Annoying creationists

[sol invictus]

Creationism was proven impossible long ago.

Is God willing to prevent evil, but not able? Then he is impotent.

Is he able, but not willing? Then he is malevolent.

Is he both able and willing? Then whence is evil?

Is he neither able nor willing? Then why call him God?

 

[sol invictus]

It’s up to you two to show that your algorithms actually represent mutation and selection. You definitely haven’t shown that n+1 selection pressures evolve more rapidly than n selection pressures when you say this:

I offered you a bet on this using your own algorithm, the one you claimed demonstrated this "fact", and you won't take it. You won't take it because you are lying, you know you are lying, and you know you will lose.

Why do you keep lying?

 

[rocketdodger]

Rocketdodger, you haven’t paid much attention to the citations posted so I’ll repeat one that show some graphics of a very simple fitness landscape for two selection conditions. I have to thank joobz for this citation though he thought varying environments had to do with the weather in this paper.
http://www.pnas.org/cgi/content/full/104/34/13711

You stupid fool. That paper discusses the effects of applying a series of goals, one after the other, to the model population. The fitness landscapes they produce, which show local maxima, are simply the result of superimposing the landscapes of each individual goal.

If you consider all the goals at once, the landscape generated is simply a huge bulge -- one convex shape, with only a global maxima.

If you disagree, then give us all an answer to my question -- given two goals A and B, each of equal weight, what distribution would constitute a local maxima? Or in words you can understand, what location on the fitness landscape?

The top image shows the trajectory ...
...snip...
This is the same reason ev becomes very slow converging for longer genomes.

This paragraph of rubbish has nothing at all to do with the actual study you cited you fool.

 

[kleinman]

Annoying Creationists

Creationism was proven impossible long ago.

Is God willing to prevent evil, but not able? Then he is impotent.

Is he able, but not willing? Then he is malevolent.

Is he both able and willing? Then whence is evil?

Is he neither able nor willing? Then why call him God?

Both you and Epicurus fail to understand that God does not allow evil to go un-judged. God has His own perfect timing for judging and punishing evil. If God judged evil at the moment that it occurs, no one would survive, but with God there is forgiveness that He is to be feared. That is not my idea; it is what the Bible says. God judges with a perfect balance of justice and mercy on His perfect time scale. Too bad you have no understanding of the rate at which God does things but read the prophecy of Habakkuk in the Bible if you want to learn about this. Habakkuk asked the same questions that Epicurus asked, the difference is Habakkuk got the answer.

Rocketdodger, you haven’t paid much attention to the citations posted so I’ll repeat one that show some graphics of a very simple fitness landscape for two selection conditions. I have to thank joobz for this citation though he thought varying environments had to do with the weather in this paper.

You stupid fool. That paper discusses the effects of applying a series of goals, one after the other, to the model population. The fitness landscapes they produce, which show local maxima, are simply the result of superimposing the landscapes of each individual goal.

If you consider all the goals at once, the landscape generated is simply a huge bulge -- one convex shape, with only a global maxima.

If you disagree, then give us all an answer to my question -- given two goals A and B, each of equal weight, what distribution would constitute a local maxima? Or in words you can understand, what location on the fitness landscape?

Rocketwhomissesthetarget almost gets it right; these authors are accelerating the evolutionary process by applying the selection pressures sequentially. However, if you look at the fourth image down, the ‘Virtual’ varying landscape, you will see what the two superimposed fitness landscape with the two goals looks like. So go home and cry in your primordial soup. Then tomorrow morning go see your optometrist because you need new glasses.

The top image shows the trajectory ...

...snip...
This is the same reason ev becomes very slow converging for longer genomes.

This paragraph of rubbish has nothing at all to do with the actual study you cited you fool.

How would you know? You don’t know anything about ev, you have admitted it already.

I am eager to participate in this discussion but I don't know the mathematical details of the topic, only general ideas. Paul, is there a good introductory source (assuming I am fluent in mathematics) where I can learn what this equation you guys are talking about represents? All this Rseq~ and Rfreq~ stuff is lost on me.

And now you are proving you are not fluent in mathematics. Where did you graduate from Rocketwhomissesthetarget, Mathishard University?

