Uncommon Descent

24 August 2007

Beyond the Edge of Evolution: The New York Times Story

Michael J Behe

Dear Readers,

As I wrote in The Edge of Evolution, Darwinism is a multifaceted theory, and to properly evaluate the theory one has to be very careful not to confuse its different aspects. Common descent, natural selection, and random mutation are separate concepts; the first two are well supported, but the power of random mutation is not. I argued that evolution — understood just as common descent — did happen, but that randomness played only a minor part. Instead, nonrandom processes — either front-loaded, guided, or somehow influenced by an intelligence — played by far the greatest part.

Unfortunately, stories in the news and on the internet regularly confuse the facets of Darwinism, ignore distinctions made in The Edge of Evolution, or misstate the arguments of intelligent design. The disregard for critical distinctions blurs the issues badly. This is the first in an occasional series of brief posts to correct confusions.

A recent New York Times story by Kenneth Chang touted a new paper inScience by the laboratory of Joseph Thornton of the University of Oregon as refuting intelligent design. Thornton’s laboratory has been interested in the evolutionary development of differences between two proteins abbreviated GR and MR. Since the two proteins are very similar, and since they bind very similar small hormone molecules, they likely developed from an ancestral gene by gene duplication and subsequent diversification. Despite Chang’s story, none of that challenges intelligent design, which agrees that minor evolutionary changes can happen by random mutation and natural selection.

The gist of the new paper is that the workers reconstructed in the lab what they thought would be the ancestral protein, as well as several later evolutionary versions of it. To get to a protein mimicking modern GR, they purposely introduced several mutations to the ancestral form. The first few mutations took the protein’s activity part of the way toward the modern activity. But adding several other mutations that they thought would increase the specific activity to that of modern GR unexpectedly caused the protein to lose all its ability to bind the hormones. So, after thinking awhile, the authors then went back and intentionally introduced other mutations which did not affect hormone binding, but which they hoped would strengthen a particular part of the protein. After deliberately strengthening that part, they found they could add the final mutations, the protein would retain its activity, and its activity would be much more similar to modern GR.

Now, dear reader, can you guess which parts of Darwin’s theory this all neglects? Of course — both random mutation and natural selection. The workers nicely showed it is quite reasonable to think that the one ancestor protein could produce two descendants, but they didn’t even try to address the question of whether it could happen by chance plus selection. Of course, getting a single amino acid mutation by chance is not a problem. But in order to have the mutation be positively selected, it has to benefit an organism. The authors (and news stories) completely ignore that — the authors didn’t measure whether duplicating the ancestral gene, and then modifying it, would benefit an organism that was used to relying on just one protein (admittedly that would be hard to do). What’s more, in order to be confident that a multi-mutation scenario reconstructs a Darwinian process, all subsequent mutations have to be positively selected, too.

But they aren’t. Although they test none of the mutations in actual organisms, the authors themselves feel that the very particular mutations they deliberately introduced, which strengthen the protein but don’t affect hormone binding, would have been neutral. That makes those mutations much, much less likely to spread in a population, to be available later for when the beneficial mutations came along. In other words, the authors themselves think the scenario involves a big stroke of luck. In theNew York Times Chang quotes Thornton: “‘These very exquisitely adapted bodies we have represent a role of the dice,’ Dr. Thornton said. ‘And they could have turned out very differently.’”

Big strokes of “luck,” however, point much more to intelligent design than to Darwinism. If evolution were guided or designed to unfold in a particular way, then very improbable events would be expected to be packed into it. The bottom line is that, while the new paper is very clever work, it offers no support at all to Darwinism. If anything, the authors careful work points strongly away from randomness. If even such minor evolutionary differences as those between GR and MR are problems for chance-driven evolution, greater evolutionary difference are almost certainly beyond the edge of random evolution.

3 August 2007

The Colbert Report

Michael J Behe

Dear Readers,

This past Thursday I was a guest on The Colbert Report, where I was interviewed about The Edge of Evolution by the inimitable Stephen Colbert.  You can watch the video here.

16 July 2007

Response to Richard Dawkins

Michael J Behe

Dear Readers,

Here I respond briefly to Richard Dawkins’ review of The Edge of Evolution in theNew York Times. I must admit I was surprised that he agreed to do it. In the past Dawkins has said that on principle he would not interact with proponents of intelligent design, because that would give us publicity. I guess when the New York Times offers writing space, principles can be reconsidered.

