Reality 1, Behe 0

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Or …

T-urf13 redux

A few months ago I posted an essay about a remarkable example of the evolution of Irreducible Complexity from scratch, via natural, unguided mechanisms. While the reaction to this essay has been pretty muted (precious little to take note of, save for one well-hidden reference on Uncommon Descent to “No Free Lunch”, citing pages that make arguments clearly refuted in the PT essay), I had no idea that a much bigger response, or target, would emerge from the Halls of ID. This would, of course, be Mike Behe’s recently-released follow-up to “Darwin’s Black Box”, entitled “The Edge of Evolution”.

More follows beneath the fold, but here’s the short version for those of us with miniscule attention spans -the previous essay refutes (or, better said, refuted) the EoE in no uncertain terms, showing that the centerpiece of the EoE, the value Behe assigns to the “probability” of occurrence of a protein interaction or binding site, does not agree with what we can and do know about the history of a bonafide multiple simultaneous mutation.

To start off with, it helps to capsulize Behe’s book. The theme of the book, indeed the very Edge of Evolution itself, is a number that Behe assigns to the probability that a protein interaction site can evolve. This number is 1 in 10^20. Behe “derives” this number from the following line of reasoning (the details have been floating around the blogosphere for a few weeks, so I’ll be brief). First, in Chapter 3, Behe discusses at some length the evolution of resistance to chloroquine in the malaria parasite Plasmodium falciparum. It has been reported that resistance to this drug involves the appearance of at least two amino acid changes. Behe argues that these need to be essentially simultaneous in appearance, and coins a term (the Chloroquine Complexity Cluster) to stand for events that involve leaps of two simultaneous mutational changes. Behe also cites a review by Nicholas White that provides an estimate of the frequency of occurrence of a “CCC” – 1 in 10^20 trials. In Chapter 7, Behe then discusses the matter of the evolution of protein binding sites. Behe reasons that the evolution of a new protein binding site will involve a modest number of amino acid changes, and that some of these changes must occur in concert; for this reason, he asserts that a single protein interaction domain is analogous in “complexity” to a CCC, and thus should be expected to occur about once in 10^20 trials. Finally, he argues that networks of more than two proteins require at least two different protein binding sites, and that selection will not act unless these changes occur simultaneously. Thus, for a trimeric complex, two sites are needed, and would be expected to occur once in 10^40 trials. In light of some general numbers (age of the universe, numbers of organisms on earth, etc.), this number would seem to lie on the other (unaccessible) side of the Edge of Evolution. This is Behe’s argument in a nutshell.

Let’s turn now to the previous PT essay. In it, we learned that the protein dubbed T-urf13 had evolved, in one fell swoop by random shuffling of the maize mitochondrial genome. We also learned some fascinating things about T-urf13. Summarizing the salient points:

T-urf13 forms heteromeric complexes in the membrane. This means that different subunits bind at least two other subunits. This means that each subunit must have at least two different protein binding sites. That’s at least two “CCC’s”.

T-urf doesn’t just form heteromers in membranes. It forms a gated ion channel. This means that each heteromeric complex must be capable of adopting at least two different conformations, of changing from one to another, and of shepherding ions through the phospholipid bilayer. This all means that the heteromers are not some non-descript clumps of polypeptide; they possess all the functionality of other, more well-known gated ion channels.

One more thing – the ion channel is gated. It binds a polyketide toxin, and the consequence is an opening of the channel. This is a third binding site. This is not another protein binding site, and I rather suppose that Behe would argue that this isn’t relevant to the Edge of Evolution. But the notion of a “CCC” derives from consideration of changes in a transporter (PfCRT) that alter the interaction with chloroquine; toxin binding by T-urf13 is quite analogous to the interaction between PfCRT and chloroquine. Thus, this third function of T-urf13 is akin to yet another “CCC”.

