This, conclusion is incorrect. The evidence does not rule out design, but neither does it demonstrate it. In this sense, Moran is over interpreting the evidence. They should both lose the debate, and they needed a third voice in the room with them.
The other problem with this debate is that it is not about IC1, but IC2. Perhaps a different one that focuses on IC1 would be more helpful, because that is what you were honing in on @bilbo.
The problem is that chloroquine resistance did evolve. So what exactly is Behe arguing against? Is he saying that a designer guided the mutations in malarial parasites to produce drug resistance?
This also brings up one of the general critiques I have of Behe’s model which is the Sharpshooter fallacy.
As an analogy, let’s say that I bet you $100 that I can hit a target the size of a half dollar with a bow from 500 yards, on the very first shot. That sounds like an impossible shot, so you take the bet. I then take aim at a dense forest 500 yards away and fire my arrow. I walk up to the tree where the arrow has embedded itself and I draw a bulls eye the size of a half dollar around the arrow. Have I won the bet?
Behe thinks that is a legitimate win. He ignores all of the other spots where the arrow could have struck and instead focuses on the one spot where it did land. How many possible two mutation beneficial changes are there in a genome? I think it would be completely nuts to say that there is just one combination of two mutations in each genome that could produce a beneficial change. In order for Behe’s argument to make any sense he needs to know how many beneficial changes there are in a genome before he can make any claims about the impossibility of beneficial changes occurring. Otherwise, he is just drawing the bulls eye around the arrow.
I will consider commenting more, after you collect the key references. I can tell you already I disagree with both Behe’s and Moran’s conclusions. There is a third way. That might be why the seemed to fight to a draw. They are both wrong on their central conclusions.
I was going to quote that too. Let’s have @Bilbo get the full set of refs in place. I note, also, that this is precisely the issue that I called Behe out on. He did not address this with Moran. It appears to be an intentional rhetorical strategy that is misleading, and it matches exactly what I have said in the past: Which Irreducible Complexity Argument?
This is why I will always be insisting on clearly stating which IC argument we are using. It appears that Behe is arguing against IC2, as if proving IC2 is impossible would also prove IC3 and IC4 are impossible. This is just an invalid argument. As a biologist, I agree that IC2 is impossibly improbable, but think the real questions are about IC3 and IC4, which Behe never really engages.
What do I mean by these ICs?
To be clear, Moran cannot possibly know if every single thing in the whole world is IC4 reducible. So he overstates the evidence. Perhaps God did involve somewhere at some time in an important way, and it either didn’t leave evidence or we have not found it yet (even in the flagellum!). That is why Moran can’t make the final claims he makes. Behe, however, never rigorously considers (though he regularly dismisses) IC3 and IC4 category explanations. This is the achilles heal of his argument, the equivocation between these four IC definitions.
To be fair, this sloppy ontological logic is found everywhere, both inside and outside of science. Most people feel that finding a natural process for a once claimed supernatural cause is evidence against the supernatural cause. Finding a natural process for producing lightning “disproves” Thor as the creator of lightning, even though Thor could create lightning in some undetectable way through natural processes. Perhaps a better way of putting it is that certain observations would disprove the necessity of supernatural causation that acts outside of natural processes. Even then, we are stuck with a possible false dichotomy, as you mention in other posts.
Behe himself has also reinforced this type of thinking. He has said on many occasions that if random mutations and selection could produce the features he cites then this would disprove intelligent design.
I’m criticizing both sides. So I think I am being fair here . That specific debate needed a third voice. I think some people at ID know this, which is why they do not want to engage with me. I’m making a far stronger argument than Moran, because I am not making unsupportable claims at the end. That cuts both ways, against both ID and New Atheism. We really should take a more humble view of science in the end. It can tell us some things, but it can’t tell us everything.
Okay then @Bilbo, here is my description fo the problem. This is only one of many problems, but this is the key one that runs through all of Behe’s work.
So, @Bilbo in Behe’s arguments in these articles, what definitions of IC is he using? If you can identify those in his statements clearly, you’ll start to see for yourself the error in his argument. His argument depends on these equivocations.
Also, do you understand this critique of Moran? Because of this statement, I cannot agree with him either. The choice is not between Behe vs. Moran, because we also have to consider a third voice, on that both @T_aquaticus and I are offering. The false choice, also, is part of how the argument works. Both are offering a false choice, and in that both are wrong.
In the second reference we find this quote, which sums it up nicely:
Moran describes the non-Darwinian pathway that Behe seems to ignore. This is why attacking “Darwinian evolution” is so misguided. What Behe is attacking is a theory that scientists abandoned long ago, and Behe also fails to address the theory of evolution as it exists today.
@Bilbo, this is where @Art’s observation becomes important. This is how Behe dismisses Moran’s points in the article linked:
So, too, with chloroquine resistance in Plasmodium falciparum . The best current statistical estimate of the frequency of de novo resistance is Nicholas White’s value of 1 in 1020 parasites. That number is now essentially fixed — no pathway to resistance will be found that is substantially more probable than that. Although with more data the value may be refined up or down by even as much as one or two orders of magnitude (to between 1 in 10^18-10^20), it’s not going very far on a log scale. Not nearly far enough to lift the shadow from Darwinism.
That summary of Whites paper is inaccurate. The really probability is far higher. This is where Behe stakes his ground and it is based on a misreading of a single paper.
Now let’s stop distracting and get back to where we left off. This discussion has nothing to do with IC1. It is an argument for IC2. Why did you abandon the IC1 argument?
Dr. Swamidass, no, I never abandoned the IC1 argument, which is that IC systems cannot evolved directly from simpler systems which do the exact same function, since by definition there are no simpler systems that do the exact function.
Actually, that is not what the definition states. Do you see how they are not equivalent?
Let us say I have a movement mechanism (M1) that takes 20 proteins, minimum to work, as far as I can tell. We would delete proteins to determine the fewest necessary, and it is 20 in this case.
Let us say I have another movement mechanism (M2) that takes 2 proteins, minimum to work, the exact same function: movement. We would delete proteins here to determine the fewest necessary, and it is 2 in this case.
What is the IC1 of M1? Is it 20 or 2? What is the IC1 of M2? Is it 20 or 2?