Other Darwinist reviewers have blustered; Dawkins is the only one who has dripped venom. I will pass on replying to that. He makes just two substantive points in his review. The first is that the success of artificial selection in things like dog breeding show the malleability of organisms, so why should Darwinian evolution be a problem? I already answered that point in my reply to Jerry Coyne. Briefly, it begs the question of what changes are occurring at the molecular level in those examples, whether simple ones or complex ones, and it begs the question of where the sophisticated molecular systems came from that we have learned control animal form and development. Dawkins seems quite reluctant to engage my argument at the molecular level; in his review he defers to other scientists for that. He himself gives the kind of argument that a 19th century naturalist might give, before the elegance of the molecular foundation of life was discovered by modern biology.

Dawkins’ second substantive point is that if I am right, then:

Behe’s calculations would at a stroke confound generations of mathematical geneticists, who have repeatedly shown that evolutionary rates are not limited by mutation. Single-handedly, Behe is taking on Ronald Fisher, Sewall Wright, J. B. S. Haldane, Theodosius Dobzhansky, Richard Lewontin, John Maynard Smith and hundreds of their talented co-workers and intellectual descendants.

It’s a flattering thought, but incorrect. If I am right it would overturn virtually no theoretical work, simply because theoreticians have not dealt with the sorts of complex, functional systems I write about. For the most part, models have considered one or two simple mutations at a time, conceptually isolated from the real-life complexity of an actual cell or organism. That’s necessary, because detailed models of complex systems would be intractable. Those (relatively) simple models can of course be very important and useful for things like predicting the spread of the sickle hemoglobin gene, or calculating from the number of neutral mutations the time since two species shared a common ancestor. But there is no theoretical evolutionary work on the production of molecular machinery.

(One of the luminaries Dawkins lists, John Maynard Smith, once briefly alluded to the kind of problem The Edge of Evolution deals with. In a letter to Nature in the early 1970s, Smith compared evolution of proteins to a word game where only one letter is allowed to be changed at a time, and misspellings are disallowed too. I cite Smith’s paper in the book.)

At the end of his review Dawkins chides me for lack of peer-reviewed publications. Talk about the pot calling the kettle black. If Dawkins himself has many peer-reviewed research publications in the last few decades, he must be writing them under a pseudonym. Dawkins’ hypocritical complaint makes a nice little example of Darwinian gate-keeping. The nebulous, wooly-minded scenarios Dawkins spins in his books, of the origins of bat echolocation, spider webs, and so on, have no real justification in peer-reviewed publications. Yet Dawkins is free to write trade books without howls of protest from the scientific community because his stories fit the way many scientists want the world to be. But if (ahem…) someone publishes a book critically analyzing the data from a different perspective, the reaction is dramatically different.

12 July 2007

Response to Kenneth R. Miller, Continued

Michael J Behe

Yesterday, in the first part of my response to Kenneth Miller’s review, in which I addressed his substantive points, I ended by showing that a reference he cited did not contain the evidence he claimed it did. In this final part, I more closely examine Miller’s tendentious style of argumentation.

Speaking of throwing around irrelevant references, Miller writes:

Telling his readers that the production of so much as a single new protein-to-protein binding site is “beyond the edge of evolution”, [Behe] proclaims darwinian evolution to be a hopeless failure. Apparently he has not followed recent studies exploring the evolution of hormone-receptor complexes by sequential mutations (Science 312, 97-101; 2006), the ‘evolvability’ of new functions in existing proteins — studies on serum paraxonase (PON1) traced the evolution of several new catalytic functions (Nature Genet. 37, 73-76; 2005) — or the modular evolution of cellular signalling circuitry (Annu. Rev. Biochem. 75, 655-680; 2006).

Now, dear reader, when Miller writes of “protein-to-protein” binding sites in one sentence, wouldn’t you expect the papers he cites in the next sentence would be about protein-to-protein binding sites? Well — although the casual reader wouldn’t be able to tell — they aren’t. None of the papers Miller cites involves protein-protein binding sites. The Sciencepaper concerns protein-steroid-hormone binding; theNature Genetics paper deals with the enzyme activity of single proteins; and theAnnual Reviews paper discusses rearrangement of pre-existing protein binding domains. What’s more, none of the papers deals with evolution in nature. They all concern laboratory studies where very intelligent investigators purposely re-arrange, manipulate, and engineer isolated genes (not whole cells or organisms) to achieve their own goals. Although such studies can be very valuable, they tell us little about how a putatively blind, random evolutionary process might proceed in unaided nature.

Miller’s snide comment, that apparently I haven’t followed these developments, seems pretty silly, since it’s so easy to find out that I followed them closely. You’d think he should have noticed that I cited the Annual Reviews article in The Edge of Evolution in Appendix D, which deals in detail with Wendell Lim’s interesting work on domain swapping. You’d think he easily might have checked and seen that I was quoted in the New York Times commenting on Joseph Thornton’s Science paper when it first came out a year ago. You’d also think he’d then have to tell readers of the review why I thought the papers weren’t pertinent. You’d be thinking wrong.

