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Doc, I never said that HIV has no possibility of evolving to 3 drug therapy. It just that the probability of someone winning three lotteries is very low, much, much lower than to two lotteries.

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But as you correctly point out in message 76, the evolution of three things doesn't have to be like winning three lotteries; it can be like one person winning a lottery, and then one of his descendants winning a lottery, and then one of his descendants winning a lottery.

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That's correct, that's the way MRSA came about. When Staph evolved resistance to penicillin, methicillin was used, when methicillin failed, the next drug was used... The use of single targeted selection pressures sequentially is the way to evolve multidrug-resistant microbes. Each step of the evolutionary process requires amplification in order to improve the probability of the next beneficial mutation occurring. When multiple selection pressures are acting simultaneously, this amplification process is disrupted. All real, measurable and repeatable examples of rmns demonstrate this.

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And selection pressures are just that, something that kills or impairs the replication of some or all members of a population. Do you think that rmns to starvation and thermal stress work differently then to targeted toxins to enzymes?

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I think that nature isn't actually designed to thwart evolution, and so is likely to be even less successful at doing so than things which are.

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I don't know what you mean by "designed". I simply tried to understand the accounting rules which govern rmns. And the importance of this is clear if you want successful and durable treatment for infectious diseases and cancers.

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To return to dinosaurs and birds, I suppose you could look at it that way and say that there were some dinosaurs that were killed or impeded in replicating for want of being able to fly. That's hardly a reason why they should not have evolved flight, is it?

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If dinosaurs wanted to fly, they will need the alleles that would enable them to do this. And there are too many genetic loci needed to be transformed for scales to become feathers by rmns. Perhaps you think there exists selection pressures which target the individual loci in a sequential manner so that scales became feathers in the same way wild variants of staphylococcus became MRSA?

This post is a response to posts 111 and 112

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And there is a straightforward explanation why that happens. Malaria can achieve populations of a trillion or more in an infected individual. When you have populations that large, the probabilities will become realistic that you will get members of that population with double beneficial mutations.

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Is there some reason why the evolution of resistance in this case can't involve two or more sequential mutations?

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Amplification requires improved fitness to reproduce. However, if the selection pressures don't drive the population to extinction, it is possible that a particular lineage which doesn't amplify but is still able to reproduce for enough generations will do enough replication trials that the necessary beneficial mutation can still occur. This is why the residual population of HIV in a well treated patient is still a danger. The vast majority of times 3 drug therapy works for HIV but the residual viral population requires monitoring for this possibility.

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What prevents reptiles (or dinosaurs if you wish) evolving into birds is the multiplication rule of probabilities.

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Well, the multiplication rule of probabilities would apply if, as you say, the mutations required for the evolution of birds had to happen simultaneously (or if some large number of them did). But do you have any evidence that this is the case?

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No, the multiplication rule applies whether the mutations occur sequentially or simultaneously. Amplification alters the value of the probabilities but the probabilities are still computed multiplicatively.

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It seems to me that you have only half an argument. On the one hand, you have seen the force of what Darwin said 150 years ago, that natura non facit saltus --- nature does not take leaps. So far we are in agreement. We can also agree why this is the case: because a simultaneous coordinated set of beneficial mutations is extraordinarily unlikely on statistical grounds. So far, so good.
But then you add the proposition that the evolution of birds must have required such a leap. And this premise appears simply to have been plucked out of thin air.

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No, what I am saying is that the creation of new alleles by rmns only works efficiently when a single gene is targeted by a single selection pressure. And that process is governed by the multiplication rule of probabilities. As soon as selection pressures target more than a single genetic locus, the process is slowed even more so because of the more complex evolutionary trajectory where the probability of each step is governed by the multiplication rule.

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That's correct, that's the way MRSA came about. When Staph evolved resistance to penicillin, methicillin was used, when methicillin failed, the next drug was used... The use of single targeted selection pressures sequentially is the way to evolve multidrug-resistant microbes.

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But as we can see from the example of HIV and malaria, applying targeted selection pressures simultaneously also leads to the evolution of resistance.

