The following is Michael Behe’s response to the essays published by Boston Review following Allen Orr’s review of Darwin’s Black Box.
Professor Orr has a mistaken notion of irreducible complexity. I thought I made that clear in my reply, but from his response I suppose I did not, so let me try again. I define irreducible complexity in Darwin’s Black Box as “a single system composed of several well-matched, interacting parts that contribute to the basic function, wherein the removal of any one of the parts causes the system to effectively cease functioning.” Orr, however, uses the term loosely to mean something like “if you remove a part, the organism will die.” In his review he talks about lungs, saying “we grew thoroughly terrestrial and lungs, consequently, are no longer luxuries?they are essential.” The problem is, if you quickly dissect lungs from an animal, many parts of it will continue to work. The liver will work for a while, muscles will twitch, and cells will metabolize until they run out of oxygen. Thus lungs are not absolutely required for the function of those other parts, not in the way that a spring is absolutely required for a standard mousetrap or nexin linkers are required for ciliary function. That’s the problem with using poorly chosen examples, especially at the whole-organ level. I am careful in my book (pp. 46-47) to say that you must look at molecular systems to see if Darwinism can explain their development. When you look at irreducibly complex molecular examples, it is clear that Darwinism has not and, I believe, cannot explain them. Orr’s main line of argument, therefore, simply misses the point.
I should also point out that, contrary to Professor Orr’s assertion, we do not know that swim bladders evolved into lungs by natural selection. There is absolutely no evidence for it. It may be likely that lungs are descended from swim bladders, but no experiment has indicated that natural selection can do the trick. In fact, no one even knows at the nuts-and-bolts molecular level what it would take. Orr simply assumes it is possible because he is not bothering with the myriad molecular difficulties that would face such a transformation.
Orr says that the parts of a mousetrap might have started out as something else, and then were changed into their current parts. I address this type of argument on page 66 of Darwin’s Black Box. Essentially this approach doesn’t help. The parts still have to be adjusted to each other at some stage, and they still don’t work until all the parts have been so adjusted. That requires intelligent activity.
Orr says we know mousetraps are designed because we have seen them being designed by humans, but we have not seen irreducibly complex biochemical systems being designed, so we can’t conclude they were. I discuss this on pp. 196-197. We apprehend design from the system itself, even if we don’t know who the designer is. For example, the SETI project (Search for Extraterrestrial Intelligence) scans space for radio waves that might have been sent by aliens. However, we have never observed aliens sending radio messages; we have never observed aliens at all. Nonetheless, SETI workers are confident, and I agree, that they can detect intelligently-produced phenomena, even if they don’t know who produced them. Orr’s criterion is also subject to a reductio ad absurdum. Suppose we flew to an alien planet and observed a deserted city. Orr’s position would hold that we can’t conclude the city was designed, because we have never seen aliens producing cities, and he would oblige us to search for an unintelligent cause for the manifestly designed city.
Orr finds it “extremely curious” that I think some systems could evolve by natural selection, but that others couldn’t. I discuss this on pp. 205-208. Simply put, some systems are more complex than others, irreducibly so. If one biochemical system looks pretty much like the other to Orr, then he isn’t going to see any problems. However, if you attend to the details of each system, as I tried to do, difficulties for Darwinism loom at many places.
Phillip Johnson can fight his own battles, but I’d just like to say I think it odd that Orr jumps on Johnson for an understandable confusion of terms. Orr seems to think that the essence of explanation is in knowing the labels that evolutionists have put on concepts, rather than on whether the concepts actually explain how life got here. It is especially odd when Orr gives no indication of understanding much about the molecular basis of life, where all the inheritable action necessarily takes place.
Jerry A. Coyne
Professor Coyne seems really to have been traumatized by being quoted in my book (page 29). He should relax. My purpose in quoting him and others was to show that many thoughtful biologists found Darwinism to be an incomplete theory of life. I did not say that Coyne or the others agreed with intelligent design. Indeed, for several of the people I quoted (Stuart Kauffman and Lynn Margulis) I specifically discuss their alternative theories to Darwinism. I start off the section by saying “A raft of evolutionary biologists examining whole organisms wonder just how Darwinism can account for their observations.” After a few other people, I quote Coyne as saying, “We conclude — unexpectedly — that there is little evidence for the neo-Darwinian view: its theoretical foundations and the experimental evidence supporting it are weak.” In Coyne’s paper, the sentence did not stop there; it continued with “and there is no doubt that mutations of large effect are sometimes important in adaptation.” I do not see, however, where that changes the sense of the sentence at all. In my manuscript I had his quote ending with an ellipsis, but the copy editor took out all ellipses in this section and put in periods, so I assume that it is in keeping with standard editorial practices. It is extremely difficult for me to understand why Coyne thinks his idea is anything other than a doubt about the efficacy of Darwinism, or what context could possibly change its plain meaning. Coyne goes on to quote the entire paragraph in which the sentence appeared, but that changes nothing of the basic thrust as far as I can see.
