In September 2005, Ken Miller, a Brown University biologist, took the witness stand during a lawsuit known as Kitzmiller v. Dover Area School District. The plaintiffs, a group of parents in Dover, Pennsylvania, objected to "intelligent design" being required to be presented as an scientific alternative to evolution. Miller, the first expert witness called by the plaintiffs, showed that the key claims made by advocates of intelligent design are false. The plaintiffs won the case, and the people of Dover voted out the members of the Dover board of education who had pushed through the intelligent design requirements.

Over three years later, advocates of intelligent design are still trying to relive the case. In late December, the Discovery Institute unleashed a three-part attack on Miller's testimony, focusing on the evolution of proteins that make blood clot. I pointed out the absurdity of their arguments with the case of the one-wheeled bike.

But there's much more to this story, as Miller noted in an email he sent to me the other day--more science and more clues to the strategies intelligent design advocates will be using in the years to come.

While Miller is the author of a number of books and a frequent lecturer, he has not yet been absorbed into the blogosphere. And so I've invited him to share his thoughts in three posts. The first appears here; I'll post the next two over the weekend. [Update: Here's part two and part three.]

One of the enduring fantasies of the intelligent design (ID) movement is the notion that it might have won the Kitzmiller v. Dover trial if it hadn’t been consistently “misrepresented” in testimony by witnesses from the scientific establishment. Even worse, they point out, when their own heroes like Scott Minnich and Michael Behe attempted to correct those Darwinist distortions, Judge Jones, that liberal, ACLU-friendly activist, paid no attention. More than three years after Kitzmiller v. Dover, Discovery Institute spokesman Casey Luskin is still trying to win the case. During the trial itself, from which Discovery stalwarts William Dembski and Steven Meyer conspicuously withdrew, Luskin stood just outside the courtroom, spinning the day’s testimony for any reporter willing to listen. Casey’s still spinning, and now he’s doing his manful best to resurrect one of Behe’s favorite arguments for “irreducible complexity” (IC), the vertebrate blood clotting cascade. The culprit in its demise at the Dover trial, of course, was me. But according to Casey, my testimony was nothing more than “Smoke-and-Mirrors.” Here’s what he says: 1) The Mirror: According to Luskin, I misrepresented Behe’s arguments (from Darwin’s Black Box) by pretending that they were “essentially identical” to those found in the ID textbook Of Pandas and People. They aren’t, according to Luskin. 2) The Smoke: Luskin claims that I then used that misrepresentation of Behe’s position to state that ID requires the entire blood clotting cascade to be irreducibly complex. Since Behe, according to Luskin, had actually limited his argument for irreducible complexity to a “particular segment” of the cascade, that’s simply “wrong.” 3) Then, another Mirror: Therefore, according to Luskin, any claim that the absence of three components of the cascade in the puffer fish refutes ID is absolutely false. 4) Finally, the Rehabilitation: Behe’s actual ideas, according to Luskin, center around an “irreducible core” of components essential for the clotting reaction. Luskin argues that the core idea, which supports the intelligent design of the system, has stood up brilliantly under scientific scrutiny. The scientific reality, of course, is entirely different. First, there’s a perfectly good reason why I compared the clotting treatment in Pandas to Darwin’s Black Box (DBB). They are indeed nearly identical, and that’s because Behe himself wrote both of them. Second, Behe actually did state that the entire pathway is irreducibly complex in DBB. Casey might have skipped over those pages, but I didn’t. Third, as a result, the absence of any components of the cascade in any organism is indeed a direct contradiction of Behe’s formulation of ID. And finally, even Luskin’s “irreducible core” has fallen apart as the result of the most recent research findings on the system. Casey seems to forget — or to ignore — the fact that Behe has never even attempted to do any scientific research to show that he is right. He ignores the fact that ID’s critics have produced a boatload of research showing Behe to be wrong while Behe himself has done no research on the system that might support Luskin. As a result, his attempts at rehabilitating the clotting cascade as an “icon” of ID are a complete failure. So, for the umpteenth time, let’s go through this again. Here are the details, one at a time. 1) The Mirror? The essence of Luskin’s argument is that my testimony on the opening days of the Dover trial misrepresented Michael Behe’s position on the irreducible complexity of blood clotting. I supposedly did this by falsely conflating Behe’s arguments with those in the ID textbook, Of Pandas and People. According to Luskin, Behe’s actual arguments (from DBB) are “much more precise.” To be specific, in DBB, according to Luskin, Behe limited “his argument for irreducible complexity to a particular segment of the blood-clotting cascade.” The interested reader might begin by comparing pages 141-146 of Pandas to pages 81-97 of DBB (click here for both clotting diagrams). As you will see, the books show the system in identical diagrams (p. 143 and 82, respectively), clearly indicating that both were derived from a common source. That source, of course, was the author of both passages, Michael Behe. More to the point, these matching diagrams show at least 16 different factors in the cascade. Both books then use these complex diagrams to frame the essence of the clotting argument in nearly identical language in both passages: All of the parts have to be present simultaneous for the system to work. Here’s how he put it in the two books:

