Behe's Trainwreck Response to Science

Behe writes: Train Wreck of a Review: A Response to Lenski et al. in Science | Evolution News

I want to remind Behe and DI that this review is just a high level summary. I explained right at the beginning of this:

Please do contact us with your questions. Think of this review like a table of contents. Remember, we only had about 750 words. There is much more coming out that explains and expands on these points. We are not even half way through this yet.

Two ID supports have come asking questions, and we have answered them in depth:

  1. Does Summers et al Validate Behe?

  2. Darwin Devolves: Miller's Coagulation Pathway Proposal

Also, we responded already Behe on the IAD mechanism (Real-Time Evolution of New Genes by Innovation, Amplification, and Divergence | Science).

  1. Leisola: Cited to Attack Darwin Devolves, Study Devolves on Close Inspection

Our answers here do not appear to be engaged by Behe, and they rebut his response before he makes it. This is unfortunate. We continue to invite Behe into dialogue with us so misfires like this can be avoided in the future.

There are a few points to emphasize…

It is a BOOK Review

This point seems to be missed by Behe. He often refers to information that is not inside his book, as if we do not know about it. We are reviewing his book, which does not mention these things. We have explained this in detail here: Does Summers et al Validate Behe?.


We covered this here: Perplexing: Michael Behe’s Critics Falsely Claim He Ignores Exaptation.

We are happy to see the the DI concedes that Behe never mentioned the word “exaptation,” confirming that we the reviewers were correct.

Much more to come on the polar bear example.

On Realtime Evolution

Regarding this reference, Behe writes:

Let me emphasize: in reviewing a book expressly advocating intelligent design, Lenski et al. can’t seem to distinguish between experiments where investigators keep their hands off and those where investigators actively manipulate a system. Perhaps they can’t see the difference.

This was a system engineered to test a specific evolutionary mechanism. Behe may misunderstand how these experiments work. His objection is very close to the third law:

No Response to Reference 2?

This is the Marten Boudry Review, which was published alongside the paper Behe based his book upon. This article lays out the the heretofore unresolved logical problems with the Irreducible Complexity argument. It is unfortunate, as this reference more clearly lays out the problems with Behe’s argument. In fact that article alone appears to be a solid rebuttal of Behe’s response to our review.

Does anyone from DI know why Behe did not respond to Reference 2? @pnelson @Agauger @bjmiller Note, that was the main reference we gave to refutations of his argument. The rest were supporting references. I want to know why Behe was unable to respond to Boudry. Hopefully he will sometime soon.

Those Polar Bears

It is worth remembering that Behe’s response to the Polar Bear’s Fat created more problems. Behe: Responding to the Polar Bear's Fat. This is his claim about ApoB:

Since few experiments can be done with grumpy polar bears, they analyzed the changes by computer. They determined that the mutations were very likely to be damaging — that is, likely to degrade or destroy the function of the protein that the gene codes for.

Two errors here:

  1. They determined that the mutations were very likely to be damaging

The authors did not determine the mutations to be damaging. They ran a program that gave some results, and they (for a good reason) came to a different conclusion. On ApoB, one of the "damaged proteins, they write it is likely to be working more effectively. This make sense, because Polar Bears need a really effective ApoB because they eat so much fat.

We suggest that the shift to a diet consisting predominantly of fatty acids in polar bears induced adaptive changes in APOB, which enabled the species to cope with high fatty acid intake by contributing to the effective clearance of cholesterol from the blood .

  1. damaging — that is, likely to degrade or destroy the function of the protein that the gene codes for.

In this context, the software program just outputs “damaging” if it is likely to be a function changing mutation. As a quirk of this program, it calls both increases and decreases in function “damaging.” It appears that Behe misunderstood how this program works. We expect many beneficial mutations to be called “damaging” by this software, but this does not mean that they are likely to degrade or destroy the function of the protein when applied to data like this.

Why this matters. Behe has advanced the hypothesis that polar bear ApoB has reduced function. We can now test this hypothesis by seeing if ApoB really is reduced or increased function. It possible that this will eventually be tested because of its relevance to human disease.

[NOTE: Real Time Evolution and Exaptation sections added on 2/22/2019]


On a personal note, not speaking for my co-authors, I want to add:

4 posts were split to a new topic: Comments on Behe’s Trainwreck Response

I knew this is how he would respond regarding the front limbs to flippers argument and he’s right about this. Your review simply cites evidence for common descent. It’s like saying, “front limbs evolved into flippers,” therefore it occured through natural processes. Yes, both the limbs and flippers were useful. Still doesn’t prove that much.