Much worse, Miller is as subtly misleading when writing about the substantive points ofThe Edge of Evolution as he is when making supercilious offhand comments. Miller writes: “Telling his readers that the production of so much as a single new protein-to-protein binding site is ‘beyond the edge of evolution’, [Behe] proclaims darwinian evolution to be a hopeless failure.” But the book says plainly that it is two, not one, binding sites that marks the edge of evolution. That was not an obscure point. Chapter 7 is entitled “The Two-Binding-Sites Rule”; Figure 7.4 has a line at two binding sites, with a big arrow pointing to it labeled “Tentative molecular edge of evolution.” What’s more, the book goes out of its way to say that Darwinism is certainly not a “hopeless failure”, that there are important biological features it clearly can explain. That’s why one chapter is called “What Darwinism Can Do”.

Regrettably, that’s Miller’s own special style. He doesn’t just sneer and thump his chest, as some other Darwinists do. He uses less savory tactics, too. His tactics include ignoring distinctions the author draws (cellular protein-protein binding sites vs. other kinds of binding sites), mischaracterizing an argument by skewing or exaggerating its claims (“so much as a single …”), and employing inflammatory, absolutist language (“[Behe] proclaims darwinian evolution to be a hopeless failure”). He turns the principle of charitable reading on its head. Instead of giving a text its best interpretation, he gives it the worst he can.

Call it the principle of malignant reading. He’s been doing it for years with the arguments of Darwin’s Black Box, and he continues it in this review. For example, despite being repeatedly told by me and others that by an “irreducibly complex” system I mean one in which removal of a part destroys the function of the system itself, Miller says, no, to him the phrase will mean that none of the remaining partscan be used for anything else — a straw man which can easily be knocked down. Unconscionably, he passes off his own tendentious view to the public as mine. People who look to Miller for a fair engagement of the arguments of intelligent design are very poorly served.

11 July 2007

Response to Kenneth R. Miller

Michael J Behe

Dear Readers,

Here I respond to the unfavorable review of The Edge of Evolution by Kenneth R. Miller inNature. Like Sean Carroll, whose review in Science I discussed earlier, he employs much bluster. But Miller goes well beyond simple bluster. I overlooked Carroll’s rhetoric and dealt only with his substantial arguments. This time I’ll do things differently. Today I’ll respond to Miller’s substantive points. Tomorrow we’ll take a closer look at his style of argumentation.

After mentioning that de novo resistance to chloroquine is found roughly once in every 1020 malaria parasites, and quoting several sentences from The Edge of Evolution where I note “On average, for humans to achieve a mutation like this by chance, we would need to wait a hundred million times ten million years,” Miller writes:

Behe, incredibly, thinks he has determined the odds of a mutation “of the same complexity” occurring in the human line. He hasn’t. What he has actually done is to determine the odds of these two exact mutations occurring simultaneously at precisely the same position in exactly the same gene in a single individual. ….

Behe obtains his probabilities by considering each mutation as an independent event, ruling out any role for cumulative selection, and requiring evolution to achieve an exact, predetermined result.

Miller makes the same mistake here that I addressed earlier when replying to Jerry Coyne’s response. The number of one in 1020 is not a probability calculation. Rather, it is statistical data. It is perhaps not too surprising that both Miller and Coyne make that mistake, because in general Darwinists are not used to constraining their speculations with quantitative data. The fundamental message of The Edge of Evolution, however, is that such data are now available. Instead of imagining what the power of random mutation and selection might do, we can look at examples of what it has done. And when we do look at the best, clearest examples, the results are, to say the least, quite modest. Time and again we see that random mutations are incoherent and much more likely to degrade a genome than to add to it — and these are the positively-selected, “beneficial” random mutations.

Miller asserts that I have ruled out cumulative selection and required Plasmodium falciparumto achieve a predetermined result. I’m flattered that he thinks I have such powers. However, the malaria parasite does not take orders from me or anyone else. I had no ability to rule out or require anything. The parasite was free in the wild to come up with any solution that might help it, by any mutational pathway that was available. I simply reported the results of what the parasite achieved. In 1020chances, it would be expected to have undergone huge numbers of all types of mutations — substitutions, deletions, insertions, gene duplications, and more. And in that astronomical number of opportunities, at best a handful of mutations were useful to it.

Miller makes two specific points:

Not only are each of these conditions unrealistic, but they do not apply even in the case of his chosen example. First, he overlooks the existence of chloroquine-resistant strains of malaria lacking one of the mutations he claims to be essential (at position 220). This matters, because it shows that there are several mutational routes to effective drug resistance.

