Annoying creationists

[delphi_ote]

I wish there weren't so many homologous genes between human and rat. This script I wrote is taking too long to run! Could someone please put all of life on Earth under more than one selection pressure? Things have evolved too much, and it's making my profession very difficult!

 

[Mr. Scott]

You kids want to talk about anything but the mathematics of mutation and selection and the empirical evidence which supports this mathematics.

This thread is about creationists who are annoying.

Who is demonstrating cognitive dissonance? It is you evolutionists who ignore the mathematical and empirical facts of life of how mutation and selection actually works.

I knew you'd throw it back at us. You are too predictable. (I'm predicting Kleinman will respond with "it is you evolutionists who are too predictable")

The fact that you don't respond at all to the proof of evolution is strong evidence your cognitive dissonance is clouding your judgement.

I assure you, evolutionists experience little cognitive dissonance since there is a mountain of consistent evidence for it.

If you want to really annoy evolutionists, present your refutation of the retrovirus evidence that humans and chimps share a common ancestor -- a point you previously ignored.

You onced brushed it off as a "coincidence" that human and chimp genomes had the same viral insertions in the same places, so I calculated the probability of this coincidence with a rough back-of-the-envelope estimate.

Number of nucleotides in the human and chimp genomes: 3 billion.

Number of endogenous retroviruses (ERVs) in the human and chimp genomes in identical positions: seven.

Chance of 1 ERV appearing in identical positions independently in chimp and human: One in three billion.

Chance of 7 ERVs appearing in identical positions independently: One in three billion to the seventh power.

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

Dr. Kleinman, I await your refutation.

 

[Belz...]

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

How could I ever be sarcastic beggaminases?

See what I mean ?

Get one of those high-schoolers into the discussion, perhaps they could explain to us what a beggaminases is.

They wouldn't need to. If you haven't understood what I meant by it, after all those times I've repeated it, then you never will.

It's very telling of your character.

Sure I realize what they show and so do you; they are cherry picked to show that combination selection pressures profoundly slow the evolutionary process.

It's nice to see you admitting to lying, Klein. There's not much else to say, now.

 

[Belz...]

Rocketdodger, do you think a war of examples would really be fair. All you evolutionists with your speculations, extrapolations and hunches against one annoying creationist with a peer reviewed and published model of random point mutations and natural selection and hundreds of empirical examples which show that combination selection pressures profoundly slow the evolutionary process.

You've got a serious case of Galileo syndrome, Alan.

Joobz, if the sun shines on lead long enough does it turn into gold?

I think you've lost it, Klein. You're just reposting the same stuff o'er and o'er even after it's been shot down.

 

[Belz...]

I wish there weren't so many homologous genes between human and rat. This script I wrote is taking too long to run! Could someone please put all of life on Earth under more than one selection pressure? Things have evolved too much, and it's making my profession very difficult!

Delphi, you're obviously ignorant of the REAL facts. Evolution is mathematically impossible. Kleinman has proved it by posting hundreds of empirical examples that show that multiple combination pressures profoundly slow evolution!

Your profession is a sham!!!

 

[Paul C. Anagnostopoulos]

Why don’t you tell us what the probability is to form a particular 100 amino acid protein is by the random addition of amino acids? Then you can tell us how natural selection will improve that probability especially when there are multiple simultaneous selection conditions acting simultaneously.

Oh now Alan, don't go all Dembski on us here. Treating a protein as a discrete combinatorial object is irrelevant to the question, since that is clearly not how they came to be. Natural selection cannot improve the probability of spontaneous assembly of a DCO because that is not what selection works on.

~~ Paul

 

[rocketdodger]

What you probably don’t realize that mutation and selection is a sorting/optimization problem that shares many features with iterative solutions to partial differential equations. The first thing you should know about these problems is that the number of sorting conditions has a profound affect on the convergence. This is what Dr Schneider’s simulation shows and this is what the hundreds of empirical examples cited of mutation and selection demonstrates. The sorting of beneficial and detrimental mutations when you have multiple selection conditions is confounded by the multiple sorting conditions.

