Michael Behe v. the critics

Irreducible Complexity and the Evolutionary Literature: A Response to Critics

Michael Behe 

Editor's note: In celebration of the 20th anniversary of biochemist Michael Behe's pathbreaking book Darwin's Black Box and the release of the new documentary Revolutionary: Michael Behe and the Mystery of Molecular Machines, we are highlighting some of Behe's "greatest hits." The following was published by Discovery Institute on July 31, 2000. Remember to get your copy of Revolutionary now! See the trailer here.

I. Summary

Although several persons have cited numerous references from the scientific literature purporting to show that the problem of irreducible complexity I pointed out in Darwin's Black Box is being seriously addressed, the references show no such thing. Invariably the cited papers or books either deal with non-irreducibly complex biochemical systems, or do not deal with them in enough detail for critical evaluation. I strongly emphasize, however, that I do not prefer it that way. I would sincerely welcome much more serious, sustained research in the area of irreducible complexity. I fully expect such research would heighten awareness of the difficulties of Darwinian evolution.

II. Web Spinners

The necessary starting point of Darwin's Black Box was the contention that, despite the common assumption that natural selection accounts for adaptive complexity, the origins of many intricate cellular systems have not yet been explained in Darwinian terms. After all, if the systems have already been explained, then there's no need to write. While most scientist-reviewers disagreed (often emphatically) with my proposal of intelligent design, most also admitted to a lack of Darwinian explanations. For example, microbiologist James Shapiro of the University of Chicago declared in National Review that "There are no detailed Darwinian accounts for the evolution of any fundamental biochemical or cellular system, only a variety of wishful speculations." (Shapiro 1996) In Nature University of Chicago evolutionary biologist Jerry Coyne stated, "There is no doubt that the pathways described by Behe are dauntingly complex, and their evolution will be hard to unravel. . . . [W]e may forever be unable to envisage the first proto-pathways." (Coyne 1996)

In a particularly scathing review in Trends in Ecology and Evolution Tom Cavalier-Smith, an evolutionary biologist at the University of British Columbia, nonetheless wrote, "For none of the cases mentioned by Behe is there yet a comprehensive and detailed explanation of the probable steps in the evolution of the observed complexity. The problems have indeed been sorely neglected -- though Behe repeatedly exaggerates this neglect with such hyperboles as 'an eerie and complete silence.'" (Cavalier-Smith 1997) Evolutionary biologist Andrew Pomiankowski agreed in New Scientist, "Pick up any biochemistry textbook, and you will find perhaps two or three references to evolution. Turn to one of these and you will be lucky to find anything better than 'evolution selects the fittest molecules for their biological function.'" (Pomiankowski 1996) In American Scientist Yale molecular biologist Robert Dorit averred, "In a narrow sense, Behe is correct when he argues that we do not yet fully understand the evolution of the flagellar motor or the blood clotting cascade." (Dorit 1997)

A prominent claim I made in Darwin's Black Box is that, not only are irreducibly complex biochemical systems unexplained, there have been very few published attempts even to try to explain them. This contention has been vigorously disputed not so much by scientists in the relevant fields as by Darwinian enthusiasts on the Internet. Several web-savvy fans of natural selection have set up extensive, sophisticated sites that appear to receive a significant amount of notice. They influence college students, reporters, and, sometimes, academic reviewers of my book such as Cal State-Fullerton biochemist Bruce Weber, who lists the addresses of the websites in his review in Biology and Philosophy as "summaries of the current research that Behe either missed or misrepresented" (Weber 1999), and Oxford physical chemist Peter Atkins, who writes:

Dr. Behe claims that science is largely silent on the details of molecular evolution, the emergence of complex biochemical pathways and processes that underlie the more traditional manifestations of evolution at the level of organisms. Tosh! There are hundreds, possibly thousands, of scientific papers that deal with this very subject. For an entry into this important and flourishing field, and an idea of the intense scientific effort that it represents (see the first link above) [sic]. (Atkins 1998)

The link Atkins refers to is a website called "Behe's Empty Box" that has been set up by a man named John Catalano, an admirer of Oxford biologist Richard Dawkins (his larger site is devoted to Dawkins' work, schedule, etc.). The Empty Box site is, I think, actually a valuable resource, containing links to many reviews, comments and other material, both critical and favorable, related to my book. One subsection of the site is entitled "Alive and Published," and contains citations to a large number of papers and books which Catalano believes belie my claim that "There has never been a meeting, or a book, or a paper on details of the evolution of complex biochemical systems." (Behe 1996) (p. 179) The citations were solicited on the web from anyone who had a suggestion, and then compiled by Catalano.

Something, however, seems to be amiss. The assertion here that very many papers have been published clashes with statements of the reviews I quoted earlier which say, for example, that "The problems have indeed been sorely neglected." (Cavalier-Smith 1997) Would reviewers such as Jerry Coyne and Tom Cavalier-Smith -- both antagonistic to my proposal of intelligent design -- be unaware of the "hundreds, possibly thousands, of scientific papers that deal with this very subject"? Both claims -- that the problems have been neglected and that the problems are being actively investigated -- cannot be correct. Either one set of reviewers is wrong, or there is some confusion about which publications to count. Which is it?

In the context of my book it is easy to realize that I meant there has been little work on the details of the evolution of irreducibly complex biochemical systems by Darwinian means. I had clearly noted that of course a large amount of work in many books and journals was done under the general topic of "molecular evolution," but that, overwhelmingly, it was either limited to comparing sequences (which, again, does not concern the mechanism of evolution) or did not propose sufficiently detailed routes to justify a Darwinian conclusion. Yet the Catalano site lists virtually any work on evolution, whether it pertains to irreducible complexity or not. For example it lists semi-popular books such as Patterns in Evolution: The New Molecular View by Roger Lewin, and general textbooks on molecular evolution such as Molecular Evolution by Wen-Hsiung Li.

Such books simply don't address the problems I raise. Molecular Evolution by Wen-Hsiung Li (Li 1997) is a fine textbook which does an admirable job of explicating current knowledge of how genes change with time. That knowledge, however, does not include how specific, irreducibly-complex biochemical systems were built. The text contains chapters on the molecular clock, molecular phylogenetics, and other topics which essentially are studies in comparing gene sequences. As I explained in Darwin's Black Box, comparing sequences is interesting but cannot explain how molecular machines arose. Li's book also contains chapters on the mechanisms (such as gene duplication, domain shuffling, and concerted evolution of multigene families) that are thought to be involved in evolution at the molecular level. Again, however, no specific system is justified in Darwinian terms.

Here is an illustration of the problem. Li spends several pages discussing domain shuffling in the proteins of the blood-clotting cascade (Li 1997). However, Li himself has not done work on understanding how the obstacles to the evolution of the clotting cascade may have been circumvented. Since those investigators who do work in that area have not yet published a detailed Darwinian pathway in the primary literature1, we can conclude that the answer will not be found in a more general text. We can further assume that the processes that text describes (gene duplication, etc.), although very significant, are not by themselves sufficient to understand how clotting, or by extension any complex biochemical system, may have arisen by Darwinian means.

Catalano's site lists other books that I specifically discussed in Darwin's Black Box, where I noted that, while they present mathematical models or brief general descriptions, they do not present detailed biochemical studies of specific irreducibly complex systems. (Gillespie 1991; Selander et al. 1991) There is no explanation on Catalano's website of why he thinks they address the questions I raised. The site also points to papers with intriguing titles, but which are studies in sequence analysis, such as "Molecular evolution of the vertebrate immune system" (Hughes and Yeager 1997) and "Evolution of chordate actin genes: evidence from genomic organization and amino acid sequences." (Kusakabe et al. 1997) As I explained in Darwin's Black Box, sequence studies by themselves can't answer the question of what the mechanism of evolution is. Catalano's compendium also contains citations to papers concerning the evolution of non-irreducibly complex systems, such as hemoglobin and metabolic pathways, which I specifically said may have evolved by natural selection. (Behe 1996) (pp. 150-151; 206-207)

III. Equivocal Terms

Another website that has drawn attention (as evidenced from the inquiries I receive soliciting my reaction to it) is authored by David Ussery (Ussery 1999), associate research professor of biotechnology at The Technical University of Denmark. One of his main goals is to refute my claim concerning the dearth of literature investigating the evolution of irreducibly complex systems. For example, in a section on intracellular vesicular transport he notes that I stated in Darwin's Black Box that a search of a computer database "to see what titles have both evolution and vesicle in them comes up completely empty." (Behe 1996) (p. 114) My search criterion, of having both words in the title, was meant to be a rough way to show that nothing much has been published on the subject. Ussery, however, writes that, on the contrary, a search of the PubMed database using the words evolution and vesicle identifies well over a hundred papers. Confident of his position, he urges his audience, "But, please, don't just take my word for it -- have a look for yourself!" (Ussery 1999)

The problem is that, as I stated in the book, I had restricted my search to the titles of papers, where occurrence of both words would probably mean they concerned the same subject. Ussery's search used the default PubMed setting, which also looks in abstracts.2 By doing so he picked up papers such as "Outbreak of nosocomial diarrhea by Clostridium difficile in a department of internal medicine." (Ramos et al. 1998) This paper discusses the "clinical evolution" (i.e., course of development) of diarrhea in hospitalized patients, who also had "vesicle catherization." Not only do the words evolution and vesicle in this paper not refer to each other, the paper does not even use the words evolution and vesicle in the same sense as I did. Since the word evolution has many meanings, and since the word vesicle can mean just a container (like the word "box"), Ussery picked up equivocal meanings.

