Answering Farina on Behe’s Work: Darwin Devolves
In three previous articles (here, here, andhere ), I began a series of four responses to You-Tuber “Professor Dave” Farina’s video review of Michael Behe’s three books. In this final post, I will turn my attention to Farina’s comments regarding Darwin Devolves.
Hemoglobin and C-Harlem
In Darwin Devolves, Behe contends that the majority of helpful mutations are deleterious rather than constructive, since there are far more ways to gain an advantage by breaking than by building something. Says the Farina video:
If Behe had bothered to look at some of the most well-documented examples of evolutionary change, he’d know that this isn’t the case. In fact, he should know this is nonsense based on examples he himself described in his other works. For example, in Edge of Evolution, Behe describes a hemoglobin allele called HbC-Harlem, which, similar to the allele that causes sickle-cell disease, confers resistance to malaria, with, as Behe describes, “the advantages but not the drawbacks of sickle.”
But this “example of evolutionary change” shows precisely the opposite of what Farina wants. As Behe explains in The Edge of Evolution, “Hereditary persistence of fetal hemoglobin (HPFH) is already widespread in Africa, ameliorating the problems of the sickle gene.”1 Surprisingly, however, “the C-Harlem gene, which builds directly on the foundation of the sickle gene and would entirely eliminate the drawbacks of the sickle mutation, has not yet turned up in Africa, where it would do the most good.”2 The reason for this is that the move from regular hemoglobin to C-Harlem would require two co-dependent mutations, whereas the sickle-cell trait requires only one. The probability of getting the sickle-celled trait in any individual is about one in a hundred million. Assuming a population size of a million people, it should thus be expected to arise spontaneously approximately every hundred generations, which is within the reach of evolutionary processes. For the two necessary mutations needed for hemoglobin C-Harlem to occur at the same time, the probability is a hundred million multiplied by a hundred million, which is 1016. As Behe summarizes, “With a generation time of ten years and an average population size of a million people, on average it should take about a hundred billion years for that particular mutation to arise — more than the age of the universe.”3Nonetheless, hemoglobin C-Harlem has arisen, and was first documented relatively recently in New York City.4 But this is because the initial sickle-cell trait was already adaptive, since it conferred resistance to the malarial parasite. Thus, natural selection can preserve the sickle-celled trait (requiring only a single mutation) first and then acquire the second mutation (building on the first), thereby giving rise to the C-Harlem trait, which confers an even greater advantage. It looks like Mr. Farina did not review this example very carefully.
Cit+ in E. coli
As Farina’s second example, he notes,
[Dr. Behe] also describes the aforementioned Cit+ trait in the E. coli of the LTEE [Richard Lenski’s long-term evolution experiment], which has a new metabolic option, without compromising any existing pathways, literally debunking himself yet refusing to acknowledge it.
I have already addressed this example (see here), so I will not belabor the point further. Suffice it to say that Behe discusses Lenski’s work at length in Chapter 7 of Darwin Devolves, and Farina fails to engage with anything Behe writes concerning the long-term evolution experiment.
De Novo Gene Birth
Another complaint in the Farina video is that,
As you are likely beginning to see, creationists [sic] have a sadistic obsession with painting evolution as some kind of destructive force, but to do so they have to ignore a long and expanding list of completely new genes rapidly evolving everywhere we look. There are many papers like this one examining the concept of de novo genes. These are new genes that originate when previously non-expressed DNA becomes protein-coding and preserved via natural selection due to promoters arising near previously non-coding sections of DNA. So, we have a section of DNA that was not a gene, which is now a gene. New genes. We used to think this was rare, but once we figured out how to look for them, by identifying protein-coding sequences that aren’t protein coding in all the most closely related species, we started finding them all over the place.