The bottom line – T-urf13 consists of at least three “CCCs”. Running some numbers, we can guesstimate that T-urf13 would need about 10^60 events of some sort in order to occur. Recalling Behe’s summation from p. 146:

“So let’s accept my earlier conservative estimation, and spell out some implications. The immediate, most important implication is that complexes with more than two different binding sites—ones that require three or more different kinds of proteins—are beyond the edge of evolution, past what is biologically reasonable to expect Darwinian evolution to have accomplished in all of life in all of the billion-year history of the world. The reasoning is straightforward. The odds of getting two independent things right are the multiple of the odds of getting each right by itself. So, other things being equal, the likelihood of developing two binding sites in a protein complex would be the square of the probability for getting one: a double CCC, 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the world in the past four billion years, so the odds are against a single event of this variety in the history of life. It is biologically unreasonable.”

That makes it pretty clear – T-urf13 is a mathematical impossibility. It simply cannot exist.

Well, this is of course absurd (although the farmers whose livelihoods were devastated by Southern corn leaf blight dearly wish that Behe was correct). Indeed, it is apparent that Behe’s “line in the sand” is badly out of touch with reality. How different is it from what actually occurs? We can run some numbers of our own and compare. The amount of arable land on the earth is on the order of 200 million hectares, or about 500 million acres (I’ll do some liberal rounding to keep things simple). A really good farmer can cram 50,000 corn plants into an acre (we won’t go into what the yields would be…). A typical corn tassel may make 50 million pollen grains (OK, a superman plant, maybe, but we’re being generous here). Finally, maize has been under cultivation for less than 10,000 years. What does this add up to? If each and every arable acre on earth had been used for corn production, at the unseemingly high planting rate of 50,000 per acre, and if somewhow we could cram four plantings in per year, then this would translate to some 10^26 pollen grains in the entire history of corn production. Of course, cmsT was probably developed over a 20 year period, and probably involved a few thousand acres and 2 or 3 generations per year. Let’s say 100,000 acres and 3 generations per year, to give us a more realistic (but still generous) estimate of 10^19 pollen grains.

Now, this isn’t the end of things. The number of interest is the number of mitochondrial genome rearrangements – the number of shufflings that occurred to give us T-urf13. Let’s stuff 1000 mitochondria into each pollen grain, and let each of them undergo a million recombinations (people who work with corn pollen may commence to groan). This translates to about 10^28 events.

Now, recall that we are talking about, not one, but a minimum of three CCC’s. Behe says 1 in 10^60, what actually happened occurred in a total event size of less that 10^30. Obviously, Behe has badly mis-estimated the “Edge of Evolution”. Briefly stated, his “Edge of Evolution” is wrong.

I’ll close this essay by noting one source of error on Behe’s part. As I have discussed, Behe asserts that the probability associated with a “CCC” is 1 in 10^20. Where does this number come from? From footnote 16 in the first excerpt given above - White, N. J. 2004. Antimalarial drug resistance. J. Clin. Invest. 113:1084-92. Here is the actual passage from the review by White that mentions the number 10^20:

“Chloroquine resistance in P. falciparum may be multigenic and is initially conferred by mutations in a gene encoding a transporter (PfCRT) (13). In the presence of PfCRT mutations, mutations in a second transporter (PfMDR1) modulate the level of resistance in vitro, but the role of PfMDR1 mutations in determining the therapeutic response following chloroquine treatment remains unclear (13). At least one other as-yet unidentified gene is thought to be involved. Resistance to chloroquine in P. falciparum has arisen spontaneously less than ten times in the past fifty years (14). This suggests that the per-parasite probability of developing resistance de novo is on the order of 1 in 10^20 parasite multiplications. “

Recall that Behe equated one CCC with a double mutation, presumably based on other work showing that two point mutations in the PfCRT gene are associated with durable resistance in the parasite. But White is not talking about double mutations in PfCRT when he tosses out the number 10^20. Rather, he is speculating about the frequency of occurrence of a multigenic trait that involves two or three genes, and more (perhaps many more) than two mutations. In other words, Behe’s use of this citation to argue that the natural frequency of occurrence of a double mutation in PfCRT is 10^20 is inappropriate. This is one reason (not the only reason, but one) why Behe’s claims are so out of touch with reality.