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And it takes huge populations and/or large numbers of generations in order for the probabilities to become realistic in these situations. Each time another selection pressure is added, the probabilities drop multiplicatively.

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I don't know what you mean by "designed".

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I mean simply that the combination therapies were designed, by us, to mess with the pathogens and indeed in particular to make it harder for them to evolve resistance. (And yet they still manage it!) Nature was, surely, not designed with the aim of thwarting evolution. No part of it is the result of a vast endeavor by teams of brilliant scientists determined to prevent dinosaurs from evolving flight.

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Do you think that starvation selection pressures can not occur simultaneously with thermal stress in nature. What do you think would happen to a population that was subjected to starvation selection pressure alone vs starvation selection pressure with thermal stress? What about diseases occurring during starvation and thermal stress, what about predation and starvation?...

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If dinosaurs wanted to fly, they will need the alleles that would enable them to do this. And there are too many genetic loci needed to be transformed for scales to become feathers by rmns.

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There are too many for them all to be transformed simultaneously, we can agree on that. If you wish to maintain that there are too many for them to have changed sequentially, over the course of millions of years, then please show your working.

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What I can show you is the empirical evidence of how mutation and selection works and the underlying physics and mathematical principles which govern this phenomenon. If you believe that dinosaurs can transform scales into feathers by rmns, let us know what the sequential selection pressures were and the targeted genetic loci which would do this.

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...the reason there is no rational way that feathers can evolve from scales by rmns is there are too many genetic loci which must be transformed simultaneously. Every evolutionary step (beneficial mutation) must amplify in order to improve the probability of another beneficial mutation occurring on some member of the lineage with that particular mutation. rmns only works efficiently when a single selection pressure targets a single gene at a time. As soon as selection pressures target more than a single genetic locus at a time, the multiplication rule of probabilities makes that probability much, much lower. We see this with every real, measurable and repeatable empirical example of rmns.

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How then do you explain the fact that real-world evidence shows that scales or scales & feathers evolved into feathers?

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Models must conform to, and hopefully explain, real world evidence or they are of little value. Or, whenever the model and the evidence disagree, it is best to reexamine the model...

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My model is based on real, measurable and repeatable examples of rmns. Perhaps you should reexamine your interpretation of the fossil record.

The following post is a response to posts 119 and 120

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Amplification requires improved fitness to reproduce. However, if the selection pressures don't drive the population to extinction, it is possible that a particular lineage which doesn't amplify but is still able to reproduce for enough generations will do enough replication trials that the necessary beneficial mutation can still occur. This is why the residual population of HIV in a well treated patient is still a danger. The vast majority of times 3 drug therapy works for HIV but the residual viral population requires monitoring for this possibility.

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Is that a no?

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Yes, but it is not a simple no. It can take thousands of generations for something like you described to happen. Evolution will have to occur at a rate of much greater than a thousand generations per beneficial mutation if scales are going to be transformed into feathers.

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No, the multiplication rule applies whether the mutations occur sequentially or simultaneously. Amplification alters the value of the probabilities but the probabilities are still computed multiplicatively.

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I presumed that by "the multiplication rule" you meant that P(A & B) = P(A) * P(B) if the events are independent. Hence for example we can use this rule to calculate the probability of me throwing six on two dice. If instead I keep rolling one die until I get a six, and then keep rolling a second die until I get a six, that's a whole different question, and the probability of me getting two sixes is in fact 1. I arrived at that result without using the multiplication rule, and indeed without using multiplication.

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Yes. But the probability problem you must solve is the probability of a beneficial mutation occurring in a given number of replications. The analogous dice rolling problem would be for example the probability of rolling at least a single 1 in a given number of rolls.

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No, what I am saying is that the creation of new alleles by rmns only works efficiently when a single gene is targeted by a single selection pressure. And that process is governed by the multiplication rule of probabilities. As soon as selection pressures target more than a single genetic locus, the process is slowed even more so because of the more complex evolutionary trajectory where the probability of each step is governed by the multiplication rule.

