There are two main problems with Intelligent Design Creationism. The first is that the IDiots never have anything positive to offer by way of explanation. They complain about how evolution can never do this or that but they never give us a better explanation based on their beliefs. The second problem is that the IDiots often get their science wrong when they complain about evolution. Sometimes this is deliberate, but in many cases it's because they just don't understand what they're criticizing. Their criticisms of evolution are based on the notion of a false dichotomy. They think that there are only two choices: their conception of evolution, or Intelligent Design Creationism. Thus, if they can refute their version of evolution it follows that creationism must be true.
People often make the claim that Intelligent Design Creationism isn't science. That may be true if you only think of it as promoting the idea of an intelligent designer but even there it depends on how you define science. However, much of the Intelligent Design Creationism literature isn't about defending creationism, it's about attacking evolution and those arguments definitely fall within the definition of science. As scientists, we have to deal with all the objections to evolution no matter what the motives of the challengers.
I think it's somewhat simplistic to dismiss all the Intelligent Design Creationist literature on the grounds that it's not science. Some of it has all the earmarks of science, it's just bad science. And bad science isn't limited to IDiots. I think there are many Theistic Evolutionists who are also guilty of promoting bad science and there are many atheist scientists who are just as guilty. The peer-reviewed scientific literature is full of examples.
Although it makes my American friends cringe, I favor teaching the controversy. It's the only way to show students the difference between good science and bad science.
Some of the Intelligent Design Creationists can craft pretty convincing arguments against evolution. It takes a lot of work to refute them. I going to give you an example of such an argument from The Edge of Evolution by Michael Behe. Let's see how you do.
The Two Binding Sites Rule
Behe's version of the history of life requires a God who intervenes quite frequently to create specific mutations that are almost impossible to account for by random mutation. Behe makes a good case for the problems with random mutation. In fact, his arguments are similar to those put forth by the mutationist camp—a group that I'm in sympathy with. Most biologists would not be able to refute Behe's arguments because they would agree with some of his false premises.
Behe's "Two Binding Sites Rule" is a good example. He argues that in order for two proteins to interact, evolution needs to create a small patch on the surface of each protein where five or six amino acid side chains become compatible with binding. Some of these changes could be neutral so they could arise independently but the analysis of hundreds of known binding sites shows that many of the mutations would be detrimental if they occurred by themselves—a single charged amino acid residue on the surface, for example.It looks like you need to wait for three or four specific mutations to occur simultaneously in order to get a moderate interaction between two proteins that did not originally bind to each other. And these can't be just any proteins, they have to be proteins where there is a selective advantage to forming a complex. The example I've chosen is a bacterial photosynthesis reaction center where four polypeptides (gold, blue, green, purple) interact with each other and with multiple cofactors (space-filling molecules) to form a very complicated structure. Presumably, there was a time in the past when some of these proteins didn't bind to each other or to the cofactors. Over time, evolution favored variants that could form the complex. How could this happen according to evolutionary theory?
Studies on in vitro mutagenesis show that the probability of forming any de novo binding site is very low. For example, it's quite difficult to engineer specific antibodies that will bind to a particular antigen. The data shows us that you need a library of more than one billion antibody molecules in order to get one that will bind. Those one billion mutations are far from random. They are engineered so that they are confined to a small patch on the surface of the antibody where it is known that other proteins can potentially bind.
Behe argues from this evidence that the probability of creating a new binding site by random mutations is exceedingly small. So small, in fact, that such mutations would only arise in very large populations after several hundred million years of evolution. He bases his argument on some experiments he describes in the first few chapters or his book.
Behe points out that it is sometimes very difficult for the malaria-causing parasite, Plasmodium falciparum, to develop resistance to some drugs used to treat malaria. That's because the resistance gene has to acquire two specific mutations in order to become resistant. A single mutation does not confer resistance and, in many cases, the single mutation is actually detrimental. P. falciparum can become resistant because the population of these single-cell organisms is huge and they reproduce rapidly. Thus, even though the probability of a double mutation is low it will still happen.
If the probability of a single mutation is about 10-10 per generation then the probability of a double mutation is 10-20. He refers to this kind of double mutation as CCC, for "chloroquine-complexity cluster," named after mutation to chloroquine resistance in P. falciparum.1 Behe's calculation is correct. If two simultaneous are required then the probability will, indeed, be close to 1 in 1020.
Let's see how this relates to the evolution of protein-protein interactions. Here's how Behe describes it on page 135 of his book.
Now suppose that, in order to acquire some new, useful property, not just one but two new protein-binding sites had to develop. A CCC requires, on average, 1020, a hundred billion billion, organisms—more than the number of mammals that has ever existed on earth. So if other things were equal, the likelihood of getting two new binding sites would be what we called in Chapter 3 a "double CCC"—the square of a CCC, or one in ten to the fortieth power. Since that's more cells than likely have ever existed on earth, such an event would not be expected to have happened by Darwinian processes in the history of the world. Admittedly, statistics are all about averages, so some freak event like this might happen—it's not ruled out by the force of logic. But it's not biologically reasonable to expect it, or less likely events that occurred in the common descent of life on earth. In short, complexes of just three or more different proteins are beyond the edge of evolution. They are lost in shape space.We're all pretty knowledgeable here but how many of you can immediately refute that argument? If you can't then you have no business accusing Behe of being stupid or silly and of dismissing his book as just another example of creationist ignorance. The correct explanation of the problem will undoubtedly appear soon in the comments. Before peeking, why not try and see how you would answer Behe if you were debating him in front of a large audience of creationists?
1. Behe may have been wrong about the specific chloroquine resistance mutation he used as an example. The two mutations may not have occurred simultaneously. Nevertheless, the principle is sound. If the single mutations are detrimental then you need both to get resistance and the probablity of two such mutations occurring together is 10-20.