Of course, there is more, much more. Lots and lots of combinatorial chemistry and protein structural research refutes Behe. As does the fact that every trait that Behe imagines as demanding multiple simultaneous mutations actually do not. Not only has Behe miscalculated the Edge of Evolution, he is actually pointing in entirely the wrong direction in looking for this edge. But these are issues for other essays. The example that is recalled here shows clearly that Behe’s claims are wrong.

As a postscript, two points of interest. It may have occurred to readers that the pre-emption of the Edge of Evolution by my essay is more than coincidence. But trust me – I’m not the Sal Bonpensiero of this on-going soap opera, who had secret access to Behe’s book ahead of time. (That having been said, I don’t think I’ll be taking boat rides with any ID bigwigs.)

No, what this all means is simpler. The earlier PT essay was a belated discussion related to Darwin’s Black Box, a pulling together of ideas that had been bounced around the internet for more than ten years. The fact that the previous essay is also a one-stop shopping mall of items that refutes the Edge of Evolution simply pushes home the message that the EoE is little more than a re-working of DBB. What is supposed to be revolutionary is actually just more of the same tired antievolutionary arguments.

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Dear Gentle Readers: At the bottom of this essay, I’m collecting links to reviews of Behe’s book The Edge of Evolution, replies to reviews and so forth. Well, now the burden is off me, and I can devote my book-reviewing time to good books,... Read More

It's been a while since I've visited the cesspool that is Uncommon Descent, a.k.a. Bill Dembski's home for wandering sycophants, toadies, and lackies. There's a good reason for this; I just get tired of the sheer stupidity that routinely assaults... Read More


Below is an example of malaria evolving resistance to a drug combo by 5 mutations. Just a repost, but it was correct the first time. Behe didn’t take into account sequential stepwise mutations and the important role of sexual recombination. Recombination is so important that few organisms don’t do it. Those few are generally considered dead ends.

raven on July 1, 2007 1:47 PM (e) This is a repost of mine from the PZ blog. Behe is wrong on the basic science. Malaria can evolve resistance to chloroquine easily and by multiple different mutations. He also did not take into account the role of stepwise sequential mutations and sexual recombination, the latter a common method for concentrating adaptive alleles from an extended gene pool into one organism.

Below is an example of malaria evolving resistance to a drug combo with a triple mutant in one gene and a double mutant in another, total 5. Whatever the limits of evolution, Behe has vastly underestimated them. Them’s the facts.

This ‘quintuple mutant’ is considered as a molecular marker for clinical failure of SP treatment of P. falciparum malaria.

A quick review of the literature reveals that malaria evolves resistance to drugs routinely. In the case below, resistance to a drug combo is associated with 5 mutations in 2 genes. One is a triple mutant in dhfr combined with a double mutant in dhps. Behe is claiming that double mutants in the chloroquine resistance gene is the edge of evolution. Here we have a simple case of a triple and a double mutation in the same organism.

His assumptions are faulty, his science is faulty, and his conclusions are false. This is your basic Demski-Meyers class fraud. Fraud and lies are the signatures of christian creo thinking, an internal contradiction that insults both the religion and science.

Malaria can accumulate multiple mutations to become resistant to many drugs without breathing hard. Science/medicine can explain these without breathing hard, standard evolution aided by sexual recombination. It’s too bad for the patients. Malaria is like TB, there are strains resistant to most drugs and strains resistant to all drugs are on the horizon. One of these days we may well be hearing about Extremely drug resistant malaria (XDR-M) and some lawyer will pick up a case somewhere and introduce it to the US, :>(.

Acta Trop. 2003 Mar;85(3):363-73. Links High prevalence of quintuple mutant dhps/dhfr genes in Plasmodium falciparum infections seven years after introduction of sulfadoxine and pyrimethamine as first line treatment in Malawi.Bwijo B, Kaneko A, Takechi M, Zungu IL, Moriyama Y, Lum JK, Tsukahara T, Mita T, Takahashi N, Bergqvist Y, Bj�rkman A, Kobayakawa T. Department of International Affairs and Tropical Medicine, Tokyo Women’s Medical University, 8-1 Kawada-Cho, Shinjuku-Ku, Tokyo 162 8666, Japan.

