Annoying creationists

[kjkent1]

Paul, it is you evolutionists who are the cannibals. I told Dr Schneider once it was revealed what his model really showed, his work would be discredited. That’s what has happened in this thread. His model even has been attributed to me.

So tell us, does Dr Schneider still say that his model simulates reality?

Thus far, after 100s of posts, the only thing that you've credibly demonstrated, is that you don't know a for-next loop from a fruit loop.

 

[delphi_ote]

Thus far, after 100s of posts, the only thing that you've credibly demonstrated, is that you don't know a for-next loop from a fruit loop.

 

[kleinman]

Annoying Creationists

a single profound selection pressure can cause extinction

Evidence contrary to your thesis that the number of selection pressures imposes a limit on evolution by natural selection..

Really? A single fatal selection pressure precludes multiple non-fatal selection pressures from slowing evolution? Then explain why the emergence of drug resistance HIV is slowed when multiple drug therapy is used.

Ev uses three selection conditions and the treatment of HIV uses three selection pressures. Both of these situations show how much only three selection conditions profoundly slow the evolutionary process.

Every triangle has three corners,

Every triangle has three sides,
No more, no less.
You don't have to guess.
When it's three you can see
It's a magic number.

Oh no, three is not a magic number, four selection pressures will slow evolution even further, five more so… It shows that only as few as three selection pressures slow evolution profoundly. Only a single selection condition evolves quickly in ev. Monotherapy quickly leads to strains of HIV resistant to that strain.

I already posted the URL to the guidelines for treatment of HIV and posted a quote from these guidelines which describes why monotherapy is not used to treat this disease with the existing drugs available.

Which is not what I asked for: a scientific biological source claiming there is a limit on the number of selection pressures to which an organism can adapt through natural selection.

Ev shows this, the guidelines for the treatment of HIV shows this. What evolutionist publication has ever considered that selection pressures actually slow evolution? This is a mathematical fact. Evolutionist have assumed that there is no limit to what natural selection can do. Ev and the HIV treatment strategy plainly demonstrate this phenomena. One from a mathematical viewpoint and the other from a clinical medical view point. Next time you publish in Science you can publish this finding.

Examples of nutrient deficiencies are so commonplace that I didn’t think I had to give any examples. In humans, multiple nutrient deficiencies are very common, for example in alcoholism, starvation, fad dieting and so on. Dietary nutrient deficiencies also occur in the wild.

And these somehow limit evolution? How? Your argument was that these multiple pressures limit evolution, was it not?

I've seen plenty of multiple minor deficiencies. They tend to do fairly little clinically, but may have effects on reproduction. I've seen plenty of multiple major deficiencies. They tend to do one thing -- lead to death. Death seems to me to be a very big part of evolution. Those who do survive the process of these multiple deficiencies tend to do so for only one reason -- variability or new mutation that allows them to survive. Funny, that.

Another evolutionist who doesn’t realize his own theory measures fitness by the ability to reproduce.

So, you are taking the position that only a single selection condition drives evolution at any given moment. Do you want to describe to us what the selection condition that evolves a gene from the beginning?

OK, I'll spell it out.......what you are describing with the antiretrovirals are selection pressures that tend to lead to the death of organisms. The fact that HIV is still around should be telling you the exact opposite of what you think it does. These pressures are immense for this particular virus. The fact that they work tells us something important -- that we have found a significantly profound pressure that has beaten back this virus somewhat. If you provide significant enough pressures you can kill or beat back anything. The number of pressures is not necessarily the magic ingredient. If we have a bacterium that uses glucose but has a pathway that can activate galactose metabolism, then the absence of glucose will not kill it. But if we remove glucose and galactose then the bacterium is in serious trouble and will likely go extinct. If we have a bacterium that will not produce quite as many offspring if glucose is not present and not as many offspring if galactose is not present, then this will not be absolutely fatal, even in the presence of both deficiencies. It is likely that some variant will arise in that situation to use another energy source eventually though. While multiple pressures may be fatal or severely limiting, other variants of different types of pressures will not. It depends critically on the type of pressures involved. Concentrating on the number and thinking of it magically is silly.

None of the treatments for HIV lead to death of the virus, these treatments only limit reproduction of the virus. So why don’t you tell us what the selection pressure is that evolves a gene from the beginning. I keep asking this question of you evolutionists and you never answer it.

And, no, I have no number of selection pressures in mind. I don't think it even makes sense to think that way as an absolute. There were undoubtedly times when one pressure for early organisms was important and other times when multiple pressures came into play.

What you don’t seem to realize is that multiple selection conditions even if not fatal confound the evolutionary process. In a simple sense, what happens if you get a beneficial mutation for one selection condition and a harmful mutation for another selection condition on the same creature. Is that creature selected for or selected against? What happens when you have numerous selection conditions? Ev shows this mathematically. Evolution becomes profoundly slow.

Just because antiretroviral drugs primarily target reverse transcriptase does not mean that each drug works in the same way. Ultimately, the strategy for the using multiple drugs is to slow the reproduction of the virus and minimize the appearance of drug resistant strains of the virus.

Um, yes, in the broad sense it does. That is what we mean when we use the term "mechanism of action". They all target the same enzyme system. They have different sites of action, so one drug may continue to work when resistance to the others forms. Eventually this will mean that none of these drugs will work. Eventually the virus is going to win. We already know it will win. It's beginning to win already. The fact that it remains viable within people who cannot stop the cocktails tells us all we need to know about how thoroughly "powerful" these drugs are. They are going to fail.

