Gloves Off — Responding to David Levin on the Nonrandom Evolutionary Hypothesis
As readers of Evolution News likely know, the National Center for Science Education is an organization dedicated to dismissing scientific criticism of Darwinian theory. Recently the group’s bimonthly publication, Reports of the National Center for Science Education (RNCSE), reviewed my book The Evolution Revolution. I was not surprised that the review by David E. Levin, who teaches in Boston University dental school’s Department of Molecular & Cell Biology, was negative. I prepared a polite reply for the RNCSE website where he published his review. I requested the opportunity to submit it, but I was not given even the courtesy of a response. Instead, Evolution News published my reply
Levin also posted his review on my book’s Amazon page. I wanted to post an answer to his absurd charges on the same page, but Amazon does not allow the author to post alongside the reviews. The most they will allow is the submission of a comment to a review. But to refute all the nonsense he wrote requires more space than Amazon allows for comments. So I offer here the following — less mild — reply.
In his review, David Levin seems to have set out to perform a hatchet job, and this required dispensing with truth. Before going into that, however, I must describe briefly the major point of my book, which he neglected to address. One would expect a review of a book to include a discussion of its major point. Perhaps he didn’t understand it or else he felt unable to refute it. Either way, he ignored it.
The major point of the book is that current evolutionary theory is a failure. It is a failure because it has never been shown that the probabilities of the alleged evolutionary events, according to the theory, are anything but negligibly small. A scientific theory cannot be established as valid unless the consequences that follow from it correspond to reality. For example, Newton’s theory of the inverse-square law of gravitation could not have been established without calculations showing that its predictions correspond quantitatively to observations. Current evolutionary theory is based on random mutations producing variation that is acted upon and directed by natural selection. Its predicted consequences are therefore random events, which are describable only by probabilities. For the theory to be properly established, these probabilities must be shown to be reasonably large. Because it has never been shown, the theory is a failure and the principle of common descent, which is based on that theory, is without support. Levin did not address this most significant point.
In the book, I present my nonrandom evolutionary hypothesis (NREH) that accounts for all the evolution that has been actually observed and which is not accounted for by modern evolutionary theory (the Modern Synthesis, or MS). Levin ridicules the NREH but does not refute it. There is too much evidence for it. A lot of evidence is cited in the book, and there is considerably more that I could add. He ridicules what he cannot refute.
Levin calls the NREH Lamarckian. But it differs significantly from Lamarkism. Lamarck taught that an animal acquired a new capability — either an organ or a modification thereof — if it had a need for it. He offered, however, no mechanism for that capability. Because Lamarck’s theory lacked a mechanism, the scientific community did not accept it. The NREH, on the other hand, teaches that the organism has an endogenous mechanism that responds to environmental stress with the activation of a transposable genetic element and often leads to an adaptive response. How this mechanism arose is obscure at present, but its operation has been verified in many species.
In the book I stated that stress, resulting from environmental change, can induce an adaptive heritable response in an organism. There is a wealth of evidence for this statement. These phenomena have been reported in bacteria (Chou et al. 2009; Stoebel et al. 2009; Stoebel and Dorman 2010; Drevinek et al. 2010; Gaffé et al., 2011), yeast (Rolfe et al., 1986; Bradshaw and McEntee, 1989), plants (Wessler, 1996; Grandbastien, 1998; Lin et al., 2007), fruit flies (Strand and McDonald, 1985; Aminetzach et al., 2005; Chung 2007), mosquitos (Chénais et al. 2012), and mammals (Liu et al., 1995). And Levin thinks there is no evidence!
Levin ignored the literature regarding the response of bacteria to stress. He writes as if the only mechanism by which bacteria respond to stress is by hypermutation. He seemed to have missed, for example, my discussion of the role of cryptic genes in evolution. Cryptic genes remain silent until activated by transposable genetic elements, which are in turn triggered by environmental stress and their activation tends to relieve the stress. Moreover, hypermutation during stress does not occur “across the genome” as Levin asserts but is targeted to specific regions (see e.g., Bridges 2001). Mutations in these specific areas have often been found to lead to an adaptation to the stressful environment. By the way, if hypermutation were to occur across the whole genome, as Levin says, it would kill the bacterium with the many errors that it would introduce in various critical functions.
He also claims there is no evidence for the heritable effects of NREH. In almost all the examples I gave of organisms responding adaptively to environmental stress, the effects are heritable. He is unaware of the literature on transgenerational effects of stress (e.g., Franklin et al. 2010; Bohacek et al. 2013; Gapp et al. 2014). His ignorance of the literature leads him to ridicule my suggestion that the effects of stress can be transmitted to the next generation. The transgenerational effect of stress, even in humans, has also been documented in recent reports (Matthews and Phillips 2010).
Good theories often start out with only partial evidence for them. A sign of a good theory is that, as time goes on, evidence is increasingly found to substantiate it. This is exactly what is happening with NREH. Since my book was published, more and more evidence of such a mechanism has appeared. RNAs in sperm from stressed mice have been reported to lead to the stress response appearing in adult offspring (Rodgers et al. 2015, Chen et al. 2016, Leslie 2016). It is not Levin’s “credulity” whose bounds he claims are strained, but his faith in Darwinian evolution, which he panics to see demolished.
I wrote in this book (as well in an earlier book) that there is no example of a random mutation that adds heritable information to the genome, and that statement still stands. The statement is important because evolution is about building up information (Spetner 1964, 1968, 1970). Some have offered what they think are counterexamples of my statement, but they are often not of random mutations at all, or they otherwise fail to be valid counterexamples.
