Koons, Part One In Wednesday's post I mentioned William Dembski's latest offering Uncommon Dissent: Intellectuals Who Find Darwinism Unconvincing. The first essay in this anthology is by Robert Koons, a professor of philosophy at the University of Texas. It is entitled “The Check is in the Mail: Why Darwinism Fails to Inspire Confidence”
I have earlier commented that the line-up of contributors to this volume was unimpressive, based on the fact that almost none of them have credentials in biology, and many don't have credentials in any branch of science. Despite this, I was vaguely optimistic that the book would offer something worth mulling over. After all, most ID books are published by Christian publishers and directed at audiences who use “intellectual” as an epithet. My hope was that the tone of the essays would be respectful, and that I would find plausible reasons for why the evidence for evolution, so persuasive to me, is not persuasive to other thoughtful people.
Sadly, that was too much to hope for. Koons' essay is, I'm sorry, awful. It is long on snarkiness and arrogance, but short on serious consideration of just what it is the biological sciences have been doing in the century and a half since Darwin.
Before considering his main argument, let us first make note of one bright spot in the essay. He writes:
Darwin himself contributed to the illicit shift in the burden of proof in his well known challenge to his critics in The Origin: “ If it could be demonstrated that any complex organ existed which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down.” It is, of course, impossible to “demonstrate” any such thing. (P.13)
I describe this quote as a bright spot because he is tactily rejecting the fundamental piller in the case for ID: the irreducible complexity of certain biochemical systems. When Michael Behe introduced this idea in Darwin's Black Box he quoted the very same line from Darwin that Koons used. It was Behe's claim that systems which could not be formed by numerous, successive, slight modifications had now been found, and they were precisely those systems involving several, well-matched parts, such that the removal of any one part rendered the system non-functional. Do a google search on Darwin's quote and you will come up with dozens of creationist web sites claiming that Darwin's challenge had been met. Yet here Koons is plainly rejecting this claim. Good for him.
Sadly, that's the only interesting line in Koons' dreary essay. We should point out that Darwin was not shifting any burden of proof and he was not challenging his critics to do anything. He was merely emphasizing the importance of gradualness within his theory. The quote comes at the end of chapter six, “Difficulties on Theory”, in which Darwin discusses potential challenges to his ideas and explains why he finds them uncompelling.
Picking up where the previous quote left off:
How could it be proved that something could not possible have been formed by a process specified no more fully than as a process of “numerous, successive slight modifications”? And why should the critic have to prove any such thing? The burden is on Darwin and his defenders to demonstrate that it is really possible for at least some of the complex organs we find in nature to be formed in this way: that is by some specific, fully articulated series of slight modifications.
Koons offers some rather specific (and laughable) thoughts on what would be required to assert with confidence that natural selection lies behind most of the complexity we see in nature. He also argues that until scientists can meet his ridiculous standards, ID should win by default. I will consider the specific points he makes in this regard in tomorrow's posting. But first, let's take up the general question of why scientists do, in fact, assert with confidence that natural selection crafted most of the complexity we find in the genomes.
The first thing to observe is that there is absolutely no reason in theory to think that natural selection can not craft a complex organ. Critiques based on the fact that natural selection is a mindless process with no foresight that acts on random variations are fundamentally misguided. The mindlessness and lack of foresight of natural selection are totally irrelevant in determining whether a particular complex structure evolved gradually. All that is relevant is whether it is possible to find a series of small steps, each one beneficial (or at least not harmful) to its bearer, leading from some ancestral species that lacked the structure to the modern species that possess it. If such a series exists than selection is a plausible explanation. If no such series exists, then selection is not a viable explanation. This was the point Darwin was making in the quote given above. Richard Dawkins makes the same point in his book Climbing Mount Improbable.
So is Koons right? Is Darwin's requirement so loose that any organ could conceivably have been formed gradually? Hardly.
People like Koons present natural selection as if it were some abstract principle invoked by scientists to avoid having to deal with the enormous complexity of biochemical systems. The reality is quite different. In attributing a complex structure to the action of selection, scientists are imposing severe explanatory constraints on themselves. Any scenario of gradual evolution must be consistent with everything that is known about the system, and inevitably makes predictions about similar systems in related animals.
To see why, let's consider a specific example: Blood clotting. This is one of the systems described by Behe as being irreducibly complex. It is also singled out by Koons in his essay. Biologist Ken Miller described a scenario for the evolution of blood clotting in his book Finding Darwin's God. Here's an excerpt from the original draft of the relevant section (the published version had been shortened due to space considerations):
Even a general scheme, like the one I've just presented, leads to a number of very specific predictions, each of which can be tested. First, the scheme itself is based on the use of well-known biochemical clues. For example, most of the enzymes involved in clotting are serine proteases, protein-cutting enzymes so-named because of the presence of a highly reactive serine in their active sites, the business ends of the protein. Now, what organ produces lots of serine proteases? The pancreas, of course, which releases serine proteases to help digest food. The pancreas, as it turns out, shares a common embryonic origin with another organ: the liver. And, not surprisingly, all of the clotting proteases are made in the liver. So, to “get” a masked protease into the serum all we'd need is a gene duplication that is turned on in the pancreas' “sister” organ. Simple, reasonable, and supported by the evidence.
