Life Sciences Icon Life Sciences

Responding to Venema’s Response to Meyer’s Response to Venema’s Response to Meyer’s Signature in the Cell: The Last in a Series (We Promise!)

We recently posted links to the exchange between Stephen Meyer and Dennis Venema regarding Signature in the Cell in Perspectives on Science & Christian Faith (PSCF), a journal of the American Scientific Affiliation. In that same issue the journal gave Venema a chance to reply to Meyer’s reply — in a courtroom setting it’s called a surrebuttal, in case you’re curious — giving Dr. Venema the last word. We ask readers’ indulgence as, in turn, ENV appropriates the last last word with a rebuttal to Venema’s surrebuttal.

Then we’re going to quit the stuff — no joke!

One main point of Venema’s original review was to provide evidence of natural selection and random mutation producing new biological evidence challenges Stephen Meyer’s thesis in Signature in the Cell. But, as Meyer explains in his reply, his argument pertinent to the origin of life is that information could not be produced by prebiological mechanisms. Meyer explains:

The balance of [Venema’s] review is spent refuting an argument that Signature in the Cell does not make and, thus, the evidence he cites is irrelevant to the main argument of the book; in short, Venema “refutes” a straw man. … I happen to think — but do not argue in Signature in the Cell — that there are significant grounds for doubting that mutation and selection can add enough new information to account for various macroevolutionary innovations. Nevertheless, the book that Venema was reviewing, Signature in the Cell, does not address the issue of biological evolution, nor does it challenge whether mutation and selection can add new information to DNA. That is simply not what the book is about. Instead, it argues that no undirected chemical process has demonstrated the capacity to produce the information necessary to generate life in the first place. The book addresses the subject of chemical evolution and the origin of life, not biological evolution and its subsequent diversification. To imply otherwise, as Venema does, is simply to critique a straw man.

ENV readers who have been following the many debates sparked by the publication of Signature in the Cell will be aware that Venema made a mistake common among reviewers of the book. And Meyer wasn’t bluffing about what his book argues. If you look at what he wrote in Signature in the Cell, he makes it explicit that his argument pertains to how information arose in the origin of life, not to the Darwinian evolution of life:

Since I was not principally concerned with whether biological evolution could generate specified information, I decided to formulate a “conservative” conservation law — one that applied only to a nonbiological context (and thus not to any information-rich initial state). My statement of the law does not say anything about whether undirected natural processes could produce an increase in specified information starting with preexisting forms of life. But it does encapsulate what repeated experience had demonstrated about the flow of information starting from chemistry and physics alone.

Here’s my version of the law of conservation of information: “In a nonbiological context, the amount of specified information initially present in a system, S, will generally equal or exceed the specified information content of the final system, Sf.

Meyer, Signature, p. 293, emphases added

In the passage quoted above, Meyer makes it excruciatingly clear that in Signature in the Cell he is explicitly restricting his thesis to the origin of the information in the first forms of life — and that in this book he is “not principally concerned” with biological evolution. Signature does very briefly discuss biological evolution in an appendix–and it is this appendix which serves as the primary section Venema cites for justifying why he he’s talking about biological evolution. But even there Meyer leaves no grounds for doubt that this is separate from his book’s basic thesis.

Despite Meyer’s patient elaboration on this point, Venema’s surrebuttal to Meyer asserts that “the basic argument of Signature requires that biological evolution be incapable of generating new information.”
But that is not the “basic argument” of Signature in the Cell, as we saw above. Meyer’s “basic argument” is restricted to the origin of life, not the diversification of life through Darwinian evolution. Venema seems intent on reviewing the appendix to Signature in the Cell, rather than the book itself.

As evidence that Venema simply doesn’t understand Meyer’s argument, consider this comment from his surrebuttal:

One might wonder: if biological evolution was viewed as a potential threat to Meyer’s argument in 1999 or 2004, why does Meyer not address any evidence for the ability of biological evolution to generate information in Signature?

The answer to Dr. Venema’s question is quite simple. In Meyer’s 1999 and 2004 articles, he was writing about whether Darwinian evolution could produce new information during the diversification of life, and did not restrict his thesis to the first life.

For example, the 2004 paper from Meyer is devoted to analyzing whether Darwinian (and other) mechanisms could produce the information required to generate all the new body plans that appear in the Cambrian explosion. That’s about 3 billion years after life appeared on earth. Likewise, Meyer’s 1999 piece is about biological evolution, in addition to chemical evolution.

