Vacuity of ID: Comments on Irreducible Complexity

Here's an interesting thing I learned from a marine biologist on a whale-watching tour last summer:

On the west coast of Canada, there are three populations of orcas (killer whales): the northern population, around Hyder/Queen Charlottes area, has as its diet, primarily mammals (seals, mostly); the southern population, just up from Seattle, eats fish; the western population, on the seaward side of Vancouver Island, is presumed from teeth and stomach contents to eat rays, skates, and sharks.

The populations don't interbreed. I'm told it's because they're songs have diverged too much for them to recognize each other as potential mates, though I suppose geography has something to do with it.

The interesting part will be the examination of their genetic divergence, and how long it will be before they are truly speciated.

Or maybe "Poof!" and they'll be three different species. Could happen...

Oops. "Their songs", not "they're songs". Apologies.

You see every time I read or see IDiots basking on the "mathematical evidence" for ID and against ToE, I remind myself of the old story about how it was mathematically proved that bumble bees cannot fly!!!! Dumbski is doing the same argument; using pseudo mathematical jargon to obfuscate arguments that he perfectly well know are baseless.

— Tyrannosaurus in Comment 97119

Nothing in biology is like what humans make, until one reduces the components down to an unreasonable level. So Denton rattles on about the "analogues" of our machines within cells---the fact is that as a discipline biology, including evolutionary biology, is busy studying how different cells are from our own machines. For one thing, biology tends not to compartmentalize what we consider to be "functions", and for another thing, biology is highly derivative in a way that human machines are not.

— Glen Davidson

the passwords were created by peoples choices

there are some serious flaws in it's claims

Salvador Cordova wrote -

"No, I do understand what the theory of evolution claims,"

Obviously, the next logical step here would be to provide some sort of evidence to back up this assertion. After all, anyone can say this. And Sal isn't just claiming to know a little about evolution. As a would-be serious critic, it is imperative that he understand what he criticizes. In fact, I already made the point that further dwelling on irrelevant computer analogies would be evidence of evasion on Sal's part.

But instead, Sal moved on to say...

"and I'm challenging that empirical reality and serious theoretical examination shows there are some serious flaws in it's claims.", and repeat some computer nonsense.

But he hasn't come close to doing what he claimed. He hasn't said a single word about empirical data, other than to make the trivial assertion that a complete step-by step evolutionary history of every protein that exists isn't available. This is akin do denying gravity by arguing that every apple that ever came off a tree hasn't been accounted for.

On the theoretical level, all Sal has offered is an extremely inapt analogy of a code-breaking algorythm. It is this very "theoretical" argument that convinces me that Sal doesn't grasp the theory of evolution. Although he disdainfully refers to "step by step" processes, his argument merely makes the obvious point that an incredibly improbable set of simultaneous events is unlikely to occur at one time.

Amazingly, astoundingly, Sal doesn't make reference to even one of the existing computer or mathematical models of evolutionary processes, not even to the decades old work of Sewell Wright. Nor does he make any reference to the theoretical work on DNA computers of about a decade or so ago.

The "password" analogy fails on so many levels it's hard to list them all.

1) The theory of evolution doesn't propose single generation leaps from one distantly related organism to another.
2) The theory of evolution doesn't propose that evolutionary steps are taken in pursuit of an ultimate goal. (Science-accepting theistic evolution positions would tend to argue that a supreme being "intended" evolution to ultimately produce consciousness, but would agree that from a human perspective, evolution is best studied as a non-magical process.)
3) Don gave an example of an algorythm which could solve passwords one step at a time (albeit due to a security flaw). This is a great deal closer to how evolution actually works, but still a far cry from it.

Computer models of evolution work on the principles of random variation, usually limited, followed by preferential selection of some variants.

I'm not even sure that Sal's arguments qualify as "straw man" arguments. Literally all he does is say "the cell is a Turing machine", without offering the slightest justification for this extraordinary claim (or even clarifying whether he means an honest-to-goodness theoretical Turing machine or merely a contemporary computer with a hard drive, RAM, keyboard, and output device). We all agree that DNA encodes information, Sal, but that doesn't mean that an amoeba is the same thing as your laptop.

Personally, I don't think that a PhD in "evolution denial" should be given out to anyone who can't first demonstrate a PhD level understanding of the theory of evolution.

Sal, I give up. You just want to repeat buzzwords, not to acknowledge anyone else's points or defend your own assertions. Just answer Lenny's 31 questions, TELL ME IF HIV CAUSES AIDS, and I'll move on.

[the] password illustration was to help the reader see the way IDists view certain biological structures like the Flagellum or a biological Turing Machine.

— Sal

For starters, [evolution] assumes the some of the very things it claims to prove, namely, that most large scale biological innovation can be reached through step-wise incremental improvements.

— Snake Oil Sal

As for the question "why do they do it?" - well, Dembski and Behe have had a lot of book sales and TV appearances out of ID, but I doubt that's it - although I'm sure it's hard to walk away from. If I was shifting units like Dembski and had to battle with my doubts, I'm not at all sure I wouldn't quietly smother them under a pillow in the dead of night.

At heart it's good old primate hierarchy, and you too can be an alpha male if you make an elite from the ignorant.

It's hard to get there through science -- to be really something in science you have to know a _lot_ and be creative, and hold your own among an awful lot of other creative, bright, inquisitive. hard working and knowledgable people. Sometimes, you need the guts to prove everyone in your peer group wrong after years of derision (primate hierarchies not being exactly absent from science either). That's hard, and most people can't do it. I love science, and I'd make a crap scientist. No, not coproliths.

To be a bit of a noise in ID, what do you need? Well, Salvador and Dave and plenty of other people have it, so I guess you should ask them. ID is nice, because you don't need to know a lot, it's forbidden to ask difficult questions (otherwise not knowing a lot might becomes a disadvantage), but you get to be smarter than all those scientists anyway! What's not to like? Plus, you get to Think Of The Children and Save Mankind From Sin -- oops, sorry, not sin. Bad thinking, perhaps, not sin. And you get a community, and the love of the President, and eternal life. No, no, sorry, not eternal life. That's... oh, what's the word, begins with an R, rhymes with real pigeon... sorry, lost it (a few years ago now).

Coming up with a theory and evidence and predictions (real ones, not ones that coincide with evolutionary predictions) and heated debate about details -- you know, like what scientists do -- would ruin the fun for everyone. You don't want to let everyone down, do you?

R

Sal and F.L. Berlinski and all the others are not going to answer questions that reveal their ignorance or misrepresentation of the facts. (political death)

Their whole M.O. is to spout some nonsense and when called on it, click the remote and move to the next channel like someone with ADD.

Posted by afdave on April 17, 2006 06:58 PM (e) ... I have an idea for a simple, fun exercise. I'm an Electrical Engineer and business man and I used to fly AF jets. I like simple, uncomplicated arguments and I like people to cut to the chase ... fast.