Coyne says my book bears the four marks of “crank science,” which I will address in turn:
1) Coyne says I did not present my views “directly to the scientific community.” Free Press sent my book out to a number of scientists for their review. One angrily told Free Press not to publish because he viewed intelligent design theory as “giving up.” Three said they thought the book meritorious and worthy of publication, although they did not agree with my conclusion of intelligent design. One scientist thought the book worthy of publication, and thought that intelligent design was possibly true. Additionally, my book was put up for competitive bidding, and several university presses were interested. They were outbid by Free Press.
2) Coyne complains that if one biochemical pathway is explained by natural selection, intelligent design advocates can just move on to another, and so ID is not falsifiable. This complaint would have some merit if Darwinists had explained any complex biochemical system. I can’t speak for others, but for myself if I were convinced that natural selection could explain a system of a certain degree of complexity, then I would assume it could explain other systems of a similar or lesser degree of complexity. However, to date it has not been able to explain the origins of functional systems of much complexity at all.
3) Coyne says Behe “likens himself to Newton, Einstein, and Pasteur.” I do not. I clearly acknowledge that the credit belongs to the scientific community as a whole, whose cumulative work makes design apparent. Here are some relevant sentences from pages 232-233:
“The result of these cumulative efforts to investigate the cell — to investigate life at the molecular level — is a loud, clear, piercing cry of “design!” The result is so unambiguous and so significant that it must be ranked as one of the greatest achievements in the history of science. The discovery rivals those of Newton and Einstein, Lavoisier and Schrödinger, Pasteur and Darwin…. The magnitude of the victory, gained at such great cost through sustained effort over the course of decades, would be expected to send champagne corks flying in labs around the world. This triumph of science should evoke cries of “Eureka” from ten thousand throats, should occasion much hand-slapping and high-fiving, and perhaps even be an excuse to take a day off…. Why does the scientific community not greedily embrace its startling discovery?”
It does not take a rocket scientist to see design; the hard work was in the day-in, day-out elucidation of the molecular workings of the cell. For someone who is as touchy as he is to possible misinterpretation, Coyne seems not to mind putting a strained interpretation on other people’s writing.
4) Coyne complains the book is “heavily larded” with quotations from evolutionists. This leads into his being upset with being quoted himself, as discussed above. That aside, however. I don’t know what to make of this statement. What is a book concerning evolution supposed to contain if not quotes from evolutionists? Quotes from accountants?
Russell F. Doolittle
Professor Doolittle is a prominent scientist, a member of the National Academy of Sciences who has worked hard on many aspects of protein structure over the course of a distinguished career. He knows more about the process of blood clotting, and more about the relationships among the protein members of the clotting cascade, then perhaps anyone else on earth. He does not, however, know how natural selection could have produced the clotting cascade. In fact, he has never tried to explain how it could have. Nonetheless, as reflected in his comments in Boston Review, he clearly thinks he has addressed the question. This results from a basic confusion, which I will try to clarify.
As Professor Doolittle points out, the sequence of amino acids in one protein might be strikingly like that in a second protein. A good example is the one he gives us — the different subunits of hemoglobin. This gave rise to the idea that the similar proteins might have descended from a common gene, when in the past the gene was duplicated. Virtually all biochemists accept this, and so do I. Many proteins of the clotting cascade are similar to each other, and similar to other non-cascade proteins, so they also appear to have arisen by some process of gene duplication. I think this is a very good hypothesis too. The critical point, however, is that the duplicated gene is simply a copy of the old one, with the same properties as the old one — it does not acquire sophisticated new properties simply by being duplicated. In order to understand how the present day system got here, a scientist has to explain how the duplicated genes acquired their new, sophisticated properties.
With hemoglobin the task of getting from a simple protein with one chain to a complex of four chains does not appear to present problems, as I discussed on pp. 206-207 of Darwin’s Black Box. In both cases the proteins simply bind oxygen, with more or less affinity, and they don’t have to interact critically with other proteins in a complex protein system. There is a fairly obvious pathway leading from a simple hemoglobin to a more complex one.
