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

Because people have already been doing that for decades, and it has nothing to do with CCC or any other such ID nonsense.;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Again, the fact that resistance disappears when chloroquine is withdrawn, and the fact that 10^20 organisms are required for resistance to arise, about the square of 10^12 for atovaquone resistance, which requires 1 mutation.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)

This would be a good idea, if it would indeed cure malaria. And I’m not saying God would then try and create resistant bugs.

Yes, I believe this is evidence that chloroquine resistance mutations are subject to negative selection. I won’t say strong selection, though.

So that would be a no. You haven’t shown us any specific mutations in specific proteins, and why those mutations are beyond the edge of evolution. All we have are empty assertions made by Behe.

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I expect combination therapies will become the norm, if the cost issues can be resolved. And if a combination could get beyond a “double-CCC” for resistance to form, the disease could be eradicated!

Yes it does. If the mutations increase resistance to an antibiotic, then if that antibiotic is present in the environment, they are beneficial by definition since they allow the carriers of those mutations to survive and reproduce better under those conditions.

Being a leaf-insect in a barren desert probably isn’t beneficial either. Many similar examples can be thought of.

That’s just what it means for a mutation to be beneficial. Mutation effects are always context-specific.

It is entirely possible there is some other circumstance where the same mutations have negative fitness effects. It is possible the mutations that give chloroquine resistance are deleterious in an environment without chloroquine, but beneficial when chloroquine is present.

That’s not an issue with evolution, that’s just what leads to ecological specialization. Some organisms evolve to be very good at specific things, but do poorly outside of that niche, others become good generalists who can do decently well in many different circumstances.


Another of your typical “These go to 11” non-answers. Not sure why I expected any better, though.

BTW, you seem to have forgotten that, in his book, Behe admits that God must have designed malaria to kill us. So how can you be so certain He would not then create parasites resistant to any drugs we might develop?

Thanks for confirming.

Why do you believe that? What do you think would have happened if, in the absence of chloroquine use, the mutations responsible for chloroquine resistance were not subject to selection and their prevalence in a population was only subject to genetic drift?

That is nothing but word salad. Exactly what did you intend to say there? Try re-wording it into something resembling coherent English.

Mainstream science, not needing any chiming from ID, has long used combination drugs in the war against malaria, bacterial infections, and cancer. Even so, incessant evolutionary process persistently challenges our best efforts. Behe’s edge of evolution has been repeated pushed back. It is worthless both in terms of theory and in terms of practical epidemiology, an ulterior motivated waste of time. Here is what evolution, as you say, actually does

Combating multidrug-resistant Plasmodium falciparum malaria

Over the past 50 years, Plasmodium falciparum has developed resistance against all antimalarial drugs used against it: chloroquine, sulphadoxine–pyrimethamine, quinine, piperaquine and mefloquine. More recently, resistance to the artemisinin derivatives and the resulting failure of artemisinin‐based combination therapy (ACT) are threatening all major gains made in malaria control. Each time resistance has developed progressively, with delayed clearance of parasites first emerging only in a few regions, increasing in prevalence and geographic range, and then ultimately resulting in the complete failure of that antimalarial.

There are recent reports of treatment failure in Cambodia, as well as along the Thai‐Myanmar and Vietnam–Cambodia borders, with treatment failing not only for artemisinin alone but also in combination with partner drugs (piperaquine or mefloquine)


Again, if you think that Behe’s idea adds anything of value, why isn’t Behe doing anything himself? Why is he only writing books aimed at people like you?


Imagine how sneaky that little bug is, developing resistance to all those drugs without ever evolving a new functional protein. It must work by magic.

No, that factor is beneficial, but the mutation overall could be harmful.

That’s ridiculous. You would then argue that a polar bear has tons of deleterious mutations because if you dropped a polar bear in the middle of the Sahara desert those mutations would be deleterious.

ALL mutations are judged in the context of the environment where they appeared.


Because we are to subdue the earth (Gen. 1:28), this would be one of the aspects needing subduing.

I would expect the mutations would be fairly persistent, since the use of chloroquine would have virtually fixed the mutations in the population.

If a combination of drugs would require a “double-CCC” (say 4-6 mutations) for resistance to form, then that disease would not be expected to form resistance, and would be eradicated.

But treatment with a combination, where a single drug of the combination is also in use, would not be effective. The combination has to be used consistently, in an area where resistance to one of the drugs has not developed.

And we would need to know if more that one mutation is involved for resistance to these drugs, singly, to know if resistance to the combination is beyond Behe’s edge of evolution.

I think Behe is also aiming at scientists, and he does mention combination therapy in his book.

You clearly don’t know what the word “fixed” means, When parasites are no longer being exposed to chloroquine, what is preventing the mutations responsible for CR from declining in prevalence in the population, do you reckon?

Chloroquine resistance requires 4-10 mutations. So what are you even talking about?

One more time:

Mutations in the chloroquine resistance transporter (PfCRT) are the primary determinant of chloroquine (CQ) resistance in the malaria parasite Plasmodium falciparum . A number of distinct PfCRT haplotypes, containing between 4 and 10 mutations, have given rise to CQ resistance in different parts of the world. Here we present a detailed molecular analysis of the number of mutations (and the order of addition) required to confer CQ transport activity upon the PfCRT as well as a kinetic characterization of diverse forms of PfCRT. We measured the ability of more than 100 variants of PfCRT to transport CQ when expressed at the surface of Xenopus laevis oocytes. Multiple mutational pathways led to saturable CQ transport via PfCRT, but these could be separated into two main lineages. Moreover, the attainment of full activity followed a rigid process in which mutations had to be added in a specific order to avoid reductions in CQ transport activity. A minimum of two mutations sufficed for (low) CQ transport activity, and as few as four conferred full activity. The finding that diverse PfCRT variants are all limited in their capacity to transport CQ suggests that resistance could be overcome by reoptimizing the CQ dosage.

There, bolded the part I want you to read this time, so hopefully you’ll see it.

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Neither single drugs nor combinations can possibly used consistently, because there are phases of the life cycle that are in mosquitoes and rats, which are not treated. Both you and Behe ignore this obvious fact.

That’s why resistance evolves so rarely, not because it requires two simultaneous mutations in the same gene.

Wouldn’t my judgment, as a scientist, be far more (10^20) relevant than yours in that context?

I don’t think he is because we don’t tolerate being lectured to by people who don’t bother to read the primary scientific literature… If Behe thinks that, he’s delusional.

If he’s aiming at scientists, why not do something other than rhetoric? You are avoiding addressing that simple question. Why?

So what? You’re making my point for me.

I’m pretty sure you’re well aware that mentioning something is not equivalent to doing something scientifically. Why are you pretending that it is?

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I’ve have often wondered why no one in ID considers the opposite approach. Say 3-4 easily selectable steps which should occur, yet do not despite extremely high probability. This could be evidence of the designer saving to maintain the integrity of the design. Your thoughts?


I mean most of the parasites in a population carry the CR mutations.

Sorry, I should have said 4-6 deleterious mutations.