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Train Wreck of a Review: A Response to Lenski et al. in Science


Last week Science unexpectedly published a scathing pre-publication review,1 by Richard Lenski and two co-authors, of my book Darwin Devolves. I have already posted a short gleeful reply,2 noting their almost complete lack of a response to the book’s main argument, but I had planned to say more. This lengthier post will address such points as they do make, grouped into four themes: supposed counter-examples they cite; stale arguments they bring up; Lenski’s own evolution work; and a clear conclusion to draw.

For readers who don’t have time to plow all the way through, here are the take-home lessons:

  • gene-level counter-examples cited by the reviewers are shamelessly question-begging; the reviewers simply gesture at genes and assume they were produced and/or integrated into living systems by random processes, but neither the reviewers nor anyone else has even tried to show that is possible;
  • organ-level counter-examples cited by the reviewers as produced by exaptive processes are similarly question-begging;
  • criticisms of my earlier books cited by the reviewers were similarly question-begging and/or relied on vague, imaginative stories;
  • the reviewers are either unaware of or ignore my many detailed replies to earlier criticisms and to papers the reviewers themselves cite;
  • as noted in my previous post, the reviewers don’t even attempt to grapple with the main argument of the book, that beneficial degradative mutations will rapidly, relentlessly, unavoidably, outcompete beneficial constructive mutations at every time and population scale.

Supposed Counter-Examples

1. exaptation

The reviewers mention two ways in which they think evolution might build novelties — exaptation and gene duplication. I’ll focus first on exaptation. The reviewers write:

Missing from Behe’s discussion is any mention of exaptation, the process by which nature retools structures for new function…. The feathers of birds, gas bladders of fish, and ossicles of mammals have similar exaptive origins.

On the contrary, in Chapter 3, “Synthesizing Evolution,” which summarizes and critiques both Darwin’s original theory and neo-Darwinism, I directly discuss Ernst Mayr’s invocation of exaptation (which he calls “change of function”). I write:3

Yet how do such elegant new biological features arise? Two broad ways that evolutionary novelties have been envisioned to occur, writes Mayr, are by “intensification of function” and “change of function.” In a change of function, a structure that was used for one purpose is adapted to serve a different one; for example, lungs may have been converted to swim [gas] bladders in fish. This is an example of what has been called [by Mayr] the “principle of tinkering.”

I later castigate Mayr for vaporous hand-waving. (The “principle of tinkering,” indeed! Not quite the same epistemic status as , say, Newton’s Laws.) Yet, like Mayr, the reviewers don’t even try to show — or cite anyone else who has tried to show — that any of the organs they mention could be produced even from pre-existing organs by a Darwinian mechanism, or by any unguided unintelligent mechanism. Despite my explicitly faulting Mayr for it, the reviewers themselves indulge in the same unreflective hand-waving.

And the unreflective hand-waving quickly descends into opaque spasms. In Darwin Devolves I write that “the hardest problem of biology — how to explain the origin of the particular, sophisticated, functional structures of life — ”4 is invisible to most evolutionary biologists. The reviewers themselves illustrate my point with gusto:

Exaptation also challenges Behe’s notion of “devolution” by showing that loss of one function can lead to gain of another. The evolutionary ancestors of whales lost their ability to walk on land as their front limbs evolved into flippers, for example, but flippers proved advantageous in the long run.

In other words, the reviewers seem to “reason,” the ancestors of whales had legs, yet whales now have flippers, so therefore the change must have been driven by random mutation and natural selection. Have they never heard the phrase non sequitur? As strange as it may seem to people outside the charmed circle, many Darwinian biologists find it difficult to distinguish the question of what occurred in biology from the question of how it occurred. The reviewers are oblivious to the fact that neither legs nor flippers nor a transition between them have ever been explained non-trivially. The key question of the book — whether changes in the history of life occurred by chance or by design — seems incomprehensible to them.

