort of biology text books you read which have "Sesame Street" and "Marvel comics" listed in their evolution sections. These, I understand, are references to American popular culture, but I am unfamiliar with the exact details, never having lived in America. Ask me about Czech and Polish animation from the 80's, instead. They showed heaps of that on Swedish TV when I was a kid.

So, the now we have the theory of evolution by “sheer coincidence”, Kotatsu, you take speculation to new levels.

So you have no actual answer, is that a correct interpretation?

Oh, that’s right, you said a reptile chased in into a tree and it would be beneficial for that reptile to grow wings. You evolutionists really practice some weird thinking.

No. Your post contains several misinterpretations. I gave you a list of a number of various realistic selection pressures, all of which could plausibly lead to a situation where mutations in genes which for instance aided in horizontal movement between trees would be advantageous compared to alleles without this advantage.

I further elaborated on how these selection pressures --- one of them alone, several in combination, or even one or several combined with selection pressures I didn't list --- would act on all genes in the genome, as evidenced by the fact that unrelated groups of animals have evolved different structures to counter the same evolutionary pressure(s). You may recall that "flying" squirrels, "flying" snakes, "flying" frogs and actually flying birds all have different structures for moving between trees, suggesting both that the need to be able to move between trees is common in the animal kingdom, and that the selection pressures inherent in this need have caused the formation of several solutions.

It is not, as you would want it to seem, a case of a predator chasing a small dinosaur up into a tree and then poof! it grows wings and flies around taunting the predator. It is a case of where succession of several hundreds or thousands of generations of various predators repeatedly chase a similar succession of prey animals into trees, and continue to chase them while in the tree, leading to what some would call an "arms race" in who is best at moving between trees, the predator or the prey. In at least some cases, the prey have had the advantage, as we can still see flying or "flying" animals today.

Please try to comprehend what I am saying, and stop misrepresent it. It is not very annoying. More annoying, by far, would be if you actually tried to understand and could poke actual holes in whatever we say. Mockery and misrepresentation, though no doubt time-honoured crafts in your world, are more silly than annoying.

What you are seeing are connections which are mathematically and empirically impossible. These are extrapolations and speculations that are contradicted by the way mutation and selection actually works.

Yet those trees are constructed using maths... In the simples tree-building algorithm, that of distance, the differences between the various sequences are simply counted, and the tree is constructed in such a way that those sequences most similar to each other are placed next to each other, and so on in a way that forms a nested hierarchy (unless, of course, all sequences are identical, which will instead result in a "comb" polytomy).

Systematics is no longer a case of doctors and professors looking at their group of animal and drawing those delightful (and remarkably often at least somewhat correct) evolutionary trees which you see in older literature, where extant group A gives rise to extant group B through the evolution of a tapered mandibular tract and a lateroventral pigmentation caused by a glandularisation of coelomocytes. These things are most commonly done at a molecular level, and is entirely automatic.

Somehow, I get the sense that, once more, you have no idea what you are talking about. Nonetheless, you talk.

When I construct a phylogenetic tree, I will see connections between the various taxa. That is why it is called a "tree". These connections and the over-all structure of the tree is based on some tree-building criterion (of which there are several), all of which are based on maths. Granted, while I can understand the maths behind some of the more basic tree-building mechanisms, I can usually not understand exactly how the more modern ones work. They are often constructed by mathematicians and not by systematicists, and mathematicians have their own obscure and bewildering language in which they present their theories. Nevertheless, they do result in trees (or, more and more often recently, networks).

As you are such a math genius, I'd like to know if you could perhaps explain what the underlying flaw in the reasoning of all those models is. Remember: "mathematically and empirically impossible" or some derivation thereof is not an explanation.

There are many unusual species which evolutionists like you speculate and extrapolate that appear by evolution. However, you are in denial about how mutation and selection actually works. Combination selection pressures confound the evolutionary process. A population can most easily evolve against a single selection pressure directed at a single gene. As soon as multiple selection pressures come into play, these multiple selection pressures confound the evolutionary process. That is what the mathematical evidence shows and that is what the empirical evidence shows.

So now it is no longer impossible for them to evolve against several selection pressures, just not as easy? And multiple selection pressures don't "slow and ultimately stop evolution" any more, but simply confounds it? Marvellous! In a few decades, we'll finally have you on our side!

So these species are merely anomalies or unusual species? How does this tie in with their distribution in the fossil layer? Why are they positioned in layer so that they give an impression of a step-wise transition from non-feathered dinosaurs, through feathered dinosaurs and what I will call "proto-birds" for lack of a better term (at least as I can recall), all the way to animals which seem bird-like enough to warrant inclusion in extant orders and, subsequently, families, genera and species? Were new unusual bird-like animals created from scratch every ten million years and then discarded when the new model came along, similar to how many old computers are thrown out?


Mr Scott has not shown that scales transform into feathers, all Mr Scott has shown is that feather can grow on birds in unusual locations when there is a mutation. Kotatsu, have you ever heard of teratomas?

I have now. However, feel free to elaborate, as I believe this may be an area where you can actually display knowledge.

Nevertheless, while waiting for that to happen, I would like to draw your attention again to the fact that while we cannot of course know the exact sequences of the dinosaur DNA, having scales differentiate into feathers due to one single mutation still implies that great changes in morphology need not be the result of several mutations in different genes. You have argued that too many mutations would be needed to transform a dinosaur into a bird, because the genes responsible for such a change would need to be changed sequentially, as multiple changes in different genes would "confound" the evolutionary process. If the difference between two such diverse character states can hang on one single mutation in birds today, it is possible that it took only one or a few mutations in ancient times as well. This shows your argument to be unfounded in at least some cases. Therefore, its power to convince is lessened somewhat.

[Kotatsu]

Of course I am Kotatsu, here is a note from your lecture: Reptile chased into tree->reptile grows wings.

Good, good. Now, your homework for next week will be to actually read what is being said to you before taking the notes. See if you can do that, and you may actually pass this class!

がんばれ!!!!!

[Belz...]

How ? Since you admit they are weaker, why would they matter all that much ?

You still haven't answered my point about the meteor, and I suspect you won't.

Uh-huh. But you must admit that the weaker ones less so.

http://http://forums.randi.org/showpost.php?p=3110656&postcount=6258


Hello ? Klein ?

[Belz...]

All of your citations and quotes definitively show that an organism population subjected to one overwhelmingly strong selection pressure will evolve quickly. Thus, you now must produce proof that this condition appears so rarely in natural environments, that evolution would not have sufficient generational time to occur.

The geological and fossil records demonstrate that evolution has occurred within the generational time available.

Yeah, that nails it, right there.

[Paul C. Anagnostopoulos]

Why can't I reproduce such a graph using ev? Because as it turns out, ev has nothing to do with selective pressures...at all... so Kleinman, how on Earth are you using ev to support your claim that "combination selection pressures profoundly slow evolution?"
Why don't you think so? You can adjust the strength of three selection criteria, or eliminate them, on the New dialog. The fact that there are three is arbitrary, but they are individually adjustable.

One problem is that Evj has no mechanism for introducing the pressures sequentially. So we can't compare what Dr. A. represented by his red and blue lines. Then again, each of Dr. A's pressures affects a different gene, whereas Evj only has one gene affected by multiple pressures, so the comparison may be moot.

~~ Paul

[Belz...]

There are many unusual species which evolutionists like you speculate and extrapolate that appear by evolution. However, you are in denial about how mutation and selection actually works. Combination selection pressures confound the evolutionary process.

Saying it is not proving it.

A population can most easily evolve against a single selection pressure directed at a single gene. As soon as multiple selection pressures come into play, these multiple selection pressures confound the evolutionary process. That is what the mathematical evidence shows and that is what the empirical evidence shows.

Not, it isn't. Not if we are to believe your own examples, anyway.

[rocketdodger]

Why don't you think so? You can adjust the strength of three selection criteria, or eliminate them, on the New dialog. The fact that there are three is arbitrary, but they are individually adjustable.


???

Which fields? I didn't see anything that suggested to me "different" selective pressures, only variations on the one (I.E. what to do on ties, etc.).

And what did Adequate use to make that graph?

[T'ai Chi]

If that causes you to reject evolution, then you have to reject all of science.


Yawn. Is this what passes for skepticism round here? If someone questions you you claim they reject all of science?

Two points: 1) one can question anothers' claims on evolution without rejecting evolution. And 2), one can in fact reject evolution and do many other sciences just fine. Remember, evolution is very specific here, not just 'change over time'.


You appear to be rejecting evolution because we do not have all the steps, that is, we have not answered all the questions.


Um you appear to be mistaken. I'm asking if you have real biology rather than some simulation.

[T'ai Chi]

It is not the "evolutionarians" of this thread who are holding this model to be a sacred standard of our way to view the world. I assume you have not read any part of the thread prior to joining in, or you would have spotted this.

You must have missed the part in a science class where people can critique a model without claiming that the people who created the model are claiming the model is Truth.

The idea of pointing out what I did about the model should have been obvious, that real biology would trump any model any day in terms of importance. For example, one complete evolutionary pathway of anything to anything else would be better than any Pascal program.

[rocketdodger]

Um you appear to be mistaken. I'm asking if you have real biology rather than some simulation.

We have numerous pieces that, taken together, constitute pretty good evidence. Given time, we hope to find all of the pieces, and judging by the increasing rate of acquisition, this will be done fairly soon.

Do you have any other ideas? Are there other mechanisms that could be responsible for life on Earth as we know it?

[CFLarsen]

Yawn. Is this what passes for skepticism round here? If someone questions you you claim they reject all of science?

Two points: 1) one can question anothers' claims on evolution without rejecting evolution.

Still up to your dishonest tactics.

Paul didn't say that you had to reject all of science merely for questioning him. He said that you have to reject all of science if you reject evolution.

And he is right. Because the moment you invoke God (because that's what you Creationists do), you don't need science for anything. All you need is "God diddit" as explanation for everything.

For biology, for geology, for astronomy, for anything that happens. Whatever you can't explain, "God diddit".

A bolt of lightening? Your explanation is "God diddit".

And 2), one can in fact reject evolution and do many other sciences just fine. Remember, evolution is very specific here, not just 'change over time'.

No, you can't reject evolution and still claim to "do" other sciences just fine. Evolution is dependent on so many other branches that it is not only hypocritical to claim that you "do" other sciences "just fine", it is also flat-out lying.

Um you appear to be mistaken. I'm asking if you have real biology rather than some simulation.

Yes, the old Creationist argument: If Evil-utionists can't point to real-life examples of Evil-ution, Evil-ution must be false.

Tough tittie, T'ai. (http://talkorigins.org/faqs/faq-misconceptions.html#observe)

[joobz]

Yes, the old Creationist argument: If Evil-utionists can't point to real-life examples of Evil-ution, Evil-ution must be false.

Tough tittie, T'ai. (http://talkorigins.org/faqs/faq-misconceptions.html#observe)

Don't forget the tactic that no matter what evidence you present, they simply claim it doesn't count. A lot like the demand for a "transitional form" demand.

I think T'ai argued himself into obscurity the moment he felt the need to invoke the pseudorandom nature of computer generated random numbers. Bringing up something so mundane and tangential to the argument is a rather embarrassing display of simpleness.

[Dr Adequate]

So, has he thought of any new lies?

[Paul C. Anagnostopoulos]

Which fields? I didn't see anything that suggested to me "different" selective pressures, only variations on the one (I.E. what to do on ties, etc.).
Click the Advanced button on the New dialog and check out the Mistake points items. You can adjust the relative strength of the pressures on missed binding sites, spurious bindings within the gene, and spurious bindings outside the gene, or you can turn them off.

It's still only one gene that is being pressured, though.

~~ Paul

[Paul C. Anagnostopoulos]

Yawn. Is this what passes for skepticism round here? If someone questions you you claim they reject all of science?
It's not just the fact that you're questioning, obviously, but which specific objections you're raising. In your case, it's "Be sure to not leave out any steps. Since you are the one claiming a scientific path for this, should be easy to provide all the steps, ..." (emphasis mine). You could raise this objection about any scientific endeavor.


Two points: 1) one can question anothers' claims on evolution without rejecting evolution. And 2), one can in fact reject evolution and do many other sciences just fine.
I don't see how (2) is the case given your specific class of objection.


Um you appear to be mistaken. I'm asking if you have real biology rather than some simulation.
So your statement above is not a rejection of evolution? What the hell are you saying then?

You must have missed the part in a science class where people can critique a model without claiming that the people who created the model are claiming the model is Truth.
But Kleinman isn't just critiquing it, is he? He's using it as the foundation of his claims.

~~ Paul

[joobz]

So, has he thought of any new lies?
Except for trying again to establish some credibility regarding his math abilities by referencing his meager publications, no.

[kjkent1]

All of your citations and quotes definitively show that an organism population subjected to one overwhelmingly strong selection pressure will evolve quickly. Thus, you now must produce proof that this condition appears so rarely in natural environments, that evolution would not have sufficient generational time to occur.
The geological and fossil records demonstrate that evolution has occurred within the generational time available.Yeah, that nails it, right there.
Thanks. I'm no scientist. But, as an attorney, I have to try to find easy-to-follow-by-a-jury-of-peers-with-no-more-than-a-high-school-education statements/questions that force a witness to either admit them under oath -- or, look foolish in their denial.

I don't necessarily agree with kleinman's ev and combinatorial therapy hypothesis. But, I'm tired of trying to introduce other affirmative evidence, because he won't discuss anything other than what he wants to discuss.

So, based on kleinman's position, this is where he's at. He can argue all day and night that combinatorial pressures confound evolutionary change. But, his own examples show that one overwhelmingly strong pressure will cause quick evolutionary change. And, as we see historical evidence that such changes occurred, it falls to kleinman to now show that natural environments do not routinely display singular overwhelming selection pressures, and/or that the fossil record is a misrepresentation of history.

ETA: Ev uses three chemical level selection pressures to determine the fitness of an organism. In such a model, the sorting problem that kleinman constantly raises is interesting. But, in the real world, an organism's ability to reproduce is not so often the product of a small chemical conundrum. It's the product of the organism's ability to successfully avoid predation before reproducing. That is the one overwhelmingly strong pressure which exists in every natural environment and it generally renders all others inconsequential by comparison.

[Belz...]

Thanks. I'm no scientist. But, as an attorney, I have to try to find easy-to-follow-by-a-jury-of-peers-with-no-more-than-a-high-school-education statements/questions that force a witness to either admit them under oath -- or, look foolish in their denial.

I think that's why so many people hate lawyers :D

So, based on kleinman's position, this is where he's at. He can argue all day and night that combinatorial pressures confound evolutionary change. But, his own examples show that one overwhelmingly strong pressure will cause quick evolutionary change.

And it should be obvious. If a selection pressure kills ALL of the organisms that haven't adapted to it, within a generation, then within that time ALL of the remaining organisms WILL have adapted to it.

And, as we see historical evidence that such changes occurred, it falls to kleinman to now show that natural environments do not routinely display singular overwhelming selection pressures, and/or that the fossil record is a misrepresentation of history.

He doesn't have to, because his "hundreds of cited empirical examples and mathematical model prove that a combination of selection pressures profoundly slow evolution". Why care for facts when you can switch to theory-thumping ?

[T'ai Chi]

You could raise this objection about any scientific endeavor.


Well please don't try to evade the specific topic here. This is a thread about evolution Paul, not physics, astronomy, hydrodynamics or any other scientific endeavor.

Specifically, you have a model for a specific part of evolution, and you think it is good. That's all fine and dandy, but do you or don't you have actual biology to prove your points?

[Dr Adequate]

I notice that T'ai Chi hasn't become coherent or rational, either.

This thread works great as a wastepaper basket, doesn't it?

[rocketdodger]

Adequate can you link me to the model you used to make that graph Kleinman is claiming to be incorrect? I am trying to reproduce the results -- they seem intuitively correct (if one has a clue about math) but I need an actual model or program or something that I can use.

[delphi_ote]

Yawn.
If you're bored, you could really change things up by answering a substantive question (http://forums.randi.org/showthread.php?postid=3100515#post3100515) about your claims.

Or, you know, keep ignoring reality. I'll just be over here pretending like I'm waiting for an answer that I know will never come...
:whistling

[Paul C. Anagnostopoulos]

Well please don't try to evade the specific topic here. This is a thread about evolution Paul, not physics, astronomy, hydrodynamics or any other scientific endeavor
For crying out loud, it's a philosophical point. You're raising an objection to biology that can just as well be raised about almost any human endeavor.


Specifically, you have a model for a specific part of evolution, and you think it is good. That's all fine and dandy, but do you or don't you have actual biology to prove your points?
Of course there is actual biology: DNA, and the information it contains. But that's not your issue, is it? Your issue is that we can't map out every step between the Big Bang and DNA. From this you conclude ... something ... that you don't actually have the guts to state plainly. Something about needing a god of the gaps. Is that the same god who fills the meteorological gaps, or is this a Greek sort of thing with lots of gods?

~~ Paul

[Paul C. Anagnostopoulos]

This thread works great as a wastepaper basket, doesn't it?
So what's the cheapest department to run at a university?

Well, the second-cheapest department is pure math. All they need is paper, pencils, and wastebaskets.

The cheapest department is philosophy: They don't need any wastebaskets.

~~ Paul

[T'ai Chi]

You're raising an objection to biology that can just as well be raised about almost any human endeavor.


Again, please stay on track. Again, we're not talking about any human endeavor, we're talking about a very specific study of evolution which you posted about.

For example. In the graph that is produced, it is interesting that at times the red 'no selection' line is just as high as the green 'selection' line has been, as well as many ups and downs on both lines, so depending on what time you arrive in the process, one can certainly say that

a) the information created by 'no selection' is as high as the information created by 'selection' has been

b) information can increase, decrease, or stay the same in either scenario

In real life, how do you ascertain where we (the collective we, the biological kingdom) are at on the timeline?


Of course there is actual biology: DNA, and the information it contains.


Well that's nice, but vague. Can you show an actual more concrete example with many details? An actual biological study in vivo?


Something about needing a god of the gaps. Is that the same god who fills the meteorological gaps, or is this a Greek sort of thing with lots of gods?


Who knows (but you). You're the one who brought up these philosophical concepts and gods afterall.

[Belz...]

Well please don't try to evade the specific topic here. This is a thread about evolution Paul, not physics, astronomy, hydrodynamics or any other scientific endeavor.

T'ai, if you stopped being your usual obtuse self you might understand that Paul's point was that NO SCIENCE EVER HAS ALL THE STEPS or ALL THE ANSWERS. Therefore you cannot use that line of argument to criticise evolution.

[Belz...]

Well that's nice, but vague. Can you show an actual more concrete example with many details? An actual biological study in vivo?

Do you want pictures, too ?

[CFLarsen]

T'ai, if you stopped being your usual obtuse self you might understand that Paul's point was that NO SCIENCE EVER HAS ALL THE STEPS or ALL THE ANSWERS. Therefore you cannot use that line of argument to criticise evolution.

That's why T'ai Chi doesn't want to talk about other sciences: Because if he admits that no other scientific area has all the answers he demands that Evolution has, he has to admit that his criticism is fundamentally flawed.

[Paul C. Anagnostopoulos]

Again, please stay on track. Again, we're not talking about any human endeavor, we're talking about a very specific study of evolution which you posted about.
And again, you are refusing to admit that you have brought up a philosophical objection that pertains to almost every other human endeavor.


For example. In the graph that is produced, it is interesting that at times the red 'no selection' line is just as high as the green 'selection' line has been, as well as many ups and downs on both lines, so depending on what time you arrive in the process, one can certainly say that ...
Which graph?

~~ Paul

[Gargoyle]

Is this thread still active!!?? :wackyeek:
I really have trouble to keep up, thats for sure...
How many times have we been through this now?

[rocketdodger]

That's why T'ai Chi doesn't want to talk about other sciences: Because if he admits that no other scientific area has all the answers he demands that Evolution has, he has to admit that his criticism is fundamentally flawed.

I don't know that he is even criticising. Usually when a person "critiques" they have something in mind for what they would prefer, as opposed to what is, and they let you know.

T'ai, however, categorically refuses to state any sort of model or theory of his own that he would prefer over what he is complaining about -- and for good reason, because he knows we would annihilate it immediately, even if by using nothing more than the same reasoning he is using to knock evolution.

What I find even more disturbing is that, by demanding everything be known about a model before we start pursuing that model, he is effectively saying nobody should ever endeavor to do anything in science. You have a hypothesis? It must be proven before you can try to prove it!

[joobz]

Maybe you on are on ignore. I'll quote you just in case.
If you're bored, you could really change things up by answering a substantive question (http://forums.randi.org/showthread.php?postid=3100515#post3100515) about your claims.

Or, you know, keep ignoring reality. I'll just be over here pretending like I'm waiting for an answer that I know will never come...
:whistling
The linked section is the following question:
Ah, but is this actually true? Is Windows less complex than e. coli? I guess you'd have to define complexity in some precise way, which I suspect you won't do. In fact, I predict you'll ignore this post altogether, because I'm discussing something substantive, and you usually flee to another thread as soon as anyone actually gets down to brass tacks

[Kotatsu]

You must have missed the part in a science class where people can critique a model without claiming that the people who created the model are claiming the model is Truth.

The idea of pointing out what I did about the model should have been obvious, that real biology would trump any model any day in terms of importance. For example, one complete evolutionary pathway of anything to anything else would be better than any Pascal program.

And, again, I must point out that Kleinman is not in any way, shape or form criticizing the model or claiming that it is at odds with reality. he claims the model is a good reflection of reality, and that the model, alone, would explain why evolution cannot happen. The numerous papers he have cited have nothing to do with his claim, really. They are a debating tactic to be able to show new readers that he has posted several hundred papers which allegedly support him, while "we" have posted many fewer.

Real biology has trumped the model. I am not arguing against you in any way in this matter. It just seems to me that you have misunderstood exactly who in this thread are arguing against the model and who is arguing for it.

[T'ai Chi]

And again, you are refusing to admit that you have brought up a philosophical objection that pertains to almost every other human endeavor.


I've admitted that you've repeatedly brought up this red herring, and reminded you that we're not talking about any other human endeavor, yes.

Still no details. Tsk.

[Belz...]

I've admitted that you've repeatedly brought up this red herring, and reminded you that we're not talking about any other human endeavor, yes.

Still no details. Tsk.

Tsk ? Are you even capable of understanding what we've been telling you ?

How can you possibly know ALL the steps ?

[rocketdodger]

Tsk ? Are you even capable of understanding what we've been telling you ?

How can you possibly know ALL the steps ?

I think T'ai Chi's point is that the theory of evolution has not been proven without a doubt, it has only been shown to be very, very, very likely -- orders of magnitude more likely than any competing theories.

If, in fact, that is his point, then I would congratulate him on being a master of the obvious.

[Foster Zygote]

Tsk ? Are you even capable of understanding what we've been telling you ?

How can you possibly know ALL the steps ?

T'ai seems to think he's hit upon something very clever here. I imagine he thinks it's one of his most devastating coup de grace lines, much like his "but the model is intelligently designed" argument (The model is also constructed within a computer so I guess T'ai Chi has also proved that we all live in the Matrix).

The only thing I really wonder about is whether he thinks it's truly reasonable to demand that all sciences produce such a ridiculously detailed proof, or if he's actually aware that he's employing an intellectually dishonest dodge by demanding the ludicrous.

[Paul C. Anagnostopoulos]

I've admitted that you've repeatedly brought up this red herring, and reminded you that we're not talking about any other human endeavor, yes.

Still no details. Tsk.
Okay, I'll ignore the fact that if you think you've shot evolution in the foot, you must also think you've shot everything else in the foot. You're the logician, dude.

So, how much detail do you want? I need to know in complete detail how much detail you require.

~~ Paul

[Belz...]

Okay, I'll ignore the fact that if you think you've shot evolution in the foot, you must also think you've shot everything else in the foot.

So, how much detail do you want? I need to know in complete detail how much detail you require.

~~ Paul

Yeah, T'ai, include ALL the steps, please.

[Foster Zygote]

Can you outline where the ability to 'answer questions' makes something right or wrong? I must have missed that in logic class.

This is the bit where T'ai Chi deliberately confuses the definition of "answer questions" as regards the context of science with "answer questions" as regards a statement in response to a query that may or may not be true.

[Foster Zygote]

I'm asking if you have real biology rather than some simulation.

I think T'ai is asking for things like examples of speciation in the laboratory or new evolutionary adaptations like Nylon eating microbes. Anyone want to take a steam shovel to this thread and dig 'em up?

[kleinman]

It is apparent from a quick perusal of posts made over the weekend that you evolutionists still don’t understand how mutation and selection works either mathematically or empirically. Since you refuse to study Dr Schneider’s simulation of random point mutations and natural selection I’ll have to continue to post real examples of how mutation and selection actually works but I don’t mind this since there is a vast number of these examples to draw from. So let’s see what you evolutionists have to say about mutation and selection. Let’s start with rocketwhomissesthetarget.
Dr Schneider has posted extensively about his ev model including a glossary of his variables used in his calculations.What does this have to do with whether or not you understand it?
Oh my rocketwhomissesthetarget, I understand how ev works, that’s why I can post hundreds of empirical examples of what Dr Schneider’s model shows. And what Dr Schneider’s model shows is that combination selection pressures profoundly slow the sorting/optimization (mutation/selection) process in his algorithm. This is how mutation and selection works in reality as well.
Why shouldn’t I cite evidence of how mutation and selection actually works? There is an abundance of this evidence available.And a complete lack of understanding regarding that evidence on your part, which is why you consistently dodge questions by simply posting more citations.
I see, you post no citations which show that n+1 selection pressures evolve more rapidly than n selection pressures and then whine when I post hundreds of citations which show that combination selection pressure profoundly slow the sorting/optimization process of mutation and selection. Just because you don’t have any mathematical or empirical evidence to support your irrational and illogical theory, don’t blame me.
Why don’t you use google and find a citation which shows that n+1 selection pressures evolve more rapidly than n selection pressures?I don't need google, I simply used all the citations you provided us:

Bacteria -- n pressures, slow mutation.
Bacteria + penicillin -- n + 1 pressures, rapid mutation.

Of course you will deny this somehow...
Sorry about this rocketwhomisses the target, you’ve got you mathematics and empirical evidence wrong. You have already admitted that bacteria in vitro will evolve resistance more quickly than bacteria in vivo. So your mathematics should look like this.
Bacteria (in vivo) – n weak selection pressures, impossibly slow evolution for common descent.
Bacteria (in vivo) + penicillin – n weak selection pressures + 1 strong selection pressure, fairly fast evolution of penicillin resistance but still impossibly slow evolution for common descent.
Bacteria (in vitro) – n-m weak selection pressures, impossibly slow evolution for common descent.
Bacteria (in vitro) + penicillin – n-m weak selection pressures + 1 strong selection pressure, faster evolution of penicillin resistance than with n selection pressures but still impossibly slow evolution for common descent.
Rocketwhomissesthetarget, I do commend you for trying to put some mathematics to your confused understanding of how mutation and selection works, keep working on it, I have great hopes that you can get it right.
Your analogy is not quite correct rocketdodger.The odds of you actually having any degrees, given your displayed maturity level, are extremely slim.
The odds are much greater that I have those degrees than your theory of evolution is mathematically possible. Not only do I have those degrees, I am licensed as both a physician and an engineer. You are going to have to find another way to defeat my arguments which disprove the theory of evolution since I have all the mathematical and empirical evidence of how mutation and selection works and you have zilch to support your view.
There are no sorting/optimization/iteration problems that work that way which converge more quickly the more sorting/optimization/iteration conditions imposed on the problem.I agree, there are not. But this has very little to do with evolution, and if you actually tried to explain why you think evolution is merely a sorting/optimization problem you would soon see this. But like I said.. you cannot explain why, because you do not know why. All you know is the nonsense you put together from random google results.
The problem you have in your argument is that Dr Schneider’s peer reviewed and published model of random point mutations and natural selection is simply a sorting/optimization algorithm and the behavior of this algorithm is exactly analogous to what is observed in reality. Sorting/optimization is exactly how mutation and selection works. Mutation and selection is the sorting of beneficial and detrimental mutations with the selection conditions defining the optimization conditions. If you have more than a single selection (optimization) condition, it profoundly slows the process. That is what the mathematics shows and that is what the empirical data shows.
I can't find the link to Kleinman's thesis and background, anyone have it handy?
I’ve already posted the title of my thesis and the publisher on this thread. Do you think you can find it, rocketwhomissesthetarget?
I have published publicly on two topics and you don’t understand the mathematics of either.I didn't bother reading your publications and judging by the number of citations, nobody else bothered reading them either or found them very useful.
I see, you claim you are going to find irregularities in my PhD thesis, let’s see you do it and prove your mathematical prowess. You would have a better chance in proving there are irregularities in 2+2=4. Joobz, you are incompetent in the mathematics of mutation and selection, ignorant of how the process works empirically and silly in your speculations of how chemistry works. You are nothing more than a big blow hard; you have no science or mathematics to back up your bizarre and strange speculations. Joobz, why don’t you put your money where your mouth is? Let’s make a wager, say $10,000. If you can find a mathematical or empirical irregularity in my PhD thesis, I’ll pay you $10,000; if you can’t you pay me $10,000. Are you ready for that, big mouth?
Hey kjkent1, if you can prove that reptiles evolved into birds one strong selection pressure at a time, go for it.At the risk of repeating myself: The geological and fossil records demonstrate that evolution has occurred within the generational time available.
Well, it didn’t happen by mutation and selection, we have mathematical and empirical evidence which show how this process works. Perhaps it happened by the string cheese theory?
I finally read up on and ran the ev program. Unfortunately, I am unable to produce a graph like Dr. Adequate, probably because (although I didn't realize it at first) he used some other model/program.

Why can't I reproduce such a graph using ev? Because as it turns out, ev has nothing to do with selective pressures...at all... so Kleinman, how on Earth are you using ev to support your claim that "combination selection pressures profoundly slow evolution?"

You said "this is what the mathematics of mutation and selection show" but so far, other than ev, you have cited no mathematics (nor presented any yourself) at all.
It’s easy to explain why you can’t generate a graph with ev like Adequate’s because Adequate’s thinking is irrational and illogical on this topic. n+1 selection pressures do not evolve more rapidly than n selection pressures.

Rocketwhomissesthetarget, you need to a little more reading about ev because there are selection pressures in the model. In addition, many of the citations which I have posted are mathematical models of the mutation and selection process which show that combination selection pressures profoundly slow the evolutionary process. Do you want me to repost those citations or do you want to read them as you look for the title and publisher of my PhD dissertation? Keep on reading rocket and perhaps you will hit the target.
Well, Kleinman is entitled to critique a model he feels is not reflective of reality, or for whatever other reason. Especially if the people who made the model are trying to convince others it is reflective of reality.You have misunderstood this thread. While more or less everyone else has understood that the model in question is just a model, which doesn't claim to model all of reality, and which certainly doesn't model all of reality, Kleinman is the person who has repeatedly claimed that it does, or, at least, that it is so accurate and so complete that results from the model, when in conflict with results from reality, counters and supersedes these, and should replace them. Kleinman's "critique" of the model is virtually non-existent, whereas the rest of us have long ago realised the limitations of the model, and act accordingly.

It is not the "evolutionarians" of this thread who are holding this model to be a sacred standard of our way to view the world. I assume you have not read any part of the thread prior to joining in, or you would have spotted this.
T’ai, you need to understand that I believe that Dr Schneider properly modeled the essential features of the mutation and selection process and it demonstrates how mutation and selection actually works. I told Dr Schneider in our discussions that once evolutionists understood what his model actually shows, his model would be discredited by evolutionists and that is exactly what his happening. Unfortunately for believers in the evolutionists world view, Dr Schneider’s model predicts how mutation and selection actually works as demonstrated in the hundreds of real citations which I have already posted, all of which show that combination selection pressures profoundly slow the evolutionary process.
No Kotatsu, these are not comments on American popular culture, they are comments on evolutionist popular culture because mutation and selection simply does not work the way you allege, the mathematics and empirical evidence of mutation and selection contradict your scientifically and mathematically baseless speculations and extrapolations.Actually being biologist, as opposed to you, I must, if I am to believe you, ask what sort of biology text books you read which have "Sesame Street" and "Marvel comics" listed in their evolution sections. These, I understand, are references to American popular culture, but I am unfamiliar with the exact details, never having lived in America. Ask me about Czech and Polish animation from the 80's, instead. They showed heaps of that on Swedish TV when I was a kid.
Kotatsu, I don’t care what you call yourself; you simply don’t understand how mutation and selection works either mathematically or empirically. This mush that you put forth doesn’t qualify as a scientific or mathematical argument of how mutation and selection actually works.
So, now we have the theory of evolution by “sheer coincidence”, Kotatsu, you take speculation to new levels.So you have no actual answer, is that a correct interpretation?
It is not a correct interpretation if you want to claim that your argument has any scientific basis. Mutation and selection does not work that way either empirically or mathematically.
Oh, that’s right, you said a reptile chased in into a tree and it would be beneficial for that reptile to grow wings. You evolutionists really practice some weird thinking.No. Your post contains several misinterpretations. I gave you a list of a number of various realistic selection pressures, all of which could plausibly lead to a situation where mutations in genes which for instance aided in horizontal movement between trees would be advantageous compared to alleles without this advantage.
Until you present something that is measurable and repeatable, you present nothing more than mush. The hundreds of citations which I have posted identify explicitly what the selection pressures are, the target genes for the selection pressures and often times identify the specific loci and mutations required for adaptation to the selection pressures. So far, all you have presented is mush.
What you are seeing are connections which are mathematically and empirically impossible. These are extrapolations and speculations that are contradicted by the way mutation and selection actually works.Yet those trees are constructed using maths... In the simples tree-building algorithm, that of distance, the differences between the various sequences are simply counted, and the tree is constructed in such a way that those sequences most similar to each other are placed next to each other, and so on in a way that forms a nested hierarchy (unless, of course, all sequences are identical, which will instead result in a "comb" polytomy).
Kotatsu, you are trying to make connections where none exist. You don’t have selection pressures which would make these transformations. Mutation and selection simply does not work the way you allege, we have mathematical and empirical evidence which show how mutation and selection actually works. This empirical evidence is measurable and repeatable.
There are many unusual species which evolutionists like you speculate and extrapolate that appear by evolution. However, you are in denial about how mutation and selection actually works. Combination selection pressures confound the evolutionary process. A population can most easily evolve against a single selection pressure directed at a single gene. As soon as multiple selection pressures come into play, these multiple selection pressures confound the evolutionary process. That is what the mathematical evidence shows and that is what the empirical evidence shows.So now it is no longer impossible for them to evolve against several selection pressures, just not as easy? And multiple selection pressures don't "slow and ultimately stop evolution" any more, but simply confounds it? Marvellous! In a few decades, we'll finally have you on our side!
Kotatsu, you are in denial. Mutation and selection is not an incomprehensible process mathematically. If you ever come to understand that this process is nothing more than a sorting/optimization problem, you would realize that your belief system is wrong. The empirical evidence of how mutation and selection works verifies this. The pictures you draw are based on a mathematically impossible theory.
Mr Scott has not shown that scales transform into feathers, all Mr Scott has shown is that feather can grow on birds in unusual locations when there is a mutation. Kotatsu, have you ever heard of teratomas?I have now. However, feel free to elaborate, as I believe this may be an area where you can actually display knowledge.
Teratomas are tumors which contain tissues not usually found in that organ. For example, these tumors can arise in the testis or ovaries and grow tissue replete with skin and hair. The point is that the potential for the growth of these tissues was already present in the genome.
Of course I am Kotatsu, here is a note from your lecture: Reptile chased into tree->reptile grows wings.Good, good. Now, your homework for next week will be to actually read what is being said to you before taking the notes. See if you can do that, and you may actually pass this class!
For some reason I don’t think I’ll ever pass your class in evolutionism or joobz’s class in alchemy.
Why can't I reproduce such a graph using ev? Because as it turns out, ev has nothing to do with selective pressures...at all... so Kleinman, how on Earth are you using ev to support your claim that "combination selection pressures profoundly slow evolution?"Why don't you think so? You can adjust the strength of three selection criteria, or eliminate them, on the New dialog. The fact that there are three is arbitrary, but they are individually adjustable.

