Biochemist Michael Behe, best known for his book Darwin's Black Box, in which he claimed that evolution via natural selection was impossible because gradual change could not evolve what he called 'irreducibly complex' structures. Behe's arguments not only have not received any support from the mainstream scientific community, but have been repeatedly debunked. Even his own department at Lehigh University have issued a formal disclaimer distancing themselves from his position:
The faculty in the Department of Biological Sciences is committed to the highest standards of scientific integrity and academic function. This commitment carries with it unwavering support for academic freedom and the free exchange of ideas. It also demands the utmost respect for the scientific method, integrity in the conduct of research, and recognition that the validity of any scientific model comes only as a result of rational hypothesis testing, sound experimentation, and findings that can be replicated by others.The department faculty, then, are unequivocal in their support of evolutionary theory, which has its roots in the seminal work of Charles Darwin and has been supported by findings accumulated over 140 years. The sole dissenter from this position, Prof. Michael Behe, is a well-known proponent of "intelligent design." While we respect Prof. Behe's right to express his views, they are his alone and are in no way endorsed by the department. It is our collective position that intelligent design has no basis in science, has not been tested experimentally, and should not be regarded as scientific.
When even your colleagues regard your views as marginal pseudoscience, it is fair to say that his views have being weighted by the experts, and found wanting.
Surprisingly, Behe accepts the evidence for common descent, which puts him in the category of people who accept the fact of evolution, but dissent on the currently accepted theory of evolution, the modern synthetic theory. This failure to differentiate between the fact of evolution and the theory of evolution lies at the heart of much special creationist confusion on the subject, and results in people thinking that problems - real or imagined - with the theory of evolution mean that the facts it explains go away. They do not. As Behe admits:
When two lineages share what appears to be an arbitrary genetic accident, the case for common descent becomes compelling, just as the case for plagiarism becomes overpowering when one writer makes the same unusual misspellings of another, within a copy of the same words. That sort of evidence is seen in the genomes of humans and chimpanzees. For examples, both humans and chimps have a broken copy of a gene that in other mammals helps make vitamin C As a result, neither humans nor chimps can make their own vitamin C.
[…]
The same mistakes in the same gene in the same positions of both human and chimp DNA. If a common ancestor first sustained the mutational mistakes and subsequently gave rise to these two modern species, that would very readily account for both why both species have them how. It's hard to imagine how there could be stronger evidence for common ancestry of chimps and humans. (Emphasis mine) [1]
So, Behe accepts common descent, and regards the genomic evidence as some of the strongest evidence for human-ape common ancestry. It is indeed puzzling that special creationists appeal to his long-discredited views on irreducible complexity, but ignore his support for common descent. As for how discredited, read on.
Debunking Irreducible Complexity
The term ‘irreducible complexity’ is not a scientific one, but rather was introduced by Behe. His assertion, that there exist organs and biochemical pathways that are too complex to have evolved via Darwinian mechanisms has been universally rejected by mainstream biologists. One of the more devastating criticisms came from the respected evolutionary biologist H. Allen Orr who wrote:
“Behe's colossal mistake is that, in rejecting these possibilities, he concludes that no Darwinian solution remains. But one does. It is this: An irreducibly complex system can be built gradually by adding parts that, while initially just advantageous, become—because of later changes—essential. The logic is very simple. Some part (A) initially does some job (and not very well, perhaps). Another part (B) later gets added because it helps A. This new part isn't essential, it merely improves things. But later on, A (or something else) may change in such a way that B now becomes indispensable. This process continues as further parts get folded into the system. And at the end of the day, many parts may all be required.