The net result is that evolution is slowed. The virus doesn’t have to win.

So tell us, what was the selection pressure that gives rise to the hemoglobin gene and molecule? If it is as Paul previously suggested, the presence of oxygen in the atmosphere, describe that selection pressure so that it can be put in ev and evolve the hemoglobin gene.

I'm sorry, but what does this have to do with anything I have said or your use of HIV as the example par excellence? I do not pretend to knowledge that I do not have. I would need to study the problem before even beginning to suggest alternatives. I do not know the history of the molecule and its progenitors well enough to say.

It has everything to do with the theory of evolution. Choose any gene, how does any gene evolve from the beginning. How do you select for something before it exists. Natural selection only can act on something that exists. Since I doubt you have carefully read this thread, I’ll explain to you what there are no selection pressures that evolve a gene from the beginning.

A gene is to evolve. The first base in the sequence for the gene is laid down on the genome. One base codes for nothing so there is nothing for natural selection to act upon. A second base added by random chance is laid down in the sequence. Still nothing to code for, natural selection can not act on this sequence. A third base in the sequence is laid down. You now have enough bases to form a codon for a single amino acid. A single amino acid has no functional use so there is still nothing for natural selection to act upon. So bases must be added randomly until you have a long enough sequence of bases to produce a functional polypeptide and then natural selection can act. Adding bases randomly yield probabilities so infinitesimally small that evolution is mathematically impossible.

It is the secondary infection that usually kills the person infected with HIV so treating the secondary infection prolonged life slightly. It wasn’t until combination therapy was introduced that real selective pressure was put on the virus (unless you count the 20 or so selective pressures you speculate are placed on the virus by the person’s own immune system). This selective pressure has altered the HIV virus. Mutated HIV reproduces at a slow rate than the wild virus.

I know the history, I watched it happen. Support for the secondary infections initially prolonged life only for short periods of time. As time progressed and before triple therapy was begun people were already living longer. The virus was already becoming less virulent before triple therapy was introduced. It mutated because it killed people too fast and less virulent strains were able to be transmitted to others. AZT caused a huge pressure on the virus to mutate. That pressure alone resulted in big changes, not all of which have or can be quantified. Triple therapy has produced changes as well. It continues to do so. Evolution has stopped, though?

Evolution has slowed sufficiently for people who suffer from HIV to live years longer. More effective and additional selection pressures on the virus may cause the virus to go extinct.

It’s not the way I define it, it is the way reality works. Certainly there is an immune response to the virus, antibodies to the virus are detected. However, this immune response is almost universally ineffective. Once the retroviral therapy is initiated, it would not surprise me that the person’s own immune system contributes to the suppression of the virus.

I'm sorry again, but I cannot understand what would possess anyone to think that the immune response is the only host reaction to the presence of the virus and the only selection pressure.

Bottom line........HIV is a bad example.

What????? What other response does a host have beside an immune response to the presence of a virus? Maybe you are talking about the sudden urge a host has to have a cup of chicken soup when exposed to a virus?

He says that selection pressures exist that transform identical genes into different genes.

When one gene is performing a function, it is under selection pressure not to adapt to another function. An unused duplicate copy of that gene, on the other hand, is free to adapt to some other function.

If the unused gene is not functioning, there is no selection.

If, however, having two copies of the same gene is more beneficial than one, the duplicate copy is not likely to adapt to a new use. The second copy is then under selection pressure to perform the same function as the original gene! I know for a fact there are tandem duplicates of tRNA genes in populus trichocarpa and arabidopsis thaliana that maintain their original function for exactly this reason.

So in one case you have no selection and in the other case selection is preventing divergence.

Paul, I did a preliminary study of the 32k case. This case does about 1,000 generations per minute. If this case takes 60,000,000 generations to converge, that would be over 40 days of cpu time. Since I can’t run my computer 24 hours/day, it would take about three months to run this case. Maybe I’ll start running this case a little at a time, just for fun. But that will have to wait until next week.

You all have a Happy Passover and joyous Easter.

 

[Dr Adequate]

Another evolutionist who doesn’t realize his own theory measures fitness by the ability to reproduce.

He evidently understands that perfectly well, you whining lying little freak. You on the other hand, seem to have overlooked the subtle little fact that it's not possible to reproduce when you're dead.

Still, congratulations on thinking of a new lie, it was most entertaining. Got any more?

 

[Dr Adequate]

Now I come to think of it, there are things which reproduce when they're dead.

Creationist arguments.

 

[Mercutio]

Now, now. They aren't dead. They smell that way naturally.










Ok, yeah, dead.

 

[delphi_ote]

Really? A single fatal selection pressure precludes multiple non-fatal selection pressures from slowing evolution? Then explain why the emergence of drug resistance HIV is slowed when multiple drug therapy is used.

As I've repeated many times, it's not the number of selection pressures (you can't really count selection pressures anyway!) The shape of the fitness landscape is what you think you're talking about here. It is possible that the topology of a fitness landscape is too steep (e.g. throwing a population of monkeys in the middle of the Pacific,) but there is no limit to the number of selection pressures to which an organism can adapt. Your theory that eventually there is a limit to the number of selection pressures to which an organism can adapt is total bunk.

Evolutionist have assumed that there is no limit to what natural selection can do.

No, they haven't.

If the unused gene is not functioning, there is no selection.

Which is why I never said the unused gene was nonfunctional. You seem to be grasping at strawmen a lot in this post.

 

[joobz]

Now I come to think of it, there are things which reproduce when they're dead.

resurrection is a central theme to ID isn't it?

