Annoying creationists

[Taffer]

Taffer Re post #5745

It was answering Henners' question as asked.

Sorry, yeah, I got that. I meant I didn't get the point of the question. :o

It does highlight something interesting, that in such a situation with very great culling of individuals and unbelievably poor chances of individuals making it to breeding, the evolutionary pressure is infavour of large breeding numbers, even if (as individuals) they are slightly less fit than a smaller number of larger offspring.

If a cod used the same biomass to produce only 100,000 smallfry (instead of 1,000,000), each could be larger, and thus individually probably have better chances of breeding; however if this individual improvement is less than tenfold, the chances of the parent's genes propagating have reduced. Given the size of the brood, this hyothetical improvement must be less than tenfold.

Sure.

For humans the converse is the case. A mother that produced 7x1lb babies in one "brood" would have less chance of any breeding than one who produced 1x7lb baby. Especially considering the extra overheads that would be associated with producing the first example.

This part of the conversation seems more interesting than the kleinmann discussion...

Agreed, it is more interesting. I'm just not quite sure what startling revelation it is making? Maybe I'm missing the point, somewhere.

[kleinman]

Now why don’t you tell us what brings about “emergence of resistance”. If it is not evolution by mutation and selection, what is it?But I was saying that selection does not change the rate of mutation per generation.
You have said that emergence of resistance is not evolution by mutation and selection so what is it?

[Henners]

Let me get this right Kleinman.

You said

That’s why the same mutations appear over and over again when particular selection pressures are put on a population.


As that seemed like biological nonsense to me, I asked:


Do you have a mechanism in mind for how selection processes cause particular mutations?

To which you replied:

Welcome to the discussion. Let’s see if I can clarify this for you. Selection pressures affect a population’s ability to reproduce. If the population is to adapt by mutation and selection, these selection pressures will increase the frequency of mutations which have beneficial affect on the fitness of the population to reproduce. Selection does not cause particular mutations to occur but it does cause beneficial mutations to increase in frequency in the population. So, consider real examples of mutation and selection, the best most well describe example is HIV subjected to drug therapy. What happens when a particular drug is used to treat HIV, resistance to this drug is often identified by particular mutations which appear in high frequency in the population. This affect is used to identify when the viral population has evolved resistance against a particular drug and that therapy has to be changed.


From which I conclude that

(a) No, you haven't a mechanism to explain how your batty ideas operate.

(b) that you didn't even understand the question.

(c) that even if you did, you think that I am stupid enough to believe that flim-flam like that constitutes an answer to the question that I asked about the biologically nonsensical statement that you made.

Now, call me old fashioned, but where I come from that would not qualify as a pass.

Selection pressures do not influence the frequency of mutations.

If you think that they do, then you have fallen down at the very first hurdle of mathematical modelling: UNDERSTANDING THE PROBLEM.

You don't.

Consequently, nothing that you say has any value whatsoever.

[Taffer]

You have said that emergence of resistance is not evolution by mutation and selection so what is it?

When did I say that?

[kleinman]

That’s why the same mutations appear over and over again when particular selection pressures are put on a population.As that seemed like biological nonsense to me, I asked:
That’s because you have no idea how mutation and selection actually works. I’ll again post one of many citations which show that particular selection pressure select for particular mutations.
http://www.blackwell-synergy.com/doi/abs/10.1111/j.1468-1293.2004.00243.x (http://www.blackwell-synergy.com/doi/abs/10.1111/j.1468-1293.2004.00243.x)
Objectives
Abacavir (ABC) selects for four mutations (K65R, L74V, Y115F and M184V) in HIV-1 reverse transcriptase (RT), both in vitro and during monotherapy in vivo. The aim of this analysis was to compare the selection of these and other nucleoside reverse transcriptase inhibitor (NRTI)-associated mutations by ABC-containing therapies in the presence and absence of concurrent lamivudine (3TC) and/or zidovudine (ZDV) and to assess the effect of these mutations on phenotypic susceptibility to the NRTIs.

Design
This study was a retrospective analysis of the patterns of NRTI-associated mutations selected following virological failure in six multicentre trials conducted during the development of ABC.

Methods
Virological failure was defined as confirmed vRNA above 400 HIV-1 RNA copies/mL. RT genotype and phenotype were determined using standard methods.

Results
K65R was selected infrequently by ABC-containing regimens in the absence of ZDV (13 of 127 patients), while L74V/I was selected more frequently (51 of 127 patients). Selection of both K65R and L74V/I was significantly reduced by co-administration of ZDV with ABC (one of 86 and two of 86 patients, respectively). Y115F was uncommon in the absence (seven of 127 patients) or presence (four of 86 patients) of ZDV. M184V was the most frequently selected mutation by ABC alone (24 of 70 patients) and by ABC plus 3TC (48 of 70 patients). Thymidine analogue mutations were associated with ZDV use. The K65R mutation conferred the broadest phenotypic cross-resistance of the mutations studied.

Conclusions
The resistance pathway selected upon virological failure of ABC-containing regimens is significantly altered by concurrent ZDV use, but not by concurrent 3TC use. These data may have important implications for the efficacy of subsequent lines of NRTI therapies.
I’ve highlighted the text in red so you can see explicitly that a particular selection pressure will select for particular mutations. Abacavir (ABC) selects for four mutations (K65R, L74V, Y115F and M184V) in HIV-1 reverse transcriptase (RT), both in vitro and during monotherapy in vivo. This is observed over and over with the use of this drug. I have posted hundreds of other citations which demonstrate this same type of behavior with different selection pressures selecting for particular mutations. This phenomenon is so common that it is used to identify when a population is resistant to a particular selection pressure. I will repost dozens of examples which show this same principle if you still don’t get the message.
You have said that emergence of resistance is not evolution by mutation and selection so what is it?When did I say that?
Taffer, I have a collection of your irrational and illogical statements you have made on this thread. Here are some of them.
One specific point, though. The time to create a triple-resistant mutant is the same in both cases you provided. If you disagree, provide evidence and citations. Until you do, I will trust my own studies, thank you.
You claim that the time to evolve resistance to three selection pressures is the same whether the pressures are sequential or simultaneous. Post your studies.
Triple antiretrovirals have nothing to do with 'macroevolution', nor do they have anything to do with the subject at hand. They are used because three antiretrovirals kill faster then one. They also decrease the risk of any one resistance evolving at a particular time, but it does not decrease the probability of triple resistance mutants arising
It is clear that monotherapy for the treatment of HIV will lead to resistance to that single drug in weeks while use of that same drug in triple drug therapy delays resistance for far longer periods, even years and decades.
To wit: emergence does not mean evolution.
So if emergence of resistance is not evolution by mutation and selection, what is it?
Emergence is not evolution, kleinman. No matter how much you wave your arms, it isn't going to make it so.
So tell us what it is Taffer, if emergence of resistance to drugs is not evolution by mutation and selection, tell us what it is. Then tell us why when combination therapy is used, it profoundly slows the evolution of resistance.

You are claiming that emergence of drug resistance is not evolution by mutation and selection and you have done this several times on this thread. If it is not evolution by mutation and selection, what is it?

For someone who is a graduate student in phylogenetics, you are demonstrating a very shallow understanding of your field.

[Paul C. Anagnostopoulos]

It is only natural to select the definition for “goal” from my Random House dictionary.

that toward which effort is directed; aim or end.

We better check if “effort” implies forethought.
Uh, effort doesn't imply forethought, but directed certainly does.


So then, why does water always flow to the lowest point? It is because that is what happens when the force of gravity exerts if force on water and this is a predictable when you understand that cause and effect relationship of gravity on matter, ...
I have no problem with cause and effect, Alan. My problem is with goal.


There are specific goals to these cause and affect relationships that are measured and repeatable. Goals do not require forethought.
Okay, sure, use goal that way. What difference will a little more misunderstanding make to your argument, anyway?


Perhaps another simple drawing will help you understand why these “perfect creature” optima are not being located in these circumstances.
You can talk about landscapes all you want. You are not answering my question about Rcapacity.


Paul, consider the following series from ev. Dr Schneider’s basic case is used and then mutation rate is increased by 1 mutation per genome/generation. You obtain the following generations for convergence.
Mutation Rate/generations for perfect creature
1/662
2/572
3/1225
4/5523
5/5,000,000 no perfect creature
Why does this model suddenly stop converging when the mutation rate goes to 5 mutations per genome per generation for this series? Is it the information content of the binding sites? Is there an Mcapacity factor?
The rate of mutations per base is too high to allow convergence. The genome is effectively scrambled on each generation.


Of course I acknowledge that ev stops converging to a perfect creature under a wide variety of circumstances but it has nothing to do with your irrational and illogical concept of the information content of a binding site.
So you don't think there is an issue with trying to cram Rfrequency bits of information in a binding site that allows fewer than that number of bits? I guess you don't, or you would not label the idea "irrational and illogical." Could you explain how Rfrequency bits of information are compressed into fewer than Rfrequency bits, except by trial and error? The data compression folks might be interested.


I can not explain the logical behavior of mutation and selection with your illogical concept of Rcapacity, but hey, your entire theory of evolution is based on speculation and extrapolation, why should you try logic now?
Ah, so you can't explain it. All you can do is accuse me of being irrational and illogical and continue to repeat your fitness landscape mantra.


This is your illogical hypothesis Paul; explain to us how the number of bits in the sequence logo affects the ability of the ev model to find a trajectory to a local optimum on the fitness landscape, a fitness landscape which you admit had perfect creature local optima?
All righty then, I'll explain it for the sixth or seventh time. You see, the binding sites require a pattern with approximately Rfrequency bits of information in order to distinguish them from all the other positions on the genome. If the binding sites are too narrow to contain Rfrequency bits, then it becomes exceedingly difficult to find such a pattern.

Rather than simply ranting "irrational and illogical," perhaps you could explain why this Rcapacity problem doesn't matter.

~~ Paul

[delphi_ote]

If he hasn't managed to figure out the forum formatting so far, do you really think he'll ever figure out evolution? :slp:

[kleinman]

It is only natural to select the definition for “goal” from my Random House dictionary.

that toward which effort is directed; aim or end.

We better check if “effort” implies forethought.Uh, effort doesn't imply forethought, but directed certainly does.
Paul, are you sure you want to discuss this topic? You think that directed effort requires forethought? Your own example of gravity and water now implies that gravity has forethought because gravity also has direction.
So then, why does water always flow to the lowest point? It is because that is what happens when the force of gravity exerts if force on water and this is a predictable when you understand that cause and effect relationship of gravity on matter, ... I have no problem with cause and effect, Alan. My problem is with goal.
The point of this discussion is whether mutation and selection as a cause and effect phenomenon has the fitness of the population as the consequence or goal of this phenomenon. What the mutation and selection phenomenon does is drive the population to different positions on the fitness landscape with the fitness of the population as the goal. You use the number of mistakes (fitness of the population) to determine which creatures reproduce in your own computer simulation. We can play around with the semantics as long as you want until you understand the governing cause and effect relationship in your own computer model. Haven’t you noticed that when you start your model with the same input parameters, it converges exactly the same way each time your run the model?
There are specific goals to these cause and affect relationships that are measured and repeatable. Goals do not require forethought.Okay, sure, use goal that way. What difference will a little more misunderstanding make to your argument, anyway?
You and others are arguing that the mutation and selection process has no “goal”. Not only does your own model converge to the same values when you use the identical input parameters, real examples of mutation and selection behave the same way. Once you established the fitness landscape and established the initial conditions for the mutation and selection process, you have profoundly limited the trajectories that population can take on the fitness landscape. Evolutionists have no comprehension that there are limitations to the trajectories that populations can take when being driven by selection pressures on a fitness landscape. Your have seen in your imagination common descent, the only problem is mutation and selection can’t do what you imagine. It is a much more limited phenomenon. Now if you want an example of misunderstanding, keep telling us how Rcapacity is the reason ev doesn’t converge.
Perhaps another simple drawing will help you understand why these “perfect creature” optima are not being located in these circumstances.You can talk about landscapes all you want. You are not answering my question about Rcapacity.
Hey Paul, Rcapacity is your fantasy trip. You can’t recognize that evolution by mutation and selection is simply an optimization problem. You realize that even if Rfrequency exceeds Rcapacity that there are still sequences of bases that will give perfect creature optima. The simple reality is that the population in ev can not evolve to those perfect creature optima unless the model starts at point on the fitness landscape that lets it take a trajectory to one of those optima. Map out the landscape and you will understand.
Paul, consider the following series from ev. Dr Schneider’s basic case is used and then mutation rate is increased by 1 mutation per genome/generation. You obtain the following generations for convergence.
Mutation Rate/generations for perfect creature
1/662
2/572
3/1225
4/5523
5/5,000,000 no perfect creature
Why does this model suddenly stop converging when the mutation rate goes to 5 mutations per genome per generation for this series? Is it the information content of the binding sites? Is there an Mcapacity factor?The rate of mutations per base is too high to allow convergence. The genome is effectively scrambled on each generation.
You can talk all you want about scrambling. Why does it suddenly not converge? You are not answering my question. There is a Mcapacity factory which prevents the model from converging.
Of course I acknowledge that ev stops converging to a perfect creature under a wide variety of circumstances but it has nothing to do with your irrational and illogical concept of the information content of a binding site.So you don't think there is an issue with trying to cram Rfrequency bits of information in a binding site that allows fewer than that number of bits? I guess you don't, or you would not label the idea "irrational and illogical." Could you explain how Rfrequency bits of information are compressed into fewer than Rfrequency bits, except by trial and error? The data compression folks might be interested.
This is not about cramming information into a binding site; it is about finding a trajectory on a fitness landscape. The appearance of a fitness landscape is extremely sensitive to the number of selection pressures. This is why the ev model easily satisfies any of the three selection conditions individually. I don’t mind talking about this issue for years. The only thing that will happen is more empirical evidence of how mutation and selection actually works will become available. You will never come up with an example of multiple selection pressures being applied simultaneously accelerating evolution.
I can not explain the logical behavior of mutation and selection with your illogical concept of Rcapacity, but hey, your entire theory of evolution is based on speculation and extrapolation, why should you try logic now?Ah, so you can't explain it. All you can do is accuse me of being irrational and illogical and continue to repeat your fitness landscape mantra.
Hey Paul, when are you going to explain why ev doesn’t converge when the Mcapacity value is reached? Are you going to chant “scrambled, scrambled, scrambled”?
This is your illogical hypothesis Paul; explain to us how the number of bits in the sequence logo affects the ability of the ev model to find a trajectory to a local optimum on the fitness landscape, a fitness landscape which you admit had perfect creature local optima?All righty then, I'll explain it for the sixth or seventh time. You see, the binding sites require a pattern with approximately Rfrequency bits of information in order to distinguish them from all the other positions on the genome. If the binding sites are too narrow to contain Rfrequency bits, then it becomes exceedingly difficult to find such a pattern.
You left out the part that ev does converge to a local optimum and that perfect creature optima do exist on the fitness landscape. So are you going to tell us there are no trajectories to those perfect creature local optima?
Rather than simply ranting "irrational and illogical," perhaps you could explain why this Rcapacity problem doesn't matter.
Now Paul, how could I think that something you say doesn’t matter even though it just represents another problem for mutation and selection converging rapidly for multiple selection conditions?
If he hasn't managed to figure out the forum formatting so far, do you really think he'll ever figure out evolution?
Delphi, I realize I’m only Y1K compliant but I do enjoy using a broad sword on your theory of evolution. Hey, did I ever thank you for introducing the concept of fitness landscape into this discussion? I’m sure you have endeared yourself to evolutionists all over the fitness landscape. Did you ever get your sock drawer organized?

[Taffer]

Taffer, I have a collection of your irrational and illogical statements you have made on this thread. Here are some of them.

Oh goodie.

You claim that the time to evolve resistance to three selection pressures is the same whether the pressures are sequential or simultaneous. Post your studies.

Why would I need to? It follows logically that the time to produce three point mutations, for example, is the same whether we are looking for all three mutations at once or one after another.

It is clear that monotherapy for the treatment of HIV will lead to resistance to that single drug in weeks while use of that same drug in triple drug therapy delays resistance for far longer periods, even years and decades.

Of course it is. And as I've said many times, this is because you are comparing three drugs versus one drug. You have to compare three drugs sequentually versus three drugs in parallel. Have you done that?

So if emergence of resistance is not evolution by mutation and selection, what is it?

Evolution is the change in allele frequencies over time. You are talking about the time until one particular mutation happens, which is unaffected by selective pressures. Hence why I use the term "emergence".

So tell us what it is Taffer, if emergence of resistance to drugs is not evolution by mutation and selection, tell us what it is.

You really are an idiot. I have stated, multiple times, that all the papers you cite show is that the time until the mutations which give rise to resistance to all the drugs in the trial increases as you add more drugs. Anyone with even a hint of scientific knowledge will understand that mutation rate is unaffected by selective pressures. This is why I made a clear difference between emergence and evolution. The time until a mutation occurs in evolution has nothing to do with evolution. Evolution acts on existing variation within a population. My point is, and always has been, that once the mutation arises, the more selective pressure on the population, the faster the allele or alleles will move to fixation. You are trying to equate the time until one mutation happens with the time until three mutations happen, then claim that evolution has been slowed down.

Then tell us why when combination therapy is used, it profoundly slows the evolution of resistance.

It doesn't slow evolution. It slows emergence. The time until resistance to all drugs naturally increases as you add more drugs. Any simpleton can see this. Any simpleton can also see that this has nothing to do with the change in allele frequency of already existant variation.

You are claiming that emergence of drug resistance is not evolution by mutation and selection and you have done this several times on this thread. If it is not evolution by mutation and selection, what is it?

Emergence of the mutations which lead to drug resistance is unrelated to selection. The change in allele frequencies of these mutations is.

For someone who is a graduate student in phylogenetics, you are demonstrating a very shallow understanding of your field.

For someone who has found a mathematical disproof of evolution, you are demonstrating a very shallow understanding of reality.

[delphi_ote]

Delphi, I realize I’m only Y1K compliant but I do enjoy using a broad sword on your theory of evolution. Hey, did I ever thank you for introducing the concept of fitness landscape into this discussion? I’m sure you have endeared yourself to evolutionists all over the fitness landscape. Did you ever get your sock drawer organized?
I felt a great disturbance in my head, as if millions of brain cells suddenly cried out in terror and were suddenly silenced. I fear something terrible has happened.

[Kotatsu]

That’s not quite correct.
1. Multiple selection pressures profoundly slow evolution.
2. Natural environments contain multiple selection pressures, none of which will evolve a gene de novo or drive the enormous transformation necessary to transform reptiles into bird.
3. Therefore, natural evolution is a much more limited process than speculated and extrapolated by evolutionists.

Nonsense. I have already provided you with a list of possible selection pressures which would do exactly that. You have not yet been able to show either that they are all nonexistant pressures, or that none of them, nor a combination of several or all of them, would be insufficient to make some reptiles evolve into birds. Further, even if the examples I listed would not be sufficient, you have not yet shown any line of reasoning or evidence that no amount of selection pressures which could feasily evolve reptiles into birds. In short, the statement highlighted in red in the quote above is a so far unsupported assertion. My guess is that it will remain unsupported for the remainder of your participation of this thread, and indeed possibly for the remainder of your life.

What I am talking about is when you look a reptiles you see birds.

The reverse is obvious to anyone who has ever been in close contact with birds (1). Just look at a Locustella, a secretary bird or an ostrich and tell me they do not resemble dinosaurs in movement, posture, behaviour and even base anatomy.

---
(1) Eating them does not necessarily count.

[Belz...]

What is the “this” are you talking about?

You must've sucked in English classes.

The "this" is the discussion. Oh, that's right. It's now just a flame wars with you.

So far, the only point you have made is that something only becomes true when it is published in a “peer reviewed” journal.

I haven't made that point. Can I yell "strawman", now ?

Then why to you subscribe to the view that reptiles evolve into birds? You have no mathematical or empirical evidence that mutation and selection can accomplish such a process.

And yet we have empirical evidence that it DID happen. So obviously something's wrong, here.

The only things you have are vague speculations and extrapolations. Mutation and selection simply does not work the way you evolutionists speculate and extrapolate.

Yeah, it MUST work the way you creationists speculate and extrapolate.

The mathematical behavior of ev and the numerous real examples of mutation and selection are not something that came out of my imagination. The former is a peer reviewed and published mathematical model and the later are measurements of mutation and selection performed by numerous scientists studying and measuring how mutation and selection actually works. Now the concept of common descent, which is something out of the imagination, does not stand up to scientific scrutiny because mutation and selection does not work that way.

That's a lot of words but it doesn't answer my question: why haven't the scientists thrown the theory of evolution out the window and publicly stated that they're working on something new ?

I don’t need to make such arguments

Yeah, we noticed.

Mutation and selection as an explanation for common descent loses to reality 4^G to 0 because 4^G describes the size of the fitness landscape and the search for multiple optima on a search space this size is profoundly slow on all but unrealistically small values of G.

Did you even READ what I said ? I said I can come up with a nth-dimensional computer model. Does that mean that reality "loses" to mathematics and is suddenly n-dimensional ?

Where is your logic? The only logic you have demonstrated is that something only becomes true when it is posted in a peer reviewed journal.

That's another bunch of words that STILL doesn't answer my point: do you think that logically impossible is the worst kind of impossible ?

Watch and see what happens.

If this is like the vaunted second coming we're going to have to wait a LOOOooong time.

Oh, I see, now you are saying that reptiles did not transform into birds? So where did birds come from?

Are you dishonest on purpose, now ? Or are you doing it unconsciously ?

You said:

"do you see reptiles transforming into birds?"

And I said this is a strawman. Obviously, I don't see reptiles transforming into birds, whatever the hell that means.

I do understand how they evolved over time, however, something that I know you can't accept because the Bibble says the world was created in six days. But if you believe what every book says, you're in a lot of trouble.

Well Belz, do you want to explain to us why particular selection pressures lead to particular mutations increasing in frequency in populations?

It's not because they have a goal, that's for sure. You seem to be stuck with Lamarckism, which is not only wierd and magical but also two centuries out of date. Selection is not an entity, it's the result of the organism's reproduction, itself the result of the fact it survives, eats enough food and finds a fertile mate (or splits in two, whatever the case).

Now Belz, just because you are annoyed does not mean you can use asterisks, that’s a violation of the member agreement.

No, it's not. The word censor worked fine, that time. I didn't do anything to circumvent it. You should read YOUR membership agreement.

What I am talking about is when you look a reptiles you see birds. Belz, here is another example of how mutation and selection works.

When you look a reptiles you see birds. What the hell does that mean, now ?

Do you deny that birds have distinctly reptilian characteristics ?

And what's this ?

http://forums.randi.org/imagehosting/thum_608047022eae7e563.jpg (http://forums.randi.org/vbimghost.php?do=displayimg&imgid=8609)

[Belz...]

I felt a great disturbance in my head, as if millions of brain cells suddenly cried out in terror and were suddenly silenced. I fear something terrible has happened.

If Klein's theory was correct, he'd have been wiped out by selection, by now.

[Belz...]

I have stated, multiple times, that all the papers you cite show is that the time until the mutations which give rise to resistance to all the drugs in the trial increases as you add more drugs. Anyone with even a hint of scientific knowledge will understand that mutation rate is unaffected by selective pressures. This is why I made a clear difference between emergence and evolution. The time until a mutation occurs in evolution has nothing to do with evolution. Evolution acts on existing variation within a population. My point is, and always has been, that once the mutation arises, the more selective pressure on the population, the faster the allele or alleles will move to fixation. You are trying to equate the time until one mutation happens with the time until three mutations happen, then claim that evolution has been slowed down.

DRBUNK'D!

[Paul C. Anagnostopoulos]

Paul, are you sure you want to discuss this topic? You think that directed effort requires forethought? Your own example of gravity and water now implies that gravity has forethought because gravity also has direction.
It has a direction, but it is not directed in the sense of seeking a goal. The direction arises from mindless application of physical laws.


You can talk all you want about scrambling. Why does it suddenly not converge? You are not answering my question. There is a Mcapacity factory which prevents the model from converging.
I answered your question precisely. The mutational load eliminates progress toward a perfect creature by scrambling the genome on each generation. It has nothing to do with a capacity, so Mcapacity is a misnomer. There certainly is mathematics to describe the problem:

http://en.wikipedia.org/wiki/Genetic_load


This is not about cramming information into a binding site; it is about finding a trajectory on a fitness landscape.
Yeah, I didn't think you'd try to explain how to compress Mfrequency bits of information into a binding site that is too narrow.


Hey Paul, when are you going to explain why ev doesn’t converge when the Mcapacity value is reached?
I've explained it numerous times. Either you are not paying attention or you don't understand it.


You left out the part that ev does converge to a local optimum and that perfect creature optima do exist on the fitness landscape. So are you going to tell us there are no trajectories to those perfect creature local optima?
No, as I've repeated many times, I am not claiming that it is impossible to evolve a perfect creature when Rcapacity is exceeeded. <-- Please take note. I am saying that it becomes precipitously difficult.


Now Paul, how could I think that something you say doesn’t matter even though it just represents another problem for mutation and selection converging rapidly for multiple selection conditions?
First you called the Rcapacity concept "irrational and illogical," but now you're saying it matters. You're a dodgeball master.

~~ Paul

[kjkent1]

Yes, I have seen all your examples of multiple selection pressures accelerating evolution. The sheer magnitude of all your citations overwhelms my measly hundreds of examples which show that combination selection pressures profoundly slow evolution. And let’s not forget your mathematical model which demonstrates your point of view. How could we forget your powerful mathematical argument?Condescension is boring, Alan -- it only proves you're an internet troll -- or an intellectual coward, for refusing to directly deal with my evidence.

I'm using the same model as you: ev. Two experiments performed by me, using ev, and posted in this thread, show serious defects in your analysis, which you cannot overcome by compounding your evidence in response, and then declaring yourself the winner via the size of your evidence pile (and, it is definitely, a "pile"). Changing the weights in ev, without turning a particular selection pressure off, changes the generational time to convergence. Therefore, according to ev, selective pressure intensity matters, it can change the rate of evolution, and NOTHING in any of your evidence, thus far considers this inescapable fact.

I'm certain you know what the limit of a function is, so you should have no trouble understanding the concept that the relative intensity of a selective pressure could easily cause only one pressure in a particular environment to dominate evolutionary activity to the point where it would render all other pressures meaningless.

So, at a minimum, your landscape model has another dimension, the importance of which you refuse to acknowledge and deal with.

None of your citations demonstrates that mutation is stopped, regardless of the selective pressures applied. Mutations remain substantially random and unpredictable. Ev does not consider anything other than point mutation. The fossil record shows evidence of evolutionary change. Genetic evidence, such as the K172 bacteria frame shift and the fusion of the 1st and 2nd chromosome in humans shows that large scale mutations occur and that they cause dramatic morphological change.

All of the above clearly demonstrates why no one takes you seriously, except yourself. If that's what you enjoy, then hang out in Clovis Urgent Care, and pretend to be important by posting on randi.org.

If you want to make a contribution to science and to society, then stop acting like a schmuck and start acting your age, doctor.

[kleinman]

You claim that the time to evolve resistance to three selection pressures is the same whether the pressures are sequential or simultaneous. Post your studies.Why would I need to? It follows logically that the time to produce three point mutations, for example, is the same whether we are looking for all three mutations at once or one after another.
You had better learn the facts before you take your exams.
It is clear that monotherapy for the treatment of HIV will lead to resistance to that single drug in weeks while use of that same drug in triple drug therapy delays resistance for far longer periods, even years and decades.Of course it is. And as I've said many times, this is because you are comparing three drugs versus one drug. You have to compare three drugs sequentually versus three drugs in parallel. Have you done that?
That’s the point Taffer; combination therapy profoundly slows the evolutionary process. If you had any understanding of the mathematics of mutation and selection you would know that it doesn’t take huge populations to evolve by mutation and selection to single selection pressures, however even with huge populations it is still extremely difficult to evolve to more than a single selection pressure. With respects to drugs administered sequentially versus concurrently, I have posted numerous studies where those very things have been done. What these studies show is that sequential use of selection pressures allows much more rapid evolution to the selection pressures than if the same selection pressures are applied concurrently. Do you want me to repost these studies?
So if emergence of resistance is not evolution by mutation and selection, what is it?Evolution is the change in allele frequencies over time. You are talking about the time until one particular mutation happens, which is unaffected by selective pressures. Hence why I use the term "emergence".
Isn’t that interesting, an evolutionist with a narrow definition for the word “evolution”. What you are missing is that when there is only a single selection pressure, the “emergence” of that single beneficial mutation occurs much more quickly and can be propagated in the population than when there are combination selection pressures requiring the “emergence” of multiple beneficial mutations simultaneously in order for them to be propagated through the population. You aren’t going to avoid the way mutation and selection actually works by playing semantics. Your theory of evolution by mutation and selection is mathematically impossible and using a narrow definition for the word “evolution” won’t change the mathematical and empirical facts of the way mutation and selection actually works. You have some homework to do before you take your exams.
Delphi, I realize I’m only Y1K compliant but I do enjoy using a broad sword on your theory of evolution. Hey, did I ever thank you for introducing the concept of fitness landscape into this discussion? I’m sure you have endeared yourself to evolutionists all over the fitness landscape. Did you ever get your sock drawer organized?I felt a great disturbance in my head, as if millions of brain cells suddenly cried out in terror and were suddenly silenced. I fear something terrible has happened.
Delphi, I keep telling you to lay off the sterno, otherwise you would have more than millions of brain cells, but let me reassure you, understanding how mutation and selection actually works it not a terrible thing.
That’s not quite correct.
1. Multiple selection pressures profoundly slow evolution.
2. Natural environments contain multiple selection pressures, none of which will evolve a gene de novo or drive the enormous transformation necessary to transform reptiles into bird.
3. Therefore, natural evolution is a much more limited process than speculated and extrapolated by evolutionists. Nonsense. I have already provided you with a list of possible selection pressures which would do exactly that. You have not yet been able to show either that they are all nonexistant pressures, or that none of them, nor a combination of several or all of them, would be insufficient to make some reptiles evolve into birds. Further, even if the examples I listed would not be sufficient, you have not yet shown any line of reasoning or evidence that no amount of selection pressures which could feasily evolve reptiles into birds. In short, the statement highlighted in red in the quote above is a so far unsupported assertion. My guess is that it will remain unsupported for the remainder of your participation of this thread, and indeed possibly for the remainder of your life.
That’s right; you did say that a predator chasing a reptile into a tree would make it beneficial for the reptile to grow wings. Doesn’t that logic turn the mathematics and empirical data which describes how mutation and selection actually works on its head.
What I am talking about is when you look a reptiles you see birds.The reverse is obvious to anyone who has ever been in close contact with birds (1). Just look at a Locustella, a secretary bird or an ostrich and tell me they do not resemble dinosaurs in movement, posture, behaviour and even base anatomy.
So when you look at birds you have reptileopomorphism? You know, you are correct, the last time I saw Jurrasic Park, the T Rex does walk just like an ostrich. I didn’t realize you had so much scientific evidence.
(1) Eating them does not necessarily count.
Is it true that when T Rex is properly prepared it tastes just like chicken?
What is the “this” are you talking about?You must've sucked in English classes.

The "this" is the discussion. Oh, that's right. It's now just a flame wars with you.
You is korrect Blz, I twartnt a ingish mager n kollige but me did dew gud in arithmatac.

You are also correct; we are having flame broiled theory of evolution at this BBQ.
So far, the only point you have made is that something only becomes true when it is published in a “peer reviewed” journal.I haven't made that point. Can I yell "strawman", now ?
Oh no, the strawman argument! What can I do? How about I post some more citations which show how mutation and selection actually works, see below.
Then why to you subscribe to the view that reptiles evolve into birds? You have no mathematical or empirical evidence that mutation and selection can accomplish such a process.And yet we have empirical evidence that it DID happen. So obviously something's wrong, here.
That empirical evidence has nothing to do with mutation and selection and has no mathematical basis. What’s wrong here is the evolutionist interpretation of the fossil record but that’s a discussion for another thread.
The only things you have are vague speculations and extrapolations. Mutation and selection simply does not work the way you evolutionists speculate and extrapolate.Yeah, it MUST work the way you creationists speculate and extrapolate.
No Belz, we look at the mathematical and empirical evidence which shows how mutation and selection actually works and it doesn’t work the way evolutionists speculate and extrapolate.
The mathematical behavior of ev and the numerous real examples of mutation and selection are not something that came out of my imagination. The former is a peer reviewed and published mathematical model and the later are measurements of mutation and selection performed by numerous scientists studying and measuring how mutation and selection actually works. Now the concept of common descent, which is something out of the imagination, does not stand up to scientific scrutiny because mutation and selection does not work that way.That's a lot of words but it doesn't answer my question: why haven't the scientists thrown the theory of evolution out the window and publicly stated that they're working on something new ?
It has only been a few years since genetic sequencing could be done with any speed or accuracy. In addition, mathematical models of mutation and selection have not been around for long either and the computational power to properly analyze these models has only been available for a few years as well. You have multiple technological improvements occurring simultaneously which enable better analysis of the mutation and selection process. It is these kinds of advances which discredit the concept of common descent. The concept of evolution by mutation and selection will not be discarded; it will just be better understood as a much more limited process than can not accomplish common descent.
Mutation and selection as an explanation for common descent loses to reality 4^G to 0 because 4^G describes the size of the fitness landscape and the search for multiple optima on a search space this size is profoundly slow on all but unrealistically small values of G.Did you even READ what I said ? I said I can come up with a nth-dimensional computer model. Does that mean that reality "loses" to mathematics and is suddenly n-dimensional ?
Belz, the mathematics agrees with the reality. Mathematically, combination selection pressures profoundly slow the evolutionary process and reality shows the same result.
Watch and see what happens.If this is like the vaunted second coming we're going to have to wait a LOOOooong time.
That’s not what I was suggesting that you watch for, I was suggesting you watch and see what happens as more and more empirical results show that combination selection pressures slow the evolutionary process by mutation and selection. It is this kind of evidence which contradicts the concept of common descent.
"do you see reptiles transforming into birds?"I do understand how they evolved over time, however, something that I know you can't accept because the Bibble says the world was created in six days. But if you believe what every book says, you're in a lot of trouble.
Your imagination shows reptiles transforming into birds but the mathematics and empirical facts which show how mutation and selection actually works shows that what you are imagining is mathematically and empirically impossible. Mutation and selection simply doesn’t work that way.
Well Belz, do you want to explain to us why particular selection pressures lead to particular mutations increasing in frequency in populations?It's not because they have a goal, that's for sure. You seem to be stuck with Lamarckism, which is not only wierd and magical but also two centuries out of date. Selection is not an entity, it's the result of the organism's reproduction, itself the result of the fact it survives, eats enough food and finds a fertile mate (or splits in two, whatever the case).
The facts are that particular selection pressures lead to particular base substitutions increasing in frequency in the gene pool. The cause and effect relationship of mutation and selection lead to repeatable results when the identical starting conditions and selection pressures are used.
Now Belz, just because you are annoyed does not mean you can use asterisks, that’s a violation of the member agreement.No, it's not. The word censor worked fine, that time. I didn't do anything to circumvent it. You should read YOUR membership agreement.
Ok
http://forums.randi.org/showthread.php?t=90347&highlight=agreement (http://forums.randi.org/showthread.php?t=90347&highlight=agreement)
10. You will not swear in your posts. This includes using swear words in a disguised form, for example, by replacing certain letters in the word with another letter, character, or image.
How about this one?
11. Posts must be on topic to the thread subject. On this Forum thread drift is expected but must follow from the discussion.
Belz, when was the last time you talked about mutation and selection?

Belz, as far as I am concerned, you can say whatever you want but so far, none of what you have said has anything to do with mutation and selection. You have shown that you know nothing about the topic but asterisk away.
What I am talking about is when you look at reptiles you see birds. Belz, here is another example of how mutation and selection works.When you look a reptiles you see birds. What the hell does that mean, now ?
Why Belz, that’s aviopomorphism.
Do you deny that birds have distinctly reptilian characteristics ?
Belz, you are seeing what you want to see, reptiles can not transform into birds by mutation and selection. It is mathematically and empirically impossible. Mutation and selection simply does not work that way.
And what's this ?http://forums.randi.org/imagehosting/thum_608047022eae7e563.jpg
An evolutionist Rorschach test.
I felt a great disturbance in my head, as if millions of brain cells suddenly cried out in terror and were suddenly silenced. I fear something terrible has happened.If Klein's theory was correct, he'd have been wiped out by selection, by now.
You got it wrong again Belz; combination selection pressures profoundly slow the evolutionary process. All the selection pressures applied by you evolutionists have not caused extinction and the goalposts have not evolved to a new local optimum.
Paul, are you sure you want to discuss this topic? You think that directed effort requires forethought? Your own example of gravity and water now implies that gravity has forethought because gravity also has direction.It has a direction, but it is not directed in the sense of seeking a goal. The direction arises from mindless application of physical laws.
Paul, the goal is the optimum fitness for the population. Selection gives direction to a local optimum. Once that point on the fitness landscape is attained, the selection pressure prevents it from moving to another local optimum unless another selection pressure changes the fitness landscape. The ultimate endpoint to these cause and effect relationships is equilibrium. It doesn’t require forethought for this goal to be attained.
You can talk all you want about scrambling. Why does it suddenly not converge? You are not answering my question. There is a Mcapacity factory which prevents the model from converging.I answered your question precisely. The mutational load eliminates progress toward a perfect creature by scrambling the genome on each generation. It has nothing to do with a capacity, so Mcapacity is a misnomer. There certainly is mathematics to describe the problem:
So let’s see what your link http://en.wikipedia.org/wiki/Genetic_load (http://en.wikipedia.org/wiki/Genetic_load) has to say:
In population genetics, genetic load or genetic burden is a measure of the cost of lost alleles due to selection (selectional load) or mutation (mutational load).
Looks like Mcapacity is a real affect, you are loading a genome to its capacity of mutations. Now why don’t you give us a Wikipedia reference to Rcapacity and show us that it has nothing to do with the shape of the fitness landscape and the starting point for finding a trajectory to a perfect creature local optimum.
This is not about cramming information into a binding site; it is about finding a trajectory on a fitness landscape.Yeah, I didn't think you'd try to explain how to compress Mfrequency bits of information into a binding site that is too narrow.
Paul, someday you will understand that evolution by mutation and selection is simply an optimization problem and that the mathematical behavior of these problems is extremely sensitive to the number of optimization conditions. Making up terms like Rcapacity will not explain away the mathematical behavior of these types of problems, but I do like watching you go through your contortionist act as you try to squirm out of what your own model shows you.
Hey Paul, when are you going to explain why ev doesn’t converge when the Mcapacity value is reached?I've explained it numerous times. Either you are not paying attention or you don't understand it.
Yes, it is the Mcapacity affect; it is the capacity of the genome to take a load of mutations. Now what is it again that the Rcapacity affect? What is it that the genome can’t take a load of?
You left out the part that ev does converge to a local optimum and that perfect creature optima do exist on the fitness landscape. So are you going to tell us there are no trajectories to those perfect creature local optima?No, as I've repeated many times, I am not claiming that it is impossible to evolve a perfect creature when Rcapacity is exceeeded. <-- Please take note. I am saying that it becomes precipitously difficult.
That’s what happens when Mcapacity is exceeded; it becomes precipitously difficult to evolve a perfect creature, too much load.
Now Paul, how could I think that something you say doesn’t matter even though it just represents another problem for mutation and selection converging rapidly for multiple selection conditions?First you called the Rcapacity concept "irrational and illogical," but now you're saying it matters. You're a dodgeball master.
I worried about your self esteem, your world view is collapsing and your own computer simulation shows why.
Condescension is boring, Alan -- it only proves you're an internet troll -- or an intellectual coward, for refusing to directly deal with my evidence.
I know that the mathematical and empirical facts which show that combination selection pressures profoundly slow the evolutionary process by mutation and selection is boring but hey, facts are facts. Now who’s the coward, someone who post under his real name or someone who posts under a pseudonym?

So let’s have some examples of how mutation and selection actually works.

http://gateway.nlm.nih.gov/MeetingAbstracts/102248881.html (http://gateway.nlm.nih.gov/MeetingAbstracts/102248881.html)
Objective: To assess the post-therapy stability of NNRTI resistance mutations selected during virologic failure of an efavirenz (EFV) containing regimen and the potential for selection of new NNRTI resistance mutations when stopping EFV therapy while fully virologically suppressed.METHODS: Plasma HIV samples from patients (pts) stopping efavirenz combination therapy (Tx) in Study DMP 266-006 were sequenced using the Visible Genetics TRUGENE HIV Genotyping Kit. Twenty-nine post-Tx samples (1-176 days after stopping EFV) from 9 pts who experienced virologic failure during EFV -containing Tx were compared to baseline and on-Tx samples. Twelve post-Tx samples (24-125 days after stopping efavirenz) from 7 pts who stopped EFV-containing Tx while fully virologically suppressed (<50 copies/mL) were compared to baseline samples.RESULTS: The K103N resistance mutation was observed in all pts virologically failing EFV/IDV or EFV/ZDV/3TC Tx. Additional mutations observed in combination with K103N included L100I, K101E, V108I, and P225H. In these pts, the K103N mutation remained detectable in the plasma virus population for 29-176 days after stopping EFV-containing Tx. Among samples from 7 pts who stopped EFV-containing Tx while fully virologically suppressed, K103N was detected in one subject post Tx. No NNRTI resistance mutations were detected in 6 subjects.CONCLUSIONS: Viruses with NNRTI resistance mutations were not detected during viral load rebound in 6/7 pts who stopped efavirenz Tx while virus replication was fully suppressed. However, in pts who failed EFV while on-Tx, viruses with the K103N resistance mutation persisted at detectable levels in the plasma virus population for 1 to >6 months post Tx.

http://www.sciencemag.org/cgi/content/abstract/269/5224/696 (http://www.sciencemag.org/cgi/content/abstract/269/5224/696)
Combinations of antiretroviral drugs that prevent or delay the appearance of drug-resistant human immunodeficiency virus-type 1 (HIV-1) mutants are urgently required. Mutants resistant to 3'-azidothymidine (AZT, zidovudine) became phenotypically sensitive in vitro by mutation of residue 184 of viral reverse transcriptase to valine, which also induced resistance to (-)2'-deoxy-3'-thiacytidine (3TC). Furthermore, AZT-3TC coresistance was not observed during extensive in vitro selection with both drugs. In vivo AZT-3TC combination therapy resulted in a markedly greater decreased in serum HIV-1 RNA concentrations than treatment with AZT alone, even though valine-184 mutants rapidly emerged. Most samples assessed from the combination group remained AZT sensitive at 24 weeks of therapy, consistent with in vitro mutation studies.
How can that be, these examples show that particular mutations appear with increased frequency subject to particular selection pressures? So, not only do combination selection pressures slow the evolutionary process, particular selection pressures select for particular mutations. Isn’t mutation and selection boring? It just shows that the theory of evolution is mathematically impossible.

[Deetee]

Is not the example of multiple selection pressure in HIV replication quite an artificial construct to compare to any situation that would be encountered in nature? After all, these are drugs that have been designed to specifically inhibit a single enzyme, reverse transcriptase.
What is the corrollary to this situation when considering evolutionary selection pressures on say an earth-bound reptile subject to predation by another organism?

[jimbob]

Kleinman
What do you mean when you say that
http://forums.randi.org/imagehosting/thum_608047022eae7e563.jpg
is "An evolutionist Rorschach test."?

I presume that "evolutionists" see something that isn't really there, so what is actually there? Something placed in stone by the prince of lies to test our your faith?

[kleinman]

Is not the example of multiple selection pressure in HIV replication quite an artificial construct to compare to any situation that would be encountered in nature? After all, these are drugs that have been designed to specifically inhibit a single enzyme, reverse transcriptase.
That is a valid question; do you raise that question to every experiment that is performed in the laboratory? The answer that question is yes, you should ask this question. These observations that combination selection pressures profoundly slow the evolutionary process are observed in numerous other “laboratory” settings such as the treatment of HBV, HCV, Malaria, TB, cancer weeds,… It is also commonly observed in the “laboratory” that single selection pressures are much easier for a population to evolve to by mutation and selection.