The paper cited above shows Ussery's misstep in an obvious way. However, there are other papers resulting from an Ussery-style search where, although they do not address the question I raised, the unrelatedness is not so obvious to someone outside the field. An example of a paper that is harder for someone outside the field to evaluate is "Evolution of the trappin multigene family in the Suidae." (Furutani et al. 1998) The authors examine the protein and gene sequences for a group of secretory proteins (the trappin family) which "have undergone rapid evolution" and are similar to "seminal vesicle clotting proteins." The results may be interesting, but the seminal vesicle is a pouch in the male reproductive tract for storing semen -- not at all the same thing as the vesicle in which intracellular transport occurs. And trappins are not involved in intracellular transport.

A second example is "Syntaxin-16, a putative Golgi t-SNARE." (Simonsen et al. 1998) This paper actually does concern a protein involved in intracellular vesicular transport. However, as the abstract states, "Database searches identified putative yeast, plant and nematode homologues of syntaxin-16, indicating that this protein is conserved through evolution." The database searches are sequence comparisons. Once again I reiterate, sequence comparisons by themselves cannot tell us how a complex system might have arisen by Darwinian means.

Instead of listing further examples let me just say that I have not seen a paper using Ussery's search criteria that addresses the Darwinian evolution of intracellular vesicular transport in a detailed manner, as I had originally asserted in my book.

It is impossible for me to individually address the "hundreds, possibly thousands" of papers listed in these websites. But perhaps I don't have to. If competent scientists who are not friendly to the idea of intelligent design nonetheless say that "There are no detailed Darwinian accounts for the evolution of any fundamental biochemical or cellular system, only a variety of wishful speculations," (Shapiro 1996) and that "We may forever be unable to envisage the first proto-pathways" (Coyne 1996), then it is unlikely that much literature exists on these problems. So after considering the contents of the websites, we can reconcile the review of Peter Atkins with those of other reviewers. Yes, there are a lot of papers published on "molecular evolution," as I had clearly acknowledged in Darwin's Black Box. But very few of them concern Darwinian details of irreducibly complex systems, which is exactly the point I was making.

IV. Kenneth Miller

In Finding Darwin's God (Miller 1999) Kenneth Miller is also anxious to show my claims about the literature are not true (or at least are not true now, since the handful of papers he cites in his section "The Sound of Silence" were published after my book appeared). Yet none of the papers he cites deals with irreducibly complex systems.

The first paper Miller discusses concerns two structurally-similar enzymes, both called isocitrate dehydrogenase. The main difference between the two is simply that one uses the organic cofactor NAD while the other uses NADP. The two cofactors are very similar, differing only in the presence or absence of a phosphate group. The authors of the study show that by mutating several residues in either enzyme, they can change the specificity for NAD or NADP. (Dean and Golding 1997) Although the study is very interesting, at the very best it is microevolution of a single protein, not an irreducibly complex system.

The next paper Miller cites concerns "antifreeze" proteins. (Logsdon and Doolittle 1997) Again, these are single proteins that do not interact with other components; they are not irreducibly complex. In fact, they are great examples of what I agree evolution can indeed do -- start with a protein that accidentally binds something (ice nuclei in this case, maybe antibiotics in another case) and select for mutations that improve that property. But they don't shed light on irreducibly complex systems.

Another paper Miller cites concerns the cytochrome c oxidase proton pump (Musser and Chan 1998), which is involved in electron transfer. In humans six proteins take part in the function; in some bacteria fewer proteins are involved. While quite interesting, the mechanism of the system is not known in enough detail to understand what's going on; it remains in large part a black box. Further, the function of electron transfer does not necessarily require multiple protein components, so it is not necessarily irreducibly complex. Finally, the study is not detailed enough to criticize, saying things such as "It makes evolutionary sense that the cytochrome bc1and cytochrome c oxidase complexes arose from a primitive quinol terminal oxidase complex via a series of beneficial mutations." In order to judge whether natural selection could do the job, we have to know what the "series of beneficial mutations" is. Otherwise it's like saying that a five-part mousetrap arose from a one-part mousetrap by a series of beneficial mutations.3

Finally Miller discusses a paper which works out a scheme for how the organic-chemical components of the tricarboxylic acid (TCA) cycle, a central metabolic pathway, may have arisen gradually. (Melendez-Hevia et al. 1996) There are several points to make about it. First, the paper deals with the chemical interconversion of organic molecules, not the enzymes of the pathway or their regulation. As an analogy, suppose someone described how petroleum is refined step by step, beginning with crude oil, passing through intermediate grades, and ending with, say, gasoline. He shows that the chemistry of the processes is smooth and continuous, yet says nothing about the actual machinery of the refinery or its regulation, nothing about valves or switches. Clearly that is inadequate to show refining of petroleum developed step by step. Analogously, someone who is seriously interested in showing that a metabolic pathway could evolve by Darwinian means has to deal with the enzymic machinery and its regulation.

The second and more important point is that, while the paper is very interesting, it doesn't address irreducible complexity. Either Miller hasn't read what I said in my book about metabolic pathways, or he is deliberately ignoring it. I clearly stated in Darwin's Black Box metabolic pathways are not irreducibly complex (Behe 1996) (pp. 141-142; 150-151), because components can be gradually added to a previous pathway. Thus metabolic pathways simply aren't in the same category as the blood clotting cascade or the bacterial flagellum. Although Miller somehow misses the distinction, other scientists do not. In a recent paper Thornhill and Ussery write that something they call serial-direct-Darwinian-evolution "cannot generate irreducibly complex structures." But they think it may be able to generate a reducible structure, "such as the TCA cycle (Behe, 1996 a, b)." (Thornhill and Ussery 2000) In other words Thornhill and Ussery acknowledge the TCA cycle is not irreducibly complex, as I wrote in my book. Miller seems unable or unwilling to grasp that point.

V. A Plea for More Research

In pointing out that not much research has been done on the Darwinian evolution of irreducibly complex biochemical systems I should emphasize that I do not prefer it that way. I would sincerely welcome more research (especially experimental research, such as done by Barry Hall -- see my discussion of Hall's work in the essay on the "acid test" at this website) into the supposed Darwinian origins of the complex systems I described in my book. I fully expect that, as in the field of origin-of-life studies, the more we know, the more difficult the problem will be recognized to be.

References:

Atkins, P. W. (1998). Review of Michael Behe, Darwin's Black Box. http://www.infidels.org/library/modern/peter_atkins/behe.html

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Behe, M. J. (1996). Darwin's black box: the biochemical challenge to evolution. (The Free Press: New York.)

Cavalier-Smith, T. (1997). The blind biochemist. Trends in Ecology and Evolution 12, 162-163.

Coyne, J. A. (1996). God in the details. Nature 383, 227-228.

Dean, A. M. and Golding, G. B. (1997). Protein engineering reveals ancient adaptive replacements in isocitrate dehydrogenase. Proc.Natl.Acad.Sci.U.S.A 94, 3104-3109.

Dorit, R. (1997). Molecular evolution and scientific inquiry, misperceived. American Scientist 85, 474-475.

Furutani, Y., Kato, A., Yasue, H., Alexander, L. J., Beattie, C. W., and Hirose, S. (1998). Evolution of the trappin multigene family in the Suidae. J.Biochem. (Tokyo) 124, 491-502.

Gillespie, J. H. (1991). The causes of molecular evolution. (Oxford University Press: New York.)

Hughes, A. L. and Yeager, M. (1997). Molecular evolution of the vertebrate immune system. Bioessays 19, 777-786.