2. gene duplication

Now for gene duplication. Lenski and companions note that I am very skeptical that gene duplication plus random mutation will lead to significant evolutionary innovations — that is, to something other than slight modification of the parent gene’s original function. However, they don’t mention that I didn’t always think that way. In the book I specifically note I have changed my mind about whether a Darwinian evolutionary pathway can lead via gene duplication from a simple myoglobin-like precursor to the sophisticated oxygen-delivery system that is hemoglobin.5 In 1996, I wrote in Darwin’s Black Box that I thought it might. In 1996, I imagined gene duplication plus random mutation/ natural selection might indeed explain increases in complexity of that degree.6 Yet, due to advances that I discuss in Darwin Devolves, I now think it doesn’t. Why did I change my mind? The reviewers don’t think readers need to hear any of that.

Instead, to show how wrong I am about the role of gene duplication/ random mutation/ natural selection, they point to “overwhelming evidence that this underlies trichromatic vision in primates (8), olfaction in mammals (9), and developmental innovations in all metazoans through the diversification of HOX genes (10).” The cited articles are from the years 1999, 2003, and 1998, respectively. And, as anyone with even a passing acquaintance with the topic would guess, the articles simply describe the occurrence of the genes. The authors of the articles don’t even try to argue — let alone experimentally investigate — that the diversification and integration of the genes into slightly different functions could have occurred through blind Darwinian processes.

The reviewers may as well have just taken my own example from the book and said, “Everyone knows Darwinian processes can produce complex hemoglobin from simpler myoglobin because myoglobin genes are similar to hemoglobin genes” and been done with it. Apparently they prefer to choose their own examples with which to beg the question.

Hemoglobin has much more sophisticated oxygen-binding capabilities than myoglobin. In contrast, the protein groups the reviewers cite — opsins (for vision), olfactory receptors (for smell), and Hox proteins — all do pretty much the same thing as each other: opsins absorb light, olfactory receptors bind odorant molecules, Hox proteins bind DNA. I have no objection to thinking the proteins within those separate classes arose by gene duplication. As for how they might be successfully folded into an organism’s biology, that is a separate question. My guess is that new odorant receptors and opsins might fit in by chance plus selection. New Hox proteins would be much, much more difficult.

Not every kind of protein has the same role so, like it or not, distinctions must be made. In a section of Chapter 9 entitled “Evolution by gene duplication revisited” I write:7

Everyone — including me — thought we knew a lot more than we did. Still, no one should now make the opposite mistake and leap to the conclusion that no development of protein function at all can occur by a classical Darwinian mechanism. As I mentioned in Chapter 6, a cichlid rhodopsin has apparently switched multiple times between two forms sensitive to different wavelengths of light, and a recent study of Andean wrens discovered a point mutation that caused its hemoglobin to bind oxygen more strongly. Those and similar simple examples are straightforward. However, whenever multiple amino acid substitutions or other mutations were needed to confer a substantially different activity on a duplicated protein, it can no longer be blithely assumed that the transition was navigated by Darwinian evolutionary processes. Some may have been, but many others not.

The reviewers seem to be like the new world monkey species Aotus trivirgatus in a paper they cite8 that has lost a functional opsin gene, leaving the species with monochromatic vision. The monkeys can see only in black and white, and the reviewers can see only in random mutation and natural selection. Yet there’s no a priori reason that chance couldn’t occur alongside design and vice versa. Those who assert that everything arose ultimately by chance carry the heavy burden of showing that is even feasible. Neither the reviewers nor any of the papers they cite even try to do so.

Worse, the reviewers don’t even pause to consider how the degradative processes I highlight in Darwin Devolves would affect any of their imagined scenarios. Degradation of genes is orders of magnitude faster than constructive changes. Would any selective pressure that could theoretically be ameliorated by gene duplication instead first be lessened by faster, more numerous degradative changes? If so, then there might be no pressure left to select the slower mutation when it eventually arrived. And when a gene did happen to duplicate, would faster degradative mutations remove any selective pressure to change it further? At each and every step, faster and more numerous degradative mutations would compete fiercely with any of the steps dreamed up by the reviewers. Yet they can’t seem to even entertain such thoughts.

