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The Edge of Evolution

post #1 of 146
Thread Starter 
Let's face it, this thread was going to happen sooner or later.

Mike Behe's new book The Edge of Evolution is out, and he basically has two points.

1. In the case of malaria, with generation sizes in the trillion trillions, all evolution has done is basically make advantageous changes that are destructive to DNA. Basically making a house safer by breaking the doorlocks.

2. Proteins, in order to bind need multiple bonding sites, and when considering tests done with antibodies, it takes, again, astronomical numbers to randomly produce these sites in matching pairs.

Both of these things he says, prove that evolution is, outside of the sorts of changes that malaria has made, not possible.

To hear the other side of the story, I went over to P.Z. Meyers' website. Very quickly PZ, Stephen Wells, and other very bright people steered my to what I think is the root of the argument. As best as I can tell, it amounts to saying 'it's not impossible' and 'look at the fossil record.'

Meyers suggested this article by Steve Carroll to counter Behe's claim:

http://www.sciencemag.org/cgi/conten.../316/5830/1427

... his two objections are:


Quote:
Behe states correctly that in most species two adaptive mutations occurring instantaneously at two specific sites in one gene are very unlikely and that functional changes in proteins often involve two or more sites. But it is a non sequitur to leap to the conclusion, as Behe does, that such multiple-amino acid replacements therefore can't happen. Multiple replacements can accumulate when each single amino acid replacement affects performance, however slightly, because selection can act on each replacement individually and the changes can be made sequentially.

Behe begrudgingly allows that only "rarely, several mutations can sequentially add to each other to improve an organism's chances of survival." Rarely? This, of course, is the everyday stuff of evolution. Examples of cumulative selection changing multiple sites in evolving proteins include tetrodotoxin resistance in snakes (3), the tuning of color vision in animals (4), cefotaxime antibiotic resistance in bacteria (5), and pyrimethamine resistance in malarial parasites (6)--a notable omission given Behe's extensive discussion of malarial drugresistance.


and...


Quote:
This lack of quantitative thinking underlies a second, fatal blunder resulting from the mistaken assumptions Behe makes about protein interactions. The author has long been concerned about protein complexes and how they could or, rather, could not evolve. He argues that the generation of a single new protein-protein binding site is extremely improbable and that complexes of just three different proteins "are beyond the edge of evolution." But Behe bases his arguments on unfounded requirements for protein interactions. He insists, based on consideration of just one type of protein structure (the combining sites of antibodies), that five or six positions must change at once in order to make a good fit between proteins--and, therefore, good fits are impossible to evolve. An immense body of experimental data directly refutes this claim. There are dozens of well-studied families of cellular proteins (kinases, phosphatases, proteases, adaptor proteins, sumoylation enzymes, etc.) that recognize short linear peptide motifs in which only two or three amino acid residues are critical for functional activity [reviewed in (7-9)]. Thousands of such reversible interactions establish the protein networks that govern cellular physiology.

Very simple calculations indicate how easily such motifs evolve at random. If one assumes an average length of 400 amino acids for proteins and equal abundance of all amino acids, any given two-amino acid motif is likely to occur at random in every protein in a cell. (There are 399 dipeptide motifs in a 400-amino acid protein and 20 20 = 400 possible dipeptide motifs.) Any specific three-amino acid motif will occur once at random in every 20 proteins and any four-amino acid motif will occur once in every 400 proteins. That means that, without any new mutations or natural selection, many sequences that are identical or close matches to many interaction motifs already exist. New motifs can arise readily at random, and any weak interaction can easily evolve, via random mutation and natural selection, to become a strong interaction (9). Furthermore, any pair of interacting proteins can readily recruit a third protein, and so forth, to form larger complexes. Indeed, it has been demonstrated that new protein interactions (10) and protein networks (11) can evolve fairly rapidly and are thus well within the limits of evolution.

I think Carroll is dodging Behe's point. First, he ducks the Behe's probabilities in the first quote, and Behe's observation that all we see in nature are the destructive, avantageous changes. Second, he dodges the point that while there are proteins out there that need only a couple binding sites, in reality there are many proteins that do need the 6 or so sites, and can't 'wait around' to build themselves one-by-one. And if you are evolving from a chimp,or higher organism, we are past evolving in the context of only those simple proteins.


So, where's the beef?

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post #2 of 146
<Vic Reeves>

You wouldddddddnnnnn'tttttt let it lie.............

You could have let it lie but you didn't let it lie.....

</Vic Reeves>
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post #3 of 146
Quote:
Originally Posted by dmz View Post

I think Carroll is dodging Behe's point. First, he ducks the Behe's probabilities in the first quote, and Behe's observation that all we see in nature are the destructive, avantageous changes. Second, he dodges the point that while there are proteins out there that need only a couple binding sites, in reality there are many proteins that do need the 6 or so sites, and can't 'wait around' to build themselves one-by-one. And if you are evolving from a chimp,or higher organism, we are past evolving in the context of only those simple proteins.


So, where's the beef?

Probabilities? Do you know anything about how antibodies are evolved in vivo? If it takes astronomical numbers of b-cells and it occurs, then by god, then there must be astronomical numbers of b-cells produced because it happens. Or is Behe actually arguing that a deity sits around and whenever someone gets an infection makes a whole bunch of b-cells that are really crappy and some that are ok?

