The validity (and testability) of Michael Behe's theories


(David Hume (nom de plume)) #1

That argument is far from sound. It is simplistic and flawed, and like the rest of the DI-based ID camp, ignores population genetics. (HT to Joao for already pointing this out on the Reclaiming Design thread.) No evolutionary geneticist (or any other kind of geneticist) has even given it a second thought. The claim that an IC system with 3+ components must be “intelligently designed” is without merit, and I think this has been discussed comprehensively in critiques of IC. I would think that Prof Venema right here at BL has done this, but haven’t checked today.

Especially in the context of the claim that ID has “produced a research program,” it is notable that IC is a topic of actual research by qualified scientists. The phrase “irreducible complexity” is rather uncommon in the literature, but it can be found in one very recent publication (abstract and title below) and is a subject of strong interest in sectors of the evolutionary biology research community, travelling under other names. (Such as complex adaptation.) I found several superb examples just now, looking only at recent articles in two of my favourite open-access journals. I pasted a few links below.

I think the DI-based ID community could do research on evolution, even productive research, if it wanted to. I don’t think it wants to, and I have written about how very badly its apparent research efforts have gone.

The papers I mentioned:

Cryptic genetic variation can make “irreducible complexity” a common mode of adaptation in sexual populations” by Trotter et al.
Abstract: The existence of complex (multiple-step) genetic adaptations that are “irreducible” (i.e., all partial combinations are less fit than the original genotype) is one of the longest standing problems in evolutionary biology. In standard genetics parlance, these adaptations require the crossing of a wide adaptive valley of deleterious intermediate stages. Here, we demonstrate, using a simple model, that evolution can cross wide valleys to produce “irreducibly complex” adaptations by making use of previously cryptic mutations. When revealed by an evolutionary capacitor, previously cryptic mutants have higher initial frequencies than do new mutations, bringing them closer to a valley-crossing saddle in allele frequency space. Moreover, simple combinatorics implies an enormous number of candidate combinations exist within available cryptic genetic variation. We model the dynamics of crossing of a wide adaptive valley after a capacitance event using both numerical simulations and analytical approximations. Although individual valley crossing events become less likely as valleys widen, by taking the combinatorics of genotype space into account, we see that revealing cryptic variation can cause the frequent evolution of complex adaptations.

Evidence that Adaptation in Drosophila Is Not Limited by Mutation at Single Sites” by Karasov et al. with accompanying commentary by Nick Barton.

Coevolution Drives the Emergence of Complex Traits and Promotes Evolvability” by Zaman et al.

Chimeric Protein Complexes in Hybrid Species Generate Novel Phenotypes” by Piatkowska et al.


Alex Berezow and Stephen Meyer talk about God and Evolution on the Michael Medved Show | The BioLogos Forum
Creation and Evolution “Research Programs” (And Why It’s So Hard to Change Perspectives) | The BioLogos Forum
#2

Hi @Humeandroid,

So there are two questions: First, is Behe’s argument sound? Second, if it is sound, does it provide a criterion for generating a research program? I’m hoping Justin Topp gives a fuller response to the second question, though I suspect that if I knew more about Lakatosian research programs, I would understand his point.

As to the first question, Behe has faithfully responded to all of his critics. Most of his responses can be found at the Discovery Institute. The ones that aren’t there can be found at his blog, here:

http://behe.uncommondescent.com

However, I don’t think he has responded to Trotter et al., yet. But otherwise, I think the reader is able to at least find responses by Behe to all his major critics and their arguments. Who wins the debate? I’ll leave that for the reader to decide.


#3

[quote=“Bilbo, post:24, topic:784”]
So there are two questions: First, is Behe’s argument sound?[/quote]
First, is Behe’s hypothesis supported by the data? You’re avoiding science. Why?

There’s a lot of research that can be done, but only if one realises that a lot of what Behe glosses over as fact really isn’t. The real question is, why isn’t Behe doing any research?