“When the system is lacking just one of the components, such as anti-hemophilic factor, severe health problems often result. Only when all the components of the system are present in good working order does the system function properly.” [Pandas, p. 145]

“… none of the cascade proteins is used for anything except controlling the formation of a blood clot. Yet in the absence of any one of the components, blood does not clot and the system fails.” [DBB, p. 86]

Writing in both books, Behe describes that as problem for evolution. Although the narrative style differs, the meaning of both passages is identical. Pandas notes similarities between some of the clotting proteins, which could be interpreted as evidence of common ancestry. However, it waves away that possibility by stating: “that even if this were the case, all of the proteins had to be present simultaneously for the blood clotting system to function” [Pandas, p. 146]. In DBB, the same issue is addressed this way: “The bottom line is that clusters of proteins have to be inserted all at once into the cascade. This can be done only by postulating a ‘hopeful monster’ who luckily gets all of the proteins at once, or by the guidance of an intelligent agent” [p. 96]. [emphasis in the original in both quotations]. In summary, there is at best only one difference between the two treatments, a passage found on page 86 of DBB:

“Leaving aside the system before the fork in the pathway, where details are less well known, the blood clotting system fits the definition of irreducible complexity. … The components of the system (beyond the fork in the pathway) are fibrinogen, prothrombin, Stuart factor, and proaccelerin.” [DBB, p. 86]

By ignoring this important difference, according to Luskin, I had misrepresented Behe and misled the Court. Behe clearly stated that the system contained just those parts past the “fork” in the pathway. How dare I pretend otherwise? Oh, the dishonesty! So, where did I get the idea that Behe’s argument for ID actually included the whole system, just like Pandas’s treatment? Easy. Unlike Mr. Luskin, I read Behe’s whole book — including the parts before and after page 86, and I took Michael Behe at his word, as you will see. 2) The Smoke? The claim that Michael Behe meant to include only a handful of components from the cascade in his “irreducibly complex” system would come as a shock to anyone who has actually read DBB. Behe describes the system in great detail, asking us to consider the whole system in all its complexity, including each of its 16 different components. In fact, Behe emphasizes how critical each and every component of the system is, pointing out that the absence of certain factors (VIII and IX) cause potentially fatal human diseases (hemophilia A and B, respectively). But then, just as Luskin points out, on page 87, he suddenly seems to retreat, limiting the system to just four factors (fibrinogen, prothrombin, Stuart factor, and proaccelerin). So any suggestion to the contrary is unfair to Behe and ID, right? Not so fast. Just keep reading. He doesn’t actually limit his “irreducible core” at all in the way that Luskin now pretends. Instead, on the very next page [p. 87] he discusses the hopelessness of evolution being able to change even a “slightly simplified system” gradually into a “complex, intact system.” Why? Because adding even a single step to the pathway is beyond the range of evolution. As Behe puts it, “From the beginning, a new step in the cascade would require both a proenzyme and also an activating enzyme to switch on the proenzyme at the correct time and place.” Then he drops the bombshell that Luskin seems not to have noticed (or, at least he wasn’t willing to tell his readers about):

“Since each step necessarily requires several parts, not only is the entire blood-clotting system irreducibly complex, but so is each step in the pathway.” [DBB, p. 87]