As I wrote in response to Coyne, however, my argument does not depend on any particular amino acid position being required, and in the paper Miller was referring to (Chen et al., 2003,Antimicrob. Agents Chemother. 47:3500-3505, apparently accidentally omitted in the Naturereview, according to Coyne) other mutations are found in the malarial strain in which position 220 remained unchanged. Miller says this matters because there are several routes to drug resistance. It matters much less than he implies. Certainly, there may be several routes, maybe permutations of pathways, too. But whether or not there are several routes, the bottom line is that resistance arises only once for every 1020 parasites.

Miller continues:

Second, and more importantly, Behe waves away evidence suggesting that chloroquine resistance may be the result of sequential, not simultaneous, mutations (Science 298, 74–75; 2002), boosted by the so-called ARMD (accelerated resistance to multiple drugs) phenotype, which is itself drug induced.

If you read that paper, however, you find that it presents no “evidence” whatsoever for cumulative mutations; rather, it merely speculates about them. What’s more, the paper makes no mention of the ARMD phenotype, and Miller says nothing about its relevance. Here Miller is simply throwing references and words around, but saying nothing meaningful.

10 July 2007

Back and Forth with Jerry Coyne, Part 3

Michael J Behe

Dear Readers,

Tonight concludes my response to University of Chicago evolutionary biologist Jerry Coyne, which began earlier this week.  As you know if you’ve been following my blog here, Professor Coyne reviewed my new book Edge of Evolution in The New Republic.  I replied to his response here, and he has responded to my reply at TalkReason.org.  Because it quickly gets awkward to include all of the context here, I’m only quoting the portions of his response that I specifically address here.  Readers who want to see the full back-and-forth should read his posted review and response.


The reviews by Ken Miller in Nature and Sean Carroll in Science cite several examples of the gradual origin of adaptations via the step-by-step accumulation of point mutations in proteins.


Hardly. Read my response to Sean Carroll’s review and my (forthcoming) response to Ken Miller’s review. Carroll begs the question of what caused changes in proteins, and Miller points to work in which investigators manipulate proteins in the lab (not to work showing what happens in nature). Frankly, I’m quite encouraged by their citations. Leaving aside their blustering rhetoric, if that’s the best that staunch, knowledgeable opponents of ID can come up with, even when writing in leading journals for a scientific audience, then I think the protein-protein binding site argument is on solid ground.


Finally, I note that Behe’s “response” completely ignores two devastating criticisms of his “scientific” theory. First, as both Dawkins and I point out, if random mutations can’t build complexity, how can they possibly have been so effective in artificial selection of plants and animals?


Because, of course, the genomes of many plants and animals already contain much developmental plasticity. Turning some existing genes or regulatory elements on or off, or tuning them up or down, or changing them slightly by simple, single mutations, can certainly affect the shapes and other properties of organisms somewhat. Artificial selection for such variants can easily explain dog breeds and such, as I noted in Chapter 9. But of course that begs the question of where the complex systems controlling the organisms’ development came from.

Now, was that really supposed to be a “devastating” criticism of my argument? Frankly, I’m a bit perplexed by this line of reply from Coyne and Dawkins. In The Edge of Evolution, and in Darwin’s Black Box before it, I strongly emphasized that modern biology shows us that life is built upon intricate molecular systems, and that to understand the limits of random mutation and thus Darwin’s theory, we have to concentrate our attention on the molecular level. I readily said that answers to questions about animal shape and other macrobiological properties would have to await elucidation of the molecular underpinnings of those properties. In The Edge of Evolution I argued that some biological levels (down to vertebrate class) could not be explained by Darwinism, but I based my argument entirely on advances in our knowledge of the complexity of the molecular developmental systems underpinning them. Even though I suspect Darwinism is also ineffective at lower biological levels, I stopped at the level of vertebrate class because, as I wrote, “at this point our reliable molecular data runs out, so a reasonably firm answer will have to await further research.”

It does not engage my argument, then, for Professors Coyne and Dawkins simply to point out that varieties of dogs come in different shapes, sizes, and colors. To actually engage my argument, a reviewer has to argue from molecular properties.


Also, as I pointed out in my review, Behe asserts quite plainly in his book that the goal of the Designer was “intelligent life.” I challenge him to provide a scientific rationale for this conclusion, which he failed to do in his response.


I don’t go into it in detail in the book (Chapter 10 was already too long), but in essence the scientific rationale is the arguments of Michael Denton in Nature’s Destiny and Ward & Brownlee in Rare Earth (which I cite). Both of those books argue that the requirements in nature for intelligent life are much greater than for “simple” life, such as bacteria. If one takes the “purposeful arrangement of parts” as empirical (scientific) evidence of design, as I do, then the intricate arrangement of parts in nature needed for intelligent life points to that as a design goal.

