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Kitzmiller v. Dover Area School District

Trial transcript: Day 11 (October 18), AM Session, Part 1


THE COURT: Good morning to all. Mr. Muise, if it's Tuesday, we must be on the blood clotting.

MR. MUISE: We will be getting to blood clotting, immunity systems, and many more complex systems, Your Honor.

THE COURT: All right. You may proceed.

MR. MUISE: Thank you.

(Whereupon, Michael Behe, Ph.D., resumed the stand and testimony continued.)



Q. Good morning, Dr. Behe.

A. Good morning.

Q. Before we do get to the blood clotting, I need to circle back to sort of cover one housekeeping matter.

MR. MUISE: If I may approach the witness, Your Honor?



Q. Sir, I've handed you what has been marked as Defendants' Exhibit No. 237, which is an article from Saier, correct?

A. That's right.

Q. Is that one of the articles that you referenced during your testimony and appeared on one of the slides regarding the type III secretory system?

A. Yes, it is.

Q. Okay. Thank you, sir. Sir, yesterday, just to sort of recap and bring us to where we need to begin this morning, I had asked you if some scientists had argued that there is experimental evidence that complex biochemical systems can arise by Darwinian processes, and I believe you indicated there were two that are offered, correct?

A. That's right.

Q. And the first one was the lac operon?

A. Yes.

Q. And we discussed that yesterday?

A. Yes.

Q. And what is the second one?

A. The second one concerns what's called the blood clotting cascade, the system for clotting blood in animals. And I should say that, emphasize again that this is the second example of an experimentally -- an experimental result that was offered as evidence against some of the arguments that I made in Darwin's Black Box.

In this one, this is directed more to the question of irreducible complexity than to the question of whether Darwinian processes can put together a complex system.

Q. Now, sir, we've put up on the slide a figure, 6-5, that appears on page 142 in the Pandas text. Can you explain what we see here?

A. That's right. This is an electron micrograph of some red blood cells caught in a meshwork of a protein called fibrin, which forms a blood clot. And most people, when they think about blood clotting, if they think about it at all, it appears to be a simple process.

When somebody cuts themself, a minor cut slows down, stops, and heals over, and it doesn't seem like -- it doesn't seem like much at all. But thorough investigation over the past 40 to 50 years has shown that the blood clotting system is a very intricate biochemical system. And I believe there's an illustration of it on the next slide.

Q. Now you referred to, I believe, a blood clotting cascade, is that correct?

A. That's right.

Q. Can you explain a little bit to us as you're explaining what we see here on this particular diagram?

A. Okay, sure. Yeah, this is a figure of the blood clotting cascade taken from the biochemistry textbook by Voet and Voet, which is widely used in colleges and universities around the country. You see all these names of things and arrows. The names of things are very complex proteins of the complexity or sometimes more complex than the hemoglobin that I showed yesterday.

In blood clotting, the material that forms the clot cannot, of course, be in its solid clotted form during the normal -- during the normal life of an animal or all of the blood would be clotted, and that would be inconsistent with its life. So the material of the clot that actual eventually forms the clot exists as something called fibrinogen, which is actually a soluble pre-cursor to the clot material.

It floats around in your bloodstream during normal times. But when a cut occurs, fibrinogen is transformed into something called fibrin, and that happens when another protein comes along and cuts off a small piece of fibrinogen, a specific piece which exposes a sticky site on it, sticky in the sense of those two proteins yesterday that I saw that -- that I showed you that had complimentary surfaces.

It exposes a sticky site on the surface of the fibrinogen, which allows the many copies of fibrinogen, now turned into fibrin, to aggregate and stick to each other, forming the blood clot.

But what is the component that cuts fibrinogen and activates it? Well, the component is another protein called thrombin. But now we've got the same problem again. If thrombin were going around cutting fibrinogen and turning it into fibrin, all the blood would clot, and that would congeal the blood and kill the animal.

So thrombin itself is an inactive form called prothrombin, so it has to be activated when a cut occurs. And that's the responsibility of another protein. And that protein exists in an inactive form, and it's -- the activation of that is the responsibility of another protein.

So in the blood -- it's called a blood clotting cascade because one component acts on the next which acts on the next which acts on the next and so on. Now notice that the blood clotting cascade actually has what are called two branches. There is one in this box up here is labeled the intrinsic pathway. And this is labeled the extrinsic pathway. So there are actually two branches to this blood clotting cascade.

Q. I believe this section is addressed in the textbook Pandas, correct?

A. Yeah, that's correct. On the left is a figure from Of Pandas and People illustrating the blood clotting cascade. And that was drawn after the illustration from the textbook by Voet and Voet. On the right-hand side is the illustration for the blood clotting cascade that appears in Darwin's Black Box.