 

[joobz]

You stupid fool. That paper discusses the effects of applying a series of goals, one after the other, to the model population. The fitness landscapes they produce, which show local maxima, are simply the result of superimposing the landscapes of each individual goal.

If you consider all the goals at once, the landscape generated is simply a huge bulge -- one convex shape, with only a global maxima.

If you disagree, then give us all an answer to my question -- given two goals A and B, each of equal weight, what distribution would constitute a local maxima? Or in words you can understand, what location on the fitness landscape?

The funny part is that kleinman's stupid lie:

I have to thank joobz for this citation though he thought varying environments had to do with the weather in this paper.

Was actually a confusion of references. I referenced both the paper he missquotes simultaneously along with the paper, "Evolution in the hypervariable environment of Madagascar" in PNAS (see link).

http://www.pnas.org/cgi/content/abstract/104/34/13723

I used those to papers to demonstrate that his assumption that
slection pressures are constant and known is completely and totally false. Since we know that weather can induce hypervariable environments and that these variable environments can accelerate evolutionary adaptation, his whole point is foolishly wrong.

He knows this. He knows better, but he'd rather believe and lie than know reality.

 

[Paul C. Anagnostopoulos]

Your last two cases converge to a local optimum with 16 mistakes rather than a zero mistake local optimum. In order for the population to evolve to a perfect creature in these cases, the population must traverse a reduced fitness trough but the selection conditions prevent this.

And that gobbledegook is called the Rcapacity problem.

~~ Paul

 

[rocketdodger]

Rocketwhomissesthetarget almost gets it right; these authors are accelerating the evolutionary process by applying the selection pressures sequentially. However, if you look at the fourth image down, the ‘Virtual’ varying landscape, you will see what the two superimposed fitness landscape with the two goals looks like.

They explicitly say, in great detail, how they temporally vary the goals back and forth in this experiment. This is not the fitness landscape produced when the model population is going for both goals at once -- they did not include that scenario in the experiment. Haven't you read the paper, Kleinman? Or did you just cite the first thing google found for you...

And if it was, it would be direct proof that your theory is wrong, because switching between the first and second goal allows the population to pull itself out of any local maxima they are in.

With regards to my earlier statement that local maxima do not exist in such graphs, I misspoke -- I was thinking of pressures as targeting single bases, rather than entire loci. In the latter case, there would be many possible combinations of mutations that would satisfy a given pressure, which would indeed lead to local optima. Unfortunately for you, Kleinman, local optima are completely irrelevant to evolutionary rate.

How would you know? You don’t know anything about ev, you have admitted it already.

Yes, I asked Paul for a reference on his program, I read it, and now I know what I wanted to know about it -- in particular, that you don't know wtf you are talking about. Congratulations on showing everyone the obvious, Kleinman.

And now you are proving you are not fluent in mathematics. Where did you graduate from Rocketwhomissesthetarget, Mathishard University?

I graduated from the University of Arizona. Where did you graduate from, Kleinman?

 

[rocketdodger]

You don’t get a yes or no answer to this question. Sometimes you can introduce penicillin to a population and it wipes out the population.

Sometimes you can introduce penicillin to a population for which it exerts no selection pressure and therefore does nothing to the population.

If you want the fastest evolution of resistance to penicillin for population which is subject to the toxic effects of this drug, you subject the population to a sub-lethal concentration of penicillin while minimizing all other selection pressures and slowly increase the concentration of penicillin. That’s how mutation and selection actually works.

Ok, lets rephrase: Will introducing a sub-lethal penicllin pressure increase the rate of evolution of penicillin resistance in a population? YES or NO?

It’s up to you two to show that your algorithms actually represent mutation and selection.

We never claimed they did. We only said they were modeled on mutation and selection. Our claim, which still stands, is that they are sorting algorithms. So far you have completely failed to show otherwise, which is pretty pathetic, considering my algorithm only has 4 steps.