One problem is that Evj has no mechanism for introducing the pressures sequentially. So we can't compare what Dr. A. represented by his red and blue lines. Then again, each of Dr. A's pressures affects a different gene, whereas Evj only has one gene affected by multiple pressures, so the comparison may be moot.
Thank you Paul for setting rocketdodger straight on this issue, it doesn’t matter that you can’t apply the selection pressures in ev sequentially, there is more than enough empirical evidence that shows how this works.
So, has he thought of any new lies?
Adequate, when are you going to stop behaving like a whining brat and start practicing mathematics again? It is now clear that the evolution by mutation and selection is nothing more than a sorting/optimization problem and that Dr Schneider’s properly demonstrates how this process works. How long are you going to cling to your incoherent, irrational and illogical view that n+1 selection pressures evolve more rapidly than n selection pressures? If you do continue to cling to the incoherent, irrational and illogical, stick around, you are my favorite annoyee and obfuscatematician.
So, has he thought of any new lies?Except for trying again to establish some credibility regarding his math abilities by referencing his meager publications, no.
Put your money where your big mouth is. You said you are going to prove irregularities in my PhD thesis, $10,000 wager says you can’t show any mathematical or empirical irregularities. What do you say big mouth? Or are you a big coward as well as a big mouth?
Adequate can you link me to the model you used to make that graph Kleinman is claiming to be incorrect? I am trying to reproduce the results -- they seem intuitively correct (if one has a clue about math) but I need an actual model or program or something that I can use.
Yeah, Adequate, give rocketdodger a link, google seems to be failing him.
Yawn.If you're bored, you could really change things up by answering a substantive question about your claims.

Or, you know, keep ignoring reality. I'll just be over here pretending like I'm waiting for an answer that I know will never come...
Yeah T’ai, like Delphi telling us that a temperature change transforms reptiles into birds, all he needs is a hundred million years and the earth as his test tube despite his own reference to Wikipedia fitness landscape contradicts his strange speculations.
Is this thread still active!!??
I really have trouble to keep up, thats for sure...
How many times have we been through this now?
I can’t help it if you evolutionists are slow at learning the mathematics of mutation and selection. Here are some more empirical examples of how the process works for those of you having trouble with the mathematics.
http://aac.asm.org/cgi/content/full/49/10/4305 (http://aac.asm.org/cgi/content/full/49/10/4305)
This is the first report to provide additional evidence that combination therapy with two small-molecule inhibitors may afford an advantage in overcoming the resistance issue. For example, we demonstrated that the frequency of resistance to the combination of A-782759 and BILN-2061 was significantly lower than the frequency of resistance to either single compound alone. In addition, the replicon containing dually resistant mutants had dramatically reduced replication compared to the wild type despite some of the single mutants having replication capacities close to or better than the wild type. Taken together, these findings support the notion that combination therapy will provide an approach to suppress the emergence of resistance and increase the efficacy of HCV therapy.
http://www.journals.uchicago.edu/CID/journal/issues/v45n11/51016/51016.html (http://www.journals.uchicago.edu/CID/journal/issues/v45n11/51016/51016.html)
Antimicrobial drug resistance in infectious agents occurs by means of several mechanisms; these include genetic changes and the acquisition of genes coding for resistance. Mycobacteria differ from most other bacteria by the presence of a cell wall with unique properties. Exchange of genes across this type of cell wall is difficult. Therefore, development of drug resistance in this group of bacteria evolves mainly from mutational events [1]. Resistance only becomes apparent if the resistant subpopulation of bacteria survives during treatment. To avoid this, patients with tuberculosis (TB) are treated with a combination of drugs. Development of resistance to one of the drugs in the regimen is not relevant to the survival of the bacterium in which that occurred, because there will always be 1 drug to which it is still susceptible. Selection of resistant mutants only happens when patients are treated with inappropriate regimens or when patients become selectively noncompliant by not taking all of the 3 or 4 drugs they were prescribed. The long duration of treatment, as well as the large amount of drugs and their gastrointestinal adverse effects, contribute to a relatively high rate of noncompliance in patients with TB.
And
Figure 1 illustrates how the F15/LAM4/KZN strain developed resistance over time. One can only speculate about the reasons for this development. A general observation in antibacterial therapy is that treatment with fixed combinations of drugs will lead to infections with organisms that are resistant to that combination. This was thought not to be applicable to M. tuberculosis for 2 reasons: (1) combination therapy would prevent in vivo survival of mutants that are resistant to one drug, and the chance of mutations leading to resistance to 2 drugs in the same cell is extremely small; and (2) the loss of fitness of drug-resistant strains limits their transmission [14, 15]. From this it follows that focussing on optimization of the TB-control programs for drug-susceptible TB will prevent resistance to spread. If the vast majority of patients fully adhere to their treatment regimens, no resistance will develop, and drug-resistant strains that develop in the small minority of persons who are not compliant will not spread.
Hey joobz after you lose $10,000 trying to find irregularities in my PhD dissertation, you can notify the authors of the above citation that evolution can not be stopped.

[joobz]

Hey joobz after you lose $10,000 trying to find irregularities in my PhD dissertation, you can notify the authors of the above citation that evolution can not be stopped.
Your delusions are getting the best of you. Why would I bother reading your ineffectual paper? 5 citations in ~25 years. 4 of those citations from your group. Meaning, that only 1 other researcher found your work worth enough to cite. Not a very impressive record at all.


but please, tell us again all about you non-linear PDEs. Or better yet, actually present your math that shows evolution is impossible. It's been a year and all we hear is boasts, but you never deliver. I wonder if this is the reason why you only had 2 publications.

[delphi_ote]

Lots of posts from T'ai Chi. Still no definition of "complex." Still no acknowledgment that this is a problem with his argument. If you're lurking, do you find this intellectually dishonest?
:whistling

[rocketdodger]

Oh my rocketwhomissesthetarget, I understand how ev works, that’s why I can post hundreds of empirical examples of what Dr Schneider’s model shows. And what Dr Schneider’s model shows is that combination selection pressures profoundly slow the sorting/optimization (mutation/selection) process in his algorithm. This is how mutation and selection works in reality as well.

Congratulations on once again utterly failing to explain why. In other words, you don't understand, you just cite.

I see, you post no citations which show that n+1 selection pressures evolve more rapidly than n selection pressures and then whine when I post hundreds of citations which show that combination selection pressure profoundly slow the sorting/optimization process of mutation and selection. Just because you don’t have any mathematical or empirical evidence to support your irrational and illogical theory, don’t blame me.

Sorry about this rocketwhomisses the target, you’ve got you mathematics and empirical evidence wrong. You have already admitted that bacteria in vitro will evolve resistance more quickly than bacteria in vivo. So your mathematics should look like this.
Bacteria (in vivo) – n weak selection pressures, impossibly slow evolution for common descent.
Bacteria (in vivo) + penicillin – n weak selection pressures + 1 strong selection pressure, fairly fast evolution of penicillin resistance but still impossibly slow evolution for common descent.
Bacteria (in vitro) – n-m weak selection pressures, impossibly slow evolution for common descent.
Bacteria (in vitro) + penicillin – n-m weak selection pressures + 1 strong selection pressure, faster evolution of penicillin resistance than with n selection pressures but still impossibly slow evolution for common descent.


...so, you are saying that n + 1 selection pressures can lead to faster evolution than n pressures... which is exactly the opposite of all your previous claims... welcome back to the Kleinman merry-go-round everyone!

The odds are much greater that I have those degrees than your theory of evolution is mathematically possible. Not only do I have those degrees, I am licensed as both a physician and an engineer.

Oh really? Where? By whom?


If you have more than a single selection (optimization) condition, it profoundly slows the process.

Why? Wait, let me guess.. "because that is what the mathematics and empirical evidence shows." OHHHH WELL THEN ITS ALL CLEARED UP, THANK YOU.

Honestly, Kleinman, I can't bring myself to believe that you could have written a paper on partial differential equations when you are completely unable to show why multiple optimization conditions would slow sorting. It is so simple.. all you have to do is think for a little and explain...

[kleinman]

Hey joobz after you lose $10,000 trying to find irregularities in my PhD dissertation, you can notify the authors of the above citation that evolution can not be stopped.Your delusions are getting the best of you. Why would I bother reading your ineffectual paper? 5 citations in ~25 years. 4 of those citations from your group. Meaning, that only 1 other researcher found your work worth enough to cite. Not a very impressive record at all.

but please, tell us again all about you non-linear PDEs. Or better yet, actually present your math that shows evolution is impossible. It's been a year and all we hear is boasts, but you never deliver. I wonder if this is the reason why you only had 2 publications.
So joobz, not only are you a big mouth who is ignorant of mathematics, you are a coward. You said you could find irregularities in my PhD thesis, put up or shut up. Here’s what you said.
As for his credentials. He's stated that he is Dr. Alan Kleinman. A physician with a PhD in engineering (I do not remember which field). He even posted a link to his thesis as proof of his degree. I could critique his PhD for irregularities in his publication track that raise interesting questions.
$10,000 wager that you can’t find any mathematical or empirical irregularities in my PhD thesis or are you just a big mouth fake? You claim to have a PhD in engineering, how much do you know about PDEs prove my thesis wrong or are you just a big faker? I think you are a faker after posting your nonsense speculations about abiogenesis.

There’s the wager you fake. Why don’t you post your name you coward and let’s have a look at your PhD thesis. Joobz, not only are you a mathematical incompetent in the mathematics of mutation and selection, you are a mathematical incompetent in PDEs. Prove otherwise and take up this $10,000 wager since you have claimed that you can find irregularities in my PhD thesis.
Lots of posts from T'ai Chi. Still no definition of "complex." Still no acknowledgment that this is a problem with his argument. If you're lurking, do you find this intellectually dishonest?
Delphi, the mathematics of mutation is not that complex, you have some understanding of the problem; otherwise you wouldn’t have posted the Wikipedia reference to fitness landscape. Why don’t you tell us how a temperature change can transform hundreds, perhaps thousands of genes simultaneously?
Sorry about this rocketwhomisses the target, you’ve got you mathematics and empirical evidence wrong. You have already admitted that bacteria in vitro will evolve resistance more quickly than bacteria in vivo. So your mathematics should look like this.
Bacteria (in vivo) – n weak selection pressures, impossibly slow evolution for common descent.
Bacteria (in vivo) + penicillin – n weak selection pressures + 1 strong selection pressure, fairly fast evolution of penicillin resistance but still impossibly slow evolution for common descent.
Bacteria (in vitro) – n-m weak selection pressures, impossibly slow evolution for common descent.
Bacteria (in vitro) + penicillin – n-m weak selection pressures + 1 strong selection pressure, faster evolution of penicillin resistance than with n selection pressures but still impossibly slow evolution for common descent....so, you are saying that n + 1 selection pressures can lead to faster evolution than n pressures... which is exactly the opposite of all your previous claims... welcome back to the Kleinman merry-go-round everyone!
Read it again rocketwhomissesthetarget.
The odds are much greater that I have those degrees than your theory of evolution is mathematically possible. Not only do I have those degrees, I am licensed as both a physician and an engineer.Oh really? Where? By whom?
You can find this information if you read the thread. Do you have to be spoon fed everything? Why don’t you tell us what your credentials are, you claim you understand how mutation and selection works, tell us why.

Attack the argument, not the arguer. This thread has calmed down a lot since I last looked in. Try to keep it that way.

[Belz...]

Oh my rocketwhomissesthetarget, I understand how ev works, that’s why I can post hundreds of empirical examples of what Dr Schneider’s model shows.

Actually, you could post those and still don't understand, so that's not a good argument.

[Paul C. Anagnostopoulos]

Read it again rocketwhomissesthetarget.
Let me see (emphasis mine):

Bacteria (in vivo) – n weak selection pressures, impossibly slow evolution for common descent.
Bacteria (in vivo) + penicillin – n weak selection pressures + 1 strong selection pressure, fairly fast evolution of penicillin resistance but still impossibly slow evolution for common descent.
Bacteria (in vitro) – n-m weak selection pressures, impossibly slow evolution for common descent.
Bacteria (in vitro) + penicillin – n-m weak selection pressures + 1 strong selection pressure, faster evolution of penicillin resistance than with n selection pressures but still impossibly slow evolution for common descent.

~~ Paul

[CFLarsen]

Tsk ? Are you even capable of understanding what we've been telling you ?

How can you possibly know ALL the steps ?

Look at it from T'ai Chi's point of view.

Since T'ai Chi argues that there is an intelligent designer - namely God, who is omniscient - it follows that any explanation that doesn't know all the steps - namely science - has to be inferior as an explanation.

T'ai Chi argues that:

1) The Intelligent Designer (God) knows all the steps.

2) Science doesn't know all the steps.

Ergo:

1) is the truth.

If in doubt, or cornered: see 1).

T'ai seems to think he's hit upon something very clever here. I imagine he thinks it's one of his most devastating coup de grace lines, much like his "but the model is intelligently designed" argument (The model is also constructed within a computer so I guess T'ai Chi has also proved that we all live in the Matrix).

Exactly. Not only is his argument unfalsifiable, it doesn't give us any answers. It only raises more questions, all of which can - and will - be answered with:

"Goddidit".

T'ai Chi may call it "intelligent designer", because he, like all Creationists, is intellectually dishonest, but he means "god".

The only thing I really wonder about is whether he thinks it's truly reasonable to demand that all sciences produce such a ridiculously detailed proof, or if he's actually aware that he's employing an intellectually dishonest dodge by demanding the ludicrous.

Judging from his previous posts, I'd say it is the latter.

[kleinman]

Oh my rocketwhomissesthetarget, I understand how ev works, that’s why I can post hundreds of empirical examples of what Dr Schneider’s model shows.Actually, you could post those and still don't understand, so that's not a good argument.
The point you are missing Belz is that Dr Schneider’s model shows that the reason it so slowly converges is the three selection conditions. If you set two of the three selection conditions to zero in the model then the remaining selection condition can evolve much, much more rapidly. That same behavior of mutation and selection is seen in reality in the numerous citations posted. That is how mutation and selection works mathematically and that is how it works empirically. Mutation and selection is simply a sorting/optimization problem. That is why Dr Schneider’s model behaves the way it does and that is why the citations posted demonstrates the same behavior. You can try to say that I don’t understand how mutation and selection works but I can produce data from a peer reviewed and published computer simulation of random point mutations and natural selection and hundreds of empirical examples which shows the same thing, that is combination selection pressures profoundly slow the evolutionary process. You can try to say the contrary but you can’t produce the mathematical data and you can’t produce the empirical evidence.
Let me see (emphasis mine):Bacteria (in vivo) – n weak selection pressures, impossibly slow evolution for common descent.
Bacteria (in vivo) + penicillin – n weak selection pressures + 1 strong selection pressure, fairly fast evolution of penicillin resistance but still impossibly slow evolution for common descent.
Bacteria (in vitro) – n-m weak selection pressures, impossibly slow evolution for common descent.
Bacteria (in vitro) + penicillin – n-m weak selection pressures + 1 strong selection pressure, faster evolution of penicillin resistance than with n selection pressures but still impossibly slow evolution for common descent.
Paul, do I have to spell this out for you? Ok, in both the in vitro and in vivo cases you have a single strong selection pressure evolving on the background of weak selection pressures. In the in vivo case, you have n weak selection pressures interfering with the evolution of the single strong selection pressure, whereas in the in vitro case, you have only n-m weak selection pressures interfering with the evolution of the single strong selection pressure. The evolution of the penicillin resistance occurs more rapidly in the in vitro case because there are fewer selection pressures than the in vivo case (the immune response and so on). Rocketdodger realizes this.

Now if you want to try and argue that putting a strong selection pressure on a population will make the weak selection pressures evolve more rapidly then you might have a point but the problem for you is that it is mathematically impossible. Weak selection pressures don’t have a strong impact on the fitness of a population to reproduce but they still interfere with the ability of that population to evolve against a strong selection pressure.

Combination selection pressures profoundly slow the ability of the population to evolve against all these pressures simultaneously. Paul, you should understand this, your own ev model shows this and reality shows this as well. Ev is simply a sorting/optimization algorithm which shows what happens when you have multiple optimization conditions acting on an evolving system simultaneously.

[Paul C. Anagnostopoulos]

Paul, do I have to spell this out for you? Ok, in both the in vitro and in vivo cases you have a single strong selection pressure evolving on the background of weak selection pressures. In the in vivo case, you have n weak selection pressures interfering with the evolution of the single strong selection pressure, whereas in the in vitro case, you have only n-m weak selection pressures interfering with the evolution of the single strong selection pressure. The evolution of the penicillin resistance occurs more rapidly in the in vitro case because there are fewer selection pressures than the in vivo case (the immune response and so on). Rocketdodger realizes this.
Aha, I get it. We're assuming that there are m fewer selection pressures in vitro than in vivo. How do we know this?

But sure, let's assume that at least some background selection pressures can interfere with the evolution of a solution to a strong selection pressure. Presumably you have mathematics to show that in the real world the situation is such that only certain (unspecified) biological mechanisms could have evolved in the time available, while other extant mechanisms could not have evolved. This mathematics would surely indicate which mechanisms could have evolved and which could not. Would you be so kind as to present the math?

~~ Paul

[Paul C. Anagnostopoulos]

The point you are missing Belz is that Dr Schneider’s model shows that the reason it so slowly converges is the three selection conditions. If you set two of the three selection conditions to zero in the model then the remaining selection condition can evolve much, much more rapidly. That same behavior of mutation and selection is seen in reality in the numerous citations posted.
So in all those citations, they are evolving two completely different mechanisms and then comparing the time required? Because that is what you're doing when you set one or two of Evj's selection conditions to zero. I don't think anyone will argue with you if you say that evolving a "simple" mechanism is easier than evolving a "more complicated" mechanism. In the case of Evj, you are comparing the time to evolve a transcription factor that recognizes any locus with one that recognizes them selectively. All three selection conditions act on a single gene.

~~ Paul

[kleinman]

Paul, do I have to spell this out for you? Ok, in both the in vitro and in vivo cases you have a single strong selection pressure evolving on the background of weak selection pressures. In the in vivo case, you have n weak selection pressures interfering with the evolution of the single strong selection pressure, whereas in the in vitro case, you have only n-m weak selection pressures interfering with the evolution of the single strong selection pressure. The evolution of the penicillin resistance occurs more rapidly in the in vitro case because there are fewer selection pressures than the in vivo case (the immune response and so on). Rocketdodger realizes this.Aha, I get it. We're assuming that there are m fewer selection pressures in vitro than in vivo. How do we know this?
I have posted citations where the scientists intentionally produce resistance to particular therapies in vitro in order to identify the particular mutations which would confer this resistance. The development of these resistant strains are done under controlled conditions and the evolution of resistance can be done in a small number of generations with proper support of the population being evolved and the minimization of other selection pressures on the population.

I have also seen this phenomenon many times in my clinical practice. There have been occasions when I have used particular recommended antibiotics for treating infections and the culture and sensitivity report comes back with the in vitro testing showing that the bacteria is resistant to the drug used yet the infection resolves. The immune system puts tremendous selection pressure on most infections. In addition, some of the citations I have posted show that drugs which when used alone may not have effect on particular populations but when used in combination with other drugs sometimes regain effectiveness.
But sure, let's assume that at least some background selection pressures can interfere with the evolution of a solution to a strong selection pressure. Presumably you have mathematics to show that in the real world the situation is such that only certain (unspecified) biological mechanisms could have evolved in the time available, while other extant mechanisms could not have evolved. This mathematics would surely indicate which mechanisms could have evolved and which could not. Would you be so kind as to present the math?
Paul, ev does present the math. Even with its strong selection pressures (only the best half of the population is allowed to reproduce every generation), the sorting process is still very slow. If you introduce other selection conditions, this would only interfere with the sorting process even more so. It is the multiple simultaneous sorting conditions which slow the evolutionary process in ev, this is strikingly apparent when you set two of the three selection conditions to zero. If you impose another selection condition in ev for example in the nonbinding site region not only do you have no binding sites but also if occurrences of 4 identical bases in a row constitutes a mistake, satisfying this additional condition would slow the sorting process for the other selection conditions.

The fundamental point here in the mathematics of mutation and selection is that the number of selection conditions dominates the mathematical behavior of these systems. Weak selection pressures may not prevent the evolution of a strong selection pressure but they do interfere with the process.
The point you are missing Belz is that Dr Schneider’s model shows that the reason it so slowly converges is the three selection conditions. If you set two of the three selection conditions to zero in the model then the remaining selection condition can evolve much, much more rapidly. That same behavior of mutation and selection is seen in reality in the numerous citations posted.So in all those citations, they are evolving two completely different mechanisms and then comparing the time required? Because that is what you're doing when you set one or two of Evj's selection conditions to zero. I don't think anyone will argue with you if you say that evolving a "simple" mechanism is easier than evolving a "more complicated" mechanism. In the case of Evj, you are comparing the time to evolve a transcription factor that recognizes any locus with one that recognizes them selectively. All three selection conditions act on a single gene.
That’s not correct Paul, the selection conditions in ev evolve sequences of bases which match the weight matrix at certain locations in the genome and eliminate these sequences in the gene and nonbinding site region. That is all that the ev sort/optimization algorithm does.

[joobz]

So joobz, not only are you a big mouth who is ignorant of mathematics, you are a coward. You said you could find irregularities in my PhD thesis, put up or shut up. Here’s what you said.
again, reading comprehension fails you.

I could critique his PhD for irregularities in his publication track that raise interesting questions. But, I see no reason to doubt him or this. As it is irrelevant. His terrible arguments and woefully terrible understanding of science is much more telling.
I know full well what I said. I was referring to the track record. I was calling your publication track of only 2 papers, neither of which had the same advisor, an irregularity. I could care less how accurate the papers were. It is obvious by their impact that they were unimportant. your inability to argue your case effectively here has been much more indicative of your skills than anything else.



$10,000 wager that you can’t find any mathematical or empirical irregularities in my PhD thesis or are you just a big mouth fake? You claim to have a PhD in engineering, how much do you know about PDEs prove my thesis wrong or are you just a big faker? I think you are a faker after posting your nonsense speculations about abiogenesis.
none of this is meaningful. Care to state where I was "fake"? can you actually present anything meaningful as an arugment, or will you resort to personal attacks?

There’s the wager you fake. Why don’t you post your name you coward and let’s have a look at your PhD thesis. Joobz, not only are you a mathematical incompetent in the mathematics of mutation and selection, you are a mathematical incompetent in PDEs. Prove otherwise and take up this $10,000 wager since you have claimed that you can find irregularities in my PhD thesis.
I see no reason to trust anything about you. it is obvious you are a dishonest person who will resort to these silly attacks because you have no foundation to any argument you make. Why would I want to share anything with you?

[rocketdodger]

You can find this information if you read the thread. Do you have to be spoon fed everything?

This is pretty ironic, coming from you of all people. I don't feel like combing through a thread with thousands and thousands of posts -- what is so hard about just telling me? I think your refusal speaks volumes about your character.


Why don’t you tell us what your credentials are, you claim you understand how mutation and selection works, tell us why.

I am a video game programmer, employed by Activision, with a B.S. in Computer Science that includes credits in molecular biology. Is that outstanding? Not at all. But it is the truth.

How does mutation and selection work? Here is an example of a coherent, well thought out, and easy to follow argument -- the kind you are incapable of producing Kleinman. I could be wrong on many points, but at least I put my ideas into a form readable by others so they have the opportunity to show me where I am wrong.

---------------------------------------------------------------------------------------

Given a population and environment, any mutation in any individual of the population can be measured by the change in relative reproductive fitness of the individual as affected by that mutation. Mutations that increase relative reproductive fitness are termed "beneficial," while those that decrease it are termed "harmful." Furthermore, the relative change in fitness can be "strong" or "weak," depending on just how large the change is.

When relative reproductive fitness is increased, an individual has a relatively higher chance to propagate its DNA to the next generation by having offspring. When decreased, the opposite occurs. These offspring, in turn, have the same fate. Over time, the changed percentages (relative to the other individuals in the population) lead to the mutation either being present in the vast majority of individuals' genomes (evolution) or hardly any (no evolution). This is "selection."

That is it. There is nothing more to evolution.

Where does "optimization/sorting" fall in this process? Clearly, the selection process can be viewed as a type of sorting, because individuals with higher relative reproductive fitness tend to be placed "ahead" of those with lower. Furthermore, the selection process can be said ` There are two important distinctions from a typical sorting algorithm, however, that are very important.

First, the individuals sort themselves, not some external entity. Thus, there is no such thing as the "sorting slowing down" -- it always proceeds at a rate determined by the species life cycle and nothing else.

Second, selection is fact not simple sorting. Rather, it is a process that can be viewed as somewhat analagous to sorting. The sorting influences the results of selection, but selection happens every generation regardless.

What does this mean for evolution and multiple selective pressures?

First of all we need to define exactly what we mean by "rate of evolution." For this discussion, it means "rate of fixation of mutations into the species' genome," or in other words, how long it takes on avearge for a given mutation to spread so that a good majority of the individuals in the population carry it.

Second, we need to define "selective pressure," which for this discussion is simply a factor in the environment that, when paired with a mutation, leads to a given change in relative reproductive fitness. A "stronger" pressure results in a larger change than a "weaker" pressure, given the same pairing.

Knowing all of this, generating some fairly accurate ideas of what will happen to a population subjected to multiple selective pressures of varying strengths is not difficult.

The individuals still sort themselves according to relative reproductive fitness, in the same amount of time as before. Those with the most/strongest beneficial mutations will tend to have the most offspring, those with the fewest/weakest beneficial mutations will tend to have the least, and vica versa for harmful mutations.

The difference is that, because a single mutation is not responsible for determining relative fitness anymore, it will take more generations for a given mutation to either spread throughout the population or disappear from the population, depending on the difference that mutation affects in relative fitness.

The change still happens, however, and furthermore, the distribution of all the mutations changes in parallel. This brings us to Adequate's graph. Because the distribution of all mutations is changing at once, in parallel, the extra time it takes for any one of them to be fixed in the genome is more than made up for. Adequate's graph shows the results that this fact leads to.

Suppose you have 50 pressures, and each of them takes on average 100 generations to result in their corresponding mutations being fixed (evolution). Then if you apply them all back to back, one at a time, it will take 50 x 100 or 5000 generations for all the mutations to be fixed and the evolution completed. Now suppose you apply them all at once. It doesn't matter that it may take much, much longer for each mutation to be fixed -- as long as they are all finished by generation 4999, the average number of generations to fixation will be less than before. And that means a faster rate of evolution. Does this actually happen? Adequate says it does, and I will whip up a little simulation of my own to see for myself. My hunch is "yes, it does."

In the context of all the studies Kleinman cites, this doesn't matter -- the goal of the pressures is to actually kill off the population, and so taking longer for a resistance mutation to be fixed is extremely damaging. If the entire population is dead by generation 2000, then obviously evolution will be profoundly slowed.

ETA: Everyone, please critique these ideas if they seem wrong in any way -- I want to show Kleinman what an intelligent discussion between educated people actually looks like.

[kjkent1]

The fundamental point here in the mathematics of mutation and selection is that the number of selection conditions dominates the mathematical behavior of these systems. Weak selection pressures may not prevent the evolution of a strong selection pressure but they do interfere with the process.This is such baloney, Alan. A pack of wolves will eat loads of sheep, regardless of the number of missing or spurious binding sites in the genomes of those sheep.

The selection pressures found in ev, are relatively equal, even where the weights are set to the extremes, vis-a-vis real life application of selective pressure.

Your examples show this, because as soon as you expose a bacteria or virus to a single wolf-sized selection pressure, resistance appears.

By analogy, if you put wolves, bears and humans into hunting down those sheep, pretty quickly, there won't be any evolutionary change, because there won't be any sheep left.

You may be terrific at doing non-linear differential equations -- but you just suck at seeing the obvious.

[Paul C. Anagnostopoulos]

I have posted citations where the scientists intentionally produce resistance to particular therapies in vitro in order to identify the particular mutations which would confer this resistance. The development of these resistant strains are done under controlled conditions and the evolution of resistance can be done in a small number of generations with proper support of the population being evolved and the minimization of other selection pressures on the population.
You're sure they are minimizing selection pressures in general, or just ones they think will interfere with what they are trying to accomplish? Are you sure they aren't introducing other pressures?


Paul, ev does present the math.
Sorry, Ev doesn't display a single math equation that I know of.


That’s not correct Paul, the selection conditions in ev evolve sequences of bases which match the weight matrix at certain locations in the genome and eliminate these sequences in the gene and nonbinding site region. That is all that the ev sort/optimization algorithm does.
Yes, indeed, when all three selection conditions are turned on. When one or two are turned off, that is not the function that evolves. The fact that evolving a different function takes fewer generations is not as interesting as you make it out to be.

~~ Paul

[kleinman]

I have posted citations where the scientists intentionally produce resistance to particular therapies in vitro in order to identify the particular mutations which would confer this resistance. The development of these resistant strains are done under controlled conditions and the evolution of resistance can be done in a small number of generations with proper support of the population being evolved and the minimization of other selection pressures on the population.You're sure they are minimizing selection pressures in general, or just ones they think will interfere with what they are trying to accomplish? Are you sure they aren't introducing other pressures?
These scientists are trying to isolate and identify the mutations that give resistance to particular drugs. Why would they introduce other selection pressures which would interfere with what they are trying to identify? They grow their populations in incubators with plenty of resources needed by the population and introduce the drugs slowly so as not to kill the entire population.
Paul, ev does present the math.Sorry, Ev doesn't display a single math equation that I know of.
Paul, you are not going to make a point here by being cute. Ev is a collection of equations and conditional statements which produces data from its sorting/optimization algorithm which simulates the mutation and selection process. Dr Schneider’s equations are there, I have seen the code and it does a good job of simulating how the mutation and selection process works.
That’s not correct Paul, the selection conditions in ev evolve sequences of bases which match the weight matrix at certain locations in the genome and eliminate these sequences in the gene and nonbinding site region. That is all that the ev sort/optimization algorithm does.Yes, indeed, when all three selection conditions are turned on. When one or two are turned off, that is not the function that evolves. The fact that evolving a different function takes fewer generations is not as interesting as you make it out to be.
Stop being silly Paul, there is no function being evolved in ev. There are only sequences of bases which satisfy the selection conditions determined by matches to the weight matrix evolving in ev. Of course you can claim that ev is evolving real binding sites, then you can explain to us what the function of a binding site is for a gene that evolves binding sites. That would be an amusing story for you to tell us.
You can find this information if you read the thread. Do you have to be spoon fed everything?This is pretty ironic, coming from you of all people. I don't feel like combing through a thread with thousands and thousands of posts -- what is so hard about just telling me? I think your refusal speaks volumes about your character.
So you want to make my character the issue in this discussion rather than what I post based on the results from ev and the hundreds of real examples of how mutation and selection actually works. How would you know what speaks volumes and what doesn’t since you are too lazy to read the volumes? Mutation and selection is not a trivial mathematical subject. Why don’t you read what Dr Schneider has written about the ev program instead of trying to figure out my PhD dissertation is all about? Then perhaps you will be prepared to carry out an intelligent discussion on the topic.
How does mutation and selection work? Here is an example of a coherent, well thought out, and easy to follow argument -- the kind you are incapable of producing Kleinman. I could be wrong on many points, but at least I put my ideas into a form readable by others so they have the opportunity to show me where I am wrong.

---------------------------------------------------------------------------------------

Given a population and environment, any mutation in any individual of the population can be measured by the change in relative reproductive fitness of the individual as affected by that mutation. Mutations that increase relative reproductive fitness are termed "beneficial," while those that decrease it are termed "harmful." Furthermore, the relative change in fitness can be "strong" or "weak," depending on just how large the change is.

When relative reproductive fitness is increased, an individual has a relatively higher chance to propagate its DNA to the next generation by having offspring. When decreased, the opposite occurs. These offspring, in turn, have the same fate. Over time, the changed percentages (relative to the other individuals in the population) lead to the mutation either being present in the vast majority of individuals' genomes (evolution) or hardly any (no evolution). This is "selection."

That is it. There is nothing more to evolution.
Rocketdodger, you are wrong about this, there is one thing more that you have to add to your description. How does this mutation and selection process work mathematically and empirically? Dr Schneider wrote a computer simulation of this process which can show you how the process works mathematically and there is a vast amount of empirical evidence which show how this process works empirically.
Where does "optimization/sorting" fall in this process? Clearly, the selection process can be viewed as a type of sorting, because individuals with higher relative reproductive fitness tend to be placed "ahead" of those with lower. Furthermore, the selection process can be said ` There are two important distinctions from a typical sorting algorithm, however, that are very important.

First, the individuals sort themselves, not some external entity. Thus, there is no such thing as the "sorting slowing down" -- it always proceeds at a rate determined by the species life cycle and nothing else.
Again rocketdodger, you are wrong about this, the environment does the sort. The individuals who have the best fitness in given environment are able to reproduce; this is not determined by the individuals themselves. If you consider for example HIV in an environment that has PIs and RTIs, only those viruses that can adapt to these selection pressures will be able to reproduce. It is an empirical fact that if you use only single drug therapy, the HIV population can evolve resistance to that single selection pressure rapidly while multiple drug therapy profoundly slows the virus population’s ability to reproduce. The sorting of beneficial and detrimental mutations is strongly dependent on the number of selection pressures. For single selection pressures, the ability of the population to sort beneficial and detrimental mutations is very easy and the sort occurs very rapidly, for multiple selection pressures, this sorting process becomes profoundly slow. This is a mathematical and empirical fact of life for mutation and selection process.
Second, selection is fact not simple sorting. Rather, it is a process that can be viewed as somewhat analagous to sorting. The sorting influences the results of selection, but selection happens every generation regardless.
Rocketdodger, mutation and selection is not somewhat analogous to sorting, it is exactly analogous. Mutation and selection is a sorting of beneficial and detrimental mutations based on the optimization of fitness of the population and these types of problems are extremely sensitive to the number of selection conditions.
First of all we need to define exactly what we mean by "rate of evolution." For this discussion, it means "rate of fixation of mutations into the species' genome," or in other words, how long it takes on avearge for a given mutation to spread so that a good majority of the individuals in the population carry it.
And the rate can be measured by the number of generations required to evolve a given number of loci for a given size genome, population, mutation rate and number of selection conditions. If read the earlier portions of this thread, you will see that was what was done with ev.
Second, we need to define "selective pressure," which for this discussion is simply a factor in the environment that, when paired with a mutation, leads to a given change in relative reproductive fitness. A "stronger" pressure results in a larger change than a "weaker" pressure, given the same pairing.
You are missing an important point. The way selection pressures affect the population is by changing the frequency of particular sequences of bases. That’s how a population finds a trajectory on the fitness landscape to a new local optimum.
Knowing all of this, generating some fairly accurate ideas of what will happen to a population subjected to multiple selective pressures of varying strengths is not difficult.

