Editor’s note: We are pleased to welcome a new contributor, Lee M. Spetner. Dr. Spetner holds a PhD in physics from MIT and is the author of The Evolution Revolution (reviewed by Casey Luskin here) and Not by Chance.

As readers of Evolution News likely know, the National Center for Science Education is an organization dedicated to dismissing all scientific criticism of Darwinian theory. Recently the group’s bimonthly publication, Reports of the National Center for Science Education, 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 requested the opportunity to reply in the journal, but received no answer. So I will offer a response here.

Unfortunately, the points Levin raises are the results of his misunderstandings or distortions of what I wrote, or his failure to read the relevant portion of the text he was commenting on. Indeed, he missed the most important point of the book.

I show that current evolutionary theory, and any derivative of it that relies on random mutations, is invalid. A scientific theory is not established as valid unless the consequences it claims 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 to observations. Current evolutionary theory is based on random genetic variation which plays the role of the raw material of natural selection. Its predicted consequences are therefore random events whose occurrence can be described only probabilistically. For the theory to be properly established, it must be shown that the occurrences of its claimed consequences have a reasonably high probability. Evolutionary theory is invalid because the probabilities of the events it predicts have not been shown to be anything but vanishingly small. Although this was alluded to in my previous work (Spetner 1997), it was not brought out explicitly there as it is in the current book. Levin either missed this point (despite its being emphasized multiple times throughout) or he declined to address it.

The nonrandom evolutionary hypothesis (NREH) introduced in The Evolution Revolution is not, as Levin asserts, a “rehash” of my earlier book. It was introduced in this book to show that a lot of new data, much of which postdated the earlier book, provide confirmation of that hypothesis. The mark of a good theory is one for which new evidence appears after the theory has been proposed. Levin applies the Lamarckian label to the NREH, and in doing so he demonstrates that he either does not understand Lamarck’s hypothesis (most people don’t), or he doesn’t understand the NREH, or both. In any case, Lamarck’s theory lacked a mechanism and for that reason was not accepted. The mechanism for the NREH is described in the book and is backed by evidence.

Levin seems to be unaware of the literature on the response of bacteria to stress. He thinks the only mechanism by which bacteria respond to stress is by hypermutation (which he refers to as elevated mutation rate). He seemed to have missed, for example, my discussion of the role of cryptic genes in evolution. Cryptic genes remain silent until activated by genetic elements, which are in turn activated by environmental stress and their activation tends to reduce that stress. Moreover, hypermutation during stress does not occur “across the genome” as Levin thinks, but is actually targeted to specific regions (see, e.g., Bridges 2001. Mutations in these specific areas lead to an adaptation to the stressful environment. By the way, if hypermutation were to occur across the whole genome, as Levin thinks it does, it would kill the bacterium with the many errors that it would cause in various critical functions.

Levin is also evidently unaware of the literature on transgenerational effects of stress (e.g., Franklin et al. 2010; Bohacek et al. 2013; Gapp et al. 2014). His lack of knowledge of the literature leads him to ridicule my suggestion that the effects of stress can be transmitted to the following generation. Ridiculing the lack of a full mechanism for a hypothesis in the early stage tends to slow the advance of scientific knowledge. It turns out that in this case good evidence of a mechanism appeared soon after my book was published. Micro RNAs in sperm from stressed mice have been reported to lead to the stress response appearing in adult offspring (Rodgers et al. 2015). My suggestion thus does not, as Levin would have it, “strain the bounds of [his] credulity” but is indeed supported by evidence.

As I stated in both this and my earlier book, there is no example of a random mutation that adds heritable information to the genome. That statement still stands. It is important because evolution is about building up information (Spetner 1964, 1968, 1970).Levin finds the statement astonishing, and it may well be to someone who believes evolutionary theory represents reality. But it happens to be true, and it indeed should astonish him because it is evidence that deals a death blow to evolutionary theory.

Levin tries in vain to refute it by charging that I have “dishonestly” changed my definition of information in going from one example to another. I shall deal with that risible charge shortly, but first I must elaborate slightly on the importance of information in mutations because it is related to the myth that macroevolution is just microevolution continued over a long time as suggested by Dobzhansky (1937). This myth, lately challenged by evolutionists (e.g., Erwin 2000; Pigliucci 2009), has been advocated for decades, with support claimed from the evolution of antibiotic resistance. It has been alleged that since such a complex adaptation as antibiotic resistance can evolve in a decade or two, one should expect many remarkable complexities to evolve in millions of years. By examining the details of antibiotic resistance, however, I have shown that no extension of it can lead to macroevolution. And this point can even be generalized — no known random mutation can build up biological information in the genome no matter how many times it, or mutations like it, occur. This fact explodes the myth.