My biggest problem with Sal's password "example" of evolution is the fact that he assumes that there is only one correct password. I assume this is because he is utterly convinced that the universe exists to bring him forward and that he is, in fact, the crown of creation and that is why it is so impossible that evolution is true - because think about the chances of Salvador existing!

The example would work much better if all you wanted is access to a computer used by billions of people. Yes, each has a password of 40 characters, but they also all have maximum privileges so any of them will do. Now it is far easier, isn't it? Particularly because if evolution is applied to this picture, all you need is to get successively closer - because you attempt thousands of combinations and select the ones that were closer to any of the solutions.

Yes, it is a pathetic example because evolution doesn't work anywhere close to password cracking programs. Of course, Sal either is so stupid that he doesn't understand the difference or is so immoral that does understand it but uses it anyway in the foolish hope that everyone else won't.

To whit: only creationists believe that the entire genetic code appeared in one go, in complete disregard of all know facts of physics, when God breathed life into clay. And all their examples do is demonstrate that their belief is completely impossible without some higher power. But none of it has anything to do with evolution, or with the actual evidence of how life came to develop on this planet.

Hope that helps,

Grey Wolf

Here's an interesting thing I learned from a marine biologist on a whale-watching tour last summer: On the west coast of Canada, there are three populations of orcas (killer whales): the northern population, around Hyder/Queen Charlottes area, has as its diet, primarily mammals (seals, mostly); the southern population, just up from Seattle, eats fish; the western population, on the seaward side of Vancouver Island, is presumed from teeth and stomach contents to eat rays, skates, and sharks. The populations don't interbreed. I'm told it's because they're songs have diverged too much for them to recognize each other as potential mates, though I suppose geography has something to do with it.

— fnxtr

The interesting part will be the examination of their genetic divergence, and how long it will be before they are truly speciated.

Lenny, am I coming across as incredibly dense?

I knew what the answer from the scientific community would be. I want the IDiots to defend themselves. I know they can't, I just wanted to see them try.

I don't know what your beliefs are Reverend Flank, but Panda's thumb has a lot of Atheists.

Yet bizarrely, you seem to think that you're scoring points on Lenny Flank by finding something religious in the book.

I'm challenging that empirical reality and serious theoretical examination shows there are some serious flaws in it's claims.

I'm also an electrical engineer and a small businessman. No, I didn't fly jets (not that I didn't want to, mind you, I was courted by the Air Force, but I didn't have the eyesight, they did, however, offer to send me to medical school, and offer I should have accepted - but I digress)

Sal found something shiny ....or he changed the channel.

Maybe he's gone off on a Ark hunt or he's seen the light and become a Scientologist (snicker) he likes a little fame. He could go on Oprah's show and jump up and down on the couch and say he thinks Dembski is hot.

What gripe, in particular, do you have with functional analysis? It seems to me that functionalism has worked rather well in psychology. Is there any scientific principle I should be made aware of that prohibits it there and elsewhere, say in biology?

Nothing in biology is like what humans make, until one reduces the components down to an unreasonable level. So Denton rattles on about the "analogues" of our machines within cells---the fact is that as a discipline biology, including evolutionary biology, is busy studying how different cells are from our own machines. For one thing, biology tends not to compartmentalize what we consider to be "functions", and for another thing, biology is highly derivative in a way that human machines are not.

There is, of course, value in the reductionism that Denton engages in, and indeed, I recall reading fairly closely an article in Nature which dealt with the syntax and semantics of DNA.

But of course this is only a model of DNA coding which is applied for our convenience, and not because we ever once invented anything like DNA informatics.

Qualifications for the Air Force depend on how desperate they are for personnel.

But of course this is only a model of DNA coding which is applied for our convenience, and not because we ever once invented anything like DNA information system.

— Glen

Apparently Sal and friends seem to think that since you can mathematically describe something (in this case using formal grammars), that description IS the thing.

I've always likened that mistake to going to Denny's and eating the menu.

Glad you liked it. I would also compare the above to the question of how the electron "knows" when to act like a particle and when to act like a wave. The erroneous question is the result of thinking that the electron becomes a particle or a wave, instead of the truth, which is that the electron behaves like an electron, and it is we who describe it as "particle-like" or "wave-like."

Sal, As an aside, while you are here, I asked for information on ID from another source in one of these threads (as I have repeatedly), and recieved deafening silence (as I have repeatedly). Perhaps you would be willing to step up to the plate for me? Namely: http://en.wikipedia.org/wiki/Scientific_Method " 1- Define the question 2- Gather information and resources 3- Form hypothesis 4- Perform experiment and collect data 5- Analyze data 6- Interpret data and draw conclusions that serve as a starting point for new hypotheses 7- Publish results " I'm sorry, but I seem to have missed some of the literature the ID scientists are putting out. I'm sure this is riveting stuff if you actually have a set of experiments refuting evolution. Could you please refer me to where I might find these, either on the internet and in print, and clearly explain what your hypothesis are and what the result of experimentation on those testable predictions were? Thanks.

Thanks, Anton, for the link to the cetacean studies. Holy crap there's a lot out there to learn. No wonder some folks run in terror and hide behind "Poof!"

fnxtr

Just wave the magic wand of mathematics and viola those pesky facts disappear.

Brave Cordova ran away
Bravely ran away, away
When reason reared its fright'ning head
He bravely turned his tail and fled
Brave, brave, brave, brave Cordova...