You don't know sh-- Kleinman.

You claim that additional optimization conditions always confound sorting/optimization problems. My program shows this to be not true in general. Can you show anyone here why the sorting/optimization algorithm used in my program is not a sorting/optimization algorithm? If not, then you are wrong.

Here it is, in short:
1) Randomly mutate x number of bases in each creature's genome.
2) Determine the fitness of each creature according to the pressures exerted on the population.
3) Reproduce, such that creatures with higher fitness have more offspring.
4) Go back to 1, stopping when the targeted mutations of all pressures have achieved 80% or more fixation in the population.

 

[kleinman]

Annoying Creationists

Sol, if you think you can use probability theory to prove the theory of evolution by mutation and selection then go for it. Since the probability above is less than about 1 in 10^400, I’ll accept your value of 1 in 10^360 probability. I don’t claim to be an expert in probability theory

OK, good - we're making progress. You admit you were wrong and that you don't understand probabilities. As for those numbers, they are yours, not mine. Where did 100 generations come from?

Sol, forget the 100 generations, show us how to use probability theory to win a million lotteries only 14 times longer than winning one lottery. You must be incredibly wealthy after winning all those lotteries.

Oh oh...D30N and N88D appeared "MOSTLY" in certain patients. But, not "ALWAYS." In some patients, K20T appeared. So, much for the hypothesis that only one mutational pathway can develop from a particular selective pressure. Kleinman loses again.

Really kjkent1? Does this explain how birds evolve into reptiles? Does this mean that genetic sequencing to identify drug resistance is wrong?

Ahem...obviously you're a bit rattled by being instantly demonstrated wrong via a peer reviewed article on your favorite HIV subject matter. Otherwise you wouldn't have written that "birds evolved into reptiles," rather than the reverse!

Kjkent1, I have never said that there can not be variants of genes. There are hundreds of forms of human hemoglobin. Just because there may be two variants of a particular gene that may confer resistance to a particular drug does not mean there is no goal for evolution as you allege. All you have shown is that there are only a small number of possible genetic sequences that improve fitness for the virus from the huge number of possible combinations available. The transformation of reptiles into birds requires a trajectory on a fitness landscape that transforms thousands of genes which always gives fitness to reproduce. When you give an example which shows only two possible variants that give improved fitness to reproduce, how do you explain the transformation of thousands of genes when you have so few variants that give improved fitness to reproduce?

I wish there weren't so many homologous genes between human and rat. This script I wrote is taking too long to run! Could someone please put all of life on Earth under more than one selection pressure? Things have evolved too much, and it's making my profession very difficult!

Really Delphi, and how many genes are not homologous? And what was the selection pressure that transformed rats into humans? You aren’t going to tell us a temperature change did that one also? You may be able to make a living finding similarities between genes in different life forms but mutation and selection didn’t transform reptiles into birds or rats into humans. You don’t have the selection pressures and even if you could imagine something like a temperature change, you can’t transform four or five genes simultaneously let alone thousands of genes. Mutation and selection doesn’t work that way mathematically or empirically. You should know that, you gave us the citation to Wikipedia and the fitness landscape. Do you care to describe the trajectory on the fitness landscape that would transform rats to humans?

You kids want to talk about anything but the mathematics of mutation and selection and the empirical evidence which supports this mathematics.

This thread is about creationists who are annoying.

And it’s way too easy to annoy you with the mathematical and empirical facts of how mutation and selection works. When are you going to tell us about the lies your parents told you?

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

How could I ever be sarcastic beggaminases?

See what I mean ?

Belz, I’m not ignoring your posts, I’m waiting for one of you evolutionists to post a citation showing that n+1 selection pressures evolves more rapidly than n selection pressures. If you want to talk about beggaminases, that alright with me.

Why don’t you tell us what the probability is to form a particular 100 amino acid protein is by the random addition of amino acids? Then you can tell us how natural selection will improve that probability especially when there are multiple simultaneous selection conditions acting simultaneously.