What protein needs 6 binding sites?

There are proteins that have multiple binding sites, certainly. But what organism NEEDS that protein to have all six?

Basically, the problem with Behe's argument (and something you have never quite gotten) is that he is too too focused on the individual interactions of the smallest components when what evolves is the entire organism (or group of individuals). There is redundancy that is the playground of evolution, without it, evolution cannot have occurred. Lack of current redundancy, however, is only an indication that it was lost at some point in the past. It is fundamentally impossible then to argue Behe's point in diploid organisms; since every organism more complex than yeast can only function with its genome duplicated (in other words, there is built in redundancy). Oops. I guess it isn't so easy to see the forest through the limited force fit myopic vision Behe and colleagues apply... Ultimately, dmz, you also haven't understood that the proteins in our genome aren't any more complex (in a real sense) than those of e. coli, there are functional equivalents at almost all levels. Again, and I have said this before, what makes humans different than chimpanzees are a few critical mutations that enormously change the REGULATION of genes. The phenotypic effect of a single mutations can be profound.

------------------------------------End of thread---------------------------------
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post #4 of 146
Thread Starter 
Quote:
Originally Posted by hardeeharhar View Post

...
Basically, the problem with Behe's argument (and something you have never quite gotten) is that he is too too focused on the individual interactions of the smallest components when what evolves is the entire organism (or group of individuals). ../

But how could you evolve the entire system if those small parts don't get on board?

In the case of HIV and malaria and E. Coli -- from ten trillion in E. Coli experiments to the 10^20 organisms in both HIV and malaria -- not a single cellular protein-protein binding site has been created. Only one in humans with sickle -- and again, it's damage.


What PZ and the others are pointing to is strictly in the realm of untested theory. But when the chips are down, when we actually can observe evolution in process, with the numbers to make it relevant, there is nothing -- broken doorlocks, that sort of thing.


Edit: I made it sound like the 'binding sites' were 6 per single protein, rather than per the chain, that's a screwup on my part.

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and in that lies not liberation but alienation, the cutting off from things as they really are. --...

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post #5 of 146
dmz.

Budding molecular biologist in his downtime.
post #6 of 146
Quote:
Originally Posted by dmz View Post

But how could you evolve the entire system if those small parts don't get on board?

In the case of HIV and malaria and E. Coli -- from ten trillion in E. Coli experiments to the 10^20 organisms in both HIV and malaria -- not a single cellular protein-protein binding site has been created. Only one in humans with sickle -- and again, it's damage.


What PZ and the others are pointing to is strictly in the realm of untested theory. But when the chips are down, when we actually can observe evolution in process, with the numbers to make it relevant, there is nothing -- broken doorlocks, that sort of thing.


Edit: I made it sound like the 'binding sites' were 6 per single protein, rather than per the chain, that's a screwup on my part.

What are you talking about?

You don't actually understand the scientific jargon you are using...

I really want to understand you confusion, and teach you something... What do you mean by binding site? What do you mean by none has been created? What do you mean by numbers and how exactly do you think these numbers are being calculated?

No protein binding sites have been created? What does that mean? Other than being obviously false (since things aren't created, at least outside of the laboratory they aren't -- my lab has 'created' protein binding sites, so what?: i am aware of several other labs that have used all natural techniques to evolve protein binding sites -- they confered the selective pressure themselves)...

In respect to parts needed before the whole... If you don't need the parts for the whole to function, then the parts can be independently evolved. That is what happens. A little evolution of there, a little evolution over here, sometimes (rarely) something great happens confering a selective advantage, most of the time nothing happens, and sometimes something bad happens (the individual, not the species, fails to propogate)...

Cellular operations are not the work of a Clockwork god, they have problems (cytokine storms for instance), they vary (superhued women and color blind men); and instead of God's creation being a beautiful set of flawless gems, nature is an ugly pile of amorphous graphite, which we think is special because if it's special then we're special...
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post #7 of 146
Thread Starter 
Quote:
Originally Posted by hardeeharhar View Post

What are you talking about?

Here, straight from the guy: on the difficutly of creating these chains at random: (p 131)

Quote:
A huge hurdle confronting Darwinian evolution is the following: Most proteins in the cell operate as specific complexes of a half dozen or more chains.7 Hemoglobin comprises a complex of two kinds of amino acid chains (alpha and beta) stuck together, but hemoglobin is relatively simple. Most cellular proteins have six or more kinds of amino acid chains. So, unless those complexes were all together from the start, then at some time in the past separate cellular proteins had to develop the ability to bind to each other. But that would be a very tricky business indeed. On the one hand if, like the octopus objects above, a protein developed a surface that stuck indiscriminately to a lot of other proteins, it would gum up the workings of the cell. It would have to be eliminated. On the other hand, most protein pairs wouldn't bind to each other at all, or bind very weakly, because their surfaces don't match closely enough. Only when a Goldilocks match randomly developed between their multidimensional surfaces would two proteins bind to each other tightly and specifically enough to make an effective pair. So we can ask, how difficult would it be for two proteins that initially did not bind to each other to develop a strong, specific interaction by random mutation and natural selection?

... he then goes on to cite a Greg Winter, who studied this probability -- finding the odds for a 'modest strength' binding you have to ''wade through ten to hundred million binding sites.'