Malawi changed its national policy for malaria treatment in 1993, becoming the first country in Africa to replace chloroquine by sulfadoxine and pyrimethamine combination (SP) as the first-line drug for uncomplicated malaria. Seven years after this change, we investigated the prevalence of dihydropteroate synthase (dhps) and dihydrofolate reductase (dhfr) mutations, known to be associated with decreased sensitivity to SP, in 173 asymptomatic Plasmodium falciparum infections from Salima, Malawi. A high prevalence rate (78%) of parasites with triple Asn-108/Ile-51/Arg-59 dhfr and double Gly-437/Glu-540 dhps mutations was found. This ‘quintuple mutant’ is considered as a molecular marker for clinical failure of SP treatment of P. falciparum malaria. A total of 11 different dhfr and dhps combinations were detected, 3 of which were not previously reported. Nineteen isolates contained the single Glu-540 mutant dhps, while no isolate contained the single Gly-437 mutant dhps, an unexpected finding since Gly-437 are mostly assumed to be one of the first mutations commonly selected under sulfadoxine pressure. Two isolates contained the dhps single or double mutant coupled with dhfr wild-type. The high prevalence rates of the three dhfr mutations in our study were consistent with a previous survey in 1995 in Karonga, Malawi, whereas the prevalences of dhps mutations had increased, most probably as a result of the wide use of SP. A total of 52 P. falciparum isolates were also investigated for pyrimethamine and sulfadoxine/pyrimethamine activity against parasite growth according to WHO in vitro standard protocol. A pyrimethamine resistant profile was found. When pyrimethamine was combined with sulfadoxine, the mean EC(50) value decreased to less than one tenth of the pyrimethamine alone level. This synergistic activity may be explained by sulfadoxine inhibition of dhps despite the double mutations in the dhps genes, which would interact with pyrimethamine acting to block the remaining folate despite dhfr mutations in the low p-aminobenzoic acid and low folic acid medium mixed with blood.

Nice essay. I can confidently predict the ID response though; so, this protein was able to evolve, but thats because of the large population size and large number of generations. There wouldn’t be such an opportunity for this to occur in species with longer generation times, like Humans. In other words, he’d argue that this example is similar to the evolution of Chloroquine resistance; just about at the edge of evolution (albeit with a modification of his numbers).

Have to squeak up here! This argument is faulty (although not as faulty as Behe’s). You are assuming that the mutation arose in response to the drug. In actuality, evolution does not work this way. Evolution does not depend on mutants arising after the challenge: all evolution does is alter the selective coefficients of existing alleles in a population. While it is indeed possible that the mutants are recent, it is more likely that the mutants existed in small numbers in the population before the drug was introduced. The altered selection regime favored them, and especially their recombinant 5-some. Behe clearly overlooked (or ignored) this factor also.

It seems to me that it is more like reality 4, Behe 0. And that’s just counting the immune system, blood clotting and the bacterial flagellum. How many other things does he claim cannot exist? Can bumble bees fly?

And exactly what alternative is he proposing? God did it! Why would God create a gated ion channel to sterilize corn? And what does God need with a starship?

djlactin makes a good point. The mutations undoubtedly did not arise in response to the presence of the toxin. However, I see nothing in the calculations that assume this. In fact, the calculations are pretty much based on the assumption that the mutations could have arisen at any time during the evolution of cultivated corn. Perhaps one could assume that the Behe calculation requires simultaneous mutations because it is in response to the toxin. That would make another error for Behe. It seems as though he just kept making unwarrented assumptions so that he could keep multiplying numbers until he thought the number was big enough to be convincing.

Raven is right. There is absolutely no reason whatsoever why this, or any other character could not arise through sequential mutations. Even if the first mutations were not selected on they could still increase in frequency by drift. That would almost guarantee that any number of mutations could be combined eventually. This is just another manifestation of the old probability of a protein calculation. Take an isolated entity, apply faulty assumptions, ignore reality completely and presto, it can’t possibly exist!

Still going on with the “improbability” argument, are they? Sorry, but if they want that argument to stick, they’ll have to prove that the creation of a particular biological system by special creation is MORE probable than the creation of the same system by evolution.