Some very serious problems in the evolution of proteins threaten the theory of evolution, and appear to disprove it. A demonstration of the seriousness of these problems therefore constitutes a disproof of the theory of evolution. In particular, the evolution of proteins having significantly different shapes (tertiary structures) than previously existing proteins appears to be impossible. Although there are other arguments against the theory of evolution, the present argument differs in several ways. Some arguments against evolution involve the improbability of abiogenesis, that is, the origin of the first life forms. These arguments are convincing, but biologists will say that some as yet undiscovered mechanism resulted in the first life forms. The biologists' argument is hard to refute in a formal way. Other arguments point to the complexity of life, and the implausibility of such a complex system evolving. For example, Behe documents the complexity of flagella and argues that they are "irreducibly complex," meaning that the system cannot function unless many parts appear, and all these parts could not have arisen at once by evolutionary processes. This is also a convincing argument, but it is hard to formalize because it does specify mathematical probabilities. Biologists will say that some as yet undiscovered mechanism resulted in the evolution of the flagellum and other structures that appear to be irreducibly complex. Other arguments involve the fact that information of the kind found in life forms does not appear by natural processes. However plausible this argument is, it does not have a formal mathematical justification. Similar comments apply to the lack of transitional forms in the fossil record, and many other arguments commonly used against the theory of evolution. The argument presented here is different, in that it involves existing genetic mechanisms, not hypothesized ones, and it involves the calculation of mathematical probabilities (or rather, improbabilities). This therefore appears to be the first argument that qualifies formally as a disproof of the theory of evolution. This argument also involves redundancies in many of its aspects. That is, under several models, the change of shape of proteins is impossible, and each model has its own set of reasonable assumptions. The difficulties presented here do not imply that proteins cannot acquire new functions by mutations; this can happen by mutations that do not significantly affect the shape of the protein. It is only the change of the shape of a protein that presents difficulties. Grishin [Grishin 01] proposes some mechanisms for the evolution of new protein folds without an explicit computation of probabilities, but this process is still problematical. The difficulties in changing the shape of proteins by evolution involve both probabilities and laws of protein structure. The evolution of proteins of new shapes by point mutations is not possible, because the change of shape of a protein would require too many mutations. If the probability of a mutation is high enough to change the shape of the protein, then many other mutations will also occur that will essentially randomize the rest of the gene and cause the newly shaped protein to be harmful to the organism. One might argue that large scale changes to a gene could result in a protein of a new shape more readily than could point mutations. However, other arguments based on laws of protein structure prevent this. The kinds of amino acids that appear on the inside and the outside of a protein are different. There can only be a small number of insertions of a part of one protein into another that do not violate the distinction between the inside and outside of the protein, and the chance that any one of these will be beneficial, is very small. The present argument is based on assumptions from the theory of evolution, according to which life began as a simple reproducing system that gradually developed into the life forms we see today. This system (or systems, if life developed multiple times) must have been very simple, because it had to originate without the benefit of evolution. In particular, it could only have had one or a very small number of proteins. From these few proteins, those in current life forms must have evolved. Each protein is produced by one (or possibly several) genes. The evolution of new proteins must have occurred by mutations to these genes. Since genetic mechanisms in current life forms are strikingly uniform, with a few modifications, it is reasonable to assume that these mechanisms have been in operation for hundreds of millions or billions of years, in the accepted evolutionary scenario. Thus the evolution of many proteins from a few must have occurred by genetic mechanisms that are still in existence. Even if special mechanisms operated in the evolution of one-celled creatures, there are undoubtedly many proteins and shapes of proteins that only appear in multicellular organisms, and these must have evolved from others by currently existing genetic mechanisms. Furthermore, because all known one-celled organisms have similar genetic mechanisms, it is reasonable to assume that these mechanisms were operating for a considerable portion of the time that these one-celled organisms evolved from simpler organisms having many fewer proteins. During this time, proteins having new shapes must have appeared. Each protein is composed of a sequence of amino acids that join together and are then called "residues." The "side chains" of the residues determine their chemical properties. These side chains are joined together by the "backbone" of the protein. Some side chains are hydrophobic (oily) and tend to cluster together inside the protein. Others are hydrophilic (water loving) and tend to occur on the outside of the protein. Some proteins function in a hydrophobic environment, such as the cell membrane; these may have more hydrophobic residues on the outside. A given shape of a protein will tend to be associated with a particular sequence of hydrophobic and non-hydrophobic side chains. Changing the shape of the protein requires changing this sequence of side chains. Even if the shape of the protein is not changed, having too many hydrophobic side chains on the outside can cause proteins to stick together, interfering with their function, as happens in sickle cell anemia. This is caused by a single mutation replacing a hydrophilic side chain on the outside of hemoglobin with a hydrophobic side chain. A protein can be in a folded or unfolded state, and if it is folded, it may fold into a variety of structures. The unfolded state is more flexible and less dense. In order to have a function in an organism, a protein must fold, and it must fold the same way sufficiently often. This means that the wild type fold (the one found in nature) must be significantly more stable than other possible folds. If the protein is modified, it may fold into a different structure, or simply not fold at all. Proteins have "active sites" where they can interact with other proteins or other substances. The geometry and composition of these sites is very highly constrained, because in order for two proteins to interact, their active sites have to match very closely in their geometry and chemical properties. A problem with the evolution of proteins having new shapes is that proteins are highly constrained, and producing a functional protein from a functional protein having a significantly different shape would typically require many mutations of the gene producing the protein. All the proteins produced during this transition would not be functional, that is, they would not be beneficial to the organism, or possibly they would still have their original function but not confer any advantage to the organism. It turns out that this scenario has severe mathematical problems that call the theory of evolution into question. Unless these problems can be overcome, the theory of evolution is in trouble.

In science's pecking order, evolutionary biology lurks somewhere near the bottom, far closer to phrenology than to physics.

Sal quote-mined thusly:

In particular, the evolution of proteins having significantly different shapes (tertiary structures) than previously existing proteins appears to be impossible.

Um...isn't Mad Cow Disease caused by a certain protein changing its shape, and thus its properties and function? So much for "appears to be impossible," eh?

Sal, honey, you got some 'splainin to do.
Specifically, justify or retract your truly idiotic assertion that evolution is a worthless theory.
Do please be sure to take into account the billions of dollars it has earned the biopharmaceutical industries.

hugs,
Shirley Knott

Raging Bee said: Sal quote-mined thusly: In particular, the evolution of proteins having significantly different shapes (tertiary structures) than previously existing proteins appears to be impossible. Um...isn't Mad Cow Disease caused by a certain protein changing its shape, and thus its properties and function? So much for "appears to be impossible," eh?

Summary: For the first time, an artificial prion, or misfolded protein, has been created that can, by itself, produce a deadly infectious disease in mice. This is thought to occur in mad cow disease. This research, if corroborated, would provide strong evidence for the protein-only hypothesis, the controversial concept that a protein alone, without the help of DNA or RNA, can cause infectious disease.

Sal: you quoted a statement that proteins can't change their shapes significantly. Mad Cow proves that statement wrong -- the protein in question changed its shape significantly. And if such a thing can happen, it can happen with bad or good results. The credibility of the arguments you quote is therefore somewhat...diminished. And your insulting phony bravado only proves your insecurity, which is a result of knowing you're in over your head and have no clue what you're talking about.

The paper Sal quotes has this telling little howler:

The biologists' argument is hard to refute in a formal way.

The "formal way" of refuting an argument is with facts, logic, research, testable hypotheses, and/or repeatable experiments. And, because they can't refute evolution in a "formal way," creationists are, often by their own admission, resorting to less "formal" ways -- i.e., no facts, no logic, no testable hypotheses, no repeatable experiments, and no peer-reviewed papers anywhere.

The fact that the paper Sal quotes contains certain old -- and discredited -- objections to evolution, and pretends they're not "really" discredited, because they "sound convincing," but are just "hard to formalize," only shows the author's dishonesty.