You definitely haven’t shown that n+1 selection pressures evolve more rapidly than n selection pressures when you say this:

We only showed that in our simulations such a thing happens. We have no intent of proving it in reality, because we don't need to. You claimed all sorting algorithms are confounded by additional sorting conditions. We showed otherwise. Mutation and selection, in reality, is irrelevant to this claim of yours as well as our disproof of it.

And for the record, you are a lying, misinforming, manipulative troll. I posted an exact set of parameters for my simulation and I addressed your concerns regarding parametric studies of it, random number seed problems, etc, multiple times. Despite this, you keep repeating the initial statement of mine regarding having forgotten the parameters I used late one night to just make sure my program ran. Doing so illustrates nothing more than what a douchebag you are.

This one you get a yes answer. See the citation and figures at the beginning of the post. I don’t think you appreciate how complex a real fitness landscape can be but there is an example of a simple fitness landscape for two selection pressures of equal magnitude for a computer simulation.

Except, this is not an example of a fitness landscape generated by two simultaneous pressures. Regardless, I was incorrect about the lack of local maxima in such graphs.

All of this has nothing to do with the rate of fixation under multiple pressures.

Now wait a minute Belz, rocketwhomissesthetarget gave the probability that evolution is true (1.0 x 10^-999999999) and the only other probability that we got here is that we were created. Since you evolutionists have shown that the sum of all probabilities is 1, it is a simple mathematical fact that probability that we were created based on rocketwhomissesthetarget’s own number is ≈ 1.

Relying on false dichotomy only illustrates how pathetically desperate you are Kleinman. Treat the two as independent events. We are still waiting for a number you feel is an accurate probability of creationism being true.

 

[kjkent1]

Both you and Epicurus fail to understand that God does not allow evil to go un-judged. God has His own perfect timing for judging and punishing evil. If God judged evil at the moment that it occurs, no one would survive, but with God there is forgiveness that He is to be feared. That is not my idea; it is what the Bible says. God judges with a perfect balance of justice and mercy on His perfect time scale. Too bad you have no understanding of the rate at which God does things but read the prophecy of Habakkuk in the Bible if you want to learn about this. Habakkuk asked the same questions that Epicurus asked, the difference is Habakkuk got the answer.

Tell that to every woman who's ever gone through labor.

God is a misogynist (Genesis 3:14-16), and a slaver (Exodus 21). You worship a monster. All history and his own writing demonstrates His incomparable evil.

 

[Kotatsu]

Oh, I thought I addressed this, several times, but I’ll address it again for you. So you have polyploidy, how do you transform those duplicated genes to a new form? Why Kotatsu, it requires mutation and selection and as we have seen over and over, transforming more than a single gene at a time profoundly slows the evolutionary process.

Cute. However, your stock answer doesn't in any way address what I am talking about, as the process I mention is independent of random point mutations and other kinds of mutations that alter the exact sequence. I am talking about the very process of polyploidisation, not what happens afterwards.

"I" transform the diploid genome into a polyploid one simply by doubling the copies of all involved chromosomes by one of several known mechanisms. When this occurs in only one of several individuals --- as is often the case --- we see diploid and polyploid individuals who have the exact same gene order and nucleotide sequences. No other mutations need to be involved. This is still evidence of common descent of these organisms.

I remind you also of the paper by Song et al. in which allopolyploids evolved "extensive genomic differences" which were expressed in at least five ecological or morphological traits. This occurred within five generations after the polyploidisation event. Apparently, these things can happen more rapidly than you can imagine.

And please don't take me on the "name the selection pressures and targeted genes" merry-go-round again --- at least not until you have read that article and understood it.

You can construct phylogenic trees based on similarities of genes. All that it shows is that living things can have some similarity in chemical structure. In order to use these phylogenic trees as evidence of common descent, you need to show how mutation and selection can accomplish the transformation from one form to another. The mathematical and empirical evidence of mutation and selection shows that it can not make the transformations.

The mathematical and empirical evidence shows that "we" can make those "transformations". I take it you have never seen an alignment of genes, have you?