 

[Ichneumonwasp]

Another evolutionist who doesn’t realize his own theory measures fitness by the ability to reproduce.

No. The point is that you are focusing on a system which has very special characteristics. Fitness may be affected in many ways. Let's say we have selection pressure one -- wolf. And we have selection pressure two -- big gonads. Little mousie with big gonads who escapes wolf long enough to reproduce before being eaten is fit. Particularly if those big gonads get him into selection pressure three, big colony of sister mice wearing white robes, promising oral sex, and lighting Grail shaped beacons.

Triple therapy for HIV is a very special case. That therapy directly targets replication -- the direct means by which the virus reproduces. There is no way for the virus to escape easily when we specifically target its ability to reproduce directly, not through the indirect means of impacting fitness through depleted resources, or whatever, that we see in nature. That is what Taffer was trying to tell you. That is why I entered this silly exchange in the first place. Triple therapy for HIV does not mimic what we tend to see in nature. It is not an issue of us not understanding what fitness means. It is an issue of us seeing that you are loading the dice in your favor and calling you on it.

None of the treatments for HIV lead to death of the virus, these treatments only limit reproduction of the virus.

And you will need to excuse me for using examples that are not directly applicable to this case in an effort to explain things within a larger context. The whole point of mentioning death scenarios is an attempt to re-orient the discussion toward a more realistic scenario. You cannot use three pressures that directly act on the molecular machinery for reproduction of an organism and pretend that this in some way replicates the natural history of three selection pressures as it relates to evolutionary change (except in very peculiar circumstances).

So why don’t you tell us what the selection pressure is that evolves a gene from the beginning. I keep asking this question of you evolutionists

I've already told you that I'm not playing that game. This discussion concerns your use of a particular example and what you think it shows. Why do you continue to try and switch the emphasis? This is a narrow discussion. You stated that triple therapy for HIV is directly analogous to what occurs in the ev program and by extension to what happens in real life when multiple pressures are put on an organism. I disagree with you. Please stay focused on the issue at hand.

What you don’t seem to realize is that multiple selection conditions even if not fatal confound the evolutionary process.

Confound the evolutionary process? What in the world could that even possibly mean?

In a simple sense, what happens if you get a beneficial mutation for one selection condition and a harmful mutation for another selection condition on the same creature. Is that creature selected for or selected against?

There is simply no way to answer that question based on the information you have provided. It depends on the actual selection pressures involved and chance.

The net result is that evolution is slowed. The virus doesn’t have to win.

What does that mean? Evolution is slowed? I don't see a stop sign sitting over Evolution. There is no slowing of evolution. There is perhaps slowing of this virus. That, in and of itself, is evolution. Your contention is nonsensical and utterly dependent on a teleological framework.

The virus will win. It already is winning. If we do not devise new strategies in the next few decades, then it will prove to be a bigger problem. Thankfully it is not as virulent now. But, there are already people in whom the virus escapes all three therapies, even when the triple therapy approach is changed and they are given a different cocktail. People still die of this disease. Most of them are so sick before the virus "gets through" that they do not spread the infection, though. So we do not currently have a crop of completely drug resistant organisms traipsing about.

It has everything to do with the theory of evolution.

Need I remind you again that we are discussing your emphasis on HIV and triple therapy. Nothing else. I am not playing that game. If we conclude this discussion, then perhaps we may move on to another topic. We need, however, to finish this topic first.

Evolution has slowed sufficiently for people who suffer from HIV to live years longer. More effective and additional selection pressures on the virus may cause the virus to go extinct.

Of course the virus could go extinct. It almost assuredly isn't, but that is beside the point. Please explain to me how the virus going extinct is not "evolution". There is no such thing as "slowing evolution". We can slow an organism down by attacking it. If it survives it may remain relatively dormant, dead, or virulent beyond anything we dreaded because it escapes our selection pressures. Slowing evolution? I have no idea what you are talking about.

What????? What other response does a host have beside an immune response to the presence of a virus? Maybe you are talking about the sudden urge a host has to have a cup of chicken soup when exposed to a virus?

You haven't bothered to notice that HIV is a parasite? Host death is a fairly significant selective pressure on parasites. Host alive means transmission opportunities. Host dead means parasite dead. Rapid host death means limited transmission while long refractory periods means more chances to replicate. Didn't you get the message of why I was speaking about the early years of this disease? We see the same thing with other infectious agents. Syphilis was an absolute scourge before it became less virulent.

 

[Ichneumonwasp]

Since this is getting so unweildy, even for a very limited discussion, here are the main points:

You claim that HIV triple therapy is a good analogy for the three selection pressures seen in the ev program.

I counter with:
1. In human hosts HIV has more than 3 selection pressures. At minimum there is triple therapy (by your definition -- 3 pressures), the host immune response, host longevity. That is a minimum of 5 pressures (167% of your stated 3). I have not even mentioned the competition for transcription and translation within the host between the reverse transcriptase and the normal host machinery -- another set of selection pressures. The reason I mentioned "probably 20", as an underestimate of, selection pressures is because, by your definition, each and every attempt at host transcription that competes with the reverse transcriptase serves as an independent selection pressure. Not a big pressure, but a pressure nonetheless.

2. The peculiar selection pressure(s) exerted by triple therapy do not mimic the typical selection pressures one would see in the wild. These are three very specific selection pressures designed to attack one (really two) specific systems. These systems are directly involved in replication of the virion. Typical selection pressures act indirectly on reproduction and affect fitness through those indirect means. These are also not independent selection pressures as I would assume is modeled in ev. They are linked together specifically by humans to attack the same system. The analogy I made earlier with death of organisms was the closest we see in nature to this paradigm. I can't think of anything else, in nature, that directly affects fitness so thoroughly as immediate death.