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Well, it seems to me that you also said something about birds, and I wondered if you had any evidence for it.

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What I have evidence of is real, measurable and repeatable examples of random mutation and natural selection. What I can tell you with mathematical certainty is that as you target more genes with selection pressures, the evolutionary process becomes too slow to support the theory of evolution. How quickly do you think a population can evolve to starvation selection pressure?

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Do you think that starvation selection pressures can not occur simultaneously with thermal stress in nature. What do you think would happen to a population that was subjected to starvation selection pressure alone vs starvation selection pressure with thermal stress? What about diseases occurring during starvation and thermal stress, what about predation and starvation?...

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Yes, many pressures are always acting on a population. Which, of course, weakens your point. A strain of bacteria evolving resistance to just one antibiotic does so in the teeth of a thousand selection pressures. Adding the antibiotic makes it a thousand and one.

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And still they evolve.

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The empirical evidence contradicts your claim. A common example is the rotation of herbicides to prevent the emergence of herbicide resistant weeds. Even if a variant has some resistance to one of the herbicides, the other herbicide suppresses its amplification. And populations can be subjected to many selection pressures and not go extinct but they won't evolve efficiently to any particular selection pressures. What you are describing is drift. That's what the surviving population of HIV subject to combination therapy is doing. If you want scales to be transformed into feathers, you need directional selection pressures, not drift.

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What I can show you is the empirical evidence of how mutation and selection works and the underlying physics and mathematical principles which govern this phenomenon.

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Well, I was already aware of that stuff. What I am unaware of is any reason why this gives us a compelling argument against the evolution of birds.

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I've never said that birds can't evolve. What I am saying is that you have too many genetic loci to transform by rmns scales into feathers.

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If you believe that dinosaurs can transform scales into feathers by rmns, let us know what the sequential selection pressures were and the targeted genetic loci which would do this.

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I don't have a description of the sequence of mutations which produced birds, which I why I have never claimed that I did and then gone on to adduce this as a proof of the evolution of birds.

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You, however, seemed to be claiming that you had a proof that no such pathway exists. If you don't, then this thread is about done.

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I debated this issue with Edward Max, supervising medical doctor of the FDA who writes essays saying that rmns can account for all the complexity of life. I critiqued one of his essays and told him that if he believed that reptiles could transform scales into feathers by rmns, it would have to be one gene at a time because that was the only way that rmns works efficiently. Max didn't understand my argument and responded by sending me a link to a paper where the researchers studied the genomes of reptiles and the genomes of birds and asked which genes would have to be transformed to turn a scale into a feather. They identified at least eight different genes which would have to be transformed. My response was, "Very interesting, how can you transform eight genes at a time subject to selection when HIV, the fastest evolving replicator known can not evolve efficiently to 3 selection pressures targeting only 2 genes?"

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Yes, but it is not a simple no. It can take thousands of generations for something like you described to happen. Evolution will have to occur at a rate of much greater than a thousand generations per beneficial mutation if scales are going to be transformed into feathers.

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Show your working?

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Study the Lenski experiment where he subjects a population of e coli to starvation selection pressure. His populations take over a thousand generations for each beneficial mutation to improve fitness against this selection pressure. His populations are not being subjected to thousands of selection pressures at the same time.

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Yes. But the probability problem you must solve is the probability of a beneficial mutation occurring in a given number of replications.

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So, we'd need to know the number of beneficial mutations, the number of generations, and also, and this would be the really awkward bit, we'd need enough data to avoid the Sharpshooter Fallacy: what we need to know is not the probability of evolving the exact birds we have, but the probability that w'd be having this sort of conversation.

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It's not all that awkward, we have empirical examples that we can measure. Weinreich did it when he measured the number of mutations required for a bacterial population to evolve resistance to an antibiotic. He found many different lineages adapted but each of the lineages required a particular set of 5 mutations. It doesn't matter what the evolutionary trajectory is, the accumulation of mutations which allow for adaptation to a particular selection pressure will always be computed by the multiplication rule of probabilities. And if amplification doesn't occur or the lineage is able to replicate for many, many generations, that probability will remain very low of that evolutionary process occurring.