False. [quote]…I think the reader is able to at least find responses by Behe to all his major critics and their arguments.[/quote]
Where will I find Behe’s response to the criticism that HIV has evolved new protein-protein binding sites in real time? Behe claimed that the number is zero, but his claim is false.

[quote]Who wins the debate? I’ll leave that for the reader to decide.
[/quote]Name a disagreement in science that was decided by debate instead of data. The data decide. Why isn’t Behe producing any, Bilbo?


#4

Hi @Joao

http://behe.uncommondescent.com/2007/11/response-to-ian-musgraves-open-letter-to-dr-michael-behe-part-4/

http://behe.uncommondescent.com/2007/11/response-to-ian-musgraves-open-letter-to-dr-michael-behe-part-5/

http://www.lehigh.edu/~inbios/pdf/Behe/QRB_paper.pdf

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2286568/


#5

Bilbo,

Thanks for showing me where Behe admitted the falsehood of his claim, but I can’t view that as a “faithful” (your word choice) response, since he glosses over what that error (a factor of infinity) does to his calculations.

Did he add that admission to the book?

Does formation of a new monopentamer involve a single binding site, or two binding sites?


#6

Hi @Joao,

If I understood Behe’s response, he would consider it a single binding site. Since his edge is two binding sites, I don’t think it affects his calculations at all. Plus he explains why a viral protein - cellular protein binding site should be in a different category from cellular protein - cellular protein binding sites.

http://behe.uncommondescent.com/2007/11/response-to-ian-musgraves-open-letter-to-dr-michael-behe-part-5/

I imagine that if a second edition The Edge of Evolution is published Behe will include a discussion of the evolution of a new HIV protein in it.


#7

[quote=“Bilbo, post:31, topic:784”]
If I understood Behe’s response, he would consider it a single binding site.[/quote]
But it isn’t a single site–it’s a pentameric channel. That means that one site on one monomer is interacting with a different site on another monomer. Two binding sites.

[quote]Since his edge is two binding sites, I don’t think it affects his calculations at all.
[/quote]What mathematical reasons would you have for saying that? Have you looked?


#8

Hi @Joao,

To quote Behe: “Only one new binding site need develop for one area of a protein which binds to a different area of the same protein, to form a homogeneous complex with, say, C5 symmetry. That is all that is required for a circularly symmetric structure to form.” That was from here:

http://behe.uncommondescent.com/2007/11/response-to-ian-musgraves-open-letter-to-dr-michael-behe-part-4/

Behe’s two binding sites rule was that if more than two new binding sites are required in order to achieve some new function, then this would be beyond the edge. Not sure what else there is to look at. Meanwhile, you haven’t responded to his argument that the evolution of viral-cellular protein interaction is significantly different from, and much easier than, the evolution of cellular-cellular protein interaction.


#9

[quote=“Bilbo, post:45, topic:784”]
To quote Behe: “Only one new binding site need develop for one area of a protein which binds to a different area of the same protein, to form a homogeneous complex with, say, C5 symmetry. That is all that is required for a circularly symmetric structure to form.”[/quote]
Quoting Behe doesn’t make him right. Moreover, you apparently didn’t read it well enough to catch the important qualifier “required.” The question neither you nor Behe are willing to address is not what is required, but whether that is what happened. Don’t we have the structure? Don’t we have the ancestral sequences? Stop playing hearsay games and engage with the evidence for yourself, Bilbo–if you dare.

It’s not a rule, it’s a hypothesis. Avoidance noted.

The math, Bilbo, for yourself. Engage your intellect. I asked you a straightforward question: what mathematical reasons would you have for saying that? Why won’t you answer?

[quote]Meanwhile, you haven’t responded to his argument that the evolution of viral-cellular protein interaction is significantly different from, and much easier than, the evolution of cellular-cellular protein interaction.
[/quote]Why should I? Behe’s false claim has nothing to do with viral-cellular protein interactions. Why are you trying to divert?

Have you considered starting with an open mind and going through the relevant data for yourself, instead of holding up someone who doesn’t bother to read the relevant primary literature as an authority?