I discussed the blood clotting cascade in one chapter of that -- of my book, and the illustration is very similar to the one in Pandas.

Q. I believe the diagram in Pandas is found on page 143?

A. Yes, that's right.

Q. Now these two diagrams, the one that appears in Darwin's Black Box and one of the blood clotting cascade appear, to my eye, to be virtually similar or almost exactly similar?

A. Yeah, they are very similar, except for the color in Pandas and so on. And that's because I wrote the discussion in Pandas and, of course, also in my own book. So the figures are very similar between the two.

Q. Now you testified yesterday that you coined the term irreducible complexity in Darwin's Black Box, which was published in 1996, is that correct?

A. Yes.

Q. So that book was published actually three years after Pandas was written, is that accurate?

A. Yes, that's correct.

Q. Is it accurate to say then that the concept of irreducible complexity was not fully developed when you had written that section in Pandas on blood clotting in 1993?

A. Yes, that's right. I was still contemplating the idea.

Q. Does Pandas, however, discuss the complexity of this system, the blood clotting system?

A. Yes, it does. It elucidates all the parts of the system.

Q. Is that discussion consistent with your discussion in Darwin's Black Box?

A. Yes, it introduces the concept of the purposeful arrangement of parts and says that's how we perceive design.

Q. That's introduced in the Pandas book?

A. Yes, uh-huh.

Q. When you talk about the purposeful arrangement of parts, that's similar to what you were discussing yesterday in your testimony, is that correct?

A. Yes.

Q. So is the scientific explanation of the blood clotting system similar to the -- the discussion in Pandas similar to the blood clotting cascade scientific explanation in Darwin's Black Box?

A. That's right, they're essentially the same. I think it's more detailed in Darwin's Black Box.

Q. In fact, you did use the similar diagrams?

A. Yes, that's correct.

Q. To explain the two?

A. Yes, uh-huh.

Q. I believe the next slide we have is, this is from your -- you discussed this and treated this as well in your book Debating Design, is that correct?

A. That's right. When I wrote Darwin's Black Box, and when Darwin's Black Box was subsequently reviewed by people, some of them looked at the argument about the blood clotting cascade and argued against what I had written in Darwin's Black Box.

And I thought that the counterarguments were themselves flawed, and so I answered some of those arguments in a variety of cites, but most recently in the chapter in that book, Debating Design, published by Cambridge University Press from the year 2004.

I wrote The Blood Clotting Cascade. Having dealt with some common misconceptions about intelligent design, I will examine two systems that were proposed as serious counterexamples of my claim of irreducible complexity. One of them discussed in that article is the blood clotting cascade.

Q. If you could then, explain to us how you refute the claims that are made that the blood clotting cascade is experimental evidence to refute irreducible complexity?

A. Okay. In the next slide, I believe that shows an excerpt from an article written by a man named Russell Doolittle entitled A Delicate Balance, which appeared in a publication called the Boston Review in 1997. Now Russell Doolittle is a very eminent scientist, a professor of biochemistry at the University of California, San Diego.

He's a member of the National Academy of Sciences, and has worked on the blood clotting system for the past 45 years or so. And this article was a part of the symposium organized by Boston Review, which again is published by MIT, and contained contributions from a number of academics, scientists discussing my book and discussing a book that had been recently published by Richard Dawkins of Oxford University.

Participants included myself, Russell Doolittle, James Shapiro, who is a professor of microbiology at the University of Chicago, Alan Orr, who is a professor of evolutionary biology at the University of Rochester, Robert DiSilvestro, who is a professor of biochemistry at Ohio State, and a number of other people as well.

And in his essay, Professor Doolittle argued that, in fact, there was experimental evidence showing that the blood clotting system was not irreducibly complex. And he said the following. Let me read the quote. Quote, Recently the gene for plaminogen (sic) -- and that's actually a typo. There should be an S there. The gene for plaminogen (sic) was knocked out of mice -- which means that it was destroyed by molecular biological methods -- and predictable, those mice had thrombotic complications because fibrin clots could not be cleared away.

Let me stop a second and explain that plasminogen is a protein that acts as a chemical scissors which cuts up and removes blood clots once the clot has finished its job. Let me resume the quote from Russell Doolittle. 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.

Let me stop again and explain that fibrinogen, remind you, is the pre-cursor of the clot material itself, the pre-cursor of those fibers. 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.

Contrary to claims about irreducible complexity, the entire ensemble of proteins is not needed. Music and harmony can arise from a smaller orchestra. So Professor Doolittle's point, if I just might briefly say, was that, if you knock out one component of the blood clotting cascade, yes, those mice have problems.

If you knock out a different component in a different line of mice, yes, those mice have problems, too. But if you make a string of mice in which both of those components were missing, then the mice are normal and the blood clotting cascade is okay. And so presumably then, that shows that the blood clotting cascade is not irreducibly complex.