So how would Behe calculate the probability of such divine intervention?

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To play devil’s advocate, I think Behe’s response to the T-urf13 example would be to demand a demonstration that the protein arose in fact by undirected mutation. In the absence of such a demonstration, he would claim that the default explanation is that T-urf13 was in fact designed.

Not to toot my own horn, but I actually had made a prediction to this effect a while ago, in a response to Behe’s incredibly weak dismissal of the evidence for adaptive immune system evolution (which came back to haunt him at the Kitzmiller trial):

…let me offer another prognostication: if an IC system was shown to have evolved to the level of detail demanded by Behe, his next step back would be to demand an account that each individual mutation was truly random with regard to fitness, as opposed as “poofed in” by the Designer.

As I see it, The Edge of Evolution is just an attempt to push the goalposts in that direction, trying to preempt any future finding for the evolution of IC systems (which at this point Behe has learned, to his own embarrassment, will certainly be forthcoming) by questioning the very premise that mutations are random with regard to fitness, until proven otherwise.

Andrea’s point did occur to me, but would this not require that God has been actively creating (poofing?) new proteins in the last few decades (not exactly sure when T-urf13 arose)? Or would he put it down to human (intelligent design) activity?

Raging Bee Wrote:

So how would Behe calculate the probability of such divine intervention?

Calculate? Given the “don’t ask, don’t tell” antics of most other IDers, it’s amazing that he even admitted that such “interventions” probably occurred “in-vivo.”

David Stanton Wrote:

In fact, the calculations are pretty much based on the assumption that the mutations could have arisen at any time during the evolution of cultivated corn.

If I’m not mistaken, even the worst case assumption would yield 10^-35 probability where Behe claims 10^-40 for the two CCC’s he must grudgingly admit. (But how we are expected to stuff that many alleles in a smaller population at any particular time beats me. More of Behe’s designer magic? :-)

Being off by several orders of magnitude still means his EoE assumptions are wrong. (Probably as Arthur Hunt says, by mistaking complex multigenic changes for single point mutations.)


But, but… that means an omnipotent deity must make an infinity number of things before breakfast. What an elegant rewrite of the angels on a pin argument.

It was some time since I laughed as hard. [I know, I know, I’m such a nerd at times. Comes with reading PT, I guess. :-P]

Behe also completely ignores the evolution of evolvability. Examples:[…]00/5624/1382[…]K3Review.pdf

Because the mechanism for evolution has a partial identity with the subject of evolution, natural self-replicating evolvers can evolve their evolutionary strategies. Indeed, recombination is an example of this… perhaps the most common. The stress-induced mechanisms are interesting though in light of evolved resistance to drugs, pesticides, etc.

Other mechanisms Behe ignores: virally-mediated horizontal gene transfer between species, rapid genetic drift during population bottlenecks, transposons and other intra-genomic sources of large-scale variability, and so on.

There are quite a few mechanisms for introducing variation.

creationism for beginners:

you tell me that you woke up this morning and dealt yourself an entire deck of cards. You have a sufficient case of Asperger’s to feel like telling me it went 10 hearts, 6 clubs, … blah blah blah … ace of spades. I point out that the chance of this happening is 1 in 52!, about ten to the power of sixty-eight. This is such an inconceivably unlikely occurrence, I call you a liar. You punch me in the nose. Hilarity ensues.


Yeah… that might be a good Asperger superpower to have :) Too bad I only got hyper-reading :)

Here’s an interesting paper I turned up today, whilst searching for something else. On the subject of Chloroquine resistance:

Das, A. and Dash, A.P. (2007) Evolutionary paradigm of chloroquine-resistant malaria in India. Trends in Parasitology, 23, 132-135.