Dear IDers reading this thread,

I should point out some comments regarding IC which our fearless leader, Casey Luskin pointed out:

Do Car Engines Run on Lugnuts? A Response to Ken Miller & Judge Jones's Straw Tests of Irreducible Complexity for the Bacterial Flagellum (Part I)

and

Do Car Engines Run on Lugnuts? A Response to Ken Miller & Judge Jones's Straw Tests of Irreducible Complexity for the Bacterial Flagellum (Continued--Part II)

I suggest the reader look at figure C in Part 2. Apt description for Ken Miller's ideas:

Figure C in part 2

Ken Miller like many PTers is pathologically persisten in making an argument with logical fallacies like the "Strawman Argument". There is even a guidebook on how to formulate such arguments, and Miller and friends would provide excellent illustrations for the guid book. The guide book can be found here:

The Swamp Battle Tactic Manual

Just remember evolution's place in the pecking order is right down there near the bottom, not at the top, and that will give you better perspective in defending this worthless theory.

Raging Bee: you quoted a statement that proteins can't change their shapes significantly. Mad Cow proves that statement wrong

Has any intelligent designer ever been shown to produce designs that are like the forms and "machines" that we find in organisms?

... A problem with the evolution of proteins having new shapes is that proteins are highly constrained, and producing a functional protein from a functional protein having a significantly different shape would typically require many mutations of the gene producing the protein. All the proteins produced during this transition would not be functional, that is, they would not be beneficial to the organism, or possibly they would still have their original function but not confer any advantage to the organism. It turns out that this scenario has severe mathematical problems that call the theory of evolution into question. Unless these problems can be overcome, the theory of evolution is in trouble.

Here is something to consider with Protein Evolution, though I do not concur with sweeping statements that there are no protein-to-protein intermediates, the few "intermediates" are sketchy and one wonders if any real intermediates really exited. That is my only obejction to the paper. This then poses a serious problem for evolution as the multi-component parts of a protein can be part of an IC barrier to Darwinian evolution: Problems in Protein Evolution

— Salvador Cordova

Pvm said: So what have you done lately Lenny to help ID activists understand either the follies of their ideas or help them understand better evolutionary theory. .... Shape up or become part of the bathroom plaster...

Your use of "change of shape" is not the same as Plaisted.

This is how Noam Chomsky and his fawning fans respond whenever he's caught lying: by insisting he actually meant something different from the statement his critics have just debunked or disproven.

It's also a standard ID/creationist dodge: the ID argument that just got smacked down wasn't the "real" "theory" of ID; and every refutation of ID only proves that ID is so, so horribly misunderstood.

I would say in defense of my friend (choke) Lenny Flank, that people like him give PT it's distinctive character. He is someone that PT should uphold as an example of what PT is all about.

— Sal

Sal,

Once again, you are not answering my question about where I can find all of the experimental studies and actual science ID is performing.

Can you expect to be a science if you either refuse to do such work or hide it from everyone? Where do I find this?

More on Plaisted's argument - i.e. calculate that something couldn't have happened, ergo it didn't happen and blissfully ignore it!

First let us use an estimate of how many "shapes" proteins have:

"Protein Eng. 1998 Aug;11(8):621-6. A re-estimation for the total numbers of protein folds and superfamilies.

Wang ZX.

National Laboratory of Biomacromolecules, Institute of Biophysics, Academia Sinica, Beijing, Peoples Republic of China.

The issue of the number of protein folds is steeped in controversy despite its significance for understanding evolution and predicting protein structure from amino acid sequence. Using various assumptions, several research groups have tackled this problem with very different results. In the present study, a more rigorous statistical approach is used to address this question. From three different data sets, the total number of protein folds is estimated to be about 650. A detailed theoretical analysis suggests that (i) a random sample of non-transmembrane protein families has been selected for crystallization and structural determination, (ii) except for about 40 folds, most protein folds occurring in nature contain about the same number of different protein families. With the estimation of the total number of protein folds, the number of naturally occurring superfamilies can then be estimated as 1150."

OK, around a thousand. Based on this, how often does this mean a new fold protein gets made, by some unlikely
occurrence? 4,000,000,000 years by 1000 folds is
one every 4,000,000 years on the whole planet!

Clearly, not getting a new protein fold would not prevent speciation - that occurs much more frequently! There are millions of species today.

Now, I also wonder, are there any differences between
humans and chimps with respect to some new protein fold?
Maybe Salvador and Plaisted would accept that amount
of microevolution?

Finally, I would like to probe Salvador's understanding of what is meant by "protein shape", and how proteins evolve. Go to the web page http://www.unc.edu/~traut/EnzymeEvolution.htm and read part A about protein evolution being modular (hint: did Plaisted calculate the probability of new "shapes" using this mechanism?). What the hell, I'll paste it here:

"A. Modules are structural and ligand-binding units

Several separate lines of data support a hypothesis that modules are small units of local structure, most commonly involved in binding specific ligands.

1. The subunit mass for many enzymes, when divided by the number of identified ligand-binding functions has a distribution around 4 - 7 kDa.

2. For the great majority of exons, the amount of polypetide coded has a distribution around 4 - 7 kDa.

3. The same modular elements are commonly used in many different proteins to form a specific type of ligand-binding site, as for ATP (next section).

The above support a hypothesis that exons code for small functional units of protein structure. Since exons may be shuffled within and between genes, both singly and in combinations, this leads to a model for protein evolution where established functional units may be used in completely novel protein environments by natural recombination and selection.

Our work has supported the above by compiling and analyzing relevant data sets for genes and for proteins."

Wamba: If proteins are so highly constrained, how is it that two versions of a protein can differ in hteor specific sequence at over 80% of their positions, and still share the same overall fold and the same function?

Taken as a whole, recent findings from biochemistry and evolutionary biology indicate that our understandingof protein evolution is incomplete, if not fundamentally flawed.

In addition to functional properties, proteins have a wide range of biophysical characteristics, such as stability, propensity for aggregation and rate of degradation. These properties are at least as important as function for cellular and organismal fitness. Proteins tolerate only narrow ranges of stability, aggregation propensity and degradation rate. Many individual missense mutations perturb these traits by amounts that are on the same order as the permissible range of values, and are consequently common causes of human genetic disease. The narrow range of tolerance of deviations from optimum characteristics and the significant effects of mutations give rise to a substantial degree of epistasis for fitness. Moreover, mutations simultaneously affect function, stability, aggregation and degradation. For these reasons, mutations might be selectively beneficial on some genetic backgrounds and deleterious on others. Mutations that change function often do so at the cost of protein stability and aggregation. Compensatory mutations therefore function by relieving the biophysical strain that is introduced by adaptive mutations.

Wamba: If proteins are so highly constrained, how is it that two versions of a protein can differ in hteor specific sequence at over 80% of their positions, and still share the same overall fold and the same function?

— Salvador T. Cordova

If the average protein has 366 positions (per PZ Myers), 20% implies 73 positions are constraining. A very crude approximation is 1 in 20^73 in terms of that constraint alone. That is substantial.