Kusakabe, T., Araki, I., Satoh, N., and Jeffery, W. R. (1997). Evolution of chordate actin genes: evidence from genomic organization and amino acid sequences. Journal of Molecular Evolution 44, 289-298.

Li, W. H. (1997). Molecular evolution. (Sinauer Associates: Sunderland, Mass.)

Logsdon, J. M., Jr. and Doolittle, W. F. (1997). Origin of antifreeze protein genes: a cool tale in molecular evolution. Proc.Natl.Acad.Sci.U.S.A 94, 3485-3487.

Melendez-Hevia, E., Waddell, T. G., and Cascante, M. (1996). The puzzle of the Krebs citric acid cycle: assembling the pieces of chemically feasible reactions, and opportunism in the design of metabolic pathways during evolution. Journal of Molecular Evolution 43 , 293-303.

Miller, K. R. (1999). Finding Darwin's God: a scientist's search for common ground between God and evolution. (Cliff Street Books: New York.)

Musser, S. M. and Chan, S. I. (1998). Evolution of the cytochrome c oxidase proton pump. Journal of Molecular Evolution 46, 508-520.

Pomiankowski, A. The God of the tiny gaps. New Scientist. 9-14-1996.

Ramos, A., Gazapo, T., Murillas, J., Portero, J. L., Valle, A., and Martin, F. (1998). Outbreak of nosocomial diarrhea by Clostridium difficile in a department of internal medicine. Enfermedades Infecciosas Y Microbiologia Clinica 16, 66-69.

Selander, R. K., Clark, A. G., and Whittam, T. S. (1991). Evolution at the molecular level. (Sinauer Associates: Sunderland, Mass.)

Shapiro, J. In the details . . . what? National Review, 62-65. 9-16-1996.

Simonsen, A., Bremnes, B., Ronning, E., Aasland, R., and Stenmark, H. (1998). Syntaxin-16, a putative Golgi t-SNARE. European Journal of Cell Biology 75, 223-231.

Thornhill, R. H. and Ussery, D. W. (2000). A classification of possible routes of Darwinian evolution. Journal of Theoretical Biology 203, 111-116.

Ussery, David (1999). A biochemist's response to "The Biochemical Challenge to Evolution".  http://www.indiana.edu/~ensiweb/behe.rev.html

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Weber, Bruce (1999). Irreducible complexity and the problem of biochemical emergence. Biology & Philosophy 14, 593-605.

Notes:

(1) See my essay on blood clotting  this website

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(2) In a later version of his review (the website has been updated several times, making it a moving target that is hard to pin down precisely), Ussery did note explicitly that one needed to search abstracts as well as titles to come up with the total of 130 papers. He then noted that a total of just four papers have both words in the title. These papers were not picked up in my search because they either were published after my search was completed in 1995, or because the papers were published before the mid 1980s (which is outside the scope of a CARL search). None of the papers affects the questions discussed in this manuscript.

(3) See my discussion of "mousetrap evolution" on  this website.

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On the royal society's peek under the hood re:Darwinism.

The Road to the Royal Society: The Problems That Matter, the Problems That Don't
Paul Nelson

Starting next Monday, November 7, the Royal Society (RS) will convene a three-day meeting   at its London headquarters that has the potential to rival -- for historical significance --   the (in)famous 1980 Field Museum gathering  on macroevolution, or the  1966 Wistar symposium on mathematical challenges to the neo-Darwinian interpretation of evolution. Structured to include open-ended roundtable discussions, the RS meeting is premised on the view that current textbook evolutionary theory falls far short of what it needs to explain, and that mechanisms and processes outside its customary purview require careful attention.

Like Sherlock Holmes's dog that did not bark in the night, however, the RS meeting is noteworthy for those speakers who were not invited. We do not mean the obvious heretics or ID bad guys, such as Mike Behe, Doug Axe, or Steve Meyer. Their absence from the program is entirely predictable, if one understands that the paradigm actually controlling the boundaries of admissible scientific dissent is not neo-Darwinian evolution, or a scientific theory at all, but the underlying philosophy of materialism or naturalism.

No, the noteworthy uninvited scientists look on casual inspection to be completely respectable, even highly distinguished. Cambridge University paleontologist Simon Conway Morris, for instance, or University of Zurich evolutionary biologist Andreas Wagner, both of whom have written extensively about how neo-Darwinian theory requires revision, are conspicuously absent from the program. Here is a speculation as to why.

Even One Part Per Billion of Teleology is One Part Too Much

Let's start with Wagner. Over the past decade, Wagner has challenged the sufficiency of neo-Darwinian theory, mainly on the grounds that random or undirected changes to any complex functional system are far likelier to end up lost in enormous non-functional regions than they are to land on the very much smaller neighborhoods where novel function or structure occur. In 2011, Wagner wrote:

...we know few of the principles that explain the ability of living things to innovate through a combination of natural selection and random genetic change. Random change by itself is not sufficient, because it does not necessarily bring forth beneficial phenotypes. For example, random change might not be suitable to improve most man-made, technological systems. Similarly, natural selection alone is not sufficient: As the geneticist Hugo de Vries already noted in 1905, 'natural selection may explain the survival of the fittest, but it cannot explain the arrival of the fittest.'"

This criticism of the neo-Darwinian premise of random change should be familiar: one finds the objection featured prominently, for example, in the arguments of the 1966 Wistar participants, not to mention the writings of ID theorists since the early 1980s. Functional complexity and randomness stand fundamentally at odds with each other. If you doubt this, ask yourself if you would like to fly on a passenger jet that had undergone, let's say, one dozen unknown random changes to its flight control system. ("But hey, we're going to take off anyway!" said the demented pilot over the intercom cheerfully, as everyone made for the exits.)

What is probably less familiar is Wagner's solution to the problem of randomness. Probabilistically favored paths, he argues, must exist through sequence and function space, to enable evolutionary processes to move from one novel island to another within the time available -- and those paths must have been built into the universe from the start. As Wagner writes at the conclusion of his 2014 book, The Arrival of the Fittest, "life's creativity draws from a source that is older than life, and perhaps older than time."

Bzzzzzzz! No Royal Society invitation for you, Andreas. Sounds like Platonism, right? And indeed it is, of a sort, anyway, as Wagner readily acknowledges. But if a universal library of Platonic forms enabled biological evolution to succeed, the materialist premise underlying neo-Darwinism must be wrong. ID skeptic and philosophical materialist Massimo Pigliucci can see where ideas of this coloring might be headed: danger, danger, Will Robinson. (He explains this week in "The Neo-Platonic Argument for Evolution Couldn't Be More Wrong.") Teleology is lurking behind those forms.

Teleology detectors also start buzzing loudly when the ideas of Simon Conway Morris come into view. Over the past 15 years, Conway Morris has contended that the "radical historical contingency" premise of neo-Darwinism -- namely, that the existence of Homo sapiens is the unexpected, unpredictable, or strictly one-off outcome of inherently random events -- is false. Rather, evolution was channeled from the start, and a species very much like Homo sapiens, if not H. sapiens itself, was destined to appear in the universe. You are not an accident of the cosmos.

Bzzzzzzz! Teleology jess don't sit right with us folks. No RS invite for Simon.

Philosophical Materialism and Its Invitation List

All joking aside, no one -- least of all, the troublemakers themselves -- really expects ID troublemakers to be invited to speak at major evolution meetings. If that happened with any regularity, or even occasionally, no one would be reading this site, because the intelligent design debate would be (1) pretty much over, (2) never started in the first place, or (3) entirely different in its nature.

But neither Andreas Wagner nor Simon Conway Morris advocates ID; in fact, both are opposed to the idea. Yet even the subtle teleology of their theories is too strong a flavor for the Royal Society. (Let me say I would love to be wrong about this speculation: it would be delightful to learn that Wagner and Conway Morris were invited by the Royal Society to speak, and couldn't make it, or declined the invitation.) Wagner's and Conway Morris's teleology would have been too strong a flavor for Darwin himself, in fact. "If I were convinced that I required such [teleological] additions to the theory of natural selection," Darwin wrote to Lyell in 1859, "I would reject it as rubbish."


But what if it's true -- namely, that teleology, or genuine purpose, is required to explain living things? Then materialism must give way to evidence. That is a problem that matters. Ultimately, the Royal Society, or anyone who wishes truly to understand the universe, must focus on the problems that matter. The ones that don't will take care of themselves.