9 July 2007

Back and Forth with Jerry Coyne, Part 2

Michael J Behe

Dear Readers,

Today I have continued my response to University of Chicago evolutionary biologist Jerry Coyne, which began yesterday and will conclude tomorrow.  Just a reminder that I’m only quoting the portions of his response that I specifically address here because it quickly gets awkward to include all of the context.  Readers who want to see the full back-and-forth should read his posted review and response.


1. There is no evolutionary expectation that complex protein-protein interactions will evolve in a parasite adapting to a new drug.


Darwinism purports to account for the complexity of cellular machinery which, along with much else, involves very many protein-protein interactions. Yet if “there is no evolutionary expectation that complex protein-protein interactions will evolve” in any particular circumstance, then for those skeptical of Darwinism, what independent reason is there to suppose the protein-protein interactions we do find in the cell evolved by random mutations? I can’t think of any. So I and a lot of other people want to decide what Darwinian processes can do based on evidence, not supposition. And the evidence is decidedly against it.

It’s myopic to view these results, as Coyne does, simply as “a parasite adapting to a new drug.” Rather, they are data that bear directly on the question, “What can Darwinian processes do given an astronomical number of opportunities?” In the past, we did not have enough data to address that question. Now we do, and observational evidence indicates the answer is, “Not much at all”. And as I show in the book, the results with malaria mirror results with E. coli and HIV, which are very different organisms in very different circumstances. In a truly enormous number of opportunities, nothing much of fundamental biochemical interest happened.


2. Behe’s probability calculations, on which his entire argument rests, are flatly wrong because they assume that adaptation cannot occur one mutation at a time.


Here is where Professor Coyne and other Darwinist reviewers really miss the boat and overlook the considerable power of the malaria results. The number I cite, one parasite in every 1020 for de novo chloroquine resistance, is not a probability calculation. Rather, it is a statistic, a result, a data point. (Furthermore, it is not mynumber, but that of the eminent malariologist Nicholas White.) I do not assume that “adaptation cannot occur one mutation at a time”; I assume nothing at all. I am simply looking at the results. The malaria parasite was free to do whatever it could in nature; to evolve resistance, or outcompete its fellow parasites, by whatever evolutionary pathway was available in the wild. Neither I nor anyone else were manipulating the results. What we see when we look at chloroquine-resistant malaria is pristine data — it is the best that random mutation plus selection was able to accomplish in the wild in 1020 tries.

Let me elaborate that last point. The fact that de novo chloroquine resistance is observed to be an event of frequency 1 in 1020 means that mutational events of greater frequency are of little help, because events of greater frequency would have been expected to occur many times in the same time interval. For example, if a single point mutation such as K76T alone in PfCRT in the wild were sufficient to confer chloroquine resistance, then resistance would occur de novo in virtually every person treated with chloroquine, as it does in almost every person treated with atovaquone. In 1020 parasites that single mutation would have been expected to have occurred about 1010 times or more. What’s more, every other possible single point mutation, at every position of the parasite’s genome, would also be expected to have occurred roughly the same number of times. And enormous numbers of other types of mutations — deletions, insertions, gene duplications, and more — in every gene of the parasite, would also have occurred. The result: a very few mutations helped the parasite a bit; the overwhelming number of mutations did not help at all.


3. The probability calculations are also wrong because Behe’s argument is based on specifying a priori: the identical pair of mutations that occur in chloroquine-resistant malaria. He neglects the possibility (indeed, the certainty) that many other mutations that cause interactions between proteins and other molecules can also be adaptive.


Coyne is wrong again, for the same reason. I did not “specify[] a priori” exactly which mutations had to occur to be adaptive. Was I somehow out in the wild in Africa and South America telling the parasite which mutations to try? The parasite was free in nature to do whatever it could. The results are not a priori; they are entirely a posteriori, observational data. Moreover, I did not “neglect the possibility” (let alone “the certainty”) of anything. Nobody told the parasite to restrict mutations just to its pfcrt gene. If other mutations could have been adaptive, Plasmodium falciparumhad 1020 chances in the wild to find them, to come up with whatever it could muster. In the malaria data, we simply observe the exceedingly modest results.

Incidentally, this bears on Coyne’s comment on Miller’s review that “one of the two mutations that Behe claims are ‘required’ for CQR is not actually required (Chen et al. 2003, reference accidentally omitted from Miller’s piece).” If you read that paper you see that, yes, A220S is not found in some resistant strains, as it is in most. (By the way, I was always quite careful in my book to state that A220S had been found in most strains, because I was quite aware of the several exceptions.) However, one also reads that the strains missing A220S have several other, novel mutations, which may be playing a comparable role in them that the mutation at position 220 plays in most other strains. My argument does not depend on exactly which changes are needed in the protein. Rather, the important point is that multiple changes appear to be required for resistance in the wild.