ETA
3. Evolution doesn't stop when a species becomes extinct (well, it stops for that species, but evolution itself does not stop). Extinction is a key ingredient in the mix. Multiple synergistic selection pressures, like triple therapy for HIV, have a high chance of leading to extinction of an organism, especially higher organisms. {It won't work for HIV because of the nature of the virus. We need another means of attacking the virus in order to promote its extinction, including better means of preventing infection.} Slowing an organism is not slowing evolution; it is part oand parcel of evolution. If you specifically target an organism's ability to produce offspring, then it will not produce as many offspring and so not produce as many distinct varieties. That is not a slowing of evolution, but an instance of evolution from the host/prey side. It means that the attack on the predator/parasite is effective and nothing else. There is nothing special about the number three. There is something special about directly attacking reproduction. Your example actually argues for the natural selection paradigm -- a perfect instance of fewer offspring, fewer varieties, so less chance for that organism to change over time. It isn't three selection presures that perform this feat. It is a synergistic effect of pressures specifically designed to stop viral replication. We might have been able to do it with one agent if they dang virus weren't so mutable to begin with. We use three not because there is something magical about the number three but because the three agents represent a compromise between toxicity and efficacy.

Therefore, HIV triple therapy is a bad example of a real-world analog to the modelling in ev.

 

[Paul C. Anagnostopoulos]

So, do you still believe that Dr Schneider’s model shows how a human genome could evolve in a billion years give or take a 100% or more? (Let’s not forget world wide populations, interspecies gene transfers and panspermia.)

I believe that's lie #12. You always forget to quote the part where he said "at this rate."

How do you know whether I am planning to run this 32k case? Let’s see, your guess is 18,000,000 generations and my guess is 60,000,000 generations. I’m starting to think this is a good case to run. I’ll have to do this one with the Pascal version of ev. It will probably take about 3 or 4 weeks to run, maybe more since I won’t be able to run the case every day. It would be fun to post intermediate results, kind of like a horse race.

By all means, run it. Rfrequency is getting close to Rcapacity, so it might take longer than my estimate. I certainly don't understand the behavior as Rfrequency approaches Rcapacity. Make sure you don't reach any definitive conclusion unless you run it three or four times, because of the variance.

~~ Paul

 

[kjkent1]

I believe that's lie #12. You always forget to quote the part where he said "at this rate."


By all means, run it. Rfrequency is getting close to Rcapacity, so it might take longer than my estimate. I certainly don't understand the behavior as Rfrequency approaches Rcapacity. Make sure you don't reach any definitive conclusion unless you run it three or four times, because of the variance.

~~ Paul

Paul,

This "Rcapacity" problem that you and Alan keep coming back to is unclear to me. Can you clarify?

 

[Dr Richard]

Since this is getting so unweildy, even for a very limited discussion, here are the main points:

You claim that HIV triple therapy is a good analogy for the three selection pressures seen in the ev program.

I counter with:
1. In human hosts HIV has more than 3 selection pressures...

I would say WAY more than 20 selection pressures acting on HIV.

HIV itself codes for 15 proteins. 15 selection pressures acting immediately as a positive or negative mutation in any gene coding for an expressed protein will affect overall fitness of the virus.

Then consider the basic life cycle of the virus:

HIV Binding to cell membrane
Penetration
Uncoating
Reverse Transcriptase
Integration
Transcription
Translation
Assembly
Extrusion
Maturation

Many of these steps will be affected by the host cell - cell membrane binding for instance, plus, as you mentioned, transcription.

If we assume every HIV protein function has only one host counterpart, that doubles us to 30 selection pressures.

Now consider the host immune response. Diffeerences in host immune response to HIV affect clinical outcome (many refs, see http://www.pnas.org/cgi/content/abstract/94/1/254 for an example) so the human immune system is a selection factor acting upon HIV. We know for instance that some individuals are naturally resistant to HIV.

So, how many genes are involved in the function of the human immune system? I have to admit I don't know; 3000 seems like a reasonable estimate .

This takes us up to 3030 selection pressures.

Now we have to see what happens when the virus spreads. As already pointed out, if the virus kills the host before being allowed to spread, the virus dies. Plus the virus must be secreted into transmissable fluids, and survive in them. Plus the virus must survive directed attempts to stop spread (abstinence, condom use, blood screening). And then it must be able to breach an epithelial membrane and survive in a new host bloodstream.

A conservative estimate now would be about 3050 selection factors.

Compared to Kleinman's three, 3050 would certainly halt evolution dead.

No questions, stops evolution in its tracks.

Which is probably why HIV continues to evolve.

Which is probably why 1% of all newly diagnosed HIV sufferers in the UK are resistant to three antiretrovirals at the time of diagnosis..

Which is probably why Kleinman has to endlessly whine about his "mathematecal proof" that evolution does not exist because the real world demonstrates it ocurring every day.

 

[Paul C. Anagnostopoulos]

This "Rcapacity" problem that you and Alan keep coming back to is unclear to me. Can you clarify?

Rcapacity is a measure of the information carrying capacity of the binding sites. An n-base site can carry 2n bits of information.