The review paper Farina cites, by Stephen Branden Van Oss and Anne-Ruxandra Carvunis, notes (as is common in review papers dealing with this subject) that, for a long time, “the consensus view was that virtually all genes were derived from ancestral genes, with Francois Jacob famously remarking in a 1977 essay that ‘the probability that a functional protein would appear de novo by random association of amino acids is practically zero’.”5 But “though de novo gene birth was once viewed as a highly unlikely occurrence, there are now several unequivocal examples of the phenomenon that have been described.”6 In other words, though it was once thought that the origins of fundamentally new genes from non-coding sequences was essentially impossible, the fact that we observe a plethora of taxonomically-restricted genes, rather than being taken as a disconfirmed prediction of evolution, is taken to show that de novo genes can be birthed by evolution quite readily after all. Evolutionary theory, remarkably, is taken to be completely insensitive to disconfirming evidence.
Moreover, though some examples of taxonomically restricted genes bear some resemblance to non-coding stretches of DNA in related species, this is not so with the majority of cases. Furthermore, there is no convincing mechanistic scenario by which non-coding DNA may be transformed into genes coding for proteins that are ready to fulfil a functional role.
Polar Bears
According to Farina,
Perhaps the best evidence that Darwin Devolves is nonsense is that Behe had to flat out lie to defend it. In a discussion of Behe’s treatment of documented adaptations in polar bears, Dr. Nathan Lents pointed out that Behe did not accurately represent the findings of a paper he cited, when he claimed that virtually all adaptations that polar bears have to their arctic climate are actually damaging in some way. In response, Behe provided a table from that paper, showing that all the documented mutations are either “possibly damaging” or “probably damaging.” But he must have thought nobody would check up on him, since Dr. Lents showed that Behe sneakily omitted two columns and many rows, and the omitted data, unsurprisingly, tell a very different story… Apart from the two restored columns, look at all those rows that say “benign,” meaning not harmful in effect. You know, the exact opposite of what Behe is claiming?
This claim has been rebutted thoroughly elsewhere (such as here). In brief, Behe nowhere denies that non-adaptive neutral mutations are common in evolution. Rather, his thesis is that the vast majority of positively selectedmutations are damaging, since there are far more ways for an organism to acquire an advantage by breaking something than there are ways to gain an advantage by building something new. In Darwin Devolves, Behe contended that “65 to 83 percent of helpful, positively selected genes are estimated to have suffered at least one damaging mutation.”7 Given that the entire chart from the Liu et al. paper, cited by Behe, is some 47 rows long and 8 columns wide, it made more sense to reproduce only the portion of the chart that was relevant to supporting his point. There is nothing duplicitous here. Behe omitted from the chart the data from the HVar algorithm (instead showing only the results of the HDiv algorithm) and also left out instances where the HDiv algorithm predicted that a mutation was benign. This served Behe’s purpose of confirming for his readers that up to 14 of the 17 genes examined (i.e., 83 percent) were probably or possibly damaging. The instances where a mutation was not predicted to be damaging (i.e., those listed as benign) do not contradict Behe’s thesis, since Behe never denied that many mutations are benign. Indeed, a significant majority of mutations are benign (e.g., the third codon position may be substituted without altering the amino acid sequence). But Behe’s thesis is that the vast majority of adaptive mutations (which make up a minority of mutations overall) are destructive rather than constructive. There is nothing in the chart that invalidates or undermines this thesis.
Conclusion
Farina’s video rebuttal directed at Behe’s work misrepresents Behe at multiple points. Moreover, Farina misreads several papers that he cites in his video, failing to understand how they intersect with Behe’s critiques of evolutionary theory. There is also little that is new to see in his video. Many of his criticisms of Behe have been made before by others and addressed in detail elsewhere. In short, despite Mr. Farina’s smug condescension and patronizing demeanor, he fails to mount a credible critique of Dr. Behe’s thesis.
Notes
Behe MJ, The Edge of Evolution: The Search for the Limits of Darwinism (Free Press, 2007), 29.
Ibid.
Ibid., 110.
Bookchin RM, Nagel RL, and Ranney HM. Structure and properties of hemoglobin C-Harlem, a human hemoglobin variant with amino acid substitutions in 2 residues of the beta-polypeptide chain. Journal of Biological Chemistry 1967; 242:248-255.
Van Oss SB, Carvunis AR. De novo gene birth. PLoS Genet. 2019 May 23;15(5):e1008160.
Ibid.
Behe MJ, Darwin Devolves: The New Science About DNA That Challenges Evolution (HarperOne, 2020), 17.