Oh now Alan, don't go all Dembski on us here. Treating a protein as a discrete combinatorial object is irrelevant to the question, since that is clearly not how they came to be. Natural selection cannot improve the probability of spontaneous assembly of a DCO because that is not what selection works on.

I’m not sure what you mean by “go all Dembski”. I raised that issue because sol invictus is going to use probability theory to prove the theory of evolution without selection. Actually, I want sol to teach us all how to win a million lotteries in only 14 times longer than winning one lottery. Sol doesn’t understand that mutation and selection is a sorting/optimization problem.

What you probably don’t realize that mutation and selection is a sorting/optimization problem that shares many features with iterative solutions to partial differential equations. The first thing you should know about these problems is that the number of sorting conditions has a profound affect on the convergence. This is what Dr Schneider’s simulation shows and this is what the hundreds of empirical examples cited of mutation and selection demonstrates. The sorting of beneficial and detrimental mutations when you have multiple selection conditions is confounded by the multiple sorting conditions.

You don't know sh-- Kleinman.

You claim that additional optimization conditions always confound sorting/optimization problems. My program shows this to be not true in general. Can you show anyone here why the sorting/optimization algorithm used in my program is not a sorting/optimization algorithm? If not, then you are wrong.

When you produce a single real example that shows n+1 selection conditions evolve more rapidly than n selection conditions, I’ll take a look at your program.

This citation demonstrated how destructive the misunderstanding that evolutionists like rocketwhomissesthetarget and their defective thinking have on understanding how mutation and selection process actually works. A proper understanding of mutation and selection process would never start with monotherapy for treating a rapidly reproducing virus. This has led to resistance strains of viruses in the gene pool making it far more difficult to find combination therapies to suppress the reproduction of the virus. The evolutionist philosophy and evolutionists misinterpretation of how mutation and selection actually works has led to the early death of many people who suffer from HIV. How much longer will you evolutionists persist with this misunderstanding of how mutation and selection actually works is up to you, but know this, your pseudo-scientific interpretation of this phenomenon has interfered with the proper understanding of the process and led to inappropriate treatment. The theory of evolution is not only wrong, it is destructive to life.
http://www.journals.uchicago.edu/CID/journal/issues/v30nS2/990304/990304.html

The response to antiretroviral therapy in human immunodeficiency virus (HIV)infected patients is limited by the emergence of drug resistance. This resistance is a consequence of the high rate of HIV mutation, the high rate of viral replication (especially when potent multidrug therapies are not used or taken reliably), and the selective effect of these drugs, which favors emergence of mutations that can establish clinical drug resistance. The introduction of highly active antiretroviral therapy (HAART), which typically includes at least 2 nucleoside reverse transcriptase inhibitors (RTIs) and a protease inhibitor or a nonnucleoside RTI, for most treatment-naive patients results in a reduction of viral load below the limit of detection determined by currently available HIV RNA assays. It is this marked reduction that results in durable viral suppression, usually only possible by the simultaneous use of 3 or 4 drugs. The RTI components of HAART are crucial for these benefits of combination therapy. Specific amino acid changes are associated with resistance to several RTIs, but new mutation complexes have been observed that can confer broad cross-resistance within this class. Genotypic and phenotypic resistance assays to measure drug resistance are being developed, but refinements in both methodology and our ability to interpret results of these assays are necessary before they are introduced into widespread clinical use.

and

The first 5 drugs approved for treatment of HIV infection were reverse transcriptase inhibitors (RTIs), all of which are nucleoside RTIs. More recently, nonnucleoside RTIs have become available, and nucleotide RTIs are being developed. Unfortunately, because these drugs were gradually introduced one at a time (starting with zidovudine in March 1987), monotherapies were routinely employed until 1994. When response was lost to 1 drug in a patient, treatments were changed to a different monotherapy. The response to the second therapy, however, was not as good as when the same drug was given to a treatment-naive patient [1, 2]. Even before the genetic mutations associated with drug resistance were identified, it seemed likely that resistance to 1 RTI diminished the response to subsequent ones.