3. guided laboratory evolution

Lenski and co-authors cite a paper on experimental evolution: “And in 2012, Andersson et al. showed that new functions can rapidly evolve in a suitable environment (11). Behe acknowledges none of these studies…” It turns out that I reviewed that paper9 shortly after it came out and posted my comments on Discovery Institute’s website. The comments are easily found with a few mouse-clicks. So much for due diligence.

My post on the paper is entitled “To Traverse a Maze, It Helps to Have a Mind.”10 It highlights the fact that the investigators actively guided the system over bumps and around corners to the desired results:

The investigators’ exceptionally intelligent manipulations are relegated to the online supplemental materials. Reading a brief part of the supplemental Materials and Methods section, entitled “Selection for bifunctional HisA mutants,” is sufficient to see the absurdity of taking the results as a model for undirected Darwinian evolution….

  • They deleted an enzyme that previous work showed could likely be replaced.
  • They added the necessary nutrient histidine because previous work showed that mutations conferring an ability to make tryptophan destroyed the ability to make histidine.
  • The added histidine would have shut off production of the protein, so they removed the genetic control element to keep it in production.
  • Later, once they found mutations to produce tryptophan, they removed histidine from the medium to encourage the production of mutations restoring histidine synthesis.

Needless to say, this ain’t how unaided nature works — unless nature is guiding events toward a goal.

Yes, “Andersson et al. showed that new functions can rapidly evolve in a suitable environment” — but under the guidance of an intelligent agent. As I write in Darwin Devolves, in his own terrific 60,000-generation evolution project, Lenski discovered the devastation wreaked by unguided, random mutation plus selection.

Let me emphasize: in reviewing a book expressly advocating intelligent design, Lenski et al. can’t seem to distinguish between experiments where investigators keep their hands off and those where investigators actively manipulate a system. Perhaps they can’t see the difference.

Stale Arguments, Unread Replies 

The reviewers recycle old hand-waving critiques of my earlier books that were either grossly inadequate or irrelevant (or both) even when they were first published, let alone today. 

1. first instance:

Behe also ignores the fact that some of his prior arguments have been dismantled (2). He includes a lengthy appendix that argues that the blood-clotting cascade is irreducibly complex, for example, but fails to mention Kenneth Miller’s simple, elegant scheme for its stepwise evolution (3) … 

Lenski’s citation #3 is to a philosophy of biology anthology from 2009,11 which reproduced a chapter by Miller originally written for an earlier (2004) book of essays published by Cambridge University Press called Debating Design.12 The title of Miller’s chapter was “The Flagellum Unspun,” which as its name implies focused on the bacterial outboard motor; it contained just a passing reference to blood clotting. I, too, contributed a chapter to the earlier book,13 which was also reproduced in the later anthology.14 My chapter was titled “Irreducible Complexity: Obstacle to Darwinian Evolution.” In it I defended both the blood clotting cascade and the flagellum against Darwinian objections, including those of Miller. The reviewers either did not see or chose to ignore my chapter. Let me emphasize: the reviewers fault me for not discussing an article Miller published in the very book in which I answered his objections with my own article.

In his 1999 book Finding Darwin’s God15 Miller did pen what one might with great charity call a “scheme” for the evolution of blood clotting, but it was so sketchy (sandwiched between a description of modern clotting cascades in vertebrates and invertebrates, the actual “scheme” comprised a single paragraph) it makes Ernst Mayr’s “principle of tinkering” look like a paradigm of scientific rigor. Miller later posted on his own website16 some material cut from his book that added more hand-waving steps. However, a similar, more clearly presented generic scenario for building a cascade was posted earlier on the Internet by a Harvard grad student.17 I pointed out the severe problems for that scenario twenty years ago.18 The reviewers don’t mention it.

