It’s always easier to refute your opponent’s position by replacing it with an outlandish straw man. The most recent issue of the Journal of Eukaryotic Microbiology contains a paper by Guillermo Paz-y-Miño of University of Massachusetts Dartmouth and Avelina Espinosa of Roger Williams University, titled “Integrating Horizontal Gene Transfer and Common Descent to Depict Evolution and Contrast It with ‘Common Design’” that takes this approach to attacking intelligent design (ID). As suggested by the title, the article attempts to critique the argument that similar features in diverse organisms can be explained by common design. It cites to both a 1996 paper by Paul Nelson in Biology and Philosophy and a response to Francis Collins published by myself and Logan Gage in Intelligent Design 101 as sources arguing for “common design.” Paz-y-Miño and Espinosa purport to discuss the evidence for the Darwinian evolution of the enzyme alcohol dehydrogenase 2 (EhADH2) in the protozoan Entamoeba histolytica, but there’s one problem: no evidence for Darwinian evolution or refutation of ID, one way or the other, is presented in the paper.
Their argument seems to be as follows:
- Set up a straw man. Claim that ID proponents argue that that Darwinism says all 2160 amino acids in EhADH2 must be created at random, all at once. Since this is highly improbable, they acknowledge it can’t happen through Darwinian processes. Then try to show that EhADH2 arose by natural selection.
- This leads into an interesting but ultimately trivial exercise in showing that the incidence of various amino acids in EhADH2 is “non-random” since they appear more (or less) often than would be predicted by the relative number of codons that code for that particular residue.
- Do the same for nucleotides, showing that the incidence of various nucleotides in EhADH2 is highly “non-random” (90% are AT but only 10% are GC but a random sequence would predict a 50/50 spread).
- Having unequivocally refuted a purely random origin of EhADH2 at both the nucleotide and amino acid levels, you come to this conclusion: “Natural selection has tinkered molecular improvements in ancestors of EhADH2 by favoring and retaining an adaptive peptide sequence that promotes optimal function, a classical trajectory from simple evolutionary pathways to complex proteins (Lynch 2005). Mutation rate coupled with natural selection and HGT coupled with common descent suffice to explain the origin and diversification of EhADH2 in the Entamoeba lineage.”
That’s basically where the purported evidence for Darwinism ends in this paper. There was a leap of logic: Where was the evidence for Darwinian evolution?
So EhADH2 has a non-random sequence. Great. Of course Darwinism doesn’t assert genes have entirely random sequences (the straw man they refute in step 1). But last time I checked, ID also predicts that genes won’t have random sequences. And while Darwinian selection predicts non-random gene sequences, not all types of non-random complexity can be produced by natural selection.
Neo-Darwinism contends that mutations are random, and that selection only selects for current–not future–functions. In that regard, if random mutations cannot blindly lead a gene along a step-by-step pathway wherein it is functional at each step and successive mutations confer some advantage, then Darwinian evolution gets stuck on adaptive peaks. (Michael Behe notes that occasionally a neutral or slightly deleterious mutation might be tolerated, but features that require more than two simultaneous mutations appear beyond the reach of neo-Darwinism in most population sizes.) But Paz-y-Miño and Espinosa never establish that the step-by-step Darwinian evolution of this gene is possible. Only one highly complicated step is mentioned (though not justified as plausible):
According to the paper, EhADH2 allegedly arose by a fusion of aldehyde dehydrogenase (ALDH) and alcohol dehydrogenase (ADH) into a bifunctonal protein, EhADH2. If functional ALDH and ADH genes existed in some ancestor, what are the odds of fusing those two genes together to produce a bifunctional chimeric gene that performs both functions? Is it probabilistically likely to occur? They don’t even attempt the calculation. Instead, they cite to a 2001 paper by Espinosa in the Journal of Biological Chemistry which took the ADH part of EhADH2 and found that it could be individually expressed to function. Then they took the ADH portion of EhADH2 and found that it too could be expressed to function, although it depended on some residues in the ADH-half of EhADH2. Thus, they feel this is sufficient to conclude that EhADH2 resulted from the fusion of ALDH and ADH. Perhaps, but what are the odds of a mutation fusing these two genes in the right fashion so both parts could remain functional? And is there a Darwinian pathway to fixing the other residues necessary for the ALDH half to properly function? They don’t say.
The least the authors could do is validate the one “fusion” step they assert took place. But they don’t. Nor do they validate any other step in the Darwinian evolution of this gene: No step-by-step account of the evolution of this gene is given or attempted.
Even if such a fusion mutation is possible, does that really explain the Darwinian origin of EhADH2? Not really; one would still also need to show that the original separate ALDH and ADH genes could evolve separately via a Darwinian pathway. Paz-y-Miño and Espinosa’s paper basically asserts that if particular amino acids and particular nucleotides appear in the gene in a non-random fashion, then descent with modification via natural selection is the correct explanation for the origin of the gene (with some horizontal gene transfer sprinkled in whenever necessary).
But non-random proportions of amino acids or nucleotides says nothing about whether natural selection or intelligent design produced the sequence. As regards the debate over Darwinism and ID, this paper pursues irrelevant exercises. Natural selection is asserted, not demonstrated. This is the epitome of taking neo-Darwinism for granted. Perhaps they should have read the warnings of evolutionary biologist Austin Hughes, who is tired of being embarrassed by bad arguments:
A major hindrance to progress has been confusion regarding the role of positive (Darwinian) selection, i.e., natural selection favoring adaptive mutations. In particular, problems have arisen from the widespread use of certain poorly conceived statistical methods to test for positive selection. Thousands of papers are published every year claiming evidence of adaptive evolution on the basis of computational analyses alone, with no evidence whatsoever regarding the phenotypic effects of allegedly adaptive mutations. … Contrary to a widespread impression, natural selection does not leave any unambiguous “signature” on the genome, certainly not one that is still detectable after tens or hundreds of millions of years. To biologists schooled in Neo-Darwinian thought processes, it is virtually axiomatic that any adaptive change must have been fixed as a result of natural selection. But it is important to remember that reality can be more complicated than simplistic textbook scenarios. … In recent years the literature of evolutionary biology has been glutted with extravagant claims of positive selection on the basis of computational analyses alone … This vast outpouring of pseudo-Darwinian hype has been genuinely harmful to the credibility of evolutionary biology as a science.
(Austin L. Hughes, “The origin of adaptive phenotypes,” Proceedings of the National Academy of Sciences USA, Vol. 105(36):13193-13194 (Sept. 9, 2008) (internal citations removed).)
In the final analysis, Paz-y-Miño and Espinosa’s article in no way refutes “common design” because ID predicts that non-random features will be reused in different organisms. Since that’s exactly what we find, how is common design, in their words “unfounded” or “improbable”? Since they haven’t demonstrated their Darwinian story is mathematically plausible by any stretch of the imagination, their short-curt argument makes premature conclusions.
It never ceases to amaze what passes as an argument for Darwinism. Apparently a non-random distribution of amino acids or nucleotides now refutes ID. Yep, because that’s what ID proponents — especially biochemists like Michael Behe or theorists like William Dembski — have been saying all along: ID predicts we’ll find a random distribution of amino acids and nucleotides. And when we don’t find it, descent with modification by natural selection is definitely the answer. Not.