and

Combination therapies that use 2 RTIs were introduced in 1994 [57]. By use of 2 drugs in initial therapy, VL reduction was greater and more durable. The use of sequential therapy (i.e., adding 1 drug to previous monotherapy after benefits are lost) results in a much lower virologic response than if 2 drugs are used in the initial therapy. When a new drug is added to a regimen that is not adequately suppressing viral replication, the only active agent may be the single new drug. The concept of greater VL reduction with more-intensive therapies was cemented in our treatment policies by the landmark studies that showed that 3- or 4-drug combination therapies that include a protease inhibitor (PI) or a nonnucleoside RTI are able to reduce VL to below levels of detection [815]. These intensive 3- or 4-drug therapy regimens have been termed highly active antiretroviral therapy (HAART).

How much longer will the faulty misunderstanding of how mutation and selection actually works be perpetuated by evolutionists so that needless deaths due to HIV, and other infectious disease and cancers because of evolution of resistance?

 

[joobz]

How much longer will the faulty misunderstanding of how mutation and selection actually works be perpetuated by evolutionists so that needless deaths due to HIV, and other infectious disease and cancers because of evolution of resistance?

Wow, that's heaping of crazy right there.

I'm not claiming you are crazy, kleinman. Only that it's becoming difficult to distinguish between a crazy person's rants and your posts.

 

[Mr. Scott]

When are you going to tell us about the lies your parents told you?

What was once in my sig is not on topic of a thread about annoying creationists. Why do you see a gotcha there?

Now, annoy us with your refutation of the endogenous retroviruses evidence that humans and chimps descended from the same ancestor.

 

[Paul C. Anagnostopoulos]

I’m not sure what you mean by “go all Dembski”.

Dembski treats the flagellum as a discrete combinatorial object in No Free Lunch. Unfortunately, it's irrelevant.

~~ Paul

 

[kleinman]

Annoying Creationists

How much longer will the faulty misunderstanding of how mutation and selection actually works be perpetuated by evolutionists so that needless deaths due to HIV, and other infectious disease and cancers because of evolution of resistance?

Wow, that's heaping of crazy right there.

For more than 50 years, the evidence of how mutation and selection actually works has been piling up, yet mathematical incompetents like you think your speculations qualify as science.

Joobz, when are you going to take me up on the $10,000 wager about your claim that you can find irregularities in my PhD thesis? You’ve opened your big mouth one too many times, put your money where your mouth is.

When are you going to tell us about the lies your parents told you?

What was once in my sig is not on topic of a thread about annoying creationists. Why do you see a gotcha there?

Why Mr Scott, you see fit to psychoanalyze me by what I write, so why can’t I psychoanalyze you by what you write. I happen to believe that what a person says reveals what is in their heart. When someone writes that they believe their parents are liars, you are revealing something about yourself. I am interested in why you would think of your parents as liars. This may explain why you embrace the false belief system of evolutionism.

Now, annoy us with your refutation of the endogenous retroviruses evidence that humans and chimps descended from the same ancestor.

It is not my job to refute every misinterpretation that you evolutionists come up with. You try to do this with a picture of a fossil; delphi and Dr Richard have tried to do this with occasional similarities found in genetic structure of different life forms. Why don’t they explain the 150,000,000 base differences between human and chimpanzee genomes all which would have to happen in only 500,000 generations with very small populations?

I have spent some time studying Dr Schneider’s peer reviewed a published mathematical model of random point mutation and natural selection which reveals an important mathematical property of this phenomenon. I have posted hundreds of empirical examples which demonstrate this phenomenon as well as other mathematical models which demonstrate the same thing. These examples show that the foundation principle for the theory of evolution, mutation and selection, does not and can not do what you claim. It is not my job to correct every misinterpretation of the physical world that you come up with. If you want to post a citation which shows that n+1 selection conditions evolve more rapidly than n selection conditions, I’ll respond to that. Otherwise, start a thread where you can speculate how endogenous retroviruses give evidence that humans and chimps descended from the same ancestor. If you do want to tell us about the lies your parents told you, we can talk about that because you need help.

