Why Behe offered a second definition of IC

Dr. Swamidass was kind enough to post a link to the article where Dr. Behe offered a second definition of IC: In Defense of the Irreducibility of the Blood Clotting Cascade | Discovery Institute

It comes in Part VI. As far as I can tell, Behe is not rejecting his first definition of IC. He is offering a second, “evolutionary,” definition in order to focus attention on the number of unselected evolutionary steps that might be needed to evolve a particular IC system. As far as I can tell, Behe is not being self-contradictory. But I will merely quote the section in its entirety, so the reader may decide for herself.

"VI. An Evolutionary Perspective on Irreducible Complexity

In Darwin’s Black Box I defined the concept of irreducible complexity (IC) in the following way.

By irreducibly complex I mean a single system which is composed of several well-matched, interacting parts that contribute to the basic function, and where the removal of any one of the parts causes the system to effectively cease functioning.
(Behe 1996, 39)

While I think that’s a reasonable definition of IC, and it gets across the idea to a general audience, it has some drawbacks. It focuses on already-completed systems, rather than on the process of trying to build a system, as natural selection would have to do. It emphasizes “parts,” but says nothing about the properties of the parts, how complex they are, or how the parts get to be where they are. It speaks of “parts that contribute to the basic function”, but that phrase can, and has, been interpreted in ways other than what I had in mind (for example, talking about whole organs that contribute to complex functions such as “living”), muddying the waters in my view. What’s more, the definition doesn’t allow for “degree” of irreducible complexity; a system either has it or it doesn’t. Yet certainly some IC systems are more complex than others; some seem more forbidding than others.

While thinking of Keith Robison’s scenario, I was struck that irreducible complexity could be better formulated in evolutionary terms by focusing on a proposed pathway, and on whether each step that would be necessary to build a certain system using that pathway was selected or unselected. If a system has to pass through one unselected step on the way to a particular improvement, then in a real evolutionary sense it is encountering irreducibility: two things have to happen (the mutation passing through the unselected step and the mutation that gives a selectable system) before natural selection can kick in again. If it has to pass through three or four unselected steps (like Robison’s scenario), then in an evolutionary sense it is even more irreducibly complex. The focus is off of the “parts” (whose number may stay the same even while the nature of the parts is changing) and re-directed toward “steps.”

Envisioning IC in terms of selected or unselected steps thus puts the focus on the process of trying to build the system. A big advantage, I think, is that it encourages people to pay attention to details; hopefully it would encourage really detailed scenarios by proponents of Darwinism (ones that might be checked experimentally) and discourage just-so stories that leap over many steps without comment. So with those thoughts in mind, I offer the following tentative “evolutionary” definition of irreducible complexity:

An irreducibly complex evolutionary pathway is one that contains one or more unselected steps (that is, one or more necessary-but-unselected mutations). The degree of irreducible complexity is the number of unselected steps in the pathway.

That definition has the advantage of promoting research: to state clear, detailed evolutionary pathways; to measure probabilistic resources; to estimate mutation rates; to determine if a given step is selected or not. It allows for the proposal of any evolutionary scenario a Darwinist (or others) may wish to submit, asking only that it be detailed enough so that relevant parameters might be estimated. If the improbability of the pathway exceeds the available probabilistic resources (roughly the number of organisms over the relevant time in the relevant phylogenetic branch) then Darwinism is deemed an unlikely explanation and intelligent design a likely one."


In this quote, he abandons IC1 as a scientifically rigorous idea, identifying it as merely a useful convenience when discussing it with the public. He also discusses its “drawbacks.” (what are they?)

Here, he points out that he has a new and better formulation of IC (IC2 in our parlance). He calls it a better formulation, except it is also a different concept.

IC1 is not the same thing as IC2. IC2 is not a better formulation of IC1. IC1 is clearly falsified, and Behe is not defending it as a valid concept here.

To be clear, IC2 has major problems too:

Nothing new here @Bilbo. Though I do appreciate the new thread on with the extended quote. Makes it clear what the issue is.

IC1 is not falsified. The problem is that it is not easily measurable. In his book, The Edge of Evolution, Behe first estimates the number of mutations it would take to form a new binding site. Based on that estimate, he concludes that Darwinian evolution cannot be expected to evolve more than two proteins. If a system requires three or more proteins, then he concludes that it is beyond the limits (“edge”) of Darwinian evolution. Since, Behe says, most cellular systems require six or more proteins, then we may conclude that they came about through non-Darwinian means.

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IC1 is very easy to measure that is its strength! IC2, on the other hand, is nearly impossible to measure.

It’s weakness is that we have clear mechanisms to explain how it arises. That is its weakness. This quote from Behe even tells you (with subtlety) he does not think it is defensible way of defining non-evolvable features.


Once again, Dr. Swamidass, Behe’s second book, The Edge of Evolution, is devoted to trying to determine the limits of Darwinian evolution. He concludes that it cannot evolve more than two proteins. If a system (IC1) requires more than two proteins, Behe concludes that it is beyond the limits (“edge”) of Darwinian evolution. Most protein complexes (IC1 systems) require six or more proteins. Behe says this is well beyond the limits of what Darwinian evolution can accomplish.