Next, if the clotting cascade really evolved the way I have suggested, then the clotting enzymes would have to be near-duplicates of a pancreatic enzyme and of each other. As it turns out, they are. Not only is thrombin homologous to trypsin, a pancreatic serine protease, but the 5 clotting proteases (prothrombin and Factors X, IX, XI, and VII) share extensive homology as well. This is consistent, of course, with the notion that they were formed by gene duplication, just as suggested. But there is more to it than that. We could take one organism, humans for example, and construct a branching “tree” based on the relative degrees of similarity and difference between each of the five clotting proteases. Now, if the gene duplications that produced the clotting cascade occurred long ago in an ancestral vertebrate, we should be able to take any other vertebrate and construct a similar tree in which the relationships between the five clotting proteases match the relationships between the human proteases. This is a powerful test for our little scheme because it requires that sequences still undiscovered should match a particular pattern. And, as anyone knows who has followed the work in Doolittle's lab over the years, it is also a test that evolution passes in one organism after another.
There are many other tests and predictions that can be imposed on the scheme as well, but one of the boldest was made by Doolittle himself more than a decade ago. If the modern fibrinogen gene really was recruited from a duplicated ancestral gene, one that had nothing to do with blood clotting, then we ought to be able to find a fibrinogen-like gene in an animal that does not possess the vertebrate clotting pathway. In other words, we ought to be able to find a non-clotting fibrinogen protein in an invertebrate. That's a mighty bold prediction, because if it could not be found, it would cast Doolittle's whole evolutionary scheme into doubt.
Not to worry. In 1990, Xun Yu and Doolittle won their own bet, finding a fibrinogen-like sequence in the sea cucumber, an echinoderm. The vertebrate fibrinogen gene, just like genes for the other proteins of the clotting sequence, was formed by the duplication and modification of pre-existing genes.
This passage comes at the end of a lenghty outline of blood clotting evolution that I recommend to everyone. Miller's writing is excellent, and he makes some rather complex biochemistry easy to understand. What Miller makes clear is that evolutionary biologists do not simply wave their hands, tell just-so stories, and call their job complete.
Miller's discussion also makes clear how we could find evidence that selection was not the crafter of some particualr complex strucure.
For example, he asserts that several of the proteins in the blood clotting cascade arose as the result of a gene duplication event. This explanation is viable only because the proteins in question show a high degree of sequence similarity. If that similarity did not exist, then Miller's scenario would not be viable.
Similarly, Miller's scenario for the formation of human blood clotting proteins has consequences for what we should find when we examine blood clotting in other vertebrates. As he indicates, those predictions are borne out. With each such successful prediction his scenario becomes more likely; just how science is supposed to proceed.
So, do complex biochemical systems in humans give the appearance of having been made from scratch out of materials unique to humans, or do they show evidence of having been cobbled together from parts that were readily available in other, related organisms? Every case studied to date has fallen into the latter category.
There are many other examples of this sort of reasoning. Darwin showed that the elaborate structures orchids use to attract pollinating insects were cobbled together from parts common in flowers. Had he found instead that they were composed of parts entirely unique to orchids, it would be much harder to attribute their formation to selection.
Stephen Jay Gould famously used the panda's thumb to illustrate the same principle.
Evidence of selection's activity comes in many other forms as well. One example that I like (because it is largely mathematical) is the role of game theory in the study of animal behavior. Game theoretic models have rendered comprehensible many formerly puzzling aspects of animal behavior. These models are based explicitly on the assumption that the behaviors in question were formed by selection. The success of these models is evidence of the correctness of that assumption.
Such examples could be multiplied endlessly. The point is that the hypothesis that natural selection is responsible for crafting complex organs has led to enormous progress in all branches of biology. This progress is strong evidence for the correctness of the hypothesis. What I have described does not even scratch the surface of what is out there. Biologists conitnue to invoke the action of natural selection because they find it enormously useful to do so.
ID proponents, unburdened by the repsonsibility of actually entering a lab and making progress on some problem of biological interest, dismiss all of this with a disgusted wave of the hand. They routinely argue that if we can not specify which genetic locus mutated when we can not have confidence that a given complex structure evolved gradually via selection. One ID proponent who argues that way is Koons, as we shall see in tomorrow's posting.