Decanonising Darwin

So, You Thought Charles Darwin Discovered Natural Selection? Wrong
Jonathan Witt 

After marshaling evidence against the theory of evolution, skeptics sometimes throw Darwin a bone so as not to seem churlish. Hey, we say in essence, natural selection does accomplish things like spreading antibiotic resistance, and Charles Darwin deserves credit for discovering the principle of natural selection even if it isn't the bauplan-building wunderkind he made it out to be.

Yet this gives Darwin too much credit.

Natural Selection Comes to Edinburgh -- Before Darwin

Long before Darwin (or Alfred Russel Wallace), James Hutton, the father of modern geology, propounded the idea of evolution by natural selection. And at least two other men followed on his heels, doing the same well before Darwin articulated the idea.

A retrospect by Paul N. Pearson in the journal Nature reports:

Following the publication of On the Origin of Species in 1859, Charles Darwin learned (and duly acknowledged) that two previous authors had anticipated the theory of evolution by natural selection. The first account to come to light was by Patrick Matthew, who had briefly outlined the mechanism in an appendix to his 1831 book On Naval Timber and Arboriculture. The second was by the physician William Wells, who had speculated on selection and human evolution in 1818.

But some 50 years ago, E. B. Bailey described a still older version of the selection theory from a 1797 manuscript by the geologist James Hutton -- now chiefly famous for his early appreciation of geological time. Unfortunately, this work, entitled the Elements of Agriculture, never appeared in print. Now a more complete, published account has come to light from 1794.

The account appears in a 1794 tome, An Investigation of the Principles of Knowledge. There Hutton wrote the following:

If an organised body is not in the situation and circumstances best adapted to its sustenance and propagation, then, in conceiving an indefinite variety among the individuals of that species, we must be assured, that, on the one hand, those which depart most from the best adapted constitution, will be most liable to perish, while, on the other hand, those organised bodies, which most approach to the best constitution for the present circumstances, will be best adapted to continue, in preserving themselves and multiplying the individuals of their race.

After quoting the passage, Pearson continues:

For example, Hutton describes that in dogs that relied on "nothing but swiftness of foot and quickness of sight" for survival, "the most defective in respect of those necessary qualities, would be the most subject to perish, and that those who employed them in greatest perfection would be best preserved, consequently, would be those who would remain, to preserve themselves, and to continue the race." But if an acute sense of smell was "more necessary to the sustenance of the animal," then "the natural tendency of the race, acting upon the same principle of seminal variation, would be to change the qualities of the animal, and to produce a race of well scented hounds, instead of those who catch their prey by swiftness." The same "principle of variation" must also influence "every species of plant, whether growing in a forest or a meadow."

One might object that this was buried deep in a long book and mostly forgotten. Perhaps, but Hutton was a major scientific figure, and he disseminated his ideas not just by book but also by lecture and conversation.

And as Pearson also notes, Wells and Matthew -- the other two men known to have articulated the idea of evolution of natural selection before Darwin had -- just so happen to have been "educated in Hutton's home town of Edinburgh, a place famous for its scientific clubs and societies."

So here's the lay of the land: Hutton was born, and died, in Edinburgh, attended the University of Edinburgh, and returned to live in the city as an adult, where he was a member of the Royal Society of Edinburgh and a leading figure in the Scottish Enlightenment. This man, the father of modern geology and a fixture of Edinburgh scientific society, propounds a theory of natural selection, and a generation later two other scientists educated in that same scientific community articulate the same idea in their works. (See a post at Genomicron by T. Ryan Gregory for more on Wells's and Matthew's early musing about natural selection.)

Darwin, keep in mind, was also educated at the University of Edinburgh. So four of the earliest articulations of the idea of natural selection are by Edinburgh men, and Darwin is the last of the four.

Darwin Rediscovers

Pearson generously reconstructs this eyebrow-raising coincidence:

It may be more than coincidence that Wells, Matthew and Darwin were all educated in Hutton's home town of Edinburgh.... Studies of Darwin's private notebooks have shown that he came to the selection principle independently of earlier authors, as he always maintained. But it seems possible that a half-forgotten concept from his student days resurfaced afresh in his mind as he struggled to explain the observations of species and varieties compiled on the voyage of the Beagle.

I suspect that's about right. I have a hard time believing that Darwin knowingly and fiendishly stole Hutton's idea and then, even in his notebooks, carefully pretended he'd never heard it before. And I find it hard to believe that the idea of natural selection was not in the air of Edinburgh when Darwin was there as a student, at least in the scientific community. Hutton was too towering a scientific figure, and the idea of natural selection popping up three times in the written works of three separate Edinburgh-trained scientists following in his wake is surely more than coincidence.

In any case, Darwin didn't discover the idea of natural selection. He either resurfaced the idea on his Beagle voyage and didn't realize he was remembering rather than discovering it; or he came upon the idea independently after three other Edinburgh men had articulated it.

And No, Darwin Doesn't Get Points for Theatrical Overstatement

But wasn't it Darwin who first realized the full power of natural selection? In his Nature article, Paul Pearson is careful to note that Hutton did not extend the idea in the way Darwin had. Hutton thought natural selection's effects were limited to generating different races or breeds within a species.

Also, neither William Wells in 1818, nor Patrick Matthew in 1831, applied the idea of natural selection beyond the species level. So the common defense of Darwin at this stage is to remind readers that it's the Victorian gentleman of Down House who gets the credit for discovering the full power and import of natural selection.

But if natural selection actually cannot produce all the biological variety we see around us, if it can only produce variety within species and just a bit beyond the species level (see Michael Behe's The Edge of Evolution), then Darwin was most original precisely where he was wrong.


Darwin did galvanize attention on the process of natural selection, but he did so in much the way those who started the legend of the Seven Cities of Gold encouraged exploration of the American Southwest. In both cases, a tall tale spurred attention and exploration. And in both cases, some worthwhile things were discovered. But the gold? Not so much.

Pre Darwinian design v. Darwinism.

Twenty Years of "Revolutionary" Machines: The Case of ATP Synthase
Evolution News & Views 




It was a Eureka! moment. When Michael Behe saw that diagram of a bacterial flagellum in his biochemistry textbook,  he says, "That's an outboard motor! That's designed. That's no chance assemblage of parts." Thousands of other students must have ignored the obvious, or else meekly accepted what their professors told them, that natural selection was capable of creating such things. But Dr. Behe self-admittedly has a stubborn streak that wouldn't tolerate simplistic answers. From such qualities a   Revolutionary was born. This year we've been celebrating the 20th year since he published  Darwin's Black Box, the book that first put intelligent design on the map.

Twenty years ago another rotary engine was to earn its discoverers the 1997 Nobel Prize in Chemistry. ATP synthase was known previously by its chemical function, but its mode of action was a black box. When Paul Boyer and John E. Walker opened the box and saw a rotary engine one tenth the size of the bacterial flagellum, they were astonished. In the years since, more details have come to light. It's hard to find any paper describing this machine that doesn't call it "amazing" or "remarkable." (Readers may wish to view our animation of ATP synthase, above.) And as Behe discovered in researching the flagellum, hardly anyone tries to explain how it could have come about by neo-Darwinian processes.

John Walker has continued research on this molecular motor since earning the Nobel. Now at age 75, he must be gratified that all the parts have been described, although details about the extraction of torque from a flow of protons remain to be understood. His latest paper, just published by the Proceedings of the National Academy of Sciences  (PNAS) with three colleagues from Cambridge, shows that the surprises keep coming.

Living cells need fuel in the form of adenosine triphosphate, or ATP, to stay alive. This fuel is generated by a molecular machine made of two motors joined by a rotor. One generates rotation by using energy provided by oxidative metabolism or photosynthesis; the other uses energy transmitted by the rotor to make ATP molecules from its building blocks, adenosine diphosphate, or ADP, and inorganic phosphate. The structure has been determined of a fungal machine, isolated from its cellular power stations, the mitochondria, where the machine operates. It provides unsuspected details of the blueprint of the machine and how it works. The working principles of the fungal machine apply to similar machines in all species.
Before now, only about 85 percent of the structure had been determined. That last 15 percent was hidden inside the membrane that anchors the machine. By extracting working motors from a fungus and combining it with counterparts from a cow's mitochondrial version, the team of Vinothkumar, Montgomery, Liu, and Walker was able to glimpse the machinery with unprecedented clarity:

As described here by cryo-EM, we have determined the structure of the entire monomeric F-ATPase complex from the mitochondria of the moderately thermophilic fungus, Pichia angusta, bound to the inhibitory region of the natural bovine inhibitor protein, IF1 (inhibitor of F1-ATPase). This structure fills significant gaps in our knowledge of the mechanism of the F-ATPase. First, it contributes to our understanding of the coupling mechanism by providing unsuspected details of the peripheral stalk and how it is attached to both the catalytic F1-domain and the membrane sector of the enzyme. Second, it provides an independent description of the transmembrane proton pathway for protons, helping both to define common features in the proton translocation mechanism in bacterial and mitochondrial F-ATPases and to explain human pathological mutations in the subunit.
That last clause reinforces Behe's concept of irreducible complexity. Mutations break things. If one of the parts is broken or missing, people get sick or die. Although there are variations in ATP synthase between bacteria and eukaryotes, particularly in the number of c-subunits in the rotor, most parts are "highly conserved" between kingdoms and species. The authors speak of parts that are "strictly conserved" or "absolutely conserved." There are so many essential parts in this machine, it cannot function unless everything is in place and matched for functional interaction.