#10

Hi @Joao,

You’re welcome to correct Behe here, if you so desire. I’ll try to understand any math you wish to communicate. Otherwise, my point remains: Behe has responded to his major critics. And if his criterion is sound, then he seems to have provided a way of conducting a research program. I’m just curious why this wouldn’t be a “Lakatosian research program.”


#11

[quote=“Bilbo, post:48, topic:784”]
You’re welcome to correct Behe here, if you so desire.[/quote]
I already did.

I’m asking what it does to the math that Behe already communicated. Do you not understand it? If so, why not just admit it?

Not substantively. Your refusal to engage mathematically constitutes implicit agreement–or at a minimum, no confidence in your claim.

[quote]And if his criterion is sound, then he seems to have provided a way of conducting a research program.[/quote]Then why isn’t anyone doing such research? And why do you call a hypothesis a “rule” or “criterion,” unless you want to avoid facing the fact that neither Behe nor anyone else has any intention of testing it?
Let’s see how well you understand the hypothesis: how many residues must be substituted to widen the substrate specificity of an enzyme to include an artificial substrate (significantly larger) without losing any ability to perform the original reaction it was “designed” to do? I hope that you understand that enzymes have to bind to their substrates.


#12

I think you’re being too charitable here. I can easily show where important data are being ignored (see Bilbo above) and have zero problem mentally entering an ID “program.”

Example: the lens of the eye and its components were designed. This makes a clear empirical prediction: the major protein components of the lens that make it refractive, the crystallins, will have no statistically-significant similarities with other proteins with different functions.

There are three crystallins that can be used to test this hypothesis.


#13

[quote=“system, post:1, topic:784”]
If one were to construct a program around it [ID], the core hypothesis would be “evolution via natural selection is insufficient to generate the diversity of life on this planet.” [/quote]
Why wouldn’t it be “life was intelligently designed”?

[quote]But this isn’t enough to build a research program,…
[/quote]I don’t see why not. There are obvious who, what, and when hypotheses that one can test empirically.


#14

Hi @Joao

HIV evolving one new binding site does not challenge Behe’s math. I would suspect that a number of ID-friendly biologists already think they have discovered IC systems that they think were designed. But getting their conclusion printed in mainstream peer-reviewed journals probably won’t happen any time soon. I would consider that a philosophical bias on the part of the journals.

If I remember correctly, Behe argued that creating a new binding site typically required 5-6 amino acid changes. Whether or not that interferes with the original function of the protein probably depends upon where the changes take place. I believe it’s usually thought that changes take place in a duplicated gene, so that interference with the orignal protein doesn’t need to occur.

But Joao, let me ask you a question. What was the original post about?


#15

[quote=“Bilbo, post:52, topic:784”]
HIV evolving one new binding site does not challenge Behe’s math.[/quote]
I asked how it changes it. Just speculate and apply the math, Bilbo. How would two change the math? I’m not asking you to agree, just apply the math.

Can you do it?

Why don’t they publish in Bio-Complexity then?

You have come to that conclusion on the basis of zero evidence! Is Behe doing anything empirical in his lab?

IIRC there was no argument, just a simple, empirical claim.

Hence my real-world question that you seem to be afraid to address: how many residues must be substituted to widen the substrate specificity of an enzyme to include an artificial substrate (significantly larger) without losing any ability to perform the original reaction it was “designed” to do?

Right in the substrate-binding site. What does Behe’s hypothesis predict?

No duplication in this case. Please apply Behe’s hypothesis and make a prediction.

[quote]But Joao, let me ask you a question. What was the original post about?
[/quote]Research programs. My point is that it’s easy to change perspectives–if one isn’t afraid of learning something. Are you?


#16

Hi @Joao,

Perhaps you have misunderstood me. My contention here has been that if Behe’s argument is sound, then he has provided a sufficient condition for conducting a research program. I have not contended that I am able to fully defend Behe’s argument. I leave that debate to the reader.