Q. Was there a particular study that Professor Doolittle is referring to?

A. Yes, it's shown on the next slide. This is the article that he was referencing in his own essay. It's entitled Loss of Fibrinogen Rescues Mice from the Pleiotropic Effects of Plasminogen Deficiency. Now if we could go to the next slide.

Now because of the phrase, rescues mice, in the title, Professor Doolittle thought that the mice missing both components were normal. But it turns out, that was a misreading of the article.

In the abstract of the article itself, the authors write, quote, Mice deficient in plasminogen and fibrinogen are phenotypically indistinguishable from fibrinogen deficient mice. Now translated that into English on the next slide.

That means that mice missing both components have all the problems that mice missing fibrinogen only have. Their blood does not clot. They hemorrhage. Female mice die during pregnancy. They are not normal. They are not promising evolutionary intermediates. So if we look at this table of the symptoms of the various strings of mice, we can see what the authors meant by that phrase, rescues mice.

Lacking plasminogen, mice can't remove blood clots once their job is done and their blood circulation gets interfered with and they develop problems such as thrombosis, ulcers, and so on. Lacking fibrinogen, they can't clot blood in the first place, and they have a different suite of symptoms.

When they lack both, they have been rescued from the symptoms of plasminogen deficiency, but only to suffer the symptoms of fibrinogen deficiency. And if you think about it for just a minute, it's easy to understand what is going on. When an animal lacks plasminogen, it can't remove blood clots and its circulation becomes impeded and it suffers problems.

Lacking fibrinogen, it can't make clots in the first place, and so hemorrhage is a problem. Lacking both, it doesn't matter that it's lacking plasminogen, because the plasminogen's job is to remove blood clots after the job is finished. But the mouse missing both components can't form clots in the first place. So there are no clots to remove.

Q. Has subsequent work verified those results?

A. Yes, here's a table of not only the work that was cited in this discussion here on plasminogen fibrinogen, but also subsequent work by the same group of scientists who knocked out other components of the blood clotting cascade, including something called prothrombin and something else called tissue factor.

And if you look at the -- under the column labeled effect, in each case the blood clotting cascade is broken. They suffer hemorrhage. They cannot clot their blood. And that is exactly the result you would expect if, in fact, the blood clotting cascade were irreducibly complex, as I had written.

Q. So Professor Doolittle's refutation of your claims was based on a misreading of the study, is that correct?

A. That's right. He misread the original paper that he pointed to. And if I could make a couple of points based on this. As I said, this study, or this essay by Professor Doolittle and the one I discussed yesterday by Professor Miller were the two examples which offered experimental evidence that either irreducible complexity was not correct or that random mutation and natural selection could explain complex biochemical systems.

But if you look at the exact studies that were offered as support for Darwinian evolution, and you look at them closely, in reality, they highlight the difficulties for Darwinian evolution. So I think this is an illustration of how a scientist's preconceptions about the truth of a theory or the validity of a theory can affect his reading of the evidence.

And one more point is that, Professor Doolittle, of course, is a very eminent scientist. Professor Miller is, too. And they're quite capable of surveying the entire scientific literature for studies that they think are problems for my argument for intelligent design.

And nonetheless, when they surveyed the whole literature, and they seemed to be motivated to look for counterexamples to intelligent design, when they do so, they offer studies such as this, which are, at best, very problematic and none of which, I would say, are arguments against intelligent design.

So in my mind, I conclude that since highly motivated capable scientists who could advance arguments or who could point to studies that have created problems for intelligent design, that they have failed to do so, makes me confident that intelligent design is a good explanation.

Q. Now these article findings, the actual findings in these articles, is that what you would expect to find for an irreducibly complex system?

A. Yes, that's right. This is completely consistent with my expectations.

Q. As far as you know, has Professor Doolittle ever acknowledged that he misread that paper?

A. Yes, he has.

Q. And if I could --

MR. ROTHSCHILD: Objection. Hearsay, Your Honor. I would move to strike.

MR. MUISE: Your Honor, he just -- he has an understanding that Professor Doolittle has indicated he has misread this paper.

MR. ROTHSCHILD: If he has a basis, I'd like to see it.

THE COURT: Well, it's his understanding, and I'm take it for that. I won't take it as a matter of fact. His understanding is, he didn't quote something that Professor Doolittle said. It's simply, I'll take it as his understanding, and you're free to cross-examine him and present rebuttal evidence, if you see fit. So it's overruled.


Q. Dr. Behe, I'd ask you to look at the exhibit binder that I had provided you yesterday. It's at your table in front of you. If you go to tab 17, please.

A. Yes.

Q. You'll see an exhibit marked Defendants' Exhibit 272. Is that the article by Russell Doolittle that you've been referring to here in your testimony?

