Editor’s note: For previous responses to Darrel Falk’s review, see here and here.

Biologist and theistic evolutionist (or, as some prefer, evolutionary creationist) Darrel Falk is no stranger to the work of Stephen Meyer. In his recent review of Return of the God Hypothesis over at BioLogos, he reports that he’s read all 1,995 pages of Meyer’s trilogy of books, Signature in the Cell, Darwin’s Doubt, and now Return of the God Hypothesis. That is commendable. Even if I disagree with Falk’s criticisms, I appreciate his willingness to read our colleague’s work and to offer a considered response. That said, Falk’s critique is surprisingly inaccurate, given his self-described familiarity with Meyer’s books, and strangely conflicted, given what he has written about Meyer’s work in the past. 

In the first place, Falk’s critique of Return of the God Hypothesis does not address the main or novel arguments that Meyer makes in his new book for a specifically theistic design hypothesis based on physics and cosmology. Instead, it offers only critiques of Meyer’s previous arguments in Darwin’s Doubt and Signature in the Cell. 

Of course, in Return of the God Hypothesis, Meyer does review those arguments from his earlier books about the evidence for intelligent design in biology. He does so in order to show how that evidence, in conjunction with evidence from physics and cosmology, provides support for theism — or a God hypothesis. So it’s not necessarily irrelevant for Falk to raise these objections in a review of Meyer’s new book. 

What is odd is that the critiques that Falk offers are ones that Meyer has already addressed either in those books or in his subsequent work, including Return of the God Hypothesis. For example, Falk claims that Meyer’s critique of the RNA world hypothesis has been superseded by new experimental results that Meyer fails to mention. But as Brian Miller shows, Meyer has addressed, and decisively refuted, exaggerated claims based on a nearly identical experiment to the one Falk cites — and he even did so in Return of the God Hypothesis on one of the pages that Falk claims to have read. Thus, we will see, as Miller’s also shows in his response, that Falk insinuates Meyer has not addressed a topic, when in reality he has done so specifically and decisively. 

In addition, in critiquing an argument about the Cambrian explosion from Darwin’s Doubt that Meyer updates in Return of the God Hypothesis, Falk dramatically changes his own tune about Meyer’s assessment of the evidence without citing any new evidence in support of his (Falk’s) own rhetorical volte-face. Moreover, Falk’s review again portrays Meyer as ignorant of relevant scientific data, this time about the alleged creative power of evolutionary mechanisms, even though Meyer already extensively discussed and evaluated the very evidence and mechanisms he is accused of failing to “appreciate.” 

New Tune on the Cambrian Explosion

Back in 2014, when Falk reviewed Darwin’s Doubt for BioLogos, Dr. Falk defended Meyer against another ID critic who claimed that Meyer had exaggerated the extent to which evolutionary biologists are rethinking or even rejecting neo-Darwinism. Did Meyer commit this error? 

“I don’t think so,” Falk wrote. “Many evolutionary developmental biologists think that we are on the verge of a significant re-organization in our thinking about the mechanics of macro-evolution.” Falk, who is a supporter of mainstream evolutionary science, further admitted that “the rapid generation of body plans de novo” in the Cambrian explosion is a “big mystery,” and that “none” of the current evolutionary models can yet explain it.

Yet now in his 2021 response to Return of the God Hypothesis, Falk claims just the opposite. Here’s what he says:

Meyer believes that the Cambrian explosion creates a major crisis for the theory of evolution; he thinks there was a significant unexplained increase in genetic information that entered the biological world at that time. I think any evolutionary biologist would, upon reading his work, say that Meyer does not fully appreciate the power of gene duplication and mutation in generating new proteins and changing the way that gene regulatory networks function.

That’s quite a change — in 2014 Falk agreed with Meyer that the Cambrian explosion is a “big mystery” for which we lack an adequate evolutionary explanation. But today, he challenges the notion that the Cambrian explosion is “unexplained,” and argues that Meyer doesn’t appreciate how new genes can evolve via duplication and mutation. What happened? Is there some dramatic new evidence that has explained how the Cambrian animals arose so abruptly or that documents the creative power of the gene duplication mechanisms? Dr. Falk certainly doesn’t cite any. 

Moreover, in Chapters 11 and 12 of Darwin’s Doubt, Meyer not only described this mechanism in detail. He also showed why it fails to provide a plausible explanation for the origin of new genes and proteins (or protein folds), let alone whole new animal body plans. 