And for the life of me, I don’t see why that proposition — that two mutations might be needed for some adaptations, and that that would be a big evolutionary impediment — is being treated by Coyne and other Darwinists with such horror. It certainly has been discussed in the evolutionary literature in the past. In my book I quote Allan Orr remarking, “Given realistically low mutation rates, double mutants will be so rare that adaptation is essentially constrained to surveying — and substituting — one-mutational step neighbors. Thus if a double-mutant sequence is favorable but all single amino acid mutants are deleterious, adaptation will generally not proceed.” All I have done is to point to an example of the situation he envisioned, to quantify it, and to argue that it’s likely to be a fairly general phenomenon. Why the shock?

8 July 2007

Back and Forth with Jerry Coyne, Part 1

Michael J Behe

Dear Readers,

University of Chicago evolutionary biologist Jerry Coyne has responded at TalkReason.org to my reply here on Amazon.com to his review of The Edge of Evolution in The New Republic. Here I will respond back — not to everything he wrote (nor to other posts and replies on that website), but only to what I think are the more important points of his original response. Because it quickly gets awkward to include all of the context, I will just quote the portions of his response that I specifically address here. Readers who want to see the full back-and-forth should read his posted review and response.


It is clear from Behe’s response on his Amazon blog to the negative reviews by Sean Carroll and myself of The Edge of Evolutionthat he really wants to score debating points, not to have a scientific discussion.


I assure Professor Coyne that I want nothing more than a frank scientific discussion. From the tone of his original review in The New Republic, I felt the same way about him regarding debating points. The tone of his response is much more civil, which I appreciate.


Both Richard Dawkins (in his review of The Edge of Evolution in The New York Times) and myself have noted Behe’s remarkable reluctance to submit his claims to peer-reviewed scientific journals. If Behe’s theory is so world-shaking, and so indubitably correct, why doesn’t he submit it to some scientific journals? (The reason is obvious, of course: his theory is flat wrong.)


Long ago I posted some of my correspondence with science journals on the Discovery Institute website. I urge readers to examine that, and decide if they agree with me. It is my conclusion, based on much experience, that broaching the topic of intelligent design in an evenhanded manner is intolerable to mainstream science journals. (On the other hand, philosophy of science journals are much more tolerant.) As one science journal editor politely wrote to me:

As you no doubt know, our journal has supported and demonstrated a strong evolutionary position from the very beginning, and believes that evolutionary explanations of all structures and phenomena of life are possible and inevitable. Hence a position such as yours, which opposes this view on other than scientific grounds, cannot be appropriate for our pages.

In fact, if one is a known ID proponent as I am, even publishing simple, extensively qualified criticisms of aspects of Darwin’s theory is extremely difficult, and a journal that does so gets pummeled by protest emails, as Protein Science did when it published a paper by David Snoke and myself.

Professor Coyne thinks he knows better about my not publishing in science journals. He writes: “The reason is obvious, of course: his theory is flat wrong.” Well, of course I disagree. Here’s a snippet from his review of Darwin’s Black Box in Nature in 1996 that I think supports my view. There he wrote:

There is no doubt that the pathways described by Behe are dauntingly complex, and their evolution will be hard to unravel. Unlike anatomical structures, the evolution of which can be traced with fossils, biochemical evolution must be reconstructed from highly evolved living organisms, and we may forever be unable to envisage the first proto-pathways. It is not valid, however, to assume that, because one man cannot imagine such pathways, they could not have existed.

So even though “we may forever be unable to envisage” how unintelligent processes could produce some “dauntingly complex” system, Coyne is not willing to concede that maybe, just maybe, unintelligent processes did not produce them. Rather, ID proponents apparently are assigned the burden of proving that no one could even imagine a pathway. Good luck. What are the chances that a manuscript on intelligent design submitted to a science journal would be published if a fellow with his views, quite common in the science community, were a reviewer?

One journal editor wrote to me: “… I am painfully aware of the close-mindedness of the scientific community to non-orthodoxy, and I think it is counterproductive.” If the science community is close-minded to “ordinary” non-orthodoxy, it is implacably close-minded to the non-orthodoxy of intelligent design. As a practical matter, given the sociological realities of the relevant scientific community, the choice for an ID scientist such as myself is either to publish outside science journals or to not publish at all.


He questions whether Jones really understood intelligent design at all, or simply adopted the plaintiff’s claims in the Dover case. In fact, it’s palpably clear from Jones’s written opinion that he saw right through Behe and his transparent creationism. And you can bet that if the verdict had gone in favor of Behe’s side, he wouldn’t be impugning Jones as “the former head of the Pennsylvania Liquor Control Board.”