Now Deetee, if you think that “natural” selection pressures in combination somehow evolve more rapidly, give us an example. The problem you have is explaining how selection pressures which target multiple genes will somehow transform rapidly by the mutation and selection process. There are no examples of this process. The reason for this is explained by the mathematics of mutation and selection. You are simply trying to optimize too many conditions simultaneously.
What is the corrollary to this situation when considering evolutionary selection pressures on say an earth-bound reptile subject to predation by another organism?
There is no corollary to earth-bound reptiles subject to predation by another organism evolving by mutation and selection. There are laboratory experiments which show that reptiles will evolve longer legs in a very short period of time by recombination and selection in response to predation. The faster running members of the population survive to breed giving a longer legged population. There is a citation earlier in the thread which describes this observation.
What do you mean when you say that http://forums.randi.org/imagehosting/thum_608047022eae7e563.jpg is "An evolutionist Rorschach test."?
You are drawing a conclusion that can not be substantiated by the mathematics and empirical evidence of how mutation and selection actually works. You see in this fossil what you want to see. The mathematics of mutation and selection and the empirical evidence of this phenomenon which has been repeated over and over by numerous scientists are much less open to the ambiguous interpretations evolutionists like to draw than from your strange interpretations of the fossil record. So content yourself with your fossil record interpretations because the mathematics of mutation and selection and the empirical evidence of this process show that your theory is mathematically impossible.

[Henners]

You are drawing a conclusion that can not be substantiated by the mathematics and empirical evidence of how mutation and selection actually works. You see in this fossil what you want to see. The mathematics of mutation and selection and the empirical evidence of this phenomenon which has been repeated over and over by numerous scientists are much less open to the ambiguous interpretations evolutionists like to draw than from your strange interpretations of the fossil record. So content yourself with your fossil record interpretations because the mathematics of mutation and selection and the empirical evidence of this process show that your theory is mathematically impossible.

Of course, it is easier by far to close your eyes very, very tight; to place and index finger in each ear, and to shout - as loud as possible - "LA-LA-LA-LA-LA-LA-LA-LA-LA-LA-LA-LA-LA-LA-LA-LA-LA-LA

[Taffer]

You had better learn the facts before you take your exams.

You had better learn about reality before claiming victory. :rolleyes:

That’s the point Taffer; combination therapy profoundly slows the evolutionary process. If you had any understanding of the mathematics of mutation and selection you would know that it doesn’t take huge populations to evolve by mutation and selection to single selection pressures, however even with huge populations it is still extremely difficult to evolve to more than a single selection pressure. With respects to drugs administered sequentially versus concurrently, I have posted numerous studies where those very things have been done. What these studies show is that sequential use of selection pressures allows much more rapid evolution to the selection pressures than if the same selection pressures are applied concurrently. Do you want me to repost these studies?

Kleinman, when will you understand that the time until a mutation occurs is unrelated to selective pressure?

Isn’t that interesting, an evolutionist with a narrow definition for the word “evolution”. What you are missing is that when there is only a single selection pressure, the “emergence” of that single beneficial mutation occurs much more quickly and can be propagated in the population than when there are combination selection pressures requiring the “emergence” of multiple beneficial mutations simultaneously in order for them to be propagated through the population. You aren’t going to avoid the way mutation and selection actually works by playing semantics. Your theory of evolution by mutation and selection is mathematically impossible and using a narrow definition for the word “evolution” won’t change the mathematical and empirical facts of the way mutation and selection actually works. You have some homework to do before you take your exams.

Aren't you smug. :rolleyes:

Kleinman, when will you understand that the time for a mutation to occur is unrelated to selective pressures?

Selection, and thus evolution, only occurs when variation exists. The time until this variation arises, the time of emergence of a particular trait, is unaffected by selection.

[Deetee]

The problem you have is explaining how selection pressures which target multiple genes will somehow transform rapidly by the mutation and selection process. There are no examples of this process.

How about this:
There are laboratory experiments which show that reptiles will evolve longer legs in a very short period of time by recombination and selection in response to predation. The faster running members of the population survive to breed giving a longer legged population. There is a citation earlier in the thread which describes this observation.


Moving on......

You are drawing a conclusion that can not be substantiated by the mathematics and empirical evidence of how mutation and selection actually works. You see in this fossil what you want to see. The mathematics of mutation and selection and the empirical evidence of this phenomenon which has been repeated over and over by numerous scientists are much less open to the ambiguous interpretations evolutionists like to draw than from your strange interpretations of the fossil record. So content yourself with your fossil record interpretations because the mathematics of mutation and selection and the empirical evidence of this process show that your theory is mathematically impossible.
I think I get the hang of this....
Me: I see that this apple is roughly spherical in shape.
You: No - not so. You see my theories on the biomechanics of fruit bud clustering render this outcome mathematically impossible, therefore you are only imagining it is spherical.

Way to go, Kleinman... best debating technique I've seen in a while.

[Taffer]

You are drawing a conclusion that can not be substantiated by the mathematics and empirical evidence of how mutation and selection actually works. You see in this fossil what you want to see. The mathematics of mutation and selection and the empirical evidence of this phenomenon which has been repeated over and over by numerous scientists are much less open to the ambiguous interpretations evolutionists like to draw than from your strange interpretations of the fossil record. So content yourself with your fossil record interpretations because the mathematics of mutation and selection and the empirical evidence of this process show that your theory is mathematically impossible.

All that the "mathematics of mutation and selection" show, kleinman, is that you understand neither.

[Paul C. Anagnostopoulos]

Looks like Mcapacity is a real affect, you are loading a genome to its capacity of mutations. Now why don’t you give us a Wikipedia reference to Rcapacity and show us that it has nothing to do with the shape of the fitness landscape and the starting point for finding a trajectory to a perfect creature local optimum.
Alan, who said Rcapacity had nothing to do with fitness landscapes? Obviously, absolutely everything that affects evolution has something to do with the fitness landscape. So you've adopted the fitness landscape mantra as a broad-brush answer to everything. But you can't see the trees for the forest: What are the specific reasons why Rcapacity is an issue? What are the specific reasons why mutational load is an issue? You reject all the details in favor of "it's a fitness landscape thing." Nature doesn't know crap-all about fitness landscapes. It just does chemistry and the details produce the results.


Yes, it is the Mcapacity affect; it is the capacity of the genome to take a load of mutations. Now what is it again that the Rcapacity affect? What is it that the genome can’t take a load of?
Cramming Rfrequency bits of information down the throat of a binding site that is too narrow.

~~ Paul

[Belz...]

Oh no, the strawman argument!

You think a strawman is an argument ? I'm saying that your pathetic assertion is a strawman fallacy. Read it up.

What can I do? How about I post some more citations which show how mutation and selection actually works, see below.

How about you don't, since it has nothing to do with the fact that you were using a strawman.

That empirical evidence has nothing to do with mutation and selection and has no mathematical basis. What’s wrong here is the evolutionist interpretation of the fossil record but that’s a discussion for another thread.

Oh, so each of the sciences that refute creationism is wrong, and the single-source Bibble is miraculously correct ?

It has only been a few years since genetic sequencing could be done with any speed or accuracy. In addition, mathematical models of mutation and selection have not been around for long either and the computational power to properly analyze these models has only been available for a few years as well.

YOU've managed to understand what it means. Why haven't other scientists ?

You are dodging the question.

Belz, the mathematics agrees with the reality. Mathematically, combination selection pressures profoundly slow the evolutionary process and reality shows the same result.

Answer the question, doctor:

I said I can come up with a nth-dimensional computer model. Does that mean that reality "loses" to mathematics and is suddenly n-dimensional ?

Your imagination shows reptiles transforming into birds but the mathematics and empirical facts which show how mutation and selection actually works shows that what you are imagining is mathematically and empirically impossible. Mutation and selection simply doesn’t work that way.

Actually I think it's fair to say that your own line of argument has proven you wrong on this.

The facts are that particular selection pressures lead to particular base substitutions increasing in frequency in the gene pool. The cause and effect relationship of mutation and selection lead to repeatable results when the identical starting conditions and selection pressures are used.

How does this relate to the issue of "goal" ?

Belz, when was the last time you talked about mutation and selection?

Last post.

Belz, as far as I am concerned, you can say whatever you want but so far, none of what you have said has anything to do with mutation and selection. You have shown that you know nothing about the topic but asterisk away.

So far, nothing I've said ? What about when I asked you about gene duplication ? Numerous times. Without an answer.

Why Belz, that’s aviopomorphism.

Troll.

Belz, you are seeing what you want to see, reptiles can not transform into birds by mutation and selection. It is mathematically and empirically impossible. Mutation and selection simply does not work that way.

Repeating it over and over does not make it true. WHY do we see those characteristics ? "You're seeing what you want to see" is the answer of a first-grade psychology teacher.

An evolutionist Rorschach test.

WHAT is it, Klein ? Answer the question. What are those things, on either side. Wings ?

You got it wrong again Belz; combination selection pressures profoundly slow the evolutionary process.

Not from what I've seen.

ll the selection pressures applied by you evolutionists have not caused extinction and the goalposts have not evolved to a new local optimum.

All those neat terms. I'm sure they mean something.

[Belz...]

Out of curiosity, what is Klein a doctor of, exactly ?

[kleinman]

Looks like Mcapacity is a real affect, you are loading a genome to its capacity of mutations. Now why don’t you give us a Wikipedia reference to Rcapacity and show us that it has nothing to do with the shape of the fitness landscape and the starting point for finding a trajectory to a perfect creature local optimum.Alan, who said Rcapacity had nothing to do with fitness landscapes? Obviously, absolutely everything that affects evolution has something to do with the fitness landscape. So you've adopted the fitness landscape mantra as a broad-brush answer to everything. But you can't see the trees for the forest: What are the specific reasons why Rcapacity is an issue? What are the specific reasons why mutational load is an issue? You reject all the details in favor of "it's a fitness landscape thing." Nature doesn't know crap-all about fitness landscapes. It just does chemistry and the details produce the results.
Paul, now that you understand that everything about mutation and selection has to do with the fitness landscape. (Thank Delphi for introducing this into the discussion). Now you need to learn that the number of selection pressures is the dominant parameter in determining the shape of the fitness landscape. What nature does is show the same type of behavior as demonstrated in the mathematics of the fitness landscape. That’s why it is so easy for me to find examples of mutation and selection which demonstrate this mathematical behavior. Now do you have a real example of Rcapacity?
Yes, it is the Mcapacity affect; it is the capacity of the genome to take a load of mutations. Now what is it again that the Rcapacity affect? What is it that the genome can’t take a load of?Cramming Rfrequency bits of information down the throat of a binding site that is too narrow.
Well, the model can take an itty-bit, it can find a local optimum despite Rfrequency > Rcapacity. That mean old fitness landscape just won’t let you get to a perfect creature local optima.
You are drawing a conclusion that can not be substantiated by the mathematics and empirical evidence of how mutation and selection actually works. You see in this fossil what you want to see. The mathematics of mutation and selection and the empirical evidence of this phenomenon which has been repeated over and over by numerous scientists are much less open to the ambiguous interpretations evolutionists like to draw than from your strange interpretations of the fossil record. So content yourself with your fossil record interpretations because the mathematics of mutation and selection and the empirical evidence of this process show that your theory is mathematically impossible.Of course, it is easier by far to close your eyes very, very tight; to place and index finger in each ear, and to shout - as loud as possible - "LA-LA-LA-LA-LA-LA-LA-LA-LA-LA-LA-LA-LA-LA-LA-LA-LA-LA
Who’s the one in LA-LA land, the one who takes a single fossil and say that it proves birds evolve from reptiles or the one who has mathematical and empirical evidence which shows how mutation and selection actually works. Henners, you are the on shutting your eyes to the mathematical and empirical facts which shows how mutation and selection actually works.
And
All that the "mathematics of mutation and selection" show, kleinman, is that you understand neither.
Taffer, you can’t tell the difference between mutation and selection and recombination and selection. You have some homework to do before you take your exams.
The problem you have is explaining how selection pressures which target multiple genes will somehow transform rapidly by the mutation and selection process. There are no examples of this process.How about this:There are laboratory experiments which show that reptiles will evolve longer legs in a very short period of time by recombination and selection in response to predation. The faster running members of the population survive to breed giving a longer legged population. There is a citation earlier in the thread which describes this observation.Moving on......
Now Deetee, why would you want to move on so quickly if you have proved that multiple selection pressures accelerate evolution? That would refute my hypothesis. The problem with the conclusion you are trying to draw here is that it is an example of recombination and selection. Recombination and selection does not select among mutations, it selects among alleles, and the alleles being selected for are the ones which affect leg length and muscle properties. This is a much smaller optimization search space than seen in the mutation and selection problem. In addition, if you think this is an example of mutation and selection, tell us which genes are targeted and what are the mutations which give the optimal fitness.
You are drawing a conclusion that can not be substantiated by the mathematics and empirical evidence of how mutation and selection actually works. You see in this fossil what you want to see. The mathematics of mutation and selection and the empirical evidence of this phenomenon which has been repeated over and over by numerous scientists are much less open to the ambiguous interpretations evolutionists like to draw than from your strange interpretations of the fossil record. So content yourself with your fossil record interpretations because the mathematics of mutation and selection and the empirical evidence of this process show that your theory is mathematically impossible.
I think I get the hang of this....
Me: I see that this apple is roughly spherical in shape.
You: No - not so. You see my theories on the biomechanics of fruit bud clustering render this outcome mathematically impossible, therefore you are only imagining it is spherical.

Way to go, Kleinman... best debating technique I've seen in a while.
Not quite Deetee, you see a single fossil and draw a sweeping conclusion. I see a mathematical model which describes mutation and selection and hundreds of empirical examples which substantiates this mathematical behavior. You have to deny the mathematical and empirical evidence in order to draw your sweeping conclusion from a single fossil. Your science is sloppy and speculative; my science is mathematically based with precise measurement of the cause and effect relationship of mutation and selection.

As I said to jimbob, content yourself with your strange interpretation of this fossil and draw the conclusion that birds evolved from reptiles because you have no mathematical or empirical evidence of mutation and selection which shows that your theory of evolution and speculations are possible.

When it comes to closing your eyes to the facts and living in LA-LA land, you evolutionists win this one in spades. Mutation and selection simply can not accomplish what you allege; you have no mathematical or empirical evidence to substantiate your allegations. In fact, the mathematical and empirical evidence contradicts your interpretations of the fossil record.

Here is another example of how mutation and selection actually works.
http://www.medpagetoday.com/HematologyOncology/LeukemiaLymphoma/tb/6437 (http://www.medpagetoday.com/HematologyOncology/LeukemiaLymphoma/tb/6437)
Frontline kinase inhibitor combination therapy could "substantially improve both the depth and durability of clinical responses," particularly in advanced phases of disease, they wrote online in the Journal of Clinical Investigation.

Furthermore, "it is likely that other cancers being treated with kinase inhibitor therapy will benefit from a similar treatment strategy," they added.

Mutations conferring kinase inhibitor resistance have become increasingly common not just in chronic myelogenous leukemia but also in gastrointestinal stromal tumor and lung cancer. As clinical experience with dasatinib grows, some patients have begun to experience relapse on second-line dasatinib, the researchers said.

One mechanism anticipated for prior studies is selection for the T315I mutation, a "gatekeeper" mutation that confers resistance to imatinib, dasatinib, and the related investigational compound nilotinib.

So, the researchers assessed it and other mutations in dasatinib failure. They studied 17 consecutive patients treated at a single center who developed dasatinib resistance after imatinib treatment.

Analysis of their blood samples at relapse showed that all patients had new mutations in the BCR-ABL protein. Twelve had the T315I mutation and one had the relatively resistant F317L mutation.
Look at that, combination selection pressures slow the evolution of cancer cells and not only that, when the cells do manage to evolve, the exact mutation at the exact location is identified. I really wish I had the vague mushy arguments you evolutionist have.

For every strange interpretation you have of the fossil record, I can post many real examples of how mutation and selection actually works and let’s not forget that we have Dr Schneider’s peer reviewed and published model of random point mutations and natural selection which shows the same. So evolutionists, post your fossils pictures and your strange interpretations and I’ll post peer reviewed and published examples of mutation and selection which show your strange interpretations are mathematically impossible. Keep your eyes closed to how mutation and selection actually works and live in LA-LA land.

[Taffer]

Taffer, you can’t tell the difference between mutation and selection and recombination and selection. You have some homework to do before you take your exams.

Kleinman, the difference exists only in your head. Reality, unfortunately for you, does not conform to your notions.

[Kotatsu]

That’s right; you did say that a predator chasing a reptile into a tree would make it beneficial for the reptile to grow wings. Doesn’t that logic turn the mathematics and empirical data which describes how mutation and selection actually works on its head.

You will recall that the list continued way past that one single example you keep coming back to. Also, I note that, again, you do not present a coherent --- or, indeed, any --- reason as to why this selection pressure would be unfeasible. Is this because of laziness or because you actually have no clue?

So when you look at birds you have reptileopomorphism? You know, you are correct, the last time I saw Jurrasic Park, the T Rex does walk just like an ostrich. I didn’t realize you had so much scientific evidence.

If by that you mean that when I see a bird, I think of it as a highly modified reptile, then yes, I do "have reptileopomorphism".

[slight derail] The thing that irritated me most about Crichton's books was how the Carnotauruses were some kind of hyper-chameleons which could blend perfectly with the background. To me, it seems too unrealistic.[/slight derail]

As to the evidence, I can comfortably lean back unto decades of published papers, books and other material on the anatomy of birds and that of dinosaurs.

Is it true that when T Rex is properly prepared it tastes just like chicken?

My guess would be that it tastes like stone, as all T rex (1) are fossilised. However, I am sure that you with your lenient way of perceiving the world of possibilities may have a different opinion, uninhibited by such base attributes are "reality".

---
(1) Since "rex" is the specific epithet, this should not begin with a capital letter.

[kleinman]

Taffer, you can’t tell the difference between mutation and selection and recombination and selection. You have some homework to do before you take your exams.Kleinman, the difference exists only in your head. Reality, unfortunately for you, does not conform to your notions.
Well let’s see what Wikipedia says:
http://en.wikipedia.org/wiki/Evolution (http://en.wikipedia.org/wiki/Evolution)
Genetic variation comes from random mutations that occur in the genomes of organisms. Mutations are changes in the DNA sequence of a cell's genome and are caused by radiation, viruses, transposons and mutagenic chemicals, as well as errors that occur during meiosis or DNA replication.[19][20][21] These mutagens produce several different types of change in DNA sequences; these can either have no effect, alter the product of a gene, or prevent the gene from functioning. Studies in the fly Drosophila melanogaster suggest that about 70 percent of mutations are deleterious, and the remainder are either neutral or have a weak beneficial effect.[22] Due to the damaging effects that mutations can have on cells, organisms have evolved mechanisms such as DNA repair to remove mutations.[19] Therefore, the optimal mutation rate for a species is a trade-off between short-term costs, such as the risk of cancer, and the long-term benefits of advantageous mutations.[23]

Large sections of DNA can also be duplicated, which is a major source of raw material for evolving new genes, with tens to hundreds of genes duplicated in animal genomes every million years.[24] Most genes belong to larger families of genes of shared ancestry.[25] Novel genes are produced either through duplication and mutation of an ancestral gene, or by recombining parts of different genes to form new combinations with new functions.[26][27] For example, the human eye uses four genes to make structures that sense light: three for color vision and one for night vision; all four arose from a single ancestral gene.[28] An advantage of duplicating a gene (or even an (entire genome) is that overlapping or redundant functions in multiple genes allows alleles to be retained that would otherwise be harmful, thus increasing genetic diversity.[29]

Changes in chromosome number may also involve the breakage and rearrangement of DNA within chromosomes. For example, two chromosomes in the Homo genus fused to produce human chromosome 2; this fusion did not occur in the chimpanzee lineage and chimpanzees retain these separate chromosomes.[30] In evolution, the most important role of such chromosomal rearrangements may be to accelerate the divergence of a population into new species by preserving genetic differences within populations.[31]

Sequences of DNA that can move about the genome, such as transposons, make up a major fraction of the genetic material of plants and animals, and may have been important in the evolution of genomes.[32] For example, more than a million copies of the Alu sequence are present in the human genome, and these sequences have now been recruited to perform functions such as regulating gene expression.[33] Another effect of these mobile DNA sequences is that when they move within a genome, they can mutate or delete existing genes and thereby produce genetic diversity.[34]
and
In asexual organisms, genes are inherited together, or linked, as they cannot mix with genes in other organisms during reproduction. However, the offspring of sexual organisms contain a random mixture of their parents' chromosomes that is produced through independent assortment. In the related process of genetic recombination, sexual organisms can also exchange DNA between two matching chromosomes.[35] These shuffling processes can allow even alleles that are close together in a strand of DNA to be inherited independently. However, as only about one recombination event occurs per million base pairs in humans, genes close together on a chromosome may not be shuffled away from each other, and tend to be inherited together.[36] This tendency is measured by finding how often two alleles occur together, which is called their linkage disequilibrium. A set of alleles that is usually inherited in a group is called a haplotype, and this co-inheritance can indicate that the locus is under positive selection (see below).[37]

Recombination in sexual organisms helps to remove harmful mutations and retain beneficial mutations.[38] Consequently, when alleles cannot be separated by recombination – such as in mammalian Y chromosomes, which pass intact from fathers to sons – harmful mutations accumulate.[39][40] In addition, recombination can produce individuals with new and advantageous gene combinations. These positive effects of recombination are balanced by the fact that this process can cause mutations and separate beneficial combinations of genes.[38] The optimal rate of recombination for a species is therefore a trade-off between conflicting factors.
Taffer, seems like the authors at Wikipedia think there is a difference between mutation and selection and recombination and selection. You had better go back and reread that chapter before you take your exams.

[Kotatsu]

It has only been a few years since genetic sequencing could be done with any speed or accuracy. In addition, mathematical models of mutation and selection have not been around for long either and the computational power to properly analyze these models has only been available for a few years as well. You have multiple technological improvements occurring simultaneously which enable better analysis of the mutation and selection process. It is these kinds of advances which discredit the concept of common descent. The concept of evolution by mutation and selection will not be discarded; it will just be better understood as a much more limited process than can not accomplish common descent.

As a phylogeneticist, I am highly intrigued by this section. Could you expand, perhaps, on the ways in which genetic sequencing will show that evolution can not accomplish common descent. What do you base this on?

This nicely ties in with my earlier but still overlooked question about how you explain nested hierarchies, such as can be found in virtually every phylogenetic tree, whether based on protein, DNA, morphological, or any other kind of data.

[Kotatsu]

Who’s the one in LA-LA land, the one who takes a single fossil and say that it proves birds evolve from reptiles or the one who has mathematical and empirical evidence which shows how mutation and selection actually works.

I would say that the one in LA-LA land is the one who believes that our present theories on how birds evolved from reptiles is based on a single fossil.

Out of curiosity, have you, Kleinman, ever heard of "China"?

[Taffer]

Well let’s see what Wikipedia says:
http://en.wikipedia.org/wiki/Evolution (http://en.wikipedia.org/wiki/Evolution)

and

Taffer, seems like the authors at Wikipedia think there is a difference between mutation and selection and recombination and selection. You had better go back and reread that chapter before you take your exams.

Kleinman, I never said there was no difference between the mechanisms of recombination and other mutations. I said there is no difference between "recombination and selection" and "mutation and selection", because those two phrases are meaningless. There is only "variation and selection".

You are extremely arrogant to assume I don't know what "recombination" and "mutation" mean.

Oh, and kleinman? Recombination is a form of mutation. Just FYI.

[kleinman]

That’s right; you did say that a predator chasing a reptile into a tree would make it beneficial for the reptile to grow wings. Doesn’t that logic turn the mathematics and empirical data which describes how mutation and selection actually works on its head.You will recall that the list continued way past that one single example you keep coming back to. Also, I note that, again, you do not present a coherent --- or, indeed, any --- reason as to why this selection pressure would be unfeasible. Is this because of laziness or because you actually have no clue?
Kotatsu, I remember your examples, that mush you presented which you didn’t define the selection pressures or the target genes for the selection pressures. You are so used to using mush to justify your theory, you think it has turned into fact.
So when you look at birds you have reptileopomorphism? You know, you are correct, the last time I saw Jurrasic Park, the T Rex does walk just like an ostrich. I didn’t realize you had so much scientific evidence.If by that you mean that when I see a bird, I think of it as a highly modified reptile, then yes, I do "have reptileopomorphism".
The only problem with this world view is that the mathematics and empirical evidence of mutation and selection shows that such transformation of their genomes can’t occur. It is mathematically impossible. I suppose you would say glass and diamond are from the same source because they have superficial similiarities.
Is it true that when T Rex is properly prepared it tastes just like chicken?My guess would be that it tastes like stone, as all T rex (1) are fossilised. However, I am sure that you with your lenient way of perceiving the world of possibilities may have a different opinion, uninhibited by such base attributes are "reality".
I guess you didn’t hear, they found a T rex fossil with soft tissue in it.
(1) Since "rex" is the specific epithet, this should not begin with a capital letter.
R->r, see Kotatsu, I can take correction, when will you take correction on the way mutation and selection actually works.

[kleinman]

Taffer, seems like the authors at Wikipedia think there is a difference between mutation and selection and recombination and selection. You had better go back and reread that chapter before you take your exams.Kleinman, I never said there was no difference between the mechanisms of recombination and other mutations. I said there is no difference between "recombination and selection" and "mutation and selection", because those two phrases are meaningless. There is only "variation and selection".
So, does the variation due to the mechanism of mutation behave the same way mathematically as does the variation which is due to recombination?

Do you believe that the process dog breeder use to obtain different types of dogs is the result of mutational variation or recombinational variation? If you claim it is mutation and recombination together, what proportion is mutation and what proportion is recombination that contributes to these variations?
You are extremely arrogant to assume I don't know what "recombination" and "mutation" mean.
I don’t have to assume this; you prove this by your posts.
Oh, and kleinman? Recombination is a form of mutation. Just FYI.
I see Taffer; one variation is as good as another. Is there no limit to how mushy the thinking of evolutionist can be? Your mathematics is non-existent and your terminology is mush.

Taffer, since you consider yourself a smart evolutionist, why don’t you give us an example of evolution by variation and selection where the process occurs more quickly when you have combination selection pressures. Oh wait, you have, you said that three selection conditions will evolve as quickly whether they are applied concurrently or sequentially. You have even said you have done the experiments yourself. So why don’t you post your data? Here, I’ll post a citation which contradicts your speculations.
http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF (http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF)
Hepatitis B virus (HBV) drug resistance to lamivudine is always accompanied by mutations in the viral polymerase gene at position 550, termed group 1 (M550V with L526M) or group 2 (M550I) mutations. The latter mutation has not been associated with famciclovir resistance. Thus, the addition of famciclovir to lamivudine therapy in persons with group 2 lamivudine resistance may lead to virus suppression. The effect of lamivudine/famciclovir combination therapy on HBV infection was monitored in 5 lamivudine-resistant patients by quantitative polymerase chain reaction and polymerase gene sequencing of serum virus. No patients treated with combination therapy had a decline in HBV load 11 log10. Continual evolution of the viral polymerase was detected in association with virologic resistance to both drugs. Cloning experiments identified the preexistence of these multidrug-resistant virus variants as minority species prior to addition of famciclovir therapy. HBV resistance to lamivudine monotherapy is associated with a complex mixture of variants that limit the efficacy of second-line nucleoside-analogue therapy. First-line potent combination therapy may reduce the emergence of HBV drug resistance.
Taffer, what is sad is when evolutionists like you spout nonsense that concurrent selection pressures evolve as rapidly as sequential selection pressures. If you had any idea of how the mathematics of mutation and selection actually works you wouldn’t allege such foolishness.

[Taffer]

So, does the variation due to the mechanism of mutation behave the same way mathematically as does the variation which is due to recombination?

I'm not quite sure what you're asking. Of course recombination behaves differently to mutation, because it is a different processes of mutation. However, what does this have to do with evolution? Selection acts on variation present in a population. It doesn't matter how that variation occurred.

Do you believe that the process dog breeder use to obtain different types of dogs is the result of mutational variation or recombinational variation? If you claim it is mutation and recombination together, what proportion is mutation and what proportion is recombination that contributes to these variations?

It is both. The genetics of coat colour, for example, is particularly complex. Since many genes are involved, both point mutation and recombination are mechanisms of mutation which affect breeding. I couldn't possibly guess as to a proportion.

I don’t have to assume this; you prove this by your posts.

Much in the same way that your posts clearly show you do not grasp evolutionary theory, I'm sure.

I see Taffer; one variation is as good as another. Is there no limit to how mushy the thinking of evolutionist can be? Your mathematics is non-existent and your terminology is mush.

Excuse me? Not only am I always clear in my terminology, but I have already posted, several times, mathematical models of selection. If you might recall, all that matters is variation.

Taffer, since you consider yourself a smart evolutionist, why don’t you give us an example of evolution by variation and selection where the process occurs more quickly when you have combination selection pressures.

I already have. Don't you remember? The only things which affect the rate of change in allele frequency over time are the starting frequency and the selective pressure. More pressure = faster change. Thus, stronger selection = faster evolution.

Oh wait, you have, you said that three selection conditions will evolve as quickly whether they are applied concurrently or sequentially. You have even said you have done the experiments yourself. So why don’t you post your data?

:rolleyes: I said I've done experiments (which any second year student will do) which clearly demonstrates that multi-drug resistance will appear quickly in the presence of multiple drugs, when that variation already exists in the population.

Here, I’ll post a citation which contradicts your speculations.[/SIZE][/FONT]
http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF (http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF)

Did you even read and understand your source? I suspect not. It states that when you use more drugs, the time until resistance to all those drugs is higher then when compared to fewer drugs. Of course it is, kleinman, no-one has ever argued any different. :rolleyes:

Taffer, what is sad is when evolutionists like you spout nonsense that concurrent selection pressures evolve as rapidly as sequential selection pressures. If you had any idea of how the mathematics of mutation and selection actually works you wouldn’t allege such foolishness.

Y'know, kleinman, if you actually understood how selection works, you wouldn't make idiotic arguments so much. Just something to think about.

[Paul C. Anagnostopoulos]

Paul, now that you understand that everything about mutation and selection has to do with the fitness landscape. (Thank Delphi for introducing this into the discussion). Now you need to learn that the number of selection pressures is the dominant parameter in determining the shape of the fitness landscape. What nature does is show the same type of behavior as demonstrated in the mathematics of the fitness landscape. That’s why it is so easy for me to find examples of mutation and selection which demonstrate this mathematical behavior. Now do you have a real example of Rcapacity?
As I've said a dozen times, Rcapacity is only an issue with Ev. However, what do you think might happen to the operation of a transcription factor if a genome suddenly doubled in size and the duplication was slightly randomized?


Well, the model can take an itty-bit, it can find a local optimum despite Rfrequency > Rcapacity.
Since absolutely any state of the genome can be called a local optimum, this sentence is without content. However, as I've said, also a dozen times, the perfect creature does not become impossible, only precipitously improbable. Why do you suppose that happens to the fitness landscape where Rfrequency > Rcapacity? What is actually going on in the fitness landscape?

~~ Paul

[Paul C. Anagnostopoulos]

Taffer, what is sad is when evolutionists like you spout nonsense that concurrent selection pressures evolve as rapidly as sequential selection pressures. If you had any idea of how the mathematics of mutation and selection actually works you wouldn’t allege such foolishness.
Where did you get this mathematics? Not from Ev, since it has no way to apply multiple selection pressures sequentially and cumulatively. (I presume you mean cumulatively, too.)

~~ Paul

[kleinman]

Paul, now that you understand that everything about mutation and selection has to do with the fitness landscape. (Thank Delphi for introducing this into the discussion). Now you need to learn that the number of selection pressures is the dominant parameter in determining the shape of the fitness landscape. What nature does is show the same type of behavior as demonstrated in the mathematics of the fitness landscape. That’s why it is so easy for me to find examples of mutation and selection which demonstrate this mathematical behavior. Now do you have a real example of Rcapacity?As I've said a dozen times, Rcapacity is only an issue with Ev. However, what do you think might happen to the operation of a transcription factor if a genome suddenly doubled in size and the duplication was slightly randomized?
Paul, Rcapacity isn’t even an issue with ev but I don’t mind talking about non-issues with you, we are already talking about a mathematically impossible theory.

I while back, some of the evolutionists got on my case when I used terminology like you have (slightly randomized) but I think I understand what you are saying. I think you mean to say the genome is slightly scrambled. I believe I posted this question or a similar one a while back. If you have and insert/deletion somewhere in the binding site/gene: I can see several possibilities. If the insertion/deletion occurs in the binding site, the gene probably will never be transcribed unless you happen to have a binding protein that happens to match the site. If the insertion/deletion occurs somewhere in the gene, you should get an entirely different amino acid sequence from the point of the insertion/deletion to the end of the gene. Who knows how this protein would function? If the insertion/deletion occurs in the stop codon, the transcription might continue until a stop codon is encountered. Again, who knows if this protein would be functional.
Well, the model can take an itty-bit, it can find a local optimum despite Rfrequency > Rcapacity.Since absolutely any state of the genome can be called a local optimum, this sentence is without content. However, as I've said, also a dozen times, the perfect creature does not become impossible, only precipitously improbable. Why do you suppose that happens to the fitness landscape where Rfrequency > Rcapacity? What is actually going on in the fitness landscape?
That’s not correct Paul. The genetic sequence can only be considered to be at a local optimum if any movement of the population on the fitness landscape reduces the populations’ fitness.

I can only speculate why it becomes so difficult for ev to find a trajectory to a perfect creature local optima when Rfrequency > Rcapacity. The way I would look for the answer would be to map out the fitness landscape for a couple cases, one where Rfrequency is much less than Rcapacity and the other when Rfrequency is greater than Rcapacity. If you want a guess on what is happening, I would look at the number of perfect creature local optima for both cases.
Taffer, what is sad is when evolutionists like you spout nonsense that concurrent selection pressures evolve as rapidly as sequential selection pressures. If you had any idea of how the mathematics of mutation and selection actually works you wouldn’t allege such foolishness.Where did you get this mathematics? Not from Ev, since it has no way to apply multiple selection pressures sequentially and cumulatively. (I presume you mean cumulatively, too.)
Paul, the empirical evidence shows this, I posted an example in the previous post and post another example at the end of this post. One of these days you should try this with ev. And yes, I do mean cumulatively.
So, does the variation due to the mechanism of mutation behave the same way mathematically as does the variation which is due to recombination?I'm not quite sure what you're asking. Of course recombination behaves differently to mutation, because it is a different processes of mutation. However, what does this have to do with evolution? Selection acts on variation present in a population. It doesn't matter how that variation occurred.
It does matter how the variation occurs if you are going to argue that reptiles can evolve into birds because recombination without error can not create new information in the gene pool and recombination with selection can cause the loss of information (alleles) from the gene pool. Now that you acknowledge that mathematics of recombination and selection behaves differently than the mathematics of mutation and selection, tell us which process allows for more rapid changes in a population.
Do you believe that the process dog breeder use to obtain different types of dogs is the result of mutational variation or recombinational variation? If you claim it is mutation and recombination together, what proportion is mutation and what proportion is recombination that contributes to these variations?It is both. The genetics of coat colour, for example, is particularly complex. Since many genes are involved, both point mutation and recombination are mechanisms of mutation which affect breeding. I couldn't possibly guess as to a proportion.
If you were to take a Chihuahua and breed it with a Great Dane (you might have to use artificial insemination), would the differences between the offspring and the parents be mostly due to mutations or mostly due to recombination?
I don’t have to assume this; you prove this by your posts.Much in the same way that your posts clearly show you do not grasp evolutionary theory, I'm sure.
Taffer, I grasp your thinking, it is vague and sloppy. You make claims about how evolution works without quantifying any of your claims.
I see Taffer; one variation is as good as another. Is there no limit to how mushy the thinking of evolutionist can be? Your mathematics is non-existent and your terminology is mush.Excuse me? Not only am I always clear in my terminology, but I have already posted, several times, mathematical models of selection. If you might recall, all that matters is variation.
And you have now acknowledged that the type of variation (mutation or recombination) behaves differently. Let’s consider the mathematical model that you posted, the Hardy-Weinberg Law. Does this model describe mutation and selection or recombination and selection?
Taffer, since you consider yourself a smart evolutionist, why don’t you give us an example of evolution by variation and selection where the process occurs more quickly when you have combination selection pressures.I already have. Don't you remember? The only things which affect the rate of change in allele frequency over time are the starting frequency and the selective pressure. More pressure = faster change. Thus, stronger selection = faster evolution.
You claim to have run experiments with bacteria and antibiotics which show that with three drugs that the bacteria take the same amount of time to evolve resistance whether the drugs are used concurrently or sequentially, give us your proof. I have posted hundreds of citations which contradict your claim.
Oh wait, you have, you said that three selection conditions will evolve as quickly whether they are applied concurrently or sequentially. You have even said you have done the experiments yourself. So why don’t you post your data?I said I've done experiments (which any second year student will do) which clearly demonstrates that multi-drug resistance will appear quickly in the presence of multiple drugs, when that variation already exists in the population.
Taffer, you are back peddling on your claim which you should do because it is wrong. Combination selection pressures profoundly slow the evolutionary process. This is shown mathematically and empirically. HIV is the best example of this since there is more data on this infection than any other. Still HIV demonstrates that multiple selection pressures profoundly slow the populations’ ability to evolve to these combination pressures. This occurs despite HIV has a short genome, huge populations, rapid reproduction rates, high mutation rates and this virus does recombination, point mutations and insertion/deletions. Still, combination selection pressures slow the evolution of this virus.
Here, I’ll post a citation which contradicts your speculations.
http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF (http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF) Did you even read and understand your source? I suspect not. It states that when you use more drugs, the time until resistance to all those drugs is higher then when compared to fewer drugs. Of course it is, kleinman, no-one has ever argued any different.
Taffer, I did read the source and if you could contradict what I am claiming the source says, you would have posted it. But I’ll post what has confused you.
Hepatitis B virus (HBV) drug resistance to lamivudine is always accompanied by mutations in the viral polymerase gene at position 550, termed group 1 (M550V with L526M) or group 2 (M550I) mutations.
These scientist start with patients who were treated with lamivudine.
The latter mutation has not been associated with famciclovir resistance. Thus, the addition of famciclovir to lamivudine therapy in persons with group 2 lamivudine resistance may lead to virus suppression.
They then propose to add famciclovir in addition to the lamivudine since none of the mutations associated with this drug are associated with famciclovir resistance.
The effect of lamivudine/famciclovir combination therapy on HBV infection was monitored in 5 lamivudine-resistant patients by quantitative polymerase chain reaction and polymerase gene sequencing of serum virus. No patients treated with combination therapy had a decline in HBV load 11 log10. Continual evolution of the viral polymerase was detected in association with virologic resistance to both drugs. Cloning experiments identified the preexistence of these multidrug-resistant virus variants as minority species prior to addition of famciclovir therapy. HBV resistance to lamivudine monotherapy is associated with a complex mixture of variants that limit the efficacy of second-line nucleoside-analogue therapy. First-line potent combination therapy may reduce the emergence of HBV drug resistance.
They then measured the effect of the combination of lamivudine (in 5 patients who already had resistant viruses) and famciclovir which is this case is effectively monotherapy. Neither drug is effective in this combination because lamivudine alone selected for resistance and the addition of famciclovir was of no benefit because already resistant viruses were in the population. Thus the authors propose that it requires potent combination therapy to reduce the emergence of HBV drug resistance.

Taffer, you have argued that combination therapy if done concurrently will evolve resistance as quickly as if the therapy is done sequentially but I am glad to see that you are finally acknowledging the mathematical and empirical facts of how mutation and selection actually works.
Taffer, what is sad is when evolutionists like you spout nonsense that concurrent selection pressures evolve as rapidly as sequential selection pressures. If you had any idea of how the mathematics of mutation and selection actually works you wouldn’t allege such foolishness.Y'know, kleinman, if you actually understood how selection works, you wouldn't make idiotic arguments so much. Just something to think about.
Taffer, the fact that you have backed off you claim that combination selection pressures evolve far more rapidly when applied sequentially than when applied concurrently shows that you can learn something about the mathematics of mutation and selection.

Taffer, here is another example of what happens when you use sequential therapy in a mutation selection system.
http://www.jci.org/cgi/content/full/117/9/2562 (http://www.jci.org/cgi/content/full/117/9/2562)
Molecularly targeted kinase inhibitor cancer therapies are currently administered sequentially rather than simultaneously. We addressed the potential long-term impact of this strategy in patients with chronic myelogenous leukemia (CML), which is driven by the fusion oncogene BCR-ABL. Analysis of BCR-ABL genotypes in CML patients who relapsed after sequential treatment with the ABL inhibitors imatinib and dasatinib revealed evolving resistant BCR-ABL kinase domain mutations in all cases. Twelve patients relapsed with the pan-resistant T315I mutation, whereas 6 patients developed novel BCR-ABL mutations predicted to retain sensitivity to imatinib based on in vitro studies. Three of these patients were retreated with imatinib (or the chemically related compound nilotinib) and responded; however, selection for compound mutants (2 or 3 BCR-ABL mutations in the same molecule) can substantially limit the potential effectiveness of retreating patients with inhibitors that have previously failed. Furthermore, drug-resistant mutations, when compounded, can increase oncogenic potency relative to the component mutants in transformation assays. The Aurora kinase inhibitor VX-680, currently under clinical evaluation based on its activity against the T315I mutation, is also effective against the other commonly detected dasatinib-resistant mutation in our analysis, V299L. Our findings demonstrate the potential hazards of sequential kinase inhibitor therapy and suggest a role for a combination of ABL kinase inhibitors, perhaps including VX-680, to prevent the outgrowth of cells harboring drug-resistant BCR-ABL mutations.
Taffer, this is how mutation and selection actually works, combination selection pressures profoundly slow the ability of a population to adapt to these selection pressures.

[kjkent1]

I know that the mathematical and empirical facts which show that combination selection pressures profoundly slow the evolutionary process by mutation and selection is boring but hey, facts are facts. I have no problem with your contention that evolution is slowed by combination selection pressures, if all of the pressures are of substantially equal intensity. That seems rather obvious.

However, to infer from this that natural environments are all full of the sort of highly targeted selection pressures that you cite to, is nonsensical. The result of such a nexus in the real world is likely extinction of a target organism.

As for your query re cowardice, you have dropped the key word from my statement: "intellectual" cowardice is the refusal to analyze one's position so as to reveal all possible conclusions. Anyone can obtain the answer they desire to any question, by simply refusing to acknowledge contrary evidence.

That's the hallmark of your posts: you have only one position: "God did it," therefore any analysis not in concert with this position must be false or kleinman's world view collapses.

I have no such predisposition. If God did it, then I'm equally fine with that, as I am with the conclusion that evolution is the product of random ignorant chance.

Therefore, you are an intellectual coward, and I am not.

So let’s have some examples of how mutation and selection actually works.

http://gateway.nlm.nih.gov/MeetingAbstracts/102248881.html (http://gateway.nlm.nih.gov/MeetingAbstracts/102248881.html)


http://www.sciencemag.org/cgi/content/abstract/269/5224/696 (http://www.sciencemag.org/cgi/content/abstract/269/5224/696)
Snore.

How can that be, these examples show that particular mutations appear with increased frequency subject to particular selection pressures? Perfect example of your reaching only the conclusion that you wish to reach, while ignoring the obvious contrary conclusion: The experiments reveal that the only viruses which survive the toxins are those which develop the required resistance. You will not see other mutations, because those mutations failed to provide sufficient resistance and the host organisms were exterminated.

I also, wouldn't dismiss the possibility that if you conducted the experiment enough times, that some other mutation might provide resistance.

But, the bottom line is that you clearly and convincingly display intellectual cowardice in nearly every post, because you won't give any opinion other than your own any credence. You treat everyone else like they're morons for not understanding what you view as obvious.

Einstein could have gotten away with such hubris. Personal information removed.