I think it probably did occur through natural processes but I completely agree with Behe that evidence for common descent is not evidence for HOW evolution occured.

I’m curious what other proposed mechanisms there are for this change. I feel like evo-devo might be of great great help here?

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It seems to me this is critical information that completely and utterly undermines Behe’s reliance on the type of “score” output by this sofware for his case.


This is a universal out. It can be claimed that any event in the past did or didn’t occur through natural processes. There’s no way to tell. And yet Behe claims to be able to tell. According to him, mutations that decrease function are natural, while those that increase function are (probably?) designed. And he uses this criterion to show that all the polar bear mutations are natural. But he’s probably wrong that they decreased function, so by his criterion he’s also probably wrong that they weren’t designed.

Anyway, what makes you think that God didn’t design reduced-function mutations too? How would you know? What makes you think that God did design increased- or altered-function mutations? They look just like any other mutation. And consider this: if mutation X to Y reduces function, then the reverse mutation Y to X would increase function. Are you saying that there’s such a bias in evolution that the first can happen naturally while the second can’t?

I suggest that any event that’s the sort of thing we expect from natural processes, such as a point mutation, should be attributed to natural processes at least as a default expectation.

How? Evo-devo doesn’t introduce any new processes. All it does, if anything, is focus attention on mutations at particular sites, notably transcription factor binding sites. But the processes that produce the raw material of evo-devo are the same ones we already know.



Well he has one heck of a problem… now that he has painted himself into a corner:

Is God the one who makes irreducibly complex mutations occur?

Or is God snoozing when he allows things to (supposedly) devolve?

Who is the prophet that knows when God’s work is evident versus non-existent?


I can’t speak for other biologists, but I think the evidence for common descent is evidence for how evolution occurred because they are one in the same. The nested hierarchy is evidence for common descent and evolutionary mechanisms because this is the pattern of similarities and differences these mechanisms would produce. Common ancestry will cause two species to share DNA sequences, and random mutations combined with other evolutionary mechanisms will produce different DNA sequences in each of the two species. Keep repeating this process and you get a (noisy) nested hierarchy.

The standard mechanisms work just fine. For example, random mutations in homeobox genes that control embryonic development can be filtered through natural selection.



No one has explained the evidence for common descent to me like that before. That makes sense. Like genetic evidence is CONSISTENT with things like whole genome duplications, hybridization, transposition, etc., all of which we know are natural. We can tell when something like one of these mechanisms occured. What you say makes a good deal of sense to me.


So what mechanism is the transition from forelimbs to flippers genetically consistent with?

Mutations in HOX genes, and the various signaling proteins that affect growth patterns of developing tissues (FGF, BMP, WNT, TGF and so on).

Mutations in these genes, and mutations in the loci that determine when and where they are expressed, have been shown in numerous different animals to cause changes in everything from body size and shape, to the locations where limbs form, the sizes and shapes of limbs, number of and shape of digits, and so on.

There are probably other genes too. I remember reading that a simple gene duplication of FGF4(a Fibroblast Growth Factor gene) is responsible for causing the “short leg” phenotype in pet dogs.


I remember reading that a simple gene duplication is responsible for causing the “short leg” phenotype in pet dogs.

A retrotransposon-induced duplication no less!



Do I need to get you the link for his 90 minute interview (or is it even longer?)?

It’s a video link, and about 1 hour and 23 minutes he starts discussing his hypothetical scenario - - where God pre-plans all the natural processes that unfold as the Universe matures…
there’s not a speck of supernatural anywhere in the process … EXCEPT that God makes his plan down to the tiniest details… and then sets everything in motion!


I understand that. But if he REALLY thinks that, then why is he arguing that if evolution proceeds naturally, it ain’t goin’ much of anywhere? If it could proceed naturally, then he would presumably be fine with all these mechanisms. But he’s clearly not. He’s one of the most confusing writers I’ve ever encountered. He says one thing then another then another. There are a lot of Behe’s and I can’t keep all of them straight.

If he would like to explain why he won’t accept these natural mechanisms even though he doesn’t see God as intervening, that would be helpful. I’m completely lost as to what he actually thinks.

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The far more interesting thing right now for me is how he handles the polar bears going forward. He is flat out wrong on a keystone example of his book. In the future, we can even demonstrate him wrong with experiments, showing polar bear apoB is increased function. This may requires several mutations, as many as 5 to 9, to have this increased function.