Professor Coyne should compare the written document signed by Judge Jones to the plaintiffs’ lawyers “finding of fact” brief, given to him about a month before he issued his opinion. Here’s a short excerpt. The lawyers’ brief reads in part:

The assertion that design of biological systems can be inferred from the “purposeful arrangement of parts” is based on an analogy to human design. According to Professor Behe, because we are able to recognize design of artifacts and objects, that same reasoning can be employed to determine biological design.
Professor Behe testified that the strength of an analogy depends on the degree of similarity entailed in the two propositions. If this is the test, intelligent design completely fails.

Jones’ opinion reads:

Indeed, the assertion that design of biological systems can be inferred from the “purposeful arrangement of parts” is based upon an analogy to human design. Because we are able to recognize design of artifacts and objects, according to Professor Behe, that same reasoning can be employed to determine biological design. Professor Behe testified that the strength of the analogy depends upon the degree of similarity entailed in the two propositions; however, if this is the test, ID completely fails.

As I said, whenever the opinion discusses expert testimony — on either side, by scientists, philosophers, or theologians — Jones simply reproduced that text (sometimes very lightly copyedited) from the lawyers’ document. I myself could happily copy from, say, a scholarly book on string theory, or Kant, or Aquinas, but my copying those words would be no evidence that I understood them. Similarly, as I said, there is no evidence Jones understood the academic issues discussed in his courtroom. Those who have hailed Jones as some sort of philosopher-king have been badly misled.

Coyne has a fair point, that I probably wouldn’t mention Jones’ former political job at the helm of the Pennsylvania Liquor Control Board if he had ruled differently. It’s a frailty of human nature that one usually doesn’t examine things too closely if they go your way. On the other hand, Coyne and other Darwinists would almost certainly make the same points I’m making now if some judge had ruled against them, and simply copied defendants’ lawyers documents in his ruling. They would certainly chide him for his lack of apparent understanding of their own arguments.

27 June 2007

Response to Critics, Part 3: Michael Ruse

Michael J Behe

Dear Readers,

Today I give you one last response for now, to Michael Ruse’s review of Edge of Evolution. After more reviews are in, I’ll compose a comprehensive response. I leave you with this for now.

Michael Ruse in The Globe and Mail

Michael Ruse is a philosopher of biology who has written over a dozen books on aspects of Darwinian thought. In his review ofThe Edge of Evolution he says a few kind words about me personally, and I will return the compliment. I like Michael Ruse and have always enjoyed our interactions (well, with one exception that I won’t mention). He is generally an amusing, fun fellow.

Yet he is unwilling or unable to engage my arguments. He spends the first third of his review, and parts thereafter, writing of young earth creationism, while stating somewhere in the middle that, oh yes, Behe is not a young earth creationist. He says that all those arguments of Darwin’s Black Box have certainly been refuted, without bothering with wearying details. And he regrets that there is more of the same pesky trivia in The Edge of Evolution: “we are still where we were with Darwin’s Black Box. The microworld is too complex to be a product of nature.” In fact, he never tells readers of the review what the book’s argument is. No sickle cell, no malaria, no nothing. Unfortunately, the review boils down to mere Darwinian posturing.

Reviews of The Edge of Evolution

Jerry Coyne, “The Great Mutator”, The New Republic, June 18, 2007.

Sean Carroll, “God as Genetic Engineer”, Science, June 8, 2007.

Michael Ruse, “Design? Maybe. Intelligent? We have our doubts”, The Globe and Mail, June 2, 2007.

26 June 2007

Response to Critics, Part 2: Sean Carroll

Michael J Behe

Dear Readers,

Yesterday I responded to Jerry Coyne’s review of my new book, The Edge of Evolution.  Today it’s Sean Carroll’s turn.

Sean Carroll in Science

Almost the same day that The Edge of Evolution was officially released Sciencepublished a long, lead review by evolutionary developmental biologist Sean Carroll, whose own work I discuss critically in Chapter 9. The review is three parts bluster to one part substance, which at least is more substance than Jerry Coyne’s essay.

Here I’ll ignore the bluster and deal with the substantive points. Carroll first covers his rhetorical bases by warning readers that “Unfortunately, [Behe’s] errors are of a technical nature and will be difficult for lay readers, and even some scientists (those unfamiliar with molecular biology and evolutionary genetics), to detect. Some people will be hoodwinked. My goal here is to point out the critical flaws in Behe’s key arguments and to guide readers toward some references.” So, you see, if Carroll’s reasoning doesn’t sound right, well, maybe that’s because you, dear reader, are too slow to understand him. If that’s the case, you’re supposed to just take his word for it.