[Paul C. Anagnostopoulos]

I while back, some of the evolutionists got on my case when I used terminology like you have (slightly randomized) but I think I understand what you are saying. I think you mean to say the genome is slightly scrambled. I believe I posted this question or a similar one a while back. If you have and insert/deletion somewhere in the binding site/gene: I can see several possibilities. If the insertion/deletion occurs in the binding site, the gene probably will never be transcribed unless you happen to have a binding protein that happens to match the site. If the insertion/deletion occurs somewhere in the gene, you should get an entirely different amino acid sequence from the point of the insertion/deletion to the end of the gene. Who knows how this protein would function? If the insertion/deletion occurs in the stop codon, the transcription might continue until a stop codon is encountered. Again, who knows if this protein would be functional.
And what about a change somewhere completely different that suddenly causes a spurious binding, or many spurious bindings? Now there may be pressure to change those spurious binding sites, or possibly to evolve a new pattern that the transcription factor matches. But, unfortunately, the genome is now twice as large and the pattern needs another bit. Can the binding site accommodate it?

It's perhaps farfetched, which is why I said that Rcapacity has nothing to do with real life.


That’s not correct Paul. The genetic sequence can only be considered to be at a local optimum if any movement of the population on the fitness landscape reduces the populations’ fitness.
Oops, yes, my mistake. But my point is that you are going to call any state that Ev gets stuck in a local optimum. That statement does not offer any explanation as to why it got stuck there.


I can only speculate why it becomes so difficult for ev to find a trajectory to a perfect creature local optima when Rfrequency > Rcapacity. The way I would look for the answer would be to map out the fitness landscape for a couple cases, one where Rfrequency is much less than Rcapacity and the other when Rfrequency is greater than Rcapacity. If you want a guess on what is happening, I would look at the number of perfect creature local optima for both cases.
I don't need to guess, Alan. I'm not the one refusing to acknowledge that there is an information-content problem when Rfrequency > Rcapacity. You will not admit that we cannot easily stuff an n-bit pattern into an m<n-bit bucket.

~~ Paul

[kleinman]

I while back, some of the evolutionists got on my case when I used terminology like you have (slightly randomized) but I think I understand what you are saying. I think you mean to say the genome is slightly scrambled. I believe I posted this question or a similar one a while back. If you have and insert/deletion somewhere in the binding site/gene: I can see several possibilities. If the insertion/deletion occurs in the binding site, the gene probably will never be transcribed unless you happen to have a binding protein that happens to match the site. If the insertion/deletion occurs somewhere in the gene, you should get an entirely different amino acid sequence from the point of the insertion/deletion to the end of the gene. Who knows how this protein would function? If the insertion/deletion occurs in the stop codon, the transcription might continue until a stop codon is encountered. Again, who knows if this protein would be functional.And what about a change somewhere completely different that suddenly causes a spurious binding, or many spurious bindings? Now there may be pressure to change those spurious binding sites, or possibly to evolve a new pattern that the transcription factor matches. But, unfortunately, the genome is now twice as large and the pattern needs another bit. Can the binding site accommodate it?
I am not going to argue that such a change is impossible and is incompatible with life because on rare occasions these types of changes occur but they usually give a creature that is not fit to reproduce. How do use this type of mutation to overcome what ev and the empirical data is showing?
It's perhaps farfetched, which is why I said that Rcapacity has nothing to do with real life.
Ev is showing a peculiar behavior as the binding site width becomes shorter and the genome length increases. Unfortunately to study why ev does this requires a huge amount of number crunching.
I can only speculate why it becomes so difficult for ev to find a trajectory to a perfect creature local optima when Rfrequency > Rcapacity. The way I would look for the answer would be to map out the fitness landscape for a couple cases, one where Rfrequency is much less than Rcapacity and the other when Rfrequency is greater than Rcapacity. If you want a guess on what is happening, I would look at the number of perfect creature local optima for both cases.I don't need to guess, Alan. I'm not the one refusing to acknowledge that there is an information-content problem when Rfrequency > Rcapacity.
You can imagine that as much as you want. I wonder when you are going to acknowledge that evolution by mutation and selection is simply an optimization problem and the rate of convergence is very sensitive to the number of optimization conditions. Delphi understands this; after all, he was the one who raised the issue of the fitness landscape. Recombination and other forms of mutations besides random point mutations don’t change this mathematical fact, not even the mutation that you propose above changes this. You have a severe mathematical conundrum for your theory.

[Taffer]

See, this is why I gave up on this thread. Kleinman refuses to acknowledge reality. I have tried many times to explain things to him, both that recombination can, and does, increase the "information" in a gene pool, and that selection has nothing to do with this. He continues to claim that the model I posted (nothing to do with Hardy-Weinberg, by the way) is "recombination and selection" rather then "mutation and selection", which is a load of rubbish. Once again, it doesn't matter how variation arises, only that it exists. The only things which affect the rate of change of an allele in a population (except for things like population drift, inbreeding, migration, etc) is selective pressure. Not only this, but the rate of change is proportional to the power of the selection. He claims I am backpeddling, yet I have never changed my claim. He claims his citations show that increase selective pressure slow evolution, whereas what they really show is that the time until resistance to all drugs in a treatment increases as you add more drugs, which is naturally true and has nothing to do with evolution. He is confused about what multiple drug therapy does; it reduces the time until all drugs are ineffective by adding more the one drug. He compares one drug to many drugs, then assumes this is the same as many drugs at the same time compared to many drugs one after another. This is, as most can see I'm sure, stupid.

Kleinman, increasing selective pressures speeds up evolution. Increasing selective pressures does not affect the rate of mutation. Thus, increasing the number of mutations one is selecting for before we consider the evolution a "success" will slow the time until all those mutations occur in one individual. This is simple probability. Equating this, however, to slowing of evolution, which is, by definition, the change in allele frequency over time, is stupid. Allele frequency can only change if that particular allele already exists in a population. Increasing drugs in a trial slows the time until an organism emerges which has resistance to all drugs. It does not slow the rate of spread of these mutations once they are already present. This is why you are wrong. And this is why I make the distinction of "emergence" versus "evolution". When we are talking about drug resistance, we are talking about the time until a particular mutation emerges. This is affected only by mutational rate. If we are wanting more mutations before we consider the traits "emerged", then it will take longer. Simple logic tells us this, and no-one has ever denied that it is so. Once these mutations have emerged, they will propagate throughout the population. This is evolution.

[Henners]

See, this is why I gave up on this thread....This is evolution.

LMSO, Taffer.

Now, do you think that kleinman's discoveries will earn that Nobel prize for him, or will he simply sink into the (wordy, oh, how very, very wordy, but boringly repetitive) obscurity that he deserves?

[Kotatsu]

Kotatsu, I remember your examples, that mush you presented which you didn’t define the selection pressures or the target genes for the selection pressures. You are so used to using mush to justify your theory, you think it has turned into fact.

The target of the selection pressures --- and the entire list is a list of selection pressures --- would be the entire genome. It is only a curious circumstance that let the arms of the dinosaurs evolve into the wings of birds, and the scales into feathers. Many other animal groups have solved the same problem in other ways, by flaps of skin, enlargements of toes, and extensions from the ribs, if memory serves.

The only problem with this world view is that the mathematics and empirical evidence of mutation and selection shows that such transformation of their genomes can’t occur. It is mathematically impossible. I suppose you would say glass and diamond are from the same source because they have superficial similiarities.

No, I am a trained chemist as well, and knows that they do not show "superficial similarities" at the level comparable to the level at which the anatomies of birds and dinosaurs show similarities.

I guess you didn’t hear, they found a T rex fossil with soft tissue in it.

But the majority are still fossilised. Thus, on average, they taste of sto-- Oh, why on Earth are we discussing this?

R->r, see Kotatsu, I can take correction, when will you take correction on the way mutation and selection actually works.

The very moment you present some actual evidence for that my current understanding of it is flawed.

[Deetee]

Has Kleinman tried to publish this hypothesis of his in any scientific journal?

[Henners]

I guess you didn’t hear, they found a T rex fossil with soft tissue in it.


Fossilised soft tissue, that is.

[Paul C. Anagnostopoulos]

Ev is showing a peculiar behavior as the binding site width becomes shorter and the genome length increases. Unfortunately to study why ev does this requires a huge amount of number crunching.
It requires no number crunching at all. It only requires that you acknowledge that the binding sites might not be wide enough to accommodate a unique pattern. I do not understand why you won't acknowledge this, since it has nothing to do with your thesis anyway. I think perhaps you simply refuse to acknowledge anything anyone here says.


You can imagine that as much as you want. I wonder when you are going to acknowledge that evolution by mutation and selection is simply an optimization problem and the rate of convergence is very sensitive to the number of optimization conditions.
Hereby acknowledged. However, you're still ignoring the trees for the forest. You've replaced "goddidit" with "fitnesslandscapedidit."

~~ Paul

[kleinman]

See, this is why I gave up on this thread. … This is evolution.
Too bad you are giving up so quickly, again. We wanted to hear what you think happens when you breed a Chihuahua and a Great Dane. Are the resultant changes in the offspring due to mutation or recombination? Oh wait, you have told us that recombination is just another form of mutation. Taffer, we will miss your enlightened views, for a while.
Now, do you think that kleinman's discoveries will earn that Nobel prize for him, or will he simply sink into the (wordy, oh, how very, very wordy, but boringly repetitive) obscurity that he deserves?
Henners, we can tell you can slog through wordy posts and find the essential point. You did it with Taffer’s post.
Kotatsu, I remember your examples, that mush you presented which you didn’t define the selection pressures or the target genes for the selection pressures. You are so used to using mush to justify your theory, you think it has turned into fact.The target of the selection pressures --- and the entire list is a list of selection pressures --- would be the entire genome. It is only a curious circumstance that let the arms of the dinosaurs evolve into the wings of birds, and the scales into feathers. Many other animal groups have solved the same problem in other ways, by flaps of skin, enlargements of toes, and extensions from the ribs, if memory serves.
Kotatsu, putting whipped cream on top of mush still gives you mush. But tell us about your memories, were you there when animals solved problems “by flaps of skin, enlargements of toes, and from extension from the ribs”, because as I have grown older, I am doing all of these things. Kotatsu, your stories are strange but I am starting to see the evidence.
The only problem with this world view is that the mathematics and empirical evidence of mutation and selection shows that such transformation of their genomes can’t occur. It is mathematically impossible. I suppose you would say glass and diamond are from the same source because they have superficial similiarities.No, I am a trained chemist as well, and knows that they do not show "superficial similarities" at the level comparable to the level at which the anatomies of birds and dinosaurs show similarities.
Ok, tell us what these anatomical similarities are between birds and dinosaurs, start with their breast bones.
I guess you didn’t hear, they found a T rex fossil with soft tissue in it.But the majority are still fossilised. Thus, on average, they taste of sto-- Oh, why on Earth are we discussing this?
Here it is, I finally start talking about fossils and you evolutionists don’t want to discuss the topic. Hey Kotatsu, how much time does it take to fossilize something?
R->r, see Kotatsu, I can take correction, when will you take correction on the way mutation and selection actually works.The very moment you present some actual evidence for that my current understanding of it is flawed.
Hey, I am not going to show you my enlarged toes, flaps of skin or extensions from my ribs, however, I will show you real examples of how mutation and selection works.
Has Kleinman tried to publish this hypothesis of his in any scientific journal?
What is it with you evolutionists? What do have against the James Randi Educational forum, Science and Medicine threads? If you are really interested, I sent a letter to the editors at Nucleic Acids Research pointing out some basic issues with Dr Schneider’s publication. They said they do not take letters to the editor.
I guess you didn’t hear, they found a T rex fossil with soft tissue in it.Fossilised soft tissue, that is.
Nope, they recovered proteins.
Ev is showing a peculiar behavior as the binding site width becomes shorter and the genome length increases. Unfortunately to study why ev does this requires a huge amount of number crunching.It requires no number crunching at all. It only requires that you acknowledge that the binding sites might not be wide enough to accommodate a unique pattern. I do not understand why you won't acknowledge this, since it has nothing to do with your thesis anyway. I think perhaps you simply refuse to acknowledge anything anyone here says.
Paul, you have already acknowledge that perfect creature optima exist even when Rfrequency > Rcapacity. Mutation and selection is all about finding trajectories to local optima. Ev finds a local optimum even when Rfrequency > Rcapacity, it just happens not to be a perfect creature local optimum. The width of the binding site affects the shape of the fitness landscape but it doesn’t affect the ability of ev to search that fitness landscape for a local optima. Construct the fitness landscape and find out why ev doesn’t easily find perfect creature local optima rather than doing your strange speculations about the information content in the binding site.
You can imagine that as much as you want. I wonder when you are going to acknowledge that evolution by mutation and selection is simply an optimization problem and the rate of convergence is very sensitive to the number of optimization conditions.Hereby acknowledged. However, you're still ignoring the trees for the forest. You've replaced "goddidit" with "fitnesslandscapedidit."
Not quite Paul, it’s “fitnesslandscapeshows” that “evolutiondidn’tdoit”.

Here’s some more examples of fitness landscapes and what combination selection pressures do to these fitness landscapes.

http://www.bumc.bu.edu/www/busm/Ll/PDFs/Gleevec.pdf (http://www.bumc.bu.edu/www/busm/Ll/PDFs/Gleevec.pdf)
The advent of combination chemotherapy has extended lifespan for many hematologic malignancies. To appreciate the significance of this fact, one need only consider that in 1970, a person diagnosed with non-Hodgkin’s lymphoma could expect to live only about a year, whereas today, combination chemotherapy and targeted molecular agents such as Rituximab, a humanized monoclonal antibody chimera against the CD20 receptor on lymphoma cells, have boosted survival and been curative in many cases.
And
Several principles have been developed to manage the troublesome occurrence of mutations in human immunodeficiency virus-1 (HIV) RT, which may be of value if applied to the case of chemoresistance in CML. An important principle in the treatment of HIV with chemical agents is the simultaneous introduction of combinations of anti-viral drugs that have not been used previously for a particular patient (41).

http://cat.inist.fr/?aModele=afficheN&cpsidt=17704985 (http://cat.inist.fr/?aModele=afficheN&cpsidt=17704985)
HCV NS3 protease variants resistant to the protease inhibitor SCH 503034 were selected. Three mutations, T54A, V170A and A156S mutations conferred low to moderate levels of resistance (<20-fold). Longer exposure (>10 passages) or selection with higher levels of compound led to the selection of a more resistant variant, A156T (>100-fold). [Lin, C., Lin, K., Luong, Y.P., Rao, B.G., Wei, Y.Y., Brennan, D.L., Fulghum, J.R., Hsiao, H.M., Ma, S., Maxwell, J.P., Cottrell, K.M., Pemi, R.B., Gates, C.A., Kwong, A.D., 2004. In vitro resistance studies of hepatitis C virus serine protease inhibitors, VX-950 and BILN 2061: structural analysis indicates different resistance mechanisms. J. Biol. Chem. 279(17), 17508-17514; Lu, L., Pilot-Matias, T.J., Stewart, K.D., Randolph, J.T., Pithawalla, R., He, W., Huang, P.P., Klein, L.L., Mo, H., Molla, A., 2004. Mutations conferring resistance to a potent hepatitis C virus serine protease inhibitor in vitro. Antimicrob. Agents Chemother. 48(6), 2260-2266.] Combination with IFN-a drastically reduced the number of emergent colonies. Resistant colonies showed no change in sensitivity to IFN-a. Although the A156T mutation conferred the highest level of resistance to SCH 503034, it significantly reduced the colony formation efficiency (CFE) of the mutant replicon RNA, and rendered replicon cells less fit than those bearing wild-type replicons. Replicon cells bearing mutation A156S were less fit than wild-type in co-culture growth competition assays but showed no impact on CFE. The V170A mutation, on the other hand, did not affect replicon fitness in either assay, which was consistent with its emergence as the dominant mutant after 12 months of continuous selection. The reduced fitness of the most resistant variant suggests that it may be rare in naive patients and that development of high-level resistance may be slow. Combination therapy with IFN-a should also greatly reduce the potential emergence of resistance.
Isn’t it amazing what combination selection pressures do to the fitness landscape? The “fitnesslandscapeshows” shows that “evolutiondidn’tdoit”.

[Belz...]

I guess you didn’t hear, they found a T rex fossil with soft tissue in it.

Was the heart still beating ? :rolleyes:

[Belz...]

Still waiting, Klein...

http://forums.randi.org/showpost.php?p=3020068&postcount=5776

[Henners]

Fossilised soft tissue, that is.

Nope, they recovered proteins.


Nope?

You are denyng that the soft tissue was fossilised.

I see your academic rigour continues at its customary wet woodbine consistency.

[Gravy]

Nope?

You are denyng that the soft tissue was fossilised.

I see your academic rigour continues at its customary wet woodbine consistency.It was soft. Here are photos. http://www.msnbc.msn.com/id/7285683/

Tasted like mastodon.

[Paul C. Anagnostopoulos]

Paul, you have already acknowledge that perfect creature optima exist even when Rfrequency > Rcapacity. Mutation and selection is all about finding trajectories to local optima. Ev finds a local optimum even when Rfrequency > Rcapacity, it just happens not to be a perfect creature local optimum.
And why is that? Apparently there is something about this question that kills your curiosity.


The width of the binding site affects the shape of the fitness landscape but it doesn’t affect the ability of ev to search that fitness landscape for a local optima.
But it does affect its ability to find the global optimum. Why is that?


The advent of combination chemotherapy has extended lifespan for many hematologic malignancies. To appreciate the significance of this fact, one need only consider that in 1970, a person diagnosed with non-Hodgkin’s lymphoma could expect to live only about a year, whereas today, combination chemotherapy and targeted molecular agents such as Rituximab, a humanized monoclonal antibody chimera against the CD20 receptor on lymphoma cells, have boosted survival and been curative in many cases.
Does this have something to do with evolution?

~~ Paul

[Deetee]

It was soft. Here are photos. http://www.msnbc.msn.com/id/7285683/

Tasted like mastodon.
No - apparently it was physiologically like an ostrich.

Nah, on second thoughts this must be mathematically impossible - we all know reptiles have no connection whatsoever to birds.

[kleinman]

I guess you didn’t hear, they found a T rex fossil with soft tissue in it.Was the heart still beating ?
http://www.smithsonianmag.com/science-nature/10021606.html (http://www.smithsonianmag.com/science-nature/10021606.html)
No, but they did find red blood cells and heme.
Still waiting, Klein...
We all know your argument; you say I put up strawmen. Post an example where combination selection pressures accelerate evolution, I’ll respond to that.
Nope, they recovered proteins.Nope?
Read the link above.
It was soft. Tasted like mastodon.
That’s mastodon without hair on it (or feathers for that matter). Hey Gravy, what’s your favorite T rex recipe?
Paul, you have already acknowledge that perfect creature optima exist even when Rfrequency > Rcapacity. Mutation and selection is all about finding trajectories to local optima. Ev finds a local optimum even when Rfrequency > Rcapacity, it just happens not to be a perfect creature local optimum.And why is that? Apparently there is something about this question that kills your curiosity.
Oh, I am curious about it but I know that the answer to this question requires computation of data points, lots of data points, like 4^G data points. Dr Schneider and you have access to far more computer power than I do. Answer your own question and see whether it changes the fact that combination selection pressures profoundly slow the evolutionary process. Just because the three selection pressures don’t converge readily when Rfrequency > Rcapacity doesn’t affect the ability of any of the individual selection pressures from converging on zero mistakes.
The width of the binding site affects the shape of the fitness landscape but it doesn’t affect the ability of ev to search that fitness landscape for a local optima.But it does affect its ability to find the global optimum. Why is that?
I’ve posed an answer, too few perfect creature local optima and too many non-perfect creature local optima for ev to find a trajectory to one of the perfect creature local optima. The only way you will know for sure is to map the fitness landscape.
The advent of combination chemotherapy has extended lifespan for many hematologic malignancies. To appreciate the significance of this fact, one need only consider that in 1970, a person diagnosed with non-Hodgkin’s lymphoma could expect to live only about a year, whereas today, combination chemotherapy and targeted molecular agents such as Rituximab, a humanized monoclonal antibody chimera against the CD20 receptor on lymphoma cells, have boosted survival and been curative in many cases.Does this have something to do with evolution?
Paul, note the title of the article “Gleevec and the emergence of chemotherapeutic drug-resistant mutations”. I’ll post the article again and point out what the author is saying.
http://www.bumc.bu.edu/www/busm/Ll/PDFs/Gleevec.pdf (http://www.bumc.bu.edu/www/busm/Ll/PDFs/Gleevec.pdf)
The advent of combination chemotherapy has extended lifespan for many hematologic malignancies. To appreciate the significance of this fact, one need only consider that in 1970, a person diagnosed with non-Hodgkin’s lymphoma could expect to live only about a year, whereas today, combination chemotherapy and targeted molecular agents such as Rituximab, a humanized monoclonal antibody chimera against the CD20 receptor on lymphoma cells, have boosted survival and been curative in many cases.
This quote points out that combination therapy slows the ability of cancer cell populations to evolve to selection pressures. Targeted selection pressures have the ability to kill cancer cells while not killing normal cells.
Several principles have been developed to manage the troublesome occurrence of mutations in human immunodeficiency virus-1 (HIV) RT, which may be of value if applied to the case of chemoresistance in CML. An important principle in the treatment of HIV with chemical agents is the simultaneous introduction of combinations of anti-viral drugs that have not been used previously for a particular patient (41).
This paragraph illustrates that the same principle for slowing the evolution of resistance in HIV can be applied to cancer cells. That principle is combination selection pressures slow the evolution of resistance.

Now Paul, Dr Schneider does work for the National Cancer Institute. He has written a model for evolution by random point mutation and natural selection. What his model shows is substantiated by empirical evidence of what happens when cancer cells are subjected to selection pressures. Instead of acknowledging this mathematical fact, Dr Schneider tries to argue that his model refutes Professor Behe’s irreducible complexity hypothesis. You evolutionists have a remarkable ability to focus in on gnats when an elephant is tromping on your head.

[Paul C. Anagnostopoulos]

This quote points out that combination therapy slows the ability of cancer cell populations to evolve to selection pressures. Targeted selection pressures have the ability to kill cancer cells while not killing normal cells.
Neither the word evolve nor evolution appear in that article.

~~ Paul

[Henners]

It was soft. Here are photos. http://www.msnbc.msn.com/id/7285683/

Tasted like mastodon.

It wasn't soft until the fossilizing minerals were dissolved away.

Try reading the text as well as looking at the pictures.

I suggest that the well-run northern expression: "Are you talking to me or chowin' a brick" is appropriate under the circumstances.

[kleinman]

This quote points out that combination therapy slows the ability of cancer cell populations to evolve to selection pressures. Targeted selection pressures have the ability to kill cancer cells while not killing normal cells.Neither the word evolve nor evolution appear in that article.
Paul, are you going to take up Taffer’s banner? Let’s consider what words show up in the article. Though the words evolve or evolution does not appear in the body of the article, the word does appear in the references in this publication.
22. Cortes J, O'Dwyer ME. Clonal evolution in chronic myelogenous leukemia. Hematol Oncol Clin North Am 2004;18:671 – 684
and
35. Wardelmann E, Merkelbach-Bruse S, Pauls K, Thomas N, Schildhaus HU, Heinicke T, Speidel N, Pietsch T, Buettner R, Pink D, Reichardt P, Hohenberger P. Polyclonal evolution of multiple secondary KIT mutations in gastrointestinal stromal tumors under treatment with imatinib mesylate. Clin Cancer Res 2006;12:1743 – 1749.
So what words appear in the body of the article?

The title has “Gleevec and the emergence of chemotherapeutic drug-resistant mutations”

Then the following words appear in the body of the article:

However, despite the early success of Gleevec treatment, resistance to the drug began to be reported very quickly, which is not surprising, given the basic principles of mutation selection in single-agent therapy.
and
The phenomenon of biological resistance to chemical agents is well known and has been widely reported in fields as diverse as insect control with pesticides and antibiotic control of microorganisms, especially tuberculosis. Primary resistance refers to innate or natural ability to resist an agent, and is of marginal interest here. Secondary, or acquired resistance, arises from the biological processes of selection under the pressure of exposure to an agent and is a significant medical problem. Mutation of specific genes within a microorganism that are responsible for the transport or metabolism of the drug, or the signaling environment within the organism, enables the acquisition of drug resistance, often with dire consequences for the health and survival of a human host infected with that microorganism (24).
Or how about this?
The elements required for the appearance of stable resistant clones of CML cells are: a mechanism for the introduction of frequent mutations, DNA replication to “stabilize” and perpetuate the mutations, the possibility that adventitious mutations exist and selective pressure to provide a proliferative advantage to the cells that harbor the adventitious mutations (25). It should be apparent that each of these elements is in place in the setting of CML under the conditions of Gleevec single agent therapy.
So Paul, wave Taffer’s “emergence of drug resistance isn’t evolution by mutation and selection” flag. That’s weirder than your Rcapacity concept. You must really enjoy squirming.

[Belz...]

We all know your argument; you say I put up strawmen. Post an example where combination selection pressures accelerate evolution, I’ll respond to that.

You said "So far, the only point you have made is that something only becomes true when it is published in a “peer reviewed” journal."

I NEVER said that, so you're attacking a position that isn't even mine.

Do you even know what a strawman is ?

Now. Answer these questions, doctor:

I said I can come up with a nth-dimensional computer model. Does that mean that reality "loses" to mathematics and is suddenly n-dimensional ?

How about gene duplication ? Can it add new information ?

Why haven't other scientists followed your example ?

What are those things on either side of the Archaeopteryx ? Wings or not

What about those birds exhibiting reptilian characteristics ?

[Kotatsu]

Kotatsu, putting whipped cream on top of mush still gives you mush. But tell us about your memories, were you there when animals solved problems “by flaps of skin, enlargements of toes, and from extension from the ribs”, because as I have grown older, I am doing all of these things. Kotatsu, your stories are strange but I am starting to see the evidence.

Obviously I was not there when they evolved those structures. That would imply me both living millions of years ago, and having a lifespan of several million years --- that is, the time it took for these structures to evolve. What I meant, however, was that if memory serves, those are some alternative structures that are in use by arboreal animals in traditionally non-flying groups today for transport between trees, for catching prey and for escape from tree-born predators.

Flying squirrels have some sort of flaps of skin between their legs, as do colugos. Interestingly, these are not to my knowledge believed to be related, which implies that this transport mechanism has evolved twice within the mammals alone. Some "flying" lizards and snakes have elongated structures along their sides which aids them in gliding --- but not actually flying --- from tree to tree. These structures are analogous to the skin flaps of flying squirrels. Finally, I seem to recall that there are at least one group of tree-living frogs that have enlarged skin around their toes with which they glide between trees, but it's been ages since I ever read something about them.

All of these are examples of structures that have evolved largely in response to some or all of the selection pressures I outlined before. Wings are just a more efficient example, as evidenced by the enormous abundance of different species and forms of birds as opposed to the lesser abundance and success of colugos, "flying" frogs and so on.

Ok, tell us what these anatomical similarities are between birds and dinosaurs, start with their breast bones.

Remind me of this when I am back home again. I am out collecting lice at the moment, and have neither the time nor the litterature to make an extensive survey of similarities between birds and dinosaurs at the moment. I will be back home in less than two weeks.

Meanwhile, compare their ears, feet, and the underlying structure of their arms.

Here it is, I finally start talking about fossils and you evolutionists don’t want to discuss the topic.

Again, I will be more than happy to discuss fossils --- particularly ones pertaining to teh transition between dinosaurs and birds --- once I return home and don't have to rely on the Internet for information. Remind me then, and we could discuss it for ages.

Hey Kotatsu, how much time does it take to fossilize something?

No longer than it takes for you to present some actual evidence for what you claim.

Hey, I am not going to show you my enlarged toes, flaps of skin or extensions from my ribs, however, I will show you real examples of how mutation and selection works.

I think I speak for everyone here when I say that I am truly grateful for every and any part of your anatomy that you keep concealed from me.

Meanwhile, could you perhaps take some time to answer my previous questions on how DNA sequencing would disprove common descent?

[rocketdodger]

Now why don’t you tell us what the internal and external pressures are?
Internal are pressures generated by the population itself, external are all others.

This can be done rapidly whereas the mutation and selection process is far slower. Let’s see if you can take your argument beyond vague mush.
Perhaps I didn't make it clear. Allow me to put it in the form of a series of questions. First, why would the influence of multiple selective pressures slow evolution? Second, given the answer to the first, given a group of n pressures, would the addition of another (bringing the sum to n + 1 pressures) always result in a slower rate? Third, given a group of n pressures, would changing the relative weights any of those pressures result in no change whatsoever in the overall rate of evolution?

If you answer those rationally, then you will see the basis of my argument, which is quite simply that you can't cram the complexity of the evolutionary process into studies done on microorganisms.

What you call an overly simplistic model demonstrates what happens in reality with multiple selection pressures, that is that they profoundly slow the evolutionary process. If you have any examples which don’t show this, why don’t you post it for us?
I will answer this when I get back into work on monday and can comb over the study so I can show you exactly what I mean. For the time being, though, I have a hunch that 1) the population being studied is microbial, and therefore extremely simple, and 2) that the selective pressures just happened to negate each other. I see no reason why multiple selective pressures that were constructive with regard to each other would slow evolution at all.

[kleinman]

We all know your argument; you say I put up strawmen. Post an example where combination selection pressures accelerate evolution, I’ll respond to that.You said "So far, the only point you have made is that something only becomes true when it is published in a “peer reviewed” journal."

I NEVER said that, so you're attacking a position that isn't even mine.
It’s good that you admit that because you had taken a ridiculous position on this issue.
Do you even know what a strawman is ?
Why does this matter, all I have to know is what a straw theory is and that is what the theory of evolution is.
I said I can come up with a nth-dimensional computer model. Does that mean that reality "loses" to mathematics and is suddenly n-dimensional ?
No, it just demonstrates you don’t understand what a dimension is mathematically.
How about gene duplication ? Can it add new information ?
Nope, it can only repeat the same information. How about if I duplicate Belz, Belz, look at that, identical twins, how much information does that add to the gene pool? Zilch.
Why haven't other scientists followed your example ?
Belz, they are. Where do you think I get all my citations? The only thing they haven’t acknowledge yet is that if combination selection pressures profoundly slow evolution, it also makes common descent mathematically impossible. Of course Belz, you can post an example of combination selection pressures accelerating evolution, that would make your posts interesting.
What are those things on either side of the Archaeopteryx ? Wings or not
Wow Belz, wings on a bird, that’s amazing!
What about those birds exhibiting reptilian characteristics ?
Belz, you have reptileopormorphism. Take two lizards and call me in the morning.
Kotatsu, putting whipped cream on top of mush still gives you mush. But tell us about your memories, were you there when animals solved problems “by flaps of skin, enlargements of toes, and from extension from the ribs”, because as I have grown older, I am doing all of these things. Kotatsu, your stories are strange but I am starting to see the evidence. Obviously I was not there when they evolved those structures. That would imply me both living millions of years ago, and having a lifespan of several million years --- that is, the time it took for these structures to evolve. What I meant, however, was that if memory serves, those are some alternative structures that are in use by arboreal animals in traditionally non-flying groups today for transport between trees, for catching prey and for escape from tree-born predators.
Well, I’m glad you clarified that point. Hey, if you are several million years old, perhaps you knew our primate precursor?
Flying squirrels have some sort of flaps of skin between their legs, as do colugos. Interestingly, these are not to my knowledge believed to be related, which implies that this transport mechanism has evolved twice within the mammals alone. Some "flying" lizards and snakes have elongated structures along their sides which aids them in gliding --- but not actually flying --- from tree to tree. These structures are analogous to the skin flaps of flying squirrels. Finally, I seem to recall that there are at least one group of tree-living frogs that have enlarged skin around their toes with which they glide between trees, but it's been ages since I ever read something about them.
Now let’s see you show us how mutation and selection did all of this because as you now know, combination selection pressures profoundly slow the evolutionary process.
All of these are examples of structures that have evolved largely in response to some or all of the selection pressures I outlined before. Wings are just a more efficient example, as evidenced by the enormous abundance of different species and forms of birds as opposed to the lesser abundance and success of colugos, "flying" frogs and so on.
You are telling the evolutionist story lacking one piece of evidence, how did mutation and selection do this when combination selection pressures profoundly slow the evolutionary process.
Ok, tell us what these anatomical similarities are between birds and dinosaurs, start with their breast bones.Remind me of this when I am back home again. I am out collecting lice at the moment, and have neither the time nor the litterature to make an extensive survey of similarities between birds and dinosaurs at the moment. I will be back home in less than two weeks.
Hey Kotatsu, remember to tell us about the similarities between bird and reptile breast bones.
Here it is, I finally start talking about fossils and you evolutionists don’t want to discuss the topic.Again, I will be more than happy to discuss fossils --- particularly ones pertaining to teh transition between dinosaurs and birds --- once I return home and don't have to rely on the Internet for information. Remind me then, and we could discuss it for ages.
Kotatsu, you keep asking me to remind you of things. How long have you had this memory problem? Oh, never mind, what were we talking about?
Hey Kotatsu, how much time does it take to fossilize something?No longer than it takes for you to present some actual evidence for what you claim.
You are correct, fossilization can be very rapid. In fact check out this site.
http://humanfossil.com/ (http://humanfossil.com/)
HumanFossil Inc's patent-pending Rapid Fossilization ProcessTM (RFP) promises to convert any biological organism into a real fossil. Instead of taking millions of years, the RFP process takes just a few weeks. Any non-living mammal, up to 250 pounds can be fossilized. Your fossil will spend the rest of eternity in the South Dakota mountains, waiting for discovery...
Hey, I am not going to show you my enlarged toes, flaps of skin or extensions from my ribs, however, I will show you real examples of how mutation and selection works.I think I speak for everyone here when I say that I am truly grateful for every and any part of your anatomy that you keep concealed from me.
There you go, I offer proof of your theory of evolution and you want me to keep it concealed. I wonder how those flaps of skin and rib extensions would work for flying?
Meanwhile, could you perhaps take some time to answer my previous questions on how DNA sequencing would disprove common descent?
That’s what the mathematics of mutation and selection is all about, it is the bookkeeping for this process. Start with human and chimpanzee genomes, there are at least 150 million base differences between the two genomes. You have about 500,000 generations to accomplish these 150 million differences. Not only do you lack the selection pressures that would accomplish these transformations, you can only transform one gene rapidly at a time by the mutation and selection process. As soon as you have combination selection pressures, the evolutionary process is profoundly slowed.
Now why don’t you tell us what the internal and external pressures are?Internal are pressures generated by the population itself, external are all others.
Ok, so how do internal versus external pressures affect the mutation and selection process differently?
[quote="Kleinman"]This can be done rapidly whereas the mutation and selection process is far slower. Let’s see if you can take your argument beyond vague mush. What you call an overly simplistic model demonstrates what happens in reality with multiple selection pressures, that is that they profoundly slow the evolutionary process. If you have any examples which don’t show this, why don’t you post it for us?[quote="rocketdodger"]I will answer this when I get back into work on monday and can comb over the study so I can show you exactly what I mean. For the time being, though, I have a hunch that 1) the population being studied is microbial, and therefore extremely simple, and 2) that the selective pressures just happened to negate each other. I see no reason why multiple selective pressures that were constructive with regard to each other would slow evolution at all.
The population is microbial (as far as I know, no one has run the model with greater than about a 100k genome) and all independent selection pressures interfere with each other in the evolutionary process, that’s the nature of this optimization problem.

By the way, this principle applies to complex organisms as well. Rats are becoming resistant to warfarin, so combinations of this chemical with other poisons are used and it interferes with these animals evolving resistance to either component. Combination herbicides are also used to prevent weeds from evolving resistance to either chemical. I have posted numerous citations which show empirically how this works, and it works the same way as with microbes.

Rocketdodger, I think you are going to find that there is no such thing as cooperative selection pressures. By the way, selection pressures are not constructive, selection pressures interfere with the fitness of a population to reproduce.

[Vintij]

Internal are pressures generated by the population itself, external are all others.

Perhaps I didn't make it clear. Allow me to put it in the form of a series of questions. First, why would the influence of multiple selective pressures slow evolution? Second, given the answer to the first, given a group of n pressures, would the addition of another (bringing the sum to n + 1 pressures) always result in a slower rate? Third, given a group of n pressures, would changing the relative weights any of those pressures result in no change whatsoever in the overall rate of evolution?

If you answer those rationally, then you will see the basis of my argument, which is quite simply that you can't cram the complexity of the evolutionary process into studies done on microorganisms.

I will answer this when I get back into work on monday and can comb over the study so I can show you exactly what I mean. For the time being, though, I have a hunch that 1) the population being studied is microbial, and therefore extremely simple, and 2) that the selective pressures just happened to negate each other. I see no reason why multiple selective pressures that were constructive with regard to each other would slow evolution at all.


Actually you can learn just as much on evidence of evolution from microbial organisms as from any larger carbon based oxygen breathing organism. Keep in mind that after the cambrian explosion 540 million years ago, prokaryotic cells dominated the earth for much longer than any eukaryotic based organism (which includes dinosaurs) infact dinosaurs and large animals ruled for less than half of the last eon or post cambrian period.

Your right about the slowing of evolution though, the only factors you must consider for that type of research would involve climate change, plate tectonics, volcanic activity and ofcourse the 4 major extinctions (most notably the permian extinction) Multiple selective pressures have no effect on the speed or even the probability of mutation within an evolutionary time period for micro-organisms. Besides, pro-karyotic cells can reproduce and duplicate much faster than eukaryotic cells and arguably have the will to survive as much as any intelligent life fullfilling Homo-sapian. As bill bryson most notably put it "the purpose of life is, to be" nothing more. That is why it is in the most literal sence not unreasonable to say that all life is one.

[Paul C. Anagnostopoulos]

Paul, are you going to take up Taffer’s banner? Let’s consider what words show up in the article. Though the words evolve or evolution does not appear in the body of the article, the word does appear in the references in this publication.
I guess I have trouble thinking of clonal mutation in a single organism as evolution. If that's an accepted use of the term, so be it. I'd be wary about drawing conclusions about species evolution from clonal evolution.

~~ Paul

[Paul C. Anagnostopoulos]

... Dr Schneider tries to argue that his model refutes Professor Behe’s irreducible complexity hypothesis.
Are you saying that the genome of a perfect creature in Ev is not irreducibly complex? That's interesting. Tell us more.

~~ Paul

[kleinman]

Paul, are you going to take up Taffer’s banner? Let’s consider what words show up in the article. Though the words evolve or evolution does not appear in the body of the article, the word does appear in the references in this publication.I guess I have trouble thinking of clonal mutation in a single organism as evolution. If that's an accepted use of the term, so be it. I'd be wary about drawing conclusions about species evolution from clonal evolution.
I think you are missing the point of that citation. What they are talking about is the selection of mutations that interfere with their drug Gleevec for the treatment of CML. These authors recognize that resistance very quickly occurs when this drug is used as monotherapy and make the analogy of the treatment of HIV and combination therapy as a way of prolonging the usefulness of their drug. Whether you are talking about clonal cancer cells, viruses or more complex organisms, these replicators are subject to the principles of mutation and selection. I expect that Dr Schneider and the people at the National Cancer Institute who fund his research understand this and this is why ev gets funding. The problem I have with Dr Schneider’s work is not the modeling he has done but the conclusions he draws from his limited analysis.
... Dr Schneider tries to argue that his model refutes Professor Behe’s irreducible complexity hypothesis.Are you saying that the genome of a perfect creature in Ev is not irreducibly complex? That's interesting. Tell us more.
I’ve listened to Professor Behe’s hypothesis and I don’t believe that Dr Schneider’s model is applicable. Dr Schneider’s model is driven by contrived selection conditions that don’t exist in reality. These selection conditions demonstrate the mathematics of mutation and selection but only in an idealized manner. The realistic aspect of the model is its demonstration of how difficult it is to navigate a fitness landscape when you have multiple selection conditions and how easy it is for a population to navigate the fitness landscape with single selection conditions. Other than that, there is no other connection to reality. Real binding sites are not being evolved on real creatures.

What I find interesting is the resistance that evolutionists have to this finding despite all the real examples of mutation and selection that work the same way as Dr Schneider’s model works.

[kjkent1]

I think you are missing the point of that citation. What they are talking about is the selection of mutations that interfere with their drug Gleevec for the treatment of CML. These authors recognize that resistance very quickly occurs when this drug is used as monotherapy and make the analogy of the treatment of HIV and combination therapy as a way of prolonging the usefulness of their drug. Whether you are talking about clonal cancer cells, viruses or more complex organisms, these replicators are subject to the principles of mutation and selection. I expect that Dr Schneider and the people at the National Cancer Institute who fund his research understand this and this is why ev gets funding. The problem I have with Dr Schneider’s work is not the modeling he has done but the conclusions he draws from his limited analysis.If you weren't blinded by your religion, you would immediately realize, that even under controlled conditions, other selective pressures must be in play in every experiment where monotherapy is present, but they are relatively insignificant to the single toxin administered. From this, you should recognize that similar circumstances could easily arise in a natural environment, causing evolution to proceed quickly.

Thus, it follows that you have proven natural evolution by mutation and natural selection, using your own theoretical underpinnings.

But, alas, you do not make this analysis. Instead, you infer only the opposite extreme of possibilities, which is that evolution must be impossible.

What I find interesting is the resistance that evolutionists have to this finding despite all the real examples of mutation and selection that work the same way as Dr Schneider’s model works.What the evolutionist resists is your inability to acknowledge that your own theory leads to a different conclusion, just as easily as it leads to the conclusion you demand:

1. A natural environment may be dominated by a single selection pressure, even though others are present -- thus producing rapid evolutionary change.

2. A natural environment may be dominated by multiple selection pressures, each of great significance -- thus producing slow evolutionary change, and perhaps even extinction.

Your facts may be exactly correct, but your conclusion does not necessarily follow. In the end, the decision remains the same as it always has: one either believes in God for reasons which cannot be verified by any scientific experiment -- or, one does not.

The Greeks had all this philosophical stuff figured out 3,000+ years ago -- yet, we all continue to quarrel over it endlessly, without respite.

"Humans is the craziest people!" -- anon

[Henners]

...selection pressures interfere with the fitness of a population to reproduce.

...typed with a straight face, no doubt.

That is probably up there along with the fly's eye and "why are there still chimps?"

[BPScooter]

I'm wondering now how "appeal to authority" arguments work. Poster comrade kleinmann appeals to "Dr. Schneider" in such a way that deference is almost expected to be due. Why is it that Schneider is the trump card sometimes, but other people don't get to snuggle up to their favorite Dr.? grumble grump

I hereby declare, for this moment and no other, the following: Kleinman, you are irritating by virtue of your relentless insultingness. I think that people like you are totally ignorant in the interpersonal and literary gifts. You're an irritating dork. Neener neener. If you had something to say, you would have said it by now.

You do appear to have knowledge and skill in some areas. I think you lack skills in presentation and defense of a thesis. It seems clear that you are convinced that contemporary biology is wrong, from root to branch--you have another interpretation of it. These posts constitute a conversation. We (I) would like to hear a testable version of it all.

Since, as you claim, evolution has been slowed unto stopped from time time over the last several million years, please clearly state the reason that we have different species and processes of speciation.

If you don't have the "balls" to state that you think a super-natural force was involved, that's weird. Everything you've stated seems to me to indicate that you believe that Natural forces are insufficient. By Natural, of course, I mean things that we can measure and speculate about.

I now apologize for this awful example of troll feeding.

[Kotatsu]

I see you have decided to bring your posts to new levels of incomprehensibility. Good work! Strangely enough, they are easier to quote this way, which may be an unwanted spin-off effect.

Well, I’m glad you clarified that point.

Good.

Now let’s see you show us how mutation and selection did all of this because as you now know, combination selection pressures profoundly slow the evolutionary process.

No, I wouldn't say that I know that that is necessarily the case in all cases. Do you remember, for example, how evolution was not slowed in the examples of moths, phytophagous insects, Limnodrilus and limpets?

Hey Kotatsu, remember to tell us about the similarities between bird and reptile breast bones.