The individuals still sort themselves according to relative reproductive fitness, in the same amount of time as before. Those with the most/strongest beneficial mutations will tend to have the most offspring, those with the fewest/weakest beneficial mutations will tend to have the least, and vica versa for harmful mutations.
That’s pretty much how the sort works rocketdodger. When you plug in the numbers like Dr Schneider did, you can watch how this process works mathematically.
The difference is that, because a single mutation is not responsible for determining relative fitness anymore, it will take more generations for a given mutation to either spread throughout the population or disappear from the population, depending on the difference that mutation affects in relative fitness.
That’s not correct rocketdodger. Every mutation has affect on the process but not nearly as much as the number of selection conditions.
The change still happens, however, and furthermore, the distribution of all the mutations changes in parallel. This brings us to Adequate's graph. Because the distribution of all mutations is changing at once, in parallel, the extra time it takes for any one of them to be fixed in the genome is more than made up for. Adequate's graph shows the results that this fact leads to.
The only problem is that Adequate has no empirical evidence for his graph. All the empirical evidence shows that when a population is trying to evolve to selection pressures in parallel, the process is profoundly slowed. So does Dr Schneider’s model, evolving all three selection conditions simultaneously takes huge numbers of generations, however any one of the selection conditions alone evolves very quickly. That’s how the mutation and selection sorting process works.
Suppose you have 50 pressures, and each of them takes on average 100 generations to result in their corresponding mutations being fixed (evolution). Then if you apply them all back to back, one at a time, it will take 50 x 100 or 5000 generations for all the mutations to be fixed and the evolution completed. Now suppose you apply them all at once. It doesn't matter that it may take much, much longer for each mutation to be fixed -- as long as they are all finished by generation 4999, the average number of generations to fixation will be less than before. And that means a faster rate of evolution. Does this actually happen? Adequate says it does, and I will whip up a little simulation of my own to see for myself. My hunch is "yes, it does."
You can run the numbers in Dr Schneider’s model. To evolve all three selection conditions simultaneously for a 16k genome takes more than 5,000,000 generations while each of the individual selection pressures when applied singly only take at most 100 generations. Your hunch is wrong.
In the context of all the studies Kleinman cites, this doesn't matter -- the goal of the pressures is to actually kill off the population, and so taking longer for a resistance mutation to be fixed is extremely damaging. If the entire population is dead by generation 2000, then obviously evolution will be profoundly slowed.
Rocketdodger, what you don’t realize is that it doesn’t take huge populations to evolve to single selection pressures. If you are going to advocate the concept of common descent, how are you going to explain the transformation of thousands of genes? All the mathematical and empirical evidence show that transforming more than a single gene at a time is extremely difficult for any size population. Here’s another example of how the process works empirically.
http://www.journals.uchicago.edu/JID/journal/issues/v181n4/990745/990745.html (http://www.journals.uchicago.edu/JID/journal/issues/v181n4/990745/990745.html)
Prolonged administration of nucleoside analogues for chronic hepatitis B may result in the emergence of hepatitis B viral polymerase mutants. To gain insight into the mechanism involved in the virus's resistance to famciclovir, the amino acid sequences of the terminal protein and reverse-transcriptase (RT) domains of the viral polymerase were determined during therapy among 28 patients. The antiviral response was independent of viral genotypes, and nonresponse to famciclovir was associated with a complex variability of the RT domain. No mutation in the YMDD motif was observed, whereas an L528M mutation was clearly selected by famciclovir treatment in 2 patients, as well as 14 novel mutations in 7 patients. Clone sequence analysis of the RT domains of patients undergoing retreatment with famciclovir and/or lamivudine showed the selection of a preexisting drug-resistant mutant in one case and indicated that sequential antiviral therapy may allow the rapid selection of resistant strains.
and
New findings were also obtained by longitudinal studies of viral sequences, obtained from PCR products and PCR clones, in 4 patients who received a second course of antiviral therapy with famciclovir and/or lamivudine (figure 4). Two cases were of particular interest in terms of drug resistance. In the first case (patient 23), an L528M mutant was found as a minor virus population before therapy and was partially selected during the first course of treatment. This mutant became rapidly dominant during the second course of famciclovir in < 6 months. In the second patient (patient 2), the L528M mutation was selected during famciclovir monotherapy. When the patient's treatment was changed to a combination of famciclovir and lamivudine, a rapid selection (6 months) of the double mutation L528M/M552V occurred, conferring resistance to both antivirals. These data demonstrate that nucleoside analogue administration may favor the outgrowth of drug-resistant mutants that preexisted as a minor viral species before therapy and that the L528M change is clearly associated with famciclovir resistance in vivo. Furthermore, these observations emphasize that sequential antiviral therapy with nucleoside analogues may allow the rapid selection of drug-resistant strains. Our observation also suggests that the selection of the L528M mutant conferring resistance to famciclovir may favor the selection of the double L528M/M552V mutant that is cross-resistant to famciclovir and lamivudine.
and
In conclusion, we report a longitudinal study of HBV polymerase sequence during antiviral treatment of chronic hepatitis B with a nucleoside analogue. Our findings give new insight in the dynamics of viral polymerase sequence evolution in relation to drug resistance. Our results have several clinical implications and suggest that antiviral response to famciclovir is independent of viral genotypes, the emergence of famciclovir-resistant strains is associated with a complex variability of the RT, and sequential antiviral therapy may allow the rapid selection of resistant strains. On the basis of these results and those obtained in lamivudine-treated patients, the selection of resistant mutants is expected to occur with any nucleoside analogue therapy. The capacity of new antiviral strategies based on combinations of inhibitors to prevent the emergence of resistant viral strains needs to be further evaluated in animal models and clinical trials.
Rocketdodger, this citation as well as the hundreds of other citations which I have posted show how mutation and selection sorting process works in real life. There are no examples of a population evolving to simultaneous selection pressures more rapidly than when the selection pressures are applied sequentially. The concept that mutations can be sorted more rapidly with simultaneous selection (sorting) conditions is mathematically irrational and illogical.

[rocketdodger]

Rocketdodger, you are wrong about this, there is one thing more that you have to add to your description. How does this mutation and selection process work mathematically and empirically?

Did you even read my post? Obviously not, because I made it very clear exactly how mutation and selection works mathematically -- mutations affect the chances their carriers have of passing them on to the next generation. It is that simple Kleinman.

Again rocketdodger, you are wrong about this, the environment does the sort.

No. The environment is an inanimate object. How you think it could possibly sort anything is beyond me.

The individuals who have the best fitness in given environment are able to reproduce; this is not determined by the individuals themselves.

So you contend that a race track sorts the field, rather than the drivers? The environment determines which individuals have the most relative fitness, but the individuals themselves do the reproducing or the dying.


Rocketdodger, mutation and selection is not somewhat analogous to sorting, it is exactly analogous.

Except for the two differences I pointed out, of course. Selection happens in O(1) time. Sorting can't happen faster than O(nlogn) time.

And the rate can be measured by the number of generations required to evolve a given number of loci for a given size genome, population, mutation rate and number of selection conditions. If read the earlier portions of this thread, you will see that was what was done with ev.

Yes. The important point is that the average rate is more important than the instantaneous rate, which you seem to agree with.

You are missing an important point. The way selection pressures affect the population is by changing the frequency of particular sequences of bases. That’s how a population finds a trajectory on the fitness landscape to a new local optimum.

The notion of a "fitness landscape" and "local optimum" are non-existent in reality. They are simply ideas used in models to help explain certain concepts. You don't even understand them to begin with, so why do you bring them up?

What exactlly is a "local optimum" in the context of a "fitness landscape?"

That’s pretty much how the sort works rocketdodger. When you plug in the numbers like Dr Schneider did, you can watch how this process works mathematically.

Except that Schneider's program is an extremely limited model that is only supposed to show the ability of populations to evolve control mechanisms for their genomes. I still don't know how you are applying it to mutation and selection in general. As Paul says, it doesn't even really include the ability to use truly different selective pressures at once.

That’s not correct rocketdodger. Every mutation has affect on the process but not nearly as much as the number of selection conditions.

What does this have to do with what I wrote?


You can run the numbers in Dr Schneider’s model. To evolve all three selection conditions simultaneously for a 16k genome takes more than 5,000,000 generations while each of the individual selection pressures when applied singly only take at most 100 generations. Your hunch is wrong.

We will see.

[Paul C. Anagnostopoulos]

These scientists are trying to isolate and identify the mutations that give resistance to particular drugs. Why would they introduce other selection pressures which would interfere with what they are trying to identify? They grow their populations in incubators with plenty of resources needed by the population and introduce the drugs slowly so as not to kill the entire population.
Okay, I'll take your word that they've got it completely under control. Who's got it under control in the real world?


Paul, you are not going to make a point here by being cute. Ev is a collection of equations and conditional statements which produces data from its sorting/optimization algorithm which simulates the mutation and selection process. Dr Schneider’s equations are there, I have seen the code and it does a good job of simulating how the mutation and selection process works.
And you're not going to make a point by saying "Ev does present the math." in response to my statement "Presumably you have mathematics to show that in the real world the situation is such that only certain (unspecified) biological mechanisms could have evolved in the time available, while other extant mechanisms could not have evolved." Note how I use the term "real world."


Stop being silly Paul, there is no function being evolved in ev. There are only sequences of bases which satisfy the selection conditions determined by matches to the weight matrix evolving in ev. Of course you can claim that ev is evolving real binding sites, then you can explain to us what the function of a binding site is for a gene that evolves binding sites. That would be an amusing story for you to tell us.
I didn't claim that Ev is evolving real binding sites, did I? I claimed that it is evolving a function, which is to match binding sites but no other positions on the chromosome. Then, when you turn off one or two selection conditions, it is not evolving that function. You have got to stop harping on my use of the word function, Alan.

2 : the action for which a person or thing is specially fitted or used or for which a thing exists : PURPOSE

~~ Paul

[Paul C. Anagnostopoulos]

You can run the numbers in Dr Schneider’s model. To evolve all three selection conditions simultaneously for a 16k genome takes more than 5,000,000 generations while each of the individual selection pressures when applied singly only take at most 100 generations. Your hunch is wrong.
Let's reword this so that it actually describes what happens:

You can run the numbers in Dr Schneider’s model. To evolve [the ability to distinguish binding sites from all other positions] for a 16k genome takes more than 5,000,000 generations while [to evolve matching at every position or no position] only takes at most 100 generations. Your hunch is wrong.

You're comparing apples and sardines.


Furthermore, these observations emphasize that sequential antiviral therapy with nucleoside analogues may allow the rapid selection of drug-resistant strains.
You know, you're emphasizing that simultaneous selection pressures make evolution more difficult, but you've cited mostly controlled lab experiments. Does your mathematical proof against evolution include the part where pressures can't happen sequentially in the real world?

~~ Paul

[rocketdodger]

You can run the numbers in Dr Schneider’s model. To evolve all three selection conditions simultaneously for a 16k genome takes more than 5,000,000 generations while each of the individual selection pressures when applied singly only take at most 100 generations. Your hunch is wrong.

You mean like setting the mistake points for each condition? I tried it with the default settings, first with one at 10 and the other two at 1 -- on average 1000 generations to convergence. With 2 out of 3 set to 10, on average it took 700 generations to convergence. With all three set to 10, it took on average 650 generations to convergence.

Does this somehow help your theory out?

[delphi_ote]

Delphi, the mathematics of mutation is not that complex, you have some understanding of the problem; otherwise you wouldn’t have posted the Wikipedia reference to fitness landscape.
Sorry, your rant here is totally irrelevant to my point (http://forums.randi.org/showthread.php?postid=3100515#post3100515).
Why don’t you tell us how a temperature change can transform hundreds, perhaps thousands of genes simultaneously?
http://i71.photobucket.com/albums/i133/delphi_ote/Scarecrow-m.jpg
How festive! Unfortunately, Halloween was last week.

[Shalamar]

Circles and Circles.

He believes evolution is wrong, therefore, it MUST be wrong.

If you are so certain, Kleinman, ignore the Jref, and submit your data to a reputable, peer reviewed publication.

[Kotatsu]

It is not a correct interpretation if you want to claim that your argument has any scientific basis. Mutation and selection does not work that way either empirically or mathematically.

In no way does this answer refer to what I asked. I was asking if you would clarify a theoretical and admittedly tangential point for me. But of course you are correct: asking you to explain anything will never result in anything with a scientific basis. I withdraw my question, and let your refusal or avoidance of answering it speak for itself.

Until you present something that is measurable and repeatable, you present nothing more than mush. The hundreds of citations which I have posted identify explicitly what the selection pressures are, the target genes for the selection pressures and often times identify the specific loci and mutations required for adaptation to the selection pressures. So far, all you have presented is mush.

The fact that several different groups of animal have countered more or less the same set of selection pressures in different ways alone shows that the process is repeatable. When faced with the selection pressures I listed before (or a subset thereof, or a combination of these, or the subset, with unlisted ones), animals will evolve a way to get from tree to tree easier, for instance to get away from an arboreal predator. Some have solved this by flying, some by gliding, some by jumping, and so on.

But I will present you, again, with the Brassica example. When different diploid species of Brassica were cross-bred, polyploid progeny occurred. These were cross-bred again, according to certain patterns (1), for five generations, and the resulting polyploid hybrids are analogous to two species of natural hybrids. In five generations of inbreeding, the plants acquired several morphological and physiological changes, including changes in leaf shape and colour, branching patterns, number of side shoots, and differences in fertility. The genetic distance between the F5 generation and the F2 generation varied between 3.7% and 9.6%. The selection pressures included having to cope with two different copies of the same gene within the same genome, having to cope with sudden polyploidisation, and several other factors which are present for all plants, such as microbial and other parasitism, pathogens, and so on. The authors used 82-89 nuclear DNA probes to detect changes in the genome, and detected changes with 23-59 of these probes, indicating, again, that no specific genes were targeted.

There are of course more details in the paper, but as you never read details and instead only post stock answers and lies, I see no reason to elaborate further.

Kotatsu, you are trying to make connections where none exist. You don’t have selection pressures which would make these transformations.

How on Earth can you make such a categorical statement? Am I to understand that you believe that regardless of what group of animal is under study, the researcher never knows any selection pressures operating on that group? Regardless of what gene he/she is working with?

The relevant selection pressures would of course change depending on the gene, the organism, and other factors. The same selection pressures wouldn't necessarily operate on a EF-1α tree as on an 18S tree. And in trees based on other genes, it is often possible to be very specific on at least some of the selection pressures operating on the gene in that organism.

Just because you don't understand phylogenies --- and this is becoming abundantly clear --- doesn't mean that the people who work with them don't.

Kotatsu, you are in denial. Mutation and selection is not an incomprehensible process mathematically. If you ever come to understand that this process is nothing more than a sorting/optimization problem, you would realize that your belief system is wrong. The empirical evidence of how mutation and selection works verifies this. The pictures you draw are based on a mathematically impossible theory.

This, again, has nothing to do with my post. I was simply making the same observation as several other people have done before me, that your arguments are changing gradually as you are overwhelmed by evidence.

For some reason I don’t think I’ll ever pass your class in evolutionism or joobz’s class in alchemy.

No, I would imagine reading comprehension would be needed for both.

---
(1) This can all be found in the paper, Song et al., 1995 (see earlier posts for complete reference).

[CFLarsen]

Just stumbled over this:

Why don’t you tell us how a temperature change can transform hundreds, perhaps thousands of genes simultaneously?

Is there any reason why temperature change can't change a gene?

[rocketdodger]

Ok I wrote a little simulation for use in investigating Kleinman's claim. I will post the source code on my website later today after I clean it up a bit.

The results show his theory to be wrong -- multiple pressures, of the same strength, eventually speed up the rate of evolution.

At first, it appeared as though Kleinman might be right -- adding selective pressures in low numbers really does slow the average rate of fixation way down. However, once a "critical mass" has been reached, adding pressures actually drives the rate back up. Eventually, with enough pressures, you get to a point where the average rate of fixation is equal to or faster than it is under only a single pressure.

[BPScooter]

rocketdodger (Dude!!!)

As a reader of this thread, I will await this long-anticpated battle of simulations. (YEAH! Dude!)

I truly hope the best simulation wins, and I will learn something about the ultimate questions that trouble my soul. (GRRR Go for it)

[I suffer from a strange disorder, I appear to type a left parenth and lose my mind, I type a right parenth and appear to be normal again. (Take Klein's simulation and give it a little selection pressure...")] Oh poops, I have a bracket problem, too...

[Kotatsu]

As a reader of this thread, I will await this long-anticpated battle of simulations. (YEAH! Dude!)

Of course, all it takes for Kleinman to ignore this is to state that it doesn't do a good job of simulating how mutation and selection really works, and all your work will have been in vain.

Nevertheless, would it be possible for you and Paul to make your simulations into robots? They could fight each other with large laser axes or something. It would be much more convincing that way.

[Belz...]

Look at it from T'ai Chi's point of view.

I refuse!

[Belz...]

The point you are missing Belz is that Dr Schneider’s model shows that the reason it so slowly converges is the three selection conditions.

I don't see how this could be the point, since this is not what we were talking about. We were talking about how understanding and posting were two different things.

The mere fact that you're talking about a subject doesn't mean you know what you're talking about.

If you set two of the three selection conditions to zero in the model then the remaining selection condition can evolve much, much more rapidly.

But why the hell would you want to do this ? What happens, instead, if you set two of the three conditions to a relatively low, non-zero value ?

That same behavior of mutation and selection is seen in reality in the numerous citations posted.

No, because you have not shown that those real-life examples have a number and relative strength of selection pressures that you can define.

That is how mutation and selection works mathematically and that is how it works empirically.

Actually, I've pointed out to you before that real things don't work mathematically.

Mutation and selection is simply a sorting/optimization problem.

You'd like that to be true, wouldn't you ?

You can try to say that I don’t understand how mutation and selection works but I can produce data from a peer reviewed and published computer simulation of random point mutations and natural selection and hundreds of empirical examples which shows the same thing

Actually, that's precisely what I'm saying. You don't understand how mutation and selection works but you can produce data from a peer reviewed and published computer simulation of random point mutations and natural selection and hundreds of empirical examples which shows the same thing according to you.

Paul, do I have to spell this out for you?

Oh, you don't need to. You've been very, very helpful at debunking your own theory. Thank you.

[Paul C. Anagnostopoulos]

You mean like setting the mistake points for each condition? I tried it with the default settings, first with one at 10 and the other two at 1 -- on average 1000 generations to convergence. With 2 out of 3 set to 10, on average it took 700 generations to convergence. With all three set to 10, it took on average 650 generations to convergence.
Kleinman is talking about setting two out of three of them to 0. Then it'll converge in only a few generations. The problem, then, is that we're not evolving a creature who distinguishes bindings sites from other positions.

~~ Paul

[Belz...]

Now if you want to try and argue that putting a strong selection pressure on a population will make the weak selection pressures evolve more rapidly then you might have a point but the problem for you is that it is mathematically impossible.

Selection pressures do not evolve. They don't even beggaminases.

[Belz...]

Stop being silly Paul, there is no function being evolved in ev. There are only sequences of bases which satisfy the selection conditions determined by matches to the weight matrix evolving in ev. Of course you can claim that ev is evolving real binding sites, then you can explain to us what the function of a binding site is for a gene that evolves binding sites. That would be an amusing story for you to tell us.

Well, I guess it all depends on whether or not the simulation's any good.

Of course, the only reason why you think it IS good is due to circular reasoning.

Rocketdodger, you are wrong about this, there is one thing more that you have to add to your description. How does this mutation and selection process work mathematically and empirically?

That WAS his description.

Again rocketdodger, you are wrong about this, the environment does the sort.

Then "predators" are part of the environment.

[Paul C. Anagnostopoulos]

But why the hell would you want to do this ? What happens, instead, if you set two of the three conditions to a relatively low, non-zero value ?
Here are a few experiments:

standard model with all mistake points = 1: 662 gens

with all mistake points = 10 (should be same): 662 gens

with missed site points = 10 (heavier pressure): 316 gens

with two spurious binding points = 10 (different heavier pressure): 1267 gens

with just gene spurious binding points = 10: 889 gens

with just nongene spurious binding points = 10: 1034 gens

So changing the relative pressures has some fairly obvious effects. More pressure on missed binding sites results in faster convergence. More pressure against spurious binding sites results in slower convergence.

Now let's turn off pressures:

(a) with missed site points = 0: 1 gen

(b) with just gene spurious binding points = 0: 707 gens

(c) with just nongene spurious binding points = 0: 405 gens

(d) with both spurious binding points = 0: 6 gens

In cases (a) and (d), no distinction evolves between binding sites and other positions, so it takes no time to produce a creature with zero mistakes. Essentially, there are no mistakes.

In cases (b) and (c), a distinction between binding sites and other positions evolves, but only for a portion of the genome. Not surprisingly, if the portion that matters is larger (case b), it takes longer.

~~ Paul

[Belz...]

Sorry, your rant here is totally irrelevant to my point (http://forums.randi.org/showthread.php?postid=3100515#post3100515).

http://i71.photobucket.com/albums/i133/delphi_ote/Scarecrow-m.jpg
How festive! Unfortunately, Halloween was last week.

Hey! That's MY strawman image. Find your own!

[kjkent1]

Here are a few experiments:

standard model with all mistake points = 1: 662 gens

with all mistake points = 10 (should be same): 662 gens

with missed site points = 10 (heavier pressure): 316 gens

with two spurious binding points = 10 (different heavier pressure): 1267 gens

with just gene spurious binding points = 10: 889 gens

with just nongene spurious binding points = 10: 1034 gens

So changing the relative pressures has some fairly obvious effects. More pressure on missed binding sites results in faster convergence. More pressure against spurious binding sites results in slower convergence.

Now let's turn off pressures:

(a) with missed site points = 0: 1 gen

(b) with just gene spurious binding points = 0: 707 gens

(c) with just nongene spurious binding points = 0: 405 gens

(d) with both spurious binding points = 0: 6 gens

In cases (a) and (d), no distinction evolves between binding sites and other positions, so it takes no time to produce a creature with zero mistakes. Essentially, there are no mistakes.

In cases (b) and (c), a distinction between binding sites and other positions evolves, but only for a portion of the genome. Not surprisingly, if the portion that matters is larger (case b), it takes longer.

~~ PaulKleinman's entire hypothesis is built on his introducing a software "bug" into ev. Using a zero value for any of the selection weights causes the population genomes to be filled with missing and/or spurious bindings, while simultaneously reporting a "perfect" creature. However, the program population is not actually evolving towards the known natural quality shared by the genomes of all independently living organisms: RSequence ~ RFrequency.

It's analogous to trying to test Einstein's E=mc2 equation by building a nuclear weapon using lead instead of U238, and then declaring Einstein wrong, because no fission occurs.

The irony of all this is that no one would argue with kleinman that exposing a population to multiple strong selective pressures will make evolution more difficult than via exposure to one selective pressure. Three against one is definitely unfair odds. But, to suggest that this means that natural evolution cannot possibly occur is frivolous/quackery.

Evolution happens and the evidence is everywhere.

[rocketdodger]

The irony of all this is that no one would argue with kleinman that exposing a population to multiple strong selective pressures will make evolution more difficult than via exposure to one selective pressure.

Actually, Adequate and I sort of are. My simulation shows that if you introduce enough strong pressures, and if you measure the rate of fixation on average, then fixation is just as fast (or even faster).

Of course this only applies to pressures that don't kill off 90% of the population, which seems to be the only kind of pressure Kleinman cares about.

[Belz...]

Actually, Adequate and I sort of are. My simulation shows that if you introduce enough strong pressures, and if you measure the rate of fixation on average, then fixation is just as fast (or even faster).

Of course this only applies to pressures that don't kill off 90% of the population, which seems to be the only kind of pressure Kleinman cares about.

Which is odd. When you wipe out 90% of a population and the rest has adapted to said pressure, then evolution has proceeded much more rapidly.

[rocketdodger]

Which is odd. When you wipe out 90% of a population and the rest has adapted to said pressure, then evolution has proceeded much more rapidly.

Well, the argument that Adequate and I are using only works if you have both a sufficient number of pressures and sufficient time for all of their targeted mutations to fixate. If the pressures are extremely lethal, the combination of them will kill off the population before any of that happens.

Which kind of begs the question why Kleinman uses this scenario in the first place -- of course there will be no evolution, the population is dead.

[kleinman]

Rocketdodger, you are wrong about this, there is one thing more that you have to add to your description. How does this mutation and selection process work mathematically and empirically?Did you even read my post? Obviously not, because I made it very clear exactly how mutation and selection works mathematically -- mutations affect the chances their carriers have of passing them on to the next generation. It is that simple Kleinman.
No you haven’t shown how mutation and selection works mathematical, you posted a hunch. Dr Schneider’s model shows mathematically how mutation and selection works and I have posted hundreds of citations which show how mutation and selection works empirically. Dr Schneider’s model and these citations show that combination selection pressures profoundly slow the mutation/selection, sort/optimization process. Your hunch shows noting about how mutation and selection actually works.
Again rocketdodger, you are wrong about this, the environment does the sort.No. The environment is an inanimate object. How you think it could possibly sort anything is beyond me.
So are you claim that sorting is done only by animate objects? Who was the animator in the primordial soup?
The individuals who have the best fitness in given environment are able to reproduce; this is not determined by the individuals themselves.So you contend that a race track sorts the field, rather than the drivers? The environment determines which individuals have the most relative fitness, but the individuals themselves do the reproducing or the dying.
Sure the track affects the race. If you have water on the track, cars with tires suitable for wet surfaces perform better than those that do not. If the track dries out, tires suitable for dry surfaces give better performance. If the population does not have the resources to reproduce in a given environment, it is not up to the population whether it lives to reproduce or die. These matters are out of the hands of the population.
Rocketdodger, mutation and selection is not somewhat analogous to sorting, it is exactly analogous.Except for the two differences I pointed out, of course. Selection happens in O(1) time. Sorting can't happen faster than O(nlogn) time.
You have introduced O(bscure) terminology. Mutation and selection is nothing more than a sorting/optimization problem but don’t let me stop you from trying to prove that n+1 selection pressures evolve more rapidly than n selection pressures. While you are at it, why don’t your write server software that performs faster as more users access the server.
And the rate can be measured by the number of generations required to evolve a given number of loci for a given size genome, population, mutation rate and number of selection conditions. If read the earlier portions of this thread, you will see that was what was done with ev.Yes. The important point is that the average rate is more important than the instantaneous rate, which you seem to agree with.
Yes, I would tend to agree with that when you are talking about stochastic processes. Often time evolutionists try to argue that a single big change can explain what is measured. The problem for evolutionists is that when there large genetic changes, they are catastrophic for the individual who has this large genetic mutation.
You are missing an important point. The way selection pressures affect the population is by changing the frequency of particular sequences of bases. That’s how a population finds a trajectory on the fitness landscape to a new local optimum.The notion of a "fitness landscape" and "local optimum" are non-existent in reality. They are simply ideas used in models to help explain certain concepts. You don't even understand them to begin with, so why do you bring them up?

What exactlly is a "local optimum" in the context of a "fitness landscape?"
Rocketdodger, don’t superimpose your lack of understanding of what a “local optimum” and “fitness landscape” are on me. If you want to understand what a fitness landscape is, consider how this concept works in ev. There are 4^G points on the fitness landscape surface. Each one of these points is one of the 4^G possible genetic sequences. Each one of the genetic sequences has a number of mistakes associated with the sequence and the selection conditions (the environment). You can construct the fitness landscape by computing the number of mistakes for all 4^G possible points on the fitness landscape. This surface has peaks and valleys which are represented by the numbers of mistakes. The highest peaks have zero mistakes and the lowest valleys could have G number of mistakes. A local optimum occurs when a population is at a particular peak. Any movement of the population away from this peak reduces the population’s fitness to reproduce. The selection conditions restrain the population from moving from the peak. Note that a local optimum does not necessarily coincide with zero mistakes.
That’s pretty much how the sort works rocketdodger. When you plug in the numbers like Dr Schneider did, you can watch how this process works mathematically.Except that Schneider's program is an extremely limited model that is only supposed to show the ability of populations to evolve control mechanisms for their genomes. I still don't know how you are applying it to mutation and selection in general. As Paul says, it doesn't even really include the ability to use truly different selective pressures at once.
I think you would get an argument from Dr Schneider about the limitations of ev. In his peer reviewed and published article on ev, he used the results to estimate the evolution of a human genome. I haven’t seen any evolutionists criticize Dr Schneider’s mathematically illogical conclusion from his model. What ev does accurately simulate is the affect of different selection conditions on the sorting of mutations. This is why it takes huge numbers of generations to evolve binding sites on all but the tiniest genomes. That’s the lesson that Dr Schneider’s model teaches. Now rocketdodger, if you want to try to define different selection conditions that will lead to faster sorting of mutations, have at it.
That’s not correct rocketdodger. Every mutation has affect on the process but not nearly as much as the number of selection conditions.What does this have to do with what I wrote?
It has everything to do with how mutation and selection actually works.
You can run the numbers in Dr Schneider’s model. To evolve all three selection conditions simultaneously for a 16k genome takes more than 5,000,000 generations while each of the individual selection pressures when applied singly only take at most 100 generations. Your hunch is wrong.We will see.
We all look forward to this. Why do I have the feeling we are in for a long, long wait?
These scientists are trying to isolate and identify the mutations that give resistance to particular drugs. Why would they introduce other selection pressures which would interfere with what they are trying to identify? They grow their populations in incubators with plenty of resources needed by the population and introduce the drugs slowly so as not to kill the entire population.Okay, I'll take your word that they've got it completely under control. Who's got it under control in the real world?
Paul, you do understand that in vitro measurements of evolution don’t include immune responses whereas the in vivo response does?
Paul, you are not going to make a point here by being cute. Ev is a collection of equations and conditional statements which produces data from its sorting/optimization algorithm which simulates the mutation and selection process. Dr Schneider’s equations are there, I have seen the code and it does a good job of simulating how the mutation and selection process works.And you're not going to make a point by saying "Ev does present the math." in response to my statement "Presumably you have mathematics to show that in the real world the situation is such that only certain (unspecified) biological mechanisms could have evolved in the time available, while other extant mechanisms could not have evolved." Note how I use the term "real world."
Paul, you are the one claiming that biological mechanisms somehow evolved. Ev does not represent the evolution of binding sites. Ev represents the evolution of sequences of bases that satisfy the conditions imposed by Dr Schneider’s selection conditions. Ev demonstrates how slow a mutation/selection sorting algorithm performs when you have more than a single selection condition. That’s the “real world” which ev demonstrates. Anything else you claim about ev including some weird function associated with these sequences of bases is nonsense.
Stop being silly Paul, there is no function being evolved in ev. There are only sequences of bases which satisfy the selection conditions determined by matches to the weight matrix evolving in ev. Of course you can claim that ev is evolving real binding sites, then you can explain to us what the function of a binding site is for a gene that evolves binding sites. That would be an amusing story for you to tell us.I didn't claim that Ev is evolving real binding sites, did I? I claimed that it is evolving a function, which is to match binding sites but no other positions on the chromosome. Then, when you turn off one or two selection conditions, it is not evolving that function. You have got to stop harping on my use of the word function, Alan.

2 : the action for which a person or thing is specially fitted or used or for which a thing exists : PURPOSE
I’ll stop harping on your use of the word “function” when you stop trying to describe what the three selection conditions in ev are doing. The selection conditions select for sequences of bases that satisfy those selection conditions and ev becomes very slow at satisfying all three selection conditions simultaneously on all but the tiniest genomes. That’s the mathematical fact of life that ev demonstrates about the mutation/selection sorting process. By the way, are you going to claim the evolution has a PURPOSE now?
You can run the numbers in Dr Schneider’s model. To evolve all three selection conditions simultaneously for a 16k genome takes more than 5,000,000 generations while each of the individual selection pressures when applied singly only take at most 100 generations. Your hunch is wrong.Let's reword this so that it actually describes what happens:

You can run the numbers in Dr Schneider’s model. To evolve [the ability to distinguish binding sites from all other positions] for a 16k genome takes more than 5,000,000 generations while [to evolve matching at every position or no position] only takes at most 100 generations. Your hunch is wrong.

You're comparing apples and sardines.
Oh really? So when you give combination therapy to someone with HIV and some drugs target one part of the genome and other drugs target other parts of the genome has nothing to do with the analogous situation where some selection conditions in ev target particular parts of the genome and other selection conditions in ev target other parts of the genome in ev? Paul, you still don’t understand that mutation and selection is nothing more than a sorting/optimization problem and Dr Schneider and your algorithm does a very good job at demonstrating how this process works. It shows what happens when you have more than a single selection condition. It slows down the process profoundly.
Furthermore, these observations emphasize that sequential antiviral therapy with nucleoside analogues may allow the rapid selection of drug-resistant strains.You know, you're emphasizing that simultaneous selection pressures make evolution more difficult, but you've cited mostly controlled lab experiments. Does your mathematical proof against evolution include the part where pressures can't happen sequentially in the real world?
Paul, simultaneous selection pressures make evolution more difficult in the real world, that is why combination therapy is used for HIV, TB, HBV, HCV, malaria, cancer, weeds,… Many of the citations I have posted are not laboratory studies; they are clinical/field studies. It is your mathematical model which shows how this works.
You can run the numbers in Dr Schneider’s model. To evolve all three selection conditions simultaneously for a 16k genome takes more than 5,000,000 generations while each of the individual selection pressures when applied singly only take at most 100 generations. Your hunch is wrong.You mean like setting the mistake points for each condition? I tried it with the default settings, first with one at 10 and the other two at 1 -- on average 1000 generations to convergence. With 2 out of 3 set to 10, on average it took 700 generations to convergence. With all three set to 10, it took on average 650 generations to convergence.

Does this somehow help your theory out?
Set two of the three selection conditions to 0 so that you have only a single selection condition and see what happens to the generations for zero mistakes (perfect creature).
Delphi, the mathematics of mutation is not that complex, you have some understanding of the problem; otherwise you wouldn’t have posted the Wikipedia reference to fitness landscape.Sorry, your rant here is totally irrelevant to my point.
So you want to draw a correlation between an intelligently designed computer program and a cell you claim came about by mutation and selection. What’s your point? Mutation and selection is not so complex, it is clear that it can’t do what you have claimed. It is mathematically impossible and your own citation to Wikipedia shows why. If my rant served to annoy you then it did the job.
Why don’t you tell us how a temperature change can transform hundreds, perhaps thousands of genes simultaneously?How festive! Unfortunately, Halloween was last week.
I take it that you have withdrawn your claim that a temperature change is able to transform reptiles into birds. How have your studies going? Have you proved that insects evolve into insects yet?
Circles and Circles.

He believes evolution is wrong, therefore, it MUST be wrong.

If you are so certain, Kleinman, ignore the Jref, and submit your data to a reputable, peer reviewed publication.
You got it wrong Shalamar, its not circles and circles; it’s a spiral that you are watching as the theory of evolution goes down the drain. Why do you devalue JREF? You don’t think an educational forum is the appropriate place to debate such an issue?
It is not a correct interpretation if you want to claim that your argument has any scientific basis. Mutation and selection does not work that way either empirically or mathematically.In no way does this answer refer to what I asked. I was asking if you would clarify a theoretical and admittedly tangential point for me. But of course you are correct: asking you to explain anything will never result in anything with a scientific basis. I withdraw my question, and let your refusal or avoidance of answering it speak for itself.
Kotatsu, we all know what your point is, you claim that entire genomes evolve simultaneously. The only problem for your view is that you have no mathematical or empirical evidence to support your view. On the other hand, I propose that evolving more than a single gene at a time profoundly slows the evolutionary process. I have mathematical and empirical evidence to support my view. Your so call science requires no mathematical or empirical evidence, my science has the mathematical and empirical evidence.
Until you present something that is measurable and repeatable, you present nothing more than mush. The hundreds of citations which I have posted identify explicitly what the selection pressures are, the target genes for the selection pressures and often times identify the specific loci and mutations required for adaptation to the selection pressures. So far, all you have presented is mush.The fact that several different groups of animal have countered more or less the same set of selection pressures in different ways alone shows that the process is repeatable. When faced with the selection pressures I listed before (or a subset thereof, or a combination of these, or the subset, with unlisted ones), animals will evolve a way to get from tree to tree easier, for instance to get away from an arboreal predator. Some have solved this by flying, some by gliding, some by jumping, and so on.