Showing how this could work is rather easy. Take COI, for example, which I have worked with previously. When examining almost any given alignment of COI, you will notice a pattern. The differences between taxa almost invariably occur in every third position. A small amount occur in the positions before those, and almost none are in the positions after the first ones. This shows us that there is a higher tolerance for variation in every third position. Not surprisingly, when we translate these sequences into amino acids, the variable positions are third positions, the less variable positions are second positions, and the least variable positions are first positions. This makes sense, because variation in third positions is least likely to change the resulting amino acid, whereas variations in second and first positions are progressively more likely to change amino acid.

Thus, if we study this gene in organisms of a given genus, we will see slight differences between them. These differences are mainly in third positions, and can be adequately explained by random point mutations. These mutations may occur at any point in the gene, of course, but as first and second positions are more likely to change the amino acid, and thus the chemical and sterical properties of the protein, they are usually selected against.

This gives us a framework for phylogenetic research. Add sufficient taxa to your matrix, and compare the differences between the sequences. Many of the third positions will differ between closely related species. Most of them differ between more distantly related organisms, and with sufficient time of separation, second positions also show differences, and even first positions. When the taxa are too distantly related, of course, there is saturation, and COI cannot be used (but there are other regions used for those levels). However, the point is that these differences, which occur precisely by random point mutation and subsequent selection, form nested hierarchies. These are usually bifurcations, as is predicted from the more common ways of speciation.

These is no point along this road in which you are correct.

The only button you have pushed is the laughter button. Are you talking about the combined weight of the citations which show that n+1 selection pressures evolve more rapidly than n selection pressures? I don’t know how I can bear all zero of your citations.

I have posted five or six examples of how you are wrong in this regard. You have dismissed them without reading them, because you cannot understand what they are about. This is not my problem, obviously, but it is wrong to say that I have presented zero citations.

Also, the pressure I was referring to was that I believe there are more people arguing against you (or at least trying to, but your childish copy-paste-dismiss routine makes that kind of hard) than there used to be. We are your selection pressures, and in this limited context, you are correct. The evolution of your arguments has slowed and will presumably stop once we are enough people.

 

[Belz...]

Now wait a minute Belz, rocketwhomissesthetarget gave the probability that evolution is true (1.0 x 10^-999999999) and the only other probability that we got here is that we were created.

Yeah, that's what I said. False dichotomy.

 

[Belz...]

Both you and Epicurus fail to understand that God does not allow evil to go un-judged.

Funny, because lots of evil goes un-judged.

God has His own perfect timing for judging and punishing evil.

Which is retarded, because he knows in advance that evil will occur, yet he chooses to let it happen to people who don't deserve it.

Why is God evil ?

If God judged evil at the moment that it occurs, no one would survive

Why ? Is every evil punishable by death ?

Why is God evil ?

but with God there is forgiveness that He is to be feared.

Well, he blew that one, didn't he ?

Too bad you have no understanding of the rate at which God does things

Well that rate must be pretty slow, considering the number of selection pressures he's probably under, right ?

 

[Mr. Scott]

My first real skepticism of abiogenesis and the theory of evolution occurred when I took courses in organic chemistry. In the laboratory we were required to synthesize a variety of more complex molecules from simpler molecules. In order to get a side group to bond to a particular site often required activating catalysts and shielding groups to prevent reactions at other sites. Often times the reactions would have to take place in strongly acidic then strongly basic solutions and visa versa. The idea that the complex organic molecules that form life can occur in some fanciful primordial soup is as joobz puts it, speculation.[/SIZE][/FONT]

Were you fine with evolution before these experiments?

How old were you when this occurred?

Were you the only one in the class who first experienced "real skepticism" during that exercise?

Aren't you again confusing abiogenesis with evolution? This discussion is about evolution after abiogenesis occurred. Many Christians and world class scientists are fine with the idea that God took care of abiogenesis and sat back while it evolved into us. Nothing I know of in the genetic or geologic evidence contradicts this possibility.

What problem do you have with the theory that God started abiogenesis and let evolution run its course on its own?

 

[sol invictus]

Well that rate must be pretty slow, considering the number of selection pressures he's probably under, right ?

 

[sol invictus]

That is not my idea; it is what the Bible says.

As little credibility as you have, kleinman, it's greater than that of some loser who wandered out into the desert 2,500 years ago and ate a bad cactus.