In order to do research, money is needed. I suspect that there isn’t a whole lot of money available to do ID research to publish in any journal, ID friendly or not. But I’m basing my opinion that mainstream journals have a philosophical bias against ID research on the anecdotal experience of Behe: http://www.discovery.org/a/450

Meanwhile, if you wish to present a full-blown critique of Behe’s argument here, feel free to do so.


#17

[quote=“Bilbo, post:54, topic:784”]
Perhaps you have misunderstood me. My contention here has been that if Behe’s argument is sound, then he has provided a sufficient condition for conducting a research program. [/quote]
Your explicit contention here was that two binding sites doesn’t change his math. I’m asking how you determined that mathematically.

But you did explicitly contend that two binding sites doesn’t change Behe’s math. Are you withdrawing that contention?

Yes, so what’s the budget of the DI? How much is Behe’s fellowship? Why would there be plenty of money for rhetoric, but none for research?

Then why did you speculate that the research has already been done? Why are you moving the goalposts from publication to funding?

I don’t see any bias against ID research, as Behe wasn’t trying to publish any research, just rhetoric. Do you not realize that Behe’s paper had ZERO research content? Do you not see the enormous gap between research and rhetoric?

Why not Bio-Complexity, then? Why do you specify “mainstream” when Behe’s on its editorial board?

[quote]Meanwhile, if you wish to present a full-blown critique of Behe’s argument here, feel free to do so.
[/quote]I think that I already have presented an empirical one, and you have implicitly accepted the validity of my critique by running away from the notion of applying his hypothesis to the real world.

Why is there any need to add to the full-blown critique in the first journal review Behe posted? The best part is this: “Meanwhile, metaphysicians should spare scientists their metaphysics and just let the scientists do their work–or join them in doing it.”

The lack of curiosity is fascinating. Why won’t Behe do any actual research to test his hypothesis?


#18

I don’t recall saying that two binding sites would change Behe’s math. I do recall saying that one binding site doesn’t challenge his math. Behe has done peer-reviewed research to support his conclusions.

http://www.lehigh.edu/~inbios/pdf/Behe/QRB_paper.pdf

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2286568/


(Mohammad Nur Syamsu) #19

Saying it is 3 is just a start. It is what the mathematics indicate. A perfectly fair line of evidence.

We already know that freedom is real and relevant in the universe, so there is obviously going to be intelligent design occurring in the universe.

I don’t agree that a scientist doesn’t use common sense. If scientists are less knowledgable about how things are chosen in the universe than somebody not educated, but who is not prejudiced against it, then they have ceased to be scientists. The risk that scientists fail to notice the relevance of freedom in the universe is far greater than any mistake or inaccuracy that may occur in grounding intelligent design research.


#20

[quote=“Bilbo, post:18, topic:2406, full:true”]
I don’t recall saying that two binding sites would change Behe’s math.[/quote]
Sorry, my error.

And I recall asking you how it changes his math, but for some reason you insist on a more violent verb.

I presume that you objected because two binding sites would make Behe’s math untenable. Would you mind explaining (mathematically, not with quotes from Behe) why one doesn’t change it, but two would apparently be catastophic? I can’t wrap my head around that mathematically.

[quote]Behe has done peer-reviewed research to support his conclusions.
http://www.lehigh.edu/~inbios/pdf/Behe/QRB_paper.pdf[/quote]
Bilbo, please! I’ve already explained to you why what Behe was unsuccessfully shopping around was not research, and now you hold up a review as “peer-reviewed research.” That’s simply not true. I’ve published 5 reviews. None were peer-reviewed. All were invited. I would never, ever hold them up as research productivity.

[quote]http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2286568/
[/quote]2004? Are you kidding? Behe has published nothing since then, and nothing empirical relevant to ID ever? He has a DI Fellowship (so he can do research) and he’s an editor of an ID journal (so he can easily publish research). What’s the problem in your opinion?

Isn’t that all the evidence we need to know that there’s nothing to see here? What do you think would happen to my NIH grant renewal application if I showed only one non-empirical paper even in three years and tried to pass off a review as research?