With the proteins of blood clotting, however, the task of adding proteins to the cascade appears to be horrendously problematic. With one protein acting on the next, which acts on the next, and so forth, duplicating a given protein doesn’t give you a new step in the cascade. Both copies of the duplicated protein will have the same target protein, which they activate, and will themselves be activated by the same protein as before. In order to explain how the cascade arose, therefore, a scientist has to propose a detailed route whereby a duplicated protein turns into a new step in the cascade, with a new target, and a new activator. Furthermore, because clotting can easily go awry and cause severe problems when it is uncontrolled, a serious model for the evolution of blood clotting has to include quantitative factors, such as how much of a clot forms, what pressure it can resist, how frequent inappropriate clots would be, and many, many more such questions.
Professor Doolittle has addressed none of these questions. He has confined his work to the question of what proteins appear to be descended from what other proteins, and is content to wave his hands and assert that, well, those systems must have been put together by natural selection somehow. The title of the reference to his work that he cites here says it all, “Reconstructing the history of vertebrate blood coagulation from a consideration of the amino acid sequences of clotting proteins.” His work concerns sequence comparisons. Doolittle has no idea of whether the clotting cascade could have been built up by natural selection.
An illustration of this fact is shown in his citing Bugge et al. (“Loss of Fibrinogen Rescues Mice from the Pleiotropic Effects of Plasminogen Deficiency,” Cell 87, 1996: 709?19). Professor Doolittle writes:
“Recently the gene for plasminogen was knocked out of mice, and, predictably, those mice had thrombotic complications because fibrin clots could not be cleared away. 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. 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.”
However, if one goes back and looks at Bugge et al, one sees that Professor Doolittle misread the paper. The mice that have had both genes knocked out do not have a functioning clotting system: they can’t form clots; they hemorrhage; females die during pregnancy. They are certainly not candidates for evolutionary intermediates.
The lesson here is not that Doolittle misread a paper, which can happen to anyone. Rather, there are two points. First, a Darwinian mindset can tend to make one glide over problems that would occur in the real world. And second, sequence information is not sufficient to conclude that a system evolved by natural selection. The sequence information that Professor Doolittle had did not stop him from mistakenly pointing to a nonviable situation as a potential evolutionary intermediate. One can go further to say that, if a scientist as prominent as Russell Doolittle does not know of a detailed route by which natural selection could produce the clotting cascade, nobody knows.
I argue that each of the steps of the clotting cascade is irreducibly complex (see Chapter 4 of my book)—requiring the rearrangement of several components simultaneously before a viable, controlled clotting system could be in place, and that is why I conclude that the cascade is a product of design. Clotting factors may be related by common descent, but the clotting cascade was not produced by natural selection.
On a different note, I’m glad Professor Doolittle likes Rube Goldberg too, but unfortunately it supplies what I think is his rock-bottom reason for deciding that natural selection produced the clotting cascade: “… no Creator would have designed such a circuitous and contrived system.” Well, Doolittle is a good scientist, but he’s no theologian, and he doesn’t serve science well when he lets his theological presuppositions influence his scientific judgment.
Douglas J. Futuyma
Professor Futuyma advances arguments that I have dealt with in my replies to Orr and Doolittle: a mistaken notion of what constitutes irreducible complexity, and a confusion of what gene duplication is able to explain. He also offers a polemic saying that I “claim a miracle in every molecule” and “Behe invites us to give up.” I do not, however, claim to see miracles—I see design. Design and intelligence are two phenomena of which we have direct experience; they are parts of the world we see every day. On the other hand, the ability of natural selection to produce complex molecular systems resides only in the mind of Futuyma and others. Far from giving up, intelligent design theory takes the world as we see it, without philosophical preconceptions. Futuyma concludes, however, that the world must have behaved in a way we have never seen it behave, all to fit his extrascientific views.
Professor Ruse asks if I have the right to appeal to design as a scientist. Well, many scientists already appeal to design. I mentioned the SETI program earlier; clearly those scientists think they can detect design (and nonhuman design at that.) Forensic scientists routinely make decisions of whether a death was designed (murder) or an unfortunate accident. Archaeologists decide whether a stone is a designed artifact or just a chance shape. And in Ruse’s own example of the downed airliner, investigators spent large amounts of effort to determine if the crash was designed. As I explain in my book (pp. 196-197) it can be easy to determine that a system was designed, but extremely difficult to determine who the designer was. I do not argue that the designer was God, although it could have been and certainly many people will think so. I argue simply for the conclusion of design itself.
I appreciate Professor Shapiro giving everyone a dose of reality in his descriptions of the enormous and interactive complexities of the cell, and certainly agree with him that they are beyond Darwinian explanation. I can’t quite understand, however, what he envisions as an explanation for the origin of those systems. He seems to imply that they somehow assemble themselves, which strikes me as having a big chicken-and-egg problem. His analogies to computers and information theory are quite congenial to intelligent design ideas. However, he draws back from that conclusion for reasons I fail to grasp. Still, I look forward to reading more of his ideas when he fleshes them out.