Certainly: There are likely to be few or none, as the specialized breastbone of modern birds is an apomorphy which it is illogical to expect to find in modern reptiles. However, several groups intermediate between the modern birds and the dinosaurs from which they have evolved show structures which are intermediate between the dinosaurian breastbone and the avian one. As predicted by evolutionary theory, they also --- again, if I remember correctly --- grow progressively more similar to that of modern birds as we approach modern times.

Now, did you look into the anatomical similarities I suggested in my last post?

Oh, never mind, what were we talking about?

You were just about to admit defeat and withdraw your silly claims after having been overwhelmed by the evidence presented that disassembles the air castle your previous notions lived in. We're all waiting.

I wonder how those flaps of skin and rib extensions would work for flying?

If you refer to those I described previously, I would guess most of them woud form very poor actual wings (though bats and pterosaurs certainly have/had the flap-of-skin type). The animals without proper wings but with these other structures are generally gliders.

That’s what the mathematics of mutation and selection is all about, it is the bookkeeping for this process. Start with human and chimpanzee genomes, there are at least 150 million base differences between the two genomes. You have about 500,000 generations to accomplish these 150 million differences. Not only do you lack the selection pressures that would accomplish these transformations, you can only transform one gene rapidly at a time by the mutation and selection process. As soon as you have combination selection pressures, the evolutionary process is profoundly slowed.

How do you know that "[we] lack the selection pressures"? I don't know what the differences between the genomes are in any detail, but I'd certainly say that there is a lot of difference in selection pressures acting on chimps and on humans.

Also, this does not significantly address my question about how genetic sequencing disproves common descent. Have you ever looked at a phylogenetic tree?

I’ve listened to Professor Behe’s hypothesis and I don’t believe that Dr Schneider’s model is applicable.

I may be overly flippant here, but I believe that is at least partly because of the fact that although it is inadequate to explain evolution as a whole, Dr Schneider's model, unlike Professor Behe's, has a basis in reality.

[Deetee]

What the evolutionist resists is your inability to acknowledge that your own theory leads to a different conclusion, just as easily as it leads to the conclusion you demand:

1. A natural environment may be dominated by a single selection pressure, even though others are present -- thus producing rapid evolutionary change.

2. A natural environment may be dominated by multiple selection pressures, each of great significance -- thus producing slow evolutionary change, and perhaps even extinction.

Your facts may be exactly correct, but your conclusion does not necessarily follow.
I've not been following this thread closely (and who could blame me after 5800 posts) but this would seem to be the crux of the issue. Why can Kleinman not see this?

Combination HIV therapy is "intelligently designed" (by humans, not god) to induce extinction in the organism by rendering it replicatively unfit.
How do we quantitate how many life forms have become extinct because of overwhelming multiple natural selection pressures as opposed to those which have rapidy evolved in the face of varying selection pressures?

[Henners]

I've not been following this thread closely (and who could blame me after 5800 posts) but this would seem to be the crux of the issue. Why can Kleinman not see this?

Combination HIV therapy is "intelligently designed" (by humans, not god) to induce extinction in the organism by rendering it replicatively unfit.
How do we quantitate how many life forms have become extinct because of overwhelming multiple natural selection pressures as opposed to those which have rapidy evolved in the face of varying selection pressures?

Over the past 50,000 years or so there are one heck of a lot of extinctions because of a single selection pressure.

kleinman probably has an authority that he can appeal to for this being about ten times the age of the planet.

[Belz...]

It’s good that you admit that because you had taken a ridiculous position on this issue.

So it WAS a strawman, now ? Or did you simply not understand what I had said ?

Why does this matter, all I have to know is what a straw theory is and that is what the theory of evolution is.

Actually, it's very important that you know the various logical fallacies so you can avoid using them. Don't you agree ?

No, it just demonstrates you don’t understand what a dimension is mathematically.

Then, pray tell, what's a dimension, mathematically, that's different from a dimension, physically ?

Nope, it can only repeat the same information. How about if I duplicate Belz, Belz, look at that, identical twins, how much information does that add to the gene pool? Zilch.

Some biologist you'd make. Once the gene is duplicated, it's quite free to mutate without being detrimental to the organism until it actually devellops a function. Once that happens, you have NEW information, agreed ?

Belz, they are. Where do you think I get all my citations? The only thing they haven’t acknowledge yet is that if combination selection pressures profoundly slow evolution, it also makes common descent mathematically impossible.

Klein, that's precisely what I'm asking, and I get the distinct impression that you are avoiding answering my question: why haven't they agreed that multiple selection pressures slow evolution if it's so obvious ?

Of course Belz, you can post an example of combination selection pressures accelerating evolution, that would make your posts interesting.

I'm not claiming that, so I don't understand why you keep asking me to do it.

Wow Belz, wings on a bird, that’s amazing!

Good, good. I'll assume you agree that those are wings.

Now, what are those things in its mouth ? Teeth ? And what are those things on its hands ? Claws ?

Belz, you have reptileopormorphism. Take two lizards and call me in the morning.

I'm sure you wouldn't even be able to give me a definition of that word.

Kleinman, you have creationist delusions. Take two origins of species and call me in the morning.

[Belz...]

Dr Schneider’s model is driven by contrived selection conditions that don’t exist in reality.

And yet it's supposed to demonstrate something ?

[Paul C. Anagnostopoulos]

I’ve listened to Professor Behe’s hypothesis and I don’t believe that Dr Schneider’s model is applicable. Dr Schneider’s model is driven by contrived selection conditions that don’t exist in reality. These selection conditions demonstrate the mathematics of mutation and selection but only in an idealized manner.
So you are drawing earth-shattering conclusions about real life from a contrived model, yet somehow irreducible complexity is not relevant to the model.


The realistic aspect of the model is its demonstration of how difficult it is to navigate a fitness landscape when you have multiple selection conditions and how easy it is for a population to navigate the fitness landscape with single selection conditions. Other than that, there is no other connection to reality.
Yet you are reaching the conclusion from this model that real evolution is impossible.

So why isn't a perfect creature in Ev an example of irreducible complexity? Let's make sure we have Behe's latest definition, from 2001:

irreducible complexity ...: a single system which is necessarily composed of several well-matched, interacting parts that contribute to the basic function, and where the removal of any one of the parts causes the system to effectively cease functioning.
Not to be confused with Dembski's definition:

A system performing a given basic function is irreducibly complex if it includes a set of well-matched, mutually interacting, nonarbitrarily individuated parts such that each part in the set is indispensable to maintaining the system's basic, and therefore original, function. The set of these indispensable parts is known as the irreducible core of the system.
Oh wait, don't forget Dembski's latest adjustment:

Along the same lines, consider an outboard motor whose basic
function is to propel a small fishing boat around a lake by means of a
gasoline- or electric-powered engine that turns a propeller. The outboard
motor is irreducibly complex and its irreducible core includes, among
other things, a propeller, an engine, and a drive shaft connecting engine to
propeller. Now, we can imagine simplifying this arrangement by replacing
the engine and drive shaft with a rubber band that, when wound up, turns
the propeller. But it’s unlikely that the level of performance attainable
from such an arrangement will propel a boat around a lake. In other words,
minimum function is unlikely to be preserved with the rubber band. Yet
even if it was, this new arrangement would not perform the primary
function in the same way as the original outboard motor: the original
outboard motor depended on the turning of rotors and not the torsion of an
elastic medium. [emphasis mine]
So here is my definition:

A system is irreducibly complex if, after you remove a component, the new system is not identical to the original system.

~~ Paul

[Belz...]

A system is irreducibly complex if, after you remove a component, the new system is not identical to the original system.

Doesn't that kind of make EVERY system irreducibly complex ?

[Paul C. Anagnostopoulos]

Doesn't that kind of make EVERY system irreducibly complex?
Indeedy-do, and that appears to be where the definition is headed. :D Now Dembski seems to be saying the the reduced system has to operate in the same manner and with the same performance as the original system. So as he waters down the definition in response to critics' analysis of specific examples, he will eventually make it a tautology. Then it will be obvious that no one need care about the idea at all.

Or something like that.

~~ Paul

[Henners]

The thing that tickles be about irreducible complexity is that, according to the definition, complex things cannot be irreducibly complex.

There are, for example, lots of bits that you can throw away off an aeroplane, and it's still an aeroplane.

The only things that are really irreducibly complex are also arbitrarily simple.

For example, the simplest know bacterial flagellum, as Young and Edis explained, might have 51 proteins in it. So that is irreducibly complex, but only until another one is discovered with, say, 48 proteins.

And on it goes.

[Belz...]

The problem with irreducible complexity is that it ignores the fact that the flagellum wasn't built that way to start with, and that the proteins were not necessarily added (evolved, I mean) one by one the way they are now.

I mentioned gene duplication. Duplicating part of your genetic material's a good way to get new information and evolving a new function. Of course, once the evolving is "done" with, it looks like no component could be removed without preventing the structure from functioning, and that's true, but it just wasn't the same structure X million years ago.

[Belz...]

Paul, do you have links to those Dembski quotes ?

[kleinman]

...selection pressures interfere with the fitness of a population to reproduce....typed with a straight face, no doubt.

That is probably up there along with the fly's eye and "why are there still chimps?"
Feel free to post any selection pressures that you know of that enhance a populations’ fitness to reproduce.
I hereby declare, for this moment and no other, the following: Kleinman, you are irritating by virtue of your relentless insultingness. I think that people like you are totally ignorant in the interpersonal and literary gifts. You're an irritating dork. Neener neener. If you had something to say, you would have said it by now.
Oh no, I’ve annoyed BPScooter. I guess you couldn’t come up with an example of multiple selection pressures accelerating evolution.
If you don't have the "balls" to state that you think a super-natural force was involved, that's weird. Everything you've stated seems to me to indicate that you believe that Natural forces are insufficient. By Natural, of course, I mean things that we can measure and speculate about.
Ask Paul who chose the thread with this name to carry on this discussion.
I see you have decided to bring your posts to new levels of incomprehensibility. Good work! Strangely enough, they are easier to quote this way, which may be an unwanted spin-off effect.
The forum screen editor changes my BBS code; I tried to fix it but decided to leave it as is. You evolutionists are good at reading tea leaves so I figured you could read that post.
Now let’s see you show us how mutation and selection did all of this because as you now know, combination selection pressures profoundly slow the evolutionary process.No, I wouldn't say that I know that that is necessarily the case in all cases. Do you remember, for example, how evolution was not slowed in the examples of moths, phytophagous insects, Limnodrilus and limpets?
Yes, I remember your vague unrepeatable examples where you don’t define the selection pressures and the target genes for those pressures. It’s convenient for you not to do this because then you don’t have to describe what mutations at what loci were required for the evolutionary process to occur. This is the kind of mushy science evolutionist practice on a regular basis.
Hey Kotatsu, remember to tell us about the similarities between bird and reptile breast bones.Certainly: There are likely to be few or none, as the specialized breastbone of modern birds is an apomorphy which it is illogical to expect to find in modern reptiles. However, several groups intermediate between the modern birds and the dinosaurs from which they have evolved show structures which are intermediate between the dinosaurian breastbone and the avian one. As predicted by evolutionary theory, they also --- again, if I remember correctly --- grow progressively more similar to that of modern birds as we approach modern times.
The evolutionist mythological story; in a land long ago things were very different… Well Kotatsu do you think mutation and selection worked differently long ago in a far away land because today combination selection pressures profoundly slow the evolutionary process.
Now, did you look into the anatomical similarities I suggested in my last post?
I will when you tell us how this relates to the mutation selection process.
Oh, never mind, what were we talking about?You were just about to admit defeat and withdraw your silly claims after having been overwhelmed by the evidence presented that disassembles the air castle your previous notions lived in. We're all waiting.
I am overwhelmed by all the evidence that shows that combination selection pressures profoundly slow evolution and the silly claim I am making is based on a peer reviewed and published model of random point mutation and natural selection. So Kotatsu, while you dream of reptiles growing feathers and wings, you can dream of me withdrawing my claims. The issue of how mutation and selection actually works is too important to allow your vague, unrepeatable, ill defined examples to contradict the mathematical and precisely defined examples I have and will continue to present.
That’s what the mathematics of mutation and selection is all about, it is the bookkeeping for this process. Start with human and chimpanzee genomes, there are at least 150 million base differences between the two genomes. You have about 500,000 generations to accomplish these 150 million differences. Not only do you lack the selection pressures that would accomplish these transformations, you can only transform one gene rapidly at a time by the mutation and selection process. As soon as you have combination selection pressures, the evolutionary process is profoundly slowed.How do you know that "[we] lack the selection pressures"? I don't know what the differences between the genomes are in any detail, but I'd certainly say that there is a lot of difference in selection pressures acting on chimps and on humans.
Tell us what those selection pressures are and the target genes for those selection pressures. You do like mush.
Also, this does not significantly address my question about how genetic sequencing disproves common descent. Have you ever looked at a phylogenetic tree?
When and if you ever understand that evolution by mutation and selection is simply an optimization problem, then you will understand that the more conditions you try to optimize by, the slower the process goes. If you try to transform more than a single gene at a time by the mutation and selection process, the probabilities of getting beneficial mutations in more than one gene simultaneously becomes infinitesimally small. You still have some work to do in order to understand anything about the mathematics of mutation and selection.
I’ve listened to Professor Behe’s hypothesis and I don’t believe that Dr Schneider’s model is applicable.I may be overly flippant here, but I believe that is at least partly because of the fact that although it is inadequate to explain evolution as a whole, Dr Schneider's model, unlike Professor Behe's, has a basis in reality.
Then why don’t you accept the result from Dr Schneider’s model that combination selection pressures profoundly slow evolution?
Your facts may be exactly correct, but your conclusion does not necessarily follow.I've not been following this thread closely (and who could blame me after 5800 posts) but this would seem to be the crux of the issue. Why can Kleinman not see this?

Combination HIV therapy is "intelligently designed" (by humans, not god) to induce extinction in the organism by rendering it replicatively unfit.
How do we quantitate how many life forms have become extinct because of overwhelming multiple natural selection pressures as opposed to those which have rapidy evolved in the face of varying selection pressures?
It’s simple Deetee; give us an example of combination “natural” selection pressures which accelerate evolution. I’ll even make it simpler for you give us an example of combination “intelligently designed” selection pressures which accelerate evolution. I’ll give you hint, if you want to accelerate the evolutionary process, use a single selection pressures which starts at a sub-lethal level and then increase the intensity of the selection pressure. What you evolutionists are so slow to grasp is that the mutation selection process is simply an optimization problem. It is extremely difficult to optimize on more than a single condition at a time.
Over the past 50,000 years or so there are one heck of a lot of extinctions because of a single selection pressure.

kleinman probably has an authority that he can appeal to for this being about ten times the age of the planet.
Henners, I thought you said there are constructive selection pressures?
No, it just demonstrates you don’t understand what a dimension is mathematically.Then, pray tell, what's a dimension, mathematically, that's different from a dimension, physically ?
The physical (space/time) dimensions are only a tiny subset of mathematical dimension. Here are a couple examples to demonstrate this difference.

In two dimensions, a circle can be defined mathematically by x^2 + y^2 = R^2. In three dimensions, a sphere can be defined mathematically by x^2 + y^2 + z^2 = R^2. In four dimensions, a hyper-sphere can be defined mathematically by w^2 + x^2 + y^2 + z^2 = R^2, and so on. To take this out of the abstract, consider heat transfer problems. In the simplest cases, temperature is a function of space and time in these systems. This simple system requires five mathematical dimensions to describe this physical system. If pressure is also an independent variable, then you require six mathematical dimensions to describe this system and so on for each independent variable you are considering.
Nope, it can only repeat the same information. How about if I duplicate Belz, Belz, look at that, identical twins, how much information does that add to the gene pool? Zilch.Some biologist you'd make. Once the gene is duplicated, it's quite free to mutate without being detrimental to the organism until it actually devellops a function. Once that happens, you have NEW information, agreed ?
Sure the duplicated gene can mutate but you know how slow the mutation selection process is with combination selection pressures. It’s a mystery to me why you evolutionists think that somehow gene duplication solves your mathematical problem with the theory of evolution. Genes are duplicated all the time, it’s called reproduction, but some how, you think if a gene is erroneously duplicated on the same genome that common descent suddenly becomes possible.
Belz, they are. Where do you think I get all my citations? The only thing they haven’t acknowledge yet is that if combination selection pressures profoundly slow evolution, it also makes common descent mathematically impossible.Klein, that's precisely what I'm asking, and I get the distinct impression that you are avoiding answering my question: why haven't they agreed that multiple selection pressures slow evolution if it's so obvious ?
Belz, I post these citations precisely because they do show that combination selection pressures profoundly slow the evolutionary process. I suspect that these authors are not familiar with Dr Schneider’s model which shows the same thing. It is only when you put the mathematical evidence together with the empirical evidence that it becomes apparent how mutation and selection actually works.
Of course Belz, you can post an example of combination selection pressures accelerating evolution, that would make your posts interesting.I'm not claiming that, so I don't understand why you keep asking me to do it.
It’s good that you don’t claim this since it is mathematically.
Wow Belz, wings on a bird, that’s amazing! Good, good. I'll assume you agree that those are wings.

Now, what are those things in its mouth ? Teeth ? And what are those things on its hands ? Claws ?
That’s more rare then hen’s teeth.
Dr Schneider’s model is driven by contrived selection conditions that don’t exist in reality.And yet it's supposed to demonstrate something ?
Yes it does Belz, it does a good job at demonstrating how slow the mutation selection process is with three selection conditions and how rapid the process becomes if you use only a single selection condition.
I’ve listened to Professor Behe’s hypothesis and I don’t believe that Dr Schneider’s model is applicable. Dr Schneider’s model is driven by contrived selection conditions that don’t exist in reality. These selection conditions demonstrate the mathematics of mutation and selection but only in an idealized manner.So you are drawing earth-shattering conclusions about real life from a contrived model, yet somehow irreducible complexity is not relevant to the model.
I wouldn’t call my conclusions earth-shattering, only theory of evolution shattering. What Dr Schneider’s model demonstrates is how difficult it is to evolve three selection conditions simultaneously and how easy it is to evolve a single selection condition, even with tiny populations. Now you have already admitted that ev does not evolve binding sites de novo, so what about ev refutes irreducible complexity? Does ev explain how the components of the DNA replicase system came about before DNA could be replicated? Ev can’t even evolve binding sites when Rfrequency > Rcapacity.
The realistic aspect of the model is its demonstration of how difficult it is to navigate a fitness landscape when you have multiple selection conditions and how easy it is for a population to navigate the fitness landscape with single selection conditions. Other than that, there is no other connection to reality.Yet you are reaching the conclusion from this model that real evolution is impossible.
That’s not my conclusion at all. I realize that evolution occurs but ev shows that it is a much more limited process than what evolutionist allege. It is the notion of common descent which ev refutes. And you know what Paul; there is lots of empirical evidence which demonstrates what ev shows.
So why isn't a perfect creature in Ev an example of irreducible complexity? Let's make sure we have Behe's latest definition, from 2001:irreducible complexity ...: a single system which is necessarily composed of several well-matched, interacting parts that contribute to the basic function, and where the removal of any one of the parts causes the system to effectively cease functioning.
Just what is the function of the binding sites? What is the interaction of the binding sites with the nonbinding site region and the gene? Ev is not the evolution of the better mousetrap. All ev does is evolve particular sequences of bases based on particular contrived selection conditions and this process is extremely slow on all but the tiniest genomes.
So here is my definition:A system is irreducibly complex if, after you remove a component, the new system is not identical to the original system.
So how does ev show the DNA replicase system is made? Ev can’t even evolve binding sites when Rfrequency > Rcapacity.
A system is irreducibly complex if, after you remove a component, the new system is not identical to the original system.Doesn't that kind of make EVERY system irreducibly complex ?
Hey, let Paul make a point. He has made so many irrational and illogical points with his Rcapacity concept that I thought I’d let him have this point. On second thought, you are correct Belz, Paul’s definition for irreducible complexity is irrational and illogical.
Doesn't that kind of make EVERY system irreducibly complex?Indeedy-do, and that appears to be where the definition is headed. Now Dembski seems to be saying the the reduced system has to operate in the same manner and with the same performance as the original system. So as he waters down the definition in response to critics' analysis of specific examples, he will eventually make it a tautology. Then it will be obvious that no one need care about the idea at all.
Now Paul, you should know something about watered down definitions. You have so much experience with your definition for ev. Let’s see, it started out ev modeled reality, then ev became a model of a part of the evolutionary landscape and then ev models 0.01% of evolution. What’s your definition now, ev refutes irreducible complexity because the binding sites interact so well with the nonbinding site region and the gene? Paul, it seems you think that ev has evolved the better mousetrap. When will ev evolve the cheese? Wait a minute; kjkent1 has taken care of that with his string cheese theory of evolution.
The problem with irreducible complexity is that it ignores the fact that the flagellum wasn't built that way to start with, and that the proteins were not necessarily added (evolved, I mean) one by one the way they are now.
Belz, since you seem to know something about this topic, why don’t you tell us how the DNA replicase system came about? In particular, could you tell us what gyrase and helicase were doing before DNA could be replicated? I asked this same question of the author of the Flagellum Unspun, Professor Miller at Brown University. Let’s hear what your answer is.

While Paul works on his cheesy definitions and Belz spins his tales, let’s give some more real examples of what ev shows, that is combination selection pressures profoundly slow the evolutionary process.

http://www.postgradmed.com/issues/2005/01_05/hauser.htm (http://www.postgradmed.com/issues/2005/01_05/hauser.htm)
Is combination therapy indicated once susceptibilities are known, or is monotherapy sufficient? Two justifications for the use of combination therapy in this situation have been given: harnessing synergy and preventing the emergence of resistance.
And
The rationale for using two antibiotics to prevent the emergence of resistance is that bacteria harboring mutations that confer resistance to one antibiotic will be quickly killed by the second antibiotic before additional resistance-conferring mutations have an opportunity to occur. However, the effectiveness of combination therapy in preventing the emergence of antibiotic resistance in P aeruginosa infections remains controversial. For example, in an observational study of 271 patients with P aeruginosa infections (17), combination therapy was not associated with a decrease in the emergence of resistance.

On the other hand, in a prospective, case-controlled observational study of patients infected with P aeruginosa, Enterobacter species, Citrobacter species, or Serratia marcescens, Jacobson and colleagues (20) found that combination therapy (an extended-spectrum cephalosporin plus an aminoglycoside) was associated with less frequent development of resistance than monotherapy (an extended-spectrum cephalosporin alone).
http://hbvadvocate.org/news/NewsUpdates_pdf/2.2_Conference_Reports/EASL_2002_Agenda/Section4/zoulim.pdf (http://hbvadvocate.org/news/NewsUpdates_pdf/2.2_Conference_Reports/EASL_2002_Agenda/Section4/zoulim.pdf)
The most important issue, when starting antiviral therapy, is to prevent drug resistance. As a rationale, the use of inhibitors with different mechanism of action and different resistance profiles should be favoured in clinical trials to obtain an additive or synergistic antiviral effect to limit the risk of emergence of drug resistant strains (3). One study showed a potential beneficial effect of the association of famciclovir and lamivudine by accelerating the kinetics of viral clearance compared to lamivudine monotherapy (36). However, the long-term effect of the combination on the selection of drug resistant mutants was not studied. Trials combining lamivudine with adefovir dipivoxil have started, but other combinations such as clevudine and emtricitabine(37), or others with entecavir, etc… may follow the same rationale. This will be the next important step of the management of chronic hepatitis B. Results of trials associating or combining sequentially lamivudine and interferon alpha are discussed in another manuscript in this issue of J. Hepatol (Schalm et al). Some studies but not all, suggest that the addition of interferon alpha to lamivudine either in association (38) or sequentially (39) may decrease the rate of lamivudine resistance. This should be confirmed in further independent trials.

http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=11594680&dopt=Citation (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=11594680&dopt=Citation)
Recent studies have shown that the kinetics of hepatitis B virus (HBV) clearance during antiviral therapy are slow, requiring long-term therapy to control viral replication. It has also been shown that emergence of resistant mutants is accelerated by high HBV replication and hepatocyte turnover, which are common features in patients with chronic HBV infection. It is therefore important to continue research on novel antiviral agents to design optimal combination strategies. The duck and woodchuck models of hepadnavirus infection are currently the best models for the investigation of the inhibitory effect of nucleoside analogues on wild-type and lamivudine-resistant mutants. Our studies revealed that these mutants have a decreased priming and elongation activity, and remain sensitive to novel nucleoside analogues. Tissue culture experiments with transient transfection of wild-type and mutant viruses also confirmed these data. Infection studies in primary hepatocytes and in animal models gave insight into the pathobiology of lamivudine-resistant mutants, as well as into the kinetics of wild-type virus clearance during antiviral therapy. Furthermore, it appears that novel strategies inducing a specific anti-HBV immune response by a DNA vaccine approach may induce viral clearance. Altogether, these results suggest that: (i) lamivudine-resistant mutants are likely to be cross-resistant to other L-cytidine analogues; (ii) antiviral therapy using a single reverse transcriptase (RT) inhibitor is likely to fail to eradicate viral covalently closed circular DNA; and (iii) new nucleoside analogues with unique mode of action (inhibition of priming or elongation of RT, or DNA polymerase activity) and activity against lamivudine-resistant strains are emerging. Combination of these new anti-HBV agents with DNA based immunization may prove useful to eradicate viral infection.
Now when are any of you evolutionists going to post a citation which shows that combination selection pressures accelerate evolution?

[Paul C. Anagnostopoulos]

For example, the simplest know bacterial flagellum, as Young and Edis explained, might have 51 proteins in it. So that is irreducibly complex, but only until another one is discovered with, say, 48 proteins.
Or until a subsystem of the flagellum is found to be useful for something else, say a secretory apparatus:

http://www.millerandlevine.com/km/evol/design2/article.html


Paul, do you have links to those Dembski quotes?
Oh gosh. His latest backpeddle can be found in:

http://www.springerlink.com/content/g527h45501l632v8/

I think his original definition is in Darwin's Black Box.

~~ Paul

[Paul C. Anagnostopoulos]

Now you have already admitted that ev does not evolve binding sites de novo, so what about ev refutes irreducible complexity?
Actually, I recall trying to get you to define what you meant by de novo, but having no success.

What does evolution de novo have to do with irreducible complexity? An IC system cannot have even one critical part removed, so the evolution of the system prior to the addition of its last component is irrelevant. The addition of that last part must have been done by magic, or else the system would be reducible by virtue of the fact that you could remove that last component.

So Ev evolves an IC system, even though it does not start from only a cloud of hydrogen gas.


That’s not my conclusion at all. I realize that evolution occurs but ev shows that it is a much more limited process than what evolutionist allege. It is the notion of common descent which ev refutes.
Ah, now it's common descent that is impossible.


Hey, let Paul make a point. He has made so many irrational and illogical points with his Rcapacity concept that I thought I’d let him have this point.
It was a joke, Alan. However, you appear to be willing to grant me my point: "Then it will be obvious that no one need care about the idea at all."

~~ Paul

[Henners]

Feel free to post any selection pressures that you know of that enhance a populations’ fitness to reproduce.

"fitness" is a technical term, kleinman. Why don't you look up what it means, replace the word "fitness" in your rather silly sentence with that definition, and then try to re-read the sentence in such a way as to make sense of it.

...and that's not all that's wrong with the sentence.

"Fitness" is not a characteristic of populations, and populations reproduce at the level of complete replacement while soft selection operates on all sides.

If you don't even understand the problem, what makes you think that you can competently model it?

[Henners]

Henners, I thought you said there are constructive selection pressures?

That is incorrect, kleinman.

I didn't say that.

You did.

I would not have made such a mind-numbingly moronic, stupid, and childish comment.

[kjkent1]

What the evolutionist resists is your inability to acknowledge that your own theory leads to a different conclusion, just as easily as it leads to the conclusion you demand:

1. A natural environment may be dominated by a single selection pressure, even though others are present -- thus producing rapid evolutionary change.

2. A natural environment may be dominated by multiple selection pressures, each of great significance -- thus producing slow evolutionary change, and perhaps even extinction.

Your facts may be exactly correct, but your conclusion does not necessarily follow.I've not been following this thread closely (and who could blame me after 5800 posts) but this would seem to be the crux of the issue. Why can Kleinman not see this?

Combination HIV therapy is "intelligently designed" (by humans, not god) to induce extinction in the organism by rendering it replicatively unfit.
How do we quantitate how many life forms have become extinct because of overwhelming multiple natural selection pressures as opposed to those which have rapidy evolved in the face of varying selection pressures?I think that kleinman "can" see that his position can just as easily lead to a conclusion which supports evolutionary change.

In fairness to kleinman, I think that he may have actually identified a reasonable distinction between micro and macro-evolution: microevolution is the result of random point changes in the genome, as modified by strong selective pressure over many generations -- while macroevolution is the result of entirely unpredictable but substantial changes: frame shifts, additions, deletions, transpositions, duplications, fusions, etc, which occasionally cause useful morphological distinctions in organisms.

And, were kleinman to actually exploit this discovery and try to publish on it, he might actually gain some measure of recognition.

As for "why" he refuses to acknowledge that point, well, I suggest, that in the most fabulously ironic fashion, kleinman is genetically predisposed to require the existence of a divine creator, due to the fact that religious fanaticism has served as a cohesive survival mechanism for human tribes during the past 100,000 years.

That is, kleinman's position is the product of the very process which he claims is impossible.

[kleinman]

Feel free to post any selection pressures that you know of that enhance a populations’ fitness to reproduce."fitness" is a technical term, kleinman. Why don't you look up what it means, replace the word "fitness" in your rather silly sentence with that definition, and then try to re-read the sentence in such a way as to make sense of it.
Well Henners, if the definition is not too technical for you, why don’t you post it. So far the only thing you have posted on this thread is that you are in LA-LA land.
"Fitness" is not a characteristic of populations, and populations reproduce at the level of complete replacement while soft selection operates on all sides.
The only thing soft on this thread is your mushy theory of evolution and you are succeeding at making it mushier and that is mushier on all sides.
If you don't even understand the problem, what makes you think that you can competently model it?
Really, now Dr Schneider’s model is now my model?
Henners, I thought you said there are constructive selection pressures?That is incorrect, kleinman.
Let’s review your evolutionist thinking. You clipped something out of one on my posts and responded as follows:
...selection pressures interfere with the fitness of a population to reproduce....typed with a straight face, no doubt.

That is probably up there along with the fly's eye and "why are there still chimps?"
Now since you evolutionists like your science to be cryptic perhaps you could decrypt your nonsense about selection pressures and fitness are? Perhaps you could even tell us what those selection pressures are?

Here, I’ll give you a start on your excursion back to reality from LA-LA land.
http://en.wikipedia.org/wiki/Fitness_%28biology%29 (http://en.wikipedia.org/wiki/Fitness_%28biology%29)
Fitness (often denoted w in population genetics models) is a central concept in evolutionary theory. It describes the capability of an individual of certain genotype to reproduce, and usually is equal to the proportion of the individual's genes in all the genes of the next generation. If differences in individual genotypes affect fitness, then the frequencies of the genotypes will change over generations; the genotypes with higher fitness become more common. This process is called natural selection.
Now Henners, tell us what a selection pressure will do to a population. Better yet, tell us what combination selection pressures do to a population. Once you give us your ridiculous mush, I’ll repost the results of Dr Schneider’s peer reviewed and published model of random point mutations and natural selection and hundreds of real empirical examples of mutation and selection which shows how this process actually works. And the way mutation and selection actually works is that combination selection pressures profoundly slow the evolutionary process. This is how mutation and selection actually works Henners, advocate of a mathematically impossible (and stupid) theory.
In fairness to kleinman, I think that he may have actually identified a reasonable distinction between micro and macro-evolution: microevolution is the result of random point changes in the genome, as modified by strong selective pressure over many generations -- while macroevolution is the result of entirely unpredictable but substantial changes: frame shifts, additions, deletions, transpositions, duplications, fusions, etc, which occasionally cause useful morphological distinctions in organisms.
Kjkent1, didn’t you know that HIV does recombination and insertion/deletions yet it still doesn’t make any difference, combination selection pressures slow evolution. So now you are proposing that unpredictable genetic changes drives macroevolution? Kjkent1, that is miraculous.

[Henners]

The only thing soft on this thread is your mushy theory of evolution and you are succeeding at making it mushier and that is mushier on all sides.

I take it that you still haven't a scoobie about what Darwinian fitness is.

That would make you, given that you have now been given the opportunity to educate yourself on the subject, not just ignorant of it, but willfully ignorant.

Why are you resorting to this kind of behaviour incidentally:
you are in LA-LA land

That is just personal abuse.

Do you have any idea how satisfying it is for me to see you comprehensively losing the argument and resorting, at the first opportunity, to playground behaviour like this?

[kleinman]

The only thing soft on this thread is your mushy theory of evolution and you are succeeding at making it mushier and that is mushier on all sides.I take it that you still haven't a scoobie about what Darwinian fitness is.
Well Henners, why don’t you educate as all on the topic?
That would make you, given that you have now been given the opportunity to educate yourself on the subject, not just ignorant of it, but willfully ignorant.
That explains why I can find hundreds of examples of mutation and selection that show that combination selection pressures profoundly show the evolutionary process and you are so smart that you can find no examples that combination selection pressures accelerate evolution. Henners, you are such an evolutionist smarty.
you are in LA-LA landThat is just personal abuse.
Hey, I’m trying to show you how mutation and selection works mathematically and empirically but if you want to be willfully ignorant and live in LA-LA land, don’t blame me.
Do you have any idea how satisfying it is for me to see you comprehensively losing the argument and resorting, at the first opportunity, to playground behaviour like this?
Well Henners, you will have to run home and tell your mother that the mean old creationist is picking on you. Maybe she can explain to you how mutation and selection works mathematically and empirically and bring you back to reality.

What a surprise, another evolutionist crybaby has found his way to this forum.

[Belz...]

In two dimensions,...

That's a nice non-answer.

I said that I can make a mathematical model that assumes more than 3 or 4 dimensions, which is basically to say that mathematical models don't always correspond to reality. You said that mathematical dimensions are not the same as physical ones. Why ?

Sure the duplicated gene can mutate but you know how slow the mutation selection process is with combination selection pressures.

That's circular reasoning, Klein. I'm offering you with an exception to your rule which leads you to think that evolution slows down to a crawl. Obviously, you can't use your conclusion to disprove the premise.

It’s a mystery to me why you evolutionists think that somehow gene duplication solves your mathematical problem with the theory of evolution. Genes are duplicated all the time, it’s called reproduction, but some how, you think if a gene is erroneously duplicated on the same genome that common descent suddenly becomes possible.

Nobody said anything about common descent. We're talking the emergence of new information in the genome. If a gene is duplicated and can mutate independently of selection pressures, which it would, since it won't be selected for or against until it devellops a function, then it CAN add new features in a population.

Belz, I post these citations precisely because they do show that combination selection pressures profoundly slow the evolutionary process. I suspect that these authors are not familiar with Dr Schneider’s model which shows the same thing.

So now your answer is that they don't know about it ? If they did they'd have the same opinion as you ? Why don't you contact them, then ?

It’s good that you don’t claim this since it is mathematically.

Are you retracting your accusation, now ?

That’s more rare then hen’s teeth.

Are those teeth and claws or aren't they, Klein ?

Yes it does Belz, it does a good job at demonstrating how slow the mutation selection process is with three selection conditions and how rapid the process becomes if you use only a single selection condition.

And yet it uses contrived selection pressures that don't exist in reality... ?

Hey, let Paul make a point.

No, I think I can speak for myself, thank you.

Dumbski seems to define irreducible complexity in so vague a term as to be meaningless, but then I wouldn't expect anything less from a creationist.

Belz, since you seem to know something about this topic, why don’t you tell us how the DNA replicase system came about? In particular, could you tell us what gyrase and helicase were doing before DNA could be replicated?

I'll do much better than that, I'll come up with something that even you can understand, as soon as I've got some time on my hands tomorrow morning. Remind me, will you ?

[Henners]

Well Henners, why don’t you educate as all on the topic?

As near as I can see kleinman, you are the only person around here in the need of such an education - and the last time I looked I didn't have a sign around my neck saying that I am the one responsible for providing it.

As far as I am concerned people who want to make an exhibition of themselves on a public forum have every right to do so.

What a surprise, another evolutionist crybaby has found his way to this forum.

Where I come from we often see behaviour like this from people who are too young for personal responsibility.

No surprise there, then.

[kleinman]

Well Henners, why don’t you educate us all on the topic?As near as I can see kleinman, you are the only person around here in the need of such an education - and the last time I looked I didn't have a sign around my neck saying that I am the one responsible for providing it.
I guess that explains why I can give the data from a peer reviewed and published model of random point mutations and natural selection and hundreds of real examples that combination selection pressures profoundly slows the evolutionary process.

And what mathematical data have you produced and what real examples have you posted which contradicts this hypothesis, zero.
As far as I am concerned people who want to make an exhibition of themselves on a public forum have every right to do so.
There is an exhibition going on here but it’s not what you think. What’s being exhibited here is the how mutation and selection actually works, both mathematically and empirically and what it shows is your theory is both mathematically and empirically impossible. Of course, you can content yourself in your mushy science and remain willfully ignorant of how mutation and selection actually works.
What a surprise, another evolutionist crybaby has found his way to this forum.Where I come from we often see behaviour like this from people who are too young for personal responsibility.
I am sure you are very civilized, you just happen to believe in a theory which is mathematically and empirically impossible. Well then why don’t you prove that you are more than just a crybaby and post some real evidence that would support your theory because so far you have addressed neither the mathematics nor the empirical data which has been cited which show that multiple selection pressures profoundly slow evolution. That would be a real surprise.

Let's keep the tone civil and attack the argument rather than the arguer.

[Kotatsu]

Yes, I remember your vague unrepeatable examples where you don’t define the selection pressures and the target genes for those pressures. It’s convenient for you not to do this because then you don’t have to describe what mutations at what loci were required for the evolutionary process to occur. This is the kind of mushy science evolutionist practice on a regular basis.

Again:
1. The relevant selection pressure that was present in the South American moths with the more derived ear structure but absent in the other moths was the presence in that area of a form of bat which used a slightly different method of hunting. This selection pressure is one of countless selection pressures operating on those moths, and acts on the entire genome. It is irrelevant to state exactly which genes it is that have changed to form these new ear structures.

2. In the example of the limpets, the added selection pressure was again the presence of a predator which used a slightly different hunting method. This also operates on the entire genome, but is expressed --- as far as the article I cited is concerned --- mainly in those genes that regulate shell thickness and versatility.

Satisfied?

The evolutionist mythological story; in a land long ago things were very different… Well Kotatsu do you think mutation and selection worked differently long ago in a far away land because today combination selection pressures profoundly slow the evolutionary process.

One of the ways in which we can tell whether or not things were different in ages past is by looking at the remnants those times have left behind. Conveniently for me, there is a vast fossil record of transitional forms between dinosaurs and birds to look at. These show a transition between the two groups of animals which is in concurrance with what I described above.

I believe mutation and selection worked the same way then as now. I also have shown you that added selection pressures do not necessarily "slow and ultimately stop" evolution.

When and if you ever understand that evolution by mutation and selection is simply an optimization problem, then you will understand that the more conditions you try to optimize by, the slower the process goes. If you try to transform more than a single gene at a time by the mutation and selection process, the probabilities of getting beneficial mutations in more than one gene simultaneously becomes infinitesimally small. You still have some work to do in order to understand anything about the mathematics of mutation and selection.

This is largely irrelevant to my question, which was something along the lines of "how does genetic sequencing disprove common descent?" Genetic sequencing is used to construct phylogenetic trees. These trees usually form nested hierarchies, with different resolutions depending on the gene or region used. This can be, and most often is, explained by common descent of the taxa involved, as that is the simplest realistic explanation to why closely related organisms have genetic sequences which are more similar to each other than they are to more distantly related taxa.

So, again, how does genetic sequencing disprove common descent?

Then why don’t you accept the result from Dr Schneider’s model that combination selection pressures profoundly slow evolution?

Within the limited framework for which his model is actually applicable, I have no strong feelings for or against its results or supposed results. There are people here better suited to evaluate its usefulness in these frameworks than I am. However, when applied to areas where I have good reason to believe it is inadequate, I will not be stupid enough to accept its results because of other peoples' religious views.

[joobz]

I guess that explains why I can give the data from a peer reviewed and published model of random point mutations and natural selection and hundreds of real examples that combination selection pressures profoundly slows the evolutionary process.
Really? Wow. I haven't read this thread in a bit. When did you start presenting data that supported your evolution is impossible theory?

[kjkent1]

Kjkent1, didn’t you know that HIV does recombination and insertion/deletions yet it still doesn’t make any difference, combination selection pressures slow evolution. So now you are proposing that unpredictable genetic changes drives macroevolution? Kjkent1, that is miraculous.Your statements are too broad.

A miracle suggests the introduction of magic: effect without causation. Randomness exists in this universe, so there's nothing miraculous about a macromutational change happening by random accident.

You have a problem understanding the position that evolution has no goal.

If 100 million years ago, a creature that looked like a reptile, was born with an extra flap of skin under its arm, and that flap was either neutral or advantageous, then the flap would likely be reproduced in future offspring.

The next major change could have been a stinger under the reptiles armpit, or it could be a hollowing of the bone structure, but it could just as easily have been one or the other, neither or both.

The point is that the transformation from reptiles to birds wasn't part of some advance planning. It could have been a transformation from a reptile into a monkey or a flea. Evolution is nothing more than the accumulation of random changes which provide advantage to the host organism so as to permit survival.

You find this miraculous. I find it the obvious result of randomness existing in the universe.

Let's use the worn out 747-junkyard analogy. The creationist says it's impossible for a tornado to churn the junkyard materials into the 747. And, I agree.

But, suppose the tornado sets down in the junkyard and stays right there for 4.5 billion years, constantly churning the junk. What do you think the odds are that "something might inadvertantly stick together to form a shape different from what was originally there?

Now, add the fact that the chemicals of life tend to stick together and combine in ways that nuts, bolts, screws, nails, transistors, refrigerators, carbarators, tires, do not.

You can only envision the absurdity of a 747 appearing in a junkyard. You don't consider the fact that it doesn't have to be a 747. It can be anything. And once that new thing appears, well, then the tornado can churn that around, too and eventually a new something may appear.

Not magic, not miracle. Just randomness operating on the basic building blocks found in our universe.

It's called evolution. You want to call it divine. You're entitled to your belief. But, your belief cannot be proven. All that is known is that randomness exists. Is there a mind behind the randomness, such that what we perceive as random is only pseudo-random? Only God, if He exists, knows the answer, and only He will ever know.

As a scientist, the best you can do is measure the universe and report your findings.

Macro-evolution happens, Alan. The record of it occuring is everywhere.

See: http://bioinfo.med.utoronto.ca/Evolution_by_Accident/Evolution_by_Accident.html

[Henners]

There is an exhibition going on here but it’s not what you think.

Do you really believe that?

...selection pressures interfere with the fitness of a population to reproduce.

I have already challenged the above statement of yours upon the grounds that it is baloney.

You have quoted a screed of wikipedia (that you clearly didn't even read - or if you did, you didn't understand) and accused me of coming from LA-LA land.

That has been the extent of your response.

Now, let me ask you...

Do you really think that a random collection of words stuck together in a mind-numbingly stupid combination is the way that you convince people that you know what you are talking about?

I repeat your baloney:

...selection pressures interfere with the fitness of a population to reproduce.

Now, are you going to deal with it, or do you want me to explain - all over again - why it is that you have not got a scoobie?

[joobz]

snip same old stuff.
Oh. So you haven't actually presented any data supporting your argument.
ok.

[OnlyTellsTruths]

kleinmans's posts are starting to make me not believe in evolution....................... who wants to guess how!

[kjkent1]

So, the evolution of HIV, Malaria and CML cancer all demonstrates that when subjected to combination selection pressures slow evolution by mutation and selection. The World Health Organization understands the implications, now if only you evolutionists realize the implications of the mathematical and empirical fact of how mutation and selection actually works. Why don’t you evolutionists use this weekend to try and figure out how mutation and selection actually works and I’ll be back next week to annoy you with more facts of how evolution by mutation and selection actually works.So, assuming that you're exactly right about microevolution, how is it that HIV appears to be the product of a macroevolutionary change?