2. second instance:

… or the fact that a progenitor fibrinogen gene has been discovered in echinoderms (4).

The investigator behind the cited reference #4 is a man named Russell Doolittle — an eminent scientist, now-retired professor of biochemistry at the University of California San Diego, and member of the National Academy of Sciences, who spent the bulk of his 50-plus-year career working on the blood clotting cascade. I discussed his work in Darwin’s Black Box in 1996,19 and I argued there that the cascade is in fact irreducibly complex. In the Appendix of Darwin Devolves20 I recount an incident from 1997 where he wrote an essay in the MIT-published Boston Review to refute me. In the essay he triumphantly described some then-recent experimental work done by other researchers:21

Recently the gene for plaminogen [sic — plasminogen is a protein that helps remove blood clots after a wound has healed] was knocked out of mice, and, predictably, those mice had thrombotic complications because fibrin clots could not be cleared away. Not long after that, the same workers knocked out the gene for fibrinogen [fibrinogen supplies the protein building material for the meshwork clot structure] in another line of mice. Again, predictably, these mice were ailing, although in this case hemorrhage was the problem. And what do you think happened when these two lines of mice were crossed? For all practical purposes, the mice lacking both genes were normal! Contrary to claims about irreducible complexity, the entire ensemble of proteins is not needed. Music and harmony can arise from a smaller orchestra.

But it turns out that Doolittle misread the paper he was discussing.22 In fact, mice missing the two cascade proteins are very sick: their blood doesn’t clot; they hemorrhage; females die during pregnancy. Promising evolutionary intermediates they are not. Please read Darwin Devolves for the details. Here I will make just two short points. 1) Russell Doolittle is a top expert on blood clotting and evolution. Yet we can quickly see from his mistake — pointing to a paper about dying mice — that he does not know how blood clotting could have evolved by a Darwinian process. (If he did know, he could easily have cited a paper describing it.) And if Russell Doolittle doesn’t know, no one knows, no one at all — most certainly including Kenneth Miller and the reviewers. The second point is equally important. 2) Russell Doolittle knows all about gene duplication, yet that knowledge was of no help at all in trying to actually explain the evolution of the blood clotting cascade.

The reviewers note that in 1990 (well before his mistaken essay quoted above was written) Doolittle discovered a gene in an invertebrate group that has a family resemblance to vertebrate fibrinogen.23 In Darwin Devolves I extensively discuss Russell Doolittle’s further fine work on the clotting cascade.24 But that work overwhelmingly consists simply of searching sequence databases for whichever clotting proteins might be found in whichever species. Such work may produce evidence pertinent to questions about common descent but, as I’ve written many times, evidence of common descent is not evidence for Darwin’s mechanism. Neither Doolittle nor anyone else has even tried to show that any imagined transitions could have occurred by random processes plus selection. Here’s an excerpt from the Appendix of the book where I discuss a few of the formidable problems facing undirected evolution of blood clotting by gene duplication:25

In order to even begin to understand how Darwinian processes might build a clotting cascade, or even just significantly modify a pre-existing one, huge roadblocks need to be addressed, such as how to maintain fine control on the fly while randomly changing a system. I wish luck to anyone with that. …

What’s more, as we’ve seen throughout this book, random mutation easily breaks or degrades genes. Since the blood clotting cascade is a finely balanced system — a seesaw of opposing protein functions that either promote or inhibit clotting — altering the balance by degrading one factor should be as effective in the short term as by strengthening another (like taking a bit of weight off one side of the seesaw instead of adding a bit to the other). And since degrading proteins is much faster and easier, that should almost always win out. …

As for Professor Doolittle, so too for the great majority of evolutionary biologists. All of these fundamental problems seem truly to be invisible to them. Evidence of common descent is routinely confused for evidence of Darwin’s mechanism.