IC2 probably helped focus Behe’s attention on the real problem: how difficult is it to evolve new binding sites? Now perhaps Behe’s estimates are wrong. So far, I don’tthink that has been demonstrated.

Hi Bilbo, old friend. Of course, there are many sorts of examples and experiments that show that Behe was and is wrong. But that may be beside the point, since Behe’s estimates are based on a number that is, for the most part, a fabrication.


In addition to @art’s point, this is not insubstantial:

This a strawman. No evolutionary biologists thinks that Darwinian evolution is sufficient to explain the complexity of what we see in life. Darwinian evolution was falsified in 1968. Why is Behe still arguing against a falsified theory?

Note, I’ve already pointed this out in that thread you seem to want me to quote to you repeatedly:

Of note, this is an issue of trustworthiness:

I proposed some new versions of IC, which might actually make Behe’s point, however, they turn out not to be tractable.

Of note @Bilbo, you still have not even attempted to fulfill a basic request:

If you would like to continue the conversation @Bilbo, please attempt to answer the question. Why do we think that IC1 has been falsified?

The point of this thread, Dr. Swamidass, was to point out that there is no contradiction between Behe’s IC1 and IC2.

I’ll get to work on those counterexamples to IC1 that you are so excited about.

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Hi Art, good to see you, too. Behe and Moran had an extended debate on this question. I think Behe prevailed. Perhaps I’m mistaken.

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The mere fact of two definitions is not contradictory. I never meant to imply this. Rather, the point is that IC1 was falsified. IC2 uses the same name, and this is what he has moved to now, while still allowing the rhetoric of IC1 to go on. This is confusing at best, though there are less charitable ways to put it.

He owes it to supporters such as yourself to clarify that IC1 is falsified, or actually engage the arguments and clear evidence against it.

No need @bilbo, unless you really want to take this further. This is really something only Behe can clear up. It is not your fault he has not been clear.

Not what I am talking about.

Here is the part of White’s review from which Behe pulled the value 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.

The bottom line is that the number bandied about by Behe et al. (1 in 10^20) is not really representative of the frequency of the CCC he discusses in the EoE.


Your post fails to state just what it is that Behe was wrong about. Further, it fails to identify the basis for your claim that “there are many sorts of examples and experiments that show that Behe was and is wrong”

But, you say, that is all beside the point. So why did you bring it up?

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That makes no sense. It’s just a definition.

Behe’s hypothesis is that structures that meet that definition can’t be evolved. That hypothesis is false, particularly as shown by nature in the case of the blood clotting cascade.

The estimate is a fabrication that has no basis in reality, but even so, he hypothesizes that Darwinian evolution, which is only part of evolution, can do that. That hypothesis is false.

No, it’s a hypothesis.

That’s a hypothesis too. Why are you and Behe pretending that all one has to do is publish a book with cherry-picked data and empty assertions, instead of doing science and testing these hypotheses?



We should remember how to describe Behe’s examples.

In fact, if Behe says this, it is with the fillowing qualifier:

unlikely to [+]

“…be evolved…”

[+] without God’s plan/design

Behe is not saying that (generally) somethings can or cant be evolved - - because he envisions a scenario where evolutionary processes produce ALL of them.

What he is doing is comparing more likely and less likely.

Yes, that’s my point. Behe presents hypotheses as conclusions.

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Understanding the limits of detecting design in ID should be commensurate with understanding the limits of what Science can disprove.

Which One Is Easier to Measure?

Before we go further @Bilbo, you might want to clarify your thoughts here, by responding to my point:

It appears you missed a very critical point about IC1 and IC2. Do you really believe that IC1 is hard to measure, but IC2 is easy to measure? Why is that? Most of us think exactly the opposite. IC1 is very easy to measure (that is its brilliance). IC2, however, is nearly impossible if not entirely impossible to measure.

Can you explain why you disagree? Or retract your statement, and acknowledge your stated reason for why he created IC2 is false. Either way works for me. Until that is settled, however, we are certainly not talking about the same things.

Is IC1 a Definition or a Hypothesis?

@Mercer, to be clear, I think both @bilbo and I are using a shorthand (at least I hope so) here. What I mean by “IC1” is precisely the hypothesis that “IC1 systems cannot evolve by Darwinian mechanisms.” You, also, are absolutely correct that Behe states this as a conclusion, without empirical justification, rather than as a hypothesis to test. Hopefully that is actually a separate issue. Though I think as this conversation plays out it will be clear.

I think that your hopes are unfounded. Nothing Bilbo has written is consistent with using that shorthand.

Unfortunately, Bilbo’s writings suggest that he is subscribing not to this being a mere hypothesis that Behe failed to state as one, but as the completely unscientific idea that ‘if something meets the definition of IC, it could not have evolved’ period.

Maybe @bilbo will clarify his understanding.


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