The endnote for that:

Quote:
10. Other proteins besides antibodies have been used to demonstrate the same point. For example, rather than antibodies, a protein called knottin was used by Winter to generate a shape-space library. About five hundred million binding sites had to be screened to find one that stuck to a test protein with modest affinity (Smith, G. R, Patel, S. U., Windass, J. D., ThorntonJ. M., Winter, G., and Griffiths, A. D. 1998. Small binding proteins selected from a combinatorial repertoire of knottins displayed on phage. J. Mol. Biol. 277:317-32).
A roughly similar result was seen when part of the sequence of a small bacterial protein was randomized to generate a library containing about forty million members, and when a library of fifty million artificial "minibodies" was probed for binding to a protein called interleukin (Nord, K., Gunneriusson, E., Uhlen, M., and Nygren, R A. 2000. Ligands selected from combinatorial libraries of protein A for use in affinity capture of apolipoprotein A-1M and taq DNA polymerase. J. Biotechnol. 80:45-54; Martin, E, Toniatti, C, Salvati, A. L, Venturini, S., Ciliberto, G., Cortese, R., and Sollazzo, M. 1994. The affinity-selection of a minibody polypeptide inhibitor of human interleukin-6. EMBO] 13:5303-9).

Also, so far, no one, even on PZ's site wants anything to do with Behe's numbers on E. Coli, HIV, and Malaria -- their lack of evolutionary progress. Is this because you feel that Malaria, etc., is not representative?

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and in that lies not liberation but alienation, the cutting off from things as they really are. --...

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post #8 of 146
Quote:
Originally Posted by dmz View Post

Here, straight from the guy: on the difficutly of creating these chains at random: (p 131)



... he then goes on to cite a Greg Winter, who studied this probability -- finding the odds for a 'modest strength' binding you have to ''wade through ten to hundred million binding sites.'


The endnote for that:



Also, so far, no one, even on PZ's site wants anything to do with Behe's numbers on E. Coli, HIV, and Malaria -- their lack of evolutionary progress. Is this because you feel that Malaria, etc., is not representative?

1) His suggestion that 'most cellular proteins have six or more kinds of amino acid chains' isn't actually true. Most do not. Some do. But that is besides the point. The question one should be asking always is 'is there a way for the cell to survive in the absense of a functioning x'? If yes considerations on the need for all of the chains to come together at the same time is irrelevent since it can be safely evolved without interference of the ability of the organism to reproduce. Ah, but he attempts to place the gottcha in there about gunking up the cellular works with non-specific binders. This does happen (think Alzheimer's plaques) but their are mechanisms that abrogate the effects -- both protinaceous (peptidases and chaperons) and non-protineaceous (inclusion body formation). Luckily for us, like dissolves like better than like dissolves dislike, in other words, bad peptides that bind non-specifically will tend to bind non-specifically to themselves more tightly than to other peptides. This has to do with repeating structural units and the energetic benefits of forming a pseudo-crystaline lattice.

Other than the first one, one could envision that all molecular complexes don't need to be generated from scratch -- once you have the scaffold for one, you have in principle the scaffold for all...

2) What numbers are you refering to? Probabilities that haven't actually been calculated? or what?
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post #9 of 146
Behe writes books for people who don't know a damned thing about science but want to fight them thar godless evilutionists.

Quote:
Also, so far, no one, even on PZ's site

Oh wow, no one on PZ's site has addressed that one issue as far as you know?

EVEN ON PZ's SITE!?
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post #10 of 146
Thread Starter 
Quote:
Originally Posted by hardeeharhar View Post

1) His suggestion that 'most cellular proteins have six or more kinds of amino acid chains' isn't actually true. Most do not. Some do. But that is besides the point. The question one should be asking always is 'is there a way for the cell to survive in the absense of a functioning x'? If yes considerations on the need for all of the chains to come together at the same time is irrelevent since it can be safely evolved without interference of the ability of the organism to reproduce. Ah, but he attempts to place the gottcha in there about gunking up the cellular works with non-specific binders. This does happen (think Alzheimer's plaques) but their are mechanisms that abrogate the effects -- both protinaceous (peptidases and chaperons) and non-protineaceous (inclusion body formation). Luckily for us, like dissolves like better than like dissolves dislike, in other words, bad peptides that bind non-specifically will tend to bind non-specifically to themselves more tightly than to other peptides. This has to do with repeating structural units and the energetic benefits of forming a pseudo-crystaline lattice.

Other than the first one, one could envision that all molecular complexes don't need to be generated from scratch -- once you have the scaffold for one, you have in principle the scaffold for all...

2) What numbers are you referring to? Probabilities that haven't actually been calculated? or what?

On the first point, that sort of 'construction' is still on paper, yes? -and that the probability of getting the moderate bond is still up in the range he is quoting?

On the second, we've have had 10^20 organisms of both HIV, and Malaria, (and 10^13 of E. Coli) but only a few (destructive) advantageous changes. Is that something that is irrelevant when we look at evolution broadly?

In our desire to impose form on the world we have lost the capacity to see the form that is there;
and in that lies not liberation but alienation, the cutting off from things as they really are. --...

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post #11 of 146
dmz:

Quote:
On the second, we've have had 10^24 organisms of both HIV, and Malaria, but only a few (destructive) advantageous changes. Is that something that is irrelevant when we look at evolution broadly?