The authors note that these motors spin at up to 350 Hz. That's a whopping 21,000 rpm! Think about that. Every rotation yields 3 ATP molecules, which are used for most energy-consuming processes in the cell.  a kinesin machine walking down a microtubule, every motion of actin in muscle, every advance of a polymerase translating DNA consumes ATP. If one ATP synthase motor generates 63,000 ATP molecules a minute, imagine how many ATP molecules are being created by thousands of the motors in a single cell. No wonder you can create up to your body weight in ATP in a single busy day.

Walk up to one of these machines in your mind's eye. It's rotating so fast it's a blur. The bottom half spins like a turbine in a hydroelectric power plant, turned not by water but by protons. The upper half assembles the ATP in three pairs of lobes that continuously run "a cycle of substrate binding, ATP formation, and product release. Thus, each 360° rotation produces three molecules of ATP." How could the scientists study something moving so fast? They couldn't. They had to slow it down with an "inhibitor protein" so they could get a good look at it.

They realized that the catalytic upper part rumbles. At top speed, the constant insertion and ejection of substrates generates lateral forces. Without a really steady brace, the machine would vibrate itself out of commission. And a steady brace is just what they found:

Although the relevant interactions are still not fully resolved, the current structure demonstrates that the attachment to the catalytic domain is much more extensive and robust than had been thought, probably involving both the N- and C-terminal domains of the OSCP [oligomycin sensitivity conferral protein] and the N-terminal regions of all three α-subunits. The structure has also provided evidence that, at the lower end of the peripheral stalk (distal from the F1-domain), the hydrophobic N-terminal region of the b-subunit is, as predicted, folded into two transmembrane α-helices, bH1 and part of bH2. It interacts with aH1 and aH2, and bH2 with aH5 and aH6, and most likely, in addition, with the loop between aH3 and aH4. It has also confirmed that the middle part of the peripheral stalk, consisting of the central α-helical pillar that is about 160 Å long and provided by bH2, is augmented by roughly parallel α-helices from subunit d and most likely from subunit h (as in the related bovine F6). Thus, it has the characteristics of a seemingly rigid and inflexible structure.
We include those details to emphasize the complexity of this machine. Without the robust stator and all its interactions, the machine could not handle the lateral forces of its high-speed operation.

But wait; there's more! The central stalk that confers stability also flexes! Why?

The second role of the peripheral stalk is to help keep the a-subunit in contact with the rotating c-ring, possibly by exerting lateral pressure toward the central axis, thereby ensuring the integrity of the transmembrane proton pathway. Subunit ATP8 may contribute here via its C-terminal region. It is known that the longer C-terminal region of bovine ATP8 extends from the membrane into the peripheral stalk, where it interacts with subunits b and d, thereby providing another brace in addition to subunit b to hold subunit a against the rotating c-ring.
In other words, as protons enter the spinning rotor on the bottom half, the stator provides lateral pressure to keep the protons from leaking out. How well-designed must that be?

Another finding concerns "supernumerary subunits" unrelated to the catalytic activity of the machine. Some of these appear to have a role in arranging multiple motors into efficient rows in the mitochondria:

The supernumerary subunits have no known direct role in ATP synthesis, but some of them mediate interactions between monomeric F-ATPase complexes in dimers [pairs of motors] of the complex that are associated in rows along the edges of the mitochondrial cristae.
The authors found another aspect that challenges Darwinian theory. Different versions of the machine work similarly despite different amino-acid sequences (and thus DNA codes) for particular parts. This was unexpected, they say:

A comparison of the current structures of the bacterial and mitochondrial enzymes (Fig. 4) illustrates their known similarities in overall architecture and in the detailed structures of the catalytic and proton translocating regions. Somewhat unexpectedly, the peripheral stalk regions of mitochondrial and bacterial enzymes are also similar, despite significant differences in subunit composition and lack of similarity in sequence of their constituent subunits.... Thus, peripheral stalks from bacteria, chloroplasts, and eukaryotes have similar designs, and presumably similar physical properties, to allow them to perform their roles in ensuring the maintenance of an intact proton pathway in the interface between rotor and stator and in keeping the stator together.
This means that function is conserved even when the sequence is not. If natural selection could not build one irreducibly complex version of a machine, how much less could it build multiple versions?


If there is any aspect of nature that should arouse our awe, it should be to find rotary engines operating with multiple well-matched parts at high speeds at fantastically tiny scales. The details of what Walker's team found can be explored in this open-access paper in PNAS. It doesn't mention "evolution" anywhere, but it does mention design (see above). We hope you will look at the pictures, read the descriptions, and notice their emotional response as they say, "The structure provides more insights into the workings of this amazing machine."

A clash of Titans. XXXV

File under "Well said" XL

"I was really too honest a man to be a politician and live." Socrates

Questioning JEHOVAH God:The Watchtower Society's commentary.

Three Questions People Would Like to Ask God:

SUSAN’S questions about God began at age seven, when her nine-year-old friend Al was hospitalized with polio and confined to an iron lung. She wrote about her experience in the January 6, 2013, issue of The New York Times.

After visiting Al in the hospital, Susan asked her mother: “Why would God do that to a little boy?”

“The priest would say God must have his reasons,” her mother replied, “but I don’t know what they could be.”

Two years later, in 1954, Jonas Salk’s polio vaccine became available, and Susan’s mother suggested that perhaps God had guided his research.

“Well, God should have guided the doctors a long time ago so that Al wouldn’t be in an iron lung,” Susan replied.

Susan summed up the account of her childhood experience by writing: “[Al] was to die only eight years later, by which time I was a committed atheist.”

Like Susan, many people who have suffered from tragedy or have witnessed it are unable to find satisfying answers to their questions about God. Some become atheists. Others may not entirely deny God’s existence, but they become skeptical.

It is not that atheists and skeptics are completely unfamiliar with religion. On the contrary, their experience with religion is often what pushes them toward disbelief. Organized religion, they may feel, has failed to answer life’s tough questions. What kind of questions? Ironically, they are often the same questions that people who claim to have faith in God struggle with. Consider three questions that many people would like to ask God, if given the chance, and the answers that the Bible provides.

1 “WHY DO YOU ALLOW SUFFERING?”

Why ask that question?

‘A loving God would prevent life’s tragedies,’ many conclude.

TO THINK ABOUT: We might find the habits and customs of people from another culture to be strange—perhaps even shocking. We could easily misinterpret their actions. For example, in one culture people feel that maintaining eye contact is a sign of sincerity; in another they see it as a sign of disrespect. Yet even in such cases, there would be no reason to say that they are wrong. Instead, we just need to get to know them better.

Could something similar happen when it comes to understanding God? Many believe that the presence of suffering proves that God does not exist. Others, though, who have come to understand why God has allowed suffering, are confident that he does exist.

WHAT THE BIBLE SAYS: God’s thoughts and ways are different from ours. (Isaiah 55:8, 9) Because of that, his actions, as well as his reasons for waiting before he acts, may at first seem strange to us.

Still, the Bible does not ask us to accept such hollow expressions as “God works in mysterious ways.” Instead, it encourages us to learn more about God, helping us to understand why and when he acts as he does.* We can even draw close to him.—James 4:8.

2 “WHY IS RELIGION FULL OF HYPOCRISY?”

Why ask that question?

‘If God appreciated sincerity,’ some might reason, ‘there wouldn’t be so much pretense among those who claim to worship him.’

TO THINK ABOUT: Imagine a son who rejects his father’s fine upbringing and leaves home to lead a corrupt life. Although the father does not approve, he allows his son to make that choice. Could those who later meet the son rightfully conclude that he had a bad father or even that he had no father at all? Of course not! Likewise, hypocrisy in religion only proves that God allows people to choose their own path in life.