Rsequence is a measure of the amount of information required to distinguish the binding sites from the rest of the genome. It is based on the size of the genome and number of binding sites. As the creatures evolve, Rsequence, the measure of the amount of information actually in their binding sites, approaches Rfrequency and then hovers there. The genetic pattern in the binding sites is illustrated by the sequence logo, and the amount of information in the sequence logo is equal to Rsequence.

If Rcapacity < Rfrequency, it becomes very difficult for Rsequence to approach Rfrequency, since the binding sites can't carry Rfrequency bits of information. It's not impossible, just more difficult. All these R variables are irrelevant if any of the mistake count parameters are set to 0, since then you are not trying to distinguish the binding sites from the rest of the genome.

Running Ev experiments where Rcapacity < Rfrequency throws another factor into the model that makes it tenuous to draw conclusions about the number of generations required to evolve a perfect creature.

~~ Paul

 

[Ichneumonwasp]

Thanks Dr. Richard. I was trying to be extremely conservative because of the nature of the debate, but that is an excellent way of explaining it.

I suppose I should keep up on HIV more, but since I don't have to deal with it on a daily basis any longer I don't or I might have know the actual drug resistance info. Thanks again for the excellent post.

 

[delphi_ote]

resurrection is a central theme to ID isn't it?

Easter is right around the corner!

 

[Paul C. Anagnostopoulos]

A little known fact: No evolution happens on Easter Sunday.

~~ Paul

 

[Mr. Scott]

A little known fact: No evolution happens on Easter Sunday.

~~ Paul

Do you mean we probably won't hear from our resident lying creationist, considering his known patterns, until Sunday night?

I recall learning about the HIV "three strikes and it's out" principle too long ago to remember where, so I'm going from memory, but based on my recollections, I think Kleinman is wrong in his interpretation and extrapolation. It's fallacious anyway to extrapolate from a simple virus to evolution of higher life forms (as it is to extrapolate from the misuse of an incomplete model of evolution to assert proof of its impossibility), but even if such extrapolation is valid, he has a fatal problem with the initial point he extrapolates from.

Here's my recollection about 3-strike HIV treatments. Someone correct me if I'm wrong.

We have three anti-HIV drugs. Each of them corresponds to a different point on the same HIV gene. This HIV gene is capable of mutating to defeat each specific attack point of each of these drugs. However, if the gene mutates at all three points of all three anti-HIV drugs, then that gene ceases to perform it's critical reproductive function.

Now, this does not show that three of any selection pressures against any organism stops its evolution. It shows the result of three carefully prepared drugs carefully targeted to three specific points in one specific gene in a specific virus for a specific, carefully planned supression effect. It is intelligently designed, not by god but by scientists who I suspect believe in evolution (oh, the irony). Real world evolution involves a helter-skelter array of selection pressures, not an intelligently designed biochemically choreographed attack.

So, I assert Dr. Kleinman's specious extrapolation of HIV treatments to all of evolution is not evidence that multiple selective pressures halt evolution. It's evidence that a species can be overwhelmed by selective pressures and become extinct. It just so happens that such extinction scenerios are a foundational principle of the theory of evolution (last I heard).

ETA: I see Ichneumonwasp has made this same basic point, which had been on my mind for months now, but decided to express before Kleinman got too carried away. Wish I had time to read every posting to this incredible thread. My regards to Ichneumonwasp, with no intent to steal thunder.

 

[Dr Adequate]

Perhaps he has some sort of primitive taboo against lying during religious holidays.

 

[kleinman]

Annoying Creationists

Did you all have a Happy Passover and joyous Easter?

Really? A single fatal selection pressure precludes multiple non-fatal selection pressures from slowing evolution? Then explain why the emergence of drug resistance HIV is slowed when multiple drug therapy is used.

As I've repeated many times, it's not the number of selection pressures (you can't really count selection pressures anyway!) The shape of the fitness landscape is what you think you're talking about here. It is possible that the topology of a fitness landscape is too steep (e.g. throwing a population of monkeys in the middle of the Pacific,) but there is no limit to the number of selection pressures to which an organism can adapt. Your theory that eventually there is a limit to the number of selection pressures to which an organism can adapt is total bunk.

Too bad your point is not supported by the results from ev or the example of using three selection pressures to treat HIV. Both the theoretical and real examples show that three non-fatal selection pressures profoundly slow the rate of evolution.

Evolutionist have assumed that there is no limit to what natural selection can do.

No, they haven't.

Ok, what is the limit?

If the unused gene is not functioning, there is no selection.

Which is why I never said the unused gene was nonfunctional. You seem to be grasping at strawmen a lot in this post.

So your unused gene is functioning? You tend to use contradictory logic quite often to defend your theory of evolution. The only thing made out of straw in this discussion is your theory of evolution and it is being blown to bits by the mathematics of ev.

Another evolutionist who doesn’t realize his own theory measures fitness by the ability to reproduce.

No. The point is that you are focusing on a system which has very special characteristics. Fitness may be affected in many ways. Let's say we have selection pressure one -- wolf. And we have selection pressure two -- big gonads. Little mousie with big gonads who escapes wolf long enough to reproduce before being eaten is fit. Particularly if those big gonads get him into selection pressure three, big colony of sister mice wearing white robes, promising oral sex, and lighting Grail shaped beacons.

Triple therapy for HIV is a very special case. That therapy directly targets replication -- the direct means by which the virus reproduces. There is no way for the virus to escape easily when we specifically target its ability to reproduce directly, not through the indirect means of impacting fitness through depleted resources, or whatever, that we see in nature. That is what Taffer was trying to tell you. That is why I entered this silly exchange in the first place. Triple therapy for HIV does not mimic what we tend to see in nature. It is not an issue of us not understanding what fitness means. It is an issue of us seeing that you are loading the dice in your favor and calling you on it.