Levin finds the statement astonishing, and it may well astonish someone who believes evolutionary theory represents reality. But it happens to be true, and I am not surprised that it astonishes him because it deals a deathblow to evolutionary theory.
Levin desperately tried to refute that statement by charging (falsely) that I have “dishonestly” changed my definition of information in going from one example to another. Before I deal with that risible charge I want to note the importance of information in evolution because it is related to the myth that macroevolution is just microevolution continued over a long time as suggested by Dobzhansky (1937).1 This myth has been promoted by evolutionists for decades. Their favorite example to bring up in support is the evolution of antibiotic resistance (ABR). It has been alleged that since such a complex adaptation as ABR can evolve in a decade or less, one should expect many remarkable complexities to evolve in millions of years. By examining the details of ABR, however, I have shown in the book that mutations leading to ABR, no matter how many millions of times they occur, cannot add any information and cannot therefore lead to macroevolution. And this point can be generalized. We know of no random mutation that can build up biological information in the genome, no matter how many times such a mutation occurs. This fact explodes the micro/macro-evolution myth.
Levin accuses me of “dishonestly” changing my definition of specificity to support my statement that no known random mutation adds information to the genome. In his attempt to discredit my book, he resorted to calling me dishonest. The reasoning on which he based this smear is nothing but ridiculous. He demonstrates that he does not understand what specificity is, nor does he understand the relationship between specificity and information.
The specificity of a biochemical reaction reflects the ability of an enzyme to discriminate. The more highly specific, the more highly discriminating it is and the more information it has. The ribitol dehydrogenase (RDH) enzyme has a high activity on ribitol and a low activity on both xylitol and L-arabitol. It is therefore quite specific to ribitol. The mutated RDH has a somewhat lower activity on ribitol and a somewhat higher activity on xylitol and L-arabitol. It therefore discriminates less well than the wild-type (unmutated) RDH between ribitol and the other two molecules. It is therefore less specific and hence contains less information. The mutation has thus reduced the specificity, and therefore the information, in the RDH.
The streptomycin molecule attaches to the matching site on a pathogenic bacterial ribosome and thereby interferes with its protein synthesis, leading to the death of the pathogen. The matching site discriminates between streptomycin and other molecules, and is therefore specific to streptomycin and this specificity represents information in the matching site. A mutation in the site destroys the match so that the streptomycin cannot attach, granting the pathogen resistance to streptomycin. The mutated site matches to no molecules and thus does not discriminate between streptomycin and other molecules. The mutated site has thus lost its specificity and has lost its information. So this mutation, too, has lost information. Levin’s assertion that it becomes more specific because it matches to zero molecules is ridiculous. To say that binding to no molecules has more information than binding to one or two is a joke. My definition of specificity and information is consistent throughout, as opposed to Levin’s (false) charge.
In referring to my discussion of pupfish evolution, Levin writes, “Spetner asserts disingenuously that ‘the DNA of those in the refuges differed from those in Devil’s Hole’, whereas the actual finding was that their genomes were nearly identical.” First of all, nearly identical is not identical. Great differences in phenotypes can stem from small percentage differences in the DNA.2 Moreover, Lema, the author of the pupfish paper, cites Wilcox and Martin (2006), who wrote that there are differences in the DNA between the fish in Devil’s Hole and the refuges. And Lema goes on to discuss possible reasons for the differences.
He further charges that I have not addressed the issue of the nested hierarchies of the phylogenetic tree, saying, “Spetner failed to address this issue at all.” He chooses to ignore an entire section I wrote on the phylogenetic tree. In contrast to his claim that “the nested hierarchies produced by anatomical and genomic comparisons agree with each other astonishingly well,” I presented a wealth of evidence showing that the trees derived from morphology and from molecular sequences fail to agree as one would expect if common descent were true.
Levin writes, “It is nothing short of astonishing that Spetner appears not to grasp the fundamental concept that descent with modification produces homologous structures, not analogous structures.” He confounds my discussion of the phylogenetic tree with this particular example of convergence. Although, as I noted in the book, the concept of convergence was invented to explain away many discrepancies in the phylogenetic trees, examples of convergence are inherently contradictions to the MS. Convergence in analogous structures is a more profound type of convergence than that in homologous structures.
With completely different types of tissues and organs, the katydid exhibits the very same mechanism for impedance matching as do the vertebrates. The authors of the study I cited on katydid hearing wrote, “Our results reveal a notable case of convergence, whereby organisms with the most remote phylogenetic histories (such as mammals and katydids), have evolved to hear in a markedly analogous way.” This is a remarkable phenomenon and cannot be explained by the random mutations and natural selection of the MS. It is one of many examples of the failure of the MS.
In short, Levin brought no valid arguments against my thesis, which remains that the current evolutionary theory is a failure, and common descent has no valid scientific basis. Microevolution is widely observed, but macroevolution is an illusionfor which there is no direct observational evidence. All that is offered is circumstantial evidence. Moreover, there is no theoretical support. Furthermore, NREH accounts for all the evolution we have observed, and for which the MS is unable to account. Rather than an honest review of my book, Levin has fabricated negative criticisms. With no valid case to make, he stooped to mendacity.
(1) This myth is, however, lately being challenged even by evolutionists (e.g., Erwin 2000; Pigliucci 2009).
(2) For example, a 10 percent change in each of 100 genes, which could account for vast phenotypic differences, would represent only a 0.0003 percent difference between two genomes of 3 billion base pairs. The two genomes would be 99.9997 percent identical — i.e., nearly identical.
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Photo credit: Airman 1st Class Kerelin Molina [Public domain], via Wikimedia Commons.