But I will present you, again, with the Brassica example. When different diploid species of Brassica were cross-bred, polyploid progeny occurred. These were cross-bred again, according to certain patterns (1), for five generations, and the resulting polyploid hybrids are analogous to two species of natural hybrids. In five generations of inbreeding, the plants acquired several morphological and physiological changes, including changes in leaf shape and colour, branching patterns, number of side shoots, and differences in fertility. The genetic distance between the F5 generation and the F2 generation varied between 3.7% and 9.6%. The selection pressures included having to cope with two different copies of the same gene within the same genome, having to cope with sudden polyploidisation, and several other factors which are present for all plants, such as microbial and other parasitism, pathogens, and so on. The authors used 82-89 nuclear DNA probes to detect changes in the genome, and detected changes with 23-59 of these probes, indicating, again, that no specific genes were targeted.

There are of course more details in the paper, but as you never read details and instead only post stock answers and lies, I see no reason to elaborate further.
More of your “more or less” mush. Why should you be surprised that recombination and selection leads to morphological and physiological changes? What are you trying to prove? Are you trying to prove that polyploidy Brassica are still Brassica and that recombination can yield morphological changes, you have succeeded. If you are trying to prove that this is an example of mutation and selection then you have failed.
Kotatsu, you are trying to make connections where none exist. You don’t have selection pressures which would make these transformations.How on Earth can you make such a categorical statement? Am I to understand that you believe that regardless of what group of animal is under study, the researcher never knows any selection pressures operating on that group? Regardless of what gene he/she is working with?

The relevant selection pressures would of course change depending on the gene, the organism, and other factors. The same selection pressures wouldn't necessarily operate on a EF-1α tree as on an 18S tree. And in trees based on other genes, it is often possible to be very specific on at least some of the selection pressures operating on the gene in that organism.

Just because you don't understand phylogenies --- and this is becoming abundantly clear --- doesn't mean that the people who work with them don't.
Just because you don’t understand how mutation and selection works doesn’t suddenly make your phylogenic trees true. You have no mechanism to allow transformations like these, mutation and selection simply can not make these types of transformations. The mathematics of mutation and selection shows this and the empirical evidence of mutation and selection shows this. I don’t have to use your kind of “more or less” terminology, I can post mathematical and empirical data which shows that evolving more than a single gene at a time becomes profoundly slow by mutation and selection.
Kotatsu, you are in denial. Mutation and selection is not an incomprehensible process mathematically. If you ever come to understand that this process is nothing more than a sorting/optimization problem, you would realize that your belief system is wrong. The empirical evidence of how mutation and selection works verifies this. The pictures you draw are based on a mathematically impossible theory.This, again, has nothing to do with my post. I was simply making the same observation as several other people have done before me, that your arguments are changing gradually as you are overwhelmed by evidence.
Your posts have nothing to do with mutation and selection. You can’t produce a measurable example which shows that multiple genes are evolving simultaneously by mutation and selection. On the other hand, I have presented hundreds of citations which show that combination selection pressures profoundly slow the evolutionary process and a peer reviewed and published model of random point mutations and natural selection which shows the same thing. The only thing that I am overwhelmed by is your lack of mathematical and empirical evidence for your view.
For some reason I don’t think I’ll ever pass your class in evolutionism or joobz’s class in alchemy.No, I would imagine reading comprehension would be needed for both.
Perhaps I have a problem with reading comprehension but it is nothing to compare with your mathematical and scientific deficiencies, more or less.
Just stumbled over this:Why don’t you tell us how a temperature change can transform hundreds, perhaps thousands of genes simultaneously?Is there any reason why temperature change can't change a gene?
You didn’t know that this is how Delphi suggests that reptiles evolved into birds? He doesn’t seem to want to explain how this happens. Perhaps you want to take up the banner?

Temperature change can certainly change a gene; in fact, it would change the properties of many enzymes since the properties of these chemicals are strongly temperature dependent. Now do want to explain to us how mutation and selection can sort the mutations necessary to evolve so many genes simultaneously when the mathematical and empirical evidence shows that evolving more than a single gene at a time by mutation and selection becomes a profoundly slow process?
Ok I wrote a little simulation for use in investigating Kleinman's claim. I will post the source code on my website later today after I clean it up a bit.

The results show his theory to be wrong -- multiple pressures, of the same strength, eventually speed up the rate of evolution.

At first, it appeared as though Kleinman might be right -- adding selective pressures in low numbers really does slow the average rate of fixation way down. However, once a "critical mass" has been reached, adding pressures actually drives the rate back up. Eventually, with enough pressures, you get to a point where the average rate of fixation is equal to or faster than it is under only a single pressure.
“critical mass”, that sounds down right nuclear. Rocketdodger has mounted an E-bomb war head to his rocket in an attempt to hit the target. I think I am going to enjoy discussing this topic. This is going to be more fun that kjkent1’s string cheese theory of evolution.

Rocketdodger, you are going to post empirical examples of your model, won’t you? Oh, that’s right, you already have reptiles evolved into birds. Don’t forget to write your server software that speeds up as more users access the system.
The point you are missing Belz is that Dr Schneider’s model shows that the reason it so slowly converges is the three selection conditions.I don't see how this could be the point, since this is not what we were talking about. We were talking about how understanding and posting were two different things.

The mere fact that you're talking about a subject doesn't mean you know what you're talking about.
Are you going to start talking about beggaminases again?
If you set two of the three selection conditions to zero in the model then the remaining selection condition can evolve much, much more rapidly.But why the hell would you want to do this ? What happens, instead, if you set two of the three conditions to a relatively low, non-zero value ?
We want to set two of the three selection conditions to zero because it demonstrates what happens to the rate of convergence for that single selection condition alone when compared to converging all three selection conditions simultaneously. Ev doesn’t quite handle relative selection pressure strengths quite correctly. In order to model this effect properly, the percent of the population which reproduces would have to vary with the selection pressure strength. As the model is written, the most fit half of the population is always allowed to reproduce no matter what the weight factors are.
That same behavior of mutation and selection is seen in reality in the numerous citations posted.No, because you have not shown that those real-life examples have a number and relative strength of selection pressures that you can define.
Sure I have Belz, for example, HIV evolves resistance very rapidly to monotherapy while three drug therapy profoundly slows the evolution of the virus. HBV, HCV, TB, malaria, cancer, weeds,… all show the same effect. These examples often contain the specific mutations required to give immunity to the particular selection pressures.
Mutation and selection is simply a sorting/optimization problem.You'd like that to be true, wouldn't you ?
It has nothing to do with what I would like, it has everything to do with what reality shows.
You can try to say that I don’t understand how mutation and selection works but I can produce data from a peer reviewed and published computer simulation of random point mutations and natural selection and hundreds of empirical examples which shows the same thingActually, that's precisely what I'm saying. You don't understand how mutation and selection works but you can produce data from a peer reviewed and published computer simulation of random point mutations and natural selection and hundreds of empirical examples which shows the same thing according to you.
Anyone who wants to run ev can and duplicate the data which shows how much more quickly a single selection condition evolves than all three selection conditions simultaneously. It’s very easy to cherry pick data which shows this as well, there is so much of it around. I do like cherries, don’t you Belz?
You mean like setting the mistake points for each condition? I tried it with the default settings, first with one at 10 and the other two at 1 -- on average 1000 generations to convergence. With 2 out of 3 set to 10, on average it took 700 generations to convergence. With all three set to 10, it took on average 650 generations to convergence.Kleinman is talking about setting two out of three of them to 0. Then it'll converge in only a few generations. The problem, then, is that we're not evolving a creature who distinguishes bindings sites from other positions.
So what Paul? Give someone who suffers from HIV a PI and do you think that resistance to RTIs will evolve? All the ev sorting algorithm does in evolve sequences which satisfy the selection conditions whether they be one or three selection conditions simultaneously.
But why the hell would you want to do this ? What happens, instead, if you set two of the three conditions to a relatively low, non-zero value ?Here are a few experiments:

standard model with all mistake points = 1: 662 gens

with all mistake points = 10 (should be same): 662 gens

with missed site points = 10 (heavier pressure): 316 gens

with two spurious binding points = 10 (different heavier pressure): 1267 gens

with just gene spurious binding points = 10: 889 gens

with just nongene spurious binding points = 10: 1034 gens

So changing the relative pressures has some fairly obvious effects. More pressure on missed binding sites results in faster convergence. More pressure against spurious binding sites results in slower convergence.

Now let's turn off pressures:

(a) with missed site points = 0: 1 gen

(b) with just gene spurious binding points = 0: 707 gens

(c) with just nongene spurious binding points = 0: 405 gens

(d) with both spurious binding points = 0: 6 gens

In cases (a) and (d), no distinction evolves between binding sites and other positions, so it takes no time to produce a creature with zero mistakes. Essentially, there are no mistakes.

In cases (b) and (c), a distinction between binding sites and other positions evolves, but only for a portion of the genome. Not surprisingly, if the portion that matters is larger (case b), it takes longer.
That’s correct, sorting on multiple conditions takes far longer than sorting on single conditions and the situation gets much worse as you lengthen the genome.
Kleinman's entire hypothesis is built on his introducing a software "bug" into ev. Using a zero value for any of the selection weights causes the population genomes to be filled with missing and/or spurious bindings, while simultaneously reporting a "perfect" creature. However, the program population is not actually evolving towards the known natural quality shared by the genomes of all independently living organisms: RSequence ~ RFrequency.
Really, I didn’t make Paul put the weight factor feature into ev. And I suppose I made hundreds of scientist post data which shows that combination selection pressures profoundly slow the evolutionary process by mutation and selection. Why don’t I post another citation which shows what kind of control I have over the scientific world since they publish the data for supporting my hypothesis.
http://aac.asm.org/cgi/content/full/48/6/2260?ck=nck (http://aac.asm.org/cgi/content/full/48/6/2260?ck=nck)

BILN 2061 is a novel, specific hepatitis C virus (HCV) NS3 serine protease inhibitor discovered by Boehringer Ingelheim that has shown potent activity against HCV replicons in tissue culture and is currently under clinical investigation for the treatment of HCV infection. The poor fidelity of the HCV RNA-dependent RNA polymerase will likely lead to the development of drug-resistant viruses in treated patients. The development of resistance to BILN 2061 was studied by the in vitro passage of HCV genotype 1b replicon cells in the presence of a fixed concentration of the drug. Three weeks posttreatment, four colonies were expanded for genotypic and phenotypic characterization. The 50% inhibitory concentrations of BILN 2061 for these colonies were 72- to 1,228-fold higher than that for the wild-type replicon. Sequencing of the individual colonies identified several mutations in the NS3 serine protease gene. Molecular clones containing the single amino acid substitution A156T, R155Q, or D168V resulted in 357-fold, 24-fold, and 144-fold reductions in susceptibility to BILN 2061, respectively, compared to the level of susceptibility shown by the wild-type replicon. Modeling studies indicate that all three of these residues are located in close proximity to the inhibitor binding site. These findings, in addition to the three-dimensional structure analysis of the NS3/NS4A serine protease inhibitor complex, provide a strategic guide for the development of next-generation inhibitors of HCV NS3/NS4A serine protease.
and
In the region of the active-site mutations, BI-1 and BI-2 are expected to project functional groups that are either structurally identical to or very similar to BILN 2061 when it is bound to the enzyme. Thus, it is expected that the losses in potency against the mutants are similar for all three serine protease inhibitors. The accurate comparison of the decrease (n-fold) in the potency of BI-2 to that of BILN 2061 is made difficult by the dramatically different potencies against the wild-type enzyme. Our results showed that any one of several single mutations results in a high level of resistance to BILN 2061. However, replicons containing either multiple mutations or single engineered mutations were still sensitive to IFN-α (Table 1 and 2), indicating that combination therapy similar to HIV treatment using several drugs with different functions and targets may help overcome drug-resistant mutations and control HCV infection.

[Belz...]

Well, the argument that Adequate and I are using only works if you have both a sufficient number of pressures and sufficient time for all of their targeted mutations to fixate. If the pressures are extremely lethal, the combination of them will kill off the population before any of that happens.

Which kind of begs the question why Kleinman uses this scenario in the first place -- of course there will be no evolution, the population is dead.

Well, all I was saying is that after a selection pressures kills off 90% of a population, suddenly 100% of the population has adapted to that pressure.

[Belz...]

No you haven’t shown how mutation and selection works mathematical, you posted a hunch. Dr Schneider’s model shows mathematically how mutation and selection works

Considering how you've addmitted that its conditions are CONTRIVED, and that it's a SIMULATION, I don't see how you can claim this. If Dodger made a program that illustrated his example, would it mathematically show anything to you ?

and I have posted hundreds of citations which show how mutation and selection works empirically.

Do you have a notepad file from which you copy-paste this bit in every one of your posts ?

So are you claim that sorting is done only by animate objects?

No, that's YOUR claim.

Mutation and selection is nothing more than a sorting/optimization problem

You wish. It'd make your position less frivolous.

While you are at it, why don’t your write server software that performs faster as more users access the server.

Now that's very interesting. If that's how you see evolution, then it's no wonder you misunderstand it so much.

The problem for evolutionists is that when there large genetic changes, they are catastrophic for the individual who has this large genetic mutation.

You're making sweeping statements, again.

I think you would get an argument from Dr Schneider about the limitations of ev. In his peer reviewed and published article on ev, he used the results to estimate the evolution of a human genome.

Can you spot the key word in your statement ?

Paul, you are the one claiming that biological mechanisms somehow evolved.

Actually the entire scientific community does. And "somehow" is misleading. But I wouldn't expect anything from someone who's idea of creation is based on two mutually-exclusive scenarios in a 3000-year old book.

Ev demonstrates how slow a mutation/selection sorting algorithm performs when you have more than a single selection condition.

Yes, it demonstrated how slow an ALGORITHM performs.

Paul, simultaneous selection pressures make evolution more difficult in the real world

Is this why we see new species arise ?

Oh, and did someone explain to you the difference between pressures all acting on a single gene and pressures acting on different ones ? Or are you going to argue that it's irrelevant, just like a pressure's relative strength ?

Mutation and selection is not so complex

Of course it isn't. But it's a lot more complex than you claim.

Just because you don’t understand how mutation and selection works doesn’t suddenly make your phylogenic trees true.

Yeah, I think they call those things "strawmen".

Are you going to start talking about beggaminases again?

Wow. I think that, so far, that's the Kleinman reply to a sentence of mine that has the LEAST to do with the sentence being replied to.

We want to set two of the three selection conditions to zero because it demonstrates what happens to the rate of convergence for that single selection condition alone when compared to converging all three selection conditions simultaneously.

Huh ? Are those selection pressures present or not ?

Ev doesn’t quite handle relative selection pressure strengths quite correctly.

Saved for posterity.

Sure I have Belz, for example, HIV evolves resistance very rapidly to monotherapy while three drug therapy profoundly slows the evolution of the virus.

Klein, you might know how many drugs are in use, but YOU HAVE NO IDEA HOW MANY OTHER PRESSURES ARE AT WORK.

It has nothing to do with what I would like, it has everything to do with what reality shows.

If that were true, you'd have given up your silly antics long ago.

[Belz...]

Anyone who wants to run ev can and duplicate the data which shows how much more quickly a single selection condition evolves than all three selection conditions simultaneously. It’s very easy to cherry pick data which shows this as well, there is so much of it around. I do like cherries, don’t you Belz?


Not your brand, no.

[Paul C. Anagnostopoulos]

I’ll stop harping on your use of the word “function” when you stop trying to describe what the three selection conditions in ev are doing.
They push the organisms toward evolving a gene that recognizes the binding sites but no other positions on the genome.


Ev represents the evolution of sequences of bases that satisfy the conditions imposed by Dr Schneider’s selection conditions.
And real evolution results in sequences of bases that satisfy the conditions imposed by the environment. Can you explain the difference to me?


By the way, are you going to claim the evolution has a PURPOSE now?
Keep your concepts straight, Alan. Evolution has no purpose. An evolved gene has a purpose, or better yet, to avoid the implication you bring up, it has a function.

Oh really? So when you give combination therapy to someone with HIV and some drugs target one part of the genome and other drugs target other parts of the genome has nothing to do with the analogous situation where some selection conditions in ev target particular parts of the genome and other selection conditions in ev target other parts of the genome in ev?
Correct, they have nothing to do with each other. In the first case, the therapies target multiple HIV genes. In the second case, there is only one gene.

In the first case, the multiple parts of the genome refer to multiple genes. In the second case, the multiple parts of the genome refer to one gene product's binding at multiple sites.

~~ Paul

[Paul C. Anagnostopoulos]

So what Paul? Give someone who suffers from HIV a PI and do you think that resistance to RTIs will evolve? All the ev sorting algorithm does in evolve sequences which satisfy the selection conditions whether they be one or three selection conditions simultaneously.
I give up, Alan. You insist on comparing two different evolutionary paths that produce different results as if one is simply an optimization of the other. Somehow we end up in the same place with one pressure instead of three. But clearly we end up in two different places.

No one is arguing that different results can require different amounts of time.

~~ Paul

[kjkent1]

Kleinman's entire hypothesis is built on his introducing a software "bug" into ev. Using a zero value for any of the selection weights causes the population genomes to be filled with missing and/or spurious bindings, while simultaneously reporting a "perfect" creature. However, the program population is not actually evolving towards the known natural quality shared by the genomes of all independently living organisms: RSequence ~ RFrequency.Really, I didn’t make Paul put the weight factor feature into ev. And I suppose I made hundreds of scientist post data which shows that combination selection pressures profoundly slow the evolutionary process by mutation and selection. Why don’t I post another citation which shows what kind of control I have over the scientific world since they publish the data for supporting my hypothesis.You didn't make up the weight factors. What you made up is the idea that ev operates to evolve a genome that matches the transcription factor when you set one of the selective weights to zero.

If you're not using ev in a manner which selects for both missing and spurious bindings, you're experiment is invalid, because what ultimately evolves is not a valid sequence logo. It's just a bunch of noise. You may choose to call that noise a different function, but it's not anything approaching a real genome.

Had Schnieder suggested that these other zero-weight selection conditions were valid, he wouldn't have been published. So, you need to lose this argument, because it's frivolous.

As for your posted examples, they all show that an overwhelming selective pressure, whether in vitro or in vivo, permits evolutionary change.

Now, do you have any evidence to show that natural environments never are subjected to a single overwhelming selective pressure over a generational period sufficient to permit an evolutionary change?

If you don't, then you LOSE, because the fossil record shows that such change has occurred in nature, which absent magic, could only have come about (according to you) through many overwhelming pressures operating sequentially.

[rocketdodger]

If you don't, then you LOSE,

He lost, and he knows it. Take a look at that last post of his! Not even so much as an attempt at an argument there -- nothing but nonsense and sarcasm.

He knows we got the better of him, and that we will easily refute anything he says, so now all he does is post jibberish and the repeated mantra of "that is what the mathematics and empirical evidence shows."

[kleinman]

No you haven’t shown how mutation and selection works mathematical, you posted a hunch. Dr Schneider’s model shows mathematically how mutation and selection worksConsidering how you've addmitted that its conditions are CONTRIVED, and that it's a SIMULATION, I don't see how you can claim this. If Dodger made a program that illustrated his example, would it mathematically show anything to you ?
Belz, virtually any mathematical model of mutation and selection will have to do some contrivance to model the selection conditions since in reality what selection pressures do is change the conformation of proteins. Dr Schneider’s contrived selection conditions still capture the consequence of multiple selection pressures on the sorting of mutations. Neither rocketdodger nor Adequate are going to successfully make a simulation that shows that n+1 selection pressures evolve more rapidly than n selection pressures that has any basis in reality. The mutation/selection sorting/optimization process simply doesn’t work that way.
and I have posted hundreds of citations which show how mutation and selection works empirically.Do you have a notepad file from which you copy-paste this bit in every one of your posts ?
Nope, don’t need to, my 7th grade typing class was preparing me for this moment in time.
So are you claim that sorting is done only by animate objects?No, that's YOUR claim.
Nope, that’s rocketwhomissesthetarget’s claim. Here, read this.
.No. The environment is an inanimate object. How you think it could possibly sort anything is beyond me.
Mutation and selection is nothing more than a sorting/optimization problemYou wish. It'd make your position less frivolous.
What’s the matter Belz, don’t you like frivol?
While you are at it, why don’t your write server software that performs faster as more users access the server.Now that's very interesting. If that's how you see evolution, then it's no wonder you misunderstand it so much.
So let’s see if we can understand how you view evolution. Things don’t evolve, they beggaminases. Now the theory of evolution is much clearer.
The problem for evolutionists is that when there large genetic changes, they are catastrophic for the individual who has this large genetic mutation.You're making sweeping statements, again.
That’s right, I’m sweeping up the theory of evolution and throwing it into the dust bin.
I think you would get an argument from Dr Schneider about the limitations of ev. In his peer reviewed and published article on ev, he used the results to estimate the evolution of a human genome.Can you spot the key word in your statement ?
The following quotes were taken from Dr Schneider’s blog web page: 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.
"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
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.
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!
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!
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.
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.
Did you spot the key word Belz?
Paul, you are the one claiming that biological mechanisms somehow evolved.Actually the entire scientific community does. And "somehow" is misleading. But I wouldn't expect anything from someone who's idea of creation is based on two mutually-exclusive scenarios in a 3000-year old book.
Belz, that’s a 3000 year old book and a peer reviewed and published model of random point mutation and natural selection and hundreds of citations that show that evolving more than a single gene by mutation and selection is a profoundly slow process, too slow for the theory of evolution to be mathematically or empirically possible.
Ev demonstrates how slow a mutation/selection sorting algorithm performs when you have more than a single selection condition.Yes, it demonstrated how slow an ALGORITHM performs.
That’s right Belz, and the empirical data shows the same thing. That’s why the theory of evolution is mathematically impossible. Evolving more than a single gene simultaneously leads to a profoundly slow process.
Paul, simultaneous selection pressures make evolution more difficult in the real worldIs this why we see new species arise ?

Oh, and did someone explain to you the difference between pressures all acting on a single gene and pressures acting on different ones ? Or are you going to argue that it's irrelevant, just like a pressure's relative strength ?
Why don’t you post some citations about these new species, identify the selection pressures and the genes which have evolved and the mutations which have led to the new species? Kotatsu has tried to do this, more or less, actually, just less.
Mutation and selection is not so complex Of course it isn't. But it's a lot more complex than you claim.
Is that why I can post hundreds of citations which show that combination selection pressures profoundly slow the evolutionary process and you have posted zero examples?
Ev doesn’t quite handle relative selection pressure strengths quite correctly. Saved for posterity.
You can save it for whatever you want. Ev does handle selection pressures well enough to demonstrate that combination selection pressures profoundly slow the evolutionary process.
Sure I have Belz, for example, HIV evolves resistance very rapidly to monotherapy while three drug therapy profoundly slows the evolution of the virus. Klein, you might know how many drugs are in use, but YOU HAVE NO IDEA HOW MANY OTHER PRESSURES ARE AT WORK.
What I do know is that all the other selection pressures at work do not have significant effect on the fitness of the virus to reproduce. Without the drugs, HIV is an early death sentence for whoever suffers from the disease. Why don’t you tell us what other selection pressures you know of against this virus?
It has nothing to do with what I would like, it has everything to do with what reality shows.If that were true, you'd have given up your silly antics long ago.
What’s the matter Belz, don’t you like to frivol?
I’ll stop harping on your use of the word “function” when you stop trying to describe what the three selection conditions in ev are doing.They push the organisms toward evolving a gene that recognizes the binding sites but no other positions on the genome.
So what again Paul? Evolving any of the three individual conditions alone give the appropriate sequences very quickly. It is only when you try to sort the mutations for all three conditions simultaneously that the sorting process becomes profoundly slow. That is the lesson that ev is demonstrating.
Ev represents the evolution of sequences of bases that satisfy the conditions imposed by Dr Schneider’s selection conditions.And real evolution results in sequences of bases that satisfy the conditions imposed by the environment. Can you explain the difference to me?
Paul, I have been saying for the past year that ev does give a plausible simulation of how the mutation and selection process works. And what ev shows is that combination selection pressures profoundly slow the sort of mutations. Ev is analogous to how mutation and selection works in reality, single selection conditions evolve far more rapidly than combination selection pressures. That is what reality shows and that is what ev shows.
By the way, are you going to claim the evolution has a PURPOSE now?Keep your concepts straight, Alan. Evolution has no purpose. An evolved gene has a purpose, or better yet, to avoid the implication you bring up, it has a function.
Paul, you put yourself in a logically impossible position. How do you select for something that has no function because until a gene exists, it has no function?
Oh really? So when you give combination therapy to someone with HIV and some drugs target one part of the genome and other drugs target other parts of the genome has nothing to do with the analogous situation where some selection conditions in ev target particular parts of the genome and other selection conditions in ev target other parts of the genome in ev?Correct, they have nothing to do with each other. In the first case, the therapies target multiple HIV genes. In the second case, there is only one gene.

In the first case, the multiple parts of the genome refer to multiple genes. In the second case, the multiple parts of the genome refer to one gene product's binding at multiple sites.
Paul, ev has no function or purpose other than to sort the genomes based on the selection pressures imposed. You have three selection pressures targeted at three different parts of the genome. One selection condition is targeted at the nonbinding site region of the genome which removes sequences that match the weight matrix; another condition is targeted to the binding site region which forces sequences which match the weight matrix and a third condition which is targeted at the genes which eliminates sequences which match the weight matrix. This is analogous to targeting different sites on the HIV genome with different selection pressures. They have everything to do with each other because that is how the mutation and selection sorting/optimization process works mathematically and that is how it works empirically. If you target different parts of a genome with different selection pressures, it profoundly slows the sorting/optimization process.
So what Paul? Give someone who suffers from HIV a PI and do you think that resistance to RTIs will evolve? All the ev sorting algorithm does in evolve sequences which satisfy the selection conditions whether they be one or three selection conditions simultaneously.I give up, Alan. You insist on comparing two different evolutionary paths that produce different results as if one is simply an optimization of the other. Somehow we end up in the same place with one pressure instead of three. But clearly we end up in two different places.

No one is arguing that different results can require different amounts of time.
Paul, the entire point of this discussion is that ev takes huge numbers of generations to evolve its three selection conditions for all but the tiniest genomes. Your theory calls for the transformations of huge numbers of genes in order for reptiles to evolve into birds. Your own model shows what happens to the sort/optimization when you have three selection conditions and real examples of mutation and selection show the same thing. I’ll post an example below which shows the difference between 1, 2, 3 and 4 selection conditions.
Really, I didn’t make Paul put the weight factor feature into ev. And I suppose I made hundreds of scientist post data which shows that combination selection pressures profoundly slow the evolutionary process by mutation and selection. Why don’t I post another citation which shows what kind of control I have over the scientific world since they publish the data for supporting my hypothesis.You didn't make up the weight factors. What you made up is the idea that ev operates to evolve a genome that matches the transcription factor when you set one of the selective weights to zero.
You must have come up with this idea in one of your alternative universes because I have never said this. What I have always said is that each of the selection conditions selects for sequences of bases which satisfy the weight matrix. I don’t believe that ev evolves transcription factors even when you use all three selection conditions.
Now, do you have any evidence to show that natural environments never are subjected to a single overwhelming selective pressure over a generational period sufficient to permit an evolutionary change?

If you don't, then you LOSE, because the fossil record shows that such change has occurred in nature, which absent magic, could only have come about (according to you) through many overwhelming pressures operating sequentially.
Sure there are selective pressures that last over a generational period sufficient to permit an evolutionary change however the evolutionary change is not going to be accomplished by mutation and selection; it is just far too slow a process for transforming more than a single gene. The diversity in the fossil record is not due to mutation and selection, it is due to recombination and selection, just as we see great diversity in dog and cat population from recombination and selection. Mutation and selection can not accomplish these types of changes in so few generations; mutation can not be sorted that quickly.

So how does mutation and selection work? Here is another citation which shows how this phenomenon works.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1681928 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1681928)
More than a decade ago, it became apparent that treatment of HIV infection with only 1 antiretroviral agent was associated with the rapid development of resistance.[1] Clinical trials conducted at that time showed that combining 2 antiretroviral agents improved virologic and immunologic responses, compared with use of a single agent. Accordingly, 2-drug combination antiretroviral therapy became the standard of care to maintain viral suppression and minimize the emergence of resistant strains and, thereby, reduce the risk of disease progression and death. Subsequent experience and clinical trials showed that 3-drug combinations were substantially more effective than 2-drug combinations. Recommended 3-drug regimens of highly-active antiretroviral therapy (HAART) generally include 2 nucleoside or nucleotide analog reverse transcriptase inhibitors (NRTIs), plus 1 nonnucleoside analog reverse transcriptase inhibitor (NNRTI) or 1 protease inhibitor (PI).
and
When given as initial HAART, 4-drug regimens have shown promising preliminary results in recently completed studies as well as ongoing, comparative trials.[40,52]
Hey rocketwhomissesthetarget, better tell these scientists not to use too many selection pressures, they may start accelerating the evolution of the virus.

[Paul C. Anagnostopoulos]

Paul, I have been saying for the past year that ev does give a plausible simulation of how the mutation and selection process works. And what ev shows is that combination selection pressures profoundly slow the sort of mutations. Ev is analogous to how mutation and selection works in reality, single selection conditions evolve far more rapidly than combination selection pressures. That is what reality shows and that is what ev shows.
Then stop telling me that Ev only results in sequences of bases that satisfy selection conditions, rather than resulting in a genetic function. Make up your mind.


Paul, you put yourself in a logically impossible position. How do you select for something that has no function because until a gene exists, it has no function?
Indeed, selection cannot operate on something that has no function. But genetic drift can.


Paul, ev has no function or purpose other than to sort the genomes based on the selection pressures imposed.
I agree. But the gene that evolves in Ev does have a function. Otherwise there would be nothing for the selection pressure to press against.


You have three selection pressures targeted at three different parts of the genome. One selection condition is targeted at the nonbinding site region of the genome which removes sequences that match the weight matrix; another condition is targeted to the binding site region which forces sequences which match the weight matrix and a third condition which is targeted at the genes which eliminates sequences which match the weight matrix. This is analogous to targeting different sites on the HIV genome with different selection pressures.
I disagree.


Paul, the entire point of this discussion is that ev takes huge numbers of generations to evolve its three selection conditions for all but the tiniest genomes.
And yet you cannot present the math that shows:

$\mathit{huge number of generations} = \mathit{too long}$


You must have come up with this idea in one of your alternative universes because I have never said this. What I have always said is that each of the selection conditions selects for sequences of bases which satisfy the weight matrix. I don’t believe that ev evolves transcription factors even when you use all three selection conditions.
What does it have to do with belief? Ev certainly does not evolve biological transcription factors. It evolves an abstraction of one. Nevertheless, the simulated gene has a function: to match the binding sites but no other positions.

Except when one or two of the mistake counts are zero, in which case the simulated gene has a different function.

~~ Paul

[kjkent1]

What does it have to do with belief? Ev certainly does not evolve biological transcription factors. It evolves an abstraction of one. Nevertheless, the simulated gene has a function: to match the binding sites but no other positions.

Except when one or two of the mistake counts are zero, in which case the simulated gene has a different function.

~~ PaulFor clarification: the "different" function, you refer to above, i.e., when a mistake count is zero, has no relationship to any known genetic behavior, as is the case when all three mistake counts are set to non-zero values.

Correct?

[CFLarsen]

You didn’t know that this is how Delphi suggests that reptiles evolved into birds? He doesn’t seem to want to explain how this happens. Perhaps you want to take up the banner?

Temperature change can certainly change a gene; in fact, it would change the properties of many enzymes since the properties of these chemicals are strongly temperature dependent. Now do want to explain to us how mutation and selection can sort the mutations necessary to evolve so many genes simultaneously when the mathematical and empirical evidence shows that evolving more than a single gene at a time by mutation and selection becomes a profoundly slow process?

Whoa. That's not what my question was about.

My question wasn't about genes changing by mutation and selection.

My question was about genes changing by temperature change.

Now, why can't hundreds of genes change, if they are subjected to temperature change?

As I understand you, if one gene is changing, the others don't change, regardless of what happens.

What mechanism causes this to happen?

Are the genes interconnected in some way?

[Cardelitre]

Lots of posts from T'ai Chi. Still no definition of "complex." Still no acknowledgment that this is a problem with his argument. If you're lurking, do you find this intellectually dishonest?
:whistling
Obviously, yes. But is that really surprising?

*back lurking*

[rocketdodger]

Ok I put up the source code at http://www.jedi-arts.com/code/jev.cpp

There is also a sample input file at http://www.jedi-arts.com/code/data.txt


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 :(

With a little experimentation you should be able to get a large number of pressures down to less than three times as slow as a single one (I have done it many times today while searching for that elusive prize of a combination). If you get better results, please post the parameters!

Also if you have any questions just ask. The source code should be pretty explanatory, though.

I can put a windows executable at that site if anyone desires it.

[Belz...]

Belz, virtually any mathematical model of mutation and selection will have to do some contrivance to model the selection conditions

Thank you, Klein. Welcome to sanity.

The mutation/selection sorting/optimization process simply doesn’t work that way.

Of course it doesn't. It's not strictly a sorting/optimisation process.

Nope, don’t need to, my 7th grade typing class was preparing me for this moment in time.

I can see you now, writing the same thing over and over on the blackboard.

"Hundreds of empirical examples showing that multiple selection pressures profoundly slow evolution. Hundreds of empirical examples showing that multiple selection pressures profoundly slow evolution. Hundreds of empirical examples showing that multiple selection pressures profoundly slow evolution. Hundreds of empirical examples showing that multiple selection pressures profoundly slow evolution. Hundreds of empirical examples showing that multiple selection pressures profoundly slow evolution. Hundreds of empirical examples showing that multiple selection pressures profoundly slow evolution. Hundreds of empirical examples showing that multiple selection pressures profoundly slow evolution..."

What’s the matter Belz, don’t you like frivol?

I just love it when an opponent chooses not to respond to another's point but resorts to "clever" sarcasm in order to draw attention away from it...

So let’s see if we can understand how you view evolution. Things don’t evolve, they beggaminases. Now the theory of evolution is much clearer.

Just to test you: what is the definition of "beggaminases" ?

That’s right, I’m sweeping up the theory of evolution and throwing it into the dust bin.

Translation: "I'm aware that I'm using logical fallacies, but that's all that's left, so now I'll use humour."

The following quotes were taken from Dr Schneider’s blog web page: 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.

BZzZT! Wrong answer! The key word was: estimate.

Belz, that’s a 3000 year old book and a peer reviewed and published model of random point mutation and natural selection and hundreds of citations that show that evolving more than a single gene by mutation and selection is a profoundly slow process, too slow for the theory of evolution to be mathematically or empirically possible.

So you ARE using the bibble ?

That’s right Belz, and the empirical data shows the same thing.

No, it doesn't. You've been consistently shown wrong on this. The fact that you're ignoring it changes nothing to the facts. Your interpretation of the empirical data is wrong, and your model doesn't represent reality. It doesn't matter how you word it. You are utterly wrong.

Why don’t you post some citations about these new species, identify the selection pressures and the genes which have evolved and the mutations which have led to the new species?

Err... why don't I not ? You're the one who's claiming that you can tell me how many selection pressures act on a certain gene. You have never done so. We HAVE seen new species. Hopefully you don't dispute that.

Is that why I can post hundreds of citations which show that combination selection pressures profoundly slow the evolutionary process and you have posted zero examples?

That has nothing to do with what I said, but I suspect neither will whatever drivel you will use to answer this sentence.

You can save it for whatever you want. Ev does handle selection pressures well enough to demonstrate that combination selection pressures profoundly slow the evolutionary process.