 

[delphi_ote]

Really Delphi, and how many genes are not homologous?

More and more the more distantly the two organisms I'm comparing have diverged from their common ancestor. It's almost as if...


Evolution is true!

 

[Mr. Scott]

Why Mr Scott, you see fit to psychoanalyze me by what I write, so why can’t I psychoanalyze you by what you write. I happen to believe that what a person says reveals what is in their heart. When someone writes that they believe their parents are liars, you are revealing something about yourself. I am interested in why you would think of your parents as liars. This may explain why you embrace the false belief system of evolutionism.

Dr. Kleinman, you are the subject of Paul's "Annoying creationists" thread! Look at the thread title! Look at the originating post! Psychoanalyzing you is fair game. Psychoanalyzing me is off-topic. Changing the subject each time you are asked a question you cannot answer is a transparent, sleazy debating tactic.

It is not my job to refute every misinterpretation that you evolutionists come up with.

Specifically, how have evolutionists misinterpreted the endogenous retroviruses evidence? You've just made this claim. Back it up.

 

[kleinman]

Annoying Creationists

Really Delphi, and how many genes are not homologous?

More and more the more distantly the two organisms I'm comparing have diverged from their common ancestor. It's almost as if...

Evolution is true!

Almost as if…? Too bad the theory of evolution isn’t the game of horseshoes. Then your “almost” would score some points. Now that we know exactly that combination selection pressures profoundly slow evolution, your “almost” doesn’t score points any more. Tell us all about the non-homologous genes between humans and chimpanzees and tell us how mutation and selection transformed these genes in 500,000 generations. Oh yes, don’t forget to tell us what the selection pressures were to achieve these transformations.

Why Mr Scott, you see fit to psychoanalyze me by what I write, so why can’t I psychoanalyze you by what you write. I happen to believe that what a person says reveals what is in their heart. When someone writes that they believe their parents are liars, you are revealing something about yourself. I am interested in why you would think of your parents as liars. This may explain why you embrace the false belief system of evolutionism.

Dr. Kleinman, you are the subject of Paul's "Annoying creationists" thread! Look at the thread title! Look at the originating post! Psychoanalyzing you is fair game. Psychoanalyzing me is off-topic. Changing the subject each time you are asked a question you cannot answer is a transparent, sleazy debating tactic.

That’s right, Paul did say this.

Sometimes these annoying creationists just piss me off:

So, you are wrong, if psychoanalyzing you pisses you off, I am on topic. However I prefer pissing you off by pointing out the mathematical and empirical facts of how mutation and selection actually works. Only an evolutionist would think that pointing out the mathematical and empirical facts of how mutation and selection actually works is sleazy but what do you expect from someone who thinks his parents are liars?

It is not my job to refute every misinterpretation that you evolutionists come up with.

Specifically, how have evolutionists misinterpreted the endogenous retroviruses evidence? You've just made this claim. Back it up.

Ok, since you don’t want to talk about your parents who you think are liars, we can talk about endogenous retroviruses. Let’s start with you explaining to us what the selection pressures these viruses cause and the target genes for these selection pressures. I like talking with you kitty cat but you should reconsider thinking of your parents as liars.

 

[rocketdodger]

When you produce a single real example that shows n+1 selection conditions evolve more rapidly than n selection conditions, I’ll take a look at your program.

Or, in other words, you are a fraud who knows none of the mathematics you claim to know and are completely unable to refute any of my mathematics.

You don't even have to look at the program, you fool -- I summarized my algorithm in that post. Here it is again:

1) Randomly mutate x number of bases in each creature's genome.
2) Determine the fitness of each creature according to the pressures exerted on the population.
3) Reproduce, such that creatures with higher fitness have more offspring.
4) Go back to 1, stopping when the targeted mutations of all pressures have achieved 80% or more fixation in the population.

You claim that additional optimization conditions always confound sorting/optimization problems. Can you show anyone here why the above algorithm is not a sorting/optimization algorithm? If not, then you are wrong.