Drug pressure in the field is believed to be responsible for the emergence of drug-resistant Plasmodium falciparum, the parasite that causes malaria. Variants of the P. falciparum chloroquine resistance transporter (pfcrt) gene have been shown to be responsible for conferring resistance to the commonly used drug chloroquine. In particular, an amino acid mutation, K76T, was shown to have a strong positive correlation with the chloroquine-resistant varieties of malaria parasites. Global studies have reported highly reduced genetic diversity surrounding K76T in the pfcrt gene, which indicates that the mutation has been a target of positive Darwinian natural selection. However, two recent studies of P. falciparum in India found high genetic diversity in the pfcrt gene, which, at first sight, do not support the role of natural selection in the evolution of chloroquine resistance in India.


“Andrea’s point did occur to me, but would this not require that God has been actively creating (poofing?) new proteins in the last few decades (not exactly sure when T-urf13 arose)? Or would he put it down to human (intelligent design) activity?”

If I understand correctly what IDists have been telling me, Behe believes in front-loading, so I guess he would claim T-urf13 has always existed.

Speaking of being dealt cards…

If you are at a poker game, how do you tell whether the hand you are dealt is due to “intelligent design” rather than being just a matter of chance?

The answer is simple: You can’t tell.

You can’t tell merely by examining the probabilities of the particular hand. You can’t reach the “intelligent design” conclusion without knowing something about the people involved, what their motivations are, what kind of card manipulations are possible, and so on.

Without information like that, you don’t know whether you have been dealt a good hand just to be set up for a bigger loss later, you don’t know whether your poor hand is just a very common chance occurrence.

Aagcobb Wrote:

If I understand correctly what IDists have been telling me, Behe believes in front-loading, so I guess he would claim T-urf13 has always existed.

Behe backpedaled from his front-loading hypothesis as soon as a critic showed him how easy it would be to test. To my knowledge he has not proposed anything else. I also asked on Talk Origins whether Behe’s book asserts, or even suggests a possible recent design event (as opposed to the usual ID implication of “Cambrian or before”). I didn’t get a reply. I will read the book someday, but I would be surprised if Behe makes it clear either way.

I’m sure that Behe personally believes that it’s evolution all the way, but I’m equally sure that he wishes that he never admitted common descent in the first place.

“However, two recent studies of P. falciparum in India found high genetic diversity in the pfcrt gene, which, at first sight, do not support the role of natural selection in the evolution of chloroquine resistance in India.”

Why a high number of variations in cloroquine resistance alleles in the same gene location would fail to support Natural Selection ?

If all those variations confer useful resistance, they will be all selected, (and obviously, have been).

What is wrong is that arguably (but demonstrably) Behe was lowballing the mutation rate in the malaria parasite.

Hi Frank J,

“I’m sure that Behe personally believes that it’s evolution all the way, but I’m equally sure that he wishes that he never admitted common descent in the first place.”

He had to. The whole reason ID was invented was to get creationist anti-evolutionary arguments into public school science classrooms. If all of your experts testify that they believe the earth is 6,000 years old and humans aren’t related to other primates, you’ve already lost. Behe’s job is to be the “real scientist” who accepts the overwhelmingly obvious fact that all life is related by common descent, thereby retaining some shred of scientific credibility, and who attempts to transfer that credibility to creationist anti-evolutionary arguments by asserting that they are grounded in science as well. Fortunately, the strategy failed spectacularly in Dover v. Kitzmiller as Behe was torn a new one on cross-examination, however the creationists haven’t given up yet. They are still promoting the same tired old creationist arguments against evolution in a spiffy new textbook which is supposed to be a “balanced” presentation of the evidence for and against evolutionary theory, but its not supposed to contain any reference to ID (I have only looked at a few excerpts on the website promoting it). Since ID is nothing but tired old creationist anti-evolutionary arguments, this is nothing but the same dog in a new suit.

Maybe I am not following this very well, but the chloroquine resistance is the “CCC” which occurs one in 10^20; however the line “Resistance to chloroquine in P. falciparum has arisen spontaneously less than ten times in the past fifty years” indicates to me that the one in 10^20 has happened several times in only fifty years.

Based on this taking a guess that it happened 5 times or so that’s once every 10 years, then even squared that’s still once every 100 years. I’m lost as to how we jump from something that theoretically happens every 100 years to something that could not happen within the lifespan of the earth?