Aside from circular reasoning, how would you know ? Since it doesn't handle those pressures adequately, how can you tell that it handles them well enough ? Exactly HOW is that not a contradiction ?

What I do know is that all the other selection pressures at work do not have significant effect on the fitness of the virus to reproduce.

Again, saved for posterity.

You have just debunked yourself.

Other pressures exist, but are of too small relative intensity to have any substantial effect in the presence of the overwhelming pressure. Ergo, evolution.

[kleinman]

Paul, I have been saying for the past year that ev does give a plausible simulation of how the mutation and selection process works. And what ev shows is that combination selection pressures profoundly slow the sort of mutations. Ev is analogous to how mutation and selection works in reality, single selection conditions evolve far more rapidly than combination selection pressures. That is what reality shows and that is what ev shows.Then stop telling me that Ev only results in sequences of bases that satisfy selection conditions, rather than resulting in a genetic function. Make up your mind.
Paul who has the bicycle with the backwards facing seat because he has back peddled so much on what he claims about ev asks me to make up my mind. Well Paul, if you want to cling to the ridiculous notion that ev evolves something with genetic function, go for it. I’ll cling to my notion that all the ev sorting algorithm does is evolve sequences of bases which satisfy the selection conditions written for the model. My, my Paul, you really have some weird ideas about what ev does but that goes well with your belief in the theory of evolution.
Paul, you put yourself in a logically impossible position. How do you select for something that has no function because until a gene exists, it has no function?Indeed, selection cannot operate on something that has no function. But genetic drift can.
Did you get your choice of colors for the paint which you use to paint yourself into a corner? So how do you get the evolution of a gene de novo? You remember what de novo means, from the beginning. There must have been a lot of drift in the primordial soup. Cyborg calls it the cruft theory of evolution.
Paul, ev has no function or purpose other than to sort the genomes based on the selection pressures imposed.I agree. But the gene that evolves in Ev does have a function. Otherwise there would be nothing for the selection pressure to press against.
Paul, you have some weird ideas what the ev sorting algorithm does.
You have three selection pressures targeted at three different parts of the genome. One selection condition is targeted at the nonbinding site region of the genome which removes sequences that match the weight matrix; another condition is targeted to the binding site region which forces sequences which match the weight matrix and a third condition which is targeted at the genes which eliminates sequences which match the weight matrix. This is analogous to targeting different sites on the HIV genome with different selection pressures.I disagree.
Make sure you click your heels together three times when you disagree with this.
Paul, the entire point of this discussion is that ev takes huge numbers of generations to evolve its three selection conditions for all but the tiniest genomes.And yet you cannot present the math that shows:
hugenumberofgenerations = toolong
That’s what so much fun for me in this discussion, I don’t have to present the math; you and Dr Schneider have already done it for me.

Do you want to go back over your estimate of how many hundreds of millions of generations it would take to evolve your function on 96 loci for a population of 100k genomes yet you only have 500,000 generations to transform 150,000,000 loci differences on a 3 billion base genome to explain the differences between humans and chimpanzees. That shows that:
Hugenumberoflociintoofewgenerations = mathematicallyimpossibletheory
You must have come up with this idea in one of your alternative universes because I have never said this. What I have always said is that each of the selection conditions selects for sequences of bases which satisfy the weight matrix. I don’t believe that ev evolves transcription factors even when you use all three selection conditions.What does it have to do with belief? Ev certainly does not evolve biological transcription factors. It evolves an abstraction of one. Nevertheless, the simulated gene has a function: to match the binding sites but no other positions.

Except when one or two of the mistake counts are zero, in which case the simulated gene has a different function.
So the function evolved in ev is an abstraction of a transcription factor. Once again you put your bicycle in reverse gear. Paul, you are the only person I know who has multiple reverse gears on your bicycle. Paul, tell us what the function of an abstraction of a transcription factor does.
What does it have to do with belief? Ev certainly does not evolve biological transcription factors. It evolves an abstraction of one. Nevertheless, the simulated gene has a function: to match the binding sites but no other positions.

Except when one or two of the mistake counts are zero, in which case the simulated gene has a different function.For clarification: the "different" function, you refer to above, i.e., when a mistake count is zero, has no relationship to any known genetic behavior, as is the case when all three mistake counts are set to non-zero values.

Correct?
There you go Paul, explain to us how a single selection pressure in ev has no function yet the three selection pressures somehow do.
Also if you have any questions just ask. The source code should be pretty explanatory, though.
Just a couple of little questions, describe to us what the selection pressures are and give us a real example of what you claim the model represents.
You didn’t know that this is how Delphi suggests that reptiles evolved into birds? He doesn’t seem to want to explain how this happens. Perhaps you want to take up the banner?

Temperature change can certainly change a gene; in fact, it would change the properties of many enzymes since the properties of these chemicals are strongly temperature dependent. Now do want to explain to us how mutation and selection can sort the mutations necessary to evolve so many genes simultaneously when the mathematical and empirical evidence shows that evolving more than a single gene at a time by mutation and selection becomes a profoundly slow process?Whoa. That's not what my question was about.

My question wasn't about genes changing by mutation and selection.

My question was about genes changing by temperature change.

Now, why can't hundreds of genes change, if they are subjected to temperature change?

As I understand you, if one gene is changing, the others don't change, regardless of what happens.

What mechanism causes this to happen?

Are the genes interconnected in some way?
So I guess you don’t want to take up Delphi’s banner that a temperature change was the selection pressure that transformed reptiles into birds. That’s what my original comment that you quoted was about.

Temperature changes certainly change the conformation of enzymes and their catalytic properties. The reason why hundreds of genes can not change simultaneously is that the mutation and selection process is a sorting/optimization problem. You can’t change hundreds of genes simultaneously by mutation and selection. Transforming two genes by mutation and selection simultaneously is a much slower process than transforming a single gene. If you have two genes evolving simultaneously with each gene needing only a single mutation and the probability of 1 in a million for the probability of each mutation, the probability of any member of the population getting both mutations simultaneously is (1/1,000,000)^2. If you are evolving a similar system with a hundred genes evolving, the probability for a member of that population getting all the proper mutations simultaneously is (1/1,000,000)^100. That’s why you can’t evolve hundreds of genes simultaneously. CFLarsen, here are a couple of examples which demonstrate empirically what happens to the mutation selection process when you have more than a single selection pressure.
http://en.wikipedia.org/wiki/Pesticide_resistance (http://en.wikipedia.org/wiki/Pesticide_resistance)
Pest resistance to a pesticide is commonly managed through pesticide rotation, which involves alternating among pesticide classes with different modes of action to delay the onset of or mitigate existing pest resistance.[9] Different pesticide classes may have different effects on a pest.[9] The U.S. Environmental Agency (EPA or USEPA) designates different classes of fungicides, herbicides and insecticides. Pesticide manufacturers may, on product labeling, require that no more than a specified number of consecutive applications of a pesticide class be made before alternating to a different pesticide class. This manufacturer requirement is intended to extend the useful life of a product.[citation needed]

Tankmixing pesticides is the combination of two or more pesticides with different modes of action in order to improve individual pesticide application results and delay the onset of or mitigate existing pest resistance.[10]
http://www.absw.org.uk/Briefings/insecticide_resistance.htm (http://www.absw.org.uk/Briefings/insecticide_resistance.htm)
Using high doses of insecticide should maximise kill of heterozygotes and this strategy was popular among theorists in the 1970s. But to be really effective, the dose was too high to be acceptable on either environmental or cost grounds. Another drawback was that uniform coverage of the crop was not assured. The high dose strategy could be revived though with transgenic plants if it is possible to maintain a high level of expression of the toxin gene. The other strategy is pyramiding which involves creating trangenic plants with genes for two different toxins. Insects resistant to one will be killed by the other, and vice versa. This provides a double hit strategy for seeing off heterozygotes and discouraging the spread of resistance genes. It also parallels the successful use of combination drug therapy in leprosy, TB and HIV/AIDS.
Combination selection pressures targeting more than a single gene profoundly slow the evolutionary process. That’s what the mathematics shows and that’s what the empirical evidence shows.

[rocketdodger]

Just a couple of little questions, describe to us what the selection pressures are and give us a real example of what you claim the model represents

The pressures are completely random, and each of them targets a single mutation. You can even set the relative fitness bonus per pressure if you wish, but that gets tedious pretty quick, so I added the ability to just set them all to a given fitness bonus.

The model is just a quick and dirty simulation of mutation and selection. It shows that additional selective pressures do not hinder the sorting mechanism like you claim it does. In particular, adding more and more pressures can easily bring the time to fixation per pressure down to within 200% of the time to fixation for a singly applied pressure. I also found a set of parameters that brought it down to be lower than for a singly applied pressure but I forgot what it was.

Needless to say, even less than 200% is not "profoundly" slowed, and is certainly not what you describe here...


You can’t change hundreds of genes simultaneously by mutation and selection. Transforming two genes by mutation and selection simultaneously is a much slower process than transforming a single gene. If you have two genes evolving simultaneously with each gene needing only a single mutation and the probability of 1 in a million for the probability of each mutation, the probability of any member of the population getting both mutations simultaneously is (1/1,000,000)^2. If you are evolving a similar system with a hundred genes evolving, the probability for a member of that population getting all the proper mutations simultaneously is (1/1,000,000)^100.


...and you claim to have a degree in engineering...

[kleinman]

Just a couple of little questions, describe to us what the selection pressures are and give us a real example of what you claim the model representsThe pressures are completely random, and each of them targets a single mutation. You can even set the relative fitness bonus per pressure if you wish, but that gets tedious pretty quick, so I added the ability to just set them all to a given fitness bonus.

The model is just a quick and dirty simulation of mutation and selection. It shows that additional selective pressures do not hinder the sorting mechanism like you claim it does. In particular, adding more and more pressures can easily bring the time to fixation per pressure down to within 200% of the time to fixation for a singly applied pressure. I also found a set of parameters that brought it down to be lower than for a singly applied pressure but I forgot what it was.

Needless to say, even less than 200% is not "profoundly" slowed, and is certainly not what you describe here...
Random mutation and random selection, just what exactly are you modeling?
You can’t change hundreds of genes simultaneously by mutation and selection. Transforming two genes by mutation and selection simultaneously is a much slower process than transforming a single gene. If you have two genes evolving simultaneously with each gene needing only a single mutation and the probability of 1 in a million for the probability of each mutation, the probability of any member of the population getting both mutations simultaneously is (1/1,000,000)^2. If you are evolving a similar system with a hundred genes evolving, the probability for a member of that population getting all the proper mutations simultaneously is (1/1,000,000)^100....and you claim to have a degree in engineering...
Actually three degrees, BS, MS and PhD. Now if you are having trouble with the mathematics above, perhaps you should take it up with this author.
http://www.blackwell-synergy.com/doi/pdf/10.1046/j.1365-3156.2001.00800.x (http://www.blackwell-synergy.com/doi/pdf/10.1046/j.1365-3156.2001.00800.x)
Resistance genes are generally assumed to be biologically less efficient than the normal susceptible type. For example, an enzyme may escape drug action by a mutation that alters the drug-binding site. As this mutation probably also affects its catalytic capacity, the mutation will be removed from the population by natural selection and their frequency in the naive, non-drug-treated, population will be determined by a mutation/selection balance (Hastings 1997; Koella 1998). If drugs are used in combination, then the frequency of parasites resistant to both drugs will be
very low. For example, if 0.1% are resistant to drug A and 0.005% are resistant to drug B, then parasites resistant to both will initially be present at a frequency of 0.1 x 0.05% = 0.00005% (assuming that the same gene cannot encode resistance to both drugs). Thus using drugs in combination from the outset may greatly increase the useful therapeutic lifespan of the drug, because lowering the starting frequency delays the point at which a significant amount of resistance emerges.
And
One important general point from the models is that use of combination therapy in their initial deployment is invariably better than introducing one drug alone, followed by introduction of the second-line drug once the first becomes ineffective (see, for example, Curtis & Otoo 1986; Smith 1990; Bonhoeffer et al. 1997; for malaria, helminths and bacteria, respectively).
And
If parasites reach high numbers within hosts, then spontaneous mutations to resistance may occur. Infections of P. falciparum may reach 10^11-10^12 individual parasites per host and it seems logical that a small subpopulation may have mutated to drug resistance (for example if the mutation rate to resistance is 10^-8 then there would be 1000±10 000 resistant parasites) which then expands to dominate the infection. This argument seems logically plausible and receives support from observations of humans treated with the antimalarial drug atovaquone, where an infection which was originally susceptible disappears below detectable levels before recrudescing as a resistant infection (Looareesuwan et al. 1996). Measurements of drug sensitivity in vitro before and after treatment show greatly increased levels of resistance in the recrudescent infection. It seems plausible that the same effects may occur in other parasites that reach high population numbers within a host. Once again the effect can be minimized or even eliminated by using drugs in combination. In the above example of 10^11 parasites, mutation rates to resistance of 10^-8, and assuming two drugs were used in combination, then resistance would arise in only 10^16 parasites, in effect rendering the frequency of spontaneous mutations negligible. The implications for the evolution of drug resistance are discussed in Lipsitch and Levin (1997) and White (1999 and references therein).
Since rocketdodger hasn’t give a real example of his simulation, I think it is worthwhile to review what Adequate said about his model.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
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.
http://forums.randi.org/images/smilies/doglaugh.gif
Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?
And
So far as I know, no-one has done the experiment.
and
[quote="Kleinman"]and too bad you don’t have any empirical examples of your silly graph ...[quote="Adequate"]As I have explained to you, I produced the model because I've not heard of this precise experiment being done.
Now we have rocketdodger’s silly model. Any chance you could give us a real example of your model rocketdodger.
http://forums.randi.org/images/smilies/doglaugh.gif

[joobz]

Unfortuantely, kleinman speaks a completely different langauge than the rest of the posters here.

Any logical well thought argument presented will be met with an equally illogical snide comment which does nothing to actually refute the argument presented him.


I still have yet to see any attempt of him to explain why his model assumptions are valid. He hopes that by ignoring this point or claiming it is irrelevant will make it magically disappear. However, it is clear to everyone that his aviodance of this (and many other points) is equal to admitting his theory is destroyed.

[rocketdodger]

It is this simple Kleinman -- look at the source code and tell us why something is incorrect.

[rocketdodger]

I still have yet to see any attempt of him to explain why his model assumptions are valid. He hopes that by ignoring this point or claiming it is irrelevant will make it magically disappear. However, it is clear to everyone that his aviodance of this (and many other points) is equal to admitting his theory is destroyed.

Yep. What is even more comical is that he doesn't realize this, and so, for instance, he will reply to this comment of yours with something like "no, it is you who have failed to explain, and are hoping the evidence that disproves evolution will magically disappear. You must be a David Copperfield fan, joobz, because you really like magic," followed by that stupid laughing dog gif.

[Paul C. Anagnostopoulos]

For clarification: the "different" function, you refer to above, i.e., when a mistake count is zero, has no relationship to any known genetic behavior, as is the case when all three mistake counts are set to non-zero values.
I can't imagine a useful biological function that would be so nonselective.

~~ Paul

[Paul C. Anagnostopoulos]

Paul who has the bicycle with the backwards facing seat because he has back peddled so much on what he claims about ev asks me to make up my mind. Well Paul, if you want to cling to the ridiculous notion that ev evolves something with genetic function, go for it. I’ll cling to my notion that all the ev sorting algorithm does is evolve sequences of bases which satisfy the selection conditions written for the model. My, my Paul, you really have some weird ideas about what ev does but that goes well with your belief in the theory of evolution.
Ev is a model, Alan. It evolves a function that models something in real life. It is an abstraction of real life. It obviously does not evolve an actual biological function, as in biology.

You must have a particular meaning of "genetic function" in mind when you make statements like the one I highlighted. Unfortunately, I don't know what that meaning is.


Did you get your choice of colors for the paint which you use to paint yourself into a corner? So how do you get the evolution of a gene de novo?
By starting with something that has a very simple function. You can interpret that statement however you want, since I have no idea what you think a "biological function" is.


That’s what so much fun for me in this discussion, I don’t have to present the math; you and Dr Schneider have already done it for me.
Wow, we're good, huh? Okay, then could you please show me where in Evj we proved:

$\mathit{hugenumberofgenerations} = \mathit{toolong}$


Do you want to go back over your estimate of how many hundreds of millions of generations it would take to evolve your function on 96 loci for a population of 100k genomes
I don't know which experiments you're referring to. What is "96 loci" and do you mean a population of 100K or a genome size of 100K? How many generations did I estimate?


So the function evolved in ev is an abstraction of a transcription factor. Once again you put your bicycle in reverse gear. Paul, you are the only person I know who has multiple reverse gears on your bicycle. Paul, tell us what the function of an abstraction of a transcription factor does.
If you think I was ever saying that Evj evolves an actual transcription factor, then clearly one or the other of us is stark raving mad. The abstraction of the transcription factor matches the binding sites on the genome, but no other positions on it. I think I've said that numerous times.


There you go Paul, explain to us how a single selection pressure in ev has no function yet the three selection pressures somehow do.
I said it had a different function. Pay attention.

~~ Paul

[kleinman]

Unfortuantely, kleinman speaks a completely different langauge than the rest of the posters here.
Joobz, could you teach us your language, speculationish.
Any logical well thought argument presented will be met with an equally illogical snide comment which does nothing to actually refute the argument presented him.
Joobz, when have you presented a logical well thought out argument? You are ignorant of the mathematics of mutation and selection and you are ignorant of the mathematics of PDEs.
I still have yet to see any attempt of him to explain why his model assumptions are valid. He hopes that by ignoring this point or claiming it is irrelevant will make it magically disappear. However, it is clear to everyone that his aviodance of this (and many other points) is equal to admitting his theory is destroyed.
I have posted hundreds of citations which show how mutation and selection actually works which contradicts your silly speculations.

Joobz, you have also claimed that you can find irregularities in my PhD thesis. The wager is still there $10,000 dollars if you can find any mathematical or empirical regularity in my thesis, or are you nothing more than a big mouth coward.
It is this simple Kleinman -- look at the source code and tell us why something is incorrect.
It’s your job to explain your model with random mutations and random selection pressures, whatever they are. You still haven’t given a real example of your model. I particularly like the thorough analysis you have done with you program when you said this.
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 :(
Could you give us a real example of your model?
For clarification: the "different" function, you refer to above, i.e., when a mistake count is zero, has no relationship to any known genetic behavior, as is the case when all three mistake counts are set to non-zero values.I can't imagine a useful biological function that would be so nonselective.
Hey, your fellow evolutionist rocketdodger has a model of mutation and selection where the mutations are random and the selection pressures are random and he claim to show that n+1 selection pressures evolve faster than n selection pressures. Paul, perhaps you could tell us what function his model evolves or do only some selection pressures evolve genes with some kind of function?

[delphi_ote]

Obviously, yes. But is that really surprising?

*back lurking*
Welcome to the board, Cardelitre. Thanks for the feedback. Don't lurk. Post your thoughts! :)

[Paul C. Anagnostopoulos]

Hey, your fellow evolutionist rocketdodger has a model of mutation and selection where the mutations are random and the selection pressures are random and he claim to show that n+1 selection pressures evolve faster than n selection pressures. Paul, perhaps you could tell us what function his model evolves or do only some selection pressures evolve genes with some time of function?
See, here's the problem, Alan. It doesn't matter what function his model evolves, as long as it shows that more selection pressures can sometimes evolve faster than fewer. This acts as a counterexample to your glib proof to the contrary. Now you must address his counterexample in your proof and prove that it has nothing to do with real life.

But you can't do that yet. First you have to prove that Ev encompasses all possible real-life scenarios and that at least some of those scenarios did not have enough time to evolve.

Sometimes you gotta do stuff in a particular order, don't you know.

~~ Paul

[delphi_ote]

So you want to draw a correlation between an intelligently designed computer program and a cell you claim came about by mutation and selection.
http://i71.photobucket.com/albums/i133/delphi_ote/fail-24.jpg
What’s your point?
That, in order to state with certainty that one thing is more complex than another thing, we need a precise definition of complexity.

Tai Chi's logic went something like this:
*Creating Windows required intelligence
*Windows was created by a human
*Creating something more complex requires more intelligence (unproven)
*A cell is more complex than Windows (unproven)
*Therefore, creating a cell requires a being more intelligent than a human

Flaws abound, but I was picking one of the flawed premises to try to get an answer out of Tai Chi... so far, none have come...

[joobz]

Yep. What is even more comical is that he doesn't realize this, and so, for instance, he will reply to this comment of yours with something like "no, it is you who have failed to explain, and are hoping the evidence that disproves evolution will magically disappear. You must be a David Copperfield fan, joobz, because you really like magic," followed by that stupid laughing dog gif.
Let's see if you are correct.

Joobz, could you teach us your language, speculationish.

Joobz, when have you presented a logical well thought out argument? You are ignorant of the mathematics of mutation and selection and you are ignorant of the mathematics of PDEs.

I have posted hundreds of citations which show how mutation and selection actually works which contradicts your silly speculations.

Joobz, you have also claimed that you can find irregularities in my PhD thesis. The wager is still there $10,000 dollars if you can find any mathematical or empirical regularity in my thesis, or are you nothing more than a big mouth coward.


avoidance of the critique.....Check.
Use of Derision and insults in attempt to mask his own inabilities....check.
Use of moronically dumb strawmen arguments.....check.
delusional lies.....check.

Yup, Rocketdodger, you are comepletely correct. The silly little man continues to embarrass himself by demonstrating his terrible understanding of evolution and math.

[CFLarsen]

So I guess you don’t want to take up Delphi’s banner that a temperature change was the selection pressure that transformed reptiles into birds. That’s what my original comment that you quoted was about.

It is up to you to present your evidence that Evolution is wrong. You are the one who argues against the scientific evidence.

Temperature changes certainly change the conformation of enzymes and their catalytic properties. The reason why hundreds of genes can not change simultaneously is that the mutation and selection process is a sorting/optimization problem. You can’t change hundreds of genes simultaneously by mutation and selection. Transforming two genes by mutation and selection simultaneously is a much slower process than transforming a single gene. If you have two genes evolving simultaneously with each gene needing only a single mutation and the probability of 1 in a million for the probability of each mutation, the probability of any member of the population getting both mutations simultaneously is (1/1,000,000)^2.

If you are evolving a similar system with a hundred genes evolving, the probability for a member of that population getting all the proper mutations simultaneously is (1/1,000,000)^100. That’s why you can’t evolve hundreds of genes simultaneously.

Why do mutations necessarily need to be the same?

CFLarsen, here are a couple of examples which demonstrate empirically what happens to the mutation selection process when you have more than a single selection pressure.
http://en.wikipedia.org/wiki/Pesticide_resistance (http://en.wikipedia.org/wiki/Pesticide_resistance)

http://www.absw.org.uk/Briefings/insecticide_resistance.htm (http://www.absw.org.uk/Briefings/insecticide_resistance.htm)

Combination selection pressures targeting more than a single gene profoundly slow the evolutionary process. That’s what the mathematics shows and that’s what the empirical evidence shows.

Ehhh....hello? Your examples are evidence of just how fast species can evolve when there is a lot of changes in a short time.

The problem with some pesticides quickly becoming less effective is precisely evidence that contradicts your argument.

[Belz...]

Notice how Kleinman completely ignores my posts, now ? He doesn't even bother with his "clever" scarcasm!

[Belz...]

Actually three degrees, BS, MS and PhD.

I'm sure I know a few high-schoolers who have a better grasp of these things than you do.

[Belz...]

I have posted hundreds of citations which show how mutation and selection actually works

Actually, you have. You just don't realise it.

[Mr. Scott]

Ok I put up the source code at http://www.jedi-arts.com/code/jev.cpp

There is also a sample input file at http://www.jedi-arts.com/code/data.txt


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 :(

With a little experimentation you should be able to get a large number of pressures down to less than three times as slow as a single one (I have done it many times today while searching for that elusive prize of a combination). If you get better results, please post the parameters!

Also if you have any questions just ask. The source code should be pretty explanatory, though.

I can put a windows executable at that site if anyone desires it.

Here's something that would be neat to try:

1) Create a meta program (metajev) that runs jev, issuing it parameters and receiving the results.

2) Have metajev start by making, say, 10 random sets of inputs for jev (population of 10).

3) Run jev on each.

4) Replace the inputs that had the one poorest result with the inputs that had the best result (10% selection pressure).

5) Apply a slight mutation to a parameter of each input set (mutation rate of one per generation).

6) Repeat 3-5 until satisfied you've found superb input sets.

Recurse, repeating 2-6 if interesting -- trying different population sizes, selection pressures, mutation rates.

Indeed, we are doing something like this already. Different evolution simulations are as we speak competing in the Annoying Creationist fitness landscape, mutating and reproducing under various selection pressures.

تطور عظيمة

[Shalamar]

Klienman, you fail at science.

Evolution has been shown to have happened. The Theory of Evolution is the statement of how it happens. If the theory were to be 'thrown into the dustbin', as you put it, it doesn't mean that evolution does not exist. The theory would be revised to show the new data. That is, after all, how science works.

I have yet to see a single point you've made that 'proves' that evolution does not exist. Your proofs are a simulation, with your concept that slow=stop.

You've also admitted to being a creationist, which likely means that you already have your conclusion, and like many creationists, you seem to erroneously think that if evolution is disproved, then creationism must be true!

Nothing is farther than the truth. And if your concept were correct, you'd publish it, prove your points, and become famous. Yet, I fail to see anywhere where the theory of evolution has been shot down.

[rocketdodger]

Here's something that would be neat to try:


That is a good idea.

[Belz...]

تطور عظيمة

Huh ?

[delphi_ote]

Huh ?
According to Google Translator "great evolution"...

[kjkent1]

If you are evolving a similar system with a hundred genes evolving, the probability for a member of that population getting all the proper mutations simultaneously is (1/1,000,000)^100. That’s why you can’t evolve hundreds of genes simultaneously.Your statement here pretty much explains why you can't "see" the obvious.

You are fixated on the idea that evolution must reach a predetermined goal. Your use of the phrase "proper genes" demonstrates this conclusively.

You think that the change from a dinosaur form to a bird form was the result of something other than just an accumulation of various unpredictable biological changes which just happened to have provided their owners a fitness advantage at a particular historical point.

Evolution is not deterministic, Alan. Two trials of an experiment using identical selection pressures will not necessarily produce the same evolutionary outcome, because the "mutation" part of the evolutionary process cannot be predicted in advance.

Birds didn't get feathers because the environment demanded feathers. Birds got feathers because there was a random mutation causing feathers (rather than, say, "armor") and the feathers just happened to be useful.

No evolutionary experiment, no matter how stringently constructed, can guarantee an identical outcome, as long as the mutations are truly random. Because, if the mutations are random, then the possible functions are also random.

The only thing that evolution guarantees is that "something" will be produced with a fitness advantage.

Also, evolution apparently guarantees that, given enough time, the genomes Rseq will approximate Rfreq. That is a measurable outcome, and the primary one which Schneider used in ev to ensure that something close to real life was evolving.

However, when you disable one or more of ev's mistake counts, the genome does not evolve so that Rseq ~ Rfreq. Instead, you hit a "perfect creature" and the program halts. That "perfect creature," however, is only perfect because you've disabled part of the selection process, so the program no longer has to evolve Rseq ~ Rfreq.

Your hypothesis is incorrectly based entirely on a bug that you have placed into ev, which prevents it from evolving anything that models real-life genetic functionality.

[Belz...]

No evolutionary experiment, no matter how stringently constructed, can guarantee an identical outcome, as long as the mutations are truly random. Because, if the mutations are random, then the possible functions are also random.

Well, they're not "truly" random, but they are random, for all intents and purposes.

Your hypothesis is incorrectly based entirely on a bug that you have placed into ev, which prevents it from evolving anything that models real-life genetic functionality.

Why doesn't that surprise me.

[rocketdodger]

OK I updated my simulation program and made it more realistic and quite a bit faster. The source code is at www.jedi-arts.com/code/jev.cpp and an example input file is at www.jedi-arts.com/code/data.txt .

The program is quite simple. It takes a population of p creatures, each with a genome of bases of size g, and exerts P pressures on it. Initially the genome is initialzed so that the targeted bases of each pressure are neutral -- the pressures do not infer any fitness change to the population at the start of generation 1.

Each generation, m mutations randomly occur in each genome. During selection, the targeted bases of the pressures are examined. If the base is the same as the pressures "match" field, f fitness is added to the creature. If the base is the same as the pressures "badMatch" field, f * badWeight fitness is subtracted from the creature. This is meant to implement the idea that a bad mutation would decrease fitness (I.E. likely kill the creature) more than a good mutation would increase fitness.

Selection is performed by summing up the fitness of the entire population, then allocating offspring according to the percentage of the total fitness each creature has. So if the total fitness is 100, and a creature has 20 fitness, 20% of the next generation is intialized with the genome of that creature.

You can play with most of the parameters, they are all documented in the source code. Under the following parameters

genome 16000
population 2048
mutation 8
fixation 0.8
fitness 1
badWeight 4
reps 4
numPressures x 5

The following data gets generated, for x = 1, 5, 10, 20, 40, and 80:

Overall rate under 1 pressures was 145.000000( 145.000000 on average per pressure ).
Overall rate under 5 pressures was 162.229996( 811.149979 on average per pressure ).
Overall rate under 10 pressures was 218.225006( 2182.250061 on average per pressure ).
Overall rate under 20 pressures was 204.338135( 4086.762695 on average per pressure ).
Overall rate under 40 pressures was 114.856873( 4594.274902 on average per pressure ).
Overall rate under 80 pressures was 56.574688( 4525.975037 on average per pressure ).

These statements mean "the overall rate under x pressures was R <fixations per generation> ( A <generations to fixation> on average per pressure ).

What does this mean? First, notice that the number of generations to fixation for a pressure monotonically increases as we add more pressures. For a single pressure it took 145 generations on average, but for 80 it took 4525 generations on average. Second, notice that the ovarall rate of fixation initially increases, then decreases. Eventually, at some point between 20 and 40 pressures, the rate of fixation passes that of a singly applied pressure.

Why? Because although each pressure takes much longer to fixate, they are all on their way to fixation at the same time -- in parallel. The factor each pressure adds to the total time to fixation is not as great as the bonus incurred by evolving against another pressure in parallel.

This demonstrates, among other things, that Kleinman is outright wrong. None of the data he has relied on goes over 4 or 5 pressures at once, so he has no way to refute this simulation (short of looking at the source code, which he won't do for reasons we all know).


Clearly, n + 1 selective pressures lead to a greater rate of fixation (evolution) than n pressures, for many values of n. Also, clearly, n pressures lead to fixation at a greater rate than a single pressure for many values of n.

Dr. Adequate is right. We are right. You are simply wrong, Kleinman. There is nothing else to say now. I did all the work of showing you, very clearly, that sorting/optimization problems are NOT always confounded by multiple sorting conditions. Particularly, when sorting happens in parallel, as it does in mutation and selection.

[Belz...]

Dodger, your model is not peer-reviewed. Klein can safely ignore it ! :rolleyes:

[rocketdodger]

wtf... I spend 4 hours writing a program that proves Kleinman is wrong, once and for all, and he disappears?

Well I guess that is a good thing...

[kjkent1]

wtf... I spend 4 hours writing a program that proves Kleinman is wrong, once and for all, and he disappears?

Well I guess that is a good thing...kleinman will return -- count on it.

Far earlier in the thread, I did some studies with ev which showed that convergence of Rseq -> Rfreq appeared to form a normal distribution curve, centered on the maximum number of selection pressures applied. And, your program supports this idea -- which should be intuitively obvious, because everything in nature that happens to biological organisms seems to take on a bell-shaped curve.

Naturally, kleinman discounted my findings as nonsense.

So, allow me to congratulate you -- you're a very talented programmer.

[delphi_ote]

wtf... I spend 4 hours writing a program that proves Kleinman is wrong, once and for all, and he disappears?
He'll be back, and your program won't change his mind. If evidence mattered at all in his decision making process, he would've recanted his position hundreds of pages ago.

I'd really like to be wrong about this.

ETA Let me second the "talented programmer" comment. Your code is sexy!

[rocketdodger]

... because everything in nature that happens to biological organisms seems to take on a bell-shaped curve.


Pretty much they do, yeah. And its not just biological, its [i]everything[i]. The Gaussian distribution is simply the mathematical effect of lots and lots of flat probability distributions applied together. So you see it even in completely unnatural phenomena as well.


So, allow me to congratulate you -- you're a very talented programmer.

Thanks (you too delphi). I am just a newbie though... only got my degree last year. You should see some of the people in my industry!

[delphi_ote]

You should see some of the people in my industry!
If you work in the industry I think you work in, yea. I'm a PhD student at a top CS school, and I'm impressed by the code coming out of that industry...

[Belz...]

ETA Let me second the "talented programmer" comment. Your code is sexy!

Nerd.

[sol invictus]

You can’t change hundreds of genes simultaneously by mutation and selection. Transforming two genes by mutation and selection simultaneously is a much slower process than transforming a single gene.
Wrong. See below.

If you have two genes evolving simultaneously with each gene needing only a single mutation and the probability of 1 in a million for the probability of each mutation, the probability of any member of the population getting both mutations simultaneously is (1/1,000,000)^2. If you are evolving a similar system with a hundred genes evolving, the probability for a member of that population getting all the proper mutations simultaneously is (1/1,000,000)^100. That’s why you can’t evolve hundreds of genes simultaneously.

What you said here is technically correct, but it's the right answer to the wrong question. You don't want to ask what the probability is that all those mutations happened in a single generation - that would be extremely unlikely. But evolution happens gradually - you want to ask what the probability is that all those mutations happened after some large number of generations. Or to turn that around: how many generations it will take on average for them all to occur?

It's easy to get the answer. Suppose for a moment we only care about one gene, and the probability per generation that gene will mutate is p. Then the number of generations t it takes for the mutation to occur is on average simply t_avg = 1/p.

Now suppose there are N mutations we want to keep track of, and for simplicity assume that each has that same probability p to occur in any given generation. It's true that the chance for them all to occur in a single generation is very small: p^N. But what's the average time it takes for all N mutations to occur? That's slightly more complicated, but the answer is the following: the chance that after t generations a given mutation has not occurred is (1-p)^t. So that chance it has occurred is 1-(1-p)^t. Then the chance that all N have occurred is (1-(1-p)^t)^N. We can use that to compute the average time exactly, or make an estimate.

For N large, the answer is approximately t_avg ~ (1/p)(d + Log[N]), where d is a number of order 1. So the time grows very slowly with N at large N, and the average time per mutation decreases at large N as Log[N]/(pN). In your example, where p = 1/1,000,000 and N = 100, the average number of generations for all 100 mutations to occur is only 5.2 10^6, or 5.2/p.

This is a simpler version of what rocketdodger did above.

Executive summary: increasing the number of mutations you're tracking does not significantly increase the typical time required for them all to occur.

[kleinman]

Paul who has the bicycle with the backwards facing seat because he has back peddled so much on what he claims about ev asks me to make up my mind. Well Paul, if you want to cling to the ridiculous notion that ev evolves something with genetic function, go for it. I’ll cling to my notion that all the ev sorting algorithm does is evolve sequences of bases which satisfy the selection conditions written for the model. My, my Paul, you really have some weird ideas about what ev does but that goes well with your belief in the theory of evolution.Ev is a model, Alan. It evolves a function that models something in real life. It is an abstraction of real life. It obviously does not evolve an actual biological function, as in biology.