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What I have evidence of is real, measurable and repeatable examples of random mutation and natural selection.

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But very little about birds.

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It doesn't matter what the replicator is, rmns works the same for all replicators. Perhaps you want to try and argue that recombination makes a difference?

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What I can tell you with mathematical certainty is that as you target more genes with selection pressures, the evolutionary process becomes too slow to support the theory of evolution.

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Well, if you have mathematical certainty, you must have some actual math. Perhaps you could demonstrate it using dinosaurs and birds as an example.

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Do you think the laws of physics and mathematical principles worked differently in the past? If so, you have some explaining to do.

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I debated this issue with Edward Max, supervising medical doctor of the FDA who writes essays saying that rmns can account for all the complexity of life. I critiqued one of his essays and told him that if he believed that reptiles could transform scales into feathers by rmns, it would have to be one gene at a time because that was the only way that rmns works efficiently. Max didn't understand my argument and responded by sending me a link to a paper where the researchers studied the genomes of reptiles and the genomes of birds and asked which genes would have to be transformed to turn a scale into a feather. They identified at least eight different genes which would have to be transformed. My response was, "Very interesting, how can you transform eight genes at a time subject to selection when HIV, the fastest evolving replicator known can not evolve efficiently to 3 selection pressures targeting only 2 genes?"

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To which the answer would be, "one locus at a time, over a long period".

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Interesting, do you want to tell us what those targeted selection pressures were and how nature applied those targeted selection pressures sequentially? We are not talking about the evolution of MRSA where we had designers designing targeted selection pressures and then applying those targeted selection pressures sequentially over a number of years.

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Let's have a look again at how fast HIV adapts, shall we?

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Reverse transcription inhibitor (RTI) mutations increased 0.5 mutations per y (STD = 0.8 mutations per y), while major protease inhibitor (PI) resistance mutations increased at a rate of 0.2 mutations per y (STD = 0.8 mutations per y) and minor PI resistance mutations increased at a rate of 0.3 mutations per y (STD = 0.7 mutations per y).
That's fast. It doesn't tell us much about dinosaurs, though, since on the one hand HIV has a higher mutation rate and population, and on the other hand the HIV is evolving to selection pressures specially designed and selected to be hard to adapt to. Still, this at least makes it look plausible that dinosaurs could evolve much more slowly than that and still produce feathers etc, since they do have an awfully long time to do it in.

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High mutation rates and huge populations and only two genetic loci targeted. People still live for decades when combination therapy is used. And that's without driving the population to extinction. On the other hand, single drug therapy gives resistant variants in a week. There's a mathematical lesson to be learned here. Populations subject to multiple simultaneous selection pressures that are not driven to extinction don't evolve efficiently to the selection pressures, they drift.

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You still have not responded to my Message 47 which deals with mathematics and shows where your entire argument is flawed.
I bet you haven't even watched that on-line lecture.

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What's the point of your hour long video?

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My model is based on real, measurable and repeatable examples of rmns. Perhaps you should reexamine your interpretation of the fossil record.

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If your model can't explain all of the real-world fossil record--that's actual data in plain English--then perhaps it needs to be reexamined.

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It is a standard creationist tactic to 1) come into a website with a magic bullet that will kill off evolution right blinkin' now and 2) to have a scheme/model/hypothesis/theory that ignores a lot of the data.

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We see these magic bullets several times a year here. Most of the posters who fit that description don't last long.

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I remember a poster, although on another website, who assured us that the odds against evolution were 1^720. He couldn't understand why we didn't take anything he said seriously.

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If you want to try and draw realistic conclusions about the fossil record, you need to take into account the mechanisms of genetic transformation. If your conclusion transcends the laws of physics, you should reconsider your conclusions.

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They identified at least eight different genes which would have to be transformed. My response was, "Very interesting, how can you transform eight genes at a time subject to selection when HIV, the fastest evolving replicator known can not evolve efficiently to 3 selection pressures targeting only 2 genes?"