Read this. Who knows, you might learn something.

http://books.google.com/books?id=lu...oi=print&ct=title&cad=one-book-with-thumbnail

Anyway, given that you have blind faith in religion, why do you need to lie about mathematics? Maybe your faith isn't so strong after all?

 

[rocketdodger]

I improved my program and now it generates results on par with what Dr. Adequate got.
Source code can be found here: www.jedi-arts.com/code/jev.cpp.
Executable (this was compiled on Vista so it might only work on 64 bit machines): www.jedi-arts.com/code/jev.exe.
Example input file (this must be placed in the same directory as the .exe): www.jedi-arts.com/code/data.txt.

Improvements --

*The ability to specify stabilizing pressures was added, so now Kleinman can't whine about us not accounting for detrimental mutations at non-targeted locations. In addition there is a "directionalWeight" parameter that allows you to jack up the relative intensity of directional pressures over the stabilizing pressures.

*The output, which was previously the average fixation rate as determined after all pressures had been fixed, is now simply the sum of all fixation activity in a given number of generations. "Fixation activity" is calculated as the inverse of the number of generations between a targeted mutation's first appearance and fixation. So for example if a targeted mutation first appears in generation 15, and gets fixed in generation 37, the fixation activity for the pressure is 1/(37 - 15). This is the most accurate measure of "rate of evolution" that I can think of.

*Because of the above change, each rep of a simulation always stops after a given number of generations, resulting in much faster simulation run times.

A selection of run results can be found at www.jedi-arts.com/code/sims.txt.

The results are clear. Regardless of the conditions, adding selective pressures can increase the amount of overall fixation in a given number of generations.

Intuitively, the additional fixation activity due to more pressures outweighs any slowdown in fixation time for each pressure. The larger the span of generations that you measure over (I used 10k generations for all of the above samples), the more profound this effect becomes.

 

[kleinman]

Annoying Creationists

Your last two cases converge to a local optimum with 16 mistakes rather than a zero mistake local optimum. In order for the population to evolve to a perfect creature in these cases, the population must traverse a reduced fitness trough but the selection conditions prevent this.

And that gobbledegook is called the Rcapacity problem.

No Paul, that’s what is called a simulation of reality. Here is a real example of this:
“Darwinian Evolution Can Follow Only Very Few Mutational Paths to Fitter Proteins”
Daniel M Weinreich, Nigel F Delaney, Mark A DePristo, Daniel L Hartl. Science. Washington: Apr 7, 2006. Vol. 312, Iss. 5770; pg. 111

Five point mutations in a particular Beta-lactamase allele jointly increase bacterial resistance to a clinically important antibiotic by a factor of ~100,000. In principle, evolution to this high-resistance Beta-lactamase might follow any of the 120 mutational trajectories linking these alleles. However, we demonstrate that 102 trajectories are inaccessible to Darwinian selection and that many of the remaining trajectories have negligible probabilities of realization, because four of these five mutations fail to increase drug resistance in some combinations. Pervasive biophysical pleiotropy within the Beta-lactamase seems to be responsible, and because such pleiotropy appears to be a general property of missense mutations, we conclude that much protein evolution will be similarly constrained. This implies that the protein tape of life may be largely reproducible and even predictable.

You have to have a trajectory on the fitness landscape which allows the population to get to that local optimum. It is your Rcapacity concept which is nonsense.

Rocketwhomissesthetarget almost gets it right; these authors are accelerating the evolutionary process by applying the selection pressures sequentially. However, if you look at the fourth image down, the ‘Virtual’ varying landscape, you will see what the two superimposed fitness landscape with the two goals looks like.

They explicitly say, in great detail, how they temporally vary the goals back and forth in this experiment. This is not the fitness landscape produced when the model population is going for both goals at once -- they did not include that scenario in the experiment. Haven't you read the paper, Kleinman? Or did you just cite the first thing google found for you...