You must have a particular meaning of "genetic function" in mind when you make statements like the one I highlighted. Unfortunately, I don't know what that meaning is.
Of course ev does not evolve any actual biological function. What ev demonstrates is how the mutation and selection sorting/optimization process is profoundly slowed when trying to sort on multiple selection conditions. The reason why you don’t know the meaning of the highlighted text is there are no selection conditions that would evolve a genetic function de novo. You tried to suggest that the presence of oxygen led to the evolution of hemoglobin. To you want to try to put some details on your speculation or are vague speculations all you need to call your theory “scientific”.
Did you get your choice of colors for the paint which you use to paint yourself into a corner? So how do you get the evolution of a gene de novo?By starting with something that has a very simple function. You can interpret that statement however you want, since I have no idea what you think a "biological function" is.
Just what is this “simple function”? What is your example of a “simple” form of hemoglobin? You are the one who is claiming that ev is an “abstraction of real life” and that ev is evolving a “function that models something in real life”. So, you tell us how this “abstraction of real life” is evolving a “function that models something in real life”.

What I claim is that ev is an idealized model of mutation and selection and what it shows is how profoundly slow the sorting/optimization process become when trying to sort by multiple selection conditions simultaneously. This is exactly what happens in all real, measurable and repeatable examples of mutation and selection. This is what ev demonstrates. So Paul, have fun trying to tell us what this “abstraction of real life” is evolving a “function that models something in real life”.
That’s what so much fun for me in this discussion, I don’t have to present the math; you and Dr Schneider have already done it for me. Wow, we're good, huh? Okay, then could you please show me where in Evj we proved: hugenumberofgenerations = toolong
From the Evolutionisdead forum:
Extrapolating your 1 mutation per genome data to a lousy 1 million population gives 254 generations. To a measly 10 million population gives 106 generations. Even with a ratio of 2000:1, that's a mere 212,000 generations.Even if I accepted your extrapolations as accurate, recall this series is based on a G=1000. Thus far, ev has shown that genome length is the dominant parameter in determining the number of generations for convergence. If your “primitive” microorganism has G=100,000 rather than 1000, and the number of generations is linearly related, the mere 212,000 generations becomes 21,200,000 generations to evolve the 16 binding sites.Heck, make is 210,000,000. At one generation per day, that's an insignificant 575,000 years.
So Paul your estimate for the number of generations to evolve 96 loci in the ev model for a population of 1 million, G=100,000 and mutation rate=1/genome/generation is 210,000,000 generations. If you assume the generation time for this population is one generation per day, you get a mere 575,000 years. Paul, do you want to do the calculation to estimate the number of years required to evolve those 96 loci for a population that reproduces once a year? Perhaps you would like to use your extrapolation technique and estimate the number of generations for a population of 1 million but with a G=1 billion instead of 100,000? This is another demonstration of why the theory of evolution by mutation and selection is mathematically impossible. Mutation and selection is simply far to slow a process.
Do you want to go back over your estimate of how many hundreds of millions of generations it would take to evolve your function on 96 loci for a population of 100k genomesI don't know which experiments you're referring to. What is "96 loci" and do you mean a population of 100K or a genome size of 100K? How many generations did I estimate?
Don’t you recall the G=1000 series we did, varying populations? Do you want me to repost that data? Paul, don’t you recall that all but the tiniest genomes take huge numbers of generations to evolve “function” in ev? And why does it take huge numbers of generations to evolve “function” in ev? It takes huge numbers of generations to evolve “function” in ev because the sorting algorithm becomes profoundly slow for the multiple sorting conditions for all but the tiniest search spaces. And Paul, that’s exactly what the empirical data for mutation and selection shows, this sorting/optimization process is profoundly slow for all but single selection conditions.
So the function evolved in ev is an abstraction of a transcription factor. Once again you put your bicycle in reverse gear. Paul, you are the only person I know who has multiple reverse gears on your bicycle. Paul, tell us what the function of an abstraction of a transcription factor does.If you think I was ever saying that Evj evolves an actual transcription factor, then clearly one or the other of us is stark raving mad. The abstraction of the transcription factor matches the binding sites on the genome, but no other positions on it. I think I've said that numerous times.
How does your abstraction relate to reality? Why does it take such huge numbers of generations to evolve your “abstraction of transcription factor matches” on all but the tiniest genomes? Even Dr Schneider knows that it would take years of CPU time to evolve your “abstraction of transcription factor matched” for a realistic G value for a free living organism. Would you like a pair of matching pants for your straight jacket?
There you go Paul, explain to us how a single selection pressure in ev has no function yet the three selection pressures somehow do.I said it had a different function. Pay attention.
Paul, you are so cute when you squirm. Why don’t you tell us what these different functions that ev is evolving when evolving only a single selection condition at a time.
Hey, your fellow evolutionist rocketdodger has a model of mutation and selection where the mutations are random and the selection pressures are random and he claim to show that n+1 selection pressures evolve faster than n selection pressures. Paul, perhaps you could tell us what function his model evolves or do only some selection pressures evolve genes with some time of function?See, here's the problem, Alan. It doesn't matter what function his model evolves, as long as it shows that more selection pressures can sometimes evolve faster than fewer. This acts as a counterexample to your glib proof to the contrary. Now you must address his counterexample in your proof and prove that it has nothing to do with real life.
When rocketdodger was asked to describe his selection pressures in his model he said this:
The pressures are completely random, and each of them targets a single mutation. You can even set the relative fitness bonus per pressure if you wish, but that gets tedious pretty quick, so I added the ability to just set them all to a given fitness bonus.
Both Adequate and rocketdodger are claiming that n+1 selection pressures evolve more rapidly than n selection pressures. Neither has been able to present a real example of this nor has any other evolutionist been able to present such an example. Both Adequate’s and rocketdodger’s assertions have no basis in reality. I’ll continue to post real examples which contradict their baseless assertions, these examples demonstrates the mathematics which your own model shows, that is combination selection pressures profoundly slow the mutation/selection, sorting/optimization process.
But you can't do that yet. First you have to prove that Ev encompasses all possible real-life scenarios and that at least some of those scenarios did not have enough time to evolve.
Paul, I’ll keep posting scenarios of how mutation and selection actually works for as long as you want. Every real measurable and repeatable example of mutation and selection shows that combination selection pressures profoundly slow the evolutionary process and we will all wait for you evolutionists to post a single real example which contradicts these findings. Paul, I almost pity you in this debate, you have no mathematical basis for your beliefs, your own model contradicts your theory and you have no empirical evidence to support your scientifically baseless theory. The only real question in this debate is which is dumb and which is dumber, abiogenesis or the theory of evolution.
Sometimes you gotta do stuff in a particular order, don't you know.
Oh, do you mean sequential selection pressures?
So you want to draw a correlation between an intelligently designed computer program and a cell you claim came about by mutation and selection.[quote="Kleinman"]What’s your point?[quote="Delphi_ote"]That, in order to state with certainty that one thing is more complex than another thing, we need a precise definition of complexity.
I suspect you are going to have some difficulty coming up with a mathematical definition for complexity because this has subjectivity associated with it. You can come up with a mathematical definition for order or disorder but something that is complex or intricate for one person may be easy to understand for another. Complexity is a qualitative property of a system. You might be able to obtain a quantitative measure for complexity by using the number of lines of computer code necessary to describe they system. Do you want to try to write a computer model for a cell? Why not try to write a computer simulation of a mitochondrion?
Tai Chi's logic went something like this:
*Creating Windows required intelligence
*Windows was created by a human
*Creating something more complex requires more intelligence (unproven)
*A cell is more complex than Windows (unproven)
*Therefore, creating a cell requires a being more intelligent than a human

Flaws abound, but I was picking one of the flawed premises to try to get an answer out of Tai Chi... so far, none have come...
I think the argument is not whether Windows or a cell is more complex than the other. It is how the order in these two complex systems came about. In one case we know absolutely that the order did not come about by mutation and selection and in the other, evolutionists argue that this order came about by random mutation and natural selection. Can random mutation and natural selection create this type of order that we see in a cell? The answer to this question is a mathematical and empirical no.
So I guess you don’t want to take up Delphi’s banner that a temperature change was the selection pressure that transformed reptiles into birds. That’s what my original comment that you quoted was about.It is up to you to present your evidence that Evolution is wrong. You are the one who argues against the scientific evidence.
What mathematical or scientific evidence have you presented? I have presented the mathematical data from a peer reviewed and published mathematical model of random point mutations and natural selection which shows that combination selection pressures profoundly slow the evolutionary process and I have presented hundreds of real empirical examples of mutation and selection, all which show that mutation and selection is profoundly slowed when you have more than a single selection pressure.
Temperature changes certainly change the conformation of enzymes and their catalytic properties. The reason why hundreds of genes can not change simultaneously is that the mutation and selection process is a sorting/optimization problem. You can’t change hundreds of genes simultaneously by mutation and selection. Transforming two genes by mutation and selection simultaneously is a much slower process than transforming a single gene. If you have two genes evolving simultaneously with each gene needing only a single mutation and the probability of 1 in a million for the probability of each mutation, the probability of any member of the population getting both mutations simultaneously is (1/1,000,000)^2.

If you are evolving a similar system with a hundred genes evolving, the probability for a member of that population getting all the proper mutations simultaneously is (1/1,000,000)^100. That’s why you can’t evolve hundreds of genes simultaneously.Why do mutations necessarily need to be the same?
Mutations don’t have to be the same; in fact there is no reason for us to believe that mutations will be the same. When a biological system is subjected to multiple selection conditions simultaneously, it becomes profoundly difficult for the population to sort beneficial and detrimental mutations in order to increase the frequency of beneficial sequences of bases. It is this false assumption that multiple genes can evolve simultaneously to multiple different selection conditions that forms the foundation for the theory of evolution.
CFLarsen, here are a couple of examples which demonstrate empirically what happens to the mutation selection process when you have more than a single selection pressure.
http://en.wikipedia.org/wiki/Pesticide_resistance (http://en.wikipedia.org/wiki/Pesticide_resistance)

http://www.absw.org.uk/Briefings/insecticide_resistance.htm (http://www.absw.org.uk/Briefings/insecticide_resistance.htm)

Combination selection pressures targeting more than a single gene profoundly slow the evolutionary process. That’s what the mathematics shows and that’s what the empirical evidence shows.Ehhh....hello? Your examples are evidence of just how fast species can evolve when there is a lot of changes in a short time.

The problem with some pesticides quickly becoming less effective is precisely evidence that contradicts your argument.
Wake up and smell the coffee CF, these articles show that rapid evolution only occurs with the use of a single pesticide. Using a second pesticide in combination with the first profoundly slows the ability of these populations to evolve against both pesticides simultaneously. It works the same for HIV, HBV, HCV, influenza, malaria, cancer, weeds,… All these populations can evolve rapidly to a single selection pressure but add additional selection pressures simultaneously and these populations can no longer evolve quickly. Mutation and selection is simply a sorting/optimization process. The process can occur quickly when only a single gene is evolving in a population, but force a population to evolve multiple genes simultaneously and this becomes a profoundly slow process. That is what the mathematical and empirical evidence of mutation and selection shows. The theory of evolution by mutation and selection is mathematically and empirically impossible.
Notice how Kleinman completely ignores my posts, now ? He doesn't even bother with his "clever" scarcasm!
How could I ever be sarcastic beggaminases?
Actually three degrees, BS, MS and PhD.I'm sure I know a few high-schoolers who have a better grasp of these things than you do.
Get one of those high-schoolers into the discussion, perhaps they could explain to us what a beggaminases is.
I have posted hundreds of citations which show how mutation and selection actually worksActually, you have. You just don't realise it.
Sure I realize what they show and so do you; they are cherry picked to show that combination selection pressures profoundly slow the evolutionary process. Too bad there are no cherries on your trees, nothing but some dry rot on your evolutionary tree.
Indeed, we are doing something like this already. Different evolution simulations are as we speak competing in the Annoying Creationist fitness landscape, mutating and reproducing under various selection pressures.
We all look forward to you posting a real example of your simulations while I continue to post real examples of what Dr Schneider’s peer reviewed and published ev model shows which is combination selection pressures profoundly slow the evolutionary process.
Evolution has been shown to have happened. The Theory of Evolution is the statement of how it happens. If the theory were to be 'thrown into the dustbin', as you put it, it doesn't mean that evolution does not exist. The theory would be revised to show the new data. That is, after all, how science works.
Sure Shalamar, microevolution exists, Dr Schneider’s computer simulation shows how it works and the hundreds of citations which I have posted substantiates what Dr Schneider’s model shows. The concept of common descent by mutation and selection is a mathematical and empirical impossibility. Mutation and selection simply doesn’t work that way.
If you are evolving a similar system with a hundred genes evolving, the probability for a member of that population getting all the proper mutations simultaneously is (1/1,000,000)^100. That’s why you can’t evolve hundreds of genes simultaneously.Your statement here pretty much explains why you can't "see" the obvious.

You are fixated on the idea that evolution must reach a predetermined goal. Your use of the phrase "proper genes" demonstrates this conclusively.
When did I use the phrase “proper genes”? There is a huge amount of evidence that particular selection pressures lead to particular mutations increasing in frequency in a population. This phenomenon is used to identify resistance to drugs, pesticides and herbicides. If evolution does not have a goal, why do the same mutations show up over and over to particular selection pressures?
You think that the change from a dinosaur form to a bird form was the result of something other than just an accumulation of various unpredictable biological changes which just happened to have provided their owners a fitness advantage at a particular historical point.

Evolution is not deterministic, Alan. Two trials of an experiment using identical selection pressures will not necessarily produce the same evolutionary outcome, because the "mutation" part of the evolutionary process cannot be predicted in advance.
Too bad that the evidence contradicts your speculations; for example, the use of particular drugs for treatment of HIV leads to increase in the frequency of particular mutations appearing in the viral population. This effect is used to identify when resistance to a particular drug has evolved.
OK I updated my simulation program and made it more realistic and quite a bit faster.
and
Clearly, n + 1 selective pressures lead to a greater rate of fixation (evolution) than n pressures, for many values of n. Also, clearly, n pressures lead to fixation at a greater rate than a single pressure for many values of n.

Dr. Adequate is right. We are right. You are simply wrong, Kleinman. There is nothing else to say now. I did all the work of showing you, very clearly, that sorting/optimization problems are NOT always confounded by multiple sorting conditions. Particularly, when sorting happens in parallel, as it does in mutation and selection.
Ok rocketdodger, here is your opportunity to give us a real example of your model. If you need help with your response, I’ll remind you what Adequate said.
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.
[quote="rocketdodger"]wtf... I spend 4 hours writing a program that proves Kleinman is wrong, once and for all, and he disappears?

Well I guess that is a good thing...
You missed me rocketdodger, how touching.
kleinman will return -- count on it.
and
He'll be back, and your program won't change his mind. If evidence mattered at all in his decision making process, he would've recanted his position hundreds of pages ago.

I'd really like to be wrong about this.
Kjkent1, for once you are correct, Delphi, you haven’t been correct on the concept of mutation and selection since you posted your citation to Wikipedia and the fitness landscape.
ETA Let me second the "talented programmer" comment. Your code is sexy!
Delphi, for your own good, lay off the sterno.

If you have two genes evolving simultaneously with each gene needing only a single mutation and the probability of 1 in a million for the probability of each mutation, the probability of any member of the population getting both mutations simultaneously is (1/1,000,000)^2. If you are evolving a similar system with a hundred genes evolving, the probability for a member of that population getting all the proper mutations simultaneously is (1/1,000,000)^100. That’s why you can’t evolve hundreds of genes simultaneously.[quote="sol invictus"]What you said here is technically correct, but it's the right answer to the wrong question. You don't want to ask what the probability is that all those mutations happened in a single generation - that would be extremely unlikely. But evolution happens gradually - you want to ask what the probability is that all those mutations happened after some large number of generations. Or to turn that around: how many generations it will take on average for them all to occur?
Welcome to the discussion sol. So let’s see what you are arguing.
It's easy to get the answer. Suppose for a moment we only care about one gene, and the probability per generation that gene will mutate is p. Then the number of generations t it takes for the mutation to occur is on average simply t_avg = 1/p.

Now suppose there are N mutations we want to keep track of, and for simplicity assume that each has that same probability p to occur in any given generation. It's true that the chance for them all to occur in a single generation is very small: p^N. But what's the average time it takes for all N mutations to occur? That's slightly more complicated, but the answer is the following: the chance that after t generations a given mutation has not occurred is (1-p)^t. So that chance it has occurred is 1-(1-p)^t. Then the chance that all N have occurred is (1-(1-p)^t)^N. We can use that to compute the average time exactly, or make an estimate.

For N large, the answer is approximately t_avg ~ (1/p)(d + Log[N]), where d is a number of order 1. So the time grows very slowly with N at large N, and the average time per mutation decreases at large N as Log[N]/(pN). In your example, where p = 1/1,000,000 and N = 100, the average number of generations for all 100 mutations to occur is only 5.2 10^6, or 5.2/p.
Sol, you have got your questions wrong. It is not how many generations it takes for all 100 mutations to occur in a population. It is how many generations it takes for all 100 mutations to show up in a single individual in the population. Then that individual has evolved to all 100 selection pressures.

Here is an example of how this computation is properly done.
http://www.billingpreis.mpg.de/hbp04/mybil.pdf (http://www.billingpreis.mpg.de/hbp04/mybil.pdf)
Despite the approval of almost 20 antiretroviral drugs and the use of combination therapy, successful treatment of HIV-infections is hampered by the emergence of drug-resistant genetic variants in response to therapy. Finding a new potent drug combination after treatment failure is considered challenging, because most accumulated mutations confer resistance to multiple drugs. We present three computational tools for the analysis and simulation of viral genomic sequences, phenotypic drug resistance, and clinical outcomes. Mtreemix is a software package for estimating and using mixture models of trees that describe probabilistically the evolution of drug resistance. Geno2pheno is a web-based system for the prediction of phenotypic resistance from viral genotypes. It also implements normalization methods that make these predictions comparable between different drugs. Finally, theo predicts virological response within a patient from the infecting viral strain and the selected drug combination. Together these models and programs provide a quantitative picture of the evolution of drug resistance and support the design of individualized antiviral therapies.
and
We mention a clinical study from De Luca, Cozzi-Lepri, Perno, Balotta, Di Giambenedetto, Orani, Mussini, Toti & d’Arminio Monforte (2003) to demonstrate the benefit of predicting phenotypic resistance for the selection of new antiretroviral regimens. These researchers analyze therapy changes accompanied by a genotypic resistance tests in 332 previously untreated patients. Phenotypes are predicted with geno2pheno for the components of the combination therapies, and each drug is scored as active if the virus is predicted susceptible to it. Using a Cox proportional hazards model, they show that patients with a combination therapy consisting of ≤ 2 active drugs have a significantly higher risk of virological failure (sustained virus load increase) than patients receiving ≥ 3 active drugs (p < 0.004). The authors also compare the performance of 11 rules-based interpretation systems and our data-driven approaches. Genotypic scoring based on the SVM predictions as implemented in geno2pheno turns out to be the only interpretation system that provides significant predictions of virological failure after 24 weeks of treatment (De Luca, Cingolani, Di Giambenedetto, Trotta, Baldini, Rizzo, Bertoli, Liuzzi,Narciso, Murri, Ammassari, Perno & Antinori 2003
These authors are answering the correct question Sol.
Here is another citation on the same topic which shows mathematically how mutation and selection works.
http://bioinformatics.oxfordjournals.org/cgi/content/full/21/21/3943 (http://bioinformatics.oxfordjournals.org/cgi/content/full/21/21/3943)
Summary: The development of drug resistance is a major obstacle to successful treatment of HIV infection. The extraordinary replication dynamics of HIV facilitates its escape from selective pressure exerted by the human immune system and by combination drug therapy. We have developed several computational methods whose combined use can support the design of optimal antiretroviral therapies based on viral genomic data.
and
Suppose we have estimated a mutagenetic tree model for the development of resistance to a certain drug. In particular, this model can be used to compute transition probabilities between mutational patterns. As described in the previous section we can predict the resistance phenotype from the genotype. Using a classifier restricted to the set of n mutations we predict each mutational pattern to be either susceptible or resistant. Now, for a given virus we may ask what the transition probability to any resistant state is. In fact, this question is crucial for minimizing the risk of resistance development with the next regimen. We refer to the genetic barrier as the probability of not reaching any resistant state after a fixed time period under therapy. This quantity can be calculated as the sum of the probabilities of all mutational patterns predicted as susceptible. Thus, a higher genetic barrier indicates that the virus is less likely to become resistant.

For example, Table 2 shows the genetic barriers to both low level and high level zidovudine resistance of the wild type virus under three different regimens, namely zidovudine monotherapy, double therapy with zidovudine plus lamivudine, and double therapy with zidovudine plus didanosine. The underlying mutagenetic tree model is the tree displayed in Figure 1 scaled to a mean sampling time of 96 weeks. As expected, the genetic barrier to zidovudine is always higher under the combination of zidovudine plus lamivudine than under zidovudine alone, because these drugs do not share any resistance mutations. More surprisingly, we find that zidovudine resistance appears to develop faster under zidovudine plus didanosine than under zidovudine monotherapy. This effect may be explained by the stronger selective pressure exerted by the double therapy and the cross-resistance profile of zidovudine and didanosine (Beerenwinkel et al., 2005b; Brun-Vezinet et al., 1997). Thus, the genetic barrier is a useful concept for designing effective treatment strategies.
and
In order to support clinical decision making on the basis of viral genomic data, we have developed and applied several computational methods and tools. Specifically, we have addressed data integration and management (Arevir database), prediction of drug resistance and co-receptor usage from genotypes (geno2pheno), modeling of the evolution of drug resistance and the genetic barrier by mutagenetic trees (mtreemix), and selection of optimal drug combinations (theo). The integration of various types of genomic, phenotypic and clinical data as well as the coupling of different computational models yields predictive models of therapy outcome that may support the design of combination therapies.
I post the above citation for two reasons. First I post this citation because of the highlighted text in the second paragraph. This is the first citation I have seen which indicates that combination therapy leads to faster evolution than monotherapy and the second point is these authors still are advocates of combination therapy. Belz, I think you are going to find the above quote is not a cherry in your bowl, only the pits but let’s see if you can extrapolate this finding to support common descent.

The nonsensical notion that n+1 selection pressures evolve more quickly than n selection pressures would lead one to believe that if you continued to add more drugs to the treatment combinations of HIV that the virus will evolve more quickly. This is mathematical nonsense which Adequate and rocketdodger a putting out.

[sol invictus]

Sol, you have got your questions wrong. It is not how many generations it takes for all 100 mutations to occur in a population. It is how many generations it takes for all 100 mutations to show up in a single individual in the population. Then that individual has evolved to all 100 selection pressures.

Nope - that's exactly what I calculated. To re-state, I answered the following question:

Suppose we start with a population of un-mutated individuals, and let's assume for simplicity that they're immortal and don't reproduce. How long do we have to wait before, say, 90% of the individuals have each undergone all N mutations, if the chance per unit time for any given mutation to occur in an individual is p?

Or asked another way, how long do we have to wait before each individual has a 90% chance of having undergone all N mutations?

Answer: t ~ log(N)/p (valid for p<<1 and N>>1).


It's mathematically the same question as the following: suppose there are N lotteries. I can buy tickets, and each ticket has a chance p of winning each of the lotteries (so one ticket might win nothing, or it might win one particular lottery (with chance p), or even all N (with chance p^N)). Question: how many tickets do I have to buy to have a 90% chance of winning ALL the lotteries?

Same answer as above: log(N)/p.

Again, to summarize: it takes hardly any longer for an individual to mutate N times than it does for it to mutate once. For example, 1,000,000 mutations will happen to one individual in only about 14 times as long as a single mutation.

[Paul C. Anagnostopoulos]

Paul, you are so cute when you squirm. Why don’t you tell us what these different functions that ev is evolving when evolving only a single selection condition at a time.
Well, let's see. If you only count mistakes points when a binding site is missed, then you are evolving a function that matches binding sites and probably every other position as well. If you only count mistake points when a spurious binding occurs, then you are evolving a function that does not match spurious positions and probably also does not match anywhere else.

Notice how those two functions are different from matching the binding sites but nowhere else. Simple, really.

~~Paul

[kleinman]

Sol, you have got your questions wrong. It is not how many generations it takes for all 100 mutations to occur in a population. It is how many generations it takes for all 100 mutations to show up in a single individual in the population. Then that individual has evolved to all 100 selection pressures.Nope - that's exactly what I calculated. To re-state, I answered the following question:

Suppose we start with a population of un-mutated individuals, and let's assume for simplicity that they're immortal and don't reproduce. How long do we have to wait before, say, 90% of the individuals have each undergone all N mutations, if the chance per unit time for any given mutation to occur in an individual is p?
This is why you are asking the wrong question. This is not simply a probability problem; it is a sorting and optimization problem as well. Only those most fit members of the population can accumulate the beneficial mutations. The harmful mutations are causing individuals to be selected out.

But for the sake of discussion, let’s consider your approach but instead of 90% of the individuals undergoing all N mutations, consider a single individual undergoing all N (100) mutations. In the first generation that individual has a (1/(1,000,000))*100 probability of getting a beneficial mutation, if that individual is gets one of those beneficial mutations, in the next generation, that individual has a (1/(1,000,000))*99 probability of getting a second beneficial mutation or a total probability of (1/(1,000,000))*100*(1/(1,000,000))*99 and so on for each additional possible beneficial mutation. The probability of a particular individual getting all one hundred beneficial mutations is (100/1,000,000)*(99/1,000,000)* … *(1/1,000,000). Sol, I’ll let you run the numbers for the probability of any individual getting all 100 beneficial mutations in 100 generations, let alone 90% of the population getting all 100 beneficial mutations. The point you are missing is that without selection, you can not improve the frequencies of genetic sequences in the population. You only have a few basic ways of improving these probabilities. You can increase population, number of generations, mutation rates (within limits) or you can reduce down the number of selection pressures.
Or asked another way, how long do we have to wait before each individual has a 90% chance of having undergone all N mutations?

Answer: t ~ log(N)/p (valid for p<<1 and N>>1).

It's mathematically the same question as the following: suppose there are N lotteries. I can buy tickets, and each ticket has a chance p of winning each of the lotteries (so one ticket might win nothing, or it might win one particular lottery (with chance p), or even all N (with chance p^N)). Question: how many tickets do I have to buy to have a 90% chance of winning ALL the lotteries?

Same answer as above: log(N)/p.

Again, to summarize: it takes hardly any longer for an individual to mutate N times than it does for it to mutate once. For example, 1,000,000 mutations will happen to one individual in only about 14 times as long as a single mutation.
So Sol, you are telling us that it only takes 14 times longer to win 100 lotteries as it takes to win 1 lottery? After all, that’s what an individual in the population has to do to get the 100 beneficial mutations and for that individual, the probability of winning one of the lotteries is decreasing with each beneficial mutation the individual wins.
Paul, you are so cute when you squirm. Why don’t you tell us what these different functions that ev is evolving when evolving only a single selection condition at a time.Well, let's see. If you only count mistakes points when a binding site is missed, then you are evolving a function that matches binding sites and probably every other position as well. If you only count mistake points when a spurious binding occurs, then you are evolving a function that does not match spurious positions and probably also does not match anywhere else.

Notice how those two functions are different from matching the binding sites but nowhere else. Simple, really.
And now you can tell us what these different functions serve other than they give sequences of bases which either match or don’t match the weight matrix. After all, that’s all that your sorting algorithm really does, simple, really.

[Paul C. Anagnostopoulos]

And now you can tell us what these different functions serve other than they give sequences of bases which either match or don’t match the weight matrix.
Your sentence is a bit muddled. The function of the modeled gene, when all three selections are present, is to match binding sites but no other positions. This is modeled using a weight matrix and a threshold. So ultimately it's all a question of math. In life, it's all a question of chemistry. Either you think modeling chemistry with math is okay, or you think it's bogus. But regardless, the math is different when all three selections are present as opposed to only one or two of them. And so therefore is the modeled function.

~~Paul

[kleinman]

And now you can tell us what these different functions serve other than they give sequences of bases which either match or don’t match the weight matrix.Your sentence is a bit muddled. The function of the modeled gene, when all three selections are present, is to match binding sites but no other positions. This is modeled using a weight matrix and a threshold. So ultimately it's all a question of math. In life, it's all a question of chemistry. Either you think modeling chemistry with math is okay, or you think it's bogus. But regardless, the math is different when all three selections are present as opposed to only one or two of them. And so therefore is the modeled function.
I’m not sure what you are having trouble understanding in my statement. Each of the selection conditions in ev does a part of the sorting requirement of the genomes. In order to get an arrangement of bases that satisfy all three sorting conditions simultaneously, it is an extremely slow process for all but the tiniest genomes. This is your so-called function. However, any individual portion of the sorting process can be done much more quickly if done independently of the other sorting conditions. A portion of your total function can be achieved by applying only a single sorting condition.

Paul, I think that modeling chemistry with mathematics is more than okay, it allows for accurate application of physical laws. That said, ev is modeling how mutation and selection sorts and optimizes in a biochemical system and doing parts of the sort individually proceeds far more rapidly than doing the total sorting conditions simultaneously. That is the only function ev demonstrates.

[rocketdodger]

Ok rocketdodger, here is your opportunity to give us a real example of your model. If you need help with your response, I’ll remind you what Adequate said.

Why don't you give us a real example of the model used in ev?

You want a war of examples? Well guess what Kleinman, none of your examples show that multiple selection pressures slow evolution in general. All they show is that many species of organisms fail to develop resistance before their population is destroyed when a few human generated pressures are applied to them. You haven't shown a single study where the pressures satisfy any of the following conditions:

1) Greater in number than 3 or 4.
2) Natural as opposed to human applied.
3) Not intended to kill the organism outright.

Thus, your little theory will hold water if and only if those three conditions hold for every population in the history of Earth. Do you think they do?

You need to use mathematics to show anything else, because of how narrow your citations are. That is why you keep running home to your gross misinterpretation of ev. On your own, you haven't even given us an equation, not one single equation, that makes any sense, to work with -- at first I suspected it was because you know we will blow it apart, but now I think its because you are a fraud and in fact know nothing about math beyond what your elementry level bible school has taught you. But you know what? It doesn't matter, because I do.

The algorithm I used in my model is exactly the algorithm used in mutation and selection. The only thing it was intended to show is that a sorting/optimization problem is not always confounded by more optimization conditions -- and it does show that, plain and simple. My program sorts by fitness and in every possible set of conditions adding more optimization conditions eventually leads to faster sorting overall. It is a mathematical fact Kleinman -- you can try to argue against this but you are just wrong.

If you dispute anything, all you have to do is take a look at the source code (which others will attest is easy to follow) and tell me where I went wrong. Please, be my guest. Surely, with your three degrees and fancy professional background, you should be able to decimate the code that I, with only a lowly bachelor's degree, came up with from scratch.




The nonsensical notion that n+1 selection pressures evolve more quickly than n selection pressures would lead one to believe that if you continued to add more drugs to the treatment combinations of HIV that the virus will evolve more quickly. This is mathematical nonsense which Adequate and rocketdodger a putting out.

And the virus would, if the population survived. It is a mathematical fact. I have provided equations to show why. You have not provided equations to show why not, nor even done so much as critique our equations and show why they might be wrong. You are just full of sh-- Kleinman, there is no other way to put it.

[kleinman]

Ok rocketdodger, here is your opportunity to give us a real example of your model. If you need help with your response, I’ll remind you what Adequate said.Why don't you give us a real example of the model used in ev?

You want a war of examples? Well guess what Kleinman, none of your examples show that multiple selection pressures slow evolution in general. All they show is that many species of organisms fail to develop resistance before their population is destroyed when a few human generated pressures are applied to them. You haven't shown a single study where the pressures satisfy any of the following conditions:

1) Greater in number than 3 or 4.
2) Natural as opposed to human applied.
3) Not intended to kill the organism outright.
Rocketdodger, do you think a war of examples would really be fair. All you evolutionists with your speculations, extrapolations and hunches against one annoying creationist with a peer reviewed and published model of random point mutations and natural selection and hundreds of empirical examples which show that combination selection pressures profoundly slow the evolutionary process. Ok, fire your best speculation since you don’t have any examples.

So, now you have a new list of conditions. So let’s consider these new conditions. 1) Greater in number than 3 or 4, I believe that if you look at some of the citations for TB, you will find that sometimes more than 4 drugs are used. If you want, I’ll go back and find these citations. In addition, there are studies already appearing with the use of 4 drug combination therapy for HIV. It wouldn’t surprise me if 5 drug therapy may be tried. Stay tuned, I’ll look for examples of this. 2) Natural as opposed to human applied; does that mean that any experiment or measurement that has human involvement no longer has validity? Rocketdodger, are you going to start supplying examples of combination natural selection pressures accelerating evolution? 3) Not intended to kill the organism outright, rocketdodger, perhaps you aren’t aware that there are no viral treatments that kill the viruses; they only impair the viruses’ ability to reproduce. Many antibacterial agents are also bacteriostatic not bacteriocidal. All selection pressures are required to do is impair the population’s ability to reproduce.
Thus, your little theory will hold water if and only if those three conditions hold for every population in the history of Earth. Do you think they do?
I think there is enough water to sink the theory of evolution. Your theory has hit an iceberg. The theory of evolution is a Titanic theory.
You need to use mathematics to show anything else, because of how narrow your citations are. That is why you keep running home to your gross misinterpretation of ev. On your own, you haven't even given us an equation, not one single equation, that makes any sense, to work with -- at first I suspected it was because you know we will blow it apart, but now I think its because you are a fraud and in fact know nothing about math beyond what your elementry level bible school has taught you. But you know what? It doesn't matter, because I have.
Oh, ev does show other things about mutation and selection, for example huge populations do not compensate as much as evolutionists like to claim. Ev shows the accelerating effect on the sort process done by mutation and selection from increasing population decreases rapidly with increasing population. You don’t have to do much interpretation here, just plot the data. I don’t have to present my own mathematics; Dr Schneider and Paul have done this already. All I have had to do is present the data from their mathematics. Why should I reinvent the wheel when Dr Schneider has properly modeled the mathematics of mutation and selection and the model has already gone through the peer review process.
The algorithm I used in my model is exactly the algorithm used in mutation and selection. The only thing it was intended to show is that a sorting/optimization problem is not always confounded by more optimization conditions -- and it does show that, plain and simple. My program sorts by fitness and in every possible set of conditions adding more optimization conditions eventually leads to faster sorting overall. It is a mathematical fact Kleinman -- you can try to argue against this but you are just wrong.
If your algorithm properly models mutation and selection, give us a real example of your model. Tell us what these random selection pressures are that you use in your model and how they accelerate the evolutionary process. I’m not asking much of you.
If you dispute anything, all you have to do is take a look at the source code (which others will attest is easy to follow) and tell me where I went wrong. Please, be my guest. Surely, with your three degrees and fancy professional background, you should be able to decimate the code that I, with only a lowly bachelor's degree, came up with from scratch.
Hey, perhaps you and Adequate have the mutation and selection process correctly modeled and n+1 selection pressures evolve more rapidly than n selection pressures so it should be easy for you to produce a real example of this. I won’t even require that you limit your example to “natural” processes, you can even use a human designed experiment.
The nonsensical notion that n+1 selection pressures evolve more quickly than n selection pressures would lead one to believe that if you continued to add more drugs to the treatment combinations of HIV that the virus will evolve more quickly. This is mathematical nonsense which Adequate and rocketdodger a putting out.And the virus would, if the population survived. It is a mathematical fact. I have provided equations to show why. You have not provided equations to show why not, nor even done so much as critique our equations and show why they might be wrong. You are just full of sh-- Kleinman, there is no other way to put it.
Too bad when you were studying for your bachelors degree, nobody told you that antiviral drugs do not kill the virus, they just impair the reproduction of the virus. Of course, if you knew this, you could present empirical examples of how mutation and selection actually works, like this:
http://qjmed.oxfordjournals.org/cgi/reprint/91/9/593.pdf (http://qjmed.oxfordjournals.org/cgi/reprint/91/9/593.pdf)
In order to support clinical decision making on the basis of viral genomic data, we have developed and applied several computational methods and tools. Specifically, we have addressed data integration and management (Arevir database), prediction of drug resistance and co-receptor usage from genotypes (geno2pheno), modeling of the evolution of drug resistance and the genetic barrier by mutagenetic trees (mtreemix), and selection of optimal drug combinations (theo). The integration of various types of genomic, phenotypic and clinical data as well as the coupling of different computational models yields predictive models of therapy outcome that may support the design of combination therapies.
Or how about this one rocketdodger which show that “natural” bacterial toxins when used in combination slow the evolution of mosquito larvae resistance.
http://aem.asm.org/cgi/content/abstract/73/19/6066 (http://aem.asm.org/cgi/content/abstract/73/19/6066)
Two mosquitocidal toxins (Mtx) of Bacillus sphaericus, which are produced during vegetative growth, were investigated for their potential to increase toxicity and reduce the expression of insecticide resistance through their interactions with other mosquitocidal proteins. Mtx-1 and Mtx-2 were fused with glutathione S-transferase and produced in Escherichia coli, after which lyophilized powders of these fusions were assayed against Culex quinquefasciatus larvae. Both Mtx proteins showed a high level of activity against susceptible C. quinquefasciatus mosquitoes, with 50% lethal concentrations (LC50) of Mtx-1 and Mtx-2 of 0.246 and 4.13 µg/ml, respectively. The LC50s were 0.406 to 0.430 µg/ml when Mtx-1 or Mtx-2 was mixed with B. sphaericus, and synergy improved activity and reduced resistance levels. When the proteins were combined with a recombinant Bacillus thuringiensis strain that produces Cry11Aa, the mixtures were highly active against Cry11A-resistant larvae and resistance was also reduced. The mixture of two Mtx toxins and B. sphaericus was 10 times more active against susceptible mosquitoes than B. sphaericus alone, demonstrating the influence of relatively low concentrations of these toxins. These results show that, similar to Cyt toxins from B. thuringiensis subsp. israelensis, Mtx toxins can increase the toxicity of other mosquitocidal proteins and may be useful for both increasing the activity of commercial bacterial larvicides and managing potential resistance to these substances among mosquito populations.
Rocketdodger, go ahead and fire some more of your strange speculations as to how mutation and selection works and I’ll fire back some real examples as to how mutation and selection works and they don’t show that n+1 selection pressures evolve more rapidly than n selection pressures.