The Creative Power of Gene Duplication and Mutation

In Darwin’s Doubt Meyer provides an extensive discussion and critique of the alleged power of the mechanism of gene duplication and mutation to produce new genes. He first accurately describes how evolutionary biologists envision the mechanism working and then he critiques it in detail. Here’s how he describes what he calls “the main neo-Darwinian model of gene evolution”: 

. . .evolutionary biologists envision new genes arising by gene duplication and subsequent mutations in the duplicated gene.” (p. 240)…typically [they] propose evolutionary scenarios in which an ancestral gene duplicates itself, and then the duplicate and the original evolve differently as the result of subsequent mutations in each gene. Next, these scenarios invoke various kinds of mutations—duplication events, exon shuffling, retropositioning, lateral gene transfer, and subsequent point mutations— as well as the activity of natural selection. The evolutionary biologists conducting these studies postulate that modern genes arose as the result of these various mutational processes—processes that they envision as having shaped genes during a long evolutionary history.

(Darwin’s Doubt, pp. 211-212)

Clearly, Meyer is aware of and accurately characterizes the standard evolutionary view that genes arise via duplication and subsequent mutation. But there’s a lot more to the story. 

Meyer shows that accounting for the origin of new genes presents neo-Darwinian evolution with a catch-22. He shows first that, according to neo-Darwinian theory, without gene duplication, any mutations that occur in functional genes will remain under selective pressure. Yet recent research in molecular biology and proteins science shows that even a modest number of mutational changes in an original functional gene will typically result in a loss of function — a loss that can result in “purifying selection” and the elimination of those genes in subsequent generations within a population. 

He then explains that many evolutionary biologists invoke gene duplication in an attempt to avoid this very problem. If a gene is duplicated, as the theory goes, then one copy can perform the original function while the other is decoupled from selection and is free to mutate without deleterious effect on the reproductive success or survival of the organism. Having a duplicate copy free of selective pressure allows the gene to eventually stumble unto a new function. 

But this leads to the other side of the catch-22. Since there is no selection pressure on, or driving, the evolution of the new gene, the evolutionary process must rely entirely on random mutations or “drift” to generate novel genes capable of producing novel protein folds. Yet as Meyer explains, this scenario encounters a different but equally severe problem, because, as he shows in Chapters 9, 10, and 12 of Darwin’s Doubt, functional amino acid sequences (especially those that encode new protein folds) are extremely rare among the vast numbers of possible amino acid combinations that correspond to a protein of a given length. 

Without some selection pressure to drive the evolution of the gene toward one of the exceedingly rare sequences capable of generating a novel protein fold, the evolutionary process must rely entirely on random mutations (or a “random walk” through sequences space) to find or generate such a new “function-ready” protein fold. But that would then require, in all probability, an exceedingly long “waiting time” for the evolutionary process to have a reasonable chance of success. Meyer then cites current research in protein science showing that the calculated waiting times associated with gene duplication and/or gene “cooption” models vastly exceed the amount of time available to the evolutionary process on planet Earth. 

Meyer first described how Michael Behe and David Snoke used standard population genetic models to calculate the expected evolutionary waiting times associated with even modest evolutionary innovations requiring a few coordinated mutational changes: 

Behe and Snoke used the principles of population genetics to assess the likelihood of various numbers of coordinated mutational changes occurring in a given period of time. . . . .[They] found that if generating a new functional gene or trait required more than two coordinated mutations, then excessively long waiting times were necessary regardless of the size of the population. If three or more coordinated mutations were necessary, their calculations generated no “sweet spots” at all. Thus, they concluded that “the mechanism of gene duplication and point mutation alone would be ineffective, at least for multicellular … species.”

(Darwin’s Doubt, pp. 241-242, 247)

He also described the experimental work of molecular biologists Ann Gauger and Douglas Axe. Axe and Gauger specifically tested the ability of evolutionary mechanisms to coopt gene duplicates in service of new functions. Meyer describes their work in detail and explains why it casts doubt on the ability of mutations acting on gene duplicates to produce novel protein folds.

[Axe] therefore effectively determined an upper bound of two for the number of coordinated mutations that could be expected to occur in a duplicate gene during the history of life on earth (taking into account the negative effects of carrying gene duplicates in the evolutionary process). He also calculated six coordinated mutations as an upper bound, neglecting the fitness cost of carrying gene duplicates. Nevertheless, in their experiments, he and Gauger could not induce a functional change in a single gene with more than six coordinated mutations. So, even that more generous — and, again, unrealistically generous upper bound — does little to render the co-option [gene duplication] hypothesis credible. Indeed, Axe and Gauger’s experiments showed that the smallest realistically conceivable step exceeded what was plausible given the time available to the evolutionary process. In their words, “evolutionary innovations requiring that many changes … would be extraordinarily rare, becoming probable only on timescales much longer than the age of life on earth.” 