How does macroevolution occur in this universe, Alan?

And, if it's by miracle, how do you, as a scientist, distinguish between miracles and random ignorant chance?

[Kotatsu]

It’s relevant if you want to put some science into your story telling. So tell us Kotatsu, what were the target genes? And what were the mutations that led to the formation of this ear structure? Countless selection pressures, countless mush.

Again, the added selection pressure acts on the entire genome. Exactly which genes are modified as a result could percievably be different if the same scenario is repeated over and over again. In this case, the genes which are specifically targeted are those which control the development of the ear/antenna structures, but as the article didn't give any names for them, and I am, as I've said, not at home at the moment, I cannot name you the exact gene.

The exact mutations are, of course, impossible to know, as we can only reconstruct hypothetical ancestor-sequences for the relevant genes (and even that is --- so I understand --- not done to any large extent these days). However, as I have explained before, determining exactly which Cs changed into Gs and so on is a pointless exercise.

Now at least you mention some targeting of genes by the selection pressures. Now, tell us how you distinguish the response of limpets to this predator as a mutation/selection response or recombination/selection response. If you suggest the former, please tell us what genes and what mutations brought this about.

I don't have the paper in front of me, but I'd wager that the likelihood that only one of those two responses were/are involved is practically nil. Unlike what you may play at in ev, these are real, sexually reproducing animals, whose lineages experience both mutation and selection and recombination and selection. These changes in shell structure would be the result of both.

Satisfied that you think mush constitutes a scientific proof. You make up stories about evolution which are unrepeatable, not measurable, and without mathematical basis. On the other hand, I present mathematically based examples of mutation and selection where the target genes are precisely defined and the exact mutations identified which confer adaptation to the selection pressures. What the mathematics and empirical data of mutation and selection shows is that combination selection pressures profoundly slow the evolutionary process.

This section seems to have no truth in it, nor anything of real value. I suggest you'd drop these cut-and-paste answers and try instead to come up with ones which are actually either true, relevant, or preferably both.

You even go so far to say that there are countless selection pressures all acting simultaneously on the entire genome when measurable examples of mutation and selection show that combination selection pressures confound the evolutionary process.

You really have no idea what a selection pressure is, do you? I could list a hundred selection pressures operating on the lifecycle of more or less any Swedish passerine, for example, and still not have reached the far end of all the actual ones. Their number is beyond counting.

Well Kotatsu, we have evidence today how mutation and selection works and all these so called transitional forms that you envision didn’t get there by mutation and selection, it is simply far to slow a process.

As you have not shown this I remain doubtful. They certainly get there somehow, and how else do you explain the gradual transition seen in above all the Chinese findings of feather-less dinosaurs, feathered dinosaurs, protoavians (I can't remember the proper name for this group), early birds and modern birds.

So what are you going to do, conclude that modern measurements of the mutation and selection process are wrong or your interpretation of the fossil record is wrong?

I will conclude that someone's measurements of mutation and selection process is flawed due to to many intellectual shortcommings to be comfortably listed in an afternoon.

You have great faith in your theory; unfortunately you have no mathematical or empirical basis or evidence to support your faith. Until you can measure it, you don’t know much about it.

No faith is needed if the evidence for a position has not been discredited by evidence for the opposite.

I have already shown you several cases making up the empirical basis for my position that added selection pressures do not "slow and ultimately stop" evolution. You, meanwhile, have not shown the opposite.

Kotatsu, hard science incorporates mathematical bookkeeping. You can construct your phylogenic trees; you just have no way from getting from one branch to another. Mutation and selection simply doesn’t work the way you imagine.

So two isolated populations will not over time accumulate slight differences in their genomes which due to their "arbitrary" distribution will appear in a phylogenetic tree as closely linked? And if one of these populations are split again, these two new populations will not experience the same so that we get a dichotomy nested into another dichotomy? Is that what you are saying?

Even within the limited framework of ev, it demonstrates what happens with multiple selection pressures. And you know what Kotatsu? It works the same way empirically. You have many doctrines in your faith system, too bad they don’t agree with how mutation and selection actually works.

Again, I have shown you in several examples that your assertion that added selection pressures "slow and ultimately stop evolution" is not necessarily correct in all cases.

Joobz, the author of cooperative chemistry and cooperative selection pressures thinks anything is possible, as long as you have enough free energy. Hey joobz, Kotatsu is a believer in your cooperative selection pressures hypothesis, she just doesn’t identify the target genes or the mutations required for her examples. Perhaps you can fill in the void in your theory.

Again, I am not a woman.

Also, pointing to a single gene in a genome of an animal and say, "Hey! Exactly here is the one and only place where selection pressure X operates!" is in many cases beyond moronic. This is seen above all in the enormous amount of ways different lineages have evolved in response to the same pressure.

To take the same example as before --- the pressure "tree-bound predator" operating on several undifferentiated populations of similar animals --- it is possible to get several other evolutionary responses than just flight and gliding (which, I would like to remind you, has evolved several times independant of each other, and not always by taking the same route (1)). Conceivably, the different populations could respond (2) by some or several of the following:
- Evolve any kind of weapon to deter the predator, be it claws, horns, beaks, loud cries, sharp teeth or any other structure
- Growing spines, shells, carapace, or other passively deterring structures.
- Evolve the mechanism of playing dead
- Evolve any form of camouflage, be it in colouration, shape, structure or other mode
- Evolve some form of poison or foul taste, either coupled to warning colouration or not
- Evolve mimicry of species (related ones or not related ones) which already possess poisons or foul tastes
- Evolve into a flatter animal or one which in any other way is harder for a predator to get a grip on
- Adopt crepuscular or nocturnal habits and spend the daytime hidden
- Adopt a habit of living in hard-to-access parts of the trees (usually the tips of branches or near the trunk, depending on the primary predator)
- Leave the trees (which, of course, exposes them to a whole new range of predators)
- Adopt a life style inside the tree, underneath its bark, or in cracks in the bark
- Adjust life cycle seasonality
- Adopt a one-species or many-species gregarious lifestyle to lessen the individual risk of being taken by the predator
- Other responses.

Note that this list is only off the top of my head, and a complete list --- were such ever to be possible to compile --- would be much longer.

---
(1) That is not, of course, to say that the evolution of flight in these animals, nor the evolution of other responses, are due only to counter predation pressures. This is singled out as a simple example, and should be interpreted as such.
(2) Naturally not all of these responses are immediately available to all groups of animals. A subset of them are, however, and the exact selection to appear in a given subset would depend largely on the initial animal.

[Belz...]

I didn’t say “mathematical dimensions are not the same as physical ones”. Read the post again and see what I actually wrote.

Why the hell are you arguing about my analogy, then ?

Mutation/selection is a cyclical process, it just becomes profoundly slow when you have multiple selection pressures.

That's what I said. It's circular reasoning because it's both your premise AND your conclusion.

You say that mutation and selection is slowed down by multiple selection pressures as shown by the ev model. We point out that the ev model does not consider gene duplication. You say that gene duplication doesn't help because mutation and seleciton is slowed down by multiple selection pressures.

Yours is dogma, Klein, not reasoning.

If you examine the results from ev when you try to use realistic parameters in the model, you will find that the emergence of new information is profoundly slow by mutation and selection.

Perhaps you've already forgotten that ev does NOT consider gene duplication, which was my whole point. Are you even reading, anymore ?

Oh, they know about it; why do you think they argue that combination selection pressures should be used to slow or stop the emergence of resistance. If you think it is so important to contact them, you do it. Tell them that a creationist is using their data to argue that combination selection pressures profoundly slow the evolutionary process. See what they’ll say.

Why are you so afraid to hear what they will say ?

Belz, I haven’t looked at the fossil. I can understand why you want to change the subject off mutation and selection.

You haven't looked at it and you say that it doesn't show what I say it shows ? That's profoundly dishonest.

Real selection pressures affect conformation of enzymes, so Dr Schneider used a set of contrived selection conditions to simulate the selection process. What this does is demonstrate is how slow the process is.

Nice dodge. What you were saying is that the model is not an adequate portrait of reality. Ergo, it's not very useful to reach your conclusion.

Yea, everything is irreducibly complex.

So the term is useless.

Bulz, you are a coward.

Reported.

I’d rather remind you that combination selection pressures profoundly slow the evolutionary process.

You don't need to remind me of your claim. Just prove it.

There is mathematical and empirical evidence this is true. Now you feel free to make up any silly story you want about the components of the DNA replicase system before DNA could be replicated. That is what evolutionists are good at doing.


http://forums.randi.org/imagehosting/thum_608046a8d2f10b671.jpg (http://forums.randi.org/vbimghost.php?do=displayimg&imgid=7279)

[Dr Adequate]

Okay, latest kleinman stats.

This week, he has posted 27068 words and, as in every other week, failed to fool a single person into agreeing with his delusions.

The only new rubbish I can see is the gibble about Archaeopteryx, and as all the reality-deniers come out with this trash, it's not much in the way of entertainment value. He's only funny when he comes up with something new, like Lie #5.

[Dr Adequate]

Now, too bad Adequate is not as good at counting with the mutation and selection, otherwise he wouldn’t have posted this huge whopper.

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

Now Adequate did get this right when he said this:

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


http://forums.randi.org/images/smilies/doglaugh.gif
Now Adequate did get this right when he said this:

I left out his whopper part of the statement “This is what my model shows.”
http://forums.randi.org/images/smilies/doglaugh.gif

A question for you. When you first started spamming the thread with lunatic bullcrap about what my model shows, the spam included the graph showing the data produced by the model, so that everyone not actually insane or retarded could instantly see that you were talking crap.

But now, though the red ink and the cartoon dog are still part of your spam, the graph which shows up your spam for the crap it is has mysteriously disappeared from your routine.

Is this because you have finally realised that you're talking crap? Did some kind person explain to you that large numbers are larger than small ones?

If so, why are you still blithering out lies about it? They aren't fooling anyone, are they?

[Dr Adequate]

Just for the benefit of latecomers.

http://img514.imageshack.us/img514/3974/genegraphhx4.jpg

Here's the description I posted of the graph.

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

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

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

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

And it does, of course, show that more optimization takes more time, which is why the number of generations increases monotonically with the number of selection pressures. I don't know how kleinman can deny this, except that the poor sod does after all have the misfortune to be kleinman.

[joobz]

Just for the benefit of latecomers.

http://img514.imageshack.us/img514/3974/genegraphhx4.jpg

Here's the description I posted of the graph.



And it does, of course, show that more optimization takes more time, which is why the number of generations increases monotonically with the number of selection pressures. I don't know how kleinman can deny this, except that the poor sod does after all have the misfortune to be kleinman.
I think he's confused by that last statement. I don't think he is able to see that the blue curve (which demonstrates simultaneous selection pressures) respresents a more rapid rate of evolution with higher selection pressures. After all, it takes a little bit of extra thought to understand that acheiving complete fixation of n alleles in fewer generations must be due to a more rapid rate of fixation(evolution).

I wonder if he bothered to realize that the ratio of "generations to fixation" at a given number of selection pressures is inversely proportional to the ratio of "rates of evolution" for the two conditions.

[Dr Adequate]

Certainly one of his problems appears to be an inability to tell the diference between rate and duration --- as though he's mixing up hours and miles per hour.

But I still can't see how even someone that grossly innumerate can't see that the number of generations is increasing with the number of selection pressures.

You just have to look at the graph. More selection pressures, more generations. Big numbers are larger than small ones.

[kleinman]

...selection pressures interfere with the fitness of a population to reproduce.I have already challenged the above statement of yours upon the grounds that it is baloney.
Henners, I am serving up a meal here but it is not baloney, it’s the theory of evolution. How would you like your meal prepared? Would you like the theory of evolution down in flames roasted? How about the theory of evolution half baked, it goes well with the other half baked notion of abiogenesis. The theory of evolution goes very well into the crock pot. Oh, I know how you would like the theory of evolution prepared, soft boiled, you evolutionists like your theories soft and mushy. I myself prefer the theory of evolution marinated in mathematics and seasoned with hundreds of real empirical examples which show how mutation and selection actually works. When you prepare the theory of evolution like that, you can cut it with a fork. Now what would you like to drink with your meal? May I suggest a favorite on this thread, evolutionist whine?
So, the evolution of HIV, Malaria and CML cancer all demonstrates that when subjected to combination selection pressures slow evolution by mutation and selection. The World Health Organization understands the implications, now if only you evolutionists realize the implications of the mathematical and empirical fact of how mutation and selection actually works. Why don’t you evolutionists use this weekend to try and figure out how mutation and selection actually works and I’ll be back next week to annoy you with more facts of how evolution by mutation and selection actually works.How does macroevolution occur in this universe, Alan?
The mathematical and empirical evidence of mutation and selection shows that macroevolution does not occur in this universe.
It’s relevant if you want to put some science into your story telling. So tell us Kotatsu, what were the target genes? And what were the mutations that led to the formation of this ear structure? Countless selection pressures, countless mush.Again, the added selection pressure acts on the entire genome. Exactly which genes are modified as a result could percievably be different if the same scenario is repeated over and over again. In this case, the genes which are specifically targeted are those which control the development of the ear/antenna structures, but as the article didn't give any names for them, and I am, as I've said, not at home at the moment, I cannot name you the exact gene.
Kotatsu, let’s consider what would happen if a selection pressure acts on every gene in a genome and let’s say there are 1,000 genes being acted on by this selection pressure and there are 10 mutations occurring on every genome per generation. Of those 10 mutations, 5 mutations improve the fitness of that creature to reproduce and 5 mutations are detrimental to the fitness of that creature to reproduce. One creature gets beneficial mutations on genes 1, 24, 332, 431 and 734 and detrimental mutations to genes 2, 33, 121, 321 and 444. Another creature gets beneficial mutations to genes 23, 46, 111, 231 and 689 and detrimental mutations to genes 243, 436, 568, 856 and 993. This process goes on for every creature for each generation. Kotatsu, the way selection works it that increases the frequency of beneficial genetic sequences in the gene pool and decreases the frequency of detrimental genetic sequences in the gene pool. If a selection pressure affects every gene on a genome, it becomes mathematically impossible to sort all the possible combinations of beneficial and detrimental mutations that can affect the genome and change the frequency of these genes in the gene pool. Mutation and selection simply does not work either mathematically or empirically. Selection pressures that act on more than a single gene are much more difficult for the population to adapt to.
The exact mutations are, of course, impossible to know, as we can only reconstruct hypothetical ancestor-sequences for the relevant genes (and even that is --- so I understand --- not done to any large extent these days). However, as I have explained before, determining exactly which Cs changed into Gs and so on is a pointless exercise.
Kotatsu, there are real examples of mutation and selection which demonstrate how the process occurs and the way it occurs shows that it doesn’t occur the way you allege.
Satisfied that you think mush constitutes a scientific proof. You make up stories about evolution which are unrepeatable, not measurable, and without mathematical basis. On the other hand, I present mathematically based examples of mutation and selection where the target genes are precisely defined and the exact mutations identified which confer adaptation to the selection pressures. What the mathematics and empirical data of mutation and selection shows is that combination selection pressures profoundly slow the evolutionary process.This section seems to have no truth in it, nor anything of real value. I suggest you'd drop these cut-and-paste answers and try instead to come up with ones which are actually either true, relevant, or preferably both.
Kotatsu, the citations I have and will continue to post are not hypothetical examples of evolution by mutation and selection, these are real examples of the process where the precise selection pressures are identified, the target genes and often the exact mutations required in order for these populations to adapt to these selection pressures are also identified.
Even within the limited framework of ev, it demonstrates what happens with multiple selection pressures. And you know what Kotatsu? It works the same way empirically. You have many doctrines in your faith system, too bad they don’t agree with how mutation and selection actually works.Again, I have shown you in several examples that your assertion that added selection pressures "slow and ultimately stop evolution" is not necessarily correct in all cases.
Kotatsu, your examples are nothing more than a demonstration of recombination and selection not mutation and selection. Predators eating limpets with thinner shells will select for thick shelled limpets and predators eating moths with poor hearing will select for moths with better hearing. You can do similar things with dog breeding. If you want dogs with longer fur, select for long haired dogs. If you want dogs with a better sense of smell, select for dogs which have the best sense of smell. Your examples have nothing to do with mutation and selection.
You say that mutation and selection is slowed down by multiple selection pressures as shown by the ev model. We point out that the ev model does not consider gene duplication. You say that gene duplication doesn't help because mutation and seleciton is slowed down by multiple selection pressures.
Belz, there is nothing special about gene duplication. It happens all the time. What makes you think there is something special about a gene duplication if it occurs accidentally on a single genome? Any transformation of an existing gene to a new gene must ultimately occur by mutation and selection and as we all know, that process is profoundly slow when you have more than a single selection condition.
Oh, they know about it; why do you think they argue that combination selection pressures should be used to slow or stop the emergence of resistance. If you think it is so important to contact them, you do it. Tell them that a creationist is using their data to argue that combination selection pressures profoundly slow the evolutionary process. See what they’ll say.Why are you so afraid to hear what they will say ?
I’m not, contact them and ask them whatever you want. In fact, why don’t you contact Dr Schneider and ask him to discuss ev? He says his model simulates reality and you say it doesn’t, why don’t you clear up this contradiction?

Good news folks, Adequate is going to explain to us all how mutation and selection actually works.
Just for the benefit of latecomers.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
Here's the description I posted of the graph.
The red line shows generations to achieve fixation of n alleles acted on by n selection pressures, the n+1th selection pressure being introduced only after the nth allele is fixed.

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

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

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
And it does, of course, show that more optimization takes more time, which is why the number of generations increases monotonically with the number of selection pressures. I don't know how kleinman can deny this, except that the poor sod does after all have the misfortune to be kleinman.
Now don’t stop there with quoting yourself Adequate, include your quote of how many real examples of your silly graph you have. Here, let me help you with this.
So far as I know, no-one has done the experiment.
And if that wasn’t enough, you said it again.
and too bad you don’t have any empirical examples of your silly graph ...[quote="Adequate"]As I have explained to you, I produced the model because I've not heard of this precise experiment being done.
Adequate, let me help you with your little problem with your silly graph. Start another thread and title it PhD in obfuscamatics seeking elegant experiment to demonstrate incredibly ridiculous graph.
http://forums.randi.org/images/smilies/doglaugh.gif
Now Adequate, while you are looking for your elegant experiment, I’ll keep posting real examples how mutation and selection actually works. We want Henners to have a delightful meal.

http://www.reg.org/NewPages/ohsuarticle.html (http://www.reg.org/NewPages/ohsuarticle.html)
[quote="HIV AND THE PATH OF LEAST RESISTANCE"]HIV is a quick change artist. Viral populations soon become genetically divergent in the infected host, and this variation is the key to its persistence in the human host. The consequences of this genetic plasticity include a remarkable capacity to develop drug resistance and to avoid immune surveillance. Lacking DNA proofreading mechanisms, RNA replication tends to be a sloppy process, with each progeny differing (on average) from its parent by one nucleotide. With an estimated 10 billion HIV1 virions produced daily in an infected person and an average of 1 mutation per 9200nucleotide genome, a strain of virus with every possible single drug resistance mutation is generated every day. Double mutants are less likely and the probability of three or more resistance mutations is extremely low. Mutations can be neutral, deleterious, or advantageous, depending in part on environmental context (e.g., host immune responses or drug treatment). Like the rat and the cockroach, HIV is an rstrategist in the game of evolution, emphasizing quantity over quality.

http://www.uspharmacist.com/index.asp?show=article&page=8_1668.htm (http://www.uspharmacist.com/index.asp?show=article&page=8_1668.htm)
The HIV-protease inhibitors (PIs) are of substantial importance in the management of HIV infection. The addition of PIs to the anti-HIV armamentarium in the mid-1990s led to the use of combination antiretroviral treatment known as highly active antiretroviral therapy (HAART) in HIV-infected patients.1,2 The latest Department of Health and Human Services (HHS) guidelines for use of antiretroviral agents in antiretroviral-naïve adults call for use of either a PI or a non-nucleoside reverse transcriptase inhibitor (NNRTI) combined with two nucleoside reverse transcriptase inhibitors (NRTIs).3 In the past decade, the PIs have had a major role in the success of HAART by suppressing viral load to undetectable levels for impressive time lengths in HIV-infected patients, contributing to a decrease in AIDS incidence in industrialized nations.4 Currently, there are eight PI products marketed in the United States (table 1).

Two more examples for you Adequate, Henners and the rest of you evolutionists which show that combination selection pressures slow the evolutionary process profoundly, that’s what the mathematics shows and that’s what the empirical evidence shows. Enjoy your meal.

[rocketdodger]

Two more examples for you Adequate, Henners and the rest of you evolutionists which show that combination selection pressures slow the evolutionary process profoundly, that’s what the mathematics shows and that’s what the empirical evidence shows. Enjoy your meal.

I don't understand why you *refuse* to think outside of the *math* you are getting from these limited HIV studies. I already asked you these questions, and you didn't answer, so I will answer them for you. They are the gist of what I am trying to get you to understand.

1) Given a population being acted upon by n selection pressures, why would the addition of another selective pressure possibly slow down evolution? (you have already answered this I think in one of your posts).

Answer -- As you showed previously, a mutation may raise fitness for one pressure and have no effect regarding another pressure. The *net* drift will be slowed in this case because the probability of getting the mutations selected for by both pressures is (on average) much lower than either one alone. Because evolution needs a net drift, evolution will be slowed in this case.

2) Given a population being acted upon by n selection pressures, will the addition of another selective pressure *always* slow down evolution?

Answer -- No.

First, the extra pressure may be a case like above, but its relative weight may be great enough to overwhelm the above explained effect. Clearly, if you have a bunch of rather trivial pressures on a population, and you throw in a devastatingly strong one, evolution will proceed much faster (and much of the population may die).

Second, if the new pressure *negates* an existing one, it effectively removes both of them from the pool as far as evolutionary drift is concerned. For example, suppose you introduce a pressure on a population that favors carbon dioxide resistance as well as heat resistance. Now add a pressure that favors cold resistance. The population might have rough time evolving to survive in hot/cold environments, because mutations adding fitness to those pressures may hinder each other, so drift with respect to those pressures will indeed be slowed. However, now there is nothing to get in the way of mutations that favor carbond dioxide resistance taking hold. Whether an individual has mutations that favor hot or cold becomes irrelevant to their advantage with respect to the remaining pressure.

Third, if the new pressure *compliments* an existing one, evolutionary drift in that direction will obviously be increased. In the above example, suppose a mutation increases fitness for *both* heat and cold resistance -- clearly drift with regard to those two pressures will be sped up.

[kleinman]

Two more examples for you Adequate, Henners and the rest of you evolutionists which show that combination selection pressures slow the evolutionary process profoundly, that’s what the mathematics shows and that’s what the empirical evidence shows. Enjoy your meal.I don't understand why you *refuse* to think outside of the *math* you are getting from these limited HIV studies. I already asked you these questions, and you didn't answer, so I will answer them for you. They are the gist of what I am trying to get you to understand.
I don’t understand why you refuse to acknowledge that it is not only HIV which shows that combination selection pressures profoundly slow the evolutionary process but it is shown with every microbe studied such as HBV, HCV, influenza virus, Malaria, bacteria, as well as more complex life forms including weeds, rodents and all other examples of mutation and selection. So why do you refuse to acknowledge both the mathematics of mutation and selection amd all of the empirical evidence of mutation and selection which show that combination selection pressures profoundly slow the evolutionary process.
1) Given a population being acted upon by n selection pressures, why would the addition of another selective pressure possibly slow down evolution? (you have already answered this I think in one of your posts).
Yes I have answered this before but I will answer it again. Each additional selection pressure which has a unique target has a probability of occurrence. The probability of all n+1 mutations occurring on a single creature is the product of the n+1 probabilities. To give you an idea of how small this product of probabilities become with multiple selection pressures, let all the probabilities for each mutation be (1/10^6), then the probability of all the necessary mutations to confer resistance against all the selection pressures occurring on a single member of the population is (1/10^6)^(n+1). This number gets much smaller if more than a single mutation is required for a given selection pressure.
Answer -- As you showed previously, a mutation may raise fitness for one pressure and have no effect regarding another pressure. The *net* drift will be slowed in this case because the probability of getting the mutations selected for by both pressures is (on average) much lower than either one alone. Because evolution needs a net drift, evolution will be slowed in this case.
Drift does not increase the frequency of sequences of bases in the population, only selection can do this. Drift can only occur if the environment can support divergence from the genetic optimum of the population for that environment. Selection increases the frequency of the optimal phenotype for the given environment.
2) Given a population being acted upon by n selection pressures, will the addition of another selective pressure *always* slow down evolution?

Answer -- No.
Rocketdodger, you have neither mathematical nor empirical evidence for your conclusion. If you think you are correct, post either or both types of evidence for your conclusion. I have posted both mathematical and empirical evidence for my conclusion.
First, the extra pressure may be a case like above, but its relative weight may be great enough to overwhelm the above explained effect. Clearly, if you have a bunch of rather trivial pressures on a population, and you throw in a devastatingly strong one, evolution will proceed much faster (and much of the population may die).
I wonder if you will ever get beyond your mushy speculations.
Second, if the new pressure *negates* an existing one, it effectively removes both of them from the pool as far as evolutionary drift is concerned. For example, suppose you introduce a pressure on a population that favors carbon dioxide resistance as well as heat resistance. Now add a pressure that favors cold resistance. The population might have rough time evolving to survive in hot/cold environments, because mutations adding fitness to those pressures may hinder each other, so drift with respect to those pressures will indeed be slowed. However, now there is nothing to get in the way of mutations that favor carbond dioxide resistance taking hold. Whether an individual has mutations that favor hot or cold becomes irrelevant to their advantage with respect to the remaining pressure.
I guess you have gotten beyond your mushy speculations, you have arrived a mushy suppositions.
Third, if the new pressure *compliments* an existing one, evolutionary drift in that direction will obviously be increased. In the above example, suppose a mutation increases fitness for *both* heat and cold resistance -- clearly drift with regard to those two pressures will be sped up.
*Complimentary* selection pressures, rocketdodger, you have moved beyond mushy speculations and suppositions to just plain weird. Selection pressures don’t *compliment* each other.

Rocketdodger, you should study the mathematics of mutation and selection, perhaps it will open your eyes to how mutation and selection actually works. Here is an example of the mathematics of mutation and selection written by some scientists at Emory University.
http://www.biology.emory.edu/research/Levin/pubs/97cycle.pdf (http://www.biology.emory.edu/research/Levin/pubs/97cycle.pdf)
ABSTRACT: The spread of bacteria resistant to antimicrobial agents calls for population-wide treatment strategies to delay or reverse the trend toward antibiotic resistance. Here we propose new criteria for the evaluation of the population-wide effects of treatment protocols for directly transmitted bacterial infections and discuss different usage patterns for single and multiple antibiotic therapy. A mathematical model suggests that the long-term benefit of single drug treatment from introduction of the antibiotic until a high frequency of resistance precludes its use is almost independent of the pattern of antibiotic use. When more than one antibiotic is employed, sequential use of different antibiotics in the population (‘‘cycling’’) is always inferior to treatment strategies where, at any given time, equal fractions of the population receive different antibiotics. However, treatment of all patients with a combination of antibiotics is in most cases the optimal treatment strategy.
It’s not just Dr Schneider’s ev model which shows that combination selection pressures profoundly slow the evolutionary process, there are many other mathematical models which show exactly the same phenomenon. And you know what else rocketdodger, the empirical evidence shows the same thing. Now if you think there are situations in nature where combination selection pressures do not slow the evolutionary process, post your example, not your speculations or suppositions.

[Kotatsu]

Kotatsu,

I think it is nice of you to state at the beginning of each response to whom it is directed. As you write more or less the same already discredited statements in each reply, this is almost the only way to see which parts it is that you consider being relevant to your discussion with me when replying.

let’s consider what would happen if a selection pressure acts on every gene in a genome and let’s say there are 1,000 genes being acted on by this selection pressure and there are 10 mutations occurring on every genome per generation. Of those 10 mutations, 5 mutations improve the fitness of that creature to reproduce and 5 mutations are detrimental to the fitness of that creature to reproduce. One creature gets beneficial mutations on genes 1, 24, 332, 431 and 734 and detrimental mutations to genes 2, 33, 121, 321 and 444. Another creature gets beneficial mutations to genes 23, 46, 111, 231 and 689 and detrimental mutations to genes 243, 436, 568, 856 and 993. This process goes on for every creature for each generation.

So... with arbitrary values of mutation rates and number of genes, as well as an arbitrary assignment of beneficial and detrimental mutations, you have now shown... what, exactly? That you know all the numbers between 0 and 9? I am afraid I have no idea why this example is relevant to anything at all, actually.

Kotatsu, the way selection works it that increases the frequency of beneficial genetic sequences in the gene pool and decreases the frequency of detrimental genetic sequences in the gene pool. If a selection pressure affects every gene on a genome, it becomes mathematically impossible to sort all the possible combinations of beneficial and detrimental mutations that can affect the genome and change the frequency of these genes in the gene pool. Mutation and selection simply does not work either mathematically or empirically. Selection pressures that act on more than a single gene are much more difficult for the population to adapt to.

Could you explain to me exactly how a selection pressure targets a single gene in a genome and at the same time has no influence at all on the other genes? If you could please do this in the context of how different animals have responded to the same selection pressure by evolving different solutions --- implying that different genes are targeted in the individual cases --- as in the theoretical overview I provided above, I would be most grateful.

Kotatsu, there are real examples of mutation and selection which demonstrate how the process occurs and the way it occurs shows that it doesn’t occur the way you allege.

Shall I take this to mean, as implied by what you are quoting from me, that you don't believe that mutation occurs by for instance G's changing into C's in a lineage?

Kotatsu, the citations I have and will continue to post are not hypothetical examples of evolution by mutation and selection, these are real examples of the process where the precise selection pressures are identified, the target genes and often the exact mutations required in order for these populations to adapt to these selection pressures are also identified.

Which is all very well in micro-organisms where this level of exactitude may be relevant. In larger organisms, this is not necessarily the case.

[Kotatsu, your examples are nothing more than a demonstration of recombination and selection not mutation and selection. Predators eating limpets with thinner shells will select for thick shelled limpets and predators eating moths with poor hearing will select for moths with better hearing. You can do similar things with dog breeding. If you want dogs with longer fur, select for long haired dogs. If you want dogs with a better sense of smell, select for dogs which have the best sense of smell. Your examples have nothing to do with mutation and selection.

I have contended that these show that added selection pressures do not "slow and ultimately stop evolution", as you have claimed. They show exactly this. Unless you can guarantee that no mutations are involved in these examples, your cut-and-pastings have little value.

[kleinman]

Kotatsu,I think it is nice of you to state at the beginning of each response to whom it is directed. As you write more or less the same already discredited statements in each reply, this is almost the only way to see which parts it is that you consider being relevant to your discussion with me when replying.
Is there anything you evolutionists don’t whine about?
let’s consider what would happen if a selection pressure acts on every gene in a genome and let’s say there are 1,000 genes being acted on by this selection pressure and there are 10 mutations occurring on every genome per generation. Of those 10 mutations, 5 mutations improve the fitness of that creature to reproduce and 5 mutations are detrimental to the fitness of that creature to reproduce. One creature gets beneficial mutations on genes 1, 24, 332, 431 and 734 and detrimental mutations to genes 2, 33, 121, 321 and 444. Another creature gets beneficial mutations to genes 23, 46, 111, 231 and 689 and detrimental mutations to genes 243, 436, 568, 856 and 993. This process goes on for every creature for each generation.So... with arbitrary values of mutation rates and number of genes, as well as an arbitrary assignment of beneficial and detrimental mutations, you have now shown... what, exactly? That you know all the numbers between 0 and 9? I am afraid I have no idea why this example is relevant to anything at all, actually.
Kotatsu, you contend that selection pressures act on entire genomes. How does this happen? What I am trying to show you and why it is relevant is that mutation selection is an optimization or sorting problem. It is mathematically and empirically impossible to sort mutations as you allege. This mush you present makes no mathematical sense.
Kotatsu, the way selection works it that increases the frequency of beneficial genetic sequences in the gene pool and decreases the frequency of detrimental genetic sequences in the gene pool. If a selection pressure affects every gene on a genome, it becomes mathematically impossible to sort all the possible combinations of beneficial and detrimental mutations that can affect the genome and change the frequency of these genes in the gene pool. Mutation and selection simply does not work either mathematically or empirically. Selection pressures that act on more than a single gene are much more difficult for the population to adapt to.Could you explain to me exactly how a selection pressure targets a single gene in a genome and at the same time has no influence at all on the other genes? If you could please do this in the context of how different animals have responded to the same selection pressure by evolving different solutions --- implying that different genes are targeted in the individual cases --- as in the theoretical overview I provided above, I would be most grateful.
Certainly I will do this for you and use your own examples to do this.

You have a predator which is consuming limpets. The advantage the predator has over the limpet is the predator can crack thin limpet shells. Those limpets whose alleles which determine the thickness of their shells are such that they create a thicker shell are at a reproductive advantage over those limpets whose alleles produce a thinner shell. The predator is selecting out alleles which produce a thinner shell and the thicker shell limpets are more fit than their thin shell counterparts. Note that in the absence of the predator, the thin shell limpet is at a reproductive advantage over their thick shell counterparts because the put less energy toward shell production and more energy toward reproduction.

This same type of analysis can be done for your moth example but I’ll leave this for an exercise for you.
Kotatsu, there are real examples of mutation and selection which demonstrate how the process occurs and the way it occurs shows that it doesn’t occur the way you allege. Shall I take this to mean, as implied by what you are quoting from me, that you don't believe that mutation occurs by for instance G's changing into C's in a lineage?
Kotatsu, you can’t even identify the genes targeted in your examples, you think the entire genome is targeted by selection pressures. Ultimately, selection pressures are manifest by changes at the genetic sequence level. Until you start making your observations and measurements at this level, everything you do is speculation.
Kotatsu, the citations I have and will continue to post are not hypothetical examples of evolution by mutation and selection, these are real examples of the process where the precise selection pressures are identified, the target genes and often the exact mutations required in order for these populations to adapt to these selection pressures are also identified.Which is all very well in micro-organisms where this level of exactitude may be relevant. In larger organisms, this is not necessarily the case.
Kotatsu, do you believe that weeds and rodents are micro-organisms? I have posted examples for these complex multi-cellular organisms and mutation and selection behaves the same for these life forms only slower than micro-organisms since they have slow reproduction rates and larger genomes. The selection pressures, targeted genes and mutations are identified in these examples as well. Your approach to the understanding of evolution has no exactitude of course that is typical for evolutionists.
Kotatsu, your examples are nothing more than a demonstration of recombination and selection not mutation and selection. Predators eating limpets with thinner shells will select for thick shelled limpets and predators eating moths with poor hearing will select for moths with better hearing. You can do similar things with dog breeding. If you want dogs with longer fur, select for long haired dogs. If you want dogs with a better sense of smell, select for dogs which have the best sense of smell. Your examples have nothing to do with mutation and selection.I have contended that these show that added selection pressures do not "slow and ultimately stop evolution", as you have claimed. They show exactly this. Unless you can guarantee that no mutations are involved in these examples, your cut-and-pastings have little value.
I know this is what you are contending but you can not identify the selection pressures, targeted genes or mutations required to accurately support your contention. This thread is a no-mush zone.

[rocketdodger]

Yes I have answered this before but I will answer it again. Each additional selection pressure which has a unique target has a probability of occurrence. The probability of all n+1 mutations occurring on a single creature is the product of the n+1 probabilities. To give you an idea of how small this product of probabilities become with multiple selection pressures, let all the probabilities for each mutation be (1/10^6), then the probability of all the necessary mutations to confer resistance against all the selection pressures occurring on a single member of the population is (1/10^6)^(n+1). This number gets much smaller if more than a single mutation is required for a given selection pressure.

You seem to think that if an individual doesn't exhibit a mutation it can't contribute to evolution... ? Why would an individual need to have all n + 1 mutations in order to propagate the mutations it does have to the next generation? Selective pressures don't do *anything* by themselves, they just modify the probability that individuals with or without a certain mutation will propagate their genetic material to the next generation.


Rocketdodger, you have neither mathematical nor empirical evidence for your conclusion. If you think you are correct, post either or both types of evidence for your conclusion. I have posted both mathematical and empirical evidence for my conclusion.

No, you have posted evidence that adding a selective pressure results in slower evolution than would otherwise result from that pressure alone. You have not in any way shown that, given a rate of evolution under n selection pressures, evolution *in general* proceeds even slower if we increase the number to n + 1.

The directed mutation and selection that occurs every day around the world in thousands of biology labs is my evidence. A cultured population is under the influence of countless selective pressures sitting in a petri dish, and evolution happens very slowly in that environment. Along comes a lab tech and starts exposing the culture to something it is averse to. All the organisms except those with mutations that confer immunity die, with the survivors having been selected for. There you go -- we have added an extra selective pressure, yet evolution proceeded much faster than would have without the addition of this pressure.


Complimentary* selection pressures, rocketdodger, you have moved beyond mushy speculations and suppositions to just plain weird. Selection pressures don’t *compliment* each other.
By which I mean two selective pressures that are simultaneously satisfied by the same mutation. You haven't heard of such a thing? Perhaps I should have said "a mutation that makes two pressures complimentary," I apologize.


It’s not just Dr Schneider’s ev model which shows that combination selection pressures profoundly slow the evolutionary process, there are many other mathematical models which show exactly the same phenomenon. And you know what else rocketdodger, the empirical evidence shows the same thing. Now if you think there are situations in nature where combination selection pressures do not slow the evolutionary process, post your example, not your speculations or suppositions.

I gave you an example. And I do not disagree that combination selection pressures profoundly slow the evolutionary process. My argument is that this is *all* they do yet you interpret such a statement as "the addition of a selection pressure to a group of existing ones always results in slower evolution than what was there without it," which is totally unfounded and clearly wrong.

[kleinman]

Yes I have answered this before but I will answer it again. Each additional selection pressure which has a unique target has a probability of occurrence. The probability of all n+1 mutations occurring on a single creature is the product of the n+1 probabilities. To give you an idea of how small this product of probabilities become with multiple selection pressures, let all the probabilities for each mutation be (1/10^6), then the probability of all the necessary mutations to confer resistance against all the selection pressures occurring on a single member of the population is (1/10^6)^(n+1). This number gets much smaller if more than a single mutation is required for a given selection pressure.You seem to think that if an individual doesn't exhibit a mutation it can't contribute to evolution... ? Why would an individual need to have all n + 1 mutations in order to propagate the mutations it does have to the next generation? Selective pressures don't do *anything* by themselves, they just modify the probability that individuals with or without a certain mutation will propagate their genetic material to the next generation.
No, that is not what I think. What I think is that when a population is trying to navigate a fitness landscape, it becomes profoundly more difficult if more than a single gene is evolving. This becomes evident if you have combination selection pressures or a single selection pressure that targets more than a single gene.
Rocketdodger, you have neither mathematical nor empirical evidence for your conclusion. If you think you are correct, post either or both types of evidence for your conclusion. I have posted both mathematical and empirical evidence for my conclusion.No, you have posted evidence that adding a selective pressure results in slower evolution than would otherwise result from that pressure alone. You have not in any way shown that, given a rate of evolution under n selection pressures, evolution *in general* proceeds even slower if we increase the number to n + 1.
Well if that is not the case, why are additional drugs used to slow the evolution of HIV or TB or cancer therapies…? You can in your imagination think that adding additional selection pressures somehow changes this mathematical reality but then you would be demonstrating you have no idea how mutation and selection actually works either mathematically or empirically.
The directed mutation and selection that occurs every day around the world in thousands of biology labs is my evidence. A cultured population is under the influence of countless selective pressures sitting in a petri dish, and evolution happens very slowly in that environment. Along comes a lab tech and starts exposing the culture to something it is averse to. All the organisms except those with mutations that confer immunity die, with the survivors having been selected for. There you go -- we have added an extra selective pressure, yet evolution proceeded much faster than would have without the addition of this pressure.
I have posted examples of this directed evolution and that way it works is to apply single selection pressures sequentially. The selection pressures are initially applied at sub-lethal intensity to eliminate the pheno-deviants and then the pressures are slowly increased to allow the population to adapt to these single selection pressures. Now if you have any examples of combination simultaneous selection pressures being used for directed evolution, post the examples.
Complimentary* selection pressures, rocketdodger, you have moved beyond mushy speculations and suppositions to just plain weird. Selection pressures don’t *compliment* each other.By which I mean two selective pressures that are simultaneously satisfied by the same mutation. You haven't heard of such a thing? Perhaps I should have said "a mutation that makes two pressures complimentary," I apologize.
Now, what you are talking about are not independent selection pressures. There are real cases of this. In particular, “convergent” therapy for the treatment of HIV in which multiple drugs are targeted to the same locus of a gene has been show not to work in slowing the evolution of the virus. It requires independent selection pressures targeting different loci in order for evolution to be slowed.
It’s not just Dr Schneider’s ev model which shows that combination selection pressures profoundly slow the evolutionary process, there are many other mathematical models which show exactly the same phenomenon. And you know what else rocketdodger, the empirical evidence shows the same thing. Now if you think there are situations in nature where combination selection pressures do not slow the evolutionary process, post your example, not your speculations or suppositions.I gave you an example. And I do not disagree that combination selection pressures profoundly slow the evolutionary process. My argument is that this is *all* they do yet you interpret such a statement as "the addition of a selection pressure to a group of existing ones always results in slower evolution than what was there without it," which is totally unfounded and clearly wrong.
Rocketdodger, give us an example of the addition of a selection pressure to a population already subjected to selection pressures where the evolutionary process does not slow down even further. While you search for your example, I’ll continue to post real examples of what combination selection pressures do to the evolutionary process. Here’s another citation for you to ponder.
http://www.jci.org/cgi/content/full/jci;113/8/1084 (http://www.jci.org/cgi/content/full/jci;113/8/1084)
Malaria, the most prevalent and most pernicious parasitic disease of humans, is estimated to kill between one and two million people, mainly children, each year. Resistance has emerged to all classes of antimalarial drugs except the artemisinins and is responsible for a recent increase in malaria-related mortality, particularly in Africa. The de novo emergence of resistance can be prevented by the use of antimalarial drug combinations. Artemisinin-derivative combinations are particularly effective, since they act rapidly and are well tolerated and highly effective. Widespread use of these drugs could roll back malaria.

[kjkent1]

Paul,

If you were to reprogram ev so that the greatest weight for a selection pressure is 65535 (or greater) instead of 100, would that break the program by overflowing integer variables, etc?

I think it would be useful to test what happens with a very large differential between the three ev selective pressures, because kleinman is relying heavily on this for his assertions.

[rocketdodger]

No, that is not what I think. What I think is that when a population is trying to navigate a fitness landscape, it becomes profoundly more difficult if more than a single gene is evolving. This becomes evident if you have combination selection pressures or a single selection pressure that targets more than a single gene.

I agree. But for evolution to occur the entire landscape doesn't need to be navigated, just a part of it...

Well if that is not the case, why are additional drugs used to slow the evolution of HIV or TB or cancer therapies…?

Because additional drugs do slow the organisms evolution... compared to those drugs being used *alone*. What you are arguing is that evolution towards resistance to a drug proceeds slower when that drug is used in combination therapy than if *the drug wasn't used at all*, and you haven't presented data to support that conclusion.


Now if you have any examples of combination simultaneous selection pressures being used for directed evolution, post the examples.

My example still stands. Selective pressures are being exerted on every population all the time. Just because they don't seem to do much doesn't invalidate them. If you think otherwise, then you have just argued against your own theory.

Now, what you are talking about are not independent selection pressures. There are real cases of this. In particular, “convergent” therapy for the treatment of HIV in which multiple drugs are targeted to the same locus of a gene has been show not to work in slowing the evolution of the virus. It requires independent selection pressures targeting different loci in order for evolution to be slowed.

Ahhhhh... so you admit that there is such a thing as multiple selection pressures that don't slow evolution... the pressures have to be "independent?"

Tell me, what exactly defines the "independence" of selection pressures? I think kotatsu has been trying to show you that you can't always, or even often, limit a selection pressure to a single loci. Selection pressures operate on the organism, and there are potentially numerous mutations that could increase the organism's fitness regarding that pressure. Given this, how can you be sure of "independence" in much more than drug resistance experiments?