What about frame shift mutations? Are you saying that a gene for a protein could not undergo a frameshift mutation, resulting in something substantially different? If you need an example, how about those nylon-digesting proteins?

— wamba

blah blah blah

— Salvador T. Cordova

Hey Sal:

All you've done this entire time is attack evolution (quite poorly I might add). You have not produced one bit of scientific evidence that supports ID (or for that matter scientific evidence that refutes ToE). I for one would be interested in seeing ID "theory" stand on its own. If ID is truly superior to "Darwinism" then produce some research that shows that its a better explanation of observed phenomenon. You can try and refute evolution all you want, but it remains useful to Biologists, while ID apparently has no value whatever. If ID can be shown to be more useful in coming up with novel solutions to biological problems; Evolution will become less prominent. Get to work doing some useful ID research Sal, because disproving Evolution in no way proves your ID creationism true.

If the average protein has 366 positions (per PZ Myers), 20% implies 73 positions are constraining. A very crude approximation is 1 in 20^73 in terms of that constraint alone. That is substantial. Further it may be true that in a protein like cytochrom-c that 70 of the 105 or so positions are "unconserved". That is we find 70 of the positions have variations across species. It does not mean automatically however that these 70 positions can willy nilly be altered and the organism survive. There is a chance neutral theory is wrong in that regard, and that the organisms need to have the protein in that configuration.

That kind of makes your computer password example, where you're looking for a single solution, look pretty retarded.

That means 70^3 different sequences

PVM asks: So what have you done lately Lenny to help ID activists understand either the follies of their ideas or help them understand better evolutionary theory. Lenny Responds: Nothing. It is quite pointless. In my 20-plus years of anti-creationist organizing, I can count on the fingers of one hand the total number of ID/creationists I have seen actually "understand the folly of their ideas".

Wamba wrote: Oops, I think that should be 3^70, which still gives a number >> 1.

So what have you done lately Lenny to help ID activists understand either the follies of their ideas or help them understand better evolutionary theory.....

The patrons gather to [1] discuss evolutionary theory, [2] critique the claims of the antievolution movement, [3] defend the integrity of both science and science education, and [4] share good conversation.

In my 20-plus years of anti-creationist organizing, I can count on the fingers of one hand the total number of ID/creationists I have seen actually "understand the folly of their ideas".

to help ID activists understand either the follies of their ideas or help them understand better* evolutionary theory,

Hey Sal, since you're so talkative now and all, perhaps you'd like to take a crack at some simple questions for me?

*ahem*

What, precisely, about "evolution" is any more "materialistic" than weather forecasting, accident investigation, or medicine?

What did the designer do, specifically. What mechanisms did it use to do whatever the heck you think it did. Where can we see it using these mechanisms today to do . . . well . . . anything.

I can't think of any scientific advance made in any area of science at any time in the past 25 years as the result of ID "research". Why is that?

Hey Sal, why is it that all of DI's funding comes from fundamentalist Christian political groups and Reconstructionist nutjobs?

You once said to me: "We do not see the Designer of life in opreation today as far as I know".

Why not, Sal? Did it climb back aboard its flying saucer and go home?

But this is also a multi-faceted battle with many fronts. We each bring something unique to the discussion, political, legislative, scientific, and educational backgrounds are all needed to combat the growing misperceptions about evolutionary theory and science in general.

Not to mention that, for whatever it's worth, no Lenny would mean no, uh, ME.

Well, I mean, I'd still be here, but I wouldn't be here...

And, don't forget, in another week or so, I won't be here, but PIZZA WOMAN will be!

no Lenny would mean no, uh, ME.

http://goodmath.blogspot.com/

Sal, check out that link. That guy's been wailing on Dembski lately. And that guy's a computer scientist with a hankerin for math, so he'll understand all those complicated things the poor dumb biologists don't. I bet you two will have amus--uh interesting...conversations.

Wamba wrote: Oops, I think that should be 3^70, which still gives a number >> 1.

— Salvador T. Cordova

3^70 out of how many sequences though? 3^70 / 20^70 = 1 out of 4.72 * 10^57 which is remote and that's on top of the 35 positions that are likely immutable (20-35 is are the numbers i've seen in literature). Oh, but I know, wamba can just refudge numbers to make it more palatable. Well done. NOTE: I acknowledge up front that 20^X is a crude approximation, a better one is obtained by including considerations for synonymous codons. But the general point of improbability remains.

geez Sal trapped in a corner and what do you do ?
Quite unseemly on your part don't you think?
Sh*t or get off the pot.

Answer Lenny's questions

And here are 2 more, how old is the earth 4.5Billion years or some wanky number dreamt up by a crackpot ?
Also do you accept Humans and Chimps have a common ancestor ?

Time to change hands Sal.

3^70 out of how many sequences though? 3^70 / 20^70 = 1 out of 4.72 * 10^57 which is remote and that's on top of the 35 positions that are likely immutable (20-35 is are the numbers i've seen in literature). Oh, but I know, wamba can just refudge numbers to make it more palatable. Well done.(emphasis mine) NOTE: I acknowledge up front that 20^X is a crude approximation, a better one is obtained by including considerations for synonymous codons. But the general point of improbability remains.

When we stated the single law of chance, "events whose probability is sufficiently small never occur," we did not conceal the lack of precision of the statement.

In conclusion, I feel it is necessary to say a few words regarding a question that does not really come within the scope of this book, but that certain readers might nevertheless reproach me for having entirely neglected. I mean the problem of the appearance of life on our planet (and eventually on other planets in the universe) and the probability that this appearance may have been due to chance. If this problem seems to me to lie outside our subject, this is because the probability in question is too complex for us to be able to calculate its order of magnitude. (emphasis mine). It is on this point that I wish to make several explanatory comments. When we calculated the probability of reproducing by mere chance a work of literature, in one or more volumes, we certainly observed that, if this work was printed, it must have emanated from a human brain. Now the complexity of that brain must therefore have been even richer than the particular work to which it gave birth. Is it not possible to infer that the probability that this brain may have been produced by the blind forces of chance is even slighter than the probability of the typewriting miracle? It is obviously the same as if we asked ourselves whether we could know if it was possible actually to create a human being by combining at random a certain number of simple bodies. But this is not the way that the problem of the origin of life presents itself: it is generally held that living beings are the result of a slow process of evolution, beginning with elementary organisms, and that this process of evolution involves certain properties of living matter that prevent us from asserting that the process was accomplished in accordance with the laws of chance. (emphasis mine) Moreover, certain of these properties of living matter also belong to inanimate matter, when it takes certain forms, such as that of crystals. It does not seem possible to apply the laws of probability calculus to the phenomenon of the formation of a crystal in a more or less supersaturated solution. At least, it would not be possible to treat this as a problem of probability without taking account of certain properties of matter, properties that facilitate the formation of crystals and that we are certainly obliged to verify. We ought, it seems to me, to consider it likely that the formation of elementary living organisms, and the evolution of those organisms, are also governed by elementary properties of matter that we do not understand perfectly but whose existence we ought nevertheless admit. (emphasis mine) Similar observations could be made regarding possible attempts to apply the probability calculus to cosmological problems. In this field, too, it does not seem that the conclusions we have could really be of great assistance.