But Signature in the Cell is different. It is restricted to studying chemical evolution and the origin of life, not biological evolution and the diversification of life. As Meyer makes clear in Signature in the Cell, Darwinian processes (e.g., natural selection acting on random mutations) require replication, and there was no replication prior to the first life. Thus Darwinian processes cannot be used to explain the origin of information in the first life. Meyer writes:

[M]any scientists recognized that Oparin’s concept of prebiotic natural selection begged the question. Natural selection occurs only in organisms capable of reproducing or replicating themselves. Yet, in all extant cells, self-replication depends on functional and, therefore, sequence-specific DNA and protein molecules. As theoretical biologist Howard Pattee explains, “There is no evidence that hereditary evolution [natural selection] occurs except in cells which already have … the DNA, the replicating and translating enzymes, and all the control systems and structures necessary to reproduce themselves.” But this fact of molecular biology posed an obvious difficulty for Oparin’s theory of prebiotic natural selection. In order to explain the origin of specified information in DNA, Oparin invoked a process that depends on preexisting sequence-specific (i.e. information-rich) DNA molecules. Yet the origin of these molecules is precisely what his theory needed to explain. As Christian de Duve explains, theories of prebiotic natural selection necessarily fail because they “need information which implies they have to presuppose what is to be explained in the first place.” (Signature, pp. 274-275.)

Venema is welcome to write all he wants about how random mutation and natural selection produce new information in a biological context, but it won’t explain how information arose in a non-biological context, before life began, before mutation and selection could operate.

OK, Let’s Talk About Biological Evolution

Yet as Meyer wrote, I too “happen to think … that there are significant grounds for doubting that mutation and selection can add enough new information to account for various macroevolutionary innovations.” So let’s talk about biological evolution.

Venema’s surrebuttal cites his own series on the BioLogos website which, so he claims, shows information arising in a biological context through natural selection and random mutation:

I discussed several examples of how evolutionary mechanisms generate biological information in my original review,4 and later in more detail as a series of blog posts for the BioLogos Foundation.5 In those sources, readers may examine the evidence that, contra Meyer, large amounts of new information have indeed arisen through the natural mechanisms of biological evolution. If a natural mechanism can produce information, then Meyer cannot claim that only intelligence produces it.

In footnote 5, Venema cites his series “Evolution and the Origin of Biological Information,” posted on the BioLogos website a few months ago. We recently posted an extensive rebuttal to that same series, Intelligent Design and the Origin of Information: A Response to Dennis Venema, which shows that the examples Venema cites (a) do not demonstrate natural selection at work and/or (b) do not demonstrate new information arising. Our rebuttal series can be found in full here, or see any of the links below for the original segments:

As for Venema’s footnote 4, this cites his initial review of Signature in PSCF. Though the footnote itself gives no specific examples of exactly where in his prior review he demonstrated new information arising in a biological context (i.e., by natural selection and random mutation), his surrebuttal later claims to have provided “evidence that refutes [Doug] Axe’s work on biological evolution.”

In his original review, Venema had claimed there is “a large body of evidence from structural biology studies that proteins do transition between varied structures and functions across evolutionary time” and thus challenged Axe’s work. Let’s look closer at a paper Venema cited on this point.

Venema cited a 2001 paper by N. V. Grishin, “Fold Change in Evolution of Protein Structures,” Journal of Structural Biology, Vol. 134:167-85. He provided no discussion to explain exactly how this paper challenged Axe. But a quick look at this paper shows that it assumes from the outset that there are Darwinian pathways, but it does not demonstrate that those pathways exist.

For example, the abstract takes the existence of Darwinian pathways as a starting assumption, stating: “The existence of evolutionarily related proteins that possess different folds brings new challenges to the homology modeling techniques….” But does the paper establish that the proteins in question actually are related through a Darwinian pathway?

Rather than showing how natural selection and random mutation might have increased the information in these genes, what the paper primarily finds is mere sequence homology. For example:

  • The paper’s discussion of the alleged evolutionary relationship between NFP and Luciferase is based entirely upon structural and sequence homologies. No step-by-step Darwinian pathway for the evolution of these proteins is given.
  • The discussion of lactate dehydrogenase (LDH) and NADH peroxidase is based upon sequence similarities. After discussing these similarities, the paper concludes “Therefore it is likely that LDH and NADH peroxidase are homologous.” But no step-by-step Darwinian pathway for the evolution of these proteins is given.
  • Likewise, the paper’s discussion of the alleged evolution of the proteins of the glutathione synthetase (ATP-grasp) is again based upon finding sequence and structural homologies. But nothing even close to a step-by-step Darwinian pathway for the evolution of these proteins is ever given.

Michael Behe reminds us why finding sequence similarity is not equivalent to finding a Darwinian pathway:

“Although useful for determining lines of descent … comparing sequences cannot show how a complex biochemical system achieved its function–the question that most concerns us in this book. By way of analogy, the instruction manuals for two different models of computer put out by the same company might have many identical words, sentences, and even paragraphs, suggesting a common ancestry (perhaps the same author wrote both manuals), but comparing the sequences of letters in the instruction manuals will never tell us if a computer can be produced step-by-step starting from a typewriter. … Like the sequence analysts, I believe the evidence strongly supports common descent. But the root question remains unanswered: What has caused complex systems to form?” (Michael J. Behe, Darwin’s Black Box: The Biochemical Challenge to Evolution, pp. 175-176 (Free Press, 1996).)

