Creationism vs. evolution debate to be topic of two-day Clarksb

Your statement that clotting too much or too little is "not necessarily fatal before the organism reaches breeding age" is considerably weaker than "has a survival advantage over" and does not imply it.

I don't see where that's a problem, since he was making two separate points, in response to two separate issues.

That's not what he said, and in any case you're oversimplyfing the issue.

First, it's hardly a "choice" between "too much or two little". Instead, the path could have been from "way too little" to "too little" to "a little too little" to "just right", for example. In that case every step would be an improvement over the last, without ever having to contrast "too little" against "too much".

Second, even if the pathway did oscillate around "just right" before homing in on it, "too little" and "too much" are hardly binary conditions. They exist on a continuum, and something along the lines of: 50% too little -> 30% too much -> 20% too little -> 10% too much -> just right would again be an example of continuous improvements.

Finally, the biggest thing that you're missing is that the clotting system can, and almost certainly did, evolve over periods where the requirements it had to meet were changing. What is "not good enough" today may have been close to "just right" back when the modern vertebrate clotting system was in an earlier stage. Thus it's a mistake to try to ponder whether the system(s) which were precursor(s) the modern vertebrate clotting sytem might be workable *in modern vertebrates*, since its precursors would have actually arisen in amphibians, and before that fish, and before that notochords, and before that invertebrates.

In short it's a fallacy to consider only whether a more primitive form of the clotting system would have been workable in modern vertebrates, since that's *not* where the earlier forms of the clotting systems evolved.

Come to think of it, this is yet *another* mistake that Behe makes, both in his examination of the vertebrate clotting system, *and* in all of his other "IC" analysis -- he never takes into account the fact that evolutionary precursors might have been "built" in *very* different conditions (i.e., in very different ancestral species). Behe only examines whether removing a component of the system would "break" it *in the modern species in which it now resides*. That quite simply is not a valid test.

I thought this might be a good time to remind everyone that Behe has responded to critics.

Behe Responds (to Doolittle and others):

http://www.arn.org/docs/behe/mb_brrespbr.htm

Professor Doolittle is a prominent scientist, a member of the National Academy of Sciences who has worked hard on many aspects of protein structure over the course of a distinguished career. He knows more about the process of blood clotting, and more about the relationships among the protein members of the clotting cascade, then perhaps anyone else on earth. He does not, however, know how natural selection could have produced the clotting cascade. In fact, he has never tried to explain how it could have. Nonetheless, as reflected in his comments in Boston Review, he clearly thinks he has addressed the question. This results from a basic confusion, which I will try to clarify.

As Professor Doolittle points out, the sequence of amino acids in one protein might be strikingly like that in a second protein. A good example is the one he gives us--the different subunits of hemoglobin. This gave rise to the idea that the similar proteins might have descended from a common gene, when in the past the gene was duplicated. Virtually all biochemists accept this, and so do I. Many proteins of the clotting cascade are similar to each other, and similar to other non-cascade proteins, so they also appear to have arisen by some process of gene duplication. I think this is a very good hypothesis too. The critical point, however, is that the duplicated gene is simply a copy of the old one, with the same properties as the old one--it does not acquire sophisticated new properties simply by being duplicated. In order to understand how the present day system got here, a scientist has to explain how the duplicated genes acquired their new, sophisticated properties.

With hemoglobin the task of getting from a simple protein with one chain to a complex of four chains does not appear to present problems, as I discussed on pp. 206-207 of Darwin’s Black Box. In both cases the proteins simply bind oxygen, with more or less affinity, and they don’t have to interact critically with other proteins in a complex protein system. There is a fairly obvious pathway leading from a simple hemoglobin to a more complex one.

With the proteins of blood clotting, however, the task of adding proteins to the cascade appears to be horrendously problematic. With one protein acting on the next, which acts on the next, and so forth, duplicating a given protein doesn’t give you a new step in the cascade. Both copies of the duplicated protein will have the same target protein which they activate, and will themselves be activated by the same protein as before. In order to explain how the cascade arose, therefore, a scientist has to propose a detailed route whereby a duplicated protein turns into a new step in the cascade, with a new target, and a new activator. Furthermore, because clotting can easily go awry and cause severe problems when it is uncontrolled, a serious model for the evolution of blood clotting has to include quantitative factors, such as how much of a clot forms, what pressure it can resist, how frequent inappropriate clots would be, and many, many more such questions.

Professor Doolittle has addressed none of these questions. He has confined his work to the question of what proteins appear to be descended from what other proteins, and is content to wave his hands and assert that, well, those systems must have been put together by natural selection somehow. The title of the reference to his work that he cites here says it all, "Reconstructing the history of vertebrate blood coagulation from a consideration of the amino acid sequences of clotting proteins." His work concerns sequence comparisons. Doolittle has no idea of whether the clotting cascade could have been built up by natural selection.

An illustration of this fact is shown in his citing Bugge et al. ("Loss of Fibrinogen Rescues Mice from the Pleiotropic Effects of Plasminogen Deficiency," Cell 87, 1996: 709-19). Professor Doolittle writes:

"Recently the gene for plaminogen was knocked out of mice, and, predictably, those mice had thrombotic complications because fibrin clots could not be cleared away. Not long after that, the same workers knocked out the gene for fibrinogen in another line of mice. Again, predictably, these mice were ailing, although in this case hemorrhage was the problem. And what do you think happened when these two lines of mice were crossed? For all practical purposes, the mice lacking both genes were normal!6 Contrary to claims about irreducible complexity, the entire ensemble of proteins is not needed. Music and harmony can arise from a smaller orchestra."

However, if one goes back and looks at Bugge et al, one sees that Professor Doolittle misread the paper. The mice that have had both genes knocked out do not have a functioning clotting system: they can’t form clots; they hemorrhage; females die during pregnancy. They are certainly not candidates for evolutionary intermediates.

The lesson here is not that Doolittle misread a paper, which can happen to anyone. Rather, there are two points. First, a Darwinian mindset can tend to make one glide over problems that would occur in the real world. And second, sequence information is not sufficient to conclude that a system evolved by natural selection. The sequence information that Professor Doolittle had did not stop him from mistakenly pointing to a nonviable situation as a potential evolutionary intermediate. One can go further to say that, if a scientist as prominent as Russell Doolittle does not know of a detailed route by which natural selection could produce the clotting cascade, nobody knows.

I argue that each of the steps of the clotting cascade is irreducibly complex (see Chapter 4 of my book)--requiring the rearrangement of several components simultaneously before a viable, controlled clotting system could be in place, and that is why I conclude that the cascade is a product of design. Clotting factors may be related by common descent, but the clotting cascade was not produced by natural selection.

On a different note, I’m glad Professor Doolittle likes Rube Goldberg too, but unfortunately it supplies what I think is his rock-bottom reason for deciding that natural selection produced the clotting cascade: "... no Creator would have designed such a circuitous and contrived system." Well, Doolittle is a good scientist, but he’s no theologian, and he doesn’t serve science well when he lets his theological presuppositions influence his scientific judgment.

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