If the causative factor does not affect reproduction, then it is not a selection pressure. It doesn’t matter whether the causative factor affects reproduction directly or indirectly for it to be a selection pressure. An environmental temperature change does not need to directly effect the temperature of a bird’s egg in order to affect the ability of the bird to reproduce.

If you think that multiple selection pressures can speed up evolution, give us some examples.

None of the treatments for HIV lead to death of the virus, these treatments only limit reproduction of the virus.

And you will need to excuse me for using examples that are not directly applicable to this case in an effort to explain things within a larger context. The whole point of mentioning death scenarios is an attempt to re-orient the discussion toward a more realistic scenario. You cannot use three pressures that directly act on the molecular machinery for reproduction of an organism and pretend that this in some way replicates the natural history of three selection pressures as it relates to evolutionary change (except in very peculiar circumstances).

Again, give us examples of multiple selection pressures that speed up evolution. Give us an example of the selection pressure that would evolve a gene from the beginning.

So why don’t you tell us what the selection pressure is that evolves a gene from the beginning. I keep asking this question of you evolutionists

I've already told you that I'm not playing that game. This discussion concerns your use of a particular example and what you think it shows. Why do you continue to try and switch the emphasis? This is a narrow discussion. You stated that triple therapy for HIV is directly analogous to what occurs in the ev program and by extension to what happens in real life when multiple pressures are put on an organism. I disagree with you. Please stay focused on the issue at hand.

No evolutionist will play that game because there are no selection pressures that evolve a gene from the beginning. The issue at hand is the mathematics of mutation and selection. If evolutionists are going to use the slogan “mutation and selection” as the mechanism that leads reptiles to morph into birds and humans and chimpanzees to morph from a primate precursor and claim this is scientific, then you need to describe the selection mechanism(s) that can do this.

What you don’t seem to realize is that multiple selection conditions even if not fatal confound the evolutionary process.

Confound the evolutionary process? What in the world could that even possibly mean?

Confound-to mingle so that the elements cannot be distinguished or separated. Hey Paul, does that sound like your definition for Rcapacity?

In a simple sense, what happens if you get a beneficial mutation for one selection condition and a harmful mutation for another selection condition on the same creature. Is that creature selected for or selected against?

There is simply no way to answer that question based on the information you have provided. It depends on the actual selection pressures involved and chance.

You need to study ev, you will get an education on this topic.

The net result is that evolution is slowed. The virus doesn’t have to win.

What does that mean? Evolution is slowed? I don't see a stop sign sitting over Evolution. There is no slowing of evolution. There is perhaps slowing of this virus. That, in and of itself, is evolution. Your contention is nonsensical and utterly dependent on a teleological framework.

The virus will win. It already is winning. If we do not devise new strategies in the next few decades, then it will prove to be a bigger problem. Thankfully it is not as virulent now. But, there are already people in whom the virus escapes all three therapies, even when the triple therapy approach is changed and they are given a different cocktail. People still die of this disease. Most of them are so sick before the virus "gets through" that they do not spread the infection, though. So we do not currently have a crop of completely drug resistant organisms traipsing about.

You affect evolution by reducing the fitness of the creature. That fitness is measured by the ability of the creature to reproduce. The virus always wins? No viruses go extinct?

It has everything to do with the theory of evolution.

Need I remind you again that we are discussing your emphasis on HIV and triple therapy. Nothing else. I am not playing that game. If we conclude this discussion, then perhaps we may move on to another topic. We need, however, to finish this topic first.

The use of triple antiviral medications to treat HIV is a very nice example of how mutation and selection works. I’m simply playing the evolutionist game by the evolutionist rules. The evolutionist computer model ev shows mathematically the same results as the real example of the treatment of HIV. These examples also show why multiple selection pressures slow evolution.

Evolution has slowed sufficiently for people who suffer from HIV to live years longer. More effective and additional selection pressures on the virus may cause the virus to go extinct.

Of course the virus could go extinct. It almost assuredly isn't, but that is beside the point. Please explain to me how the virus going extinct is not "evolution". There is no such thing as "slowing evolution". We can slow an organism down by attacking it. If it survives it may remain relatively dormant, dead, or virulent beyond anything we dreaded because it escapes our selection pressures. Slowing evolution? I have no idea what you are talking about.

Extinction does not lead to evolution, extinction is the end of a genetic line. The reason you have no idea what I’m talking about is that you don’t understand the mathematics of ev. Ev is an evolutionist written, peer reviewed and published model of random point mutation and natural selection. Once you have an understanding of this model, you will understand my arguments, that is if you don’t go into denial like Paul has.

What????? What other response does a host have beside an immune response to the presence of a virus? Maybe you are talking about the sudden urge a host has to have a cup of chicken soup when exposed to a virus?

You haven't bothered to notice that HIV is a parasite? Host death is a fairly significant selective pressure on parasites. Host alive means transmission opportunities. Host dead means parasite dead. Rapid host death means limited transmission while long refractory periods means more chances to replicate. Didn't you get the message of why I was speaking about the early years of this disease? We see the same thing with other infectious agents. Syphilis was an absolute scourge before it became less virulent.

If parasites kill their host before they can complete their life cycle then they will go extinct. Syphilis is no longer an absolute scourge because of the advent of antibiotics, also the selective pressure on the host has selected out those who can’t mount a strong immune response against the bacteria.

You claim that HIV triple therapy is a good analogy for the three selection pressures seen in the ev program.