Got that? The “entire blood-clotting system” is “irreducibly complex,” and “so is each step in the pathway.” Which Michael Behe should we believe? The pre-Dover trial one who described the whole magnificent system as an argument for ID? Or the one who flip-flops to a tiny core of just four proteins? Or the one who flip-flops again a page later, and once again says that the “entire blood-clotting system” and each of its steps are irreducibly complex? I wasn’t blowing any “smoke” when I characterized Behe’s views as pertaining to the entire clotting pathway in both books. What I was actually doing, unlike Luskin, was taking Behe’s claims in their totality. Behe really did argue that the whole system is irreducibly complex, and that it would be impossible for evolution to add so much as a single step to it. That’s why I testified to the effect those missing clotting factors in the pufferfish were a fatal blow to Behe’s argument. And so they are. The only mirror I held up to the Court was the one that reflected Behe’s own written arguments in Pandas and DBB. 3) The Judge? Luskin seems surprised that the Judge paid no attention to Behe’s attempts to “correct” my testimony on this point. After all, isn’t the blood-clotting argument in DBB more carefully qualified than the one in Pandas? Well, it may be. It certainly is more detailed, since it is intended for readers a bit older than your average 14-year-old. But there is something very strange, and even distressing, about Luskin’s contention that the obvious failings of the arguments in Pandas are somehow less important than the ones in DBB. Why is it OK to give high school readers an argument about the irreducible complexity of the entire cascade that you know to be false (as Luskin admits), just as long as you modify that argument in another book? Luskin seems to have forgotten that the Dover trial was about an issue much more important than the fate of ID…. It was about what should be taught to high school science students. And, in that respect, the arguments in Pandas were the ones that really mattered. And those arguments, as my friend Casey Luskin has implicitly admitted in his first web posting, were completely wrong. Too bad he didn’t spin that message at the trial. 4) An “Irreducible Core?” Here’s where things get really, really interesting. Luskin maintains that the “irreducible core” is a “long-standing concept within ID thinking,” and argues that this concept is well-supported by current research on the system. Well, is it? Does the blood-clotting system really contain an “irreducible core?” Not even close. Luskin’s own sketch of that core highlights seven (count ‘em) components in that core (click here for that image. The core is the red box in his diagram). Those seven components are:

Tissue Factor Factor VIII (Antihemophilic Factor) Factor X (Stuart Factor) Factor V (Proaccelerin) Factor II (Prothrombin) Factor XIII (Fibrin Stabilizing Factor) Fibrinogen

According to Luskin, these form an “irreducible core” without which blood clotting would not be possible. Once again, ID fails, and the culprit isn’t a liberal judge, the ACLU, or even a slick-talking smoke-and-mirrors biology prof. It’s nature itself, in the form of a collaboration between a nasty little beast called the lamprey (Petromyzon marinus), and a pioneering scientist who has spent his career working out the evolution of the clotting cascade. That scientist is Russell Doolittle of the University of California at San Diego Diego (which, as it happens, is the very same university where Casey got two degrees in Earth Science while simultaneously founding and managing his creationist “Intelligent Design and Evolution Awareness” [IDEA] Club). His 2008 paper [Doolittle et al, 2008] reports on a careful search through the lamprey genome. The lamprey, as luck would have it, has a perfectly functional clotting system, and it lacks not only the three factors missing in jawed fish, but also Factors IX and V. Now, Luskin could object that Factor IX wasn’t part of his “core,” but Factor V certainly was. And, as Behe pointed out at length, the absence of factor IX causes potentially-fatal hemophilia in humans, which was part of his argument for the irreducible complexity of the whole system. The lamprey genome does contain a single gene, somewhat related to Factor X and Factor V, but not identical to either. As the paper’s authors put it: “In summary, the genomic picture presented here suggests that lampreys have a simpler clotting scheme than later diverging vertebrates. In particular, they appear to lack the equivalents of factors VIII (or V) and IX, suggesting that the gene duplication leading to these factors, synchronous or not, occurred after their divergence from other vertebrates.” [p. 195]. To make things even worse for Luskin’s “core,” a previous study from Doolittle’s lab [Jiang & Doolittle, 2003] had already shown that the bits and pieces (protein domains) of most of the clotting factor proteins are present in a primitive, invertebrate chordate. This is exactly what one would expect from an evolutionary trajectory leading to the current system in vertebrates — the assembly of a complex pathway from pre-existing parts. So, what are we left with? Nothing more than a vain attempt to pretend that ID’s collapse in the Dover case was the result of misrepresentation and deception. For Mr. Luskin and his employers at the Discovery Institute, the generation of sound and fury continues, but in scientific terms, their continuing noise signifies nothing more than the utter emptiness of their failed ideas.

(Tomorrow: The fingerprint of evolution left in whale DNA.)

References: Pallen MJ, Matzke NJ. (2006). “From The Origin of Species to the origin of bacterial flagella.” Nature Reviews Microbiology, 4: 784-790. Bottaro A, Inlay MA, Matzke NJ (2006) “Immunology in the spotlight at the Dover 'Intelligent Design' trial.” Nature Immunology 7: 433 – 435. Doolittle RF, Jiang Y, Nand J. (2008) “Genomic evidence for a simpler clotting scheme in jawless vertebrates.” J. Mol. Evol. 66:185-96. Jiang Y, Doolittle RF (2003) “The evolution of vertebrate blood coagulation as viewed from a comparison of puffer fish and sea squirt genomes.” PNAS 100: 7527-7532 Semba U, Shibuya Y, Okabe H, Yamamoto T (1998) Whale Hageman factor (factor XII): prevented production due to pseudogene conversion. Thromb. Res. 90: 31–37. [Image courtesy of Ken Miller]