Levin, as I said, accuses me of “dishonestly” changing my definition of specificity to support my statement that no known random mutation adds information to the genome. He used an impolite adverb. As I shall show, however, he arrived at this charge through faulty reasoning.

He apparently agrees with me that when a mutation reduces the activity of the enzyme ribitol dehydrogenase on ribitol and increases it on the related sugar molecules of xylitol and L-arabitol, the enzyme has become less specific — the specificity of the enzyme, and consequently its information content, has decreased. The specificity of an enzyme in binding its substrate stems from the specificity of the portion of the amino-acid chain forming the binding site of the enzyme. If this binding site is degraded by a random mutation, the ability to bind is reduced, or even lost entirely. If it is reduced, then the enzyme’s activity on that substrate is usually weakened, and other molecules, similar in structure to the substrate, may then also come to weakly bind. This weakening of the bond to the main substrate, accompanied by a new ability of other molecules to bind, is a manifestation of a loss of specificity. Levin, as I said, apparently agrees with this.

It is generally understood that the specificity of an enzyme is crucial to its function. “One of the fundamental functions of an enzyme is to provide specificity by limiting the range of substrates which are catalytically productive” (Bone et al. 1989). So in losing specificity something important has been lost. A microevolutionary event that loses specificity cannot lead to macroevolution no matter how many times it repeats and continues to lose specificity.

But Levin does not agree that in my example of antibiotic resistance to streptomycin the matching site in the ribosome has lost specificity. He makes the absurd charge that since the mutation in the bacterial ribosome has ruined the match (it doesn’t bind at all), the ribosome now binds to fewer molecules (namely zero!) than it did before (namely one!) and therefore qualifies as more specific because it binds to fewer molecules! This is sophistry in the extreme. When a mutation increases the range of molecules bound by an enzyme as described above, the specificity of the enzyme is reduced and consequently its information content is lowered. When a mutation ruins the match of an antibiotic to the ribosome it does not bind any molecules. In this case the binding function of the ribosome is lost. The enzyme thus relates to all molecules equally. Its specificity has been reduced to zero.

Levin thus resorts to rather peculiar reasoning to make his claim that I changed my definition of specificity. I did not change my definition; in both cases specificity is reduced; in neither case, can the mutations extend to macroevolution.

Levin chides me for rejecting common descent without addressing what he calls the “cornerstone” of the evidence for it. He is testifying here that he did not properly read the book he claims to be reviewing. I indeed addressed the evidence of what he calls “nested hierarchies” of organisms (usually known as the phylogenetic tree). His knowledge of the phylogenetic tree is faulty and out of date. “The” phylogenetic tree is a construct supposed to show the alleged genealogy of living organisms arranged according to their similarities — anatomical, morphological, chemical. The branches ramify to show evolutionary diversification. Any animal organ or system or even a molecule can be used to construct a tree by placing the animals having the most similarity in that organ, system, or molecule on the same branch; those with somewhat less similarity on an adjacent branch and so on. It had been expected that trees based on different organs or physiological systems would be identical, and that would be evidence for common descent.

Some researchers in the life sciences, who are not necessarily knowledgeable about evolution (including Levin), think that the various trees based on different biological systems or on protein- and DNA-sequence data yield the same tree. Life scientists once thought that trees based on anatomy and on the molecular sequences of proteins and DNA would be the same, but they were wrong (Nichols 2001; Degnan and Rosenberg 2006; Degnan and Rosenberg 2009; Heled and Drummond 2010; Rosenberg and Degnan 2010). They thought at least there would be consistency among the trees based on the DNA sequences of different genes, but again they were wrong. They then hoped that if they used the whole genome instead of individual genes, the data might average out and things would be better. In fact, it only made matters worse (Jeffroy et al. 2006; D�valos et al. 2012). All this is discussed in my book. Levin is mistaken about what he calls the “cornerstone” of the evidence for common descent.