Alan, “Resistance to chloroquine in P. falciparum has arisen spontaneously less than ten times in the past fifty years” –that we know of. There are presumably an unknown number of other chloroquine-resistant malaria critters that haven’t been sequenced yet, deep in the jungle/savanna.

True it could be significantly more frequent, and may apply to other species.

My point is really the reverse, even if it only happens once in fifty years, how does this begin to approach the “edge of evolution”? even if you cube the probability aren’t we talking in time frames where a thousand years is nothing?

Yes, it took less than 50 years for the malaria parasite to counter the chloroquine drug (and only a fraction of the malaria potential victims were treated with that drug), and apparently the parasite is still coming up with other versions of the resistance gene. The conclusion is that overcoming a new chemical is child’s play for Evolution, as already demonstrated in antibiotics resistance.

The whole rationale for the “Edge of Evolution” falls apart.

Aagcobb Wrote:

He had to. The whole reason ID was invented was to get creationist anti-evolutionary arguments into public school science classrooms. If all of your experts testify that they believe the earth is 6,000 years old and humans aren’t related to other primates, you’ve already lost.

While YEC, even if packaged as “designer-free” and strictly scientific (e.g. “radiologic dating if flawed”) may be impossible to defend without invoking Genesis (and I’m not sure that’s the case), OEC-without-common-descent is not. If “Edwards v. Aguillard” were the only reason to change the strategy, most anti-evolution activists, if not Behe too, would have just taken the strategy of Schwabe or Senapathy, and tried to defend “no common descent” in a strictly “designer-free” manner. The problem is that such approaches would simply make claims that don’t hold up to scrutiny, so for that reason, not religious reasons, they would have had little chance at being taught in public schools. Unless someone also thinks that Cold Fusion is not taught for “religious reasons.”

I have contended for years that, before “Edwards v. Aguillard,” leading anti-evolutionists were already aware that, designer or not, nothing other than evolution holds up. So one approach (Behe’s) was to concede as much to evolution as possible (Behe probably knew that his target audience would mostly “tune out” his concessions, a la “Morton’s Demon”). The other was simply to play “don’t ask, don’t tell” with the whats and whens, as well as the designer’s identity. I suspect that Behe sometimes wishes that he never let the cat out of the bag, but OTOH, while other IDers can get away with “don’t ask, don’t tell,” a biochemist might not be let off the hook so easily. So for that reason, he never had much of a choice.

Before anyone catches my apparent contradiction, I should say that my earlier comment about being “sure” that Behe at least sometimes wishes that he didn’t admit common descent is only my personal “gut feeling”. I often make the point, when fellow critics confidently state what anti-evolution activists “believe”, that we really can’t really know what others privately think - especially if they are activists with a vested interest in promoting what they don’t necessarily believe. So for this case I should just say that I “suspect,” even if my suspicion is strong enough to warrant stronger words.

The notion that a metaphysical question hinges on a statistical calculation is ludicrous. The desperation of the creationists is seen in their retreat to a view that God only exists in universes in which no other explanation is possible – God exists because the universe is finely tuned or because the ToE isn’t explanatory. What a pathetic deity that is.

Reading Darwin’s Black Box for the first time, something struck me as downright silly.

In the opening chapter, Behe says he believes that there was a common ancestor. Which, of course, MUST be due to ID. But he also believes that molecular mechanisms like the rhodopsin and flagella MUST also be due to ID. There is no way that our common ancestor had every single possible protein. So the intelligent designer must have interfered several times during life on earth. (Actually, more than several, considering T-urf13!)

Behe refuses to say anything about what he believes this intelligent designer may have done, and tosses around some examples like Crick’s alien theory to make him seem more “open”. But really, only a designer who was constantly watching over us could have directed evolution in the way that Behe insists. That is God. Behe is the PhD Trojan Horse that creationists are using to destroy us all.

Something bugs me about this article. T-urf13 is a mitochondrial gene, it is inherited maternally. Why do you count the number of pollen grains? Their mitochondria do not contribute to the offspring, the offspring’s mitochondria are the same as their mother’s, so it would be more accurate (and genetically correct) to count the corn seeds.

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