No, it is entirely relevant.

The question is, what significance are you assigning to that big number? What is it about that big number that you think is important?
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post #12 of 146
Quote:
Originally Posted by groverat View Post

Behe writes books for people who don't know a damned thing about science but want to fight them thar godless evilutionists.



Oh wow, no one on PZ's site has addressed that one issue as far as you know?

EVEN ON PZ's SITE!?

It's because they know the emperor has no new binding sites and they're terrified of this new, penetrating analysis.

Don't you know, Groverat? There's all this evidence that flatly contradicts evolution, so the faithful have to pretend like it doesn't exist and assiduously ignore it even when thrust beneath their noses.
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post #13 of 146
Quote:
Originally Posted by dmz View Post

On the first point, that sort of 'construction' is still on paper, yes? -and that the probability of getting the moderate bond is still up in the range he is quoting?

On the second, we've have had 10^20 organisms of both HIV, and Malaria, (and 10^13 of E. Coli) but only a few (destructive) advantageous changes. Is that something that is irrelevant when we look at evolution broadly?

Define "large" quantitatively?

So Behe dusts off the Irreducible Complexity argument, again!

What's new under the sun?

Let's see how ID works, shall we?

So you can't answer all my questions (and infinite permutations thereof) wrt your "theory of evolution" (nee science) therefore doG (nee shit) happens!

Every eye fixed itself upon him; with parted lips and bated breath the audience hung upon his words, taking no note of time, rapt in the ghastly fascinations of the tale. NOT!
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post #14 of 146
Thread Starter 
Quote:
Originally Posted by franksargent View Post

Define "large" quantitatively?

So Behe dusts off the Irreducible Complexity argument, again!

What's new under the sun?

Let's see how ID works, shall we?

So you can't answer all my questions (and infinite permutations thereof) wrt your "theory of evolution" (nee science) therefore doG MUST exist!


Behe cites that the number of living organisms, ever, is ~10^40. When you look at HIV viruses, and Malaria organisms, both in the 10^20 range, I think if darwinist predictions were going to come true, that you would be seeing that already. But we don't -- what evolution is showing in those two cases is that it can do very little.

I just read an article on the explosion of RNA research in this week's The Economist -- crazy stuff. There are some rumblings on dual-coding DNA, and junk DNA, too. The levels of complexity, and the associated probabilities, are never going to be better than right now, it's only going to get worse for darwinists.

Eventually ID will save darwinists from themselves, it will be the only thing that keeps the theory alive. The numbers will crush it on it's own.

As far as running for the 'safety' of the fossil record, knock yourself out. The problem with the fossil record, statistically speaking, is that over the course of history, the 'working' creatures are a tiny fraction compared to the 'missing links.' If you look at the numbers, all that you should be seeing in the fossil record are missing links. But you don't, you find nearly none, and even those are subject to what is a missing link/what is simply an extinct species.

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and in that lies not liberation but alienation, the cutting off from things as they really are. --...

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post #15 of 146
addabox:

Even at PZ's site!
If the answer to every little question, no matter how irrational or poorly-founded, isnot there, where could it be!?!?


dmz:

Quote:
Behe cites that the number of living organisms, ever, is ~10^40. When you look at HIV viruses, and Malaria organisms, both in the 10^20 range, I think if darwinist predictions were going to come true, that you would be seeing that already. But we don't -- what evolution is showing in those two cases is that it can do very little.

Who made these "darwinist predictions" we are busy criticizing, pray tell?
(What you mean to say is, "See me build a straw man. See me set a straw man on fire!")

Well, if god was real then he'd give me $20 billion but since I don't have $20 billion there is no god, hurrrr!

Quote:
I read an article on the explosion of RNA research in The Economist -- and there is some rumblings on dual-coding DNA, and junk DNA. The levels of complexity, and the associated probabilities, are never going to be better than right now, it's only going to get worse for darwinists.

Why would great complexity and "junk" DNA be bad for "darwinists"?

Quote:
As far as running for the 'safety' of the fossil record, knock yourself out. The problem with the fossil record, statistically speaking, is that over the course of history, the 'working' creatures are a tiny fraction compared to the 'missing links.' If you look at the numbers, all that you should be seeing in the fossil record are missing links. But you don't, you find nearly none, and even those are subject to what is a missing link/what is simply an extinct species.

Do you know how fossils form? Do you understand the delicacy and tenuousness of the process?

Should we expect to see fossils of all transitional forms? Should we expect to see fossils of any transitional forms?

Also... "nearly" none? Are you saying that we have found transitional forms?
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post #16 of 146
I wonder why finer grained insights into the mechanisms of cellular biology would be a "problem" for "Darwinists"?

After all, we also have accrued, over time, a great deal more "complexity" in our understanding of the nature of matter and energy and the structures of the universe.

Would you argue that the elaborate interaction of forces that account for the large scale structures we see across galaxies makes a case for intelligent design?

Or, more properly, does the fact that we now have a far more detailed awareness of the processes driving those structures than when the universe was more of a black box, as far as we knew, make a better case for intelligent design?

Does the evolution of our model of the atom, from tidy miniature solar system to seething probabilistic force field, also make an ever better case for God's hand? After all, the sub-atomic world as we currently view it is nothing if not complicated, certainly far more complicated than we imagined a century ago.