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Quite easily, actually. A population of millions (+-) of dinos over a span of millions of years can easily progress from undifferentiated tubular follicle collars developed out of the old keratinocytes being pushed out, through the inner, basilar layer of the follicle collar differentiating into longitudinal barb ridges with unbranched keratin filaments, while the thin peripheral layer of the collar become the deciduous sheath, forming a tuft of unbranched barbs with a basal calamus, through the helical displacement of barb ridges arising within the collar and the barbules pairing within the peripheral barbule plates of the barb ridges, creating branched barbs with rami and barbules, then through having differentiated distal and proximal barbules producing a closed, pennaceous vane with a closed vane that develops when pennulae on the distal barbules form a hooked shape to attach to the simpler proximal barbules of the adjacent barband, and finally, developmental novelties giving rise to additional structural diversity in the closed pennaceous feather.**

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With millions of dinos over millions of years nature (mutation and selection) can do such things.

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Your comparison with HIV is bogus since the drug cocktails are selected specifically to kill HIV and when the virus evolves a resistance to one another is put in its place. The evolution of feathers did not have that level of artificial pressure applied and had plenty of time to experiment with incremental developments on millions of genomes over millions of years.

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You do believe in millions of years, do you not?

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** Thanks Wiki

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What antiviral medication kills the virus? Effective treatment of HIV still leaves populations at least in the hundreds of thousands. Isn't that enough for rmns to work to evolve resistance? Horses have keratin as well. So perhaps you want to tell us what those selection pressures were that transform keratinocytes from scale producers to feather producers?Millions of years? Did you hear about the guy who went to the natural history museum? While on tour, the tour guide said, "This dinosaur skeleton is one million and six years old"! And the guy says to the tour guide, "What, how do you know that this dinosaur skeleton is one million and SIX years old"??? And the tour guide said, "I came to work here six years ago and the dinosaur skeleton was a million years old then"!

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What's the point of your hour long video?

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I figured you hadn't viewed it.

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You want the point? Here's the abstract:

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Mathematical computer models of two ancient and famous genetic networks act early in embryos of many different species to determine the body plan. Models revealed these networks to be astonishingly robust, despite their 'unintelligent design.' This examines the use of mathematical models to shed light on how biological, pattern-forming gene networks operate and how thoughtless, haphazard, non-design produces networks whose robustness seems inspired, begging the question what else unintelligent non-design might be capable of.
In other words, your model is countered completely by this one. But of course creationists won't accept that, if they even take the time to view the on-line lecture which most won't.

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I watched the first 5 minutes and listened to a description of what they were going to talk about and then a moderater talking about how great the next lecture was going to be. You complain that I don't get to the point. So give us an empirical example of what they claim their model is showing.If you want to look at a good computer simulation, look at Tom Schneider's EV simulation or rmns. But don't take Schneider's superficial analysis of his algorithm, do a thorough analysis of his computer program including varying the mutation rates, population sizes, genome lengths and most importantly, the complexity of his selection conditions. His model not only demonstrates how rmns works, it can also be used to demonstrate how drift works (if you do a thorough analysis which Schneider didn't do).

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If you want to create realistic models about the fossil record, you need to take into account the fossil record! If your models, no matter how elegant, fail to account for the real-world evidence they are destined for the trash heap of science.

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If you want to make realistic interpretations of the fossil record, you need to take into account the mechanisms of genetic transformation.