Didn’t you know, joobz cited this article however he didn’t read it, he thought varying environments had to do with the weather. So let’s see what these authors have to say:
http://www.pnas.org/cgi/content/full/104/34/13711

Simulations of biological evolution, in which computers are used to evolve systems toward a goal, often require many generations to achieve even simple goals. It is therefore of interest to look for generic ways, compatible with natural conditions, in which evolution in simulations can be speeded. Here, we study the impact of temporally varying goals on the speed of evolution, defined as the number of generations needed for an initially random population to achieve a given goal. Using computer simulations, we find that evolution toward goals that change over time can, in certain cases, dramatically speed up evolution compared with evolution toward a fixed goal. The highest speedup is found under modularly varying goals, in which goals change over time such that each new goal shares some of the subproblems with the previous goal. The speedup increases with the complexity of the goal: the harder the problem, the larger the speedup. Modularly varying goals seem to push populations away from local fitness maxima, and guide them toward evolvable and modular solutions. This study suggests that varying environments might significantly contribute to the speed of natural evolution. In addition, it suggests a way to accelerate optimization algorithms and improve evolutionary approaches in engineering.

And that’s what I have been saying for months now, single selection pressures evolve quickly. Single selection pressures toward a single goal applied sequentially is the only way you can achieve accelerated evolution. As soon as you combine selection pressures, the trajectory is confounded and the entire sorting/optimization process is profoundly slowed.

Oh, I thought I addressed this, several times, but I’ll address it again for you. So you have polyploidy, how do you transform those duplicated genes to a new form? Why Kotatsu, it requires mutation and selection and as we have seen over and over, transforming more than a single gene at a time profoundly slows the evolutionary process.

Cute. However, your stock answer doesn't in any way address what I am talking about, as the process I mention is independent of random point mutations and other kinds of mutations that alter the exact sequence. I am talking about the very process of polyploidisation, not what happens afterwards.

Why don’t you mention that the majority of the examples of aneuploidy are harmful.

"I" transform the diploid genome into a polyploid one simply by doubling the copies of all involved chromosomes by one of several known mechanisms. When this occurs in only one of several individuals --- as is often the case --- we see diploid and polyploid individuals who have the exact same gene order and nucleotide sequences. No other mutations need to be involved. This is still evidence of common descent of these organisms.

Wheat evolving by polyploidisation into wheat is an example of “common descent”? So are you now going to make the leap and tell us that reptiles evolved into birds by polyploidisation? You evolutionists do love you speculations and extrapolations.

You can construct phylogenic trees based on similarities of genes. All that it shows is that living things can have some similarity in chemical structure. In order to use these phylogenic trees as evidence of common descent, you need to show how mutation and selection can accomplish the transformation from one form to another. The mathematical and empirical evidence of mutation and selection shows that it can not make the transformations.

The mathematical and empirical evidence shows that "we" can make those "transformations". I take it you have never seen an alignment of genes, have you?

If you have the mathematical and empirical evidence, why are you always trying to inoculate yourself from having to specify the selection pressures and target genes to these pressures? I continue to post measurable and repeatable examples of mutation and selection which show combination selection pressures profoundly slow the evolutionary process while you continue to fail to post examples of mutation and selection which show otherwise and the examples you do post don’t define the selection pressures or the target genes for these selection pressures.

The only button you have pushed is the laughter button. Are you talking about the combined weight of the citations which show that n+1 selection pressures evolve more rapidly than n selection pressures? I don’t know how I can bear all zero of your citations.

I have posted five or six examples of how you are wrong in this regard. You have dismissed them without reading them, because you cannot understand what they are about. This is not my problem, obviously, but it is wrong to say that I have presented zero citations.

None of your citations define the selection pressures and the target genes for these selection pressures. You post citations are not repeatable or measurable. The hundreds of citations I have and will continue to post more of all show how mutation and selection actually works. And the way this sorting/optimization problem works is that combined selection pressures have a profound slowing on the sorting of beneficial and detrimental mutations. The mutation and selection process can only sort mutations for a single selection condition targeting a single gene with any rapidity. As soon as two or more genes are targeted, the process is profoundly slowed. That’s how mutation and selection works mathematically and that’s how mutation and selection works empirically.

Now wait a minute Belz, rocketwhomissesthetarget gave the probability that evolution is true (1.0 x 10^-999999999) and the only other probability that we got here is that we were created.