Ironically, of course, back then it was simplicity and orderliness that were taken for the evidence of God the watchmaker, properly assembling the parts with grace and economy. The complexity that is now brandished as evidence of higher intelligence was then regarded as simply lack of understanding, the assumption being that nature was, above all, simple, if only we had the wit to see.
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post #17 of 146
Thread Starter 
Quote:
Originally Posted by addabox View Post

I wonder why finer grained insights into the mechanisms of cellular biology would be a "problem" for "Darwinists"?

After all, we also have accrued, over time, a great deal more "complexity" in our understanding of the nature of matter and energy and the structures of the universe.

Would you argue that the elaborate interaction of forces that account for the large scale structures we see across galaxies makes a case for intelligent design?

Or, more properly, does the fact that we now have a far more detailed awareness of the processes driving those structures than when the universe was more of a black box, as far as we knew, make a better case for intelligent design?

Does the evolution of our model of the atom, from tidy miniature solar system to seething probabilistic force field, also make an ever better case for God's hand? After all, the sub-atomic world as we currently view it is nothing if not complicated, certainly far more complicated than we imagined a century ago.

Ironically, of course, back then it was simplicity and orderliness that were taken for the evidence of God the watchmaker, properly assembling the parts with grace and economy. The complexity that is now brandished as evidence of higher intelligence was then regarded as simply lack of understanding, the assumption being that nature was, above all, simple, if only we had the wit to see.

If RNA proves to be as big as some say, it will mean more excruciating complexity to explain away. The same if Junk DNA becomes something other than 'junk'.

Also, let's not forget sin and the curse when we look at torn up/damaged systems. Don't get me wrong, none of this proves ID right, or that God exists. What I think will happen is the numbers will eventually get so sour that darwinists will have to step back and admit they believe what they believe for dogmatic reasons. (Which would be fine with me.)

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and in that lies not liberation but alienation, the cutting off from things as they really are. --...

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post #18 of 146
Quote:
Originally Posted by dmz View Post

If RNA proves to be as big as some say, it will mean more excruciating complexity to explain away. The same if Junk DNA becomes something other than 'junk'.

Also, let's not forget sin and the curse when we look at torn up/damaged systems. Don't get me wrong, none of this proves ID right, or that God exists. What I think will happen is the numbers will eventually get so sour that darwinists will have to step back and admit they believe what they believe for dogmatic reasons. (Which would be fine with me.)

Again, why would more complexity be "excruciating", and why would it have to be "explained away"?

And, again, how is any of this different from the gradually unfolding story of science, in general?

For instance, I've yet to hear a creationist, upon learning of the latest theories on dark matter, exclaim, "See how complicated our model of the universe is getting? Pretty soon those astrophysicists are just going to have to throw in the towel and admit that God made it, to his own fiendishly complicated specs."
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post #19 of 146
Quote:
Originally Posted by dmz View Post

Behe cites that the number of living organisms, ever, is ~10^40. When you look at HIV viruses, and Malaria organisms, both in the 10^20 range, I think if darwinist predictions were going to come true, that you would be seeing that already. But we don't -- what evolution is showing in those two cases is that it can do very little.

I just read an article on the explosion of RNA research in this week's The Economist -- crazy stuff. There are some rumblings on dual-coding DNA, and junk DNA, too. The levels of complexity, and the associated probabilities, are never going to be better than right now, it's only going to get worse for darwinists.

Eventually ID will save darwinists from themselves, it will be the only thing that keeps the theory alive. The numbers will crush it on it's own.

As far as running for the 'safety' of the fossil record, knock yourself out. The problem with the fossil record, statistically speaking, is that over the course of history, the 'working' creatures are a tiny fraction compared to the 'missing links.' If you look at the numbers, all that you should be seeing in the fossil record are missing links. But you don't, you find nearly none, and even those are subject to what is a missing link/what is simply an extinct species.

You would have to provide a link to these estimates. 10^20/10^40 appears to be a small number (to me), but if HIV/Malaria add up to 10^20 for just those two, I can't even begin to imagine what the total would be for all organic life. BTW, I really don't know what you are implying in your first paragraph.

As to the fossil record, given the 10^40 number of total historical living organisms, how many of these have we dug up in total (and yes, most of them would, by their very nature, be very small (mass versus number PDF/CDF)) so far? And why must what we have dug up so far be predominately "missing links?" I'd expect the "missing links" to be the exception (e. g. very hard to find since we don't know where to look a priori) rather than the rule.

When you look at the geologic record, and note the inherent lack of temporal/spatial granularity, it becomes apparent, that we may forever be missing some very big pieces from the evolutionary puzzle that forms the geologic record.

For instance what happens when Earth is bombarded with cosmic rays (as our solar system passes through the arms of our galaxy)? What happens when the magnetic polarity changes? Solar flares? Catastrophic events? Tectonic activity? Climate change? Naturally occurring invasive species?
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post #20 of 146
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Originally Posted by addabox View Post

I wonder why finer grained insights into the mechanisms of cellular biology would be a "problem" for "Darwinists"?

After all, we also have accrued, over time, a great deal more "complexity" in our understanding of the nature of matter and energy and the structures of the universe.