 

[Lord Emsworth]

This thread is about creationists who are annoying.



I knew you'd throw it back at us. You are too predictable. (I'm predicting Kleinman will respond with "it is you evolutionists who are too predictable")

The fact that you don't respond at all to the proof of evolution is strong evidence your cognitive dissonance is clouding your judgement.

I assure you, evolutionists experience little cognitive dissonance since there is a mountain of consistent evidence for it.

If you want to really annoy evolutionists, present your refutation of the retrovirus evidence that humans and chimps share a common ancestor -- a point you previously ignored.

You onced brushed it off as a "coincidence" that human and chimp genomes had the same viral insertions in the same places, so I calculated the probability of this coincidence with a rough back-of-the-envelope estimate.

Number of nucleotides in the human and chimp genomes: 3 billion.

Number of endogenous retroviruses (ERVs) in the human and chimp genomes in identical positions: seven.

Chance of 1 ERV appearing in identical positions independently in chimp and human: One in three billion.

Chance of 7 ERVs appearing in identical positions independently: One in three billion to the seventh power.

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

Dr. Kleinman, I await your refutation.

If you are interested in ERVs etc, then you might find pleasure in reading this thead on ForU.ms: http://foru.ms/t6048362-200000-ervs.html

Seven orthologous ERVs? Ahem, ...

 

[Belz...]

Belz, I’m not ignoring your posts, I’m waiting for one of you evolutionists to post a citation showing that n+1 selection pressures evolves more rapidly than n selection pressures.

Easy.

Dinosaurs live and die for millions of years, with n selection pressures affecting them.

Meteor hits. Selection pressures: n+1. Lots of death. Suddenly mammals are all over the place.

If you want to talk about beggaminases, that alright with me.

Yes, let's talk about that. Remember what it means ?

 

[kjkent1]

Kjkent1, I have never said that there can not be variants of genes. There are hundreds of forms of human hemoglobin. Just because there may be two variants of a particular gene that may confer resistance to a particular drug does not mean there is no goal for evolution as you allege. All you have shown is that there are only a small number of possible genetic sequences that improve fitness for the virus from the huge number of possible combinations available. The transformation of reptiles into birds requires a trajectory on a fitness landscape that transforms thousands of genes which always gives fitness to reproduce. When you give an example which shows only two possible variants that give improved fitness to reproduce, how do you explain the transformation of thousands of genes when you have so few variants that give improved fitness to reproduce?

In the current example there are demonstrably at least two pathways to resistance (maybe more, no way to know without repeating the experiment at least a few million times).

But, let's suppose that every selective pressure has only 2 possible evolutionary pathways. I'll leave it to you to figure out how fast the number of possible outcomes reaches to practical infinity (2^100 = ~1.27E30).

You're not giving the numbers their due. Evolution is demonstrably not goal oriented. We know that mutations are not always single point, and that sometimes long pieces of DNA duplicated and those strings can create new functions. The fact that the experiments with HIV that you cite don't find these duplications, doesn't mean that they don't occur, or that they won't occur, if you were to repeat the experiment long enough.

You only need one novel change to set a species off in a new direction. The fossil and genetic record of extinct and existing species shows that such novel changes have occurred, we have evidence that such mutations are possible, we have evidence that multiple pathways can result from one selective condition -- what more do you want?

That was rhetorical. I know what you want. You want me to put some base chemicals into a petri dish, bake it for 45 minutes at 350, and then open the oven door and pull out a giraffe.

That's not gonna happen, Alan. So, your belief system is safe.

 

[sol invictus]

Sol, forget the 100 generations, show us how to use probability theory to win a million lotteries only 14 times longer than winning one lottery. You must be incredibly wealthy after winning all those lotteries.

I already did - if you can find me a million lotteries where each ticket has a chance to win all of them. That's not so common in real lotteries... but the math is identical to the case we were discussing, which is why I mentioned it.

In any case you've already agreed my formula was correct, and yours was wrong. Are you flipflopping again?