“The point is there's no guarantee that improvements will remain mere improvements. Indeed because later changes build on previous ones, there's every reason to think that earlier refinements might become necessary. The transformation of air bladders into lungs that allowed animals to breathe atmospheric oxygen was initially just advantageous: such beasts could explore open niches—like dry land—that were unavailable to their lung-less peers. But as evolution built on this adaptation (modifying limbs for walking, for instance), we grew thoroughly terrestrial and lungs, consequently, are no longer luxuries—they are essential. The punch line is, I think, obvious: although this process is thoroughly Darwinian, we are often left with a system that is irreducibly complex. I'm afraid there's no room for compromise here: Behe's key claim that all the components of an irreducibly complex system "have to be there from the beginning" is dead wrong. [2]
As Orr notes, this evolutionary explanation is hardly new, and has an impeccable pedigree, being advanced by the Nobel laureate and geneticist Hermann Muller as early as 1918:
“Most present-day animals are the result of a long process of evolution, in which at least thousands of mutations must have taken place. Each new mutant in turn must have derived its survival value from the effect which it produced upon the “reaction system” that had been brought into being by the many previously formed factors in cooperation; thus a complicated machine was gradually built up whose effective working was dependent upon the interlocking action of very numerous different elementary parts or factors, and many of the characters and factors which, when new, were originally merely an asset finally became necessary because other necessary characters and factors had subsequently become changed so as to be dependent on the former. It must result, in consequence, that a dropping out of, or even a slight change in any one of these parts is very likely to disturb fatally the whole machinery; for this reason we should expect very many, if not most, mutations to result in lethal factors, and of the rest, the majority should be “semi-lethal” or at least disadvantageous in the struggle for life, and likely to set wrong any delicately balanced system, such as the reproductive system.” [3] (Emphasis mine)
Muller’s argument answered Behe’s question about how complex organs could have evolved nearly 80 years before it was first advanced, a telling example of the poverty of research in most creationist material.
The classic example of irreducible complexity given by Behe - that of the evolution of the vertebrate blood clotting system - is not regarded by biologists as posing any problem for evolution. Russell Doolittle, a biologist who is recognised world-wide as an expert in blood coagulation and whose work was cited by Behe has forcefully refuted Behe’s argument:
Here are a few of his comments that I found most irritating.
On page IV-29 the author bold-facedly claims that "the (Doolittle) article does not explain.. how clotting might have originated and subsequently evolved." and then in italics "..no one on earth has the vaguest idea how the coagulation cascade came to be."
I disagree. I have a good idea, shared by most workers in the field, and it is a matter of the (important) details that we are trying to establish.
On page IV-24, Behe underscores that no "causative factors are cited." "What exactly is causing all this springing and unleashing?" Gene duplications, of course, the frequency of which is difficult to measure (I often note that "duplication begets more duplication," for reasons of the misalignment of similar sequences), but which is turning out to be enormously more common than expected.
Causation is tricky. Sometimes environmental or internal benefits are obvious. Often however, the rule for survival is "no harm, no foul," with adaptations occurring subsequently. For the moment, they don't even have to be slightly improved.
As for the "enormous luck needed", we are now into the crux of all evolutionary problems, which is to say, what is the probability of survival? Population geneticists are attempting to answer such questions in general terms (see, e.g., J. B. Walsh, Genetics, 139, 421-428, 1995). In fact, the product of most gene duplications, which are the heart of the evolutionary process, are doomed to random oblivion (see enclosed, Doolittle, Science, 1981).
Also, on page IV-26, he states, "the crucial issues of how much? how fast? when? where?" are not addressed. These are relevant and not unknowable matters. There is a wonderful article about to appear in Molecular Phylogenetics by D. Gumucio et al on how fetal hemoglobin has evolved in primates and that also outlines exactly the regulatory circumstances that allow its differential expression. Finally, my "model" does give some important numbers. The power of sequence-based analysis is that it reveals the order of appearance of new proteins, even when the sequences are limited to one or a few species. As noted above, it also has the power to make predictions about the occurrence of proteins in different creatures. [4]
Doolittle's scathing condemnation of Behe's "irreducible complexity" is hardly isolated - as I mentioned earlier, even his colleagues in the Department of Biological Sciences at Lehigh University in Pennsylvania have distanced themselves from his ideas. Placing confidence in a broken reed such as "irreducible complexity" is ill-advised.