A. Yes, that's correct. This is a web version.

MR. ROTHSCHILD: Objection, Your Honor. I want to make clear, I think that's not the acknowledgment of the mistake, it's just the article that's being referred to. I just want to clarify that.

MR. MUISE: I think the question was pretty clear.


Q. That's the article in the Boston Review that you're referring to?

A. Yes, this is Russell Doolittle's article in the Boston Review.

THE COURT: Does that resolve the objection?

MR. ROTHSCHILD: Yes. I just want to clarify, this was not Dr. Doolittle's acknowledgment of a mistake.


THE COURT: All right.


Q. Dr. Behe, does anyone else know how the blood clotting cascade can be explained in Darwinian fashion and other proposed examples or explanations?

A. No, that's one of the very nice things about science is that, if there is no explanation in the science library in scientific literature, and if leaders in the field do not know how something could have come about, and presumably they know the literature very, very well, then one can be confident that not only do they not know how something could have been done, but nobody else in the world knows how that could have been done as well. And that's important to keep in mind because some people claim that nonetheless.

Q. And that's my next question. There have been individuals that nonetheless have made such claims, and do you have some slides to bring that up?

A. Yes, that's correct. On the next slide is an excerpt from an article by a man named Michael Ruse. Michael Ruse is a professor of philosophy of science currently at Florida State University. And in particular, he's a philosopher interested in Darwinian thought.

And he's written many books on Darwin, his ideas, the history around them, and so on. And several years after my book came out in 1998, Professor Ruse wrote an article entitled Answering the Creationists, Where They Go Wrong and What They're Afraid Of, and had it published in a magazine called Free Inquiry. And he said the following in the article.

Quote, For example, Behe is a real scientist, but this case for the impossibility of a small-step natural origin of biological complexity has been trampled upon contemptuously by the scientists working in the field. They think his grasp of the pertinent science is weak and his knowledge of the literature curiously, although ventsly, outdated.

For example, far from the evolution of clotting being a mystery, the past three decades of work by Russell Doolittle and others has thrown significant light on the ways in which clotting came into being. More than this, it can be shown that the clotting mechanism does not have to be a one-step phenomenon with everything already in place and functioning. One step in the cascade involves fibrinogen, required for clotting, and another, plaminogen -- there's that typo, missing the S -- required for clearing clots away.

And he goes on in his article to quote that passage from Russell Doolittle's Boston Review essay that I showed on the slide a couple slides ago. So this excerpt, in my view, shows that Professor Ruse relies completely on Professor Doolittle's explanation for the blood clotting cascade and has no independent knowledge of his own.

As a matter of fact, the fact that the same typo, the same misspelling of plasminogen occurs in Professor Ruse's essay makes me think that he relied on Professor Doolittle even for the spelling of the components of the cascade. So the point is that, even though Professor Ruse is a prominent academic concerned with Darwin and Darwinian thought, he has no knowledge that Professor Doolittle does not have concerning the blood clotting cascade.

Q. Do you have another example, sir?

A. Yes, another person has written on this, a man named Neil Greenspan, who is a professor of pathology at Case Western Reserve University, and he wrote an article in a magazine called The Scientist in the year 2002 entitled Not-so-intelligent Design. In the article, he writes the following. Quote, The Design advocates also ignore the accumulating examples of the reducibility of biological systems. As Russell Doolittle has noted in commenting on the writings of one ID advocate -- and perhaps I can be forgiven if I think he means me -- mice genetically altered so they lack either thrombin or fibrinogen have the expected abnormal hemostatic phenotypes. However, when the separate knockout mice are bred, the double knockouts apparently have normal hemostasis, reducible complexity after all, at least in the laboratory.

So the reasoning here exactly mimics the reasoning of Russell Doolittle in his Boston Review article. And let me just point out here that he talks about thrombin or fibrinogen, but the study was actually on plasminogen and fibrinogen. So again, I think this illustrates that even a scientist has -- even a scientist writing publicly on this topic, even a scientist writing publicly on this topic in order to argue against intelligent design has no more knowledge of this than Professor Doolittle has.

And once more, I think this speaks to the point of how firmly a theory can guide persons' thinking. I think the fact that Professor Ruse relied so heavily on Professor Doolittle, and Professor Greenspan did, too, and apparently they did not even go back and read the article on blood clotting that was being disputed, shows that they are so confident in Darwinian evolution that they don't think they have to, you know, check the facts.

They can rely on the authority of a person like Professor Doolittle. So I think that shows the grip of a theory on many people's thinking.

Q. Do you have an additional example?

A. Yes, one other excerpt here. In 1999, the National Academy of Sciences issued a booklet called Science and Creationism. And in it, they write the following, quote, The evolution of complex molecular systems can occur in several ways. Natural selection can bring together parts of a system for one function at one time, and then at a later time, recombine those parts with other systems of components to produce a system that has a different function.