Rocketdodger, give us an example of the addition of a selection pressure to a population already subjected to selection pressures where the evolutionary process does not slow down even further.
I did. Just because you refuse to realize that a petri dish full of bacteria is under the influence of selective pressures prior to any human interference doesn't mean it in fact isn't.

[kleinman]

No, that is not what I think. What I think is that when a population is trying to navigate a fitness landscape, it becomes profoundly more difficult if more than a single gene is evolving. This becomes evident if you have combination selection pressures or a single selection pressure that targets more than a single gene.I agree. But for evolution to occur the entire landscape doesn't need to be navigated, just a part of it...
This is what you haven’t come to understand yet. The fitness landscape becomes much more complex when you have more than a single selection condition. This is why combination therapy works at all for HIV, one of the fastest reproducing, smallest genome creature with a very high mutation rate. Even navigating a small portion of the landscape with three selection pressures becomes much more difficult for the virus.
Well if that is not the case, why are additional drugs used to slow the evolution of HIV or TB or cancer therapies…?Because additional drugs do slow the organisms evolution... compared to those drugs being used *alone*. What you are arguing is that evolution towards resistance to a drug proceeds slower when that drug is used in combination therapy than if *the drug wasn't used at all*, and you haven't presented data to support that conclusion.
Again, what you don’t realize about the mutation and selection process is that you don’t need huge populations to evolve against a single selection pressure. Ev demonstrates this and the empirical data demonstrates this as well. Monotherapy can suppress HIV for a few weeks but the remaining population can easily evolve against this single selection pressure. Large populations are much more important when evolving against combination selection pressures.
Now if you have any examples of combination simultaneous selection pressures being used for directed evolution, post the examples.My example still stands. Selective pressures are being exerted on every population all the time. Just because they don't seem to do much doesn't invalidate them. If you think otherwise, then you have just argued against your own theory.
You haven’t presented an example, you have presented speculations and suppositions.
Now, what you are talking about are not independent selection pressures. There are real cases of this. In particular, “convergent” therapy for the treatment of HIV in which multiple drugs are targeted to the same locus of a gene has been shown not to work in slowing the evolution of the virus. It requires independent selection pressures targeting different loci in order for evolution to be slowed.Ahhhhh... so you admit that there is such a thing as multiple selection pressures that don't slow evolution... the pressures have to be "independent?"
The example of convergent therapy for HIV does not represent multiple selection pressures. A single mutation causes resistance to multiple drugs. There are other examples such as with Pseudomonas which has the capability to evolve resistance against multiple different antibiotics even when not exposed to the antibiotics because the bacteria acquires the ability to pump these drugs out. These “non-independent” selection pressure cases are rare. Are you going to try to construct your theory of evolution around these rare cases? Good luck rocketdodger.
Tell me, what exactly defines the "independence" of selection pressures? I think kotatsu has been trying to show you that you can't always, or even often, limit a selection pressure to a single loci. Selection pressures operate on the organism, and there are potentially numerous mutations that could increase the organism's fitness regarding that pressure. Given this, how can you be sure of "independence" in much more than drug resistance experiments?
Independent selection pressures target either different genes or different loci of the same gene. An example of non-independent selection pressures is MRSA. Once the bacteria are resistant to methicillin, virtually all the drugs in the penicillin family are useless, or if the bacteria are sensitive to penicillin, combining penicillin with amoxicillin would not constitute independent selection pressures because they both target the same loci on the same gene.
Rocketdodger, give us an example of the addition of a selection pressure to a population already subjected to selection pressures where the evolutionary process does not slow down even further.I did. Just because you refuse to realize that a petri dish full of bacteria is under the influence of selective pressures prior to any human interference doesn't mean it in fact isn't.
The vast majority of selection pressures are stabilizing selection pressures which prevent a gene from diverging too far from its optimum. It is the directional selection pressures which move a population to a new location on the fitness landscape. If you have two or more directional selection pressures acting on a population, it becomes much more difficult for the population to find a trajectory to this new location. That is how mutation and selection works mathematically and that’s who it works empirically.

[Henners]

Originally Posted by Kleinman

Henners, I am serving up a meal here but it is not baloney, it’s the theory of evolution. How would you like your meal prepared? Would you like the theory of evolution down in flames roasted? How about the theory of evolution half baked, it goes well with the other half baked notion of abiogenesis. The theory of evolution goes very well into the crock pot. Oh, I know how you would like the theory of evolution prepared, soft boiled, you evolutionists like your theories soft and mushy. I myself prefer the theory of evolution marinated in mathematics and seasoned with hundreds of real empirical examples which show how mutation and selection actually works. When you prepare the theory of evolution like that, you can cut it with a fork. Now what would you like to drink with your meal? May I suggest a favorite on this thread, evolutionist whine?


Nice creative writing.

Now, the point was that you said:...selection pressures interfere with the fitness of a population to reproduce.

I told you that was baloney.

You then posted a definition from Wikipedia. I'm not certain why you would want to post independent confirmation that your statement was, indeed, baloney.

Yet you did.

I think you didn't even read it. If you did read it, you certainly didn't even understand it.

Maybe you should have gone to SpecSavers.

Baloney again, as they say.

Just like spam, only not as big, and not as clever.

So, well done, that man. You put up a good front.

However, in the words of the great John Stewart (no, not him, John Stewart), "you've got your backside..."

[rocketdodger]

Again, what you don’t realize about the mutation and selection process is that you don’t need huge populations to evolve against a single selection pressure. Ev demonstrates this and the empirical data demonstrates this as well. Monotherapy can suppress HIV for a few weeks but the remaining population can easily evolve against this single selection pressure. Large populations are much more important when evolving against combination selection pressures.

This has nothing to do with the sentence it is supposed to be <?> a response to.


You haven’t presented an example, you have presented speculations and suppositions

No. It is an example, and it happens daily around the world. Just because it doesn't fit into your theory doesn't mean it isn't an example.

The example of convergent therapy for HIV does not represent multiple selection pressures.
Each therapy used by itself would be a selection pressure. If you don't want to call the combination of them "multiple" pressures then fine, call it whatever you want. But then you have to accept that adding an additional pressure to an existing group might result in some of them aggregating to form this <whatever you call it>.

Independent selection pressures target either different genes or different loci of the same gene. An example of non-independent selection pressures is MRSA. Once the bacteria are resistant to methicillin, virtually all the drugs in the penicillin family are useless, or if the bacteria are sensitive to penicillin, combining penicillin with amoxicillin would not constitute independent selection pressures because they both target the same loci on the same gene.

Sounds great. In no way is a counter-argument, though, because as I and others have been telling you over and over, you can't reliably target individual genes or loci with selection pressures unless those pressures are things like drugs (which is probably why you refuse to think outside these drug resistance studies).

The vast majority of selection pressures are stabilizing selection pressures which prevent a gene from diverging too far from its optimum. It is the directional selection pressures which move a population to a new location on the fitness landscape.

Which is already a step back from your original claim, I am glad you are starting to understand.


If you have two or more directional selection pressures acting on a population, it becomes much more difficult for the population to find a trajectory to this new location. That is how mutation and selection works mathematically and that’s who it works empirically.

Absolutely. My argument is that you contend, for example, that if we have pressures {A, B, C, D} and we add {E}, the new evolutionary rate {A,B,C,D,E} will be slower than {A,B,C,D}. There is no math or experiments to prove that this is true in general. The experiments and math you are citing ONLY show that {A,B,C,D,E} will be slower than {E} by itself.

[kleinman]

...selection pressures interfere with the fitness of a population to reproduce.I told you that was baloney.
So Henners, if selection pressures don’t interfere with a populations ability to reproduce, then what do they do?

You have to do more than cold cuts to make your argument. So far all you have done is give us some evolutionist whine.

[Henners]

...selection pressures interfere with the fitness of a population to reproduce.


The point is, you believe that is a valid statement, kleinman.

What does that reveal about what you believe?

...about what you know?

...about what you understand?

I've never seen a valid mathematical model in my life that is based on a comprehensive failure to understand the system being modelled.

You say you have Mathematics? So what? You have not got a scoobie about the system you think is being modelled. You less advanced than someone who thinks that you can add up two apples and get a banana.

[Henners]

So Henners, if selection pressures don’t interfere with a populations ability to reproduce, then what do they do?

Well, kleinman, you know as well as I do that you already posted a wikipedia definition of "fitness" that you obviously didn't understand.

Why don't you go and read it yourself and try to understand it this time.

You have asked for it to be explained to you several times now.

Are you 12?

[kleinman]

...selection pressures interfere with the fitness of a population to reproduce.The point is, you believe that is a valid statement, kleinman.
Yup, and the point you are making is that you have absolutely no idea of how the mathematics of mutation and selection works and you are doing a good job at it.
I've never seen a valid mathematical model in my life that is based on a comprehensive failure to understand the system being modelled.
Well Henners, Dr Schneider created the model and it has been peer reviewed and published. It does not surprise me that now that you have some idea what it shows you would try to discredit Dr Schneider’s work. So why don’t you tell us what the problem is with ev. Why does it take such huge number of generations to evolve its selection conditions on all but the tiniest genomes? Can you do anything more than whine?
You say you have Mathematics? So what? You have not got a scoobie about the system you think is being modelled. You less advanced than someone who thinks that you can add up two apples and get a banana.
Henners, not only to I have the mathematics to back up my hypothesis, I have the empirical data which shows that combination selection pressures profoundly slow the evolutionary process. But Henners, you do have evolutionist whine to support your position.

[Mercutio]

Neat article in today's NY Times (http://www.nytimes.com/2007/10/09/science/09clea.html?_r=1&ref=science&oref=slogin), about bacteria growing in NASA's "clean rooms".
Samples of air and surfaces in the clean rooms at three National Aeronautics and Space Administration centers revealed surprising numbers and types of robust bacteria that appear to resist normal sterilization procedures, according to a newly published study.
How many selection pressures are involved in "normal sterilization procedures", I wonder? Must be enough to profoundly slow evolution, don't you think? Well, perhaps, if you are looking only at the evolution of some bacteria, but ignoring others.
Dr. Catharine A. Conley, a biologist who is the acting planetary protection officer at NASA headquarters, said the agency had long suspected that the organisms previously detected in clean rooms did not represent the full range that were there. Current cleaning techniques kill most common microbes, she said, and the resulting lack of competition could contribute to the number and diversity of the durable survivors found by the genetic testing approach. Wait a minute--you mean, the fact that multiple selection pressures can profoundly impact the numbers of one species might actually benefit other species? Sounds like multiple selection pressures are speeding evolution, at least of the survivors...

[Belz...]

Belz, there is nothing special about gene duplication. It happens all the time. What makes you think there is something special about a gene duplication if it occurs accidentally on a single genome? Any transformation of an existing gene to a new gene must ultimately occur by mutation and selection and as we all know, that process is profoundly slow when you have more than a single selection condition.

No, it isn't, Klein, because your selection pressures DO NOT act on the duplicated gene.

You should know this.

I’m not, contact them and ask them whatever you want. In fact, why don’t you contact Dr Schneider and ask him to discuss ev? He says his model simulates reality and you say it doesn’t, why don’t you clear up this contradiction?

You have yourself stated that ev doesn't model reality adequately.

[kjkent1]

Wow! The last string of kleinman posts is quite interesting. Apparently, there are dependent, independent, directional, and non-directional selection pressures acting on organisms -- and all of these different factors effects evolutionary development.

But, what about relative intensity? Why doesn't intensity factor into the equation?

After all, if there are 1,000 selective pressures, and one is 10,000 times stronger in its effect on the organism than all the others, it is trivially obvious that that one pressure will account for nearly all of the directional pressure, and thus increase the organism's evolutionary change.

Indeed, this is exactly what we see in every one of kleinman's examples, i.e., a single therapeutic pressure, when combined with all of the natural pressures ordinarily weighing on an organism, causes the organism to rapidly develop resistance.

And, so, once again, kleinman's ultimate conclusion is falsified by his own data.

Too bad, so sad.

[Belz...]

You have a predator which is consuming limpets. The advantage the predator has over the limpet is the predator can crack thin limpet shells. Those limpets whose alleles which determine the thickness of their shells are such that they create a thicker shell are at a reproductive advantage over those limpets whose alleles produce a thinner shell.

But several genes may be involved in constructing the shell...

Some of them may even be redundant.

[Belz...]

Well if that is not the case, why are additional drugs used to slow the evolution of HIV or TB or cancer therapies…?

You really do only focus on the examples that seem to support your position.

Now if you have any examples of combination simultaneous selection pressures being used for directed evolution, post the examples.

He just did.

[Belz...]

Well Henners, Dr Schneider created the model and it has been peer reviewed and published.

What's in question is your interpretation of the results, Klein.

[kleinman]

Samples of air and surfaces in the clean rooms at three National Aeronautics and Space Administration centers revealed surprising numbers and types of robust bacteria that appear to resist normal sterilization procedures, according to a newly published study.How many selection pressures are involved in "normal sterilization procedures", I wonder? Must be enough to profoundly slow evolution, don't you think? Well, perhaps, if you are looking only at the evolution of some bacteria, but ignoring others.
You evolutionists really love vague mush to try to substantiate your mathematically impossible theory of evolution.
Dr. Catharine A. Conley, a biologist who is the acting planetary protection officer at NASA headquarters, said the agency had long suspected that the organisms previously detected in clean rooms did not represent the full range that were there. Current cleaning techniques kill most common microbes, she said, and the resulting lack of competition could contribute to the number and diversity of the durable survivors found by the genetic testing approach.Wait a minute--you mean, the fact that multiple selection pressures can profoundly impact the numbers of one species might actually benefit other species? Sounds like multiple selection pressures are speeding evolution, at least of the survivors...
Wow Mercutio, they discovered bacteria which evolve into bacteria. Now if you could only identify the simultaneous selection pressures and genes which are evolving then you would have an example of simultaneous selection pressures accelerating evolution.
Belz, there is nothing special about gene duplication. It happens all the time. What makes you think there is something special about a gene duplication if it occurs accidentally on a single genome? Any transformation of an existing gene to a new gene must ultimately occur by mutation and selection and as we all know, that process is profoundly slow when you have more than a single selection condition.No, it isn't, Klein, because your selection pressures DO NOT act on the duplicated gene.

You should know this.
My selection pressure? The only selection pressure I am exerting is on the theory of evolution and look; it is trying to evolve before it goes extinct. Belz, one of the many things you don’t understand about evolution by mutation and selection is that if a mutation occurs to a gene that is not acted on by a selection pressure; it does not change the frequency of that sequence of bases in the gene pool.
I’m not, contact them and ask them whatever you want. In fact, why don’t you contact Dr Schneider and ask him to discuss ev? He says his model simulates reality and you say it doesn’t, why don’t you clear up this contradiction?You have yourself stated that ev doesn't model reality adequately.
Belz, what I have said is that Dr Schneider’s selection conditions are contrived but they do give a reasonable simulation of the mathematical behavior of the mutation selection process. The reason I say this is that we see the same type of behavior in real systems evolving by mutation and selection.
Wow! The last string of kleinman posts is quite interesting. Apparently, there are dependent, independent, directional, and non-directional selection pressures acting on organisms -- and all of these different factors effects evolutionary development.
You sure don’t know much about genetics, do you kjkent1. Go back and run ev on a case which will converge. The selection pressures initially are directional, changing the random sequences of bases to sequences which satisfy the selection conditions. Once the selection conditions are satisfied, these selection conditions become stabilizing conditions which prevent the sequences of bases from reverting to random sequences. Turn off selection in the model and watch what happens to the sequences of bases. In order to transform a population, you need directional selection pressures. Every gene has stabilizing pressures acting on them which prevent the gene from diverging so that they no longer function properly. Stabilizing selection pressures prevent divergence of genetic sequences.
You have a predator which is consuming limpets. The advantage the predator has over the limpet is the predator can crack thin limpet shells. Those limpets whose alleles which determine the thickness of their shells are such that they create a thicker shell are at a reproductive advantage over those limpets whose alleles produce a thinner shell.But several genes may be involved in constructing the shell...

Some of them may even be redundant.
That may be true but you are selecting for alleles, not mutations. Your search space is much smaller for alleles which may only number in the hundreds while mutations have a search space which may number in the millions or billions.
Well if that is not the case, why are additional drugs used to slow the evolution of HIV or TB or cancer therapies…?You really do only focus on the examples that seem to support your position.
Nobody is stopping you from posting citations which support your position. The only problem for you is there are no citations which support your position. Combination selection pressures profoundly slowing evolution by mutation and selection is a mathematical and empirical fact. That is why it is so easy for me to find citations which support my position.
Now if you have any examples of combination simultaneous selection pressures being used for directed evolution, post the examples.He just did.
Are you talking about Mercutio’s citation from the NY Times? You evolutionists do love your mush.
Well Henners, Dr Schneider created the model and it has been peer reviewed and published.What's in question is your interpretation of the results, Klein.
Hey Belz, my interpretation of the results from Dr Schneider’s model is that it shows combination selection pressures profoundly slow evolution by mutation and selection. And guess what Belz; I’ve cherry picked some more citations just for you.

http://www.recombinomics.com/News/12220501/H5N1_Tamiflu_Resistance_Mutants.html (http://www.recombinomics.com/News/12220501/H5N1_Tamiflu_Resistance_Mutants.html)
The first reported human H5N1 case in mainland China was successfully treated with amantadine, suggesting combination therapy may be useful in H5N1 cases that do not have resistance polymorphisms.

http://www.jpgmonline.com/article.asp?issn=0022-3859;year=2006;volume=52;issue=4;spage=277;epage=2 80;aulast=Shanks (http://www.jpgmonline.com/article.asp?issn=0022-3859;year=2006;volume=52;issue=4;spage=277;epage=2 80;aulast=Shanks)
The growing problem of drug resistance has greatly complicated the treatment for falciparum malaria. Whereas chloroquine and sulfadoxine/pyrimethamine could once cure most infections, this is no longer true and requires examination of alternative regimens. Not all treatment failures are drug resistant and other issues such as expired antimalarials and patient compliance need to be considered. Continuation of a failing treatment policy after drug resistance is established suppresses infections rather than curing them, leading to increased transmission of malaria, promotion of epidemics and loss of public confidence in malaria control programs. Antifolate drug resistance (i.e. pyrimethamine) means that new combinations are urgently needed particularly because addition of a single drug to an already failing regimen is rarely effective for very long. Atovaquone/proguanil and mefloquine have been used against multiple drug resistant falciparum malaria with resistance to each having been documented soon after drug introduction. Drug combinations delay further transmission of resistant parasites by increasing cure rates and inhibiting formation of gametocytes. Most currently recommended drug combinations for falciparum malaria are variants of artemisinin combination therapy where a rapidly acting artemisinin compound is combined with a longer half-life drug of a different class. Artemisinins used include dihydroartemisinin, artesunate, artemether and companion drugs include mefloquine, amodiaquine, sulfadoxine/pyrimethamine, lumefantrine, piperaquine, pyronaridine, chlorproguanil/dapsone. The standard of care must be to cure malaria by killing the last parasite. Combination antimalarial treatment is vital not only to the successful treatment of individual patients but also for public health control of malaria.
And
Combination chemotherapy's principles remain the same whether one is treating cancer or malaria. Full doses of effective drugs in combination should be used to result in cure and to avoid the generation of drug-resistance. Combination chemotherapy for falciparum malaria is currently available and should be the standard of care. Artemisinin compounds (an alternative possibly being quinine) are combined with a variety of partners to include mefloquine, pyronaridine, piperaquine, amodiaquine, chlorproguanil-dapsone and lumefantrine. Actual treatment regimens are undergoing rapid evolution and so a list of updated websites is provided rather than a table of treatment regimens which will be superseded in the future.
Life is a bowl of cherries, isn’t it Belz.

[kjkent1]

You sure don’t know much about genetics, do you kjkent1. Go back and run ev on a case which will converge. The selection pressures initially are directional, changing the random sequences of bases to sequences which satisfy the selection conditions. Once the selection conditions are satisfied, these selection conditions become stabilizing conditions which prevent the sequences of bases from reverting to random sequences. Turn off selection in the model and watch what happens to the sequences of bases. In order to transform a population, you need directional selection pressures. Every gene has stabilizing pressures acting on them which prevent the gene from diverging so that they no longer function properly. Stabilizing selection pressures prevent divergence of genetic sequences.Nice dodge -- I do appreciate the condescension. Regardless, the purpose of my comments were to demonstrate that you are intentionally ignoring the property of selective intensity, because it is inescapable that it has an effect on convergence of Rseq -> Rfreq, and that none of your citations consider the property, because all of those citations use selection pressures of relatively equivalent intensity to obtain results.

So, I'll just ask you straight out: what is the difference in the generational time in convergence to an organism faced with one selection pressure vis-a-vis an organism faced with two selection pressures, one of which is 10,000x stronger than the other?

[kleinman]

You sure don’t know much about genetics, do you kjkent1. Go back and run ev on a case which will converge. The selection pressures initially are directional, changing the random sequences of bases to sequences which satisfy the selection conditions. Once the selection conditions are satisfied, these selection conditions become stabilizing conditions which prevent the sequences of bases from reverting to random sequences. Turn off selection in the model and watch what happens to the sequences of bases. In order to transform a population, you need directional selection pressures. Every gene has stabilizing pressures acting on them which prevent the gene from diverging so that they no longer function properly. Stabilizing selection pressures prevent divergence of genetic sequences.Nice dodge -- I do appreciate the condescension. Regardless, the purpose of my comments were to demonstrate that you are intentionally ignoring the property of selective intensity, because it is inescapable that it has an effect on convergence of Rseq -> Rfreq, and that none of your citations consider the property, because all of those citations use selection pressures of relatively equivalent intensity to obtain results.

So, I'll just ask you straight out: what is the difference in the generational time in convergence to an organism faced with one selection pressure vis-a-vis an organism faced with two selection pressures, one of which is 10,000x stronger than the other?
The implication for a weak selection pressure is that it has little effect on the reproductive fitness of a population. What a strong selection pressure does is reduce the diversity of the population. Only those members who have some reproductive advantage for that strong selection pressure can survive and reproduce.

The selection pressures that Dr Schneider has designed are strong selection pressures because they eliminate half the population each generation, yet the remaining population is still able to reproduce. This is somewhat like the case of HIV where the selection pressures used in treatment of the virus do not kill the virus but simply limit the population’s ability to reproduce. An extremely intense selection pressure simply means that very few members of the population are able to reproduce thus only their genes remain in the gene pool.

[rocketdodger]

I finally grokk Kleinman -- he is a religious nutter who somehow heard about "combination selection pressures profoundly slowing evolution," did some (a very little) research, latched onto the idea that the possiblity of slow evolution proves creationism, and is vomiting over and over the same ineffective arguments and incorrect conclusions.

He doesn't really understand the experiments he cites, he doesn't really understand the evolutionary process, he doesn't really understand experimental biology, and most of all he refuses to even consider to learn any of what he doesn't know, as evidenced by a total absence of rational responses to all of our valid arguments.

Kleinman, what the heck is your point dude? Everyone here agrees with you that multiple drug therapies *can* slow down the evolution of microbe populations due to the combination of selective pressures -- you don't need to shove this in our faces over and over. Move past that idea... you have been doing nothing but barfing out citations to back up a claim we don't dispute.

I can predict the format of the next hundred Kleinman posts:
<one of us> - "how does x prove y in the general case?"
<kleinman> - "you sad sorry evolutionist, multiple drug therapy profoundly slows the evolution of <some microbe nobody really cares about in this argument> due to combination selection pressures. Evolution is finished!"

[kleinman]

Kleinman, what the heck is your point dude? Everyone here agrees with you that multiple drug therapies *can* slow down the evolution of microbe populations due to the combination of selective pressures -- you don't need to shove this in our faces over and over. Move past that idea... you have been doing nothing but barfing out citations to back up a claim we don't dispute.
Well hey dude? I guess you missed the citations which I posted which show the same affect of combination selection pressures on rodents, and the same affect of combination pressures on weeds. Each of these examples show that combination selection pressures affect complex organism is the same way as they do for microorganisms.

And then dude, ev wasn’t designed to demonstrate the affects of antibiotics on microorganisms. Yet ev’s three selection pressures profoundly slow the evolutionary process in this case as well. What a bummer for the theory of evolution.

Now dude, why don’t you show us an example of any combination selection pressures which behave differently than all the citations I have posted previous. When you realize you can’t find any examples of combination selection pressures which behave differently than in the citations which I have posted, then perhaps you will understand that evolution by mutation and selection is simply an optimization problem. The more conditions you try to optimize for the slower the process goes. That is why mutation and selection is a much more limited process than what you evolutionists allege. Far out man, far out.

[kjkent1]

The implication for a weak selection pressure is that it has little effect on the reproductive fitness of a population. What a strong selection pressure does is reduce the diversity of the population. Only those members who have some reproductive advantage for that strong selection pressure can survive and reproduce.

The selection pressures that Dr Schneider has designed are strong selection pressures because they eliminate half the population each generation, yet the remaining population is still able to reproduce. This is somewhat like the case of HIV where the selection pressures used in treatment of the virus do not kill the virus but simply limit the population’s ability to reproduce. An extremely intense selection pressure simply means that very few members of the population are able to reproduce thus only their genes remain in the gene pool.That's all it means?

Every one of your cites is a comparison of the fast resistance which appears in the target organism when faced with only one artificially induced extremely intense selection pressure, vis-a-vis the slow resistance which appears in the target organism when faced with multiple relatively equal intense selection pressures.

Now, all of a sudden, you're doing a head fake on one of the ceterpieces of your entire theory. Your cites prove that in an environment where one selective pressure dominates, evolution proceeds quickly.

You've pretty much shot yourself in the chest with your own data.

[kleinman]

The implication for a weak selection pressure is that it has little effect on the reproductive fitness of a population. What a strong selection pressure does is reduce the diversity of the population. Only those members who have some reproductive advantage for that strong selection pressure can survive and reproduce.

The selection pressures that Dr Schneider has designed are strong selection pressures because they eliminate half the population each generation, yet the remaining population is still able to reproduce. This is somewhat like the case of HIV where the selection pressures used in treatment of the virus do not kill the virus but simply limit the population’s ability to reproduce. An extremely intense selection pressure simply means that very few members of the population are able to reproduce thus only their genes remain in the gene pool.That's all it means?
Sorry to disappoint you kiddo, but that’s all there is to it. That’s why mathematics is so useful to science. It gives a way to way to study the interactions of multiple different variables and how they affect the behavior of other variables.
Every one of your cites is a comparison of the fast resistance which appears in the target organism when faced with only one artificially induced extremely intense selection pressure, vis-a-vis the slow resistance which appears in the target organism when faced with multiple relatively equal intense selection pressures.
What you still don’t understand is there is no difference mathematically or empirically whether selection pressures are “artificial” or “natural”. Do you think penicillin is an “artificial” selection pressure?
Now, all of a sudden, you're doing a head fake on one of the ceterpieces of your entire theory. Your cites prove that in an environment where one selective pressure dominates, evolution proceeds quickly.
Evolution against a single selection pressure also proceeds rapidly in ev. That’s what started this whole discussion. Why does ev evolve so slowly on all but the tiniest genomes? It’s the three selection conditions which slow down the model and that’s what happens in reality. No head fake or moving of the goal posts here kjkent1. This is simply brute force mathematics right through the center of the line.
You've pretty much shot yourself in the chest with your own data.
Too bad for your theory that I’m wearing a vest made of mathematics and it is bullet proof.

This is not just a gap in your theory of evolution; the effect of combination selection pressures on the rate of evolution is in direct contradiction to the theory. Your theory is mathematically impossible.

[balrog666]

That's all it means?

Every one of your cites is a comparison of the fast resistance which appears in the target organism when faced with only one artificially induced extremely intense selection pressure, vis-a-vis the slow resistance which appears in the target organism when faced with multiple relatively equal intense selection pressures.

Now, all of a sudden, you're doing a head fake on one of the ceterpieces of your entire theory. Your cites prove that in an environment where one selective pressure dominates, evolution proceeds quickly.

You've pretty much shot yourself in the chest with your own data.


It's only a flesh wound!

http://www.intriguing.com/mp/_pictures/grail/large/HolyGrail017.jpg

[kleinman]

That's all it means?

Every one of your cites is a comparison of the fast resistance which appears in the target organism when faced with only one artificially induced extremely intense selection pressure, vis-a-vis the slow resistance which appears in the target organism when faced with multiple relatively equal intense selection pressures.

Now, all of a sudden, you're doing a head fake on one of the ceterpieces of your entire theory. Your cites prove that in an environment where one selective pressure dominates, evolution proceeds quickly.

You've pretty much shot yourself in the chest with your own data.It's only a flesh wound!
I suppose there are evolutionists who will believe that reptiles evolved into birds one gene at a time to selection pressures that only existed in a land long ago and far away but no longer exist in these modern times.

[kjkent1]

I suppose there are evolutionists who will believe that reptiles evolved into birds one gene at a time to selection pressures that only existed in a land long ago and far away but no longer exist in these modern times.You keep ignoring the point. Your cites and ev both prove that in an environment where one selection pressure dominates, evolution proceeds rapidly to whatever local optimum exists in that particular environment.

You've been saying this for 100s of posts, so there's no sense in denying it now.

Thus, if there are many natural environments wherein one selective pressure dominates, then this fact explains how evolution proceeds in nature.

And, the empirical evidence is that such environments exist, because if they didn't, then there wouldn't be any evolved life forms, except via God's divine will (which you can't invoke as an affirmative proof, because it can't be affirmatively proven).

Got evidence to prove that natural environments always have multiple selection pressures of relatively equal strength? If not, you're done.

[kleinman]

I suppose there are evolutionists who will believe that reptiles evolved into birds one gene at a time to selection pressures that only existed in a land long ago and far away but no longer exist in these modern times.You keep ignoring the point. Your cites and ev both prove that in an environment where one selection pressure dominates, evolution proceeds rapidly to whatever local optimum exists in that particular environment.
Now this is a strange argument you are trying to make since I have been making this point for hundreds of posts. This is an example of microevolution. So let’s see what kind of contortions you are going to go through.
You've been saying this for 100s of posts, so there's no sense in denying it now.
Yes sir, I confess my guilt.
Thus, if there are many natural environments wherein one selective pressure dominates, then this fact explains how evolution proceeds in nature.
Ah yes, the string cheese theory of evolution, 10^500 alternative natural environments in which billions and billions of genes are evolving to transform reptiles into birds.

Kjkent1, perhaps you could explain something to me. Why is it when a read your posts I start hearing the theme song for Twilight Zone?
And, the empirical evidence is that such environments exist, because if they didn't, then there wouldn't be any evolved life forms, except via God's divine will (which you can't invoke as an affirmative proof, because it can't be affirmatively proven).
Wait a minute, now I’m hearing the theme song for the Three Stooges. Woo, woo, woo, knuck, knuck, knuck.
Got evidence to prove that natural environments always have multiple selection pressures of relatively equal strength? If not, you're done.
Oh no, I’m not done, however the theory of evolution is well done, in fact it is so well done, it is burned to a crisp. Sorry about that Henners, I burned your meal; at least you have something to drink.

[kjkent1]

Now this is a strange argument you are trying to make since I have been making this point for hundreds of posts. This is an example of microevolution. So let’s see what kind of contortions you are going to go through.So, now you claim that even given sequential environments each with a single dominant selective pressure, evolution is impossible.

Why, only moments before, your contention was that the differential in generational change between single pressure dominant environments and multiple pressure environments was your proof that evolution is impossible.

Definitely a huge goal post move, here. Make up your mind, Alan.

Ah yes, the string cheese theory of evolution, 10^500 alternative natural environments in which billions and billions of genes are evolving to transform reptiles into birds.Ad hominem -- reported to moderators.

Kjkent1, perhaps you could explain something to me. Why is it when a read your posts I start hearing the theme song for Twilight Zone?Ad hominem -- reported to moderators.
Wait a minute, now I’m hearing the theme song for the Three Stooges. Woo, woo, woo, knuck, knuck, knuck.Ad hominem -- reported to moderators.

Is this how you address your patients, Alan? Rather juvenile if you ask me.

[rocketdodger]

Well hey dude? I guess you missed the citations which I posted which show the same affect of combination selection pressures on rodents, and the same affect of combination pressures on weeds. Each of these examples show that combination selection pressures affect complex organism is the same way as they do for microorganisms.

Exactly the response I predicted...

And then dude, ev wasn’t designed to demonstrate the affects of antibiotics on microorganisms. Yet ev’s three selection pressures profoundly slow the evolutionary process in this case as well. What a bummer for the theory of evolution.

and again...

Now dude, why don’t you show us an example of any combination selection pressures which behave differently than all the citations I have posted previous. When you realize you can’t find any examples of combination selection pressures which behave differently than in the citations which I have posted, then perhaps you will understand that evolution by mutation and selection is simply an optimization problem. The more conditions you try to optimize for the slower the process goes. That is why mutation and selection is a much more limited process than what you evolutionists allege. Far out man, far out.

and again.

You completely failed to address the main argument against your bablygook, which is simply this:

What the studies show
-------------------------------------------
If pressure p is the strongest pressure in a set, evolution under the effects of the set will be slower than if p was acting on the population alone.


What you incorrectly think the studies show
-------------------------------------------
If pressure p is the weakest pressure in a set, evolution under the effects of the set will be slower than if p was acting on the population alone.

[chillzero]

Folks, a gentle reminder to please respond to the arguments and not the individual arguing them.

[Kotatsu]

Is there anything you evolutionists don’t whine about?

We are not Borg. I, for one, do not whine about being bitten by shrikes and sparrowhawks --- something that's happened quite often recently. However, how am I to know if kjkent, Mercutio or Dr. Adequate, when placed in the same circumstances, would whine about it afterwards?

Kotatsu, you contend that selection pressures act on entire genomes. How does this happen? What I am trying to show you and why it is relevant is that mutation selection is an optimization or sorting problem. It is mathematically and empirically impossible to sort mutations as you allege. This mush you present makes no mathematical sense.

I contend that some selection pressures do, yes. Or at least that they are not necessarily limited to one single gene. If for example a new predator is introduced into an area, and this new predator uses a different hunting method than all other predators in the area, then this new selection pressure will operate on all of the prey genome. Any mutation in any gene that provides a boon to the animal will --- theoretically --- be transmitted to the next generation. It doesn't matter where in the genome the gene is, as long as it does provide the added benefit. This is exemplified for instance in the list of possibly responses to a tree-born predator I provided before. In this sense, the selection pressure operates on the whole genome.

It is also intuitively reasonable to assume this, as many selection pressures, if intense enough, will make the individual die. If this happens, the entire genome of that individual will die, not just the genes which the selection pressure works on.

You have a predator which is consuming limpets. The advantage the predator has over the limpet is the predator can crack thin limpet shells. Those limpets whose alleles which determine the thickness of their shells are such that they create a thicker shell are at a reproductive advantage over those limpets whose alleles produce a thinner shell. The predator is selecting out alleles which produce a thinner shell and the thicker shell limpets are more fit than their thin shell counterparts. Note that in the absence of the predator, the thin shell limpet is at a reproductive advantage over their thick shell counterparts because the put less energy toward shell production and more energy toward reproduction.

But, as Belz has pointed out, what if there are several genes which are involved in the construction of the shell? Conceivably, there could be one gene which controls extraction of calcium from the limpet's food, one (or even several, depending on the exact mechanisms) which controls transportation of it to the correct place, one which controls deposition of it, and --- though I am not sure exactly what the shell consists of --- perhaps several others which control extraction, transport and deposition of other materials in the shell. Then how does the selection pressure act on only one of them to the exclusion of the others?

This same type of analysis can be done for your moth example but I’ll leave this for an exercise for you.

This example is of an even more complex structure, with even more opportunities for many genes to be involved. I would leave the implications of this for you to work out, but I know you are more likely to ignore them.

Kotatsu, you can’t even identify the genes targeted in your examples, you think the entire genome is targeted by selection pressures. Ultimately, selection pressures are manifest by changes at the genetic sequence level. Until you start making your observations and measurements at this level, everything you do is speculation.

So you don't believe that mutation occurs by for instance G's changing into C's in a lineage? Is that a correct interpretation of your evasive answer to my question?

Kotatsu, do you believe that weeds and rodents are micro-organisms? I have posted examples for these complex multi-cellular organisms and mutation and selection behaves the same for these life forms only slower than micro-organisms since they have slow reproduction rates and larger genomes. The selection pressures, targeted genes and mutations are identified in these examples as well. Your approach to the understanding of evolution has no exactitude of course that is typical for evolutionists.

I would like to draw your attention to the word "necessarily". In some cases, depending on the study, that level of exactness would be relevant also in larger, more complex animals. However, just because they are more complex --- consisting of more than one cell, for instance --- it can often be not only irrelevant, but also impossible to locate the gene on which a specific selection pressure's effects are being studied. Therefore, it is not necessary to specify the exact mutations in this gene in all cases.

However, again, in systematics we can study these changes over a larger time frame, and the results are invariably nested hierarchies which suggest a common descent brought about by gradual evolution. I have no or little experience with whole-genome sequencing (which is generally too expensive to carry out to any large degree in my field), but I understand these also produce nested hierarchies.

I know this is what you are contending but you can not identify the selection pressures, targeted genes or mutations required to accurately support your contention. This thread is a no-mush zone.

I have done so repeatedly. Go back and check my other posts.

I suppose there are evolutionists who will believe that reptiles evolved into birds one gene at a time to selection pressures that only existed in a land long ago and far away but no longer exist in these modern times.

If you find one of those evolutionists, tell him/her to come here so we can meet him/her.

[Kotatsu]

Now this is a strange argument you are trying to make since I have been making this point for hundreds of posts. This is an example of microevolution. So let’s see what kind of contortions you are going to go through.

Just a quick thought: if the local maximum under a certain set of selection pressures makes the organism in question change substantially into something else --- from sea-living to land-living, for instance --- would this also fall under your concept of micro-evolution, Kleinman? In other words, will gradual changes from one local maximum to another always be micro-evolution, or can it --- if even theoretically --- be something more?

[Belz...]

My selection pressure? The only selection pressure I am exerting is on the theory of evolution and look; it is trying to evolve before it goes extinct.

I'm getting really tired of you picking on one erroneous word in my sentences and using that as an excuse to ignore my points while patting yourself on the back for your cleverness.

Belz, one of the many things you don’t understand about evolution by mutation and selection is that if a mutation occurs to a gene that is not acted on by a selection pressure; it does not change the frequency of that sequence of bases in the gene pool.

Didn't I mention, more than once, that once this gene evolves a function it will be affected by the pressures ?

Belz, what I have said is that Dr Schneider’s selection conditions are contrived but they do give a reasonable simulation of the mathematical behavior of the mutation selection process.

So they're not very good but they're good enough for you ?

That may be true but you are selecting for alleles, not mutations.

Actually, we're selecting individuals for reproduction, but hey! Who's really interested in real stuff ?

Nobody is stopping you from posting citations which support your position.

I'm quite content to point out how ridiculous your theory is while OTHER people present citations of their own.

The only problem for you is there are no citations which support your position.

Well, none that you'll adress, anyway. We've seen that.

Combination selection pressures profoundly slowing evolution by mutation and selection is a mathematical and empirical fact.

Translation: "my conclusion invalidates the premise!"

Are you talking about Mercutio’s citation from the NY Times? You evolutionists do love your mush.

That's your rebuttal ?

Hey Belz, my interpretation of the results from Dr Schneider’s model is that it shows combination selection pressures profoundly slow evolution by mutation and selection.

Yes, that is exactly what I meant by "your interpretations are in question."

Life is a bowl of cherries, isn’t it Belz.

Well, it's SOME kind of vegetable, for sure.

[Belz...]

I suppose there are evolutionists who will believe that reptiles evolved into birds one gene at a time to selection pressures that only existed in a land long ago and far away but no longer exist in these modern times.

I don't think you've been reading this very well.

Ah yes, the string cheese theory of evolution, 10^500 alternative natural environments in which billions and billions of genes are evolving to transform reptiles into birds.

Now you're making it sound like those alternatives are each equal in probability. Typical creationist nonsense.

[kleinman]

Now this is a strange argument you are trying to make since I have been making this point for hundreds of posts. This is an example of microevolution. So let’s see what kind of contortions you are going to go through.So, now you claim that even given sequential environments each with a single dominant selective pressure, evolution is impossible.
Correctomundo, or should I say correctoenvironmento. Now I am open to correction if you can demonstrate what the thousands of sequential environmental changes are. Woo, woo, woo, knuck, knuck, knuck.
Why, only moments before, your contention was that the differential in generational change between single pressure dominant environments and multiple pressure environments was your proof that evolution is impossible.
Wrongomundo, or should I say wrongoenvironmento. I have never said that evolution is impossible, what I have said is the theory of evolution by mutation and selection is mathematically impossible. Let’s put some more precision is this statement. What is mathematically impossible is the concept of common descent in the theory of evolution. Actually I think that evolutionist terminology is backwards on this concept, it should be called common ascent.
Definitely a huge goal post move, here. Make up your mind, Alan.
How would you know my mind? You haven’t arrived at the ball park yet.
Ah yes, the string cheese theory of evolution, 10^500 alternative natural environments in which billions and billions of genes are evolving to transform reptiles into birds.Ad hominem -- reported to moderators.
To the moderators: I confess that I am an annoying creationist.
Kjkent1, perhaps you could explain something to me. Why is it when a read your posts I start hearing the theme song for Twilight Zone?Ad hominem -- reported to moderators.
To the moderators: I confess that I am an incorrigible annoying creationist.
Wait a minute, now I’m hearing the theme song for the Three Stooges. Woo, woo, woo, knuck, knuck, knuck.Ad hominem -- reported to moderators.
To the moderators: Three strikes.
Is this how you address your patients, Alan? Rather juvenile if you ask me.
Why kjkent1, this is exactly how I talk with my patients. If they come in with a bad back, I tell them I was trained at the Three Stooges School of back care. Moe is the doctor and Curley is the patient.
Moe: Tell me, how long have you had a weak back?
Curley: Oh, about a week back.
You completely failed to address the main argument against your bablygook, which is simply this:

What the studies show
-------------------------------------------
If pressure p is the strongest pressure in a set, evolution under the effects of the set will be slower than if p was acting on the population alone.