[Paul C. Anagnostopoulos]

I’m not sure what you are having trouble understanding in my statement. Each of the selection conditions in ev does a part of the sorting requirement of the genomes. In order to get an arrangement of bases that satisfy all three sorting conditions simultaneously, it is an extremely slow process for all but the tiniest genomes. This is your so-called function. However, any individual portion of the sorting process can be done much more quickly if done independently of the other sorting conditions. A portion of your total function can be achieved by applying only a single sorting condition.
But a portion of a whole function is not the same function as the whole function, is it? Lots of things in life are made easier by only doing part of the whole task.

~~Paul

[Olowkow]

Just gotta love this reply by P.Z. Meyers to an inane email from a Mr. Wood, which can be seen in its entirety on Pharyngula (scienceblogs.com/pharyngula/2007/08/i_get_email_5.php#more):

Somebody is seriously overcompensating, aren't they? That's some piece of twisty-turny logic couched in arch and overwrought language. Just a suggestion, Mr Wood: you can't fill a vacuum with pedantry, no matter how much you try to shovel in.

Let me help. I get this argument all the time: "you wouldn't be so angry if the Designists/Creationists/Illuminati/Holocaust Deniers/Second Gunmen/Flat Earthers weren't right!" It's a very silly rationale, and no, writing it in a more longwinded style doesn't help.

There's a simple reason why biologists get pissed off with creationists, and it has nothing to do with a "first person ontology" — it's that we have the hard work, the data, the experiments, the whole dang enchilada of the "objective facts of the matter," and pretentious pissants like Mr Wood think nothing of overlooking their own self-admitted ignorance of evolution to pronounce a verdict based entirely on their half-assed psychoanalysis of the universe. We can see quite clearly (especially in this instance) what it is that drives a person to oppose Darwin (as if ol' Chuck had anything to do with the issue at this point): it is the arrogance of incompetence, the self-satisfied smugness of preening ********, the sanctimony of pious lackwits, the insufferable stupidity of pompous windbags who think they can rationalize their superstitions by seeking justification in a kind of gasified cold reading.

Your bubble-headed ******** doesn't bamboozle me, Mr Wood — I think the only person your verbose drivel might persuade is another superficial drone who mistakes diarrhea for depth.

[Foster Zygote]

Just gotta love this reply by P.Z. Meyers to an inane email from a Mr. Wood, which can be seen in its entirety on Pharyngula (scienceblogs.com/pharyngula/2007/08/i_get_email_5.php#more):

Somebody is seriously overcompensating, aren't they? That's some piece of twisty-turny logic couched in arch and overwrought language. Just a suggestion, Mr Wood: you can't fill a vacuum with pedantry, no matter how much you try to shovel in.

Let me help. I get this argument all the time: "you wouldn't be so angry if the Designists/Creationists/Illuminati/Holocaust Deniers/Second Gunmen/Flat Earthers weren't right!" It's a very silly rationale, and no, writing it in a more longwinded style doesn't help.

There's a simple reason why biologists get pissed off with creationists, and it has nothing to do with a "first person ontology" — it's that we have the hard work, the data, the experiments, the whole dang enchilada of the "objective facts of the matter," and pretentious pissants like Mr Wood think nothing of overlooking their own self-admitted ignorance of evolution to pronounce a verdict based entirely on their half-assed psychoanalysis of the universe. We can see quite clearly (especially in this instance) what it is that drives a person to oppose Darwin (as if ol' Chuck had anything to do with the issue at this point): it is the arrogance of incompetence, the self-satisfied smugness of preening ********, the sanctimony of pious lackwits, the insufferable stupidity of pompous windbags who think they can rationalize their superstitions by seeking justification in a kind of gasified cold reading.

Your bubble-headed ******** doesn't bamboozle me, Mr Wood — I think the only person your verbose drivel might persuade is another superficial drone who mistakes diarrhea for depth.

Welcome. And thanks for the chuckles.

[joobz]

I see kleinman still hasn't justified any of his model assumptions nor has he presented ANY reports that support his half baked, Evolution is too slow=stop idea.

[kleinman]

I’m not sure what you are having trouble understanding in my statement. Each of the selection conditions in ev does a part of the sorting requirement of the genomes. In order to get an arrangement of bases that satisfy all three sorting conditions simultaneously, it is an extremely slow process for all but the tiniest genomes. This is your so-called function. However, any individual portion of the sorting process can be done much more quickly if done independently of the other sorting conditions. A portion of your total function can be achieved by applying only a single sorting condition.But a portion of a whole function is not the same function as the whole function, is it? Lots of things in life are made easier by only doing part of the whole task.
Of course things are made easier when you break down a complex task into simpler parts but Paul, any one of the three selection conditions sorts at least 10’s of thousands of times faster than all three conditions together for a 16k genome. And then you have this notion that thousands of genes can be transformed by mutation and selection to evolve reptiles into birds all without any goal. Your model shows what happens to the mutation and selection sorting/optimization process with just three selection conditions. Paul, evolutionbymutationandselectiondidn’tdoit.
Let me help. I get this argument all the time: "you wouldn't be so angry if the Designists/Creationists/Illuminati/Holocaust Deniers/Second Gunmen/Flat Earthers weren't right!" It's a very silly rationale, and no, writing it in a more longwinded style doesn't help.
Welcome to the discussion Olowcow. You certainly seem to be a bit angry with a lot of people. Stick with the discussion, we’ll lift your spirits with a little discussion of the mathematics of mutation and selection and the empirical evidence which substantiates this mathematics.
There's a simple reason why biologists get pissed off with creationists, and it has nothing to do with a "first person ontology" — it's that we have the hard work, the data, the experiments, the whole dang enchilada of the "objective facts of the matter," and pretentious pissants like Mr Wood think nothing of overlooking their own self-admitted ignorance of evolution to pronounce a verdict based entirely on their half-assed psychoanalysis of the universe. We can see quite clearly (especially in this instance) what it is that drives a person to oppose Darwin (as if ol' Chuck had anything to do with the issue at this point): it is the arrogance of incompetence, the self-satisfied smugness of preening ********, the sanctimony of pious lackwits, the insufferable stupidity of pompous windbags who think they can rationalize their superstitions by seeking justification in a kind of gasified cold reading.
Olowcow, it’s only your first post and you are already annoyed. If you are trying out for the job of my favorite annoyee, Adequate already has it. I can’t help it if you evolutionists have already done my work for me. Next time you formulate a mathematically impossible theory, don’t write mathematical simulations of your theory and don’t run the experiments and collect data which show that the mathematical model is correct. Just stick with your speculations and extrapolations and your mathematically impossible world view will be a bit more secure.
Your bubble-headed ******** doesn't bamboozle me, Mr Wood — I think the only person your verbose drivel might persuade is another superficial drone who mistakes diarrhea for depth.
Olowcow, do you have anything to say about the mathematics of mutation and selection? Perhaps you want to break the long drought you evolutionists have had and give us an example of n+1 selection pressures evolving more rapidly than n selection pressures.
I see kleinman still hasn't justified any of his model assumptions nor has he presented ANY reports that support his half baked, Evolution is too slow=stop idea.
Joobz, you have claimed you are going to find irregularities in my PhD dissertation, $10,000 wager says that you can’t find any mathematical or empirical irregularities. Joobz, didn’t you read this citation?
http://www.blackwell-synergy.com/doi/pdf/10.1046/j.1365-3156.2001.00800.x (http://www.blackwell-synergy.com/doi/pdf/10.1046/j.1365-3156.2001.00800.x)
Resistance genes are generally assumed to be biologically less efficient than the normal susceptible type. For example, an enzyme may escape drug action by a mutation that alters the drug-binding site. As this mutation probably also affects its catalytic capacity, the mutation will be removed from the population by natural selection and their frequency in the naive, non-drug-treated, population will be determined by a mutation/selection balance (Hastings 1997; Koella 1998). If drugs are used in combination, then the frequency of parasites resistant to both drugs will be
very low. For example, if 0.1% are resistant to drug A and 0.005% are resistant to drug B, then parasites resistant to both will initially be present at a frequency of 0.1 x 0.05% = 0.00005% (assuming that the same gene cannot encode resistance to both drugs). Thus using drugs in combination from the outset may greatly increase the useful therapeutic lifespan of the drug, because lowering the starting frequency delays the point at which a significant amount of resistance emerges.
And
One important general point from the models is that use of combination therapy in their initial deployment is invariably better than introducing one drug alone, followed by introduction of the second-line drug once the first becomes ineffective (see, for example, Curtis & Otoo 1986; Smith 1990; Bonhoeffer et al. 1997; for malaria, helminths and bacteria, respectively).
And
If parasites reach high numbers within hosts, then spontaneous mutations to resistance may occur. Infections of P. falciparum may reach 10^11-10^12 individual parasites per host and it seems logical that a small subpopulation may have mutated to drug resistance (for example if the mutation rate to resistance is 10^-8 then there would be 1000±10 000 resistant parasites) which then expands to dominate the infection. This argument seems logically plausible and receives support from observations of humans treated with the antimalarial drug atovaquone, where an infection which was originally susceptible disappears below detectable levels before recrudescing as a resistant infection (Looareesuwan et al. 1996). Measurements of drug sensitivity in vitro before and after treatment show greatly increased levels of resistance in the recrudescent infection. It seems plausible that the same effects may occur in other parasites that reach high population numbers within a host. Once again the effect can be minimized or even eliminated by using drugs in combination. In the above example of 10^11 parasites, mutation rates to resistance of 10^-8, and assuming two drugs were used in combination, then resistance would arise in only 10^16 parasites, in effect rendering the frequency of spontaneous mutations negligible. The implications for the evolution of drug resistance are discussed in Lipsitch and Levin (1997) and White (1999 and references therein).
These authors seem to think they can eliminate drug resistance using combination selection pressures. Joobz, you better tell them that slow doesn’t mean stop.

[rocketdodger]

I am just going to stop writing as much, because I see that you pick and choose what you want to respond to in order to dodge the issue at hand, Kleinman.

You claimed that additional optimization conditions always confound sorting / optimization problems. My program shows this to be not true in general. Can you show anyone here why the sorting/optimization algorithm used in my program is, in fact, not a sorting / optimization algorithm?

Here it is, in short:
1) Randomly mutate x number of bases in each creature's genome.
2) Determine the fitness of each creature according to the pressures exerted on the population.
3) Reproduce, such that creatures with higher fitness have more offspring.
4) Go back to 1, stopping when the targeted mutations of all pressures have achieved 80% or more fixation in the population.

[sol invictus]

This is why you are asking the wrong question. This is not simply a probability problem; it is a sorting and optimization problem as well. Only those most fit members of the population can accumulate the beneficial mutations. The harmful mutations are causing individuals to be selected out.

Those effects make this process faster, not slower, because individuals with the beneficial mutations will breed more than those without. I'm ignoring that.

But for the sake of discussion, let’s consider your approach but instead of 90% of the individuals undergoing all N mutations, consider a single individual undergoing all N (100) mutations.

If we ask after how much time does an individual have a 90% chance of having all N mutations, it's the same question - so fine.

In the first generation that individual has a (1/(1,000,000))*100 probability of getting a beneficial mutation, if that individual is gets one of those beneficial mutations, in the next generation, that individual has a (1/(1,000,000))*99 probability of getting a second beneficial mutation or a total probability of (1/(1,000,000))*100*(1/(1,000,000))*99 and so on for each additional possible beneficial mutation. The probability of a particular individual getting all one hundred beneficial mutations is (100/1,000,000)*(99/1,000,000)* … *(1/1,000,000).

You're confusing yourself. That's supposed to be the probability after how much time?

Sol, I’ll let you run the numbers for the probability of any individual getting all 100 beneficial mutations in 100 generations, let alone 90% of the population getting all 100 beneficial mutations.

Whoa there, slow down. If the chance of any given mutation is only 1/1,000,000, after 100 generations it's very unlikely any mutations have occurred. What my calculation showed was that however long you have to wait for one mutation, you don't have to wait much longer for many more. It's 1/p that sets that timescale, so in the case p is 1/1,000,000, you'll need to wait around 1,000,000 generations for even one mutation.


The point you are missing is that without selection, you can not improve the frequencies of genetic sequences in the population. You only have a few basic ways of improving these probabilities. You can increase population, number of generations, mutation rates (within limits) or you can reduce down the number of selection pressures.

Again, selection makes this process faster, not slower. I'm just ignoring it for now for simplicity.

So Sol, you are telling us that it only takes 14 times longer to win 100 lotteries as it takes to win 1 lottery? After all, that’s what an individual in the population has to do to get the 100 beneficial mutations and for that individual, the probability of winning one of the lotteries is decreasing with each beneficial mutation the individual wins.

Nope - I'm saying it only takes 14 times longer to win a million lotteries. To win a 100 would only take around 5 times as long. Counterintuitive, huh?

But it's true - and the reason is you're playing all the lotteries at once, and the odds of not winning even one decrease exponentially with the number of chances, once the number is greater than 1/p. So you're extremely unlikely not to have won any given lottery after that point, which is why winning many doesn't take much longer at all (and that exponential also explains where the log comes from).

[kjkent1]

There is a huge amount of evidence that particular selection pressures lead to particular mutations increasing in frequency in a population. This phenomenon is used to identify resistance to drugs, pesticides and herbicides. If evolution does not have a goal, why do the same mutations show up over and over to particular selection pressures?You think that the change from a dinosaur form to a bird form was the result of something other than just an accumulation of various unpredictable biological changes which just happened to have provided their owners a fitness advantage at a particular historical point.

Evolution is not deterministic, Alan. Two trials of an experiment using identical selection pressures will not necessarily produce the same evolutionary outcome, because the "mutation" part of the evolutionary process cannot be predicted in advance.Too bad that the evidence contradicts your speculations; for example, the use of particular drugs for treatment of HIV leads to increase in the frequency of particular mutations appearing in the viral population. This effect is used to identify when resistance to a particular drug has evolved.

Mutational patterns and correlated amino acid substitutions in the HIV-1 protease after virological failure to nelfinavir- and lopinavir/ritonavir-based treatments.

Garriga C, Pérez-Elías MJ, Delgado R, Ruiz L, Nájera R, Pumarola T, Alonso-Socas Mdel M, García-Bujalance S, Menéndez-Arias L; Spanish Group for the Study of Antiretroviral Drug Resistance.

Centro de Biología Molecular Severo Ochoa, CSIC-Universidad Autónoma de Madrid, Cantoblanco, Madrid, Spain.

Human immunodeficiency virus type 1 (HIV-1) antiviral drug resistance is a major consequence of therapy failure and compromises future therapeutic options. Nelfinavir and lopinavir/ritonavir-based therapies have been widely used in the treatment of HIV-infected patients, in combination with reverse transcriptase inhibitors. The aim of this observational study was the identification and characterization of mutations or combinations of mutations associated with resistance to nelfinavir and lopinavir/ritonavir in treated patients. Nucleotide sequences of 1,515 subtype B HIV-1 isolates from 1,313 persons with different treatment histories (including naïve and treated patients) were collected in 31 Spanish hospitals over the years 2002-2005. Chi-square contingency tests were performed to detect mutations associated with failure to protease inhibitor-based therapies, and correlated mutations were identified using statistical methods. Virological failure to nelfinavir was associated with two different mutational pathways. D30N and N88D appeared mostly in patients without previous exposure to protease inhibitors, while K20T was identified as a secondary resistance mutation in those patients. On the other hand, L90M together with L10I, I54V, A71V, G73S, and V82A were selected in protease inhibitor-experienced patients. A series of correlated mutations including L10I, M46I, I54V, A71V, G73S, and L90M appeared as a common cluster of amino acid substitutions, associated with failure to lopinavir/ritonavir-based treatments. Despite the relatively high genetic barrier of some protease inhibitors, a relatively small cluster of mutations, previously selected under drug pressure, can seriously compromise the efficiency of nelfinavir- and lopinavir/ritonavir-based therapies. (c) 2007 Wiley-Liss, Inc.

PMID: 17854027 [PubMed - indexed for MEDLINE]

Oh oh...D30N and N88D appeared "MOSTLY" in certain patients. But, not "ALWAYS." In some patients, K20T appeared.

So, much for the hypothesis that only one mutational pathway can develop from a particular selective pressure. Kleinman loses again.

[Mr. Scott]

I am just going to stop writing as much, because I see that you pick and choose what you want to respond to in order to dodge the issue at hand, Kleinman.


Where previously I'd agree this was a debating tactic of Kleinman (and creationists in general), I now see he's exhibiting the psychological phenomenon known as Cognitive Dissonance (http://en.wikipedia.org/wiki/Cognitive_dissonance). Sufferers of this cope with conflicting information by ignoring information that conflicts with their established beliefs. In this example Kleinman, who's believed in biblical creation since he was too young to think for himself, ignores the decisive proof of evolution to relieve the uncomfortable feeling caused by attempting to reconcile these dissonant ideas. I'd be more sympathetic if he didn't resort to deliberate, smirking viscous denigration of those who disagreed with his infantile beliefs.

Cognitive dissonance is a psychological term describing the uncomfortable tension that may result from having two conflicting thoughts at the same time, or from engaging in behavior that conflicts with one's beliefs, or from experiencing apparently conflicting phenomena.

In simple terms, it can be the filtering of information that conflicts with what one already believes, in an effort to ignore that information and reinforce one's beliefs.

[joobz]

Joobz, you have claimed you are going to find irregularities in my PhD dissertation, $10,000 wager says that you can’t find any mathematical or empirical irregularities.
Obviously this is a lie and everyone knows it. I've addressed this point, but you choose to pretend otherwise. This, among other lies, simply exposes your entire method. You ignore truth and present idiotic statements. All this does is make you appear to be a complete inept moron. Coupled with all the science you present, which is horrificly dumb, I'm starting to believe you are a complete inept moron. Are you?

[kleinman]

I am just going to stop writing as much, because I see that you pick and choose what you want to respond to in order to dodge the issue at hand, Kleinman.
That’s correct, and the issue at hand is you have claimed you have written a simulation of mutation and selection which shows that n+1 selection pressures evolve more rapidly than n selection pressures. Now it’s time for you to post a real example of your alleged model.
This is why you are asking the wrong question. This is not simply a probability problem; it is a sorting and optimization problem as well. Only those most fit members of the population can accumulate the beneficial mutations. The harmful mutations are causing individuals to be selected out.Those effects make this process faster, not slower, because individuals with the beneficial mutations will breed more than those without. I'm ignoring that.
You are also ignoring the fact that selection pressures reduce the fitness to reproduce.
In the first generation that individual has a (1/(1,000,000))*100 probability of getting a beneficial mutation, if that individual is gets one of those beneficial mutations, in the next generation, that individual has a (1/(1,000,000))*99 probability of getting a second beneficial mutation or a total probability of (1/(1,000,000))*100*(1/(1,000,000))*99 and so on for each additional possible beneficial mutation. The probability of a particular individual getting all one hundred beneficial mutations is (100/1,000,000)*(99/1,000,000)* … *(1/1,000,000).You're confusing yourself. That's supposed to be the probability after how much time?
That’s 100 generations sol, each additional generation will improve that probability less than an additively.
Sol, I’ll let you run the numbers for the probability of any individual getting all 100 beneficial mutations in 100 generations, let alone 90% of the population getting all 100 beneficial mutations.Whoa there, slow down. If the chance of any given mutation is only 1/1,000,000, after 100 generations it's very unlikely any mutations have occurred. What my calculation showed was that however long you have to wait for one mutation, you don't have to wait much longer for many more. It's 1/p that sets that timescale, so in the case p is 1/1,000,000, you'll need to wait around 1,000,000 generations for even one mutation.
The chance of any given mutation is always 1/1,000,000. The chance of any beneficial mutation for a given individual is the sum of the probabilities for each of the possible beneficial mutations.
The point you are missing is that without selection, you can not improve the frequencies of genetic sequences in the population. You only have a few basic ways of improving these probabilities. You can increase population, number of generations, mutation rates (within limits) or you can reduce down the number of selection pressures.Again, selection makes this process faster, not slower. I'm just ignoring it for now for simplicity.
You are also ignoring that you are not computing the probability of a given individual getting all 100 beneficial mutations.
So Sol, you are telling us that it only takes 14 times longer to win 100 lotteries as it takes to win 1 lottery? After all, that’s what an individual in the population has to do to get the 100 beneficial mutations and for that individual, the probability of winning one of the lotteries is decreasing with each beneficial mutation the individual wins.Nope - I'm saying it only takes 14 times longer to win a million lotteries. To win a 100 would only take around 5 times as long. Counterintuitive, huh?

But it's true - and the reason is you're playing all the lotteries at once, and the odds of not winning even one decrease exponentially with the number of chances, once the number is greater than 1/p. So you're extremely unlikely not to have won any given lottery after that point, which is why winning many doesn't take much longer at all (and that exponential also explains where the log comes from).
The problem with your calculation is that you are using 1/p (1/1,000,000) as your number. To win this lottery, the individual has to adapt to 100 selection pressures each with a 1/p = 1/1,000,000. The individuals don’t get to play with all these selection pressures. Counterintuitive, huh?

But it’s true, even two strong selection pressures are sufficient to stop most populations from evolving. Even for the very fast replicating virus HIV with high mutation rate, 3 selection pressures profoundly slow the evolutionary process. The exponential gain from selection only occurs with single selection pressures. Once you add additional selection pressures, the different selection conditions confound the sorting process.
Too bad that the evidence contradicts your speculations; for example, the use of particular drugs for treatment of HIV leads to increase in the frequency of particular mutations appearing in the viral population. This effect is used to identify when resistance to a particular drug has evolved.Mutational patterns and correlated amino acid substitutions in the HIV-1 protease after virological failure to nelfinavir- and lopinavir/ritonavir-based treatments.
And then kjkent1 posts this from his reference:
D30N and N88D appeared mostly in patients without previous exposure to protease inhibitors, while K20T was identified as a secondary resistance mutation in those patients. On the other hand, L90M together with L10I, I54V, A71V, G73S, and V82A were selected in protease inhibitor-experienced patients. A series of correlated mutations including L10I, M46I, I54V, A71V, G73S, and L90M appeared as a common cluster of amino acid substitutions, associated with failure to lopinavir/ritonavir-based treatments. Despite the relatively high genetic barrier of some protease inhibitors, a relatively small cluster of mutations, previously selected under drug pressure, can seriously compromise the efficiency of nelfinavir- and lopinavir/ritonavir-based therapies. (c) 2007 Wiley-Liss, Inc.
Oh oh...D30N and N88D appeared "MOSTLY" in certain patients. But, not "ALWAYS." In some patients, K20T appeared.

So, much for the hypothesis that only one mutational pathway can develop from a particular selective pressure. Kleinman loses again.
Really kjkent1? Does this explain how birds evolve into reptiles? Does this mean that genetic sequencing to identify drug resistance is wrong? Of course it does because kjkent1 says this:
Evolution is not deterministic, Alan. Two trials of an experiment using identical selection pressures will not necessarily produce the same evolutionary outcome, because the "mutation" part of the evolutionary process cannot be predicted in advance.
Kjkent1, does this mean that HIV can now digest nylon?
I am just going to stop writing as much, because I see that you pick and choose what you want to respond to in order to dodge the issue at hand, Kleinman. Where previously I'd agree this was a debating tactic of Kleinman (and creationists in general), I now see he's exhibiting the psychological phenomenon known as Cognitive Dissonance. Sufferers of this cope with conflicting information by ignoring information that conflicts with their established beliefs. In this example Kleinman, who's believed in biblical creation since he was too young to think for himself, ignores the decisive proof of evolution to relieve the uncomfortable feeling caused by attempting to reconcile these dissonant ideas. I'd be more sympathetic if he didn't resort to deliberate, smirking viscous denigration of those who disagreed with his infantile beliefs.
You kids want to talk about anything but the mathematics of mutation and selection and the empirical evidence which supports this mathematics. Mr Scott, neither you or rocketdodger who claim that n+1 selection pressures evolve more rapidly than n selection pressures are able to produce any empirical evidence of this claim. Who is demonstrating cognitive dissonance? It is you evolutionists who ignore the mathematical and empirical facts of life of how mutation and selection actually works.

Mr Scott, I noticed you removed the line from your posts about the lies your parents told you. Do you now believe your parents?
Joobz, you have claimed you are going to find irregularities in my PhD dissertation, $10,000 wager says that you can’t find any mathematical or empirical irregularities.Obviously this is a lie and everyone knows it. I've addressed this point, but you choose to pretend otherwise. This, among other lies, simply exposes your entire method. You ignore truth and present idiotic statements. All this does is make you appear to be a complete inept moron. Coupled with all the science you present, which is horrificly dumb, I'm starting to believe you are a complete inept moron. Are you?
Sure you made this claim. Don’t you remember? Here, let me remind you.
http://forums.randi.org/showpost.php?p=3112268&postcount=6267 (http://forums.randi.org/showpost.php?p=3112268&postcount=6267)
… I could critique his PhD for irregularities in his publication track that raise interesting questions. …
So not only are you incompetent in the mathematics of mutation and selection, you are incompetent in the mathematics of PDEs. So are you going to take the $10,000 wager that you can’t find any mathematical or empirical irregularities in my PhD thesis or are you going to continue being a big mouth coward? I believe you will continue to be a big mouth coward. I think you are a fake joobz; no engineer could be so incompetent in mathematics. As for your skills as a chemist, this post of yours reveals you are a fake as well.
Envision a system of millions of forming and destructive chemical reactions. Now, envision that intermediates of there reactions associate through non-covalent means and that this complex becomes protected against the destructive reactive pathway, perhaps by a reversible precipitation. These new complexes result in a localized increased of new chemical species. These chemical species then progress in a new series of reaction... that is what I mean through cooperative means. I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?

So, while you evolutionists look for citations which show that n+1 selection pressures evolve more rapidly than n selection pressures, I’ll keep posting citations which show that combination selection pressures profoundly slow the evolutionary process.
http://www.blackwell-synergy.com/doi/full/10.1046/j.1365-2672.92.5s1.10.x (http://www.blackwell-synergy.com/doi/full/10.1046/j.1365-2672.92.5s1.10.x)
infections are caused by high bacterial numbers of 10^9 to 10^10 cfu ml1, which means that significant numbers of single-step mutations are likely to arise conferring low level antibiotic resistance. In the presence of suboptimal, low antibiotic concentrations at the site of infection (Table 5), these single-step mutations may confer survival advantage leading to their selection, multiplication, clinical treatment failure and/or spread. It is desirable to maintain antibiotic concentrations at the site of infection at levels which are high enough to ensure that two mutations are required to confer useful survival value. Consequently, the chances of these double mutations occurring are statistically minimal and the mutant prevention concentration (MPC) has been reached. (Drlica 2001) For example, if the chances of a single mutation arising and conferring survival value are 10^7 then the chances of a double mutation conferring survival value are 10^14. Given that few, if any, infections are caused by bacterial numbers as high as > 10^10 to 10^11 then this implies that double mutations are highly unlikely to occur in individual patients. The clinical evidence, albeit incomplete, bears this out although it has to be accepted that these mutation rates are extrapolated from in vitro work and mutation rates appear to be more frequent in vivo, when exposed to antibiotics (Table 4).
Current pharmacodynamic-based dosing schedules for quinolones (in particular the new quinolones) and aminoglycosides may achieve MPCs against selected pathogens in easily accessible sites. This, however, does not necessarily apply to the whole dosing interval, nor in sequestered sites of infection. A well-recognized way round this is combination therapy, particularly when treating with aminoglycoside. This approach has been used for many years.

Theoretically, using two antibiotics simultaneously will negate the need to achieve MPC concentrations, but the two drugs must have similar pharmacokinetic properties to ensure continued presence of both at supra-MIC concentration over the dosing interval. This is clearly not the case with the current trend of once daily aminoglycoside dosing. There are also problems with antituberculous therapy although this approach has been used for many years with varying degrees of success in the treatment of tuberculosis. The main reasons for using combination therapy in the past, however, were the desire to achieve greater bactericidal activity by synergistic interaction with β-lactam and to broaden the spectrum of therapy.
Sol, do you see why you can’t look at mutation and selection as a simple probability problem?

http://www.mja.com.au/public/issues/186_04_190207/sas10773_fm.pdf (http://www.mja.com.au/public/issues/186_04_190207/sas10773_fm.pdf)
The concept of combination therapy has long been established as the paradigm of therapy for a number of chronic infections. In the late 1940s, it was first shown that combination therapy with streptomycin and p-aminosalicylic acid could prevent the rapid emergence of streptomycin resistance during therapy for tuberculosis.4 More recently, the HIV pandemic has given us greater insights into the management of chronic viral diseases. Studies such as the Delta trial using hard clinical endpoints (eg, mortality) unequivocally demonstrated the superiority of combination dual antiviral therapy over monotherapy. Moreover, these early studies showed that initiating dual therapy in treatment-naïve patients gave a superior outcome compared with using a second drug in treatment-experienced patients, proving that an upfront combination that prevented resistance was superior to sequential monotherapy.5 More recently, it has been shown that triple therapy for HIV infection (ie, adding a protease inhibitor) is superior to dual therapy, thereby further strengthening the case for combination therapy.6 By contrast, current Australian (Section 100) and international prescribing guidelines for HBV infection either mandate or recommend lamivudine monotherapy for HBV in treatment-naïve patients, resulting in the almost inevitable development of antiviral resistance and setting the scene for the emergence of multidrug resistance.
So why does combination treatment work? It works because multiple selection conditions confound the ability of the population to evolve to the multiple sorting conditions simultaneously.

Now if any of you evolutionist want to post an example of n+1 selection conditions evolving more rapidly than n selection conditions, that would make this an interesting debate. Perhaps if joobz took up my $10,000 wager with him, that would make this discussion a bit more interesting but I doubt it, we all know what joobz is.

[joobz]

So not only are you incompetent in the mathematics of mutation and selection, you are incompetent in the mathematics of PDEs. So are you going to take the $10,000 wager that you can’t find any mathematical or empirical irregularities in my PhD thesis or are you going to continue being a big mouth coward? I believe you will continue to be a big mouth coward. I think you are a fake joobz; no engineer could be so incompetent in mathematics. As for your skills as a chemist, this post of yours reveals you are a fake as well.

http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?
So your answer is that you are a raving idiot?
Is this why you only had 2 journal publications, neither with the same advisor?
Is this why you are unable to actually justify your assumptions of your idiotic theory?

[kleinman]

So not only are you incompetent in the mathematics of mutation and selection, you are incompetent in the mathematics of PDEs. So are you going to take the $10,000 wager that you can’t find any mathematical or empirical irregularities in my PhD thesis or are you going to continue being a big mouth coward? I believe you will continue to be a big mouth coward. I think you are a fake joobz; no engineer could be so incompetent in mathematics. As for your skills as a chemist, this post of yours reveals you are a fake as well.

http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?So your answer is that you are a raving idiot?
Is this why you only had 2 journal publications, neither with the same advisor?
Is this why you are unable to actually justify your assumptions of your idiotic theory?
So not only are you are incompetent in the mathematics of mutation and selection, incompetent in the mathematics of PDEs, you are also incompetent in doing literature searches. If you had any competence at all, you would find that I have more than 2 journal publications. Care to make a wager on that issue as well or has the Madagascar rain forest waterlogged your brain.