The administrator states that I haven't abided by forum policy by posting links without description.
The basic science and mathematics of random mutation and natural selection - PubMed
The mathematics of random mutation and natural selection for multiple simultaneous selection pressures and the evolution of antimicrobial drug resistance - PubMed
Random recombination and evolution of drug resistance - PubMed
I have given layman's descriptions for the two papers on rmns, I'll repeat the description here:Let's say that in order for your family to survive, your family must win two lotteries. And the probability of winning the first lottery is 1 in a million and the probability of winning the second lottery is 1 in a million. For you to win both lotteries, that probability will be 1 in a million times 1 in a million, 1 in a trillion, a very low probability. But let's say you are lucky enough to win one of the lotteries and now you are very wealthy and because of all your wealth, you can raise a very large family. And now all your descendants start buying tickets to the second lottery. As soon as you have enough descendants, you will have a reasonable probability that your family will win both lotteries.Now let's extend this idea to a real example of random mutation and natural selection. Let's say I want to treat someone with an infection with an antibiotic. And let's say the bacteria I'm treating need 3 mutations to become resistant to the antibiotic. It's very unlikely that in a single replication that a bacterium will get all 3 mutations but let one lucky member get the first beneficial mutation. Now that member has to replicate for many generations so there are millions of members with that mutation and then there is a reasonable probability that one of those members will get the second beneficial mutation. That new member must now replicate for many generation so there are millions of members with the first 2 mutations and then some lucky member gets the third beneficial mutation and now is resistant to the antibiotic. So random mutation and natural selection works in a cycle of beneficial mutation followed by amplification of that mutation (increase in number of those with that mutation) to improve the probability of the next beneficial mutation occurring.But what happens if we use two drugs? Let's say the first drug requires mutations A, B, and C and the second drug requires mutation X, Y and Z. Even if some lucky member gets mutation A, the second drug interferes with the amplification of that member. And if some lucky member gets mutation X, the first drug interferes with the amplification of that member. It is this principle that has led to the successful treatment of HIV.The second paper on rmns extends this concept with computing the joint probability of two (or more) simultaneous beneficial mutations occurring when multiple simultaneous selection pressures are acting on a population. This is conceptually similar to computing the probability that someone will win two lotteries.The third paper concerns the mathematics of random recombination. I haven't discussed this paper yet but will now give the layman's version. Random recombination is very similar to a random card drawing problem. In this case, you have a population with various different alleles. The probability of two particular alleles showing up in a descendant by recombination is dependent on the relative frequencies of the different alleles.Now I apologize that these papers are behind a paywall but the open source cost is prohibitive for me. If you have access to any medical school library or good college library, which subscribes to this journal, you can get the papers for free. WRT giving copies of the papers to the administrator, I have to check with the editor of the journal to see if this violates copyright agreement.

The following message is a response to message 129, 130, 132

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Study the Lenski experiment where he subjects a population of e coli to starvation selection pressure. His populations take over a thousand generations for each beneficial mutation to improve fitness against this selection pressure. His populations are not being subjected to thousands of selection pressures at the same time.

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Well, they are, as I pointed out; it's just that most of these are conservative. As would of course be the case with dinosaurs.

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But to even start applying this to dinosaurs we'd need to know how many beneficial mutations get your from dinosaurs to birds and how long it took.

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Are you arguing that conservative selection pressures are what transformed dinosaurs into birds. It's not just scales to feathers, it's mouths to beaks, limbs to wings, muscles suited for weight bearing into muscles suited for flight, bones suited for weight bearing into bones suited for flight..., all the alleles which differentiate reptiles from birds. Lenski's starvation selection pressure experiment targets only a few genes and it takes thousand of generations per beneficial mutation.

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It's not all that awkward, we have empirical examples that we can measure.

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But examples of something else. In order to do the working in the dinosaur-to-bird case, we'd need to know these things about dinosaurs and birds. How many beneficial mutations? How many generations? What mutation rate? What is the strength of the selection pressures? Which operated concurrently and which consecutively? How many other evolutionary pathways would have struck us as equally remarkable?

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I have empirical examples of rmns for microbes, plants, insects, rodents, cancers, some of these examples are for clonal replicators, some for sexually reproducing replicators. All show the same thing, there ability to evolve against selection pressures efficiently only occurs when there is a single selection pressure targeting a single gene. When more than a single selection pressure is acting, the probabilities of evolving against these selection pressures drop multiplicatively.

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It doesn't matter what the replicator is, rmns works the same for all replicators.

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Right, but in order to do the math we need the actual data.

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By analogy, the formula area = width height works the same for all rectangles, but in order to apply it to any particular rectangle we would need to know the particular width and height.

