On Human Origins, Smithsonian Teaching Resources Oversell Evolution

Evolution News thinks that Smithsonian teaching resources oversell evolution. What’s your view?


Sarah Chaffee, the DI employed author of that fetid piece of anti-science propaganda, is repeating bog-standard ID-Creationist PRATTs.

She complains the explanation for the evolution of fish antifreeze proteins is wrong because it is not macroevolution. Never mind it wasn’t offered as an example of macroevolution. Same for the adaptation in Tibetans for high altitude breathing. Another whine that’s not macroevolution.

She agrees adaptations for skin color are microevolution but complains it doesn’t show a “meaningful gain of information”, whatever that vague undefined buzzterm means.

She rehashes Behe’s long discredited claims about malaria evolving drug resistance needs an Intelligent Designer and that evolution can’t produce new information, only lose it. Behe’s nonsense has been beaten into the proverbial fine pink mist many times; refutations are easy to find online.

She finishes off by repeating the same nonsensical opening claim; the Smithsonian’s examples do not explain human origins. By themselves of course they don’t. They are simply a few of the thousands of scientific facts concerning human origins and were never offered as a complete explanation.


I think that could be a good model post for discussion. Being personally unfamiliar with what information is presented and how it is presented I’d have to reserve judgment on whether evolution is being oversold.

Do people see the post at EN has being anti-evolution and if so, why?

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That’s weird… I read The Edge of Evolution and I clearly remember Behe using malarial resistance as an example of evolution, not design. I don’t have the book, so I can’t say the page number, but I recall him saying that it was an expectation that every ten years it would happen and the drugs would have to be cycled in and out.

Okay, I pulled the text from the article. This is what it says:

The third unit delves into malaria, one of the leading causes of death in the world. In a description for students of a scientific experiment, it talks about how resistance to the drug chloroquine came about because of a change in an amino acid in the PfCRT protein — lysine changed to threonine. This sounds a lot like what Michael Behe discusses regarding malaria in The Edge of Evolution . Yet, the authors try to use this discussion to build their case for human evolution when in fact malaria demonstrates the opposite: how little evolution can accomplish even in organisms with huge populations and short generation times. The G6PD deficiency shows a loss of information that is beneficial — not the emergence of a new protein or anything similar to that.

What they are saying here is that the mutation of malaria is very much to be expected in evolution, but is not a poster-child for significant change over time, especially in comparison to human evolution… (descent of man?)

Thanks @Timothy_Horton that is a helpful summary of your assessment, and what is in the article. Thank you.

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I think @Michael_Callen has a point. It seems rather that Behe is pointing to the difficult if evolving Malaria resistance as validation of his mathematical claims, because it is evolved, not designed.

Here’s a good technical rebuttal to Behe’s Edge of Evolution claim that a double CCC complex for conferring drug resistance to malaria is impossible to evolve and must be designed.

Mutation Combinations for Chloroquine Resistance

Note that Behe also claimed in EOE that malaria itself was “Designed”.

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That’s exactly it… His point here was that this was a single mutation in a location where it was readily accepting as compared to some changes that would require three or four mutations to take place.

I’m not defending either perspective, but only clarifying what they were discussing in both the book and the article.

Hey, Tim. I don’t believe that’s what the book said… I wish I still had a copy… this site is referring to a “double” CCC complex, which it refers to as a made-up term. I have a feeling that this page follows the original section which spoke of the resistance being expected. That, due to the shortness of the life cycle, the population sizes, and the relative ease of the mutation, that it was expected to occur about every ten years.

That said, I don’t doubt that he would say that malaria was “designed”… just that this particular example wasn’t used in this regard. Do you have the book? I’d really like to know… You know this stuff and I do not… It’s this part here:

In a description for students of a scientific experiment, it talks about how resistance to the drug chloroquine came about because of a change in an amino acid in the PfCRT protein — lysine changed to threonine.

This does not sound like the CCC complex issue. I think it is something different. I wish I still had the book and could cite the page, though.

14 posts were split to a new topic: Quote Mining Behe?

Behe doesn’t argue that. He argues that a double mutation is just about the maximum that evolution can accomplish even in a species with as large a population as P. falciparum.


Oh, and Behe is right on this point, as far as I know(*). The fact that clinically significant chloroquine resistance only arose a handful of times over decades of the drug’s use does mean that the mutations required are quite unlikely.

(*) And I’m probably the only malaria geneticist in the room.

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I don’t know @glipsnort. What does “unlikely” mean quantitatively?

Behe cites a back-of-the-envelope calculation of once per 10^20 parasite cells, which is in the right ballpark. I think that was assuming that 10% of malaria cases were treated with chloroquine, which would be ~50 million cases per year; assuming 10^12 parasites per case, that would yield one successful resistant parasite every other year.

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