What then?

If not for his book, he would just argue that God infused this information into a brown bears genome. However, in this case, he can’t go there without directly contradicting his book. The insanity of that switch, however, is that there is nothing telling us that this isn’t the case. In fact, if he is correct about devolution, polar bear apoB must be the product of ID.

Which exposes an absurdity in this proposal. In evolution in the wild, we see complexity increases all the time. All the time. Behe wants to dismiss all these as infusions of information OR examples of devolution. He, however, cannot distinguish one from the other. Then, if we show complexity increases in the lab, he calls it a designed experiment. So he has set up a situation where he can dismiss any contradicting evidence for a shifting set of reasons.

Except for polar bears. There, he put down his flag. Now what is going to do?

Speaking of Polar Bears, @Joel_Duff, where does Behe fit in your diagnostic?


Once again, getting back to the polar bears, these guys are phenomenally adapted to their environment. It appears Behe is offering up that they evolved entirely by natural processes, without God’s guidance or “information infusions.” If this is what unguided evolution can do, that is quite a lot.


Tangentially related to the question of the nature of polar bear adaptations to their environment and diet, I was looking into an on-going argument about the health-effects of certain high-fat diets on humans.

In particular, the simultaneously much maligned and praised “Atkins” style diets, high in protein and animal fats from animal meat have occasionally seen renewed popularity. An argument I have often come across on the pro-meat/fat side of the debate is the fact that Eskimos who persist for extended periods of time on extremely high-fat diets derived from whale and seal blubber don’t seem to exhibit any adverse health effects such as increased rate of heart disease, high LDL cholesterol and so on.

This argument is invoked to rebut the claim that diets high in animal (saturated) fats are the cause of heart disease, or that high blood cholesterol is a cause of (as opposed to caused by) heart disease.

So the argument basically goes that, if it was really the case that eating lots of saturated fats cause heart disease (and/or high LDL blood cholesterol), then we should expect to see this manifest in much higher rates of heart disease in eskimo populations who eat lots of seal and whale blubber.

This got wondering, what is the fatty acid composition of whale and seal blubber?

It took me a while, and I’ll have to go dig up some references again if somebody wants to see them, but I managed to find some articles where the fatty acid composition of (in this case whale) blubber was analyzed. Turns out whale blubber is actually very high in healthy polyunsaturated fats, ala fish-oils you also find in fatty fish like Salmon, Herring and so on, which is known to actually increase good HDL blood cholesterol, and decrease bad LDL cholesterol, and which in countless studies is positively correlated with good cardiovascular health.

This of course completely undermines this particular argument for the pro-animal-fat side of the debate.

In light of this it is possible that some of the polar bear adaptations to a high fat diet does not necessarily imply selection against heart disease, but rather just adaptations to fat transport and metabolism. Getting fat out of the bloodstreams and into muscles and adispose tissues simply for reasons of improved storage and ease of use. The fatty acid composition of a diet high in whale and seal blubber could in effect all by itself reduce the risk of heart disease.


@Rumraket good thoughts. It is also possible that:

  1. Eskimos have a better balance between calorie consumption and utilization, and this reduces risks.

  2. Eskimos are genetically adapted so as to better process fats, similar to how we were considering so for polar bears.

I’m skeptical of the unsaturated fats being protective the way you suggest, but these are all valid hypothesis to test. As for selecting for better processing of fat vs. against heart disease, these might merely be two sides of the same coin. I’m not sure they are seperable in meaningful way.

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Makes sense. I wouldn’t claim to know which of these options, if any, are the case.

I’m skeptical of the unsaturated fats being protective the way you suggest, but these are all valid hypothesis to test.

I’m just relaying what I have often read, that there is evidence that suggests that some types of fats actually have a protective effect against other types of fats. Particularly the types of fats found in different types of nuts, like hazel, walnuts, and almonds. And fatty fish.

As for selecting for better processing of fat vs. against heart disease, these might merely be two sides of the same coin. I’m not sure they are seperable in meaningful way.

I see what you mean. Selection for improved lipid handling would inadvertently also be protective against heart disease.

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Yes, I am a medical doctor. I know about this hypothesis, and I have skepticism towards it as an explanation of Eskimos lower cardiovascular risk. Caloric balance has a huge impact, as does intermittent fasting. So I’d expect those to be the reason. At the very least that is the null hypothesis for me.