Yeah, that's what I said. False dichotomy.

We are all waiting for you to tell us any other possible way that we got here. Maybe you can make it a false trichotomy?

Both you and Epicurus fail to understand that God does not allow evil to go un-judged.

Funny, because lots of evil goes un-judged.

How do you know? Do you think the fiend god gets away with evil?

My first real skepticism of abiogenesis and the theory of evolution occurred when I took courses in organic chemistry. In the laboratory we were required to synthesize a variety of more complex molecules from simpler molecules. In order to get a side group to bond to a particular site often required activating catalysts and shielding groups to prevent reactions at other sites. Often times the reactions would have to take place in strongly acidic then strongly basic solutions and visa versa. The idea that the complex organic molecules that form life can occur in some fanciful primordial soup is as joobz puts it, speculation.

Were you fine with evolution before these experiments?

I never really gave much thought to the topic but now that I work in a profession which must deal with mutation and selection, I’ve decided to study the process in more detail. In addition, many evolutionists use the theory to argue there is no God. It is clear now that the theory of evolution by mutation and selection is mathematically and empirically impossible. The mutation and selection sorting/optimization process simply does not work the way evolutionists allege.

I improved my program and now it generates results on par with what Dr. Adequate got.

Then you get what Adequate got for all his real examples he posted of his model.

And here is for all the data you have posted which shows that n+1 selection pressures evolve more quickly than n selection pressures.

http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=11448283&dopt=AbstractPlus

CONTEXT: The continued release of human immunodeficiency virus type 1 (HIV-1) into plasma at very low levels during highly active antiretroviral therapy (HAART) can be detected using specialized techniques, but the nature and significance of this low-level viremia, especially as related to acquisition of drug resistance mutations, are unclear. OBJECTIVE: To determine genetic resistance profiles of low-level plasma HIV-1 in patients with prolonged viral suppression (<50 copies/mL of plasma HIV-1 RNA) while receiving HAART. DESIGN AND SETTING: Cross-sectional study conducted at a US academic hospital from November 1999 to February 2001 using a novel method for amplification of low levels of viral genomes in plasma. PATIENTS: Eighteen HIV-1-infected patients (7 children and 11 adults), enrolled in a longitudinal study of HIV-1 reservoirs, who had suppression of viral replication while receiving protease inhibitor-containing combination therapy. Two patients (1 adult and 1 child) with less optimal suppression of viral replication were included to assess virus predominating when plasma HIV-1 RNA levels are low but detectable (<1000 copies/mL). Follow-up analyses were conducted in 3 patients. MAIN OUTCOME MEASURE: Detection of drug resistance mutations in clones amplified from low-level plasma virus. RESULTS: Viral sequences were amplified from 8 of the 18 patients with simultaneous plasma HIV-1 measurements of less than 50 copies/mL and from 2 patients with 231 and 50 copies/mL. Clones from 3 treatment-naive patients with less than 50 copies/mL of plasma HIV-1 RNA showed continued release, for as long as 42 months, of wild-type drug-sensitive virus. The 7 patients with prior nonsuppressive therapy, with viral loads below 50 copies/mL and during "blips" to 231 and 64 copies/mL, had only resistance mutations consistent with pre-HAART therapy (although reverse transcriptase inhibitor mutations may have continued to occur). New HAART-related mutations were seen in a control patient with prior viral load levels of about 400 to 1000 copies/mL. For phylogenetic analysis, sequences were available for both resting CD4(+) T cells and plasma HIV for 7 of 10 patients and showed patient-specific clustering of sequences and a close relationship between virus in the plasma and the latent reservoir. CONCLUSIONS: Based on the samples that could be amplified, low-level viremia in children and adults receiving HAART with prolonged suppression of viremia to less than 50 copies/mL of HIV-1 RNA may result primarily from archival, pre-HAART virus, reflecting earlier treatment conditions, and does not appear to require development of new, HAART-selected mutations reflecting partial resistance to therapy. Low-level viremia below 50 copies/mL may represent less of a concern regarding impending drug failure of current HAART regimens. However, the archival drug-resistant virus may be relevant regarding future treatment strategies.