Further work by Doolittle has merely confirmed that the blood clotting pathway is in fact readily explained in evolutionary terms, and is not (contrary to Behe’s assertions) irreducibly complex. Ken Miller, a cell biologist and expert witness at the Kitzmiller v. Dover Trial that ruled comprehensively against intelligent design has pointed out:
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 [an intelligent design advocate] 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. [5]
Why there is no Edge of Evolution - the debunking of Behe's second book
Eight years after Darwin's Black Box, Behe and physicist David Snoke published a paper in the journal Protein Science in which they attempted to justify their claim that Darwinian evolution could not "account for the evolution of complex biochemical systems." [6] Far from sealing the fate of evolution, as some special creationists claimed, the paper was widely savaged, with the paper by respected geneticist Michael Lynch:
In summary, the conclusions derived from the current study are based on a model that is quite restrictive with respect to the requirements for the establishment of new protein functions, and this very likely has led to order-of-magnitude underestimates of the rate of origin of new gene functions following duplication. Yet, the probabilities of neofunctionalization reported here are already much greater than those suggested by Behe and Snoke. Thus, it is clear that conventional population-genetic principles embedded within a Darwinian framework of descent with modification are fully adequate to explain the origin of complex protein functions. [7]
and the Panda's Thumb article by molecular pharmacologist Ian Musgrave, molecular biologist Steve Reuland, and computational evolutionary geneticist Reed Cartwright:
We began this essay with a quotation from Behe complaining that a paper describing an evolutionary simulation (Lenski et al. 2003) had “precious little real biology” in it. What we see here is that Behe and Snoke’s paper is acutely vulnerable to the same criticism. A theoretical model is useful to the extent that it accurately represents or appropriately idealizes the processes that occur in the phenomenon being studied. Although it is worthwhile to investigate the importance of neutral drift, Behe and Snoke have in our opinion over-simplified the process, resulting in questionable conclusions.
Their assumptions bias their results towards more pessimistic numbers. The worst assumption is that only one target sequence can be hit to produce a new function. This is probably false under all circumstances. The notion that a newly arisen duplicate will remain selectively neutral until the modern function is firmly in place is also probably false as a general rule. Their assumption that 70% of all amino acid substitutions will destroy a protein’s function is much too high. And finally, we have shown that their flagship example does not require a large multi-residue change before being selectable.
And ironically, despite these faulty assumptions, Behe and Snoke show that the probability of small multi-residue features evolving is extremely high, given the types of organisms that Behe and Snoke’s model applies to. When we use more realistic assumptions, though many bad ones still remain, we find that the evolution of multi-residue features is quite likely, even when there are smaller populations and larger changes involved. In fact, the times required are within the estimated divergence times gleaned from the fossil record. We can therefore say, with confidence, that the evolution of novel genes via multi-residue changes is not problematic for evolutionary theory as currently understood. [8]
Despite the poor review this argument received, Behe expanded on this theme in his follow-up book The Edge of Evolution: The Search for the Limits of Darwinism, which while conceding the reality of common descent asserted that Darwinian evolution was incapable of producing the diversity of life we see today. Unsurprisingly, given the poor reception of his previous book and the paper co-authored with Snoke, The Edge of Evolution was critically slated. It's fatal flaws, as evolutioanry geneticist and developmental biologist Sean Carroll pointed out in his book review for Science was:
...minimizing the power of natural selection to act cumulatively as traits or molecules evolve stepwise from one state to another via intermediates. Behe states correctly 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 multiple-amino acid replacements therefore can't happen. Multiple replacements can accumulate when each single amino acid replacement affects performance, however slightly, because selection can act on each replacement individually and the changes can be made sequentially.Behe begrudgingly allows that only “rarely, several mutations can sequentially add to each other to improve an organism's chances of survival.” Rarely? This, of course, is the everyday stuff of evolution. Examples of cumulative selection changing multiple sites in evolving proteins include tetrodotoxin resistance in snakes (3), the tuning of color vision in animals (4), cefotaxime antibiotic resistance in bacteria (5), and pyrimethamine resistance in malarial parasites (6)—a notable omission given Behe's extensive discussion of malarial drugresistance.
Behe seems to lack any appreciation of the quantitative dimensions of molecular and trait evolution. He appears to think of the functional features of proteins in qualitative terms, as if binding or catalysis were all or nothing rather than a broad spectrum of affinities or rates. Therefore, he does not grasp the fundamental reality of a mutational path that proteins follow in evolving new properties.
This lack of quantitative thinking underlies a second, fatal blunder resulting from the mistaken assumptions Behe makes about protein interactions. The author has long been concerned about protein complexes and how they could or, rather, could not evolve. He argues that the generation of a single new protein-protein binding site is extremely improbable and that complexes of just three different proteins “are beyond the edge of evolution.” But Behe bases his arguments on unfounded requirements for protein interactions. He insists, based on consideration of just one type of protein structure (the combining sites of antibodies), that five or six positions must change at once in order to make a good fit between proteins—and, therefore, good fits are impossible to evolve. An immense body of experimental data directly refutes this claim. There are dozens of well-studied families of cellular proteins (kinases, phosphatases, proteases, adaptor proteins, sumoylation enzymes, etc.) that recognize short linear peptide motifs in which only two or three amino acid residues are critical for functional activity [reviewed in (7–9)]. Thousands of such reversible interactions establish the protein networks that govern cellular physiology.
