The biochemistry of blood clotting is irreducibly complex, indicating that it must have been designed.
(Talk.Origins quotes in blue)
1. The blood clotting systems appears to be put together by using whatever long polymeric bridges are handy. There are many examples of complicated systems made from components that have useful but completely different roles in different components. There is also evidence that the genes for blood clotting (indeed, the whole genome) duplicated twice in the course of its evolution (Davidson et al. 2003). The duplication of parts and co-opting of parts with different functions gets around the "challenge" of irreducible complexity evolving gradually.
This is based on comparative studies that assume Evolution in their conclusions, no place do they demonstrate that such processes can actually occur. While the duplication and co-opting of parts would indeed help, it does not solve the challenge of irreducible complexity evolving gradually. The organism still needs have all the right parts together in the same place and correctly assembled. That problem is not addressed by Talk Origins.
2. Blood clotting is not irreducibly complex. Some animals -- dolphins, for example -- get along fine without the Hagemann factor, a component of the human blood clotting system which Behe includes in its "irreducible" complexity. Doolittle and Feng (1987) predicted that "lower" vertebrates would lack the "contact pathway" of blood clotting. Work on the genomes of the puffer fish and zebrafish have confirmed this
- This would seem to simply show that dolphins and other animals which lack the Hagemann factor have a blood clotting chemistry that is different from humans. That’s not a surprise from a creation perspective, particularly given the fact that dolphins live in water while humans live on land.
- The most this shows is that Behe erred on this one point.
- The fact that some animals do not need the Hagemann factor for blood clotting says nothing about humans. If humans can get along without it, then Talk Origins would have a point, but otherwise the Hagemann factor could still be part of the irreducible complexity of human blood.
Behe's Response to this Objection
In fact, this objection to Behe’s argument for the irreducible complexity of the blood-clotting cascade is entirely beside the point. In the Kitzmiller v. Dover case, Behe, in his testimony, dealt explicitly with this ‘rebuttal’ as expressed by Dr. Ken Miller. Here is the relevant portion of Behe’s testimony, running from page 25, line 9 to page 30, line 5 (A = Behe):
- Q. -- and Doolittle and Davidson, et al, to argue against the irreducible complexity of the blood clotting system. Do you agree with his assessment of those studies?
- A. No, I do not.
- Q. And you have some diagrams to explain this further, sir?
- A. Yes, I do. This is a slide from Professor Miller's presentation showing work from Jiang and Doolittle. And he also shows a diagram of the blood clotting cascade. And notice again, it's a branched pathway with the intrinsic pathway and the extrinsic pathway. And Professor Miller makes the point that in DNA sequencing studies of something called a puffer fish, where the entire DNA of its genome was sequenced, and scientists looked for genes that might code for the first couple components of the intrinsic pathway, they were not found.
And so Professor Miller demonstrated that by -- if you could push to start the animation -- Professor Miller demonstrated that by having those three components blanked out in white. Nonetheless, puffer fish have a functioning clotting system. And so Professor Miller argued that this is evidence against irreducible complexity.
But I disagree. And the reason I disagree is that I made some careful distinctions in Darwin's Black Box. I was very careful to specify exactly what I was talking about, and Professor Miller was not as careful in interpreting it. In Darwin's Black Box, in the chapter on blood clotting cascade, I write that, a different difference is that the control pathway for blood clotting splits in two. Potentially then, there are two possible ways to trigger clotting.
The relative importance of the two pathways in living organisms is still rather murky. Many experiments on blood clotting are hard to do. And I go on to explain why they must be murky. And then I continue on the next slide. Because of that uncertainty, I said, let's, leaving aside the system before the fork in the pathway, where some details are less well-known, the blood clotting system fits the definition of irreducible complexity. And I noted that the components of the system beyond the fork in the pathway are fibrinogen, prothrombin, Stuart factor, and proaccelerin. So I was focusing on a particular part of the pathway, as I tried to make clear in Darwin's Black Box. If we could go to the next slide. Those components that I was focusing on are down here at the lower parts of the pathway. And I also circled here, for illustration, the extrinsic pathway. It turns out that the pathway can be activated by either one of two directions. And so I concentrated on the parts that were close to the common point after the fork.
So if you could, I think, advance one slide. If you concentrate on those components, a number of those components are ones which have been experimentally knocked out such as fibrinogen, prothrombin, and tissue factor. And if we go to the next slide, I have red arrows pointing to those components. And you see that they all fall in the area of the blood clotting cascade that I was specifically restricting my arguments to. And if you knock out those components, in fact, the blood clotting cascade is broken. So my discussion of irreducible complexity was, I tried to be precise, and my argument, my argument is experimentally supported.
- Q. Now just by way of analogy to maybe help explain further. Would this be similar to, for example, a light having two switches, and the blood clotting system that you focus on would be the light, and these extrinsic and intrinsic pathways would be two separate switches to turn on the system?
- A. That's right. You might have two switches. If one switch was broke, you could still use the other one. So, yes, that's a good analogy.
- Q. So Dr. Miller is focusing on the light switch, and you were focusing on the light?
- A. Pretty much, yes.
- Q. I believe we have another slide that Dr. Miller used, I guess, to support his claim, which you have some difficulties with, is that correct?
- A. Yes, that's right. Professor Miller showed these two figures from Davidson, et al, and from Jiang, et al, Jiang and Doolittle, and said that the suggestions can be tested by detailed analysis of the clotting pathway components. But what I want to point out is that whenever you see branching diagrams like this, especially that have little names that you can't recognize on them, one is talking about sequence comparisons, protein sequence comparisons, or DNA nucleotide sequence comparisons. As I indicated in my testimony yesterday, such sequence comparisons simply don't speak to the question of whether random mutation and natural selection can build a system. For example, as I said yesterday, the sequences of the proteins in the type III secretory system and the bacterial flagellum are all well-known, but people still can't figure out how such a thing could have been put together. The sequences of many components of the blood clotting cascade have been available for a while and were available to Russell Doolittle when he wrote his essay in the Boston Review. And they were still unhelpful in trying to figure out how Darwinian pathways could put together a complex system. And as we cited yesterday, in Professor Padian's expert statement, he indicates that molecular sequence data simply can't tell what an ancestral state was. He thinks fossil evidence is required. So my general point is that, while such data is interesting, and while such data to a non-expert in the field might look like it may explain something, if it's asserted to explain something, nonetheless, such data is irrelevant to the question of whether the Darwinian mechanism of random mutation and natural selection can explain complex systems.
- Q. So is it your opinion then, the blood clotting cascade is irreducibly complex?
- A. Yes, it is.
Thus, this objection doesn’t even deal with Behe’s case for the IC of the blood-clotting cascade; it completely and utterly misses the target. As he points out in his testimony, Behe expressly limited his argument in Darwin’s Black Box to a specific sector of this biochemical pathway. This ostensible rebuttal to Behe addresses an entirely different sector; one that Behe explicitly excluded from his case for the IC of the cascade.
If Darwinists wish to rebut Behe, they must address the case that he actually makes rather than a mischaracterization of it. As it is, Behe’s attribution of IC to the blood-clotting cascade stands – unscathed by this misdirected and irrelevant attack.
3. Irreducible complexity is not an obstacle to evolution and doesn't imply design.
This statement is bogus, being based on flawed logic.
This includes the impossible demand that those who hold to the position that irreducible complexity implies design disprove all possible evolutionary scenarios, even those that have not been invented yet.