What you incorrectly think the studies show
-------------------------------------------
If pressure p is the weakest pressure in a set, evolution under the effects of the set will be slower than if p was acting on the population alone.
I’m a little negative about the positive but I am positive about the negative.
Is there anything you evolutionists don’t whine about?We are not Borg. I, for one, do not whine about being bitten by shrikes and sparrowhawks --- something that's happened quite often recently. However, how am I to know if kjkent, Mercutio or Dr. Adequate, when placed in the same circumstances, would whine about it afterwards?
Kotatsu, there’s an old saying that goes, “there is no education in the second kick of a mule”.
Kotatsu, you contend that selection pressures act on entire genomes. How does this happen? What I am trying to show you and why it is relevant is that mutation selection is an optimization or sorting problem. It is mathematically and empirically impossible to sort mutations as you allege. This mush you present makes no mathematical sense.I contend that some selection pressures do, yes. Or at least that they are not necessarily limited to one single gene. If for example a new predator is introduced into an area, and this new predator uses a different hunting method than all other predators in the area, then this new selection pressure will operate on all of the prey genome. Any mutation in any gene that provides a boon to the animal will --- theoretically --- be transmitted to the next generation. It doesn't matter where in the genome the gene is, as long as it does provide the added benefit. This is exemplified for instance in the list of possibly responses to a tree-born predator I provided before. In this sense, the selection pressure operates on the whole genome.
When you make these types of speculations, you abandon scientific method. Your own examples are better explained by recombination and selection. If you are going to contend that a predator is going to apply selection pressure to the prey’s entire genome, you need to find some way to measure how mutation and selection can evolve the entire genome. The mathematical problem you will encounter is, if every gene in the genome is evolving simultaneously; you have to sort beneficial and detrimental mutations that are being mixed though out the entire genome in different locations in each member of the population. It becomes impossible for the population to find any trajectory to a new optimum. Mutation and selection is an extremely slow process for more than a single gene. This is why your examples are more logically explained to be examples of recombination and selection.
It is also intuitively reasonable to assume this, as many selection pressures, if intense enough, will make the individual die. If this happens, the entire genome of that individual will die, not just the genes which the selection pressure works on.
Even if the selection pressures do not cause extinction, more than a single selection pressure still slow evolution by mutation and selection, that is what the mathematics shows and that is what the empirical evidence of mutation and selection shows.
You have a predator which is consuming limpets. The advantage the predator has over the limpet is the predator can crack thin limpet shells. Those limpets whose alleles which determine the thickness of their shells are such that they create a thicker shell are at a reproductive advantage over those limpets whose alleles produce a thinner shell. The predator is selecting out alleles which produce a thinner shell and the thicker shell limpets are more fit than their thin shell counterparts. Note that in the absence of the predator, the thin shell limpet is at a reproductive advantage over their thick shell counterparts because the put less energy toward shell production and more energy toward reproduction.But, as Belz has pointed out, what if there are several genes which are involved in the construction of the shell? Conceivably, there could be one gene which controls extraction of calcium from the limpet's food, one (or even several, depending on the exact mechanisms) which controls transportation of it to the correct place, one which controls deposition of it, and --- though I am not sure exactly what the shell consists of --- perhaps several others which control extraction, transport and deposition of other materials in the shell. Then how does the selection pressure act on only one of them to the exclusion of the others?
It would not surprise me if there are several, perhaps dozens of genes involved in the manufacture of the limpet shell. Selecting alleles which produce a thicker shell is a much simpler mathematical problem than selecting mutations that might somehow produce a thicker shell. It still hasn’t sunk in with you that recombination and selection is a very rapid way of changing the characteristics of a population while mutation and selection is a profoundly slow process. I asked Taffer this question before he abandoned the discussion, perhaps you would try to answer the question. If you breed a Chihuahua with a Great Dane, is the variation in the offspring due to recombination or mutation?
This same type of analysis can be done for your moth example but I’ll leave this for an exercise for you.This example is of an even more complex structure, with even more opportunities for many genes to be involved. I would leave the implications of this for you to work out, but I know you are more likely to ignore them.
Which do you think is more complex, the sense of hearing or the sense of smell? You can breed dogs and get blood hounds which have a superior sense of smell than other breeds. I am sure there are many genes involved but it hasn’t taken many generations to do this by recombination and selection.
Kotatsu, you can’t even identify the genes targeted in your examples, you think the entire genome is targeted by selection pressures. Ultimately, selection pressures are manifest by changes at the genetic sequence level. Until you start making your observations and measurements at this level, everything you do is speculation.So you don't believe that mutation occurs by for instance G's changing into C's in a lineage? Is that a correct interpretation of your evasive answer to my question?
What I believe is that you can’t produce measurable evidence of your hypothesis, you present only speculation and there is a much more reasonable explanation for your examples and it is not mutation and selection.
Kotatsu, do you believe that weeds and rodents are micro-organisms? I have posted examples for these complex multi-cellular organisms and mutation and selection behaves the same for these life forms only slower than micro-organisms since they have slow reproduction rates and larger genomes. The selection pressures, targeted genes and mutations are identified in these examples as well. Your approach to the understanding of evolution has no exactitude of course that is typical for evolutionists.I would like to draw your attention to the word "necessarily". In some cases, depending on the study, that level of exactness would be relevant also in larger, more complex animals. However, just because they are more complex --- consisting of more than one cell, for instance --- it can often be not only irrelevant, but also impossible to locate the gene on which a specific selection pressure's effects are being studied. Therefore, it is not necessary to specify the exact mutations in this gene in all cases.
Only an evolutionist would claim that it is not necessary to specify exact mutations because when you do, it shows your theory to be mathematically impossible. Kotatsu, good science requires repeatable experiments and measurements. You provide neither.
However, again, in systematics we can study these changes over a larger time frame, and the results are invariably nested hierarchies which suggest a common descent brought about by gradual evolution. I have no or little experience with whole-genome sequencing (which is generally too expensive to carry out to any large degree in my field), but I understand these also produce nested hierarchies.
The problem with your hypothesis is that the fundamental mechanism which you claim brings about common descent does not work the way you allege. Mutation and selection can now be measured with mathematical precision and it is now known how profoundly slow the process is with combination selection pressures. You can do your systematics but you have no way to transform comparable genes.
I know this is what you are contending but you can not identify the selection pressures, targeted genes or mutations required to accurately support your contention. This thread is a no-mush zone.I have done so repeatedly. Go back and check my other posts.
I understand your argument; you contend that a predator applies selection pressure to the prey’s entire genome. There is nothing measurable or repeatable in your example. The citations which I post precisely define the selection pressures and targeted genes and in many cases specify the exact mutations required for the population to adapt to these selection pressures. There is a difference between the mush you present and the mathematically precise examples I have cited.
I suppose there are evolutionists who will believe that reptiles evolved into birds one gene at a time to selection pressures that only existed in a land long ago and far away but no longer exist in these modern times.If you find one of those evolutionists, tell him/her to come here so we can meet him/her.
We know your hypothesis Kotatsu. A predator chased a reptile into a tree and the reptile’s entire genome transformed to grow wings and feathers.
Now this is a strange argument you are trying to make since I have been making this point for hundreds of posts. This is an example of microevolution. So let’s see what kind of contortions you are going to go through.Just a quick thought: if the local maximum under a certain set of selection pressures makes the organism in question change substantially into something else --- from sea-living to land-living, for instance --- would this also fall under your concept of micro-evolution, Kleinman? In other words, will gradual changes from one local maximum to another always be micro-evolution, or can it --- if even theoretically --- be something more?
Kotatsu, you can have profound changes in the morphological properties of a population by recombination and selection. This is already demonstrated by our dog breeding example. What you can’t get by mutation and selection are huge changes in many genes simultaneously. This is the mathematical conundrum that you face with how the mutation and selection process actually works. Multiple selection pressures profoundly slow the evolutionary process.
My selection pressure? The only selection pressure I am exerting is on the theory of evolution and look; it is trying to evolve before it goes extinct.I'm getting really tired of you picking on one erroneous word in my sentences and using that as an excuse to ignore my points while patting yourself on the back for your cleverness.
You have only one erroneous word in your sentences?
Belz, one of the many things you don’t understand about evolution by mutation and selection is that if a mutation occurs to a gene that is not acted on by a selection pressure; it does not change the frequency of that sequence of bases in the gene pool.Didn't I mention, more than once, that once this gene evolves a function it will be affected by the pressures ?
Now that’s correct, only a gene which has function will be subject to selection pressures. So do you want to explain to us how a gene can evolve de novo? Were you not also going to refute Professor Behe’s hypothesis of irreducible complexity by telling us what the proteins for the DNA replicase system were doing before DNA could be replicated? Tell us what gyrase and helicase were doing before DNA could be replicated.
Belz, what I have said is that Dr Schneider’s selection conditions are contrived but they do give a reasonable simulation of the mathematical behavior of the mutation selection process.So they're not very good but they're good enough for you ?
Yup, it is also good enough for Dr Schneider and the peer reviewers at Nucleic Acids Research as well. What Dr Schneider’s selection conditions do is demonstrate mathematically how slow the mutation and selection process occurs when you have multiple selection conditions.
That may be true but you are selecting for alleles, not mutations.Actually, we're selecting individuals for reproduction, but hey! Who's really interested in real stuff ?
Whether it is humans who are doing the selection for breeding purposes or “natural” selection, the mathematics is not changed.
Nobody is stopping you from posting citations which support your position.I'm quite content to point out how ridiculous your theory is while OTHER people present citations of their own.
What other citations? Kotatsu presents examples of recombination and selection and can’t define the selection pressures or target genes. Kotatsu thinks that all it takes is for a reptile to be chased into a tree and that’s enough selection pressure to make it grow wings and feathers.
The only problem for you is there are no citations which support your position.Well, none that you'll adress, anyway. We've seen that.
I like addressing Kotatsu’s citations; they demonstrate how recombination and selection work in “nature”. Now if one of you evolutionists would present an example of combination selection pressures accelerating evolution by mutation and selection, that would be a challenge.
Combination selection pressures profoundly slowing evolution by mutation and selection is a mathematical and empirical fact.Translation: "my conclusion invalidates the premise!"
That must be a translation into evolutionish.
Are you talking about Mercutio’s citation from the NY Times? You evolutionists do love your mush.That's your rebuttal ?
Bacteria growing in a supposed clean room are an example of multiple selection pressures accelerating evolution by mutation and selection. You need to translate that from evolutionish to English.
Hey Belz, my interpretation of the results from Dr Schneider’s model is that it shows combination selection pressures profoundly slow evolution by mutation and selection.Yes, that is exactly what I meant by "your interpretations are in question."
Well then, why don’t I post some more citations which substantiate my interpretation of the mathematics?
Life is a bowl of cherries, isn’t it Belz.Well, it's SOME kind of vegetable, for sure.
Hey Belz, if a predator goes after a cherry in a tree, will the cherry grow wings and feathers?
I suppose there are evolutionists who will believe that reptiles evolved into birds one gene at a time to selection pressures that only existed in a land long ago and far away but no longer exist in these modern times.I don't think you've been reading this very well.
I told you, I twarn’t an inglish magor in kollige.
Ah yes, the string cheese theory of evolution, 10^500 alternative natural environments in which billions and billions of genes are evolving to transform reptiles into birds.Now you're making it sound like those alternatives are each equal in probability. Typical creationist nonsense.
I know Belz, so here’s some more of this typical nonsense for you to ponder.
http://www.eanmat.org/Newsletters/nwsltt05.doc (http://www.eanmat.org/Newsletters/nwsltt05.doc)
Malaria Control in East Africa is facing an enormous challenge. The reason is the speed with which resistance to pyrimethamine-sulfadoxine [‘Fansidar’, ‘SP’ ‘PSD’] has emerged and spread. As first-line treatment for non-severe malaria, Kenya only officially changed from chloroquine to SP in 1998, and Tanzania is in the process, yet there is evidence that this ‘new’ treatment is already nearing the end of its ‘Useful Therapeutic Life’ [UTL]. The new molecular biological technology is helping to assess the progression of SP resistance. There are four mutations in the dihydrofolate reductase [DHFR] gene known to be associated with SP resistance, and two mutations in the dihydropteroate synthase [DHPS] gene which further increase the resistance level. 3 out of 4 of the DHFR mutations and both of the DHPS mutations are already prevalent in Kenya, and probably in Tanzania and Uganda also. At some study sites in Kenya and Tanzania it has been shown that 20-40% of SP-treated patients remain slide-positive on day 7, which means that < 50% of infections are being cleared by SP treatment. Our preliminary EANMAT data for SP efficacy are compatible with these results.

So, the question must be posed: “How long will SP last, and what will we use next?”. Chloroquine lasted so long in Africa that the possibility of a short UTL for its replacement has been overlooked. But in Africa, we have the advantage of a historical perspective: we can look at Southeast Asia, or South America, and see what happened there. SP lasted about 5 years, once it became widely used, and was replaced by mefloquine; a much more expensive drug, and one which has an even longer elimination half-life than SP, and thus a very strong selective pressure for resistance. In Thailand, mefloquine efficacy started to fall steeply within a few years of implementation. However, in combination with artemisinin the progression of mefloquine resistance has been halted: good evidence that, in Africa, we should be thinking of using antimalarial drugs in combination, to get the longest UTL [see White et al, 1999].

Our choice of a replacement for SP is heavily restricted by cost, and combinations will always be more expensive than ‘monotherapy’ [see box]. Lapdap, mefloquine or quinine monotherapy are the cheapest options, but carry great dangers. Lapdap, like SP, is an antifolate antimetabolite. At present, it clears SP-resistant infections, but the selection of one more DHFR mutation will produce resistant parasites: a potential disaster which should be faced now. The best way to avoid ruining such a useful drug is through combination: Lapdap-artesunate. Quinine is effective, but will patients take a full, 7-day course? If not, the selection of quinine resistance is likely, and this will threaten our standard treatment of severe, life-threatening malaria. Mefloquine is effective in Africa, but it is absolutely certain that mefloquine monotherapy will select resistance very quickly: within a short time, malaria control units will be facing the same problem: what do I use next?. Further; mefloquine-resistant P. falciparum is cross-resistant to quinine: apart from the rapid loss of treatment for outpatients, quinine treatment for severe, inpatient malaria will start to become ineffective. We can go further; it is a fair statement that every effort should be made to ensure that mefloquine monotherapy never replaces SP as first line treatment in Africa.
Now aren’t these authors writing nonsense? They seem to think that combination therapy for the treatment of malaria will somehow slow the evolution of resistance. Aren’t they silly Belz?

[joobz]

Just a friendly reminder. The assumptions that Kleinman makes in his argument are as foolows:
1.) Mutation rate remains constant
2.) Mutation rate is known
3.) Number of selection pressures for all species for all time in all areas is known
4.) Number of selection pressures is constant
5.) Slection pressure magnitude is constant and equal for all pressures
6.) Point mutations are the only mutation/adaptation mechanism
7.) defining selection pressure is unimportant
8.) slow equals stop


Even just one bad assumption would invalidate his argument, there are at least 8.

[kjkent1]

Correctomundo, or should I say correctoenvironmento. Now I am open to correction if you can demonstrate what the thousands of sequential environmental changes are. Woo, woo, woo, knuck, knuck, knuck.
Do you deny that the environment of the Earth has changed over the past 4 billion years?

The sequential environments that have resulted in the present-day existence of birds have occured exactly as the geological record shows them to have changed.

PS. Ad hominem -- reported to moderators.

[kjkent1]

Just a friendly reminder. The assumptions that Kleinman makes in his argument are as foolows:
1.) Mutation rate remains constant
2.) Mutation rate is known
3.) Number of selection pressures for all species for all time in all areas is known
4.) Number of selection pressures is constant
5.) Slection pressure magnitude is constant and equal for all pressures
6.) Point mutations are the only mutation/adaptation mechanism
7.) defining selection pressure is unimportant
8.) slow equals stop


Even just one bad assumption would invalidate his argument, there are at least 8.You may want to consider adding (9) "Mutation is non-random."

[rocketdodger]

I’m a little negative about the positive but I am positive about the negative.

And this shows that you don't know what you are talking about -- the first case is *implied* by the second...


Now aren’t these authors writing nonsense? They seem to think that combination therapy for the treatment of malaria will somehow slow the evolution of resistance. Aren’t they silly Belz?[/SIZE][/FONT]

Yet another microbial disease treatment citation, about an issue nobody disagrees with you on, fronted as an actual argument. Are you completely ignoring what we are telling you? WE DON'T DISAGREE THAT COMBINATION THERAPY SLOWS EVOLUTION. *Nobody* is arguing against that.

[Kotatsu]

When you make these types of speculations, you abandon scientific method. Your own examples are better explained by recombination and selection. If you are going to contend that a predator is going to apply selection pressure to the prey’s entire genome, you need to find some way to measure how mutation and selection can evolve the entire genome. The mathematical problem you will encounter is, if every gene in the genome is evolving simultaneously; you have to sort beneficial and detrimental mutations that are being mixed though out the entire genome in different locations in each member of the population. It becomes impossible for the population to find any trajectory to a new optimum. Mutation and selection is an extremely slow process for more than a single gene. This is why your examples are more logically explained to be examples of recombination and selection.

When I do these speculations, I am essentially forming a hypothesis which I could then --- theoretically, because I have neither the time nor the inclination to pursue this myself --- test empirically. As I have observed a phenomenon --- evolution --- I believe it is prudent first to explore possible way for the phenomenon to work based on established knowledge. I do not feel this is to abandon the scientific method. It is just a case of stopping midway, because I haven't got the opportunity to carry the experiment through.

Also, I agree that none of my examples are pure cases of mutation and selection. However, neither are they pure cases of recombination and selection, as the differences between alleles need to arise in some way.

If you are going to contend that a predator does not exert a selection pressure on the entire genome, you will have to explain why different animals find different solutions to the same problem. You will also have to explain how the selection pressure of the predator somehow excludes parts of the genome.

Your perceived sorting problem is easily countered by the fact that inheritance of a good enough allele --- that is one which gives a significant edge against one of the more overbearing of the countless selection pressures that acts on the organism --- can allow survival of several detrimental mutations in other genes, if the benefit of the beneficial one is large enough. This is because selection pressures can be of different intensities.

It would not surprise me if there are several, perhaps dozens of genes involved in the manufacture of the limpet shell. Selecting alleles which produce a thicker shell is a much simpler mathematical problem than selecting mutations that might somehow produce a thicker shell.

But the difference between two homologous genes are differences in mutation, are they not? I do not in any way contend that the animals actively select between changing a C into a G and changing it into an A.

If you breed a Chihuahua with a Great Dane, is the variation in the offspring due to recombination or mutation?

Both. But not necessarily in equal amounts.

Which do you think is more complex, the sense of hearing or the sense of smell?

I would say this depends entirely on the sophistication of the organs involved, which in turn depends on what animals you are comparing. To make a general statement on this would probably be unconsciously biased towards those animals with which I am most familiar.

You can breed dogs and get blood hounds which have a superior sense of smell than other breeds. I am sure there are many genes involved but it hasn’t taken many generations to do this by recombination and selection.

Fortunately for my moth example, being done quickly is not a requirement, as I have several million years to work with.

What I believe is that you can’t produce measurable evidence of your hypothesis, you present only speculation and there is a much more reasonable explanation for your examples and it is not mutation and selection.

So shall I take that as a confirmation that you don't believe that mutation occurs by for instance G's changing into C's in a lineage?

Only an evolutionist would claim that it is not necessary to specify exact mutations because when you do, it shows your theory to be mathematically impossible. Kotatsu, good science requires repeatable experiments and measurements. You provide neither.

It follows, then, that only an evolutionist would be justified in stating anything at all. Especially because a large part of what the evolutionist studies are extinct organisms, where the genes present or absent, evolving or not evolving, and so on, would be entirely impossible to know anything about anyway. Only the evolution of the phenotype would be possible to study in those cases.

The problem with your hypothesis is that the fundamental mechanism which you claim brings about common descent does not work the way you allege. Mutation and selection can now be measured with mathematical precision and it is now known how profoundly slow the process is with combination selection pressures. You can do your systematics but you have no way to transform comparable genes.

Please elaborate. If I have a theoretical organism which I can sequence, and let that reproduce for some time, periodically sequencing the same gene, mutations would accumulate. This would translate in a phylogenetic tree to a nested hierarchy. This is independent of the speed of evolution, as genes evolving at different speeds simply give resolution on different taxonomic levels. Precisely where is the flaw?

We know your hypothesis Kotatsu. A predator chased a reptile into a tree and the reptile’s entire genome transformed to grow wings and feathers.

Of course not. What use would a set of wings be inside the cells attached to the genome?

Kotatsu thinks that all it takes is for a reptile to be chased into a tree and that’s enough selection pressure to make it grow wings and feathers.

This is not a true representation of what I have said. I have given you a long list of possible selection pressures to grow feathers out of scales.

[kleinman]

Just a friendly reminder. The assumptions that Kleinman makes in his argument are as foolows:
1.) Mutation rate remains constant
2.) Mutation rate is known
3.) Number of selection pressures for all species for all time in all areas is known
4.) Number of selection pressures is constant
5.) Slection pressure magnitude is constant and equal for all pressures
6.) Point mutations are the only mutation/adaptation mechanism
7.) defining selection pressure is unimportant
8.) slow equals stop


Even just one bad assumption would invalidate his argument, there are at least 8.
Just a friendly reminder to the inventor of cooperative chemistry as an explanation for abiogenesis and cooperative selection pressures as an explanation for common descent, you have yet to post a single real example which would refute my hypothesis. However, I do encourage you to post citations because every time you do, they support my hypothesis.

Correctomundo, or should I say correctoenvironmento. Now I am open to correction if you can demonstrate what the thousands of sequential environmental changes are. Woo, woo, woo, knuck, knuck, knuck.Do you deny that the environment of the Earth has changed over the past 4 billion years?
Have you ever lived in the Midwest? The weather changes about four times an hour. That must be the place where all the lizards transform into birds.
The sequential environments that have resulted in the present-day existence of birds have occured exactly as the geological record shows them to have changed.
So that’s where daffy duck came from.
When you make these types of speculations, you abandon scientific method. Your own examples are better explained by recombination and selection. If you are going to contend that a predator is going to apply selection pressure to the prey’s entire genome, you need to find some way to measure how mutation and selection can evolve the entire genome. The mathematical problem you will encounter is, if every gene in the genome is evolving simultaneously; you have to sort beneficial and detrimental mutations that are being mixed though out the entire genome in different locations in each member of the population. It becomes impossible for the population to find any trajectory to a new optimum. Mutation and selection is an extremely slow process for more than a single gene. This is why your examples are more logically explained to be examples of recombination and selection.When I do these speculations, I am essentially forming a hypothesis which I could then --- theoretically, because I have neither the time nor the inclination to pursue this myself --- test empirically. As I have observed a phenomenon --- evolution --- I believe it is prudent first to explore possible way for the phenomenon to work based on established knowledge. I do not feel this is to abandon the scientific method. It is just a case of stopping midway, because I haven't got the opportunity to carry the experiment through.
So at least now you admit your speculations have neither mathematical nor empirical basis. Why don’t you study ev and get a mathematical basis for how mutation and selection actually works?
I’m a little negative about the positive but I am positive about the negative.And this shows that you don't know what you are talking about -- the first case is *implied* by the second...
Not quite rocketdodger, it doesn’t matter whether selection pressures are weaker or stronger when acting simultaneously, they will still interfere with each other when compare to the selection pressures acting alone.
Now aren’t these authors writing nonsense? They seem to think that combination therapy for the treatment of malaria will somehow slow the evolution of resistance. Aren’t they silly Belz?Yet another microbial disease treatment citation, about an issue nobody disagrees with you on, fronted as an actual argument. Are you completely ignoring what we are telling you? WE DON'T DISAGREE THAT COMBINATION THERAPY SLOWS EVOLUTION. *Nobody* is arguing against that.
Well then rocketdodger, here’s a few citations which show the same phenomenon occurs with weeds and last I heard, weeds are not microorganisms.
http://www.blackwell-synergy.com/doi/abs/10.1046/j.1365-3180.2003.00355.x (http://www.blackwell-synergy.com/doi/abs/10.1046/j.1365-3180.2003.00355.x)
A simulation study was conducted to examine the effect of pattern of herbicide use on development of resistance to two herbicides with different modes of action in finite weed populations. The effects of the size of the treatment area (analogous to initial weed population), germination fraction and degree of self-pollination in the weed were investigated. The results indicate that the probability of developing resistance to one or both herbicides decreases as the size of the area/initial population decreases. For treatment areas of 100 ha or less with an initial weed seedbank of 100 seeds m2 and initial frequencies of the resistance genes of 106, development of resistance to both herbicides (double-resistance) is uncommon within 50 years for all types of weeds if both herbicides are used in all years (used in combination). If herbicides are used in alternate years (rotated) double-resistance almost always occurs in 100 ha areas but is uncommon in areas of 1 ha or less. The results suggest that adoption of practices that limit movement of weeds in conjunction with using herbicides in combination rather than in rotation can substantially delay development of herbicide resistance.

http://www.extension.umn.edu/distribution/cropsystems/DC6077.html (http://www.extension.umn.edu/distribution/cropsystems/DC6077.html)
Apply herbicides in tank-mixed, prepackaged, or sequential mixtures that include multiple sites of action. Both herbicides, however, must have substantial activity against potentially resistant weeds for this strategy to be effective. Remember that in the past, weeds that were selected for herbicide resistance often were not the primary target species. It may be expensive to apply herbicide combinations that duplicate a wide spectrum of weed control activity. Many of the more economical herbicide combinations may not be adequate. Table 10 is a cross reference list of package mixtures and their corresponding sites of action.

http://www.weeds.iastate.edu/mgmt/qtr98-4/resistanceupdate.htm (http://www.weeds.iastate.edu/mgmt/qtr98-4/resistanceupdate.htm)
The use of herbicides with multiple sites of action, applied either as tank mixes, premix formulations, or sequential applications, may provide some benefit in managing resistance. A second herbicide will only reduce selection pressure if it is effective on the same weed species as the first product. For example, Bicep contains two herbicides with two different sites of action, Dual and atrazine. This combination should be effective at reducing selection pressure on pigweed since both Dual and atrazine are active on this species. This combination would be less likely at reducing the potential for Dual resistance in foxtail since the rate of atrazine found in Bicep provides little control of foxtail. Thus, when using multiple sites of action, it is critical to evaluate how much overlap in activity among the herbicides being used is present. In most situations there will be several species in which only one of the herbicides is placing selection pressure on the population, and therefore selecting for resistant biotypes.
Now how can that be rocketdodger? Combination selection pressures slow the evolution of herbicide resistance with weeds. There must be some kind of mistake.

[Belz...]

Only an evolutionist would claim that it is not necessary to specify exact mutations because when you do, it shows your theory to be mathematically impossible.

Only a creationist would claim that God's ways are mysterious because otherwise, you'd be able to question his claims.

You have only one erroneous word in your sentences?

Thank you for illustrating my point. You have nothing left but childish responses.

Now that’s correct, only a gene which has function will be subject to selection pressures. So do you want to explain to us how a gene can evolve de novo?

Where exactly did I lose you ? We were talking about gene duplication just two posts ago.

Were you not also going to refute Professor Behe’s hypothesis of irreducible complexity by telling us what the proteins for the DNA replicase system were doing before DNA could be replicated?

No, I wasn't.

So they're not very good but they're good enough for you ?

Yup

I do believe I can rest my case, now.

Whether it is humans who are doing the selection for breeding purposes or “natural” selection, the mathematics is not changed.

I'm not talking about mathematics. I'm talking about reality. Individuals die, not genes. Genes only get passed on if the entire organism survives.

What other citations? Kotatsu presents examples of recombination and selection and can’t define the selection pressures or target genes.

Obviously, you're working backwards from a conclusion, since every example that goes against your beliefs is not really mutation, in your eyes.

Kotatsu thinks that all it takes is for a reptile to be chased into a tree and that’s enough selection pressure to make it grow wings and feathers.

I think the only person in this thread who has argued Lamarckism at any time is you.

That must be a translation into evolutionish.

Actually, it's english, a language that creationists have a lot of trouble grasping.

You're the one who said that point mutations could not produce the variety we have today, because evolution was "profoundly slowed" by multiple selection pressures. Of course, when I pointed out that other sources of mutation are available, which would work against this slowing down, you replied that they can't because multiple selection pressures "profoundly slow" the evolutionary process.

Now, how is that NOT circular ?

Bacteria growing in a supposed clean room are an example of multiple selection pressures accelerating evolution by mutation and selection. You need to translate that from evolutionish to English.

What the hell are you talking about, now ?

Well then, why don’t I post some more citations which substantiate my interpretation of the mathematics?

No need, since they all bring us back to square 1, anyway.

Hey Belz, if a predator goes after a cherry in a tree, will the cherry grow wings and feathers?

I've got a better one for you, if a predator goes after a cherry in a tree, will God give the cherry wings and feathers ?

I know Belz, so here’s some more of this typical nonsense for you to ponder.

That has nothing to do with what I said. Why am I not surprised ?

[jimbob]

Back to the "sub-optimal peaks"

That is exactly what you do see in evolved systems. I am thinking about this because of another thread.

Could a half-competent designer improve on the "design" of the mamalian eye, by shifting the blood supply behind the retina?

Is that likely to happen with evolution? No.

When talking about entire organisms, and not traits, these different local optima represent the beginning of speciation.

[rocketdodger]

Not quite rocketdodger, it doesn’t matter whether selection pressures are weaker or stronger when acting simultaneously, they will still interfere with each other when compare to the selection pressures acting alone.

Kleinman, here is a final knockout argument that, if you can't understand it, then you genuinely do not know anything about what you have claimed for the duration of this thread.

1) Naturally occuring organisms (which includes pathogens and weeds and platypuses and anything else you want to include) are under numerous selective pressures all the time -- there is no escaping it. As you contend, a great deal of these are stabilizing. This does not matter -- there is no difference between a stabilizing pressure and a destabilizing one according to evolution; both of them effect reproductive fitness in exactly the same way. This is not something you can disagree with because it is implicit in the formal definition of evolution.

2) Naturally occuring organisms do not rapidly, or even at all, evolve defenses against destructive human activity (such as drugs, herbicides, etc) without the presence of humans or that activity. There was no such thing as penicillin resistance in most human pathogenic bacteria when penicllin was first discovered -- only the naturally occuring bacteria that are pathogenic to penicllin producing fungi had that evolved trait. You cannot disagree with this because it is implicit in in the formal definition of evolution.

3) Evolved defenses against human destructive activity are not all, or even in a majority of cases, an example of recombination and selection -- it is from mutation and selection. This is a fact you have to agree with because you claim all of the studies you cited are based on mutation and selection processes.

4) Naturally occuring organisms, when exposed to our activity, evolve defenses against it (another fact you have to agree with due to your cited material).

5) The rate of evolution toward these defenses is vastly greater *after* such organisms are exposed compared to prior (or else there would be no such thing as evolved resistances for your cited studies to even examine, so you also have to agree here).

6) Since such organisms were already under the influence of multiple selection pressures when our destructive activity introduced a new pressure, and the rate of evolution towards resistance to such activity increased as a result, COMBINATION SELECTION PRESSURES DO NOT ALWAYS SLOW THE RELATIVE RATES OF EVOLUTION. They *can*, which is ALL the studies you cite show.

[Kotatsu]

Why don’t you study ev and get a mathematical basis for how mutation and selection actually works?

Because ev is inadequate when it comes to studying real organisms. Why don't you try to understand what we are telling you instead of ignoring it or making derisive or belittling comments?

[kleinman]

Only an evolutionist would claim that it is not necessary to specify exact mutations because when you do, it shows your theory to be mathematically impossible.Only a creationist would claim that God's ways are mysterious because otherwise, you'd be able to question his claims.
Did I say this? You can question God’s claims all you want.
You have only one erroneous word in your sentences?Thank you for illustrating my point. You have nothing left but childish responses.
Nothing left but a peer reviewed and published mathematical model of random point mutations and natural selection and hundreds of real empirical examples which show that combination selection pressures profoundly slow the evolutionary process.
Now that’s correct, only a gene which has function will be subject to selection pressures. So do you want to explain to us how a gene can evolve de novo?Where exactly did I lose you ? We were talking about gene duplication just two posts ago.
You haven’t lost me. You quite correctly noted that selection can not act on a gene which is not functioning and therefore there is no way to evolve a gene de novo.
Were you not also going to refute Professor Behe’s hypothesis of irreducible complexity by telling us what the proteins for the DNA replicase system were doing before DNA could be replicated?No, I wasn't.
Don’t you remember when you said this?
Belz, since you seem to know something about this topic, why don’t you tell us how the DNA replicase system came about? In particular, could you tell us what gyrase and helicase were doing before DNA could be replicated?I'll do much better than that, I'll come up with something that even you can understand, as soon as I've got some time on my hands tomorrow morning. Remind me, will you ?
You wouldn’t be dodging a question would you? Evolutionists never dodge questions, do they Belz?
So they're not very good but they're good enough for you ?YupI do believe I can rest my case, now.
Belz, you have to have a case before you can rest it.
Whether it is humans who are doing the selection for breeding purposes or “natural” selection, the mathematics is not changed.I'm not talking about mathematics. I'm talking about reality. Individuals die, not genes. Genes only get passed on if the entire organism survives.
Belz, both the mathematics and the reality of recombination and selection remain unchanged where it is humans doing the selection or “nature” doing the selection.
What other citations? Kotatsu presents examples of recombination and selection and can’t define the selection pressures or target genes.Obviously, you're working backwards from a conclusion, since every example that goes against your beliefs is not really mutation, in your eyes.
Belz, work it in whatever direction you want, combination selection pressures profoundly slow the evolutionary process. If Kotatsu believes these are examples of mutation and selection, let Kotatsu identify the selection pressures and target genes for these pressures. In case you didn’t notice, Kotatsu posted that the hypothesis being supported by these citations is speculation without mathematical or empirical basis.
That must be a translation into evolutionish.Actually, it's english, a language that creationists have a lot of trouble grasping.
Especially the way evolutionist use the language.
You're the one who said that point mutations could not produce the variety we have today, because evolution was "profoundly slowed" by multiple selection pressures. Of course, when I pointed out that other sources of mutation are available, which would work against this slowing down, you replied that they can't because multiple selection pressures "profoundly slow" the evolutionary process.

Now, how is that NOT circular ?
It’s not circular because the hundreds of citations posted are not limited to random point mutations and still demonstrate the same behavior as the ev computer simulation.
Bacteria growing in a supposed clean room are an example of multiple selection pressures accelerating evolution by mutation and selection. You need to translate that from evolutionish to English.What the hell are you talking about, now ?
Mercutio’s citation.
Well then, why don’t I post some more citations which substantiate my interpretation of the mathematics?No need, since they all bring us back to square 1, anyway.
That’s your problem Belz; you are only working in two dimensions. You need to be working in a cube or perhaps even a hypercube. Read the citations, then perhaps you can make your way to hypercube 2.
Hey Belz, if a predator goes after a cherry in a tree, will the cherry grow wings and feathers?I've got a better one for you, if a predator goes after a cherry in a tree, will God give the cherry wings and feathers ?
Ask God yourself.
I know Belz, so here’s some more of this typical nonsense for you to ponder.That has nothing to do with what I said. Why am I not surprised ?
When you start talking about the mathematics of mutation and selection and the empirical evidence of the phenomenon then it will have something to do with what you say and then we can get you to hypercube 2.
Back to the "sub-optimal peaks"

That is exactly what you do see in evolved systems. I am thinking about this because of another thread.

Could a half-competent designer improve on the "design" of the mamalian eye, by shifting the blood supply behind the retina?

Is that likely to happen with evolution? No.

When talking about entire organisms, and not traits, these different local optima represent the beginning of speciation.
If you want an example of a population reproducing at suboptimal fitness, consider HIV when suppressed by effective three drug therapy.
Why don’t you study ev and get a mathematical basis for how mutation and selection actually works?Because ev is inadequate when it comes to studying real organisms. Why don't you try to understand what we are telling you instead of ignoring it or making derisive or belittling comments?
Isn’t that interesting, you know nothing about the mathematics of mutation and selection and when a peer reviewed and published model of random point mutations and natural selection comes along, you immediately discount it because it doesn’t fit with your preconceived speculations.
Not quite rocketdodger, it doesn’t matter whether selection pressures are weaker or stronger when acting simultaneously, they will still interfere with each other when compare to the selection pressures acting alone.Kleinman, here is a final knockout argument that, if you can't understand it, then you genuinely do not know anything about what you have claimed for the duration of this thread.

1) Naturally occuring organisms (which includes pathogens and weeds and platypuses and anything else you want to include) are under numerous selective pressures all the time -- there is no escaping it. As you contend, a great deal of these are stabilizing. This does not matter -- there is no difference between a stabilizing pressure and a destabilizing one according to evolution; both of them effect reproductive fitness in exactly the same way. This is not something you can disagree with because it is implicit in the formal definition of evolution.
Yes I can disagree with what you are saying here. Stabilizing selection pressures tend to remove phenodeviants from the population where as destabilizing (directional) selection pressures change shape of the fitness landscape and the local optimum for the population on the fitness landscape. This is right out of the textbook.
2) Naturally occuring organisms do not rapidly, or even at all, evolve defenses against destructive human activity (such as drugs, herbicides, etc) without the presence of humans or that activity. There was no such thing as penicillin resistance in most human pathogenic bacteria when penicllin was first discovered -- only the naturally occuring bacteria that are pathogenic to penicllin producing fungi had that evolved trait. You cannot disagree with this because it is implicit in in the formal definition of evolution.
How do you know that was no bacteria in the environment that evolved penicillin resistance before humans started using penicillin? Rocketdodger, do you think nothing evolved until humans got involved in the process? So if evolution of organisms require selection pressures to evolve, what was the selection pressure that transformed reptiles into birds?
3) Evolved defenses against human destructive activity are not all, or even in a majority of cases, an example of recombination and selection -- it is from mutation and selection. This is a fact you have to agree with because you claim all of the studies you cited are based on mutation and selection processes.
Now it is true that humans use targeted selection pressures. An autoclave may be a good way to kill bacteria but it would not be very useful to treat strep throat. Likewise, herbicides would not be very useful if they killed the crop as well.
4) Naturally occuring organisms, when exposed to our activity, evolve defenses against it (another fact you have to agree with due to your cited material).
And note that these citations show that combination selection pressures impair these populations’ ability to evolve against these pressures.
5) The rate of evolution toward these defenses is vastly greater *after* such organisms are exposed compared to prior (or else there would be no such thing as evolved resistances for your cited studies to even examine, so you also have to agree here).
Sure, no (directional) selection pressure, no evolution.
6) Since such organisms were already under the influence of multiple selection pressures when our destructive activity introduced a new pressure, and the rate of evolution towards resistance to such activity increased as a result, COMBINATION SELECTION PRESSURES DO NOT ALWAYS SLOW THE RELATIVE RATES OF EVOLUTION. They *can*, which is ALL the studies you cite show.
You are jumping to a conclusion. The populations which humans subject to new selection pressures are already at a local optimum. Something which has not been discussed extensively on this thread is that when we subject populations to selection pressures and the populations are able to adapt to these pressures, the new local optimum often time does not give a population that can reproduce as well as the original population. For example HIV which has evolved resistance to drugs often times yields a population of viruses that can not reproduce as well as the wild virus.
Rocketdodger, here a few examples of combination selection pressures slowing the evolution of rodents.
http://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1047&context=vpc16 (http://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1047&context=vpc16)
ABSTRACT: Coumatetralyl (Racumin ) has been known since 1957 as a multiple dose anticoagulant and has been used successfully over many decades. In the seventies and especially the eighties, rats developed an increased resistance to anticoagulants in certain regions of Central Europe. Also, the addition of vitamin K to animal feed (especially to chicken feed) has reduced the efficacy against rats and mice in farm buildings. Combinations of anticoagulants with different types of vitamin D are generally described to increase the efficacy of action against rodents. It was found that especially the combination of coumatetralyl with cholecalciferol (vitamin D3) could overcome the above mentioned problems. Cholecalciferol causes hypercalcemia and, therefore, has a different mode of action compared to anticoagulants. The combination of these active ingredients leads to an obvious increase in efficacy against rodents, even under difficult conditions. The formulation with optimal rodenticidal efficacy contains 0.04 % coumatetralyl and 0.025 % cholecalciferol mixed in rolled oats.

http://www.springerlink.com/content/gl091616ggx0lmbe/ (http://www.springerlink.com/content/gl091616ggx0lmbe/)
Abstract Resistance to 4-hydroxycoumarin anticoagulant rodenticides has been a problem in some local foci for a number of years. One method of managing resistance could be to use synergists in conjunction with anticoagulants. We investigated the effect of administering cholecalciferol and coumatetralyl alone and in a synergistic mixture to anticoagulant-resistant rats by monitoring plasma factor X concentrations. The study showed that the efficacy of the compounds was significantly improved when they were used together. This synergistic effect led to an increased mortality in female rats that had been treated with both compounds compared to both a control group and groups of rats that had received the compounds singly. An unexpected result from this work was that cholecalciferol when given on its own to rats caused a decrease in plasma factor X concentration. We hypothesise that this effect was due to a vitamin D-induced increase in production of vitamin K-dependent proteins leading to a saturation of the carboxylation process and hence to a significant number of factor X molecules being under-carboxylated and therefore dysfunctional. It is suggested that the reduction in factor X levels is a major component of the increased efficacy of the anticoagulant/calciferol mixture and also that effects on other vitamin K-dependent proteins, e.g. matrix GLA protein, may play a role in the increased mortality seen in female rats.

This work illustrates that synergists could be utilised in managing anticoagulant resistance. There are also possible implications for human patients on anticoagulant therapy who may be receiving increased amounts of vitamin D analogues through, for example, dietary supplements.

http://www.sciencemag.org/cgi/content/abstract/180/4087/741 (http://www.sciencemag.org/cgi/content/abstract/180/4087/741)
Strains of wild rats that are resistant to the anticoagulant action of coumarins and derivatives of indandione have been discovered in a number of geographic areas. These rats have now been shown to be more susceptible than normal rats are to the anticoagulant action of the vitamin K antagonist, 2-chloro-3-phytyl-1,4-naphthoquinone. This compound, either alone or in combination with warfarin, would appear to be an effective rodenticide in areas where resistance to the indirect anticoagulants is a problem.

[rocketdodger]

Stabilizing selection pressures tend to remove phenodeviants from the population
... because those phenodeviants exhibit reduced reproductive fitness under the pressures...

where as destabilizing (directional) selection pressures change shape of the fitness landscape and the local optimum for the population on the fitness landscape.
... which means reduced reproductive fitness for certain phenotypes under the pressures ...

How do you know that was no bacteria in the environment that evolved penicillin resistance before humans started using penicillin? Rocketdodger, do you think nothing evolved until humans got involved in the process?

wow... seriously, did you even read my post before you wrote that rebuttal? I explicitly and in very plain English said that there were -- "Only the naturally occuring bacteria that are pathogenic to penicllin producing fungi had that evolved trait."


the new local optimum often time does not give a population that can reproduce as well as the original population. For example HIV which has evolved resistance to drugs often times yields a population of viruses that can not reproduce as well as the wild virus.

This statement, as you wrote it, it completely contradicts everything you have claimed about evolution so far. If the mutants exhibit REDUCED reproductive fitness, then there would be no selection for them...

I will assume you mean "can reproduce as well as the original population under the original conditions," in which case, who cares?


You are jumping to a conclusion.


It is not my conclusion, it is yours. Don't you see that? I made it plain and simple in those 5 statements preceeding the conclusion that I am using *exactly* your own arguments.


The populations which humans subject to new selection pressures are already at a local optimum.


Asserting that every such population was perfectly and completely stationary at a local optimum is absurd ... if only because we have never seen a perfectly stationary population in all of science. You are sliding down the hill, Kleinman, tearing at anything you think will stop your fall, but everything you touch crumbles.


Something which has not been discussed extensively on this thread . . .

Since this has nothing to do with my argument, I take it to mean that you realize the futility of your claims. I doubt you care, but at least every other reader here can see that you were brought down by your very own arguments.

[kleinman]

Stabilizing selection pressures tend to remove phenodeviants from the population... because those phenodeviants exhibit reduced reproductive fitness under the pressures...
Correct
where as destabilizing (directional) selection pressures change shape of the fitness landscape and the local optimum for the population on the fitness landscape.... which means reduced reproductive fitness for certain phenotypes under the pressures ...
Again, correct
How do you know that was no bacteria in the environment that evolved penicillin resistance before humans started using penicillin? Rocketdodger, do you think nothing evolved until humans got involved in the process?wow... seriously, did you even read my post before you wrote that rebuttal? I explicitly and in very plain English said that there were -- "Only the naturally occuring bacteria that are pathogenic to penicllin producing fungi had that evolved trait."
I’m not sure what you mean by your (highlighted) sentence.
the new local optimum often time does not give a population that can reproduce as well as the original population. For example HIV which has evolved resistance to drugs often times yields a population of viruses that can not reproduce as well as the wild virus.This statement, as you wrote it, it completely contradicts everything you have claimed about evolution so far. If the mutants exhibit REDUCED reproductive fitness, then there would be no selection for them...
It is reduced reproductive fitness when compared to wild virus in an unchallenged or environment without the selection pressures. Often times when microbes evolve to antimicrobial agents the evolved form does not reproduce as rapidly as the un-evolved form did before it was subjected to the selection pressures. The evolved gene is not as efficient as the “wild” form of the gene but is more efficient than the wild form the gene in the environment with the selection pressure. The evolutionary process does not necessarily evolve a better functioning enzyme but only one which can still perform in the presence of the selection pressure.
I will assume you mean "can reproduce as well as the original population under the original conditions," in which case, who cares?
It should matter to you because selection is all about the efficient use of energy for reproduction.
You are jumping to a conclusion.It is not my conclusion, it is yours. Don't you see that? I made it plain and simple in those 5 statements preceeding the conclusion that I am using *exactly* your own arguments.
My conclusion is actually quite simple. It is that combination selection pressures profoundly slow the evolutionary process. The mathematics shows this and the empirical evidence shows this as well. You complained that I only posted examples of this with microbes, but I have posted (and reposted) examples of much more complex organisms such as weeds and rodents. There are also examples with pesticides as well. You may be trying to use my arguments but you don’t have the mathematics or the empirical examples to contradict my hypothesis.