3. third instance:

Behe doubles down on his claim that the evolution of chloroquine resistance in malaria by random mutations is exceedingly unlikely because at least two mutations are required, neither of which is beneficial without the other. His calculations have already been refuted (5), and it has long been known that neutral and even deleterious mutations can provide stepping stones to future adaptations.

I responded to the cited reference #5 in 2009 with a letter26 that was published in the journal Genetics along with a reply by the authors, Durrett and Schmidt.27 I followed up that exchange with further responses that can easily be found on the web.28 The reviewers tell readers nothing about that. Briefly, in my replies I showed that Durrett and Schmidt, two mathematicians, misunderstood some of the biology of the system (which they acknowledged), and when that mistake was rectified their calculations agreed pretty closely with my own. As for “even deleterious mutations” providing stepping stones, I happily agree. In fact a major point of my book The Edge of Evolution was that the development of chloroquine resistance by the malarial parasite likely required two mutations, the first of which was deleterious. (I am mystified as to why the reviewers can’t see that their first sentence in the quote above answers the last half of their second sentence.) Yet the need for a neutral or deleterious step in an evolutionary pathway will greatly slow Darwinian evolution, as it did in the case of chloroquine resistance.

4. fourth instance:

Indeed, a 2014 study, unmentioned by Behe, reported discovery of two genetic paths through which malaria has evolved chloroquine resistance through multiple steps (6).

I blogged extensively on that paper soon after it was published.29 In fact I touted that terrific study of Summers et al (2014)30 far and wide, because it confirmed my surmise in The Edge of Evolution that two mutations were required before any chloroquine resistance occurred. (How hard can it be to type “Behe” and “Summers” into a search engine?) As they wrote in their abstract, “A minimum of two mutations sufficed for (low) CQ transport activity.” The need for two specific mutations neatly explains the approximately billion-fold increase in difficulty for the parasite to evolve resistance to chloroquine versus other antimalarial drugs, such as atovaquone, which require only one. (The fact that there may be several paths to the resistant state is a red herring because, as the paper showed, all paths pass through the deleterious step. Otherwise the de novo origin of chloroquine resistance would be much more frequent than it is, similar to that of atovaquone.) It also illustrates the feebleness of the Darwinian mechanism when confronted with the need for even the tiniest amount of coordination — just two simple point mutations. The difficulties go up exponentially with the number of mutations required.

So let me emphasize that the reviewers fault me for not mentioning a paper that I had in fact publicly and extensively written about, and which strongly supports my arguments.

Alleged “Deriding” of Lenski’s Terrific Long-Term Evolution Experiment

Richard Lenski has done wonderful work with his now-thirty-year-long project that follows the growth and evolution of E. coli cultures in his laboratory.31 However, he does not own the interpretation of those publicly reported results. He himself interprets them within a standard Darwinian framework. Fine, he is certainly free to do so. However, in Darwin Devolves I do not assume as he does that it’s Darwinism all the way down. I explain that, while the results do confirm the ability of random mutation and natural selection to produce beneficial small-scale changes (mostly by degradation of pre-existing genes), they also show why larger constructive changes are beyond its reach.

1. random is as random does

Lenski and co-authors write in the review:

There are indeed many examples of loss-of-function mutations that are advantageous, but Behe is selective in his examples. He dedicates the better part of chapter 7 to discussing a 65,000-generation Escherichia coli experiment, emphasizing the many mutations that arose that degraded function — an expected mode of adaptation to a simple laboratory environment, by the way — while dismissing improved functions and deriding one new one as a “sideshow” (1).