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If we were to assume that birds evolved as fast as HIV does, then you, Kleinman, wouldn't have a leg to stand on. But we know that they don't. So in order for us to figure out how much water your argument holds, it's kind of important to have some actual data about birds.

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Even if birds could evolve as quickly as HIV does, the theory of evolution does not have a chance. Are you going to argue that combination therapy doesn't work for the treatment of HIV? Even HIV with its high mutation rate, huge populations, the fact that it does recombination can not evolve efficiently when selection pressures target only two genes at a time. HIV obeys the laws of probability just like every other replicator. It's the multiplication rule the kills the theory of evolution.

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Perhaps you want to try and argue that recombination makes a difference?

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Well, everything that's different about the two cases makes a difference. Though I seem to remember that HIV is diploid and undergoes recombination.

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HIV does do recombination but it has no significant effect on evolving drug resistance. I did the mathematics for that case. The mathematics for that case is analogous to a random card drawing problem. Unless the resistance alleles are in high relative frequency in the population, the probability of recombination for two different beneficial alleles is low.

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Interesting, do you want to tell us what those targeted selection pressures were and how nature applied those targeted selection pressures sequentially?

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Once again --- I don't go about telling people that I've found such an evolutionary pathway.

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You, on the other hand, claim to have a proof that there is no such pathway. That's for you to demonstrate.

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(What on earth you mean by "targeted" in this context I cannot begin to imagine, perhaps you could explain?)

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Of course, you don't know what the selection pressures are which would transform a reptile into a bird because they don't exist. You could prove me wrong by naming the selection pressures but then we could test the concept.And targeted selection pressures are those pressures which target a single genetic loci. Examples of these are antimicrobial agents, herbicides, many modern anti-cancer agents. Non-targeted selection pressures are those which target more than a single genetic locus. Examples of this are starvation, radiation, bleach, alkylating anti-cancer agents, etc. It is the targeted selection pressures when used singly which are most easily evolved to by rmns. The non-targeted selection pressures like bleach are not easily adapted to if at all.

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High mutation rates and huge populations and only two genetic loci targeted. People still live for decades when combination therapy is used. And that's without driving the population to extinction. On the other hand, single drug therapy gives resistant variants in a week. There's a mathematical lesson to be learned here. Populations subject to multiple simultaneous selection pressures that are not driven to extinction don't evolve efficiently to the selection pressures, they drift.

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And yet as I have pointed out, everything is subject to multiple simultaneous selection pressures, yet and many things do in fact evolve efficiently. This empirical observation beats your "mathematical lesson" (which does not appear to involve any mathematics).

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Don't hide your empirical examples, but make sure they are real, measurable and repeatable examples of rmns.

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Effective treatment of HIV still leaves populations at least in the hundreds of thousands. Isn't that enough for rmns to work to evolve resistance?

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Yes.

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So three drug combination therapy does not work for the treatment of HIV? You'd better notify the WHO, CDC, FDA, and NBA

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If you could manage to prove that the Earth isn't old, that would be a much more effective answer to evolution than anything you've shown us so far. You would need to start a new thread so as not to annoy the moderators.

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I really haven't studied the age of the earth and techniques used to compute this. It has taken me a decade to unravel the bloody mess that evolutionists have made with the rmns phenomenon. I would say one thing about evolutionist estimates of the age of things. If the T Rex fossils that still have soft tissue and red blood cells are really 70 million years old, would these evolutionists apply the physical laws that allow this to happen to my freezer so that when I forget something in there for 6 months so it won't be totally ruined.

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It is easy to argue that in an ideal case a population will evolve more efficiently if it is presented with a number of selection pressures concurrently than if they are presented consecutively.
Consider a set of potential adaptive mutations to n selection pressures, each of which (for convenience) we shall take to have a chance 1/q in each generation of arising and going on to fixation.

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I'm going to stop you right there because you are making the same error in physics which Haldane and Kimura make in their models of substitution and fixation. Fixation is neither necessary nor sufficient for rmns to work. Do you understand why? I'll give you empirical examples of this after you think about this for a while and explain to you why you are wrong if you can't figure it out yourself.