Genes can be duplicated, altered, and then amplified through natural selection. The complex biochemical cascade resulting in blood clotting has been explained in this fashion.

Let me make a comment on this. Professor Doolittle is a member of the National Academy of Sciences. There is no other member of the National Academy who knows anything more about blood clotting than Professor Doolittle. But if Professor Doolittle does not know how Darwinian processes could have produced the blood clotting cascade, as I think is evident from his pointing to an inappropriate paper in his attempt to refute a challenge to Darwinian evolution, then nobody in the National Academy knows either. I should also -- well, I'll --

Q. Do they cite any papers or experiments to support this claim, the National Academy of Sciences, in this particular booklet?

A. No. That's a very interesting point. They simply assert this. They do not cite any paper in any journal to support this. And it's an interesting point, if I may say so. I've heard said earlier in this trial that not every utterance by a scientist is a scientific statement.

And that's something that I entirely agree with. And it's also true that not every utterance by a scientist even on science is a scientific statement. And it's also true that not even, not every proclamation, or not every declaration by a group of scientists about science is a scientific statement.

Scientific statements have to rely on physical evidence. They have to be backed up by studies. And simply saying that something is so does not make it so. In fact, this statement of the National Academy is simply an assertion. It is not a scientific statement.

Q. Does the National Academy of Sciences, in this document that you referenced, give any other examples of complex biochemical systems that have been explained?

A. This is the only example that they point to.

Q. In his testimony, Dr. Miller has pointed to the work of, I believe, you pronounce is Jiang, J-i-a-n-g --

A. Yes.

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.

Q. Now Professor Pennock had testified that he was co-author on a study pertaining to the evolution of complex features. Does this study refute the claim of irreducible complexity?

A. No, it does not.

Q. And I believe we put up a slide indicating the paper that was apparently by Lenski and Pennock, correct?

A. That's right. Richard Lenski, and Professor Pennock was co-author, and several other co-authors as well. This is the first page of that article. Let me reemphasize that the last two systems that I talked about, the lac operon and the blood clotting cascade were ones in which experiments were done on real biological organisms to try to argue against intelligent design and irreducible complexity.

This study of Lenski is a computer study, a theoretical study not using live organisms, one which is conducted by writing a computer program and looking at the results of the computer program.

If I could have the next slide. This is an excerpt from the abstract of that paper. Let me read parts of it. It says, quote, A long-standing challenge to evolutionary theory has been whether it can explain the origin of complex organismal features, close quote. Let me just stop there to emphasize that these workers admit that this has been a long-standing problem of evolutionary theory.

MR. ROTHSCHILD: Objection. This mischaracterizes the document.

THE COURT: Elaborate on that objection.

MR. ROTHSCHILD: I'm sorry?

THE COURT: Elaborate on the objection. You say he's mischaracterizing --

MR. ROTHSCHILD: This is a long-standing challenge not a long-standing problem.

THE COURT: Well, I think he's characterizing something and not necessarily reading from it. What are you objecting to?

MR. ROTHSCHILD: I think he's mischaracterizing it. That's my objection.

THE COURT: Again, you'll have him on cross. This is direct examination. I'll overrule the objection. You may proceed.


Q. Dr. Behe, just for reference, the article you are referring to is published in 2003, is that correct?

A. That's correct, yes.

Q. Continue, please.

A. So apparently, this had not been explained up until at least the publication of this paper. The authors continue, quote, We examined this issue using digital organisms, computer programs that self-replicate, mutate, compete and evolve. Let me close quotes there.

You have to remember that the labeling of these things as organisms is just a word. These things are not flesh and blood. These things are little computer programs. There are strings of instructions. And a comparison of these to real organisms is kind of like comparing an animated character in some movie to a real organism.

So the authors go on. And the next slide, please. And this is the first figure on the first page of their article. And I just want to emphasize, this is just an illustration emphasizing that these -- there are computer instructions. Each one of these are little computer instructions; swap, nand, nand, shift R. They have no similarity to biological features, biological processes. You see over here little strings of ones and zeroes.

These are characters in a computer memory. These are not anything biological. Let me say that, theoretical studies of biology can oftentimes be very useful. And I'm certainly not denigrating the use of computer in studying biology. But one has to be careful, very careful that one's model, computer model mimics as closely as possible a real biological situation. Otherwise, the results one obtains really don't tell you anything about real biology.

And I think that the Lenski paper, it does not mimic biology in the necessary way. And that's shown on the next slide.

Q. Let me just, to clarify. So a crucial question is whether or not it's a good model for biological process, is that correct?