I counter with:
1. In human hosts HIV has more than 3 selection pressures. At minimum there is triple therapy (by your definition -- 3 pressures), the host immune response, host longevity. That is a minimum of 5 pressures (167% of your stated 3). I have not even mentioned the competition for transcription and translation within the host between the reverse transcriptase and the normal host machinery -- another set of selection pressures. The reason I mentioned "probably 20", as an underestimate of, selection pressures is because, by your definition, each and every attempt at host transcription that competes with the reverse transcriptase serves as an independent selection pressure. Not a big pressure, but a pressure nonetheless.

Any of the selection pressures you allege are so weak that the sum of all pressures have no affect on the outcome of the disease when compared to the affect of triple antiviral therapy.

2. The peculiar selection pressure(s) exerted by triple therapy do not mimic the typical selection pressures one would see in the wild. These are three very specific selection pressures designed to attack one (really two) specific systems. These systems are directly involved in replication of the virion. Typical selection pressures act indirectly on reproduction and affect fitness through those indirect means. These are also not independent selection pressures as I would assume is modeled in ev. They are linked together specifically by humans to attack the same system. The analogy I made earlier with death of organisms was the closest we see in nature to this paradigm. I can't think of anything else, in nature, that directly affects fitness so thoroughly as immediate death.

You are making a distinction where none exists. A selection pressure by definition is one which affects the ability of a creature to reproduce. Ultimately, all these pressures act somewhere at the genetic level. Whether the pressure acts directly on enzymes involved in reproduction of the genome or at some other metabolic step which is required for the creature to survive, they all affect the fitness of a creature to reproduce. If you starve a creature, you deprive the creature of the required energy and materials needed to reproduce. This is an example of multiple selection pressures. If you deprive a creature of a single essential nutrient, you impair the reproduction of that creature with a single selection pressure.

3. Evolution doesn't stop when a species becomes extinct (well, it stops for that species, but evolution itself does not stop). Extinction is a key ingredient in the mix. Multiple synergistic selection pressures, like triple therapy for HIV, have a high chance of leading to extinction of an organism, especially higher organisms. {It won't work for HIV because of the nature of the virus. We need another means of attacking the virus in order to promote its extinction, including better means of preventing infection.} Slowing an organism is not slowing evolution; it is part oand parcel of evolution. If you specifically target an organism's ability to produce offspring, then it will not produce as many offspring and so not produce as many distinct varieties. That is not a slowing of evolution, but an instance of evolution from the host/prey side. It means that the attack on the predator/parasite is effective and nothing else. There is nothing special about the number three. There is something special about directly attacking reproduction. Your example actually argues for the natural selection paradigm -- a perfect instance of fewer offspring, fewer varieties, so less chance for that organism to change over time. It isn't three selection presures that perform this feat. It is a synergistic effect of pressures specifically designed to stop viral replication. We might have been able to do it with one agent if they dang virus weren't so mutable to begin with. We use three not because there is something magical about the number three but because the three agents represent a compromise between toxicity and efficacy.

Therefore, HIV triple therapy is a bad example of a real-world analog to the modelling in ev.

As I said previously to Delphi, there is nothing special about three selection pressures other than it only takes three selection pressures to profoundly slow evolution. This is what ev shows and this is what the example of triple therapy for HIV shows. Four or more selection pressures only slow the process more so. The more ways you try to select and sort on, the more slowly the process occurs.

So, do you still believe that Dr Schneider’s model shows how a human genome could evolve in a billion years give or take a 100% or more? (Let’s not forget world wide populations, interspecies gene transfers and panspermia.)

I believe that's lie #12. You always forget to quote the part where he said "at this rate."

Silly Paul, “at this rate”, didn’t you forget to mention that this rate is based on a genome only 256 bases long with a mutation rate 100 times faster than you see in HIV. The latest case you ran which evolved the same number of binding sites and loci took over 6 million generations. Plug those numbers into Dr Schneider’s equations an you get 6 trillion years to evolve a human genome. Of course, that still only a 16k genome. What happens when you compute the rate of information gain on a 500k genome?

How do you know whether I am planning to run this 32k case? Let’s see, your guess is 18,000,000 generations and my guess is 60,000,000 generations. I’m starting to think this is a good case to run. I’ll have to do this one with the Pascal version of ev. It will probably take about 3 or 4 weeks to run, maybe more since I won’t be able to run the case every day. It would be fun to post intermediate results, kind of like a horse race.

By all means, run it. Rfrequency is getting close to Rcapacity, so it might take longer than my estimate. I certainly don't understand the behavior as Rfrequency approaches Rcapacity. Make sure you don't reach any definitive conclusion unless you run it three or four times, because of the variance.

I know you don’t understand the mathematics of ev. It is the multiple selection pressures which slow the convergence of the model. As I said previously, this is analogous to a large database sorting problem. The more conditions you try to sort on and the larger the database, the slower the sorting process occurs. Ev can select and sort when the genome is small (a relatively small database) but as the genome is lengthened, the slower the select and sort occurs. If you reduce the number of sorting conditions (reduce the number of selection pressures) you can markedly speed up the process. That is what the mathematics of ev is saying and that effect is demonstrated by the use of triple antiviral medications for the treatment of HIV.

By all means, run it. Rfrequency is getting close to Rcapacity, so it might take longer than my estimate. I certainly don't understand the behavior as Rfrequency approaches Rcapacity. Make sure you don't reach any definitive conclusion unless you run it three or four times, because of the variance.