He criticizes my rejection of common descent. I reject common descent because it is based on only circumstantial evidence. The drawback to circumstantial evidence is that it needs a valid theory to connect the evidence with the conclusion, and evolutionary theory is invalid, as I explain at length in my first chapter. There is thus no valid evidence for common descent — and certainly not what Levin calls its “cornerstone.” The alleged evolutionary events that have happened in the past have not been observed directly — they have only been inferred from circumstantial evidence (without a valid theory to make the connection). So the only evolution we can learn from is what we can observe, namely the many examples of rapid evolution that we see. Levin calls my assertion incorrect because he does not understand why we cannot rely on the inferences from unobserved events of the past (yes, fossils have been observed but events inferred from them have not).

Levin evidently has a shallow understanding of evolution. He must think that his university studies in the life sciences automatically qualify him in evolutionary studies. A knowledge of evolution does not come through osmosis from studying molecular biology. He is not aware, for example, of the general understanding that there are several levels of convergence in evolution. Convergence is understood to occur not only among homologous organs but among analogous organs as well. The article in which the authors reported their study on the comparison of the auditory system between katydids and mammals had “convergent evolution” in its title. The authors wrote (Montealegre-Z, F. et al. 2012):

Thus, two phylogenetically remote organisms, katydids and mammals, have evolved a series of convergent solutions to common biophysical problems, despite their reliance on very different morphological substrates. [Emphasis added.]

In their conclusion, they 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.

David Levin finds this example of convergence amusing — but his amusement stems from his own lack of understanding.

Levin, in short, has produced no valid negative criticisms of my book. That he tried and found none turns his attempt at a negative review into a positive one.

References:

Bohacek, J. et al. (2013) Transgenerational epigenetic effects on brain functions. Biological Psychiatry 73: 313-320.

Bone, R. et al. (1989). Structural plasticity broadens the specificity of an engineered protease. Nature 339: 191-195.

Bridges, B. A. 2001 Hypermutation in bacteria and other cellular systems. Philosophical Transactions of the Royal Society (London) 356: 29-39.

D�valos, L. M. et al. (2012) Understanding phylogenetic incongruence: lessons from phyllostomid bats. Biological Reviews 87(4): 991-1024.

Degnan J. H. and N. A. Rosenberg (2006) Discordance of species trees with their most likely gene trees. PLoS Genetics 2(5): 762-768.

Degnan J. H. and Rosenberg N. A. (2009) Gene tree discordance, phylogenetic inference and the multispecies coalescent. Trends in Ecology and Evolution 24(6): 332-340.

Dobzhansky, T. G. (1937) Genetics and the Origin of Species. Columbia University Press.

Erwin, D. H. (2000) Macroevolution is more than repeated rounds of microevolution. Evolution and Development 2 (2): 78-84.

Franklin, T. B. et al. (2010) Epigenetic transmission of the impact of early stress across generations. Biological Psychiatry 68: 408-415

Gapp, K. et al. (2014) Early life epigenetic programming and transmission of stress-induced traits in mammals: How and when can environmental factors influence traits and their transgenerational inheritance? Bioessays 36 (5): 491-502.

Heled, J. and A. J. Drummond (2010) Bayesian inference of species trees from multilocus data. Molecular Biology and Evolution 27(3): 570-580.

Montealegre-Z, F. et al. (2012) Convergent evolution between insect and mammalian audition. Science 338: 968-971.

Nichols R. (2001) Gene trees and species trees are not the same. Trends in Ecology and Evolution 16: 358-364.

Pigliucci , M. (2009) An Extended Synthesis for Evolutionary Biology. Annals of the New York Academy of Science 1168: 218-228.

Rodgers, A. B. et al., (2015) Transgenerational epigenetic programming via sperm microRNA recapitulates effects of paternal stress. Proceedings of the National Academy of Sciences USA 112 (44): 13699-13704.

Rosenberg, N. A. and J. H. Degnan (2010) Coalescent histories for discordant gene trees and species trees. Theoretical Population Biology 77: 145-151.

Spetner, L. M. (1964). Natural selection: an information-transmission mechanism for evolution. Journal of Theoretical Biology 7: 412?419.

Spetner, L. M. (1968). Information transmission in evolution. IEEE Transactions on Information Theory IT?14: 3?6.

Spetner. L. M. (1970). Natural selection versus gene uniqueness. Nature 226: 948?949.

Spetner. L. M. (1997) Not by Chance! Shattering the Modern Theory of Evolution. Brooklyn: Judaica Press.

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