A. Yes, that's right.

Q. And you don't believe this is one?

A. No, I think it misses the point and it assumes what should be proven instead. And let me try to explain that with an excerpt from the article itself. The authors write in their discussion, quote, Some readers might suggest that we stacked the deck by studying the evolution of a complex feature that could be built on simpler functions that were also useful, close quote.

Let me stop there to comment that, yes, that is exactly what I would suggest, that they stacked the deck. They built a model in which there was a continuous pathway of functional Features very close together in probability, which is exactly the question that's under dispute in real biological organisms. Is there such a pathway in real biological organisms?

So to assume that in your computer model is stacking the deck. Let me go back to the abstract. They continue, quote, However, that is precisely what evolutionary theory requires. Now I'll close quote there, and let me comment on that.

Just because your theory requires something does not mean it exists in nature. James Clerk Maxwell's theory required ether. Ether does not exist. So just because a theory requires it is no justification for saying that building a model shows something about biology.

Q. Dr. Behe, if you could, just so we're clear on the record, because I'm not sure if we have it that clear, can you identify the title and the specifics of this article, so we're clear on what specific article you're referring to?

A. Yes, this is an article by Lenski, Ofria, Pennock, and Adami published in the year 2003. The title is The Evolutionary Origin of Complex Features published in the journal Nature, volume 423, pages 139 to 144.

Q. Thank you. And the authors go on to say in their discussion, indeed, our experiments showed that the complex feature never evolved when simpler functions were not rewarded. This is not surprising to me. This shows the difficulty of irreducible complexity. If you do not have those closely stacked functional states, if you have to change a couple things at once before you get a selectable property, then I have been at pains to explain, that's when Darwinian theory starts to fail, not when you have things close together.

And to build them into your model is, again, begging the question. The fact that when they do not build that into their model, they run into problems that complex features then don't evolve. That is exactly what I would expect. I would cite this as evidence supporting my own views.

Q. Have other scientists made similar criticisms?

A. Yes. A couple years ago, there was an article published by two scientists named Barton and Zuidema published in a journal called Current Biology. The title of the article is Evolution, The Erratic Path Towards Complexity.

And much of the article is a commentary on the work by Lenski and co-workers. And if I could just read a couple excerpts from that article. They make a couple interesting points. The authors say, complex systems, systems whose function requires many interdependent parts, that is irreducible complexity systems in my view, are vanishingly unlikely to arise purely by chance.

Darwin's explanation of their origin is that natural selection establishes a series of variants, each of which increases fitness. This is an efficient way of sifting through an enormous number of possibilities, provided there is a sequence of ever-increasing fitness that leads to the desired feature, close quote.

So that's the exact -- that's the big question. Is there such a pathway, or is it, as it certainly appears, that one has to make large numbers of changes before one goes from a functional selectable state to a second functional selectable state? And Barton and Zuidema continue in their discussion.

They say, in Lenski's artificial organisms, the mutation rate per site is quite high. So, in other words, if I might make my own comment, they are using -- they are using factors which are not common for biological organisms.

Now picking up with the paper again. So that favorable pairs can be picked up by selection at an appreciable rate. This would be unlikely in most real organisms because, in these, mutation rates at each locus are low. In other words, again, they are building into the model exactly the features they need to get the result they want.

But building it into your model does not show that that's what exists in nature. And Barton and Zuidema comment further, quote, Artificial life models such as Lenski, et al's, are perhaps interesting in themselves, but as biologists, we are concerned here with the question of what artificial life can tell us about real organisms.

It's -- it can be productive and it can be interesting to do such studies as Lenski, et al, did. But the big question is, do they tell us anything about real organisms? And I am very skeptical that this study does so.

Q. Now have you done some work yourself that's somewhat similar?

A. Yes, indeed. A year ago, as I mentioned earlier in my testimony, David Snoke and myself published a paper in the journal Protein Science entitled Simulating Evolution by Gene Duplication of Protein Features that Require Multiple Amino Acid Residues.

In this, we also -- it was essentially a theoretical study using computer programs to try to mimic what we thought would occur in biology. But we tried, as closely as possible, to mimic features of real proteins and real mutation rates that the professional literature led us to believe were the proper reasonable values.

And when we used those values, the short, the gist of the matter is that, once -- if there is not a continuous pathway, if one has to make two or three or four amino acid changes, those little changes from that figure of two interacting proteins that I talked about yesterday, if one has to make several changes at once, then the likelihood of that occurring goes -- drops sharply in the length of time, and the number of organisms in a population that one would need to have that goes up sharply.

Q. Would it be fair to say that your model is closer to biological reality?

A. Well, I certainly think so.

Q. Now Dr. Miller testified that the immune system is being explained by Darwinian theory. Do you agree with that?

A. No, I do not.

Q. And so I'd ask you if you could explain why not?

A. Yes. On the next slide is a -- is the first slide of Professor Miller's discussion of this topic and his presentation simply showing a model of an immunoglobulin protein. And here is kind of a little cartoon version of the same thing, the immunoglobulin protein.

