Behe's review in context, or what's the point?

by Paul S. Braterman, University of Glasgow; Professor Emeritus, University of North Texas

As you know by now, Behe has actually had a paper published in a peer-reviewed scientific journal (Behe M.J., Quarterly Review of Biology 85(4), 2010, 419-415). Well, not exactly a paper, more of a literature review. Well, not exactly a literature review, more a review of previous reviews, reinterpreting their findings according to his own criteria. The publication itself is shoddy piece of work. I have written numerous reviews myself, and would never have dreamed of basing them on earlier reviews, rather than my own up-to-date literature search. But let that pass.

Behe constructs an elaborate apparatus for classifying mutations as “gain”, “modification”, or “loss” of what he calls a Functional Coded Element (FCT). The definition is skewed to make “gain” as difficult to prove as possible. The process needs to be understood at the molecular level, rather than simply in terms of phenotype expression. This enables him to dismiss as of unproven relevance the Lenski group’s famous demonstration of E.Coli acquiring the ability to metabolise citrate under anaerobic conditions. Moreover, advantageous removal of inhibition is treated as “loss”, but advantageous disruption of a function by IS duplication and insertion is classified as “modification”, rather than “gain”. Using these restrictive and asymmetric criteria, Behe classifies most sufficiently well-understood mutations in laboratory-bred bacteria as loss or modification, although he does recognise a few gains.

Why bother with this eccentric-seeming enterprise? Here we need to look at the broader context of Behe’s involvement with the Discovery Institute.

The context makes him a colleague of William Dembski, who notoriously claims that undirected evolution cannot even in principle generate novel information. So Behe is concerned to minimise the importance of cases where evolution has demonstrably done just that. The techniques he uses invite analysis along the lines of the deconstruction by Boudry et al. of creationist strategy, which (through good luck, or cruel judgement, who knows?) appeared in the same issue of Quarterly Review of Biology as the article under discussion. (Boudry M., Blancke S., Braeckman J., Quarterly Review of Biology 85(4), 2010, 473-482.)

The advocates of supernatural causation start with the bold initial claim: that organisms cannot acquire new functions by natural processes, since new information cannot be generated without the intervention of an intelligence. Notice that this is a claim that such things cannot happen, even in principle.

But there are numerous well-known counterexamples, many of them discussed in this review.

The next stage is rhetorical dismissal of such counterexamples. Here the strategies include limiting the search (ignoring the massive creative role of gene duplication and polyploidy in eukaryotes, and of horizontal transfer followed by selection in bacteria themselves), narrowing the criteria (new functions don’t count unless they can be demonstrated to arise from additions, rather than any other kinds of alterations, to the molecular machinery), and inventing additional constraints (creation of a new category, the FCT, classifying the process as a loss if either material or function is lost at any stage in the change being discussed, dismissing changes in function as mere transformations, rather than novelties). This stage switches the emphasis from what is possible in principle, to the demand that each case be demonstrated in practice, and fully analysed in detail, at the molecular level.

Finally, any counterexamples still surviving this moving of the goalposts and restricting and tilting of the playing field are dismissed as untypical, and therefore unimportant. Another leap of logic, as the present case shows. For even if losses (according to Behe’s criteria) outnumber gains, losses are in general unlikely to be dramatic without being lethal—there are some obvious well-known exceptions, such as the evolution of parasitism—whereas dramatic gains such as gene duplication, horizontal gene transfer, or polyploidy, can and do have the most profound effects imaginable.

The whole process is a study in indirection, closely related to the technique of the stage magician. We are supposed to nod our heads wisely, and agree that real and difficult problems have been raised, rather than noticing displacement of our attention away from the initial claim. This, let me remind you, was that something is impossible even in principle, and was more than adequately refuted by the very first counterexample.

The ultimate in indirection is the promulgation of a new rule, rising phoenix-like from the ashes of the old, while pretending to the same level of significance. In the present case we have, to quote the article’s peroration:

This reasoning can be concisely stated as what I call “The First Rule of Adaptive Evolution”:

Break or blunt any functional coded element whose loss would yield a net fitness gain.

It is called a “rule” in the sense of being a rule of thumb. It is a heuristic, useful generalization, rather than a strict law; other circumstances being equal, this is what is usually to be expected in adaptive evolution

(Emphasis in the original)

In other words, when it is advantageous to lose an element of the molecular machinery, selection pressures are likely to lead to its loss.

Did we really need 27 pages of prime journal space to tell us this?