I don’t “dismiss improved functions.” Rather, as I explicitly state, my focus is on distinguishing beneficial degradative mutations from beneficial constructive mutations. That is, do most beneficial mutations help by constructing new “functional coded elements” (abbreviated FCTs, — for example, genes or control elements) or by degrading old ones? That’s simply an exercise in counting the number of beneficial mutations that fall into each category. As I originally wrote in The Quarterly Review of Biology,32 by far the most frequent beneficial mutations reported in the literature are ones that degrade FCTs. — Sorry! Don’t blame me! That’s just the way it is.

I didn’t intend to hurt Lenski’s feelings by calling the widely reported citrate mutation33 that his lab isolated a “side show.” Rather, I just meant to put that mutation in perspective. Here’s an extended quote from Darwin Devolves for context:34

But the stark lesson of this chapter by far overrides any squabbling about the significance of this or that particular mutation. To see why, consider the other mutations the citrate-eater has suffered along its evolutionary journey. Like all of the culture lines, the citrate-using bacteria have lost the ability to metabolize ribose, suffered killing “mobile element” mutations to other genes, and fixed degradative point mutations in even more. And, like five other replicate cell lines, the citrate-user has turned into a mutator, with a greatly degraded ability to repair its DNA. Whatever the bug’s fate from here, it has irrevocably lost the services of perhaps a dozen genes.

But that’s not all. In order to best accommodate the gene rearrangement that gave it the talent to eat citrate, several other mutations were found that fine-tuned its metabolism. (Quandt, E. M., et al. 2015. Elife: 4.e09696.) Even before the critical mutation occurred, a different mutation in a gene for a protein that makes citrate in E. coli degraded the protein’s ability to bind another metabolite abbreviated NADH, which normally helps regulate its activity. Another, later mutation to the same gene decreased its activity by about 90%. Why were those mutations helpful? As the authors write, “when citrate is the sole carbon source, [computer analysis] predicts optimal growth when there is no flux through [the enzyme]. In fact, any [of that enzyme] activity is detrimental…” And if something is detrimental, random mutation will quickly get rid of it. Further computer analysis by the authors suggested that the citrate mutant would be even more efficient if two other metabolic pathways that were normally turned off were both switched on. They searched and discovered that two regulatory proteins that usually suppress those pathways had been degraded by point mutations, the traffic lights now stuck on green.

Interesting as it is, the ambiguous citrate mutation that started the hoopla is a side show. The overwhelmingly important and almost completely unnoticed lesson is that genes are being degraded left and right, both when they directly benefit the bacteria and when they do so indirectly in support of another mutation. The occasional, particularly noticeable modification-of-function or gain-of-FCT mutation can’t turn back the tide of damaging and loss-of-FCT ones.

The critical distinction to grasp is that beneficial degradative mutations are a completely different sort of beast from beneficial constructive ones. Helpful degradative mutations will arrive very rapidly and in much larger numbers than constructive ones. That’s simply because it is much easier and faster to degrade a gene than to improve one constructively. What’s more, beneficial degradative mutations are relentless. They will appear before, during, and after any constructive mutation, and compete fiercely with it for selection. And once a degradative mutation is established in a population, for all intents and purposes the degraded gene is gone forever.

Lenski is rightly proud of his work, and naturally wants to accentuate the positive. I, however, am interested in the question of whether Darwinian processes could have constructed the sophisticated machinery of life, so I consider the results from a different angle.

2. “degraded function — an expected mode of adaptation to a simple laboratory environment, by the way”

a. rationalizing results

The “expectation” that degradative mutations would dominate laboratory evolution experiments is an entirely post-hoc rationalization. Consider, for example, it was only in 2013 that PLoS Genetics published a paper titled “Bacterial adaptation through loss of function” in which researchers systematically demonstrated that breaking genes could almost always be beneficial in some environment or other. I write in Darwin Devolves:35

In the only work I’ve seen that does focus on loss of function mutations as a general class, interesting in its own right, in 2013 researchers from Princeton and Columbia universities surveyed the literature and then conducted experiments of their own to see which bacterial genes could be broken and the bug would grow better. [Hottes, A. K., et al. 2013. Bacterial adaptation through loss of function. PLoS Genetics 9:e1003617.] They showed that “at least one beneficial [loss-of-FCT] mutation was identified in all but five of the 144 conditions considered.” In other words, a bacterium could improve its lot by breaking a gene in over 96% of environmental circumstances examined…. 