So joobz, if the sun shines long enough on lead, does it turn into gold?
http://forums.randi.org/images/smilies/doglaugh.gif
Here joobz, let me show you how to find and post a citation supporting a hypothesis that combination selection pressures profoundly slow the evolutionary process.
http://www.blackwell-synergy.com/doi/full/10.1046/j.1365-3156.2001.00800.x (http://www.blackwell-synergy.com/doi/full/10.1046/j.1365-3156.2001.00800.x)
Mathematical models of the evolution of drug resistance in infectious diseases are predominantly concentrated in three main areas: antimalarial, antibiotic and anthelmintic resistance. There appears to be little or no cross-reference between them. This literature was examined to identify factors that influence the evolution of drug resistance irrespective of the species and drug under study. The aim is to provide non-technical readers with a basic qualitative understanding of the issues and pitfalls involved in designing drug treatment regimens to minimize the evolution of resistance. The principal factors determining the rate at which resistance evolves appear to be (i) the starting frequency of resistance, (ii) the level and pattern of drug use, (iii) the drug's pharmacokinetic properties, (iv) the number of genes required to encode resistance, (v) the level of sexual recombination in the parasite population, (vi) intrahost dynamics and, in particular, whether 'crowding' effects are present, (vii) the genetic basis of resistance and (viii) the number of individual parasites in an infection. The relative importance of these factors depends on the biology of the organisms under consideration and external factors such as the extent to which the infrastructure of health care delivery constrains the practicalities of drug regimens.
That’s you joobz, the non-technical reader (are you a reader joobz?).
Resistance genes are generally assumed to be biologically less efficient than the normal susceptible type. For example, an enzyme may escape drug action by a mutation that alters the drug-binding site. As this mutation probably also affects its catalytic capacity, the mutation will be removed from the population by natural selection and their frequency in the naive, non-drug-treated, population will be determined by a mutation/selection balance (Hastings 1997; Koella 1998). If drugs are used in combination, then the frequency of parasites resistant to both drugs will be very low. For example, if 0.1% are resistant to drug A and 0.005% are resistant to drug B, then parasites resistant to both will initially be present at a frequency of 0.1 × 0.05%=0.00005% (assuming that the same gene cannot encode resistance to both drugs). Thus using drugs in combination from the outset may greatly increase the useful therapeutic lifespan of the drug, because lowering the starting frequency delays the point at which a significant amount of resistance emerges.
and
One important general point from the models is that use of combination therapy in their initial deployment is invariably better than introducing one drug alone, followed by introduction of the second-line drug once the first becomes ineffective (see, for example, Curtis & Otoo 1986; Smith 1990; Bonhoeffer et al. 1997; for malaria, helminths and bacteria, respectively).
and
The Holy Grail of drug development is to discover a drug to which resistance cannot evolve. It appears impossible to select resistance in vitro to the antimalarial artemisinine and one explanation is that the drug may disrupt iron metabolism in a manner that can only be overcome by (impossible) mutations that transcend the laws of physical chemistry. Figure 1, the calculations on starting frequency made above, and prior experience with other drugs suggest that such a seductively optimistic interpretation be judged with caution. Figure 1 shows that the frequency of resistance may be extremely low during much of the evolution of resistance and it is very difficult to detect these low levels. This is not to say that such drugs cannot be developed, merely to stress that the working hypothesis must be that resistance is present, albeit at low frequencies, and that drug deployment should be designed with this in mind. A similar effect is seen with the antimalarial quinine where it is very difficult to select for resistance in vitro. One plausible explanation is that quinine has widespread metabolic effects, several genes may be required to encode resistance, and starting frequencies of resistance may, therefore, be very low. The calculations of starting frequency made above assumed a one gene/one drug relationship but can be extended to take account of numerous metabolic effects. Continuing the above calculation, if resistance to metabolic effect A is 0.1%, resistance to effect B is 0.05% and resistance to effect C is 0.01%, then the frequency of parasites resistant to the total effects of the drug is 0.000000005%.
An increasing number of genes required to encode resistance has two effects, one direct and one indirect, which delay the emergence of resistance. The first, indirect, effect is that the starting frequency of resistance is decreased: if gene A is present at frequency f(a) and gene B at frequency f(b) and both are required to encode resistance, then the starting frequency of resistance is much lower, i.e. f(a) multiplied by f(b). The second, direct, effect occurs in organisms that are sexual or partially sexual. The greater the number of genes, the greater the loss of resistance during sexual recombination (Figure 3) and the slower the development of resistance (Hastings 1997). The most common and convenient method of increasing the number of genes required to encode resistance is to combine several drugs into a mixture (e.g. Peters 1984, 1998; White 1999 and references therein).
This citation is just for you joobz, the non-technical reader who lacks the mathematical skills to understand how mutation and selection works. The more genes which must evolve simultaneously the slower the process, understand rubberband? These authors have the audacity to think that the evolution of resistance not only can be slowed, it can be stopped, ring a bell ding-a-ling?

So joobz, I wager you $10,000 that you can’t back up your claim that I have irregularities in my PhD thesis or for that matter in any of my publications, even the ones you can’t find, either mathematical or empirical. Are you going to take up the wager or are you just a big mouth coward?

[joobz]

Nice job. Keep the crazy coming!
Perhaps you'll eventually justify your model assumptions.
Perhaps you'll eventually explain away the evidence for evolution.
Perhaps you'll tell us again how probablity can be greater than 1.
Perhaps you'll tell us all about how nuclear and chemical reactions are the same.
Perhaps you'll eventually explain why hardly anyone referenced your publications.

I have a feeling the last 3 points are related.

[kleinman]

Nice job. Keep the crazy coming!
Perhaps you'll eventually justify your model assumptions.
Perhaps you'll eventually explain away the evidence for evolution.
Perhaps you'll tell us again how probablity can be greater than 1.
Perhaps you'll tell us all about how nuclear and chemical reactions are the same.
Perhaps you'll eventually explain why hardly anyone referenced your publications.

I have a feeling the last 3 points are related.
Let’s see, you attribute Dr Schneider’s model to me. You are wrong.

Whatever concocted interpretation of the evidence you allege for the theory of evolution does not include the mathematics of mutation and selection and the vast amount of empirical evidence which contradicts your mathematical irrational and illogical theory. You are wrong.

Hey, you are correct; I made a mistake about the effects of increasing population on the probabilities of a mutation occurring at a particular locus. I thought that doubling the population would double the probability but this probability is not additive, it only makes the theory of evolution less likely. I acknowledged Myriad’s correction of my error. Now when are you going to take up the $10,000 wager that you can not find any mathematical or empirical irregularities in my PhD thesis or any of my other publications? Oh, that’s right; you are a non-technical big mouth who makes claims that he can’t backup.

Oh, and I see, any chemical reaction is possible as long as you have enough free energy but there is not enough free energy in the sun to turn lead into gold?
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, when are your going to tell us how to form ribose non-enzymatically? Then you can tell us what the half life of ribose is if you miraculously could tell us how the ribose could form. You do remember what the half life of ribose is, don’t you? Or is that too technical of a question for someone of your technically challenged abilities? You are wrong again.

Then lastly, you would never reference my publications because you are mathematically incompetent, you have no idea how to do the mathematics, you after all are non-technical but you are an expert speculationist, but don’t let that stop you from taking up my $10,000 wager with you that you can’t prove your claim about any of my publications. You are wrong. Let’s see you put your money where your big mouth is.

Since we all know you are nothing more than a big blow hard, let me once again show you how to post a citation to support a hypothesis that combination selection pressures profoundly slow the evolutionary process.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1865999 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1865999)
Mutation is the basis of adaptation. Yet, most mutations are detrimental, and elevating mutation rates will impair a population's fitness in the short term. The latter realization has led to the concept of lethal mutagenesis for curing viral infections, and work with drugs such as ribavirin has supported this perspective. As yet, there is no formal theory of lethal mutagenesis, although reference is commonly made to Eigen's error catastrophe theory. Here, we propose a theory of lethal mutagenesis. With an obvious parallel to the epidemiological threshold for eradication of a disease, a sufficient condition for lethal mutagenesis is that each viral genotype produces, on average, less than one progeny virus that goes on to infect a new cell. The extinction threshold involves an evolutionary component based on the mutation rate, but it also includes an ecological component, so the threshold cannot be calculated from the mutation rate alone. The genetic evolution of a large population undergoing mutagenesis is independent of whether the population is declining or stable, so there is no runaway accumulation of mutations or genetic signature for lethal mutagenesis that distinguishes it from a level of mutagenesis under which the population is maintained. To detect lethal mutagenesis, accurate measurements of the genome-wide mutation rate and the number of progeny per infected cell that go on to infect new cells are needed. We discuss three methods for estimating the former. Estimating the latter is more challenging, but broad limits to this estimate may be feasible.
and
A treatment strategy for preventing the evolution of significant or complete resistance could be combination therapy with several mutagens or with a mutagen in combination with other antiviral drugs.
Joobz, you better tell these authors that slowing evolution does not mean stop. Here is another citation for you joobz which shows that combination selection pressures profoundly slow the evolutionary process.
http://www.journals.uchicago.edu/JID/journal/issues/v189n7/31334/31334.web.pdf (http://www.journals.uchicago.edu/JID/journal/issues/v189n7/31334/31334.web.pdf)
Limited studies have suggested that, in areas where drug usage has decreased, the spread of resistance has also decreased [36, 37]. These findings are in agreement with our observation in eastern Sudan and emphasize the need for better drug deployment policies, to combat evolution of drug resistance. For example, the use of combination therapy in this region would reduce the risk of multidrug resistance emerging and spreading, helped by the short transmission seasons, when drug pressure, the low number of paraiste generations during this period, and natural section against resistance alleles allow for only 1 or 2 parasite generations. Such information is important for predicting the spread of drug resistance in areas where multiple clones of P. falciparum infection are common.
Hey joobz, did I miss addressing any of your ridiculous speculations? Joobz, do you want me help you find some references for your speculations on abiogenesis? Try doing a google search of the SciFi channel.

[joobz]

Kleinman, you never fail. I write a few sentences and you respond with paragraphs of stupidity.

Thank you for making my night.

[kleinman]

Kleinman, you never fail. I write a few sentences and you respond with paragraphs of stupidity.

Thank you for making my night.
Oh, I get it, slow doesn’t equal stop, slow equals joobz, slow to understand how mutation and selection actually works.

[rocketdodger]

That’s correct, and the issue at hand is you have claimed you have written a simulation of mutation and selection which shows that n+1 selection pressures evolve more rapidly than n selection pressures. Now it’s time for you to post a real example of your alleged model.


You claimed that additional optimization conditions always confound sorting / optimization problems. My program shows this to be not true in general. Can you show anyone here why the sorting/optimization algorithm used in my program is, in fact, not a sorting / optimization algorithm?

[sol invictus]

But for the sake of discussion, let’s consider your approach but instead of 90% of the individuals undergoing all N mutations, consider a single individual undergoing all N (100) mutations. In the first generation that individual has a (1/(1,000,000))*100 probability of getting a beneficial mutation, if that individual is gets one of those beneficial mutations, in the next generation, that individual has a (1/(1,000,000))*99 probability of getting a second beneficial mutation or a total probability of (1/(1,000,000))*100*(1/(1,000,000))*99 and so on for each additional possible beneficial mutation. The probability of a particular individual getting all one hundred beneficial mutations is (100/1,000,000)*(99/1,000,000)* … *(1/1,000,000).

That’s 100 generations sol, each additional generation will improve that probability less than an additively.

OK, let's focus on this nice concrete statement of yours - which is completely wrong. You are claiming the following: that, if there are 100 mutations, each with probability 10^{-6} per generation, the odds of all 100 occurring after 100 generations are (100*10^{-6})*(99*10^{-6})*... = 100! 10^{-600}. This is wrong - it's off (in this case) by a mere 40 orders of magnitude. It's the kind of mistake someone that doesn't understand probability at all would make.

There are many ways to see why it's wrong. Let's take the first step. You seem to be under the misapprehension that 100*10^{-6} is the probability that one mutation will take place in the first generation. Tell me - is that the prob. for one and only one mutation? Because that's the wrong answer. What about exactly two mutations? Nope, wrong again.

In case you'd like to know, the probability that one and only one mutation took place in the first generation is 100 p (1-p)^99. The probability that at least one mutation took place is 1-(1-p)^100. No mutations at all? (1-p)^100. Shall I go on?

How much math have you studied?

The correct answer was in my previous post. If there are N mutations, each with probability p, and G generations, the odds that all N mutations have occurred after G generations are (1-(1-p)^G)^N. That's extremely basic, and can be derived in five minutes by anyone with any passing knowledge of probabilities. I'd be happy to explain the derivation again if you'd like to learn how to do it yourself.

Once again, the time required for all N mutations to happen grows extremely slowly with N. This is an absolutely fundamental fact in this debate, and I recommend you attempt to understand it.

[kleinman]

That’s 100 generations sol, each additional generation will improve that probability less than an additively.OK, let's focus on this nice concrete statement of yours - which is completely wrong. You are claiming the following: that, if there are 100 mutations, each with probability 10^{-6} per generation, the odds of all 100 occurring after 100 generations are (100*10^{-6})*(99*10^{-6})*... = 100! 10^{-600}. This is wrong - it's off (in this case) by a mere 40 orders of magnitude. It's the kind of mistake someone that doesn't understand probability at all would make.
Sol, if you think you can use probability theory to prove the theory of evolution by mutation and selection then go for it. Since the probability above is less than about 1 in 10^400, I’ll accept your value of 1 in 10^360 probability. I don’t claim to be an expert in probability theory, what I claim is that I know something about the mathematics of mutation and selection and the empirical data which supports this mathematics. So let’s see you use probability theory to prove otherwise. Why don’t you tell us what the probability is to form a particular 100 amino acid protein is by the random addition of amino acids? Then you can tell us how natural selection will improve that probability especially when there are multiple simultaneous selection conditions acting simultaneously. Let’s see if your knowledge of probability theory extends to the mathematics of mutation and selection.

[kleinman]

How much math have you studied?
Most of my mathematical experience is in solving non-linear partial differential equations by iterative techniques. As I said above, I claim no expertise in probability theory but mutation and selection is an iterative problem. What you probably don’t realize that mutation and selection is a sorting/optimization problem that shares many features with iterative solutions to partial differential equations. The first thing you should know about these problems is that the number of sorting conditions has a profound affect on the convergence. This is what Dr Schneider’s simulation shows and this is what the hundreds of empirical examples cited of mutation and selection demonstrates. The sorting of beneficial and detrimental mutations when you have multiple selection conditions is confounded by the multiple sorting conditions. Without selection, the ability to increase frequencies of beneficial sequences is eliminated.

[sol invictus]

Sol, if you think you can use probability theory to prove the theory of evolution by mutation and selection then go for it. Since the probability above is less than about 1 in 10^400, I’ll accept your value of 1 in 10^360 probability. I don’t claim to be an expert in probability theory

OK, good - we're making progress. You admit you were wrong and that you don't understand probabilities. As for those numbers, they are yours, not mine. Where did 100 generations come from?

You might ask yourself how many generations of organisms have there been in the last 3 billion years (or do you think it's only been 6,000 years?). Quite a few more than 100, don't you agree? Quite a few more than 1,000,000, in fact. Which means that an essentially infinite number of mutations with odds of far less than 1/1,000,000 have occurred.

So let’s see you use probability theory to prove otherwise. Why don’t you tell us what the probability is to form a particular 100 amino acid protein is by the random addition of amino acids? Then you can tell us how natural selection will improve that probability especially when there are multiple simultaneous selection conditions acting simultaneously. Let’s see if your knowledge of probability theory extends to the mathematics of mutation and selection.

You're making exactly the same mistake all over again. The odds of generating that protein are extremely small if it has to happen all in one shot. But it doesn't - because evolution didn't happen all at once.

Or even all in six days.

[kjkent1]

Oh oh...D30N and N88D appeared "MOSTLY" in certain patients. But, not "ALWAYS." In some patients, K20T appeared.
So, much for the hypothesis that only one mutational pathway can develop from a particular selective pressure. Kleinman loses again.Really kjkent1? Does this explain how birds evolve into reptiles? Does this mean that genetic sequencing to identify drug resistance is wrong?Ahem...obviously you're a bit rattled by being instantly demonstrated wrong via a peer reviewed article on your favorite HIV subject matter. Otherwise you wouldn't have written that "birds evolved into reptiles," rather than the reverse!

But, back on point, the article demonstrates how evolution can take different paths from the same selective condition, due to the unpredictable nature of mutations. Which does, in fact, show how substantial morphological change can occur over time, when such unpredictable mutations provide a fitness advantage.

Perhaps as important, though, this little dialog proves that you can't admit when you're just plain wrong on a point. You asked me to provide evidence that more than one resistance mechanism could arise from the same selective pressure, and I did.

Your response, instead of admitting the evidence falsifies your contention, was to ridicule it.

That just makes you an intellectual coward, Alan, because you can't admit the possibility of error and learn from it. That is a truly inadmirable characteristic -- especially for a physician and a scientist.

[delphi_ote]

I wish there weren't so many homologous genes between human and rat. This script I wrote is taking too long to run! Could someone please put all of life on Earth under more than one selection pressure? Things have evolved too much, and it's making my profession very difficult!

[Mr. Scott]

You kids want to talk about anything but the mathematics of mutation and selection and the empirical evidence which supports this mathematics.

This thread is about creationists who are annoying.

Who is demonstrating cognitive dissonance? It is you evolutionists who ignore the mathematical and empirical facts of life of how mutation and selection actually works.

I knew you'd throw it back at us. You are too predictable. (I'm predicting Kleinman will respond with "it is you evolutionists who are too predictable")

The fact that you don't respond at all to the proof of evolution is strong evidence your cognitive dissonance is clouding your judgement.

I assure you, evolutionists experience little cognitive dissonance since there is a mountain of consistent evidence for it.

If you want to really annoy evolutionists, present your refutation of the retrovirus evidence that humans and chimps share a common ancestor -- a point you previously ignored.

You onced brushed it off as a "coincidence" that human and chimp genomes had the same viral insertions in the same places, so I calculated the probability of this coincidence with a rough back-of-the-envelope estimate.

Number of nucleotides in the human and chimp genomes: 3 billion.

Number of endogenous retroviruses (ERVs) in the human and chimp genomes in identical positions: seven.

Chance of 1 ERV appearing in identical positions independently in chimp and human: One in three billion.

Chance of 7 ERVs appearing in identical positions independently: One in three billion to the seventh power.

Probability chimps and humans share a common ancestor, going just by the seven ERV insertions, is about 99.99999999999999999999999999999999999999999999999 999999999999999999% (65 nines after the decimal place) It's true!

Dr. Kleinman, I await your refutation.

[Belz...]

Notice how Kleinman completely ignores my posts, now ? He doesn't even bother with his "clever" scarcasm!

How could I ever be sarcastic beggaminases?

See what I mean ?

Get one of those high-schoolers into the discussion, perhaps they could explain to us what a beggaminases is.

They wouldn't need to. If you haven't understood what I meant by it, after all those times I've repeated it, then you never will.

It's very telling of your character.

Sure I realize what they show and so do you; they are cherry picked to show that combination selection pressures profoundly slow the evolutionary process.

It's nice to see you admitting to lying, Klein. There's not much else to say, now.

[Belz...]

Rocketdodger, do you think a war of examples would really be fair. All you evolutionists with your speculations, extrapolations and hunches against one annoying creationist with a peer reviewed and published model of random point mutations and natural selection and hundreds of empirical examples which show that combination selection pressures profoundly slow the evolutionary process.

You've got a serious case of Galileo syndrome, Alan.

Joobz, if the sun shines on lead long enough does it turn into gold?

I think you've lost it, Klein. You're just reposting the same stuff o'er and o'er even after it's been shot down.

[Belz...]

I wish there weren't so many homologous genes between human and rat. This script I wrote is taking too long to run! Could someone please put all of life on Earth under more than one selection pressure? Things have evolved too much, and it's making my profession very difficult!

Delphi, you're obviously ignorant of the REAL facts. Evolution is mathematically impossible. Kleinman has proved it by posting hundreds of empirical examples that show that multiple combination pressures profoundly slow evolution!

Your profession is a sham!!!

[Paul C. Anagnostopoulos]

Why don’t you tell us what the probability is to form a particular 100 amino acid protein is by the random addition of amino acids? Then you can tell us how natural selection will improve that probability especially when there are multiple simultaneous selection conditions acting simultaneously.
Oh now Alan, don't go all Dembski on us here. Treating a protein as a discrete combinatorial object is irrelevant to the question, since that is clearly not how they came to be. Natural selection cannot improve the probability of spontaneous assembly of a DCO because that is not what selection works on.

~~ Paul

[rocketdodger]

What you probably don’t realize that mutation and selection is a sorting/optimization problem that shares many features with iterative solutions to partial differential equations. The first thing you should know about these problems is that the number of sorting conditions has a profound affect on the convergence. This is what Dr Schneider’s simulation shows and this is what the hundreds of empirical examples cited of mutation and selection demonstrates. The sorting of beneficial and detrimental mutations when you have multiple selection conditions is confounded by the multiple sorting conditions.

You don't know sh-- Kleinman.

You claim that additional optimization conditions always confound sorting/optimization problems. My program shows this to be not true in general. Can you show anyone here why the sorting/optimization algorithm used in my program is not a sorting/optimization algorithm? If not, then you are wrong.

Here it is, in short:
1) Randomly mutate x number of bases in each creature's genome.
2) Determine the fitness of each creature according to the pressures exerted on the population.
3) Reproduce, such that creatures with higher fitness have more offspring.
4) Go back to 1, stopping when the targeted mutations of all pressures have achieved 80% or more fixation in the population.

[kleinman]

Sol, if you think you can use probability theory to prove the theory of evolution by mutation and selection then go for it. Since the probability above is less than about 1 in 10^400, I’ll accept your value of 1 in 10^360 probability. I don’t claim to be an expert in probability theoryOK, good - we're making progress. You admit you were wrong and that you don't understand probabilities. As for those numbers, they are yours, not mine. Where did 100 generations come from?
Sol, forget the 100 generations, show us how to use probability theory to win a million lotteries only 14 times longer than winning one lottery. You must be incredibly wealthy after winning all those lotteries.
Oh oh...D30N and N88D appeared "MOSTLY" in certain patients. But, not "ALWAYS." In some patients, K20T appeared. So, much for the hypothesis that only one mutational pathway can develop from a particular selective pressure. Kleinman loses again.Really kjkent1? Does this explain how birds evolve into reptiles? Does this mean that genetic sequencing to identify drug resistance is wrong?Ahem...obviously you're a bit rattled by being instantly demonstrated wrong via a peer reviewed article on your favorite HIV subject matter. Otherwise you wouldn't have written that "birds evolved into reptiles," rather than the reverse!
Kjkent1, I have never said that there can not be variants of genes. There are hundreds of forms of human hemoglobin. Just because there may be two variants of a particular gene that may confer resistance to a particular drug does not mean there is no goal for evolution as you allege. All you have shown is that there are only a small number of possible genetic sequences that improve fitness for the virus from the huge number of possible combinations available. The transformation of reptiles into birds requires a trajectory on a fitness landscape that transforms thousands of genes which always gives fitness to reproduce. When you give an example which shows only two possible variants that give improved fitness to reproduce, how do you explain the transformation of thousands of genes when you have so few variants that give improved fitness to reproduce?
I wish there weren't so many homologous genes between human and rat. This script I wrote is taking too long to run! Could someone please put all of life on Earth under more than one selection pressure? Things have evolved too much, and it's making my profession very difficult!
Really Delphi, and how many genes are not homologous? And what was the selection pressure that transformed rats into humans? You aren’t going to tell us a temperature change did that one also? You may be able to make a living finding similarities between genes in different life forms but mutation and selection didn’t transform reptiles into birds or rats into humans. You don’t have the selection pressures and even if you could imagine something like a temperature change, you can’t transform four or five genes simultaneously let alone thousands of genes. Mutation and selection doesn’t work that way mathematically or empirically. You should know that, you gave us the citation to Wikipedia and the fitness landscape. Do you care to describe the trajectory on the fitness landscape that would transform rats to humans?
You kids want to talk about anything but the mathematics of mutation and selection and the empirical evidence which supports this mathematics.This thread is about creationists who are annoying.
And it’s way too easy to annoy you with the mathematical and empirical facts of how mutation and selection works. When are you going to tell us about the lies your parents told you?
Notice how Kleinman completely ignores my posts, now ? He doesn't even bother with his "clever" scarcasm!How could I ever be sarcastic beggaminases?See what I mean ?
Belz, I’m not ignoring your posts, I’m waiting for one of you evolutionists to post a citation showing that n+1 selection pressures evolves more rapidly than n selection pressures. If you want to talk about beggaminases, that alright with me.
Why don’t you tell us what the probability is to form a particular 100 amino acid protein is by the random addition of amino acids? Then you can tell us how natural selection will improve that probability especially when there are multiple simultaneous selection conditions acting simultaneously.Oh now Alan, don't go all Dembski on us here. Treating a protein as a discrete combinatorial object is irrelevant to the question, since that is clearly not how they came to be. Natural selection cannot improve the probability of spontaneous assembly of a DCO because that is not what selection works on.
I’m not sure what you mean by “go all Dembski”. I raised that issue because sol invictus is going to use probability theory to prove the theory of evolution without selection. Actually, I want sol to teach us all how to win a million lotteries in only 14 times longer than winning one lottery. Sol doesn’t understand that mutation and selection is a sorting/optimization problem.
What you probably don’t realize that mutation and selection is a sorting/optimization problem that shares many features with iterative solutions to partial differential equations. The first thing you should know about these problems is that the number of sorting conditions has a profound affect on the convergence. This is what Dr Schneider’s simulation shows and this is what the hundreds of empirical examples cited of mutation and selection demonstrates. The sorting of beneficial and detrimental mutations when you have multiple selection conditions is confounded by the multiple sorting conditions.You don't know sh-- Kleinman.

You claim that additional optimization conditions always confound sorting/optimization problems. My program shows this to be not true in general. Can you show anyone here why the sorting/optimization algorithm used in my program is not a sorting/optimization algorithm? If not, then you are wrong.
When you produce a single real example that shows n+1 selection conditions evolve more rapidly than n selection conditions, I’ll take a look at your program.

This citation demonstrated how destructive the misunderstanding that evolutionists like rocketwhomissesthetarget and their defective thinking have on understanding how mutation and selection process actually works. A proper understanding of mutation and selection process would never start with monotherapy for treating a rapidly reproducing virus. This has led to resistance strains of viruses in the gene pool making it far more difficult to find combination therapies to suppress the reproduction of the virus. The evolutionist philosophy and evolutionists misinterpretation of how mutation and selection actually works has led to the early death of many people who suffer from HIV. How much longer will you evolutionists persist with this misunderstanding of how mutation and selection actually works is up to you, but know this, your pseudo-scientific interpretation of this phenomenon has interfered with the proper understanding of the process and led to inappropriate treatment. The theory of evolution is not only wrong, it is destructive to life.
http://www.journals.uchicago.edu/CID/journal/issues/v30nS2/990304/990304.html (http://www.journals.uchicago.edu/CID/journal/issues/v30nS2/990304/990304.html)
The response to antiretroviral therapy in human immunodeficiency virus (HIV)infected patients is limited by the emergence of drug resistance. This resistance is a consequence of the high rate of HIV mutation, the high rate of viral replication (especially when potent multidrug therapies are not used or taken reliably), and the selective effect of these drugs, which favors emergence of mutations that can establish clinical drug resistance. The introduction of highly active antiretroviral therapy (HAART), which typically includes at least 2 nucleoside reverse transcriptase inhibitors (RTIs) and a protease inhibitor or a nonnucleoside RTI, for most treatment-naive patients results in a reduction of viral load below the limit of detection determined by currently available HIV RNA assays. It is this marked reduction that results in durable viral suppression, usually only possible by the simultaneous use of 3 or 4 drugs. The RTI components of HAART are crucial for these benefits of combination therapy. Specific amino acid changes are associated with resistance to several RTIs, but new mutation complexes have been observed that can confer broad cross-resistance within this class. Genotypic and phenotypic resistance assays to measure drug resistance are being developed, but refinements in both methodology and our ability to interpret results of these assays are necessary before they are introduced into widespread clinical use.
and
The first 5 drugs approved for treatment of HIV infection were reverse transcriptase inhibitors (RTIs), all of which are nucleoside RTIs. More recently, nonnucleoside RTIs have become available, and nucleotide RTIs are being developed. Unfortunately, because these drugs were gradually introduced one at a time (starting with zidovudine in March 1987), monotherapies were routinely employed until 1994. When response was lost to 1 drug in a patient, treatments were changed to a different monotherapy. The response to the second therapy, however, was not as good as when the same drug was given to a treatment-naive patient [1, 2]. Even before the genetic mutations associated with drug resistance were identified, it seemed likely that resistance to 1 RTI diminished the response to subsequent ones.
and
Combination therapies that use 2 RTIs were introduced in 1994 [57]. By use of 2 drugs in initial therapy, VL reduction was greater and more durable. The use of sequential therapy (i.e., adding 1 drug to previous monotherapy after benefits are lost) results in a much lower virologic response than if 2 drugs are used in the initial therapy. When a new drug is added to a regimen that is not adequately suppressing viral replication, the only active agent may be the single new drug. The concept of greater VL reduction with more-intensive therapies was cemented in our treatment policies by the landmark studies that showed that 3- or 4-drug combination therapies that include a protease inhibitor (PI) or a nonnucleoside RTI are able to reduce VL to below levels of detection [815]. These intensive 3- or 4-drug therapy regimens have been termed highly active antiretroviral therapy (HAART).
How much longer will the faulty misunderstanding of how mutation and selection actually works be perpetuated by evolutionists so that needless deaths due to HIV, and other infectious disease and cancers because of evolution of resistance?

[joobz]

How much longer will the faulty misunderstanding of how mutation and selection actually works be perpetuated by evolutionists so that needless deaths due to HIV, and other infectious disease and cancers because of evolution of resistance?
Wow, that's heaping of crazy right there.

I'm not claiming you are crazy, kleinman. Only that it's becoming difficult to distinguish between a crazy person's rants and your posts.

[Mr. Scott]

When are you going to tell us about the lies your parents told you?

What was once in my sig is not on topic of a thread about annoying creationists. Why do you see a gotcha there?

Now, annoy us with your refutation of the endogenous retroviruses evidence that humans and chimps descended from the same ancestor.

[Paul C. Anagnostopoulos]

I’m not sure what you mean by “go all Dembski”.
Dembski treats the flagellum as a discrete combinatorial object in No Free Lunch. Unfortunately, it's irrelevant.

~~ Paul

[kleinman]

How much longer will the faulty misunderstanding of how mutation and selection actually works be perpetuated by evolutionists so that needless deaths due to HIV, and other infectious disease and cancers because of evolution of resistance?Wow, that's heaping of crazy right there.
For more than 50 years, the evidence of how mutation and selection actually works has been piling up, yet mathematical incompetents like you think your speculations qualify as science.

Joobz, when are you going to take me up on the $10,000 wager about your claim that you can find irregularities in my PhD thesis? You’ve opened your big mouth one too many times, put your money where your mouth is.
When are you going to tell us about the lies your parents told you?What was once in my sig is not on topic of a thread about annoying creationists. Why do you see a gotcha there?
Why Mr Scott, you see fit to psychoanalyze me by what I write, so why can’t I psychoanalyze you by what you write. I happen to believe that what a person says reveals what is in their heart. When someone writes that they believe their parents are liars, you are revealing something about yourself. I am interested in why you would think of your parents as liars. This may explain why you embrace the false belief system of evolutionism.
Now, annoy us with your refutation of the endogenous retroviruses evidence that humans and chimps descended from the same ancestor.
It is not my job to refute every misinterpretation that you evolutionists come up with. You try to do this with a picture of a fossil; delphi and Dr Richard have tried to do this with occasional similarities found in genetic structure of different life forms. Why don’t they explain the 150,000,000 base differences between human and chimpanzee genomes all which would have to happen in only 500,000 generations with very small populations?

I have spent some time studying Dr Schneider’s peer reviewed a published mathematical model of random point mutation and natural selection which reveals an important mathematical property of this phenomenon. I have posted hundreds of empirical examples which demonstrate this phenomenon as well as other mathematical models which demonstrate the same thing. These examples show that the foundation principle for the theory of evolution, mutation and selection, does not and can not do what you claim. It is not my job to correct every misinterpretation of the physical world that you come up with. If you want to post a citation which shows that n+1 selection conditions evolve more rapidly than n selection conditions, I’ll respond to that. Otherwise, start a thread where you can speculate how endogenous retroviruses give evidence that humans and chimps descended from the same ancestor. If you do want to tell us about the lies your parents told you, we can talk about that because you need help.

[delphi_ote]

Really Delphi, and how many genes are not homologous?
More and more the more distantly the two organisms I'm comparing have diverged from their common ancestor. It's almost as if...

:shocked::shocked::shocked::shocked::shocked:
Evolution is true!
:shocked::shocked::shocked::shocked::shocked:

[Mr. Scott]

Why Mr Scott, you see fit to psychoanalyze me by what I write, so why can’t I psychoanalyze you by what you write. I happen to believe that what a person says reveals what is in their heart. When someone writes that they believe their parents are liars, you are revealing something about yourself. I am interested in why you would think of your parents as liars. This may explain why you embrace the false belief system of evolutionism.

Dr. Kleinman, you are the subject of Paul's "Annoying creationists" thread! Look at the thread title! Look at the originating post! Psychoanalyzing you is fair game. Psychoanalyzing me is off-topic. Changing the subject each time you are asked a question you cannot answer is a transparent, sleazy debating tactic.

It is not my job to refute every misinterpretation that you evolutionists come up with.

Specifically, how have evolutionists misinterpreted the endogenous retroviruses evidence? You've just made this claim. Back it up.

[kleinman]

Really Delphi, and how many genes are not homologous?More and more the more distantly the two organisms I'm comparing have diverged from their common ancestor. It's almost as if...
http://forums.randi.org/images/smilies/mazeguyemotions/shocked.gif
Evolution is true!
http://forums.randi.org/images/smilies/mazeguyemotions/shocked.gif
Almost as if…? Too bad the theory of evolution isn’t the game of horseshoes. Then your “almost” would score some points. Now that we know exactly that combination selection pressures profoundly slow evolution, your “almost” doesn’t score points any more. Tell us all about the non-homologous genes between humans and chimpanzees and tell us how mutation and selection transformed these genes in 500,000 generations. Oh yes, don’t forget to tell us what the selection pressures were to achieve these transformations.
Why Mr Scott, you see fit to psychoanalyze me by what I write, so why can’t I psychoanalyze you by what you write. I happen to believe that what a person says reveals what is in their heart. When someone writes that they believe their parents are liars, you are revealing something about yourself. I am interested in why you would think of your parents as liars. This may explain why you embrace the false belief system of evolutionism.Dr. Kleinman, you are the subject of Paul's "Annoying creationists" thread! Look at the thread title! Look at the originating post! Psychoanalyzing you is fair game. Psychoanalyzing me is off-topic. Changing the subject each time you are asked a question you cannot answer is a transparent, sleazy debating tactic.
That’s right, Paul did say this.
Sometimes these annoying creationists just piss me off:
So, you are wrong, if psychoanalyzing you pisses you off, I am on topic. However I prefer pissing you off by pointing out the mathematical and empirical facts of how mutation and selection actually works. Only an evolutionist would think that pointing out the mathematical and empirical facts of how mutation and selection actually works is sleazy but what do you expect from someone who thinks his parents are liars?
It is not my job to refute every misinterpretation that you evolutionists come up with.Specifically, how have evolutionists misinterpreted the endogenous retroviruses evidence? You've just made this claim. Back it up.
Ok, since you don’t want to talk about your parents who you think are liars, we can talk about endogenous retroviruses. Let’s start with you explaining to us what the selection pressures these viruses cause and the target genes for these selection pressures. I like talking with you kitty cat but you should reconsider thinking of your parents as liars.

[rocketdodger]

When you produce a single real example that shows n+1 selection conditions evolve more rapidly than n selection conditions, I’ll take a look at your program.

Or, in other words, you are a fraud who knows none of the mathematics you claim to know and are completely unable to refute any of my mathematics.

You don't even have to look at the program, you fool -- I summarized my algorithm in that post. Here it is again:

1) Randomly mutate x number of bases in each creature's genome.
2) Determine the fitness of each creature according to the pressures exerted on the population.
3) Reproduce, such that creatures with higher fitness have more offspring.
4) Go back to 1, stopping when the targeted mutations of all pressures have achieved 80% or more fixation in the population.

You claim that additional optimization conditions always confound sorting/optimization problems. Can you show anyone here why the above algorithm is not a sorting/optimization algorithm? If not, then you are wrong.

[Lord Emsworth]

This thread is about creationists who are annoying.



I knew you'd throw it back at us. You are too predictable. (I'm predicting Kleinman will respond with "it is you evolutionists who are too predictable")

The fact that you don't respond at all to the proof of evolution is strong evidence your cognitive dissonance is clouding your judgement.

I assure you, evolutionists experience little cognitive dissonance since there is a mountain of consistent evidence for it.

If you want to really annoy evolutionists, present your refutation of the retrovirus evidence that humans and chimps share a common ancestor -- a point you previously ignored.

You onced brushed it off as a "coincidence" that human and chimp genomes had the same viral insertions in the same places, so I calculated the probability of this coincidence with a rough back-of-the-envelope estimate.

Number of nucleotides in the human and chimp genomes: 3 billion.

Number of endogenous retroviruses (ERVs) in the human and chimp genomes in identical positions: seven.

Chance of 1 ERV appearing in identical positions independently in chimp and human: One in three billion.

Chance of 7 ERVs appearing in identical positions independently: One in three billion to the seventh power.

Probability chimps and humans share a common ancestor, going just by the seven ERV insertions, is about 99.9999999