WHAT THE BIBLE SAYS: God hates religious hypocrisy. (Jeremiah 7:29-31; 32:35) At the same time, he allows people to exercise free will. Many who claim to believe in God choose to follow man-made religious teachings and their own brand of morality.—Matthew 15:7-9.

In contrast, religion that God approves is not hypocritical.* Jesus said: “By this all will know that you are my disciples—if you have love among yourselves.” (John 13:35) This love must be “without hypocrisy.” (Romans 12:9) Most religions have failed to live up to that standard. During the 1994 genocide in Rwanda, for example, tens of thousands of religious people slaughtered members of their own faith, simply because those people were of a different tribe. In contrast, Jehovah’s Witnesses did not share in the massacre, and many of them protected fellow believers and others, even risking their life to do so. Such selfless acts prove that religion can be free of hypocrisy.

3 “WHY ARE WE HERE?”

Why ask that question?

Some may wonder: ‘Why do humans live for only 80 or 90 years and then die? What is the purpose of such a brief existence?’

TO THINK ABOUT: Many who do not believe in God still recognize the need to account for the complexity, intricacy, and order of the natural world. They perceive that our planet, other planets, and the moon are configured in just the right way to sustain life on earth. They describe the natural laws that govern the universe as being fine-tuned, perfectly set so that even the slightest alteration would make life on earth impossible.

WHAT THE BIBLE SAYS: While many people view our relatively brief life span as proof that there is no God, the natural world gives ample evidence that there is a Creator. (Romans 1:20) He had a purpose in making these things, and the reason for our existence is closely linked to his purpose. God created humans to live forever on the earth, and he has not abandoned his purpose.—Psalm 37:11, 29; Isaiah 55:11.

While we can discern God’s existence and even some of his qualities through the natural world, God did not intend for us to perceive his purpose that way. For us to know God’s purpose, and hence the meaning of our existence, we need communication from God. In the Bible he ­communicates with us, using simple, direct terms.* JEHOVAH'S Witnesses invite you to take a fresh look at the answers found there.

For the reason why God allows suffering, see chapter 11 of the book What Does the Bible Really Teach? published by Jehovah’s Witnesses. Also available at www.jw.org.

For more information, see chapter 15 of the book What Does the Bible Really Teach? published by Jehovah’s Witnesses. Also available at www.jw.org.

For more information, see chapter 3 of the book What Does the Bible Really Teach? published by Jehovah’s Witnesses. Also available at www.jw.org.

HE FOUND ANSWERS TO HIS QUESTIONS:

As a boy, Harry never understood why a loving God permitted suffering. As a young man, he witnessed firsthand the horrors of war and asked, “If there is an almighty Creator, why would he permit such conditions to afflict so many people, especially innocent children?”

Despite his university education and his examination of various religions, Harry’s questions persisted. After wrestling with the issue for years, he concluded that “perhaps there was no God after all.”

Harry kept an open mind when he heard what the Bible had to say on the matter. He learned that God is not the source of wickedness; rather, God hates it and feels pain when others suffer. (Proverbs 6:16-19; Isaiah 63:9; James 1:13) Harry found out that ultimately all pain and suffering can be traced to humans’ rejecting God’s authority and using their free will to decide for themselves what is right and what is wrong. (Deuteronomy 32:4, 5; James 1:14, 15) He also saw that God did not stand back and take an ‘I told you so’ posture. Instead, God immediately set in motion arrangements to eradicate wickedness and suffering. He will completely undo all the damage that has been done. Harry came to realize that in the meantime, God has provided comfort and support to help individuals endure.—Genesis 3:15; Romans 8:20, 21; Revelation 21:4.

These answers did more than satisfy Harry’s curiosity about a fundamental question. They helped him to weather the emotional turmoil he later experienced when tragedy touched him personally.

For some the circus is no laughing matter.

Saving Darwin?

Does Karl Giberson represent the new face of American evangelicals, “accepting” Darwin?
November 23, 2015 Posted by News under Christian Darwinism, Intelligent Design

As some might hope? Where would that leave evangelicals now that Darwin is being re-evaluated in so many other places?

Dragging in here late, with the last of the religion coverage for the week:

Further to: “Karl Giberson? But at this point who cares what Darwin’s Christian huffs at Huffpo? (We all rate a better informed class of critic. Especially now.)

There we looked at Nazarene process theologian Karl Giberson’s fact-free claims about the Discovery Institute, sponsor of ID theorists …

Sounded odd, but he had been in the files for years. So I went back to see what else one might learn about a figure on the Christian lecture circuit who wants to “save Darwin.”

From my notes:

–  Giberson helped genome mapper Francis Collins found Templeton-funded Darwin apologist group (2008), BioLogos. He has served as vice-president (2008–2010) Collins resigned from BioLogos when appointed NHS director in 2008. However, in 2011, Giberson also left both BioLogos and Eastern Nazarene College in Boston, where he had taught physics.

– He considers Darwin’s theory of evolution to be “confirmed beyond a reasonable doubt by science,” though as Bill Dembski notes, “No theory is that good.”

– In 2008, Karl Giberson wrote a book called Saving Darwin (Harper One, 2008). That positions him clearly, considering that, as far-left The Nation (2012) noted, Christian Alvin Plantinga, non-materialist atheist Thomas Nagel, and materialist atheist Jerry Fodor (well-known philosophers all) agree on doubting Darwin. And it is becoming a trend.

– In the book  co-authored with Collins, The Language of Science and Faith (IVP Books, 2011), readers are told, “We avoid using the ‘E-word.’” [evolution]

Theistic evolution is the belief that God created life using natural processes, working within the natural order, in harmony with its laws. So, why don’t we simply use the term evolution to describe our view? We don’t use the term, at least not at this point in our discussion, because it is associated with negative ideas, including atheism, and many readers would have a constant uncomfortable feeling while thinking about it. The word evolution carries emotional baggage that we are tossing overboard. (pp. 19–20)

Of course, the history of the word “evolution” is not emotional baggage. It is the best evidence for what the word usually means: 78% of evolutionary biologists are pure naturalist atheists.

– Giberson, along with Collins, seems to display a deep attachment to Darwinism that comes out in his theology. For example, in response to the question of whether God planned us in any sense, Giberson and Collins are quite clear in The Language of Science and Faith, that God is not in the details like us:

… we hope readers will agree with us that the relevant part of our origins is not the story of how we acquired the specific details of our body plan—ten fingers, two ears, one nose—or how we lack a marsupial pouch to carry our newborns, or why potty-training takes so long. Nothing about these details is critical to what makes us human. Our humanness is embedded more holistically in our less tangible aspects and could certainly be embodied in creatures that looked nothing like us …

Many may find this thought unsettling and strangely at odds with their understanding of creation, which celebrates that God created us “in his image.”We suggest that this is due to the influence that actual artistic images have had on our view of God and ourselves Because God became incarnate in Jesus, who looks like us, we all too quickly slip into the assumption that God also looks like us. (p. 201, p. 204-5. )

This feels disingenuous. The question isn’t whether God looks like us (a notion with which the Scriptures are clearly comfortable) but whether God intends us to look the way we do. On a Darwinist reckoning, no. On a Christian reckoning, yes.

– In Saving Darwin, Giberson offers a doctrine of the fall of man that most orthodox Christians would not recognize:

Selfishness, in fact, drives the evolutionary process. Unselfish creatures died, and their unselfish genes perished with them. Selfish creatures, who attended to their own needs for food, power, and sex, flourished and passed on these genes to their offspring. After many generations selfishness was so fully programmed in our genomes that it was a significant part of what we now call human nature. ( p. 12.)

In other words, the fall was not a human choice after all. And salvation now means getting the better of that selfish gene.

– More significantly, Giberson also tells us, “Jesus would believe in evolution and so should you.” Jesus thus stands revealed as a mere man among men—a good, honest man who wants to believe the correct things. As it happens, orthodox Christians regard him as the Word who created the entire cosmos. In that case, for Jesus, belief is superfluous. He knows how he made life.

– There has been conflict among Nazarenes in recent years over “emergent” (open, process) theology, as denominational news stories attest, with some asking, about Giberson, “What is this guy doing teaching in an allegedly evangelical school?”

– Process/open theology affirms that

1) love is uniquely exemplified by God, 2) love is the human ethical imperative, 3) God and creatures enjoy free and mutually-influencing relations, 4) and the future is open and not settled.

Open theology affirms that God knows everything that may happen in the future. God knows all possibilities. But God does not know with absolute certainty what every free creature will someday actually do.