Would you argue that the elaborate interaction of forces that account for the large scale structures we see across galaxies makes a case for intelligent design?

Or, more properly, does the fact that we now have a far more detailed awareness of the processes driving those structures than when the universe was more of a black box, as far as we knew, make a better case for intelligent design?

Does the evolution of our model of the atom, from tidy miniature solar system to seething probabilistic force field, also make an ever better case for God's hand? After all, the sub-atomic world as we currently view it is nothing if not complicated, certainly far more complicated than we imagined a century ago.

Ironically, of course, back then it was simplicity and orderliness that were taken for the evidence of God the watchmaker, properly assembling the parts with grace and economy. The complexity that is now brandished as evidence of higher intelligence was then regarded as simply lack of understanding, the assumption being that nature was, above all, simple, if only we had the wit to see.

You asked three rhetorical questions, the answer is the same for all three. They don't.

The main differences between our PRESENT understanding of the universe (nee physics/inorganic) versus life (biology/organic) is the finite speed of light (our ability to see back in time directly), a much more rigorous system of mathematics to describe non-living matter, and the fact that we cannot create an independent ecosystem (apart from our Earthly existence) and wait a few billion years to see what happens.
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post #21 of 146
Just because you can't fathom something to be possible doesn't make it impossible. It just means that your capacity for understanding random probability is poor. Or you're in denial of the obvious. Either way, you're dumb.
post #22 of 146
I would just like to note that vast, vast majority of people I know have no problem reconciling evolution and god. The two are simply not mutually exclusive.
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post #23 of 146
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Originally Posted by addabox View Post

Again, why would more complexity be "excruciating", and why would it have to be "explained away"?

And, again, how is any of this different from the gradually unfolding story of science, in general?

For instance, I've yet to hear a creationist, upon learning of the latest theories on dark matter, exclaim, "See how complicated our model of the universe is getting? Pretty soon those astrophysicists are just going to have to throw in the towel and admit that God made it, to his own fiendishly complicated specs."

Science is science -- it is what it is. You look, you study, it's its own thing. A theory on how what we see has come together is what's at issue.

If darwinists begin to make enough predictions that prove false -- vestigial organs [as useless] come to mind -- if Junk DNA turns out to be not junk, for instance, then darwinism will prove to be a handicap when approaching science. It will also make the timetables of evolution more dense, remember it's only 100,000-200,000 generations from us to chimps.

On the Pharyngula forums, the mantra was: it's not impossible to do all these things because it's not that complicated. The only differences between chimps and humans is a question of degrees. Sure, there's 60 million differences in the genome, but we can cut that in half since we know chimps have evolved since then, and then reduce that more since a lot of those differences are in Junk DNA, so when you really look at it, it only takes a couple hundred changes per generation to bridge the difference.

That assumes it can be done, and lets' be honest the "proving" is held together exclusively by the fossil record.

But lets' grant that it's biologically feasible under current assumptions, what if RNA is a big as some say it will be? And when the next discovery happens? At the moment, the last thing the darwinist zeitgeist probably wants, is to find complexity on a order of magnitude higher than what we know now.


Edit: and it's Sean Carroll, not Steve. The [my] mind is the first thing to go.

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post #24 of 146
post #25 of 146
Thread Starter 
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Originally Posted by franksargent View Post

You would have to provide a link to these estimates. 10^20/10^40 appears to be a small number (to me), but if HIV/Malaria add up to 10^20 for just those two, I can't even begin to imagine what the total would be for all organic life. BTW, I really don't know what you are implying in your first paragraph.

The 10^40 was organisms, which wouldn't include viruses like HIV. (And don't forget these are 'squared' functions, 10^20 obviously isn't half of 10^40, etc.)

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post #26 of 146
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Originally Posted by Flounder View Post

...[the] vast, vast majority of people I know have no problem reconciling evolution and god.

Ha -- as far as his fellow scientists are concerned, isn't that Behe's sin?

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post #27 of 146
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Originally Posted by dmz View Post

if Junk DNA turns out to be not junk, for instance, then darwinism will prove to be a handicap when approaching science.

Ummm, junk DNA doesn't, in particular, have a whole lot to do with 'darwinism' (i'm not even sure what you regard that term to mean though). It's molecular biology. Although I can see how you could be confused. Evolution is the core theme that units all of biology. Virtually every aspect of biology relies on it to one extent or another.
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post #28 of 146
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Originally Posted by dmz View Post

On the first point, that sort of 'construction' is still on paper, yes? -and that the probability of getting the moderate bond is still up in the range he is quoting?

What construction? No. It happens -- and tight binding between proteins is EASY, cyt c is a promiscuous binder to negatively charged patches on its binding partners. Specific binding is a challenge. But you don't need specific binding to get things rolling -- cyt c is perhaps the most important electron transfer protein in biology and all it uses is a patch of positively charged residues on its surface. The most important protein uses the simplest system. We are finding more and more that proteins will non-specifically associate more often than not...

Quote:
On the second, we've have had 10^20 organisms of both HIV, and Malaria, (and 10^13 of E. Coli) but only a few (destructive) advantageous changes. Is that something that is irrelevant when we look at evolution broadly?

