The Problems & Successes of Intelligent Design (w/ Dr. Joshua Swamidass)

How’d you find out? :slight_smile:

Details still in flux. It will be recorded.

Cameron has your name in the promos he is doing for the conference.

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What do you want to hear me talk about?

One thing you said in the video, Dr. Swamidass, that I would like to hear more about here, is that evolution can get through several unselected steps, re Behe’s last 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.”

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@swamidass Can you explain what Behe’s original definition of irreducible complexity was and what he changed it to with sources where he did this?

See here: Which Irreducible Complexity?

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Unselected is different than selected-against/deleterious.

The CCC is not about unselectable steps, but about cases where intermediate steps are selected against.

We observe changes with multiple unselected steps all the time in simulations and in laboratory experiments. The rare cases that require strongly deleterious steps may indeed be extremely difficult to evolve. But there is no evidence this is required, for example, in the ape to human transition, as Behe himself acknowledges.

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Never mind the fact that there is conclusive evidence that it is not required for the evolution of chloroquine resistance, the very example on which Behe based his CCC concept.

https://www.pnas.org/doi/abs/10.1073/pnas.1322965111

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Yes, so then Behe’s edge of evolution, of two new protein-protein binding sites, with 3-4 deleterious steps each, would seem reasonable? Not strongly deleterious steps, necessarily, but deleterious nonetheless…

But Summers et al. state that two mutations seem to be required, on each of two paths, for resistance to develop.

It’s just that no known attribute of any organism is known to require 3-4 deleterious steps. So while we can all imagine some hypothetical hurdle that would prevent evolution, there is no evidence such a hurdle obtains in reality, and we have only found evidence against such hurdles where scientists have looked.

But neither require any deleterious mutations to reach that resistance.

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Can you cite any real world adaptations that required 3-4 deleterious steps? If so, can you please cite all of the specific DNA sequences involved and the specific mutations with population data to back up the deleteriousness of the mutations?

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I think a great application of Behe’s edge of evolution would be to use cocktails of drugs to combat malaria, for instance, where a double-CCC (chloroquine complexity cluster) would be required to obtain resistance. Since we know the specific DNA sequences etc. in regard to various medicines.

There is evidence they are deleterious (resistance disappearing after removal of chloroquine, resistance arising in 1 in 10^20 organisms), do you have evidence that they are not deleterious?

Please provide that evidence.

It’s the green and blue arrows here. All high-resistance states can be reached without requiring any deleterious mutations.
https://www.pnas.org/doi/full/10.1073/pnas.1322965111

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So the answer to my question is “No”? You can’t name a single demonstrable adaptation that is beyond the edge of evolution as defined by Behe?

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Why would we even need to do that? Behe thinks double CCC mutations are impossible, so why worry about them? Or are you saying God is going to start using his magic to create resistant bugs, but drug cocktails are more powerful than God?

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For anyone who has not been following my earlier attempt to educate Lee, he is basing this on the following paper:

In 1993, Malawi became the first African country to replace chloroquine with sulfadoxine-pyrimethamine nationwide in response to high rates of chloroquine-resistant falciparum malaria. To determine whether withdrawal of chloroquine can lead to the reemergence of chloroquine sensitivity, the prevalence of the pfcrt 76T molecular marker for chloroquine-resistant Plasmodium falciparum malaria was retrospectively measured in Blantyre, Malawi. The prevalence of the chloroquine-resistant pfcrt genotype decreased from 85% in 1992 to 13% in 2000. In 2001, chloroquine cleared 100% of 63 asymptomatic P. falciparum infections, no isolates were resistant to chloroquine in vitro, and no infections with the chloroquine-resistant pfcrt genotype were detected. A concerted national effort to withdraw chloroquine from use has been followed by a return of chloroquine-sensitive falciparum malaria in Malawi. The reintroduction of chloroquine, ideally in combination with another antimalarial drug, should be considered in areas where chloroquine resistance has declined and safe and affordable alternatives remain unavailable.

He believes this shows that the chloroquine resistant strain is subject to strong negative selection. I’m not joking, just ask him.

Taq did not ask for an application. He asked whether you can cite any real world adaptations. How about responding to the question asked?

So why isn’t Behe doing that?

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Because people have already been doing that for decades, and it has nothing to do with CCC or any other such ID nonsense.

http://apps.who.int/iris/bitstream/handle/10665/66952/WHO_CDS_RBM_2001.35.pdf;jsessionid=4CEAA6AA0EC3BD073BD13DA8787BABF6?sequence=1

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Again, the fact that resistance disappears when chloroquine is withdrawn, and the fact that 10^20 organisms are required for resistance to arise, about the square of 10^12 for atovaquone resistance, which requires 1 mutation.

But just because resistance functionality is increasing, doesn’t mean the mutations are not deleterious.

“With the criterion of two protein-protein binding sites, we can quickly see why stupendously complex structures such as the cilium, the flagellum, and the machinery that builds them are beyond Darwinian evolution. The flagellum has dozens of protein parts that specifically bind to each other; the cilium has hundreds. The IFT particle itself has sixteen proteins; even complex A, the smaller subset of IFT, has half a dozen protein parts, enormously beyond the reach of Darwinian processes. In fact, drawing the edge of evolution at complexes of three different kinds of cellular proteins means that the great majority of functional cellular features are across that line, not just the most intricate ones that command our attention such as the cilium and flagellum. Most proteins in the cell work as teams of a half dozen or more.” (The Edge of Evolution, p. 146)