Note: This summary is from the page of Thomas Jay Oord, a Nazarene theologian supported by Giberson.

Process theology would be most helpful to anyone promoting Darwinian evolution as an account of the history of the human race among Christians. But most evangelicals have rejected it in the past, due to its sharply diminished view of the sovereignty of God.

However, in 2011 Christianity Today went to considerable trouble to highlight—favourably, it seemed—Giberson’s approach to origins, grounded in process theology. As I used to write for that mag, I took an interest, and will unpack that episode next Sunday if possible.

Meanwhile, is Christianity Today onto something, that a Darwinized human origins story is gaining ground among American evangelicals? Or what?

Note: Giberson currently has a Web site, “Exploring America’s creation-evolution controversy* * probably not going to hell,” which doubtless updates any of the forgoing. – O’Leary for News

On Spaceship earth.

Molecular biology v. Darwinism

Look at All that Goes into Translating a Gene
Evolution News & Views 

In Nature, Marlene Oeffinger gives readers a tour of the ribosome, in particular how it is built. This wonder of the cell translates messenger RNA into proteins. Prepare to be astonished. Here’s the overture:

Production of the cell's translational apparatus, the ribosome, requires the orchestrated function of hundreds of proteins. A structure of its earliest precursor yields unprecedented insight into ribosome formation. [Emphasis added.]
For the first movement, she calls forward an ensemble of scientists led by Markus Kornprobst. They published in the journal Cell a composition about the “pre-ribosome” in eukaryotes. The 3-D structure of this protein, revealed through cryo-electron microscopy, shows that it engulfs the “pre-rRNA” (one of the large, complex RNA molecules that will comprise the ribosome) during construction. The pre-ribosome itself has about 70 assembly factors. Are we sounding irreducibly complex yet? The work has only begun. Oeffinger comments,

The structure reveals, for the first time and in stunning detail, the arrangement of and interactions between many proteins that have been implicated in ribosome assembly, shedding light on a crucial step in early ribosome formation.
Keep in mind we are only looking so far at one crucial step in early ribosome formation.

In the nucleolus, three of four ribosomal RNAs undergo assembly before leaving to work in the cytoplasm. Many other proteins, called ribosome biogenesis factors, will be involved in construction of the pre-ribosome. (Remember, this is just for the pre-ribosome.) As the complexity grows, tension increases in the orchestration:

During its transcription, the long pre-rRNA is assembled with r-proteins, ribosome biogenesis factors and small nucleolar RNAs to form a large 90S pre-ribosome. Following the first stage of pre-rRNA processing, the complex splits into two pre-ribosomes, dubbed pre-40S and pre-60S, which are eventually exported to the cytoplasm where they undergo further maturation steps and then join as 40S and 60S subunits to form the mature ribosome.
Along with the identities of the biogenesis factors came the realization that they numbered a vast 200 to 300 in eukaryotes. In the yeast Saccharomyces cerevisiae, the 90S pre-ribosome alone contains about 70 ribosome biogenesis factors -- almost as many as the number of proteins in a mature ribosome. Hence, a recurring question in the field is: why does ribosome production require so many accessory proteins?

Kornprobst’s team provided a partial answer. All these dozens of proteins are involved in multi-part complexes that work together to build the pre-ribosome.

The requirement for so many extra proteins is explained by the authors' observation that many accessory proteins are arranged around the folded pre-rRNA molecule in previously defined multi-protein complexes called UTP-A, UTP-B and UTP-C. Of these, UTP-A and UTP-B form a scaffold, within which the newly transcribed pre-rRNA is encased and so can be securely processed, modified and assembled with r-proteins.
Explained, perhaps, but not simplified! Oeffinger’s cartoon illustration of these complexes shows the pre-rRNA being threaded into a mold formed by UTP-A, UTP-B, and another factor named U3. “Encased within this mould, the pre-rRNA is safely folded and processed,” she explains. But then, we still only have the Pre-40S and Pre-60S parts of the ribosome constructed.

The role of this scaffold is reminiscent of the way in which chaperone proteins aid folding of other proteins -- a common process that prevents aggregation of proteins into non-functional structures. But although chaperone-mediated protein folding has been long established, the idea of chaperone moulds is new to RNA biology.
Keep that in mind as we talk later about the implications for the origin of life. That little U3 factor, by the way, has two functions. Half of it forms part of the scaffold. The other half is buried deep within the pre-ribosome, “presumably interacting with the pre-rRNA.” It clings to a spacer molecule that gets cleaved from the pre-rRNA. This step “is crucial for the separation of the processed 90S pre-rRNAs into pre-40S and pre-60S complexes, and the progression of ribosome production.”

We’re getting into gory details on purpose. We need to hear the complex counterpoint going on, so that the standing ovation at the end of the composition will be deserved. Remember, we are still just trying to get the “pre-ribosome” finished. Bear with us:

Kornprobst and colleagues also identified the position of the pre-18S rRNA (which will become the rRNA component of the 40S subunit) in their structure. When comparing the pre-18S structure with that of the mature 18S rRNA, the authors observed that the molecule underwent progressive folding, beginning in the domains closest to the site where transcription began. In the 90S, these regions were folded to resemble the mature 18S, whereas domains farther from the transcriptional start site were seemingly still in transitory states. This observation fits well with a previous model of hierarchical rRNA assembly.
All this and we still don’t have a working ribosome yet -- just a pre-ribosome. At this point, though, we can give hearty applause for the first movement of the symphony. Oeffinger is sure thrilled with it.

Kornprobst and colleagues have visualized in detail what, until now, has been seen through electron microscopy only as small black balls on strings of pre-rRNA. Holding a magnifying glass to the early steps of ribosome biogenesis, the authors have finally revealed a role for the multitude of ribosome biogenesis factors as a chaperone mould that provides a secure environment for the processing and folding of pre-rRNA.
The rest of the story is bound to be good. For now, we can ponder these members of a large orchestra playing together, interacting in complex sequential ways, and ask some important questions. Chiefly, could any of this have arisen by chance?

Origin-of-life researchers sometimes leap from random building blocks to a cell, or a replicator, without considering all the factors involved. They think RNA is the magic molecule that can fulfill the dual roles of metabolism and coding. Simplistic accounts, like this one on Phys.org, make it seem an “RNA World” could have preceded the DNA-protein world of life as we know it.

Actual RNA, though, is extremely delicate and nearly impossible to form in water. With copious amounts of guidance and protection by intelligent investigators in a lab, RNA can do simple things like cut itself in half or make crude copies of parts of itself. What it cannot do is code for proteins that can help it assemble. That’s putting the cart before the horse. If it needs proteins to guide and protect it into a hierarchical sequence of stages leading up to a mature ribosome, you can’t invoke raw RNA as a stepping stone for what it has to have to exist.

And no fair attributing sentience to the RNA molecules. In a sense, they’re dumb. They have no goal, and no desire to organize on a cell-making project. Some origin-of-life researchers have a bad habit of envisioning the molecules wanting to get together to form a cell. RNA starts out holding some code and metabolic function, they will say, then it “hands off” the coding to DNA and the metabolism to proteins. For a materialist, that’s cheating.

Italian biochemist Pier Luigi Luisi calls the RNA World scenario a “baseless fantasy.” See his reasons in an interview with Susan Mazur in her book The Origin of Life Circus (pp. 360-363 in particular), where he dismisses it as so unrealistic on several levels that he states that a new start is needed, a “beginner’s mind revolution” away from the RNA-DNA-centric models.

The real problem is to make ordered sequences of amino acids, and of course ordered sequences of nucleic acids – and on that the prebiotic RNA world is absolutely silent. But this view of the prebiotic RNA world is still the most popular. I think it is a case of social science psychology more than science itself (p. 363).
We do know of a cause, however, that is capable of sequencing building blocks into ordered structures. It can organize dozens of complex parts that can interact in detailed ways, in a hierarchical structure, working in sequence toward a goal. That cause (need it be said again?) is intelligence.


Intelligence is not magic. It is a cause we know and use every day. It is a cause that is necessary and sufficient for these kinds of highly ordered operations. Because of this, and because blind chance is utterly incapable of such things, intelligence is the cause that we should use in our scientific explanations.

Is there still cause for doubt?

Do New Ediacaran Fossils Muffle the Cambrian Explosion?
Evolution News & Views 

Whenever the mainstream journals discuss the Cambrian explosion, you can expect three things:

They will try to explain the Cambrian radiation using only unguided material causes like oxygen, temperature or chemistry. Mind and intelligence is forbidden.