A brief comment on the original work by a news writer shows that the simple distinction between beneficial and constructive mutations has clicked for at least one person: “This study changes the widely held view [my emphasis] that loss-of-function mutations are maladaptive.” [Stower, H. 2013. Molecular evolution: Adaptation by loss of function. Nature Reviews Genetics 14:596.]

Like many people, evolutionary biologists revise their expectations in light of experience (or experimental results). The reviewers are doing that here, perhaps unwittingly.

b. in the wild, too

What’s more, I devote a good chunk of Chapter 7 to demonstrating that loss-of-function mutations dominate not only in “a simple laboratory environment” but also in the wild. In Chapter 9 I write:36

In the real world, any possibly-beneficial, degradative mutations will arrive rapidly, in force, to alleviate any selective pressure on an organism — aeons before the first multi-residue feature even appears on the scene. (Figure 9-5) The result is that every degradative change and every damaging single-step mutation would be tested multiple times as a solution, or as part of a solution, to whatever selective pressure a species was facing, and, if helpful, would spread to fixation well before a beneficial multi-residue feature even showed up. Where Darwinian processes dominate, the biological landscape would be expected to be littered with broken-but-helpful genes, damaged-yet-beneficial systems, degraded-organisms-on-crutches, ages before any fancy machinery was even available. That’s exactly what we saw in Chapter 7 with laboratory E. coli, natural Yersinia pestis, wild polar bears, tame dog breeds and all other organisms so far examined.

Whatever mutation helps alleviate some selective pressure by any means will immediately begin to spread. Degradative mutations can often help relieve selective pressure, and they arrive orders of magnitude faster than constructive mutations, both in the laboratory and in the wild.

Drawing a Conclusion

Can any important conclusion be drawn from this train wreck of a review? Consider that Richard Lenski is perhaps the most qualified scientist in the world to review the argument of Darwin Devolves. Lenski has spent decades overseeing the most extensive, most acclaimed laboratory evolution experiment conducted to date, for which he was elected a member of the National Academy of Sciences. His own work is a major focus of Darwin Devolves. He could easily and casually have pointed out any problems with the argument all by himself, merely by wielding Darwin’s putatively powerful theory and his own expertise. Yet he and his co-authors spend the entire review deriding the author, barely mentioning Lenski’s own work, recounting old criticisms by other people, and leaning heavily on aged theoretical conjectures instead of new experimental results.

The implication is clear. Just as Russell Doolittle unwittingly showed, simply by his mistaken citation, that no explanation for the origin of the blood clotting cascade existed, so the reviewers show that there is no answer to the problems for unguided evolution described in Darwin Devolves. Although it serves a useful role in understanding changes at the margins of biology, as an explanation for the overarching structure of life Darwin’s theory is defunct.