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Perhaps a simpler take on the issues.
Hard selection is the fastest way to achieve fixation of a single allele. However, because it relies on a declining population - and the rate of decline is directly tied to the strength of selection - it does not work any faster in parallel, nor is it sustainable.

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Soft selection is slower but it does not rely on a declining population. So it is sustainable and it can work in parallel. Soft selection, then, can be more efficient than hard selection because it can work sustainably and in parallel.

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Fixation is neither necessary nor sufficient for rmns to work. This notion of fixation is based on an erroneous application of a physical principle. Do you think that natural selection is a conservative phenomenon?

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See if you can find an error in the physics or mathematics.

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Um, what do any of these papers have to do with the topic at hand? In fact, from the abstracts, you seem to accept a priori the previous work that establishes evolutionary theory. Much of it is mathematical in nature. Surely you aren't saying that because we can mathematically describe how randomness works (which is what probability in general and chaos theory in particular are about), that somehow means we have a deterministic system, are you? If you think you have something that countermands what we understand about how evolution works, it would help if you would put it here.

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Use your words. Argument by footnote is not helpful.

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Be specific.

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I notice you didn't answer my questions. I directly stated that I wanted to hear your answers. I did not ask them for my health. I'll reduce it to the last example:

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You have a trait that is in a single-gene, two-allele, dominant/recessive scenario. The recessive trait only appears when the individual is homozygous recessive. Otherwise, the dominant trait appears. Those who express the recessive trait do not reproduce.

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The recessive trait currently is seen in 1 in 1,000 individuals. How many generations would need to pass in order to reduce the occurrence to 1 in 1,000,000?

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What is p? What is q?

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These papers are totally apropo to the discussion. I am total pro-evolution, I'm just anti the theory of evolution. These papers correctly describe the physics and mathematics of rmns including the mathematics or rmns to multiple simultaneous selection pressures, as well as a paper on random recombination. I've already posted the layman's description of how this phenomenon works several times on this thread but you with your skill in probability theory might be interested in the mathematics which goes along with it. All real, measurable and repeatable examples of rmns obey the mathematics in these publications.rmns has nothing to do with chaos theory. Before they called it chaos theory, they called it ill-conditioned mathematics. I published papers on an ill-conditioned problem years ago and rmns is far from being ill-conditioned.And there are actually two different random trials in the rmns phenomenon, the first random trial is the replication where p=the probability that an error does not occur at a particular site in the genome and q=the probability that an error does occur at a particular site in the genome. Now the mutation itself also is a random trial. In this case, it is not a binomial probability. The mutation can be a substitution of a base, an insertion, a deletion, double insertion,...

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So perhaps you want to tell us what those selection pressures were that transform keratinocytes from scale producers to feather producers?

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So you're one of those "Darwin", "Darwinism" naysayers that are stuck (or purposefully want to be stuck) on the idea that all traits of all organisms must be the product of selection. This is a glowing ignorance of the Theory of Evolution. Natural Selection is not the sole determinant of phenotypic features. Every detail of every organism is not the product of selection pressures.

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I suggest you take a few months off to research and learn the limits of selection and what other vectors are known to produce novel features in a phenotype. Most of the fine details, and even some major ones, of the phenotype are not adaptive through selection pressures.

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I'm one of those sayers that says Darwin got it half right.

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"I came to work here six years ago and the dinosaur skeleton was a million years old then"!

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Cute. Nice way to dodge the question.

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Are you a YEC?

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[ABE] BTW, That dino skeleton had better be considerably more than 1 million and six years old.

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I've never really studied the age of the earth issue, I'm too busy unraveling the bloody mess evolutionists have made with the rmns phenomenon. I do think it is really weird to think that a T Rex red blood cell could last 70 million years.

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How do you take an ancestor which has scales and all the genes which produce scales and transform all those scale producing genes into genes which would produce feathers?

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Well, all modern birds (that I, personally, know of) have both scales and feathers. I'm therefore not to sure what you're asking.

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Do all modern reptiles also have genes for scales and feathers as well?