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 two-amino acid motif is likely to occur at random in every protein in a cell. (There are 399 dipeptide motifs in a 400-amino acid protein and 20 × 20 = 400 possible dipeptide motifs.) Any specific three-amino acid motif will occur once at random in every 20 proteins and any four-amino acid motif will occur once in every 400 proteins. That means that, without any new mutations or natural selection, many sequences that are identical or close matches to many interaction motifs already exist. New motifs can arise readily at random, and any weak interaction can easily evolve, via random mutation and natural selection, to become a strong interaction (9). Furthermore, any pair of interacting proteins can readily recruit a third protein, and so forth, to form larger complexes. Indeed, it has been demonstrated that new protein interactions (10) and protein networks (11) can evolve fairly rapidly and are thus well within the limits of evolution.
Is it possible that Behe does not know this body of data? Or does he just choose to ignore it? Behe has quite a record of declaring what is impossible and of disregarding the scientific literature, and he has clearly not learned any lessons from some earlier gaffes. He has again gone “public” with assertions without the benefit (or wisdom) of first testing their strength before qualified experts. [9]
Damning as Carroll's criticism are, his most important point is in the final paragraph quoted above. Behe's arguments are made in defiance of the established scientific literature, do not represent solid, peer-reviewed arguments that have survived the test of time, and when they are made on arguments that have made it into the peer-reviewed literature, they have been solidly criticised and dismissed. This is characteristic of how special creationist and intelligent design advocates operate. They bypass the peer-reviewed literature and peddle snake oil to the masses, rather than offer an argument that has been scrutinised by the mainstream scientific community, subjected to scrutiny, and come out unscathed. What they are doing is not science, but Christian apologetics, and pretty shabby apologetics at that.
Conclusion
It is ironic that our community appeals to Behe's views on irreducible complexity and the 'edge of evolution' despite the fact that both have been debunked repeatedly, and are regarded as risible nonsense, while ignoring his support for common descent, the one main area where Behe and the mainstream community are in essential agreement. Certainly, anyone who appeals to Behe for support for their anti-evolutionary arguments is relying in a most fragile of reeds that will readily pierce the hand of anyone unwise enough to lean on it.
References
1. Behe M The Edge of Evolution. The Search for the Limits of Darwinism (2007, Free Press) pp 71-72
2. Orr, H.A (December 1996/January 1997). "Darwin v. Intelligent Design (Again): The latest attack on evolution is cleverly argued, biologically informed—and wrong". Boston Review 22:(6)
3. Muller, H. J. "Genetic variability, twin hybrids and constant hybrids, in a case of balanced lethal factors." Genetics (1918) 3:422-499
4. Brayton E “Two of Behe’s Reviewers Speak Out” Dispatches From the Culture Wars October 27, 2005.
5. Miller K “Smoke and Mirrors, Whales and Lampreys: A Guest Post by Ken Miller” The Loom January 2 2009
1. Behe M The Edge of Evolution. The Search for the Limits of Darwinism (2007, Free Press) pp 71-72
2. Orr, H.A (December 1996/January 1997). "Darwin v. Intelligent Design (Again): The latest attack on evolution is cleverly argued, biologically informed—and wrong". Boston Review 22:(6)
3. Muller, H. J. "Genetic variability, twin hybrids and constant hybrids, in a case of balanced lethal factors." Genetics (1918) 3:422-499
4. Brayton E “Two of Behe’s Reviewers Speak Out” Dispatches From the Culture Wars October 27, 2005.
5. Miller K “Smoke and Mirrors, Whales and Lampreys: A Guest Post by Ken Miller” The Loom January 2 2009
6. Behe M.J., Snoke D.W. "Simulating evolution by gene duplication of protein features that require multiple amino acid residues." Protein Sci. (2004) 13:2651-64.
7. Lynch M "Simple evolutionary pathways to complex proteins" Protein Sci. (2005) 14: 2217–2225
8. Musgrave, I.F., Reuland S., Cartwright R.A. "Theory is as Theory Does." Panda's Thumb October 11, 2004.
9. Carroll S.B. "Books: God as Genetic Engineer" Science (2007) 316:1427-1428