Salvador T. Cordova Said... LOL! Just like a Darwinist to appeal to Mad Cow disease prions as a selective improvement.

We're talking about evolvability of an extant functional protein, not random assembly of such a protein from scratch.

— Someone schooling Sal

I agree, registered user, it will be quite a task for Sal or anyone else to address let alone rebut the reverse ordination refutation.

Sal, just Google "reverse ordination refutation" and follow the link. It's very straightforward.

Sal, uh, doesn't do research.

He just brainlessly parrots whatever the Isaac Newton of Information Theory tells him.

Sal, just Google "reverse ordination refutation" and follow the link. It's very straightforward.

— Anton Mates

Seriously Sal you are trying to refute the vacuity of ID and you don't know what the reverse ordination refutation is?

Just admit it you do not have a clue.

Then of course there is the ridiculous stochastic heuristic fallacy that Heddle, Dembski and Berlinski all fall into.

As though numbers had thoughts or preconceived notions of their own existence.

Sal do Chimpanzees have a common ancestor with humans?

And how old is the earth?

For everyone around here you will note Sal is a very desperate religious apologist and has difficulty answering even the simplest questions

True. It leads directly to this thread.

— Rilke's Granddaughter

Don wrote: Someone schooling Sal wrote: We're talking about evolvability of an extant functional protein, not random assembly of such a protein from scratch.

Duplicate the gene which codes the protein and mutate it and perhaps by chance the gene gets later activated (for no good reason except to rescue a failed theory) and then we hope some function evolves which can fix it in the population. Yeah, nothing like a just so story.

— Sal

Wow, that was fast. Sal's attempts at mathematically supporting his claims vanished like fairy gold at sunrise.

Ah Sal DarLogic ?
Performing science again without science ?
Sal performs The Group attribution error
or succumbs to the the False consensus effect

These guys here have quite a collection
http://www.absoluteastronomy.com/reference/list_of_cognitive_biases

A model for the evolution of insulin mainly in terms of adaptive processes is discussed. The model depends critically on the relationship of sequence changes to the three-dimensional structure and the role of various parts of this structure in the conversion of the proinsulin molecule to the active form, the storage of insulin, its transport to the site of action and its interaction with a receptor.

The regulation of a gene depends on the binding of transcription factors to specific sites located in the regulatory region of the gene. The generation of these binding sites and of cooperativity between them are essential building blocks in the evolution of complex regulatory networks. We study a theoretical model for the sequence evolution of binding sites by point mutations. The approach is based on biophysical models for the binding of transcription factors to DNA. Hence we derive empirically grounded fitness landscapes, which enter a population genetics model including mutations, genetic drift, and selection. RESULTS: We show that the selection for factor binding generically leads to specific correlations between nucleotide frequencies at different positions of a binding site. We demonstrate the possibility of rapid adaptive evolution generating a new binding site for a given transcription factor by point mutations. The evolutionary time required is estimated in terms of the neutral (background) mutation rate, the selection coefficient, and the effective population size. CONCLUSIONS: The efficiency of binding site formation is seen to depend on two joint conditions: the binding site motif must be short enough and the promoter region must be long enough. These constraints on promoter architecture are indeed seen in eukaryotic systems. Furthermore, we analyse the adaptive evolution of genetic switches and of signal integration through binding cooperativity between different sites. Experimental tests of this picture involving the statistics of polymorphisms and phylogenies of sites are discussed.

I present here a personal perspective on more than three decades of research into the structural biology of the insulin-receptor interaction. The solution of the three-dimensional structure of insulin in 1969 provided a detailed understanding of the insulin surfaces involved in self-assembly. In subsequent years, hundreds of insulin analogues were prepared by insulin chemists and molecular biologists, with the goal of relating the structure to the biological function of the molecule. The design of methods for direct receptor-binding studies in the 1970s, and the cloning of the receptor in the mid 1980s, provided the required tools for detailed structure-function studies. In the absence of a full three-dimensional structure of the insulin-receptor complex, I attempt to assemble the existing pieces of the puzzle generated by our and other laboratories, in order to generate a plausible mechanistic model of the insulin-receptor interaction that explains its kinetics and negative cooperativity. Copyright 2004 Wiley Periodicals, Inc.

The recent characterization of diverse vertebrate genomes has revealed the importance of gene duplication in vertebrate evolution. Evidence suggests that a genome duplication event occurred on the lineage leading to teleost fish-species that are often used to understand human biology. The existence of a genome duplication event complicates the use of fish as a model for human diseases as there are often two fish homologues for a single copy human gene. Often the second homologue has not been recognized. Our searches of the near complete zebrafish and fugu fish genomes indicate that both species have two insulin genes. Phylogenetic analysis indicates that the two genes are likely the product of the fish-specific genome duplication. The maintenance of two insulin genes within the fish suggests that the two genes have different functions. Thus the well-characterized insulin genes in some fish species may not be complete homologues of the human insulin gene.

All vertebrates possess anatomical features not seen in their closest living relatives, the protochordates (tunicates and amphioxus). Some of these features depend on developmental processes or cellular behaviours that are again unique to vertebrates. We are interested in the genetic changes that may have permitted the origin of these innovations. Gene duplication, followed by functional divergence of new genes, may be one class of mutation that permits major evolutionary change. Here we examine the hypothesis that gene duplication events occurred close to the origin and early radiation of the vertebrates. Genome size comparisons are compatible with the occurrence of duplications close to vertebrate origins; more precise insight comes from cloning and phylogenetic analysis of gene families from amphioxus, tunicates and vertebrates. Comparisons of Hox gene clusters, other homeobox gene families, Wnt genes and insulin-related genes all indicate that there was a major phase of gene duplication close to vertebrate origins, after divergence from the amphioxus lineage; we suggest there was probably a second phase of duplication close to jawed vertebrate origins. From amphioxus and vertebrate homeobox gene expression patterns, we suggest that there are multiple routes by which new genes arising from gene duplication acquire new functions and permit the evolution of developmental innovations.