He goes on the next slide to take an excerpt from my book where in a chapter where I discussed the immune system and argue that, in fact, it is not well-explained by Darwinian processes but, in fact, is better explained by design.

Q. Can you explain that Sisyphus reference?

A. Yeah, okay. Sisyphus. I said, Sisyphus himself would pity us. That was just a literary flourish there. Sisyphus is a figure from mythology who was doomed for eternity to have to roll a bolder up a hill, and whenever he got to the top of the hill, the bolder would roll back, and he would have to start all over again.

This was meant to indicate frustration. And I argued that Darwinian attempts at explanations would be similarly frustrating.

Q. I just want to make a point clear. You said there were two examples where those who claim that irreducible complexity does not work or is not a valid explanation, they use experimental evidence, and that was the blood clotting system and the lac operon. How does the immunity system, is that experimental evidence or is that a theoretical claim?

A. No, this is mostly a theoretical claim. There is no experimental evidence to show that natural selection could have produced the immune system. And I think that's a good example of the different views that people with different theoretical frameworks bring to the table.

If we could show the next slide. Professor Miller shows this slide from a reference that he cited by Kapitonov and Jurka, and he has titled Summary, Between 1996 and 2005, each element of the transposon hypothesis has been confirmed. He has this over this diagram.

But again, as I mentioned previously, whenever you see diagrams like this, we're talking about sequence data, comparison of protein, sequences, or gene sequences between organisms. And such data simply can't speak to the question of whether random mutation and natural selection produced the complex systems that we're talking about.

So Professor Miller -- so, in my view, this data does not even touch on the question. And yet Professor Miller offers as compelling evidence. And one more time, I view this as the difference between two people with two different expectations, two different theoretical frameworks, how they view the same data.

And I'd like to take a little bit of time to explain why such studies do not impress me. And I'll do so by looking at one of the papers that Professor Doolittle -- I'm sorry, Professor Miller, that's his name, cited in his presentation, Kapitonov and Jurka, that was published this year.

I just want to go through, and just kind of as a quick way to show why I am not persuaded by these types of studies. I want to excerpt some sentences from this study to show what I consider to be the speculative nature of such studies.

For example, in this excerpt, the authors say, something indicates that they may be important. This may indicate. It may be encoded. It might have been added. If so, it might have been derived. Alternatively, it might have been derived from a separate unknown transposon. It was probably lost. And we have a lot more of those, one more slide at least.

It says, we cannot exclude the possibility. In any case, the origin appears to be a culmination of earlier evolutionary processes. If so, this might have been altered. Again, without going into the detail of the article, I just wanted to emphasize those phrases to point out what I consider to be the very speculative nature of such papers.

Here's what I view to be the problem. The sequence of the proteins are there. The sequence of the genes are experimentally determined. And the question is, what do we make of that information? People like Professor Miller and the authors of this paper working from a Darwinian framework simply fit that data into their framework.

But to me, that data does not support their framework. It does not offer experimental evidence for that framework. They're simply assuming a background of Darwinian random mutation and natural selection and explaining it -- or fitting it into that framework, but they're not offering support for it.

Q. Dr. Behe, is there another paper that scientists point to for the support that the immune system can be explained by this Darwinian process?

A. Yes, there is. There is one more that I have to discuss. Here is a recent paper, again the year 2005, by Klein and Nikolaidis entitled The Descent of the Antibody-Based Immune System by Gradual Evolution. And on the next slide is an excerpt from the initial part of their discussion where they say, quote, According to a currently popular view, the Big Bang hypothesis, the adaptive immune system arose suddenly, within a relatively short time interval, in association with the postulated two rounds of genome-wide duplications.

So these people, Klein and Nikolaidis, are going to argue against what is the currently popular view among immunologists and people who study the immune system on how that system arose.

Q. And what is the Big Bang hypothesis that's referred to here?

A. Well, that's kind of a label that they put on to kind of indicate the fact that the immune system appears in one branch of animals, the vertebrates, and any obvious pre-cursors or functional parts of such a system do not appear to be obvious in other branches of animals.

So it seems like the immune system arose almost complete in conjunction with the branching of vertebrates from invertebrate.

Q. Do scientists acknowledge that or treat that as a problem for Darwin's theory?

A. Well, in my experience, no, nobody treats such a thing as a problem for Darwin's theory.

Q. Do you consider it a problem?

A. I certainly consider it a problem. But other scientists who think that Darwinian evolution simply is true don't consider much of anything to be a problem for their theory.

Q. Why do you consider it a problem?

A. Because the -- as Darwin insisted, he insisted that adaptations had to arise by numerous successive slight modifications in a very gradual fashion. And this seems to go against the very gradual nature of his view.