(Darwin’s Doubt, p. 253)

So Meyer clearly described, addressed, and critiqued the gene duplication hypothesis and he did so by citing novel experimental and theoretical work that Falk does not himself address let alone refute. Clearly, Meyer fully understands (i.e., “appreciates”) the claims that evolutionary biologists make about the creative power of the gene duplication mechanism. Unfortunately, Dr. Falk does not appear to have appreciated or even addressed the powerful critique that Meyer developed of those claims. 

Gene Regulatory Networks

And what about gene regulatory networks (GRNs)? Does Meyer fail to “appreciate” this topic or is this another case where Meyer is being critiqued for ignoring a topic that he actually addressed in detail? In fact, it is the latter. Meyer describes GRNs, or developmental gene regulatory networks (dGRNs), in detail in both in Darwin’s Doubt and Return of the God Hypothesis. Here’s how he described them in his latest book:

Developmental gene regulatory networks comprise networks of genes and gene products (DNA-binding proteins and regulatory RNAs) that control the timing and expression of genetic information during animal development. The components in these networks transmit signals (known as transcriptional regulators or transcription factors) that influence the way individual cells develop and differentiate. For example, exactly when a signaling molecule gets transmitted often depends upon when a signal from another molecule is received, which in turn affects the transmission of still others—all beautifully coordinated to perform specific time-critical functions. These networks of genes and gene products function much like integrated circuits and ensure that the developing organism produces the right proteins at the right times to service the right types of cells during embryological development.

(Return of the God Hypothesis, p. 311)

Moreover, Meyer explains in detail why dGRNs pose a problem for evolutionary explanations of the origin of new body plans:

Even modest mutation-induced changes to the genes in the core of the dGRN produce either no change in developmental trajectory (due to a preprogrammed redundancy) or catastrophic (most often lethal) effects within developing animals. Disrupt the central control nodes and the developing animal does not shift to a different viable, stably heritable body plan. Rather, the system crashes, and the developing animal usually dies or, if it survives, is severely malformed. 

(Return of the God Hypothesis, p. 314)

In support of these claims, Meyer cites the authoritative research of the late Caltech developmental biologist Eric Davidson. He notes that Davidson candidly acknowledged the catastrophic consequences of modifying dGRNs. As Meyer notes, quoting Davidson:

Davidson emphasized that “there is always an observable consequence if a dGRN subcircuit is interrupted. Since these consequences are always catastrophically bad, flexibility is minimal.” 

Meyer then explained why the immutability of dGRNs pose an acute difficulty for evolutionary explanations of the origin of novel body plans:

Building new animal body plans requires not just new genes and proteins, but new dGRNs. But to build a new dGRN from a preexisting one requires altering the preexisting dGRN — the very thing Davidson showed does not occur without catastrophic consequence. Given this, how could a new animal body plan — and the new dGRNs necessary to produce it — ever evolve from a preexisting body plan and dGRN? Davidson himself made clear that no one really knows. Although many evolutionary theorists have speculated about early “labile” (highly flexible) dGRNs, no developing animal that biologists have observed exhibits the kind of elasticity that the evolution of new body plans requires. Davidson, when discussing these hypothetical labile dGRNs, thus acknowledged that evolutionary biologists are speculating “where no modern dGRN provides a model.” 

(Return of the God Hypothesis, pp. 314-315)

In his critique of Meyer, Falk does not venture to offer an explanation for how the evolutionary process might have generated the new dGRNs needed to produce new animal body plans. Nor could he do so, since leading experts in developmental biology such as Davidson have acknowledged that what we know about developmental gene regulatory networks presents a major impediment to the evolutionary innovation of novel body plans. Instead, Falk presents our knowledge of dGRNs as a major reason to regard the mystery of the Cambrian explosion as solved and then faults Meyer for not appreciating that alleged fact. 

A Deep Understanding

In his review, Falk portrays Meyer as ignorant of the importance of dGRNs and gene duplication in evolutionary biology. Yet as we have seen, Meyer’s work displays a deep understanding of both dGRNs and the mechanism of gene duplication. Meyer also makes detailed criticisms of the creative power of various evolutionary mechanisms that are predicated on this knowledge — criticisms that Falk neither acknowledges nor refutes. 

I appreciate that Dr. Falk and his colleagues at BioLogos would like to engage in a productive “dialogue” with proponents of intelligent design — and with Stephen Meyer specifically. Nevertheless, productive dialogue cannot occur when one party misrepresents the position, or fails to acknowledge the arguments, of the other. Nor can productive dialogue occur when one party claims the other is ignorant of ideas and proposals that the other party has described and critiqued decisively and at length.