“[M]odern Darwinists point to evidence of common descent and erroneously assume it to be evidence of the power of random mutation.” (Michael J. Behe, The Edge of Evolution: The Search for the Limits of Darwinism, p. 95 (Free Press, 2007).)

The closest the paper gets to discussing Darwinian pathways is with the following statement, which is basically just an assertion: “As a single event, such an indel/substitution may not affect a protein fold significantly, but gradual consecutive events could transform the structure beyond recognition.” This is followed by diagrams purporting to show “the evolution of protein structures.” The diagrams compare protein structure and sequence, identifying which sections would need to be changed — on a broad structural level — to convert one protein into another. Step-by-step sequence changes are not given. The odds of various proposed insertion or deletion mutations occurring are never calculated. Proposed selective advantages for specific or general/ambiguous changes are never given. No Darwinian pathways are given at all.

In short, Grishin (2001) doesn’t establish what Venema claims it does.

In one case, a hypothetical example of protein evolution is offered, but the paper acknowledges that this does not match known biological reality: “Unfortunately, in the current set of available protein structures it is not possible to find a convincing example of such a path composed entirely of evolutionarily related proteins. … Again, the path shown in Figs. 4a-4h does not necessarily reflect the actual evolutionary events but rather illustrates some principles that are possible in protein evolution and could be implemented in protein design.” In fact, the paper acknowledges that true step-by-step pathways of protein evolution are currently elusive:

However, these experiments do not really model the evolution that occurs through gradual, step-by-step changes, with all intermediates being fully foldable proteins (Blanco et al., 1999). To create such an evolutionarily relevant path from all-a to all-b domains would be the next challenge for protein designers.

Whatever this paper demonstrates, it definitely does not establish that “evolutionary mechanisms generate biological information.”

Talking vs. Doing

But there’s another, more important point to make about papers like this one cited by Venema. At best, Venema’s citation of Grishin (2001) is just talking about protein evolution through armchair analyses. In contrast, Doug Axe and other Biologic Institute scientists are doing empirical laboratory tests to directly study these questions.

As one example, a 2011 study by Axe and Ann Gauger published research that attempted to convert one protein into a closely related protein – the kind of transformation which evolutionists claim happened easily in the history of life. Axe and Gauger studied two proteins, Kbl and BioF, with different functions but highly similar structures. Through mutational analysis, they found that a minimum of seven independent mutations — and probably many more — would be necessary to convert Kbl into the function of its allegedly close relative, BioF. Per Axe’s 2010 BIO-Complexity paper, they report that this is beyond the edge of evolution:

The extent to which Darwinian evolution can explain enzymatic innovation seems, on careful inspection, to be very limited. Large-scale innovations that result in new protein folds appear to be well outside its range. This paper argues that at least some small-scale innovations may also be beyond its reach. If studies of this kind continue to imply that this is typical rather than exceptional, then answers to the most interesting origins questions will probably remain elusive until the full range of explanatory alternatives is considered.

(Ann K. Gauger and Douglas D. Axe, “The Evolutionary Accessibility of New Enzyme Functions: A Case Study from the Biotin Pathway,” BIO-Complexity, Vol. 2011(1) (2011).)

Axe has already replied to many of Venema’s criticisms of his work here. The main result of Axe’s work is the finding that functional proteins are extremely rare in sequence space. This calls into pretty serious question the ability of any unguided search mechanism to find functional sequence folds. That holds true regardless of whether we’re talking about prebiotic processes like Meyer did in Signature in the Cell or postbiotic processes like Darwinian evolution. So Meyer was justified in citing Axe’s research in Signature in the Cell even though his book didn’t deal with biological evolution. And Venema’s citation of papers like Grishin (2001) do not refute Axe.

Nor do such papers refute the basic thesis of Meyer’s book. After all, how can natural selection and random mutation explain how information arose in the first life, if there was no selection or mutation prior to the origin of life?

Casey Luskin

Associate Director and Senior Fellow, Center for Science and Culture
Casey Luskin is a geologist and an attorney with graduate degrees in science and law, giving him expertise in both the scientific and legal dimensions of the debate over evolution. He earned his PhD in Geology from the University of Johannesburg, and BS and MS degrees in Earth Sciences from the University of California, San Diego, where he studied evolution extensively at both the graduate and undergraduate levels. His law degree is from the University of San Diego, where he focused his studies on First Amendment law, education law, and environmental law.



Dennis VenemaStephen Meyer