No. HIV has had as many advantageous changes as we would be right to ask of it -- resistance to every new type of drug we throw at it without a real change in its function -- this non-sentient organism is out smarting us big brained intelligent designers (fancy that). E. coli mutates at a much much lower level, and yet still we have observed spontaneous changes that are selectively advantageous. And as we all know malaria still gets the job done (most common infection other than certain viruses) even though it has had to change to avoid drug treatments.

I think your point is that these changes appear destructive. But what does that mean? Is that actually even a real measure outside of human conception? If the organism survives and continues to do what it does, is it right to call any change destructive?
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post #29 of 146
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Originally Posted by dmz View Post

Ha -- as far as his fellow scientists are concerned, isn't that Behe's sin?

The vast majority of scientists I know have no problem with it either. The false dichotomy of that choice really bothers me. They're separate topics, to me.
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post #30 of 146
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Originally Posted by Flounder View Post

Ummm, junk DNA doesn't, in particular, have a whole lot to do with 'darwinism' (i'm not even sure what you regard that term to mean though). It's molecular biology. Although I can see how you could be confused. Evolution is the core theme that units all of biology. Virtually every aspect of biology relies on it to one extent or another.

I would have to say that is false, as Dick Dawkins points out, we are dealing with the appearance of exquisite design. So when you go poking around you have to act in terms of predictability, and 'lucid' functionality.

Junk DNA would only be a failed prediction -- it falls that way -- based on darwinist dogma. The actually process of discovery is a separate thing.

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post #31 of 146
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Originally Posted by dmz View Post

The 10^40 was organisms, which wouldn't include viruses like HIV. (And don't forget these are 'squared' functions, 10^20 obviously isn't half of 10^40, etc.)

10^-20 = 10^20/10^40, and it's exponential (to an exponent).
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post #32 of 146
Quote:
Originally Posted by dmz View Post

Science is science -- it is what it is. You look, you study, it's its own thing. A theory on how what we see has come together is what's at issue.

If darwinists begin to make enough predictions that prove false -- vestigial organs [as useless] come to mind -- if Junk DNA turns out to be not junk, for instance, then darwinism will prove to be a handicap when approaching science. It will also make the timetables of evolution more dense, remember it's only 100,000-200,000 generations from us to chimps.

On the Pharyngula forums, the mantra was: it's not impossible to do all these things because it's not that complicated. The only differences between chimps and humans is a question of degrees. Sure, there's 60 million differences in the genome, but we can cut that in half since we know chimps have evolved since then, and then reduce that more since a lot of those differences are in Junk DNA, so when you really look at it, it only takes a couple hundred changes per generation to bridge the difference.

That assumes it can be done, and lets' be honest the "proving" is held together exclusively by the fossil record.

But lets' grant that it's biologically feasible under current assumptions, what if RNA is a big as some say it will be? And when the next discovery happens? At the moment, the last thing the darwinist zeitgeist probably wants, is to find complexity on a order of magnitude higher than what we know now.


Edit: and it's Sean Carroll, not Steve. The [my] mind is the first thing to go.

I'm all for discovery, wherever it leads us.

We don't know exactly if it's 100,000 or 1,000,000 generations, we are currently making inferences based on the fossil record. We could make linear assumptions, or they could be highly nonlinear, based on highly constricted (e. g. small seed populations), which skews the genetic pool greatly, competition for resources, etceteras.
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post #33 of 146
Thread Starter 
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Originally Posted by hardeeharhar View Post

What construction? No. It happens -- and tight binding between proteins is EASY, cyt c is a promiscuous binder to negatively charged patches on its binding partners. Specific binding is a challenge. But you don't need specific binding to get things rolling -- cyt c is perhaps the most important electron transfer protein in biology and all it uses is a patch of positively charged residues on its surface. The most important protein uses the simplest system. We are finding more and more that proteins will non-specifically associate more often than not...



No. HIV has had as many advantageous changes as we would be right to ask of it -- resistance to every new type of drug we throw at it without a real change in its function -- this non-sentient organism is out smarting us big brained intelligent designers (fancy that). E. coli mutates at a much much lower level, and yet still we have observed spontaneous changes that are selectively advantageous. And as we all know malaria still gets the job done (most common infection other than certain viruses) even though it has had to change to avoid drug treatments.

I think your point is that these changes appear destructive. But what does that mean? Is that actually even a real measure outside of human conception? If the organism survives and continues to do what it does, is it right to call any change destructive?

I understand that, in terms of darwinist perspective, that we would not know if we were actually seeing something forming, because it happens very slowly. But in both HIV and malaria, we have advantagous changes that are only turning off things, literally breaking things, etc., nothing new has ever been generated. That's my point.

On the protein binding, what I meant is that the actual building of these chains remains on paper, not something where you can set up real-world or even favorable conditions and see them form. Or that they would form, but at the incidence Behe suggests. But in any case, we haven't seen this happen in HIV, E. Coli, or malaria, either.

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post #34 of 146
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Originally Posted by franksargent View Post

10^-20 = 10^20/10^40, and it's exponential (to an exponent).

yes, that's what the little ' thingies are for around 'squared' -- you ninny!

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post #35 of 146
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Originally Posted by franksargent View Post

I'm all for discovery, wherever it leads us.

We don't know exactly if it's 100,000 or 1,000,000 generations...

But we do. Those are commonly held numbers, some go as high as 300,000 but that's about it.