  1. Lents, N.H., Swamidass, S.J., Lenski, R.E. 2019. The end of evolution? Science 363: 590-590.
  2. Behe, M.J. 2019. Woo-hoo! In Science Review of Darwin Devolves, Lenski Has No Response to My Main Argument.
  3. Behe, M.J., 2019. Darwin Devolves: The New Science About DNA that Challenges Evolution. HarperOne, New York, pp 80-81
  4. Behe 2019, 225
  5. Behe 2019, 214.
  6. Behe, M.J., 1996. Darwin’s Black Box: the Biochemical Challenge to Evolution. The Free Press, New York, pp. 206-207.
  7. Behe 2019, 214-215.
  8. Dulai, K.S. et al. 1999. The evolution of trichromatic color vision by opsin gene duplication in New World and Old World primates. Genome Res. 9: 629.
  9. Näsvall, J., et al. 2012. Real-time evolution of new genes by innovation, amplification, and divergence. Science 338: 384-387.
  10. Behe, M.J. 2012. To traverse a maze, it helps to have a mind.
  11. Miller, K.R. 2009. The Flagellum Unspun: The Collapse of Irreducible Complexity, in: Rosenberg, A., Arp, R. (Eds.), Philosophy of Biology: an Anthology. Wiley-Blackwell, Chichester, West Sussex, U.K., pp. 439-455.
  12. Miller, K.R. 2004. The Flagellum Unspun: The Collapse of Irreducible Complexity, in: Dembski, W.A., Ruse, M. (Eds.), Debating Design: from Darwin to DNA. Cambridge University Press, Cambridge, pp. 81-97.
  13. Behe, M.J. 2004. Irreducible Complexity: Obstacle to Darwinian Evolution, in: Dembski, W.A., Ruse, M. (Eds.), Debating Design: from Darwin to DNA. Cambridge University Press, Cambridge, pp. 352-370.
  14. Behe, M.J. 2009. Irreducible complexity: obstacle to Darwinian evolution, in: Rosenberg, A., Arp, R. (Eds.), Philosophy of Biology: an Anthology. Wiley-Blackwell, Chichester, West Sussex, U.K., pp. 427-438.
  15. Miller, K.R. 1999. Finding Darwin’s God: a Scientist’s Search for Common Ground Between God and Evolution. Cliff Street Books, New York, pp. 156-157.
  16. Miller, K.R. The evolution of vertebrate blood clotting.
  17. Robison, K. 1996. Darwin’s Black Box: Irreducible complexity or irreproducible irreducibility?
  18. Behe, M.J. 2000. In defense of the irreducibility of the blood clotting cascade: Response to Russell Doolittle, Ken Miller and Keith Robison.
  19. Behe 1996, Chapter 4.
  20. Behe 2019, 294-298.
  21. Doolittle, R.F. 1997. A delicate balance. Boston Review, pp. 28-29.
  22. Bugge, T.H., et al. 1996. Loss of fibrinogen rescues mice from the pleiotropic effects of plasminogen deficiency. Cell 87: 709-719.
  23. Xu, X., Doolittle, R.F., 1990. Presence of a vertebrate fibrinogen-like sequence in an echinoderm. Proceedings of the National Academy of Sciences USA 87: 2097-2101.
  24. Behe 2019, 298-301.
  25. Behe 2019, 300.
  26. Behe, M.J. 2009. Waiting longer for two mutations. Genetics 181: 819-820.
  27. Durrett, R., Schmidt, D. 2009. Reply to Michael Behe. Genetics 181: 821-822.
  28. Behe, M.J. 2009. Waiting longer for two mutations.
  29. Behe, M.J. 2014. A key inference of The Edge of Evolution has now been experimentally confirmed.
  30. Summers, R.L., et al. 2014. Diverse mutational pathways converge on saturable chloroquine transport via the malaria parasite’s chloroquine resistance transporter. Proceedings of the National Academy of Sciences USA 111: E1759-E1767.
  31. Good, B.H., et al. 2017. The dynamics of molecular evolution over 60,000 generations. Nature 551: 45-50.
  32. Behe, M.J. 2010. Experimental evolution, loss-of-function mutations, and “The First Rule of Adaptive Evolution”. Quarterly Review of Biology 85: 1-27.
  33. Blount, Z.D., Borland, C.Z., Lenski, R.E. 2008. Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli. Proceedings of the National Academy of Sciences USA 105: 7899-7906.
  34. Behe 2019, p 188-190
  35. Behe 2019, p 191
  36. Behe 2019, pp 248-249

Photo: A train wreck, 1895, Montparnasse Station, Paris, via Wikimedia Commons.