In addition to the two complete genome duplication events, our results showed that subsequent local duplications, rearrangements, and gene losses corroded the regions in question. This corrosion might eventually disguise the paralogous patterns. For example, an analysis of regions flanking the INSL3 and RLN3 genes on human chromosome 19p revealed that additional duplication, together with rearrangements, contributed to the formation process. This duplication took place before the bony fishes diverged from the main vertebrate branch and, of course, after the suggested tetraploidization events. This finding provides support for the 2R hypothesis as compatible with duplications occurring either before or after the proposed genome duplications

Studies on the evolutionary pathway of the insulin gene family suggest that insulin and insulin-like growth factor (IGF) became distinct molecules only after the vertebrates arose. A single molecule with identity to both insulin and IGF was reported in amphioxus. To study the origin of insulin, we selected tunicates because their ancestors are thought to be a nodal point in the evolution of vertebrates. This is the first report of separate insulin and IGF molecules from invertebrates. Two cDNAs were isolated from the tunicate Chelyosoma productum: One cDNA encodes a distinct preproinsulin with B, C, and A domains, whereas the other encodes tunicate preproIGF, including all five domains in their proper sequence. Both mRNAs are expressed in the nervous system, digestive tract, heart, and possibly the gonad but not in branchial basket or tunic. Hence, insulin and igf genes have similar expression patterns. In situ methods confirm the polymerase chain reaction evidence that tunicate insulin and igf mRNAs are expressed in cortical cells of the neural ganglion. We conclude that insulin and IGF have maintained separate gene lineages in both vertebrate and protochordate evolution and, thus, a distinct evolutionary history of more than 600 million years.

Hi there, long-time listener, first-time caller.

Sal Says : "Evolvability from existing proteins? Haha... What happens? Change a few amino acids, oops, cripes the organism is dead. Kinda hard to evolve a dead creature...Did it ever occur to you guys that starting from scratch is actually a less laughable scenario than trying to evolve an existing protein to a radically different one? DarLogic at it's finest."

Since Mr. van Meurs has already shown you some interesting sights in the world of insulin evolution, I thought I might point out some other ,older faves. Here's an oldie but goodie, Sal-baby, you wack-a-doo krazy kreashunist kat:
http://www.pnas.org/cgi/content/full/94/8/3485 Chen et al. demonstrate that an Antifreeze Glycoprotein (AFGP)gene from the Antarctic notothenioid Dissostichus mawsoni derives from a gene encoding a pancreatic trypsinogen. There are now known at least four types of fish AFPs (antifreeze proteins) , all apparently unrelated to each other (AFPs types I, II, III, and AFGP). In the case of "type II" AFP's, they are found in at least three fish: Atlantic herring , smelt , and sea ravens. These AFP's arose from C-type lectin genes. (Eek! More ...evilushuns!!!)

I found this interesting , not only because of the evolutionary implications, but also because protease proenzymes (zymogens) like trypsinogen act as autocatalytic systems in organisms like me and you, Sal: Trypsinogen enters the small intestine, and gets a peptide bond cloven and breaks down into trypsin. Trypsin itself then cleaves lysine peptide bonds, and so, once a small amount of trypsin is generated, it participates in cleavage of its own zymogen, generating -- more trypsin! Fascinating, eh, Sal?

Sal, really, now. Do you ever read anything other than Chick tracts? The literature is replete with such examples, as even a cursory search by a non-biologist like me shows. Get your bleedin' head out of your bleedin' bum and let your bloody brains breathe, Sal. Oh, and have a *NICE* day.

P.S. Would you view this as "large-scale" cooption? I mean...gosh, it kept the li'l fishies alive and all.

Hi there, Long-time listener, first-time caller.

Sal Says : "Evolvability from existing proteins? Haha... What happens? Change a few amino acids, oops, cripes the organism is dead. Kinda hard to evolve a dead creature...Did it ever occur to you guys that starting from scratch is actually a less laughable scenario than trying to evolve an existing protein to a radically different one? DarLogic at it's finest."

Since Mr. van Meurs has already shown you some interesting sights in the world of insulin evolution, I thought I might point out some other ,older faves. Here's an oldie but goodie, Sal-baby, you wack-a-doo krazy kreashunist kat: http://www.pnas.org/cgi/content/full/94/8/3485

Chen et al. demonstrate that an Antifreeze Glycoprotein (AFGP) gene from the Antarctic notothenioid Dissostichus mawsoni derives from a gene encoding a pancreatic trypsinogen. There are now known at least four types of fish AFPs (antifreeze proteins) , all apparently unrelated to each other (AFPs types I, II, III, and AFGP). In the case of "type II" AFP's, they are found in at least three fish: Atlantic herring , smelt , and sea ravens. These AFP's arose from C-type lectin genes. (Eek! More ...evilushuns!!!)

I found this interesting , not only because of the evolutionary implications, but also because protease zymogens like trypsinogen act as autocatalytic systems in organisms like me and you, Sal: Trypsinogen enters the small intestine, and gets a peptide bond cloven and breaks down into trypsin. Trypsin itself then cleaves lysine peptide bonds, and so, once a small amount of trypsin is generated, it participates in cleavage of its own zymogen, generating -- more trypsin! Fascinating, eh, Sal?

Sal, really, now. Do you ever read anything other than Chick tracts? The literature is replete with such examples, as even a cursory search by a non-biologist like me shows. Get your bleedin' head out of your bleedin' bum and let your bloody brains breathe, Sal. P.S. Would you view this as an example of cooption? I mean, gosh , it kept the li'l fishies alive and all.

Hey Sal, if ID is science, then why does it get all its funding from fundamentalist Christian political groups and Reconstructionist wackos?

Thanks in advance for not answering my simple question.

We're talking about evolvability of an extant functional protein, not random assembly of such a protein from scratch.

— me

Sigh ... Sal made THAT false assumption again?

Pvm cited in favor of gene duplication: And an oldie Holland PW, Garcia-Fernandez J, Williams NA, Sidow A. Gene duplications and the origins of vertebrate development. Dev Suppl. 1994;:125-33.

Pvm cited in favor of gene duplication: And an oldie Holland PW, Garcia-Fernandez J, Williams NA, Sidow A. Gene duplications and the origins of vertebrate development. Dev Suppl. 1994;:125-33.

— Sal

PvM, These articles assume the very thing they wish to prove. We call that circular reasoning. I'm afrraid your offerings only prove that Darwinists think circular reasoning is a valid mode of deduction. Salvador

These articles assume the very thing they wish to prove.
No, they don't.
Do you ever get tired of saying the same things over and over? I swear Sal, if Nature hadn't published that goofy picture of you, I'd take even odds that you did not in fact exist, and were a cut-rate chat-bot.

As it is, I'll still take it at 3:1.

Perhaps Sal can start by explaining what in these papers is circular and how such circularity affects the scientific nature.