This "Rcapacity" problem that you and Alan keep coming back to is unclear to me. Can you clarify?

Yes Paul, explain Rcapacity to all of us. If you want, you can use the definition for “confound”.

Compared to Kleinman's three, 3050 would certainly halt evolution dead.

3050 selection pressures? Do you want to explain why 3053 selection pressures works so well at slowing the reproduction of the virus?

Which is probably why 1% of all newly diagnosed HIV sufferers in the UK are resistant to three antiretrovirals at the time of diagnosis..

Which is probably why Kleinman has to endlessly whine about his "mathematecal proof" that evolution does not exist because the real world demonstrates it ocurring every day.

So Dr Richard, are you advocating monotherapy for the treatment of HIV?

This "Rcapacity" problem that you and Alan keep coming back to is unclear to me. Can you clarify?

Rcapacity is a measure of the information carrying capacity of the binding sites. An n-base site can carry 2n bits of information.

Rsequence is a measure of the amount of information required to distinguish the binding sites from the rest of the genome. It is based on the size of the genome and number of binding sites. As the creatures evolve, Rsequence, the measure of the amount of information actually in their binding sites, approaches Rfrequency and then hovers there. The genetic pattern in the binding sites is illustrated by the sequence logo, and the amount of information in the sequence logo is equal to Rsequence.

If Rcapacity < Rfrequency, it becomes very difficult for Rsequence to approach Rfrequency, since the binding sites can't carry Rfrequency bits of information. It's not impossible, just more difficult. All these R variables are irrelevant if any of the mistake count parameters are set to 0, since then you are not trying to distinguish the binding sites from the rest of the genome.

Running Ev experiments where Rcapacity < Rfrequency throws another factor into the model that makes it tenuous to draw conclusions about the number of generations required to evolve a perfect creature.

Set the weight factors for spurious binding sites to 0 and ev has no trouble evolving sequences of bases that satisfy the threshold for the weight matrix no matter how long the genome is. Your binding sites are evolved but you still have spurious binding sites. You haven’t satisfied the other selection conditions. It is the multiple selection conditions which confounds the evolutionary process.

This is a database sorting problem, the more sorting conditions and the larger the database, the slower the process goes. That’s the mathematics that ev demonstrates for the slogan “mutation and natural selection”. This is why the theory of evolution is mathematically impossible. Well that and the fact that there are no selection processes to evolve genes from the beginning.

A little known fact: No evolution happens on Easter Sunday.

Do you mean we probably won't hear from our resident lying creationist, considering his known patterns, until Sunday night?

Mr Scott, I neither need to nor want to lie about this. I have the Dr Schneider’s mathematics, peer reviewed and published which shows exactly why macroevolution does not occur, Easter Sundays or any other day of the week. Ev shows that multiple selection pressures slow and ultimately stop evolution and there are no selection pressures which can evolve a gene from the beginning. The treatment of HIV demonstrates the former and no evolutionists can refute the later.

We have three anti-HIV drugs. Each of them corresponds to a different point on the same HIV gene. This HIV gene is capable of mutating to defeat each specific attack point of each of these drugs. However, if the gene mutates at all three points of all three anti-HIV drugs, then that gene ceases to perform it's critical reproductive function.

That’s not quite right. If the virus succeeds in mutating at all three points, the resultant strain of the HIV virus is a slower reproducing virus than the wild strain of the virus.

Now, this does not show that three of any selection pressures against any organism stops its evolution. It shows the result of three carefully prepared drugs carefully targeted to three specific points in one specific gene in a specific virus for a specific, carefully planned supression effect. It is intelligently designed, not by god but by scientists who I suspect believe in evolution (oh, the irony). Real world evolution involves a helter-skelter array of selection pressures, not an intelligently designed biochemically choreographed attack.

Dr Richard says there are a helter-skelter of 3050 selection pressures against the virus. Doesn’t seem to slow the reproduction of the virus very much. They must not be much of selection pressures. By definition, selection pressures affect the ability of the virus to reproduce. It doesn’t matter whether they are intelligently designed or environmental in origin. The example of the use of triple antiviral therapy for the treatment of HIV is a perfect example how mutation and selection works.

So Mr Scott, do you want to show us how a helter-skelter array of selection pressures speed up evolution?

So, I assert Dr. Kleinman's specious extrapolation of HIV treatments to all of evolution is not evidence that multiple selective pressures halt evolution. It's evidence that a species can be overwhelmed by selective pressures and become extinct. It just so happens that such extinction scenerios are a foundational principle of the theory of evolution (last I heard).

That’s right, multiple selection pressures slow the evolutionary process and can and do lead to extinction. So do you want to explain how a helter-skelter array of selection pressures speed up evolution? Maybe you want to define three different selection conditions that Paul can put into ev and evolve three different sequences of bases that satisfy those conditions. The process is profoundly slow with the selection conditions that Dr Schneider intelligently designed.

What you and the other evolutionists are having trouble seeing is that mutation and selection is analogous to sorting a database. The larger the database and the more sorting conditions, the slower the process goes. It doesn’t matter whether you intelligently design the sorting conditions or whether the sorting conditions are helter-skelter, except that the helter-skelter conditions will be slower. That is what the mathematics of ev is showing and that is what the real example of the treatment of HIV is showing.

I see Ichneumonwasp has made this same basic point, which had been on my mind for months now, but decided to express before Kleinman got too carried away. Wish I had time to read every posting to this incredible thread. My regards to Ichneumonwasp, with no intent to steal thunder.

You are not stealing his thunder, you are stealing his blunder.