What you are having difficulty understanding is that evolution by mutation and selection is simply an optimization or sorting problem. The more conditions you try to optimize or sort by, the more complex the process becomes. The dominant parameter in this problem is the number of selection conditions. The genome length also has a strong affect on the rate of convergence with short genomes the easiest to sort or optimize and the process becomes more difficult on longer genomes. Huge populations do help somewhat but strong selection pressures drive the population down. This is why creatures like HIV which have short genomes, large populations and rapid reproduction rates are among the most rapid evolving forms. Still, three selection pressures profoundly slow the rate of evolution of the virus. Two selection pressures accomplish this with more complex life forms like weeds and rodents. That’s what the mathematics shows and that’s what the empirical data shows. Your argument has neither to back it up.
The populations which humans subject to new selection pressures are already at a local optimum.Asserting that every such population was perfectly and completely stationary at a local optimum is absurd ... if only because we have never seen a perfectly stationary population in all of science. You are sliding down the hill, Kleinman, tearing at anything you think will stop your fall, but everything you touch crumbles.
If the populations which humans are subjecting to selection pressures are not at local optima, that means these populations are already trying to evolve to at least one selection pressure at the time humans add further selection pressures. This means these populations have even more selection pressures to evolve to simultaneously.

Rocketdodger, what I am touching is the theory of evolution and it is crumbling. The reason why the theory of evolution is crumbling is the way mutation and selection actually works. Every example of mutation and selection shows this, whether it is examples from virology and bacteriology, or parasitology or oncology or agriculture, they all show the same thing. Combination selection pressures profoundly slow the evolutionary process. And let’s not forget, that’s what the mathematics shows as well, not just Dr Schneider’s ev computer simulation but also computer simulations from numerous investigators who have also examined this phenomenon.
Something which has not been discussed extensively on this thread . . . Since this has nothing to do with my argument, I take it to mean that you realize the futility of your claims. I doubt you care, but at least every other reader here can see that you were brought down by your very own arguments.
My arguments are futile except for the mathematical basis and vast amount of empirical evidence which supports my argument. Now you are making the same type of argument only you don’t have the mathematical or empirical evidence.

[joobz]

Just a friendly reminder to the inventor of cooperative chemistry as an explanation for abiogenesis and cooperative selection pressures as an explanation for common descent, you have yet to post a single real example which would refute my hypothesis. However, I do encourage you to post citations because every time you do, they support my hypothesis.
Yup, you still can't justify your assumptions, which means you are still horribly wrong.

[kleinman]

Just a friendly reminder to the inventor of cooperative chemistry as an explanation for abiogenesis and cooperative selection pressures as an explanation for common descent, you have yet to post a single real example which would refute my hypothesis. However, I do encourage you to post citations because every time you do, they support my hypothesis.Yup, you still can't justify your assumptions, which means you are still horribly wrong.
You are right joobz, I can’t justify my hypothesis except with a peer reviewed and published model of random point mutations and natural selection and hundreds of real examples which substantiate this justification. Here are a few more citations which show that combination selection pressures profoundly slow the evolutionary process. Too bad joobz that you don’t have any citations to post to support your view.

http://www.cnio.es/eventos/descargas/Meeting/160329_524,38_booklet.pdf (http://www.cnio.es/eventos/descargas/Meeting/160329_524,38_booklet.pdf)
These findings in extensive preclinical studies led to dozens of clinical trials of C225,both as monotherapy and in combination with chemotherapy or radiotherapy. Results from Phase I and II trials involving thousands of patients are promising, and data from two Phase III trials have been reported. In a randomized study C225 was added to therapy for patients with colorectal cancer progressing on Irinotecan chemotherapy, or chemotherapy alone was continued. The results for combination treatment were 22.9% partial response and 4.1 months time to progression; the results for chemotherapy alone were 10.8% partial response and 1.5 months time to progression. In a Phase III study of radiotherapy plus or minus C225 for patients with locally advanced head and neck cancer, the combination therapy extended median survival to 54 months, whereas radiation alone extended median survival 28 months – a highly significant difference.

http://www.genesdev.org/cgi/content/full/genesdev;17/24/2998 (http://www.genesdev.org/cgi/content/full/genesdev;17/24/2998)
If we look ahead to an era of molecularly based cancer diagnostics coupled with a wide selection of kinase inhibitors, what degree of clinical success might we anticipate? For cancers like CML and GIST, where the kinase abnormality is thought to play an initiating role, partial or complete remissions should be possible if the drug effectively inhibits its kinase target without significant toxicity. The major obstacles are likely to be the emergence of drug resistance, which would be managed best by combination therapy with a second agent whose choice would be based on the mechanism of resistance. With CML, this might be a second BCR-ABL kinase inhibitor. Conversely, there are likely to be other cancers in which the kinase abnormality occurs late during tumor progression and may be present in only a subset of the tumor cells. The clinical expectation here would be a partial remission followed by relapse due to continued growth of a subclone lacking the relevant molecular lesion (Fig. 4). Finally, there may be cases in which the beneficial effect of a kinase inhibitor on a relevant target is overcome by a second genetic lesion in a compensatory signaling pathway. Indeed, the sensitivity of a breast cancer cell line to an EGFR inhibitor is reversed when coupled with loss of the PTEN tumor suppressor gene (Bianco et al. 2003). The message, quite clearly, is that the optimum use of kinase inhibitors in oncology can only be achieved if coupled with detailed molecular characterization of tumor tissues. Presently, the ability to conduct this characterization uniformly across clinical trials is the rate-limiting step to rapid progress.

http://www.translational-medicine.com/content/5/1/38 (http://www.translational-medicine.com/content/5/1/38)
Background
Ocular melanoma is the leading intraocular malignancy. There is no effective treatment for metastatic ocular melanoma. We sought a treatment targeting the tumor microenvironment as well as the tumor cells.

Methods
Migration of HUVEC cells, the ability of HUVEC cells to form tubes, and proliferative capacity of a human ocular melanoma cell line were tested in the presence of lenalidomide and sorafenib alone and in combination. The compounds were also tested in a rat aortic ring assay and were tested in a highly aggressive human ocular melanoma xenograft model.

Results
Lenalidomide and Sorafenib inhibit HUVEC ability to migrate and form tubes and when used in combination the inhibition is increased. The agents alone and in combination inhibit outgrowth in the rat aortic ring model. The combination of the agents improved the inhibition over either single agent. In a xenograft model, combination therapy inhibited tumor growth over inhibition by single agent alone in a significant fashion (p < 0.004: lenalidomide and p < 0.0035: sorafenib). Furthermore, spontaneous lung metastasis development was completely inhibited in the combination treated animals. Sixty percent of vehicle treated animals developed lung metastases compared to 50% of lenalidomide treated animals, and 33% of sorafenib treated animals.

Conclusion
Lenalidomide and sorafenib are effective at targeting endothelial cells, inhibiting growth of ocular melanoma cells and can inhibit growth of tumors in a xenograft model as well as inhibit development of metastases. Combining these agents works in an additive to synergistic way to inhibit the growth of tumors and development of metastases.

[joobz]

You are right joobz, I can’t justify my hypothesis except with a peer reviewed and published model of random point mutations and natural selection and hundreds of real examples which substantiate this justificationby pretending the papers I quote don't show that life can still adapt and evolve except under the most extreme conditions where extinciton occurs.
I know, I know.

Note - The above quote is altered from kleinman's original post. If you are going to use this technique please ensure that it is entirely obvious (in case your post is quoted with no context that you have made such an alteration.

[Kotatsu]

Isn’t that interesting, you know nothing about the mathematics of mutation and selection and when a peer reviewed and published model of random point mutations and natural selection comes along, you immediately discount it because it doesn’t fit with your preconceived speculations.

This is incorrect. I dismiss it because it doesn't model quite a lot of relevant mechanisms by which evolution occurs. Therefore, it is an inadequate basis on which to base any conclusions on the likelihood and mechanisms of evolution as a whole.

[Belz...]

You haven’t lost me. You quite correctly noted that selection can not act on a gene which is not functioning and therefore there is no way to evolve a gene de novo.

Actually, I never said that. What I'm saying is the exact opposite.

Don’t you remember when you said this?

First off, you didn't remind me, as I asked. Second, I never talked about the specific example you asked for. You're quite apt at putting words in other people's mouths.

Evolutionists never dodge questions, do they Belz?

Of course they do. All types of people dodge questions, just as all types of people eat and bathe. What's your point ?

Belz, you have to have a case before you can rest it.

I do.

Belz, both the mathematics and the reality of recombination and selection remain unchanged where it is humans doing the selection or “nature” doing the selection.

It's very interesting that between reality and mathematics you choose the latter. Reality cannot lost, Klein.

Belz, work it in whatever direction you want

No, I'll follow my conclusion from the premises, thank you.

combination selection pressures profoundly slow the evolutionary process.

Since when is it only combination, now ? I thought it was point mutations a while ago ?

In case you didn’t notice, Kotatsu posted that the hypothesis being supported by these citations is speculation without mathematical or empirical basis.

We could say the same about Genesis. Does that convert you to Buddhism, now ?

It’s not circular because the hundreds of citations posted are not limited to random point mutations and still demonstrate the same behavior as the ev computer simulation.

It doesn't matter whether or not you are correct. It IS circular because you assume your conclusion when looking at the premises.

That’s your problem Belz; you are only working in two dimensions. You need to be working in a cube or perhaps even a hypercube. Read the citations, then perhaps you can make your way to hypercube 2.

Okay, that's completely nuts. Please make some sense.

Ask God yourself.

I might as well ask Bugs Bunny.

It's very interesting that you're just as critical of your own claims as you are of others'.

[Belz...]

2) Naturally occuring organisms do not rapidly, or even at all, evolve defenses against destructive human activity

They don't evolve it, but I would think that, in some cases at least, the defense already exists, if only through blind luck.

[rocketdodger]

They don't evolve it, but I would think that, in some cases at least, the defense already exists, if only through blind luck.

Right thats why I inlcuded "not rapidly." The point of that, err, point, was that Kleinman can't claim *all* the populations in his studies started out with evolved defenses against the pressures introduced in the studies. Basically just covering my tracks in anticipation of a possible insane response by him.

[kleinman]

You are right joobz, I can’t justify my hypothesis except with a peer reviewed and published model of random point mutations and natural selection and hundreds of real examples which substantiate this justificationby pretending the papers I quote don't show that life can still adapt and evolve except under the most extreme conditions where extinciton occurs.I know, I know
Joobz, I don’t have to alter your quotes to try making my points.
Envision a system of millions of forming and destructive chemical reactions. Now, envision that intermediates of there reactions associate through non-covalent means and that this complex becomes protected against the destructive reactive pathway, perhaps by a reversible precipitation. These new complexes result in a localized increased of new chemical species. These chemical species then progress in a new series of reaction... that is what I mean through cooperative means. I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?

See joobz, no strikeout, no altered text, just your unadulterated speculations with no scientific basis. Anytime you want to get out of the rain from your Madagascar rainforest, continue to post your unscientific nonsense.
Isn’t that interesting, you know nothing about the mathematics of mutation and selection and when a peer reviewed and published model of random point mutations and natural selection comes along, you immediately discount it because it doesn’t fit with your preconceived speculations.This is incorrect. I dismiss it because it doesn't model quite a lot of relevant mechanisms by which evolution occurs. Therefore, it is an inadequate basis on which to base any conclusions on the likelihood and mechanisms of evolution as a whole.
Well, let’s count the number of relevant mechanisms in your model of mutation and selection. Why Kotatsu, it’s zero, and from your careful analysis of your mathematical model, you can determine what are the relevant mechanism by which evolution occurs. So Dr Schneider’s model with a single mechanism, random point mutations, is not relevant to make any conclusions and your model with zero mechanisms is relevant to make all kinds of conclusions. The only difference is that I can back up my conclusion that Dr Schneider’s model shows combination selection pressure profoundly slows the evolutionary process with hundreds of real examples which demonstrates this mathematical finding. And Kotatsu, your unscientific approach to this problem is to say that it is not relevant to specify which genes are targeted from which selection pressures. Kotatsu, you practice myth telling, not scientific method which tries to use precise measurements and find mathematical relationships between variables.
You haven’t lost me. You quite correctly noted that selection can not act on a gene which is not functioning and therefore there is no way to evolve a gene de novo.Actually, I never said that. What I'm saying is the exact opposite.
Oh really? How does a selection pressure act on a gene which is not functioning? How does a selection pressure form a gene de novo? If a gene is not functioning or does not exist, what determines if something beneficial or detrimental is occurring by a mutation?
Don’t you remember when you said this?First off, you didn't remind me, as I asked. Second, I never talked about the specific example you asked for. You're quite apt at putting words in other people's mouths.
Belz, I took your words directly from your post. No strikeout or modifications like joobz does. You claimed you would explain to us what the components of DNA replicase system were doing before DNA could replicate and now you are claiming that selection can act on a gene which is not functioning or on a non-existent gene. Don’t dodge the questions, answer them Belz.
Evolutionists never dodge questions, do they Belz?Of course they do. All types of people dodge questions, just as all types of people eat and bathe. What's your point ?
My point is that I have a mathematical and empirical basis to claim that combination selection pressures profoundly slow the evolutionary process by mutation and selection and this makes the concept of common descent mathematically impossible (the centerpiece of the theory of evolution).

In addition, Professor Behe’s hypothesis of irreducible complexity shows that the spontaneous appearance of the DNA replicase system is impossible. A ridiculous number of complex proteins would somehow have to spontaneously appear, assemble themselves into a complex structure before DNA could be replicated. The formation of any one of these proteins spontaneously is nothing short of pure fancy.
Belz, you have to have a case before you can rest it.I do.
Yes, you do have a case, speculationitis, denialophilia, hyperextraplopia, and amathematica sciencea, you have a case of evolutionism.
Belz, both the mathematics and the reality of recombination and selection remain unchanged where it is humans doing the selection or “nature” doing the selection.It's very interesting that between reality and mathematics you choose the latter. Reality cannot lost, Klein.
Belz, in case you haven’t noticed, I have both the mathematical and empirical evidence to support my hypothesis. Check below to see some more of the empirical evidence.
Belz, work it in whatever direction you wantNo, I'll follow my conclusion from the premises, thank you.
What premise do you have?
combination selection pressures profoundly slow the evolutionary process. Since when is it only combination, now ? I thought it was point mutations a while ago ?
The empirical examples cited are not limited to point mutations. Some mutations done by HIV are insertion and deletions and have been documented. HIV also does recombination, this also has been documented. Despite this, combination selection pressures slow the evolution of this virus.
In case you didn’t notice, Kotatsu posted that the hypothesis being supported by these citations is speculation without mathematical or empirical basis.We could say the same about Genesis. Does that convert you to Buddhism, now ?
At least now you are finally admitting that evolutionism is nothing more than a religion. Most evolutionarians try to claim their belief system is scientific but look how they whine when scientific method is applied to your belief system.
It’s not circular because the hundreds of citations posted are not limited to random point mutations and still demonstrate the same behavior as the ev computer simulation.It doesn't matter whether or not you are correct. It IS circular because you assume your conclusion when looking at the premises.
What’s the problem Belz, evolutionist propose a theory and look for evidence to substantiate the theory. The problem for you evolutionists is that mathematics shows you have false premises. Mutation and selection simply doesn’t work the way you allege.
That’s your problem Belz; you are only working in two dimensions. You need to be working in a cube or perhaps even a hypercube. Read the citations, then perhaps you can make your way to hypercube 2.Okay, that's completely nuts. Please make some sense.
Never mind, stay in two dimensions, stay at square 1.
Ask God yourself.I might as well ask Bugs Bunny.
Bugs Bunny is not omniscience; he’s always asking “What’s up doc?”
They don't evolve it, but I would think that, in some cases at least, the defense already exists, if only through blind luck. Right thats why I inlcuded "not rapidly." The point of that, err, point, was that Kleinman can't claim *all* the populations in his studies started out with evolved defenses against the pressures introduced in the studies. Basically just covering my tracks in anticipation of a possible insane response by him.
I never made that claim rocketdodger. The only claim that I am making is that combination selection pressures profoundly slows evolution, not just for microbes but even more so for more complex organisms. If you had any understanding of the mathematics of mutation and selection you would understand this as well.
Here are a couple more citations which show that combination selection pressures profoundly slow the evolutionary process.

http://www.blackwell-synergy.com/links/doi/10.1046/j.1365-2893.2001.00265.x (http://www.blackwell-synergy.com/links/doi/10.1046/j.1365-2893.2001.00265.x)
Recent results of clinical trials suggest that combination of interferon and ribavirin exhibits an enhanced antiviral effect in the treatment of chronic hepatitis C. To investigate the effect of ribavirin on hepatitis C virus (HCV) infection, we analysed the evolution of the genetic heterogeneity of HCV in relation to the anti-HCV humoral response in patients treated by ribavirin alone. The study population included 35 patients with liver biopsy proven chronic hepatitis C infected with HCV genotype 1. Among them, 26 were treated with ribavirin for at least 12 months and nine untreated patients served as a control group. Serum samples were analysed before and at 6 and 12 months of therapy. Three regions of the HCV genome, i.e. HVR1, a domain of NS5A including part of the interferon sensitivity determining region (ISDR), and a segment of NS5B, were amplified by RT-PCR using specific primers. The PCR products were then studied using single-strand conformation polymorphism (SSCP) analysis followed by either direct sequencing, or cloning and sequencing. In parallel, the humoral anti-E1 response was studied using an ELISA (Innotest HCV E1Ab, Innogenetics). The results of HCV genome analysis showed no significant effect on the amino acid sequence evolution of the HVR1, NS5A and NS5B regions of HCV. Analysis of a phylogenetic tree from the major quasispecies variants showed the absence of correlation with ribavirin response, and the absence of selection of viral strains during ribavirin treatment. A trend towards a decrease in the anti-E1 Ab response was also observed. Altogether these results suggest that ribavirin may not exhibit a direct antiviral effect, but may trigger a favourable response to interferon by modulating the immune response against HCV.
Here is another citation dedicated to Dr Schneider and his crew over at the National Cancer Institute.
http://bloodjournal.hematologylibrary.org/cgi/content/abstract/110/7/2242 (http://bloodjournal.hematologylibrary.org/cgi/content/abstract/110/7/2242)
Mutations in the kinase domain (KD) of BCR-ABL are the most prevalent mechanism of acquired imatinib resistance in patients with chronic myeloid leukemia (CML). Here we examine predisposing factors underlying acquisition of KD mutations, evidence for acquisition of mutations before and during therapy, and whether the detection of a KD mutation universally implies resistance. We also provide a perspective on how the second-line Abl inhibitors dasatinib and nilotinib are faring in the treatment of imatinib-resistant CML, especially in relation to specific KD mutations. We discuss the growing importance of the multi-inhibitor–resistant 315T>I mutant and the therapeutic potential that a 315T>I inhibitor would have. Last, we assess the potential of Abl kinase inhibitor combinations to induce stable responses even in advanced CML and interpret the emerging data in the context of CML pathogenesis.

[Belz...]

Oh really? How does a selection pressure act on a gene which is not functioning?

It doesn't. In fact, I said exactly the opposite.

Gosh, you really are bad at reading.

I said that once a gene is duplicated, it becomes free from selection pressures until it evolves a new function, and nothing prevents that mutations accumulate on this duplicated gene until that happens.

Try imagining that OTHER beneficial mutations may result in the duplicated gene being passed on.

Belz, I took your words directly from your post. No strikeout or modifications like joobz does. You claimed you would explain to us what the components of DNA replicase system were doing before DNA could replicate and now you are claiming that selection can act on a gene which is not functioning or on a non-existent gene. Don’t dodge the questions, answer them Belz.

I have never claimed this. You are hallucinating.

In addition, Professor Behe’s hypothesis of irreducible complexity shows that the spontaneous appearance of the DNA replicase system is impossible.

Who ever said it was spontaneous ?

Yes, you do have a case, speculationitis, denialophilia, hyperextraplopia, and amathematica sciencea, you have a case of evolutionism.

At least I don't pray to evolution, like you do with your theory.

Belz, in case you haven’t noticed, I have both the mathematical and empirical evidence to support my hypothesis. Check below to see some more of the empirical evidence.

I've noticed the exact opposite.

What premise do you have?

If you could follow the conversation, you'd remember. I'm getting tired of repeating myself.

At least now you are finally admitting that evolutionism is nothing more than a religion.

I have never admitted this. You may not modify my quotes, but you are adding content nonetheless.

What’s the problem Belz, evolutionist propose a theory and look for evidence to substantiate the theory. The problem for you evolutionists is that mathematics shows you have false premises. Mutation and selection simply doesn’t work the way you allege.

You CANNOT USE THE CONCLUSION to argue against the premises, Klein.

Bugs Bunny is not omniscience; he’s always asking “What’s up doc?”

Yeah, but he's just as real as God.

[rocketdodger]

Correct
Again, correct
Since you agree with both of those statements, which prove the correctness of my earlier one, the fact that you actually posted a rebuttal against my earlier statement shows you can't even keep track of your own logic, never mind everyone elses.


I’m not sure what you mean by your (highlighted) sentence.
It means that there are of course bacteria that have naturally evolved resistance against penicillin, and they are surely pathogenic to penicillin producing fungi (or else they wouldn't have been under that selection pressure, and hence couldn't evolve according to it). This isn't entirely correct, because there could be many other organisms that happen to live in or near such fungi that don't actually attack the fungi yet have still developed resistance. In any case, my point is that the set of human pathogenic bacteria is not a subset of the set of bacteria that already have immunity to penicillin.


The evolutionary process does not necessarily evolve a better functioning enzyme but only one which can still perform in the presence of the selection pressure.
Which is all it needs to do ...

It should matter to you because selection is all about the efficient use of energy for reproduction.
...under the selection pressures affecting the population... which is exactly what you just said. Yet another example of you introducing an obvious fact, which I never disputed or even mentioned, in order to make it appear as if I don't understand evolution -- as if I didn't know all of this before you made the post. Pathetic.

My conclusion is actually quite simple. It is that combination selection pressures profoundly slow the evolutionary process. The mathematics shows this and the empirical evidence shows this as well.

NO. Your conclusion is, as you have admitted slowly over the last group of posts, that "combination directional (and only directional) selection pressures profoundly slow the evolutionary process of a population that was completely stationary at a local optimum (I.E. only under the influence of non-directional pressures) prior to the addition of the directional pressures."

Even if this WERE true (and it isn't, because there is no such thing as a pressure that is only "directional" or a "stationary" population), it is a MUCH weaker claim than your original and hence your corollary that in the natural world evolution is too slow to have produced what we see today, even over billions of years, is no longer supported in any way.

You cannot deny that combination pressures *in general* may accelerate evolution, because that is the positive control of every study you cite. So, to mash these studies until they fit your theory, you redefine "directional" and "stationary" on a per-dataset basis. Unfortunately, that isn't how science works (or even logic, for that matter) -- you need to use a *consistent* defintion for everything. Since you are not, and refuse to, you are just spouting nonsense now.


You complained that I only posted examples of this with microbes, but I have posted (and reposted) examples of much more complex organisms such as weeds and rodents. There are also examples with pesticides as well.

... which is why I included "weeds evolving defenses against pesticides" in my statements...

Yet another example of you re-stating the obvious in an attempt to make it look like the other side doesn't know what they are talking about.

You may be trying to use my arguments but you don’t have the mathematics or the empirical examples to contradict my hypothesis.

What are you talking about? I am using the *exact same* mathematics and the *exact same* empirical examples you are using to FORMULATE your hypothesis. I explicitly told you that I am using the studies YOU cite as my evidence.

What you are having difficulty understanding . . . Your argument has neither to back it up.

That block of gibberish, which is basically your entire theory summed up, has nothing to do with the last few posts of mine. Yet again, you are purposefully avoiding addressing the valid points in our counter-arguments and instead repeating tangential statements that you have already made time and time again.

If the populations which humans are subjecting to selection pressures are not at local optima, that means these populations are already trying to evolve to at least one selection pressure at the time humans add further selection pressures. This means these populations have even more selection pressures to evolve to simultaneously.

Yet they still develop resistance orders of magnitude more rapidly than if humans weren't present ... which proves that combination pressures can speed up the evolutionary process ... which is why you of course claim that there have been NO SUCH POPULATIONS, ever, in human history ... which is clearly rubbish.


And let’s not forget, that’s what the mathematics shows as well, not just Dr Schneider’s ev computer simulation but also computer simulations from numerous investigators who have also examined this phenomenon.

... if you ignore the data, in those exact same studies, that suggests otherwise, not the least of which are the positive controls. Do you have *any* scientific education at all, Kleinman?

Now you are making the same type of argument only you don’t have the mathematical or empirical evidence.

My argument is that the positive controls of the studies you cite refute your hypothesis directly. The evidence I provide is the exact definition and model of evolution that you use and the exact same studies you have cited in this thread. So ... if we are using the same evidence, why would you make a statement like this? Because you have no clue what you are talking about.

[rocketdodger]

See joobz, no strikeout, no altered text, just your unadulterated speculations with no scientific basis. Anytime you want to get out of the rain from your Madagascar rainforest, continue to post your unscientific nonsense.

...except that this is a documented phenomenon that is used, among elsewhere, in the synthesis of organic chemicals. If you know how to read, Kleinman, I suggest brushing up on basic college level chemistry and first year organic chemistry before you even consider making posts like this.

[Belz...]

Will Kleinman ever learn to make one post for each poster he's responding to ?

Stay tuned.

[kjkent1]

... which is why I included "weeds evolving defenses against pesticides" in my statements...N.B.: kleinman's study re weeds concludes that resistance is "uncommon after 50 years."

Thus, resistance does evolve in some cases, despite the use of multiple selective pressures.

This is a typical process of an intenet "troll":

1. State a position
2. Ignore or ridicule contrary facts and/or arguments
3. Restate the original position
4. Goto 2.

[kleinman]

Oh really? How does a selection pressure act on a gene which is not functioning?It doesn't. In fact, I said exactly the opposite.

Gosh, you really are bad at reading.

I said that once a gene is duplicated, it becomes free from selection pressures until it evolves a new function, and nothing prevents that mutations accumulate on this duplicated gene until that happens.

Try imagining that OTHER beneficial mutations may result in the duplicated gene being passed on.
So, let’s see if I can get right what you are writing now. How does, a gene evolve a new function when there is no selection pressure operating on it? How does this duplicated gene increase in frequency in the gene pool without selection acting on it?

I’ll let you evolutionists work on the imaginations, I’d rather concentrate on the mathematics and what is measurable.
Belz, I took your words directly from your post. No strikeout or modifications like joobz does. You claimed you would explain to us what the components of DNA replicase system were doing before DNA could replicate and now you are claiming that selection can act on a gene which is not functioning or on a non-existent gene. Don’t dodge the questions, answer them Belz.I have never claimed this. You are hallucinating.
Now you are claiming that evolution occurs without selection. You have claimed above that a duplicated gene evolves without selection. I highlighted your line in red. Belz, you really need to make up your mind.
In addition, Professor Behe’s hypothesis of irreducible complexity shows that the spontaneous appearance of the DNA replicase system is impossible.Who ever said it was spontaneous ?
You have, you said that evolution occurs without selection. Check out your line above in red. Of course if you want to change your mind, that’s ok, just tell us what the selection pressures were that evolved the components of the DNA replicase system.
Yes, you do have a case, speculationitis, denialophilia, hyperextraplopia, and amathematica sciencea, you have a case of evolutionism.At least I don't pray to evolution, like you do with your theory.
Belz, you are showing great wisdom not praying to your theory of evolution, after all, it’s a mathematically impossible theory.
Belz, in case you haven’t noticed, I have both the mathematical and empirical evidence to support my hypothesis. Check below to see some more of the empirical evidence.I've noticed the exact opposite.
Just use your imagination, better yet, check out the measurements numerous scientists have made of the process of mutation and selection in the citations posted which show that combination selection pressures profoundly slow the evolutionary process. If you still have trouble noticing the facts, try out Dr Schneider’s ev computer simulation of random point mutations and natural selection. You can learn something about the process of evolution by mutation and selection by studying this model.
What premise do you have?If you could follow the conversation, you'd remember. I'm getting tired of repeating myself.
I am following the conversation, you don’t have any premises; you only have imaginations. Of course, now you claim evolution occurs without selection. That’s cyborg’s cruft theory of evolution.
At least now you are finally admitting that evolutionism is nothing more than a religion.I have never admitted this. You may not modify my quotes, but you are adding content nonetheless.
Now your theory is no longer a religion, it is just something that exists in your imagination. Will you ever make up your mind?
What’s the problem Belz, evolutionist propose a theory and look for evidence to substantiate the theory. The problem for you evolutionists is that mathematics shows you have false premises. Mutation and selection simply doesn’t work the way you allege.You CANNOT USE THE CONCLUSION to argue against the premises, Klein.
I’m not, I’m using mathematics and the empirical evidence to argue against your religion, no wait, now I’m arguing against your imaginations. Is there anything real in the theory of evolution? Yes, there is, that is combination selection pressures profoundly slow the process.
Bugs Bunny is not omniscience; he’s always asking “What’s up doc?”Yeah, but he's just as real as God.
Just because you have a theory that makes as much sense as if it was written by Daffy Duck does not mean you can impose Bugs Bunny as proof of your theory. B’da, B’da, B’da, that’s all folks for the theory of evolution.
I’m not sure what you mean by your (highlighted) sentence.It means that there are of course bacteria that have naturally evolved resistance against penicillin, and they are surely pathogenic to penicillin producing fungi (or else they wouldn't have been under that selection pressure, and hence couldn't evolve according to it). This isn't entirely correct, because there could be many other organisms that happen to live in or near such fungi that don't actually attack the fungi yet have still developed resistance. In any case, my point is that the set of human pathogenic bacteria is not a subset of the set of bacteria that already have immunity to penicillin.
How do you know that humans have never been infected by bacteria that have already “naturally” evolved resistance to penicillin?
The evolutionary process does not necessarily evolve a better functioning enzyme but only one which can still perform in the presence of the selection pressure.Which is all it needs to do ...
Then how do you extrapolate this process to the evolution of birds from reptiles? Perhaps you use Belz’s technique, use your imagination.
It should matter to you because selection is all about the efficient use of energy for reproduction....under the selection pressures affecting the population... which is exactly what you just said. Yet another example of you introducing an obvious fact, which I never disputed or even mentioned, in order to make it appear as if I don't understand evolution -- as if I didn't know all of this before you made the post. Pathetic.
What is pathetic is the way you evolutionists take the obvious way these phenomena work and then extrapolate this to the evolution of birds from reptiles. It is obvious that combination selection pressures profoundly slow the evolutionary process, so what are the selection pressures that transform reptiles into birds. There are no selection pressures that would do this and if there were, they would have to act one at a time transforming one gene at a time. That is obvious.
My conclusion is actually quite simple. It is that combination selection pressures profoundly slow the evolutionary process. The mathematics shows this and the empirical evidence shows this as well.NO. Your conclusion is, as you have admitted slowly over the last group of posts, that "combination directional (and only directional) selection pressures profoundly slow the evolutionary process of a population that was completely stationary at a local optimum (I.E. only under the influence of non-directional pressures) prior to the addition of the directional pressures."

Even if this WERE true (and it isn't, because there is no such thing as a pressure that is only "directional" or a "stationary" population), it is a MUCH weaker claim than your original and hence your corollary that in the natural world evolution is too slow to have produced what we see today, even over billions of years, is no longer supported in any way.

You cannot deny that combination pressures *in general* may accelerate evolution, because that is the positive control of every study you cite. So, to mash these studies until they fit your theory, you redefine "directional" and "stationary" on a per-dataset basis. Unfortunately, that isn't how science works (or even logic, for that matter) -- you need to use a *consistent* defintion for everything. Since you are not, and refuse to, you are just spouting nonsense now.
Rocketdodger, if you had read the thread before entering the discussion, you would realize that there have been extensive discussions about directional and stabilizing selection pressures. Ev demonstrates how directional pressures become stabilizing pressures. I do claim that combination selection pressures always slow evolution when compared to the selection pressures applied singly. You evolutionists have not been able to produce a single case either mathematically or empirically. Rocketdodger, someday you have to face the mathematical and empirical facts of life.
You complained that I only posted examples of this with microbes, but I have posted (and reposted) examples of much more complex organisms such as weeds and rodents. There are also examples with pesticides as well.... which is why I included "weeds evolving defenses against pesticides" in my statements...

Yet another example of you re-stating the obvious in an attempt to make it look like the other side doesn't know what they are talking about.
Rocketdodger, I reposted examples of combination rodenticides, also if you had read this thread where combination insecticides impair the ability of insects to evolve resistance against these selection pressures. Combination selection pressures work the same on all life forms; they profoundly slow the evolutionary process from the simplest forms to the most complex life forms. The most obvious finding is that the simplest life forms with short genomes, huge populations and rapid reproduction times have the least difficult time evolving against combination selection pressures. More complex life forms have a more difficult time evolving against combination selection pressures. Dr Schneider’s ev model demonstrates this as well as seen by what happens with the convergence rate as you lengthen the genome in the model.
You may be trying to use my arguments but you don’t have the mathematics or the empirical examples to contradict my hypothesis.What are you talking about? I am using the *exact same* mathematics and the *exact same* empirical examples you are using to FORMULATE your hypothesis. I explicitly told you that I am using the studies YOU cite as my evidence.
Really, so you are arguing that combination selection pressures accelerate evolution? How do you get that out of ev and the citations posted?
What you are having difficulty understanding . . . Your argument has neither to back it up.That block of gibberish, which is basically your entire theory summed up, has nothing to do with the last few posts of mine. Yet again, you are purposefully avoiding addressing the valid points in our counter-arguments and instead repeating tangential statements that you have already made time and time again.
You have no counter argument. The mathematics of ev shows that combination selection pressures profoundly slows the convergence of the model and the empirical evidence shows the same fact. You have already agreed to this fact with microbes and now with weeds, it also works that way with rodenticides, insecticides and cancer therapies. This is the mathematical and empirical fact of life how mutation and selection works and if you understood that mutation and selection is simply an optimization problem, then this fact of life would become obvious to you.
If the populations which humans are subjecting to selection pressures are not at local optima, that means these populations are already trying to evolve to at least one selection pressure at the time humans add further selection pressures. This means these populations have even more selection pressures to evolve to simultaneously.Yet they still develop resistance orders of magnitude more rapidly than if humans weren't present ... which proves that combination pressures can speed up the evolutionary process ... which is why you of course claim that there have been NO SUCH POPULATIONS, ever, in human history ... which is clearly rubbish.
What makes you think that bacteria evolve resistance orders of magnitude more rapidly than if humans weren’t present? Post your citations which show your speculations have either an empirical or mathematical basis.
And let’s not forget, that’s what the mathematics shows as well, not just Dr Schneider’s ev computer simulation but also computer simulations from numerous investigators who have also examined this phenomenon.... if you ignore the data, in those exact same studies, that suggests otherwise, not the least of which are the positive controls. Do you have *any* scientific education at all, Kleinman?
Who is ignoring the data; I have posted hundreds of citations which show that combination selection pressures profoundly slow the evolutionary process. If you think these citations are saying something different, you are free to quote whatever you want.
Now you are making the same type of argument only you don’t have the mathematical or empirical evidence.My argument is that the positive controls of the studies you cite refute your hypothesis directly. The evidence I provide is the exact definition and model of evolution that you use and the exact same studies you have cited in this thread. So ... if we are using the same evidence, why would you make a statement like this? Because you have no clue what you are talking about.
What positive controls are you talking about? Many of the citations posted are the results of double blind studies and they all show that combination selection pressures profoundly slow the evolutionary process. That’s what the mathematics shows and that’s what the empirical evidence demonstrates.
See joobz, no strikeout, no altered text, just your unadulterated speculations with no scientific basis. Anytime you want to get out of the rain from your Madagascar rainforest, continue to post your unscientific nonsense....except that this is a documented phenomenon that is used, among elsewhere, in the synthesis of organic chemicals. If you know how to read, Kleinman, I suggest brushing up on basic college level chemistry and first year organic chemistry before you even consider making posts like this.
Don’t forget rocketdodger, not only does the Madagascar rainforest accelerate evolution, so does plate tectonics. Those cooperative selection pressures sure do accelerate evolution.
Will Kleinman ever learn to make one post for each poster he's responding to ?
No, and don’t be so lazy, read the entire thread.
... which is why I included "weeds evolving defenses against pesticides" in my statements...N.B.: kleinman's study re weeds concludes that resistance is "uncommon after 50 years."

Thus, resistance does evolve in some cases, despite the use of multiple selective pressures.

This is a typical process of an intenet "troll":

1. State a position
2. Ignore or ridicule contrary facts and/or arguments
3. Restate the original position
4. Goto 2.
Kjkent1, how could I ignore your string cheese theory of evolution? It is obvious to everyone that there are 10^500 alternative universes. There goes that theme song for Twilight Zone again.

Kjkent1, would you feel better if I moved the goalposts?

[kjkent1]

Kjkent1, how could I ignore your string cheese theory of evolution? It is obvious to everyone that there are 10^500 alternative universes. There goes that theme song for Twilight Zone again.


Kjkent1, would you feel better if I moved the goalposts?It's rather pathetic that you just followed the exact steps in the algorithm that I stated.

You ignored my statement about the weed resistance only being uncommon, rather than non-existent. And, then you followed by ridiculing me, rather than facing up to the contrary evidence.

I don't need 10500 universes to falsify your conclusion. There is no barrier to a single selection pressure maintaining beneficial changes in multiple genes, so sequential change is not required. Only a dominant selection pressure in the environment is required.

And, each of your citations, including ev, show that evolution proceeds rapidly under the stress of a dominant selection pressure.

Moreover, environments change, so the course of evolution will be channeled along the course of environmental change, which sometimes may be relatively stable, and other times may be severe.

In the end, the geological evidence proves the environmental change and the fossil evidence proves that the organisms evolved. Assuming that your evidence is correct and a dominant selective pressure is required to cause evolution to proceed at a sufficiently rapid pace, then it is trivially obvious to infer from the evidence that most environments do, in fact, have a single dominating selective pressure, because if they did not, then there would be no evolutionary change, as evinced by the fossil record.

That is, unless you invoke divine intervention. Which is fine by me, but it ain't scientific.

So, if you want to prove your theory, then you'll either have to show that most environments are not dominated by a single selective pressure, or that the geological and fossil records are both false.

[Belz...]

So, let’s see if I can get right what you are writing now. How does, a gene evolve a new function when there is no selection pressure operating on it? How does this duplicated gene increase in frequency in the gene pool without selection acting on it?

If you had bothered to read my FOLLOWING sentence, instead of hand-waving it because it contains a word you don't like, you'd have your answer.

I’ll let you evolutionists work on the imaginations, I’d rather concentrate on the mathematics and what is measurable.

Don't worry, creationists do A LOT of imagining.

Now you are claiming that evolution occurs without selection.

No, you're the one who's claiming that blue bananas write monkey browns at 8 foot noses.

Would you please stop putting words in my mouth ?

You have claimed above that a duplicated gene evolves without selection.

No, I've claimed that a duplicated gene MUTATES without selection.

You DO know what "evolution" means, don't you ?

You have, you said that evolution occurs without selection.

No, I didn't. I couldn't, because that's part of the definition of evolution.

Belz, you are showing great wisdom not praying to your theory of evolution, after all, it’s a mathematically impossible theory.

You are not showing equal wisdom in respect to your fairy godling.

Just use your imagination

I thought imagining was a big no-no ?

Besides, why would I want to IMAGINE that you have arguments ?

I am following the conversation, you don’t have any premises

Klein, you're simply not very good at this. You are using your conclusion, that evolution is "profoundly" slowed by said process, based on falses premises, to hand-wave a NEW premise that I've included into the equation; namely that there are OTHER sources of mutation. That's not logical.

Now your theory is no longer a religion, it is just something that exists in your imagination. Will you ever make up your mind?

About what ? You're the one who keeps inventing what I think.

I’m not, I’m using mathematics and the empirical evidence to argue against your religion, no wait, now I’m arguing against your imaginations.

I think you're getting delusional.

Just because you have a theory that makes as much sense as if it was written by Daffy Duck does not mean you can impose Bugs Bunny as proof of your theory. B’da, B’da, B’da, that’s all folks for the theory of evolution.

I think I've seriously lost you in my last post. When did I offer Bugs Bunny as proof of anything ?

[Belz...]

The mathematics of ev shows that combination selection pressures profoundly slows the convergence of the model and the empirical evidence shows the same fact.

Wasn't I clear about what you can show with mathematics vs reality ?

Oh, that's right. You hand-waved that, too.

[Belz...]

So, if you want to prove your theory, then you'll either have to show that most environments are not dominated by a single selective pressure, or that the geological and fossil records are both false.

Don't you know ? The fossil record was created by me (the devil) to fool all of you into doubting God!!!

[joobz]

Joobz, if the sun shines on lead long enough does it turn into gold? You are back to equating chemical and nuclear reactions. :boggled:
See joobz, no strikeout, no altered text, just your unadulterated speculations with no scientific basis. Anytime you want to get out of the rain from your Madagascar rainforest, continue to post your unscientific nonsense.There are actually 9 strikes against you.

1.) Mutation rate remains constant
2.) Mutation rate is known
3.) Number of selection pressures for all species for all time in all areas is known
4.) Number of selection pressures is constant
5.) Slection pressure magnitude is constant and equal for all pressures
6.) Point mutations are the only mutation/adaptation mechanism
7.) defining selection pressure is unimportant
8.) slow equals stop
9.) Mutation is non-random

It's the end of an inning.

[rocketdodger]

How do you know that humans have never been infected by bacteria that have already “naturally” evolved resistance to penicillin?
I don't, and I never claimed otherwise -- look up the defintion of "subset" Kleinman.

Then how do you extrapolate this process to the evolution of birds from reptiles?

I don't need to, because that is not what this argument is about. It is about your claim that combination selection pressures profoundly slow evolution. That is quite different from a claim like "evolution is too slow to have produced birds from reptiles."

It is obvious that combination selection pressures profoundly slow the evolutionary process,


I do claim that combination selection pressures always slow evolution when compared to the selection pressures applied singly.

These are two very different claims. The second is backed up by the studies you cite, and that is why I have argued that very point over and over (read my previous posts carefully if you don't think so). The first is not backed up in any way by any valid evidence in the entire world of science.


Combination selection pressures work the same on all life forms; they profoundly slow the evolutionary process from the simplest forms to the most complex life forms.

... yet you go back to spamming it over and over ...

Really, so you are arguing that combination selection pressures accelerate evolution? How do you get that out of ev and the citations posted?

The fact that we need studies to figure out how to prevent organisms from evolving defenses against our methods implies that evolution occurs rapidly -- otherwise we wouldn't need such studies in the first place. That is what a positive control is in science, Kleinman -- the state we are measuring our experiments against.


What makes you think that bacteria evolve resistance orders of magnitude more rapidly than if humans weren’t present? Post your citations which show your speculations have either an empirical or mathematical basis.

You make me think that. When you say "combination selection pressures profoundly slow evolution" that means without combination selection pressures the evolutionary process occurs at a rate that can be profoundly slowed. If you don't know what "profound" means then you shouldn't use it in your statements.

If you want to argue that this occurs without the influence of people, then tell me how the populations in all your cited studies could be at a local optimum yet still be evolving rapidly.

What positive controls are you talking about? Many of the citations posted are the results of double blind studies and they all show that combination selection pressures profoundly slow the evolutionary process.

Compared to what? Compared to the rate fizz pops in a freshly poured coke? No -- compared to the evolutionary process when there are not "combination selection pressures." This is a positive control, and it is in every study you have cited.

Don’t forget rocketdodger, not only does the Madag