“Antibiotic interactions that select against resistance”
Remy Chait, Allison Craney, Roy Kishony. Nature. London: Apr 5, 2007. Vol. 446, Iss. 7136; pg. 668, 4 pgs

Multidrug combinations are increasingly important in combating the spread of antibiotic-resistance in bacterial pathogens. On a broader scale, such combinations are also important in understanding microbial ecology and evolution. Although the effects of multidrug combinations on bacterial growth have been studied extensively, relatively little is known about their impact on the differential selection between sensitive and resistant bacterial populations. Normally, the presence of a drug confers an advantage on its resistant mutants in competition with the sensitive wild-type population. Here we show, by using a direct competition assay between doxycycline-resistant and doxycycline-sensitive Escherichia coli, that this differential selection can be inverted in a hyper-antagonistic class of drug combinations. Used in such a combination, a drug can render the combined treatment selective against the drug's own resistance allele. Further, this inversion of selection seems largely insensitive to the underlying resistance mechanism and occurs, at sublethal concentrations, while maintaining inhibition of the wild type. These seemingly paradoxical results can be rationalized in terms of a simple geometric argument. Our findings demonstrate a previously unappreciated feature of the fitness landscape for the evolution of resistance and point to a trade-off between the effect of drug interactions on absolute potency and the relative competitive selection that they impose on emerging resistant populations.

So here is an example where combination selection pressures not only slow the evolutionary process, it reverses the evolutionary process.

 

[Belz...]

We are all waiting for you to tell us any other possible way that we got here. Maybe you can make it a false trichotomy?

Just because you can't think of a third way doesn't mean there isn't one.

But that's besides the point, as anyone who's ever studied logic knows. You can't prove a theory by disproving another one.

Funny, because lots of evil goes un-judged.

How do you know?

Because to claim otherwise would be an argument from ignorance.

Do you think the fiend god gets away with evil?

He doesn't, because he doesn't exist.

 

[rocketdodger]

So you are only putting up single sentence dodges now. Getting tired of writing bullsh--, Kleinman? Just in case anyone might forget, I will recap the issues you keep dodging.

You claim sorting algorithms are always slowed by additional sorting conditions. Dr. Adequate and I have written independent programs which use sorting algorithms yet are not slowed by additional sorting conditions. You demand real world examples -- our programs are real world examples you fool. This issue is completely unrelated to evolution. It is about your claims regarding sorting algorithms.

You claim the probabililty of creation is greater than the probability of evolution. You have failed to come up with any sort of independent value for the probability of creation. Because you can't come up with a value, you rely on a false dichotomy. We are still waiting for you to show us how to generate a value independent of evolution.

You claim that the studies you cite show multiple selective pressures to slow evolution profoundly. They do no such thing. What they show is that lethal pressures, when combined, prevent populations from evolving resistance -- by killing them. If a population dies, obviously there will be no more evolution. The few studies you do cite that do not use lethal pressures fail to measure anything that could be construed as a "rate" of evolution.

You claim that the ev program can be used to generate data regarding the effects of the number of selective pressures on a population. The ev program only features 3 pressures, and they target the same loci. Only a fool would consider this a large enough input domain for generalizations about selective pressures in general. Furthermore, the model used in the ev program was never intended to show anything about selective pressures. Paul, the programmer who wrote the java version, has told you this. Yet, in your foolish vanity you presume to think you know, better than he does, what is in the source code.

 

[rocketdodger]

And that’s what I have been saying for months now, single selection pressures evolve quickly. Single selection pressures toward a single goal applied sequentially is the only way you can achieve accelerated evolution. As soon as you combine selection pressures, the trajectory is confounded and the entire sorting/optimization process is profoundly slowed.

My god, you are so dense. Did you not read the paper? They sped up evolution, compared to a single pressure, by temporally alternating the application of two pressures. If you think this finding helps your case, you are truly insane.

So here is an example where combination selection pressures not only slow the evolutionary process, it reverses the evolutionary process.

Evolution can't be reversed, you fool, any more than you can walk a negative distance. In that study they simply inverted the direction of a selective pressure. You seriously need to 1) read and 2) think before you cite.