Q. Now has this paper been held up by scientists as refuting claims against intelligent design?

A. Yes, it has. As a matter of fact, Professor Miller cited it in his expert report, although he didn't refer to it in his testimony. Additionally, I attended a meeting on evolution at Penn State in the summer of 2004 where one of the authors, Juan Kline, spoke on his work, and he interpreted it in those terms.

Q. Now we have some quotes, I believe, from this paper that you want to highlight?

A. Yes. Again, I want to pull out some excerpts from that paper just to show you why I regard this as speculative and unpersuasive. For example, they start with, by saying, quote, Here, we sketch out some of the changes and speculate how they may have come about. We argue that the origin only appears to be sudden. They talk about something as probably genuine.

It probably evolved. Probably would require a few substitutions. It might have the potential of signaling. It seems to possess. The motifs presumably needed. One can imagine that a limited number. It might have been relatively minor. Quote, The kind of experimental molecular evolution should nevertheless shed light on events that would otherwise remain hopelessly in the realm of mere speculation. They're talking about experiments that have yet to be done.

Next slide, I have even more such quotations. These factors are probably genuine. Nonetheless. They might have postdated. Nevertheless. Albeit. It seems. This might have been. These might represent. They might have been needed. This might have functioned. This might have. And this might have contributed.

So again, this is just a shorthand way of trying to convey that, when I read papers like this, I do not see any support for Darwin's theory. I read them as speculative and -- but nonetheless, people who already do believe in Darwin's theory fit them into their own framework.

Q. Now Dr. Miller cited numerous papers in his testimony to support his claims on irreducible complexity, the type III secretory system, and so forth. Have you done a review of those papers and have some comments on them that you prepared slides for?

A. Yes, I did. I went through many of the papers that Professor Miller cited, as many as I could, and simply, as a shorthand way of trying to indicate or trying to convey why I don't regard any of them as persuasive, I simply did a search for the phrases, random mutation, which is abbreviated here in this column, RM, and the phrase, natural selection.

Random mutation, of course, and natural selection are the two elements of the Darwinian mechanism. That is what is at issue here. And so this is, you know, this is, of course, a crude and perhaps shorthand way, but nonetheless, I think this illustrates why I do not find any of these papers persuasive.

When I go through the papers that Professor Miller cited on the blood clotting cascade, Semba, et al, Robinson, et al, Jiang and Doolittle, there are no references to those phrases, random mutation and natural selection.

Q. Some of your indications on this slide, you have 0 with asterisks and some without. Is there a reason for that?

A. Yes. The papers that have asterisks, I scanned by eye. I read through them visually. Ones that do not have an asterisk, I was able to do a computer search for those phrases because they are on the web or in computer readable form. I have a number of other such tables.

On the next one are references that Professor Miller cited on the immune system. And again, none of these references contain either those phrases, random mutation and natural selection. There were a couple more references on the immune system that Professor Miller cited, and they didn't contain those phrases either.

In references for the bacterial flagellum and the type III secretory system, there was one paper by Hauch, a review in 1998 that did use the phrase natural selection. However, that phrase did not occur in the body of the paper. It was in the title of one of the references that Hauck listed.

And on the next slide, I think there are papers cited by Professor Miller on common descent of hemoglobin. And again, those phrases are not there. I think there's another slide or two, if I'm not mistaken. This is the one on what he described as molecular trees, Fitch and Margoliash, from 1967. And I didn't find the phrase there either. So again, this is a shorthand way of showing why I actually considered these off-the-point and unpersuasive.

Q. So all these papers that are being used to provide evidence for Darwin's theory of evolution, in particular, the mechanism evolution of natural selection, yet they don't mention random mutation or natural selection in the body of the works?

A. That's correct.

Q. Could you summarize the point then, Dr. Behe, that you are making with, referring to these studies and the comments you made about the speculative nature of some of these studies?

A. Yes. Again, much of these studies, in my view, are speculative. They assume a Darwinian framework. They do not demonstrate it. And certainly, you know, certainly scientists should be free to speculate whatever they want. You know, science usually starts with speculation, but it can't end with speculation.

And a person or, and especially a student, should be able to recognize and differentiate between speculation and actual data that actually supports a theory.

Q. So it would be beneficial to point this sort of feature that you just described, point that out to students?

A. I very much think so.

MR. MUISE: Your Honor, we're going to be moving again into another subject, and it appears to be close to the time for a break.

THE COURT: Yeah, why don't we take a break at this point. I think that makes good sense. We'll break for 20 minutes at this juncture, and we'll return and pick up direct examination at that point.

(Whereupon, a recess was taken at 10:11 a.m. and proceedings reconvened at 10:36 a.m.)


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