Unfortunately, his word is demonstrably questionable. He claims that

Behe’s chief error is minimizing the power of natural selection to act cumulatively… Behe states correctly [my emphasis] that in most species two adaptive mutations occurring instantaneously at two specific sites in one gene are very unlikely and that functional changes in proteins often involve two or more sites. But it is a non sequitur to leap to the conclusion, as Behe does, that such multipleamino acid replacements therefore can’t happen.

But I certainly do not say that multipleamino acid replacements “can’t happen”. A centerpiece of The Edge of Evolution is that it can and did happen. I stress in Chapter 3 that in the case of malarial resistance to chloroquine, multiple necessary mutations did happen in the membrane protein PfCRT. I also of course emphasize that it took a huge population size, one that would not be available to larger organisms. But Carroll seems uninterested in making distinctions.

Carroll cites several instances where multiple changes do accumulate gradually in proteins. (So do I. I discuss gradual evolution of antifreeze resistance, resistance to some insecticides by “tiny, incremental steps — amino acid by amino acid — leading from one biological level to another”, hemoglobin C-Harlem, and other examples, in order to make the critically important distinction between beneficial intermediate mutations and detrimental intermediate ones.) But, as Carroll might say, it is a non sequitur to leap to the conclusion that all biological features therefore can gradually accumulate. Incredibly, he ignores the book’s centerpiece example of chloroquine resistance, where beneficial changes do not accumulate gradually.

As a “second fatal blunder”, he asserts I overlook proteins that bind to “short linear peptide motifs” of two or three amino acids. I’ll get to that in a second. Notice, however, that here he is writing simply of a sub-class of protein binding sites, and never gets around to dealing with the question of how the majority of binding sites, those with interacting folded domains, developed. I assume that’s because he has no answer.

Carroll lets his imagination run wild. He thinks it would be child’s play for random processes to develop binding sites, at least for the sub-category of short peptide motif binding:

Very simple calculations indicate how easily such motifs evolve at random. If one assumes an average length of 400 amino acids for proteins and equal abundance of all amino acids, any given twoamino acid motif is likely to occur at random in every protein in a cell.

Wow, every protein in the cell will have a binding site! Methinks Carroll has just stumbled over an embarrassment of riches. If every protein (or even a large fraction of proteins) had such a binding site, then binding would essentially be non specific. (It would be much like, say, the case of the digestive enzyme trypsin, which binds and cuts proteins wherever there is the amino acid lysine or arginine.) As I make clear in The Edge of Evolution, the problem the cell faces is not just to have protein binding sites (which could simply be large hydrophobic patches), but to bindspecifically to the right partner.

In fact, if one takes the trouble to look up the references Carroll cites, one sees that a short amino acid motif is not enough for function in a cell. For example, Budovskaya et el (Proc. Nat. Acad. Sci USA 102, 13933-8, 2005) show that the majority of proteins in the yeast Saccharomyces cerevisiae containing a motif recognized by a particular protein kinase were not phosphorylated by the enzyme. What does that mean? It just means that the simple motifs, while necessary for binding, are not sufficient. Other features of the proteins are necessary, too, features which Sean Carroll ignores.

In his enthusiasm Carroll seems not to have noticed that, as I discuss at great length in my book, no protein binding sites — neither short linear peptide motifs nor any other — developed in a hundred billion billion (1020) malarial cells. Or in HIV. Or E. coli. Or in human defenses against malaria, save that of sickle hemoglobin. Like Coyne, Carroll simply overlooks observational evidence that goes against Darwinian views. In fact, Carroll seems unable to separate Darwinian theory from data. He writes that “what [Behe] alleges to be beyond the limits of Darwinian evolution falls well within its demonstrated [my emphasis] powers”, and “Indeed, it has beendemonstrated [my emphasis] that new protein interactions (10) and protein networks (11) can evolve fairly rapidly and are thus well within the limits of evolution.”

Yet if one looks up the papers he cites, one finds no “demonstration” at all. Those papers show, respectively, that: A) different species have different protein binding sites (but, although the authors assume Darwinian processes, they demonstratenothing about how the sites arose); or B) different species have different protein networks (but, again, the authors demonstrate nothing about how the networks arose). Like Jerry Coyne, Sean Carroll simply begs the question. Like Coyne, Carroll assumes whatever exists in biology arose by Darwinian processes. Apparently Darwinism has eroded Coyne’s and Carroll’s ability to separate data from theory.

In fact, the data I cite in The Edge of Evolution is a real demonstration. While we have studied them, in a truly astronomical number of chances, a variety of microbes developed precisely none of the sophisticated cellular mechanisms that Darwinist imaginations ascribe to random mutation and selection. That data demonstratesrandom mutation doesn’t explain the elegance of cellular systems.