Faizal_Ali
(Faizal Ali)
December 22, 2025, 1:54pm
251
Umm, you either have a very short memory, or are counting on the rest of us doing so. Here, for at least the third time that I have pointed it out to you, is Art Hunt’s own response:
11 years ago (give or take), I posted an essay on The Panda’s Thumb that discussed what I believed to me some serious flaws in Doug Axe’s 2004 paper in the Journal of Molecular Biology, or rather, flaws in the ways that the ID community have used the conclusions from that study. Over the years, there have supposedly been some responses from Axe to my essay, but in all reality, to my knowledge, Axe has never addressed the central criticisms I discussed. Joshua has been kind enough to give me a place to revisit this, and maybe elicit a relevant response from the ID community – perhaps Axe, perhaps Anne Gauger, perhaps Brian Miller (the latter two of whom have both avoided my essay with what amount to ad hominem remarks.) What I will do here is: to as briefly as possible, recapitulate my central criticisms so that readers here may understand some of the issues; and raise some new concerns that arose (in my mind) a few years ago, after reading another of Axe’s papers.
For starters, let…
More specifically, here is one particular point that, on its own, completely demolishes Axe’s entire argument:
As I said above, in reading some of Axe’s later work, I realized that the assays he used in his JMB paper are not really suited to the task at hand. In all of the work I am aware of, Axe uses growth of E. coli on ampicillin as a proxy for beta-lactamase activity; as far as I know, he has never published results of direct enzyme assays of any of the beta-lactamase variants he is studying. (I am more than happy to be corrected in this regard, and would be glad to update the following with the data I am asking for below.). Anyone who has plated transformed E. coli on ampicillin or other beta-lactams knows that this isn’t a very quantitative method, and certainly not suited to quantitatively distinguishing enzyme variants with differing activities. More to the point of the JMB paper, Axe’s BioComplexity paper shows that, in cases where enzyme activity may be very low, this assay cannot reliably distinguish between low and zero enzyme activity. This is very important – I believe the conditions used by Axe in the 2004 JMB paper cannot distinguish between mutants with low but significant activities and those with no activity. In other words, the accuracy of Axe’s estimates in the 2004 paper cannot be known, and he may be wrong by tens and tens of orders of magnitude or more.
No one, neither you nor anyone from the ID camp (including Axe himself) has responded to this point. Can you explain why?
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