In summary, our data indicate that recruitment of CRYZ by the lens was not the result of neutral evolution but rather derives from a selective mechanism. We would further suggest that a primary factor underlying this selective pressure may be the marked elevation in reduced pyridine nucleotides that occurs in the lens as a result of high CRYZ expression. As has been shown previously, lenses with relatively low levels of reduced pyridine nucleotides appear to be more susceptible to UV radiationinduced oxidative damage than do lenses containing high concentrations of pyridine nucleotides (C. Rao and Zigler 1992). While the molecular mechanism of enzyme/ crystallin recruitment may vary, the fact that the large majority of recruited proteins bind pyridine nucleotides may be of paramount importance. We believe that greater consideration should be given to the possibility that enzyme/crystallin recruitment is, in general, an adaptive process and that enzyme/crystallins may provide specific benefits to the lens. Evidence for Independent Recruitment of &-crystallin/Quinone Reductase (CRYZ) as a Crystallin in Camelids and Hystricomorph Rodents Pedro Gonzalez, P. Vasantha Rae, Susan B. Nun"ez,-t_a nd J. Samuel Zigler, Jr. Mol. Biol. Evol. 12(5):773-781. 1995 .

As has been suggested for other cases (1, 2), the primary selective pressure for this gene recruitment may have been the modification of the optical properties of the lens in an ancestor of elephant shrews, "diluting" the specialized g-crystallins, to help make a softer accommodating lens. Other benefits may have been protection against the toxic effects of aldehydes resulting from light-induced oxidation of lens components, or generalized anti-oxidant and UV-filtering effects though sequestration of NAD(H) or retinoids in the lens (1, 28, 43, 44). While there may have been selective advantages for the recruitment of ALDH1/h-crystallin in lens, there is no clear advantage to its collateral recruitment as the major ALDH1 expressed in other parts of the eye A Retinaldehyde Dehydrogenase as a Structural Protein in a Mammalian Eye Lens GENE RECRUITMENT OF h-CRYSTALLIN Caroline Graham, Jason Hodin, and Graeme Wistow Journal of Biological Chemistry Vol. 271, No. 26, Issue of June 28, pp. 15623---15628, 1996.

Sal says: " These articles assume the very thing they wish to prove. We call that circular reasoning. I'm afrraid your offerings only prove that Darwinists think circular reasoning is a valid mode of deduction."

Well, let's look at the number of fallacies explicit or implicit in those two sentences , Sal-baby.

You mention one citation by PvM, then say "These articles" as if you adressed each example presented to you. You fail to show that even the one article you name contains circular reasoning. By implication, since you use the collective "these," you are falsely implying that all PvM's examples are invalid, but you haven't shown that.

You leap from these fallacious claims to yet another one: That your assertion alone ( without evidence ) of "circularity" enables you to say you have "proven" something...when you have not shown anything at all. You then move from PVM to "Darwinists", indicting a whole range of people without showing you have a basis for that indictment.

Now stand back and look at the collection of fallacies you used, Sal. To what purpose did you use them? Answer: To show that "Darwinists" argue illogically and ivalidly.

I count at least 5 distinct fallacies in two measly sentences comprising 32 words. And you never *really* address the actual articles cited -- you wave your hands and hope they go away?

I forgot to add: after you've substantively addressed Mr. van Meurs' articles, you may address the one I cited. Please do so. (Oh, and in the previous post, it should be "invalidly")

I'm afrraid your offerings only prove that Darwinists think circular reasoning is a valid mode of deduction.

Perhaps Sal can start by explaining what in these papers is circular and how such circularity affects the scientific nature.

Sal, your audience is awaiting your presentation of data to support your claims. Or will ID remain scientifically vacuous yet once again?
Don't worry, we have the patience... 10 years and more and counting....

only 10 years PvM
why not give them until the second coming?
2000 years plus whatever billions of years until its lights out for the universe of circular reasoning is sure to produce something?

Here is a tip Sal the one true test of circular reasoning is it produces mere words and nothing else useful EXACTLY like creationism.

The reason you (Sal) think that creationism is true and science is false is because you are functionally incapable of determining the truth and the reason for that is you believe a lie (creationism) to be true. The reason that lie is created, by religious cults, is to manipulate its followers for fun and profit.... no other reason,the one tried and true method used by priest's since Adam was a boy.
You have heard of Jim Jones and Scientology and the other cults have you not?
In fact Sal all religions have a cult methodology to inculcate their followers. The way it is done is by manipulating the followers perception of reality, in short form their minds so that the cult determines what is real and what is not by means of social realism otherwise known as cultural engineering...but then you already know that (good christian soldier) Sal, don't you?
You will do whatever HQ says with no questions asked, just like the good little soldier, salute and execute, no thinking required (or asked for in your case) Sal.
If you were able to think you would realize that practically everything the creo's tell you is false about science, happens to be true in the real world.

Sal you not only have no idea what circular reasoning is, along with every other topic you have ever expounded on here at PT, I'm beginning to think you are genuinely stupid, your brains are practically useless for anything except saying yes Mr. Dembski.

Keep down the insults and give Sal at least a chance to reply. Perhaps he may even surprise us.

Keep down the insults and give Sal at least a chance to reply. Perhaps he may even surprise us.

Pvm cited in favor of gene duplication: Holland PW, Garcia-Fernandez J, Williams NA, Sidow A. Gene duplications and the origins of vertebrate development. Dev Suppl. 1994;:125-33. These[sic] articles[sic] assume the very thing they wish to prove. We call that circular reasoning. I'm afrraid your offerings only prove that Darwinists think circular reasoning is a valid mode of deduction.

Today, for those keeping track, is day 3 since Sal was asked to back up this:

Maybe the chatbot software needed an upgrade:
TurboGoalposts v.3:16, now QuoteMine Enhanced!

4 days and counting Sal. What better evidence to show that ID is scientifically vacuous as the silence from Sal...

This is rich from an ID activist. It's ID which calls something complex and thus designed without showing that it matches the complexity criterion. On the other hand real science observes the fact of gene duplications, and understands how such duplications may find various fates. The fact that we find such exquisite examples of for instance hox gene duplications which explain the many 'innovations' in life show that rather than circular reasoning, these findings support an evolutionary paradigm. Sal may object that science is 'circular' in the sense that the data support the theory but that's the power of real science. Sal may doubt that natural selection is sufficient in explaining these data and I would agree, natural selection is one of various mechanisms which can cause variation to become (permanently) part of the genome. As science is uncovering neutral variations are another important contributor, also biology's dark matter of cryptic genetic variation may play a role. Then we have selective sweeps were other alleles can become fixated because of a selective sweep elsewhere. Perhaps Sal's real problem is that he does not appreciate how real science works. After all being a YECer in spite of all the contrary evidence suggests that there may be some deeper issues here. Perhaps Sal can start by explaining what in these papers is circular and how such circularity affects the scientific nature. And finally, Sal can provide us with the ID hypotheses in this area? Let him show how vacuous ID is compared to science.

Circular reasoning? That's something that can happen in attempts at deductive reasoning. But support via evidence is not deductive reasoning, and so "circularity" doesn't apply to it.

Henry

Jason Rosenhouse and I have returned to the topic of Salvador's claims.