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post #36 of 146
Quote:
Originally Posted by dmz View Post

I just read an article on the explosion of RNA research in this week's The Economist -- crazy stuff. There are some rumblings on dual-coding DNA, and junk DNA, too. The levels of complexity, and the associated probabilities, are never going to be better than right now, it's only going to get worse for darwinists.

Actually, you don't know the probabilities. I personally know a researcher who has figured out that the dual coding DNA is simplified by the codon use of nature. What this means is that the complexity you are seeing now was the simplest thing to do when the life ball got rolling -- having pieces of dna that code for two proteins in two different directions or offset gives a selective advantage to early life. And yet a billion years later, some creationist thinks that this change in understanding of how OUR dna works means that there is something wrong with evolution because it didn't predict (from what? who knows) that these things would exist. The point being... they are probably some of the oldest aspects of life due to their apparent pervasiveness. in other words, just because we recently discovered these aspects of dna, doesn't mean they just evolved.

Quote:
But you don't, you find nearly none, and even those are subject to what is a missing link/what is simply an extinct species.

1) Missing links, so to speak, will not be radically different than the two links around them or even the progenitor species or terminal.

2) Fossils are HARD to make; certain conditions much be matched. This means that our fossil record for deserts or high plains or etc will NEVER be complete.

3) Without genetic work the fossils of two different currently extant birds might suggest that they are the same species, when in point of fact they aren't. It comes down to the definition of species, really. In ideal conditions a human and a chimpanzee might be able to mate to form a viable offspring -- but no one now would claim that they are the same species, perhaps we should. Species currently has a functional definition involving proximity, likelihoods etc, which is simply something we CANNOT use to look at the fossil record. We need a better definition -- which will undoubtedly lead to creationists claiming that the field post is being moved...

4) Aren't all missing links extinct species?
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post #37 of 146
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Originally Posted by hardeeharhar View Post

2) Fossils are HARD to make; certain conditions much be matched. This means that our fossil record for deserts or high plains or etc will NEVER be complete.

Ken Hamm, is that you?














Just kidding, I get your point.

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post #38 of 146
Quote:
Originally Posted by dmz View Post

yes, that's what the little ' thingies are for around 'squared' -- you ninny!

X^2 is "squared" not trying to nitpick, no biggie, I know what you meant.
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post #39 of 146
Quote:
Originally Posted by dmz View Post

I understand that, in terms of darwinist perspective, that we would not know if we were actually seeing something forming, because it happens very slowly. But in both HIV and malaria, we have advantagous changes that are only turning off things, literally breaking things, etc., nothing new has ever been generated. That's my point.

No. HIV cannot spare to turn off things -- every mutation HIV conferring resistance to a drug has been on an actively used protein (and it doesn't matter that these organisms are turning off things anyway -- that means the things that aren't being used can be further modified, evolved to match some new needed function). Scientists are realizing this and trying to out design HIV's built in evolutionary device buy forcing new drugs to look as much like natural substrates as possible so that it would be all but impossible for HIV to mutate a resistance. But you know what, it might work a little better, but I suspect it will fail just the same. HIV is SOOOO smart.

Quote:
On the protein binding, what I meant is that the actual building of these chains remains on paper, not something where you can set up real-world or even favorable conditions and see them form. Or that they would form, but at the incidence Behe suggests. But in any case, we haven't seen this happen in HIV, E. Coli, or malaria, either.

Yes... you can and people have. Using a leaky polymerase people have done amazing things in the modification of protein function (there are other methods, of course, but the polymerase reactions are the most natural off them) selected, but not designed. In order to see anything on a laboratory time scale you have to increase the rate of mutation 10^6 to 10^9 times. This barely gets you over the preservation of function tendencies nature has evolved.

Why Behe thinks that e. coli or malaria is evolving any faster than than it has in the past, I will never know....

I also have to point out that MOST scientists aren't looking for spontaneous gain of function when they work with any of these organisms... I don't know of a single one looking at evolution at the scale of bacteria in any event...

Evolution is used as a theory to explain observed results... And like the young universal gravitation it has its yips that proclaim that it must be false because the moon hasn't crashed into the earth, and when the scientists respond that actually the moon is moving away from earth due to tidal effects, they proclaim that the end is nigh for gravitation...
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post #40 of 146
Quote:
Originally Posted by dmz View Post

I understand that, in terms of darwinist perspective, that we would not know if we were actually seeing something forming, because it happens very slowly. But in both HIV and malaria, we have advantagous changes that are only turning off things, literally breaking things, etc., nothing new has ever been generated. That's my point.

On the protein binding, what I meant is that the actual building of these chains remains on paper, not something where you can set up real-world or even favorable conditions and see them form. Or that they would form, but at the incidence Behe suggests. But in any case, we haven't seen this happen in HIV, E. Coli, or malaria, either.

Destructive or advantagous, who cares, oh that's right, we humans care.

Things change, that's the basic point, beyond that, we humans confer value judgments, that nature doesn't a priori.

The whole species thing is a moot point beyond some arbitrary granularity defined by humans, several hundred years ago.

The fossil record is replete with various hominids, our species being the last from that branch.

Are we a "virus" or "pox" on the rest of the ecosystem? That's a value judgement, a human construct. I'd prefer to just call it what it is, evolution.
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