They will use anthropomorphic words or appeal to magic, saying that the Cambrian animals appeared, developed, innovated, arose, emerged, filled new ecological niches, or engaged in an evolutionary arms race.

They will completely ignore the argument in Stephen Meyer's book Darwin's Doubt: that the sudden appearance of the Cambrian animals required vast amounts of information expressed hierarchically in new cell types, tissues, organs, and body plans. Since this is beyond the capabilities of neo-Darwinism, and the only cause we know that can produce this kind of information is intelligence, the Cambrian explosion provides powerful evidence for intelligent design.

The journal Geology just published new research dealing with the Ediacaran period -- that lazy world of sessile marine animals that preceded the Cambrian. Let's see if they live up to our expectations or have something new to say. Unless they find a gradual neo-Darwinian path from Precambrian microbes to trilobites, appealing to only material causes, without using magic words, we will have to call Strike Three.

Pour Sand, Add Cement, Mix

Derek E. G. Briggs, a Darwin proponent we called out last October, lends his name to a paper by lead author Lidya Tarhan and three others writing in Geology, "Exceptional preservation of soft-bodied Ediacara Biota promoted by silica-rich oceans." Tarhan's team took a closer look at the type sequence in Australia where the Ediacarans were first identified. Their goal was to understand how such soft creatures could be perfectly preserved as fossils in sandstone. In short, they propose that if you add the right silica cement to the sandy seafloor fast enough, you can get beautiful molds and casts of creatures before they decay.

Here we present evidence from the Ediacara Member of South Australia that Ediacara-style preservation was due to rapid, early-stage precipitation of silica cements, facilitated by the high silica saturation state of the oceans prior to the appearance of prolific silica biomineralizers. An early silicification model provides a coherent, mechanistic and empirically supported explanation for the widespread preservation of soft-bodied organisms of Ediacaran-early Paleozoic age as sandstone casts and molds. The prevalence of early silicification confirms that Ediacara-style fossil assemblages can provide an accurate window into life on the Ediacaran seafloor that can be used to reconstruct critical steps in the development and diversification of early animal ecosystems. [Emphasis added.]
You see right off the bat their focus is on the fossilization process, not on evolution. If you can explain the creatures' preservation, they say, you can "reconstruct critical steps in the development and diversification of early animal ecosystems." But that doesn't follow. It's only a half-truth. You might open a window on the conditions that existed when they were fossilized, but you can't leap from there to a theory of how animals "developed" (euphemism for evolved) and "diversified" (another evolutionary euphemism).

In a nutshell, their premise is that a "taphonomic window" (opportunity for fossilization) opened in Precambrian days that permitted a unique kind of "Ediacaran-style preservation," as can be seen in their beautifully detailed photos of Ediacarans, those mysterious frond-like and pillow-like multicellular colonies illustrated in Illustra's film Darwin's Dilemma. This taphonomic window persisted for "hundreds of millions of years" well into the Ordovician.

So why don't we find Ediacarans after the Cambrian explosion? As the story goes, the new critters used up the cement. Modern oceans are undersaturated in silica, thanks to drawdown by diatoms, sponges, and radiolarians. That wouldn't have been the case back in the Ediacaran. With more dissolved silica in the water, the Precambrian creatures could have been cemented in the sand, forming casts and molds before their tissues decayed away. But later, the silica-hungry newcomers broke the molds; that's why the Ediacarans stopped being preserved. Most likely this reflected a global change in the chemistry of the oceans. What are the implications of their model?

Evidence for early silicification across a wide range of tissue types demonstrates the importance of a global and persistent environmental control on fossilization, i.e., high marine silica concentration. Resolving this long-standing taphonomic paradox allows genuine evolutionary signals (e.g., extinction events) to be distinguished from preservational artifacts. An early silicification taphonomic model indicates that the geologically abrupt appearance and subsequent disappearance of the Ediacara Biota is a valid evolutionary signal. It also provides the first empirical support for the contention that Ediacara-style fossil assemblages truly reflect the diversity, trophic complexity, and community-level ecology of Earth's oldest fossil animal ecosystems.
That's not helpful. For Darwinians, that is. They just said that the abrupt appearance and disappearance of the Ediacarans "is a valid evolutionary signal." Meyer agrees that the Ediacarans appeared explosively (DD, pp. 86-88), and disappeared before the Cambrian explosion. He would only disagree that this is a valid evolutionary signal. Next.

Signals in the Desert

In a desolate area east of Death Valley, a team of scientists found "Two new exceptionally preserved body fossil assemblages from Mount Dunfee, Nevada, USA" (Geology). They were hopeful this site would shed light on the Cambrian explosion, because

Evaluation of hypotheses that relate environmental to evolutionary change across the Ediacaran-Cambrian transition has been hampered by a dearth of sections that preserve both the last appearance of Ediacaran body fossils and the first appearance of Treptichnus pedum [an index fossil for the start of the Cambrian] within carbonate-rich strata suitable for chemostratigraphic studies. Here, we report two new exceptionally preserved latest Ediacaran fossil assemblages from the Deep Spring Formation at Mount Dunfee, Nevada (USA). Further, we report these occurrences in a high-resolution carbon isotope chemostratigraphic framework, permitting correlation on a regional and global scale.
It's a significant find. They've got the latest Ediacaran all the way to the first Cambrian. In between, they identified a "worm world" of ichnofossils (trails and burrows), some small shelly fossil traces, and -- get this -- the "carbon isotope excursion" that evolutionists believe indicates a global change in ocean chemistry and the carbon cycle. Their detailed geological cross-sections show this transition across 100 meters of strata. They can correlate some fossils with similar ones from China. It's a perfect setup to refute Darwin's Doubt.

The data presented here represent the tightest relationship documented to date between the negative δ13C excursion and biological turnover at the Ediacaran-Cambrian boundary, consistent with an environmental disturbance eliminating the last of the Ediacaran biota and paving the way for the Cambrian radiation.
Alas, things are not so simple. Once again, they agree that the Ediacarans went extinct before the Cambrian event. That means those weird sessile creatures didn't have anything to do with the new Cambrian body plans. The Nevada site lacks the frond-like and mattress-like creatures for which the Ediacaran period is best known. As for Cloudina, (once considered a "small shelly fossil" but later reclassified), its classification as a metazoan living in the Ediacaran period seems questionable. It looks like a pile of cups, and has no organs or specialized tissues. It went extinct at the base of the Cambrian, so it cannot have been an ancestor to the new Cambrian phyla. T. pedum is hardly a better contender; it's known by its burrows, and probably lacked hard parts.

The team's geological chart shows lots of strata between the first and second fossil assemblages where transitional forms could be hiding, but they're not there. You have Ediacarans, then blank space, then some tubular things, then the Cambrian index fossil T. pedum higher up. No evolution is obvious. No pre-trilobites. No pre-Anomalocaris. A Darwinian would be batting the air to consider this outcrop helpful for explaining the Cambrian Explosion.

As for that carbon isotope excursion, we've observed that its significance is questionable, since it doesn't correlate tightly around the world. At best it is an effect of the explosion, not the cause of it. Similarly, T. pedum shows up in different places around the world, so it's not exactly a precise marker either. Moreover, their correlations of the few worm-like body fossils with similar ones in China appear dubious. And embarrassingly, one fossil they call Conotobus used to be considered an ancestor to Cloudina, but here in Nevada it appears in strata above its descendent! So as noteworthy as the Nevada site is, it leaves the Cambrian explosion completely unexplained. Another strikeout.

Summing Up

The editors of Geology put the best spin on things that they can. James D. Schiffbauer, a geologist from the University of Missouri, reviews the papers in a piece titled, "The age of tubes: A window into biological transition at the Precambrian-Cambrian boundary." He recalls his delight at reading Wonderful Life, Stephen Jay Gould's marvelous description of the Burgess Shale. He remembers his astonishment at the newly discovered Ediacaran fauna in 1992, wondering what it meant for evolution. He says that the Ediacaran-Cambrian interval "has become one of the most intensively studied time slices in the geological and paleontological records." Then he laments:

The past twenty years have brought significant new data to the table regarding the Ediacaran-Cambrian Earth system and biosphere, but a great many questions remain unanswered. Foremost of which, the pattern(s) of and mechanism(s) for biotic change during the Ediacaran-Cambrian transition are still largely unresolved.
Did these two papers offer new hope? Well, they helped rule out some unworkable ideas, like the "Cheshire Cat" theory that posited the Ediacarans disappeared gradually. No, Schiffbauer admits, "we observe that the fossil record of Ediacara organisms was truncated at this transition -- whether by disappearance of their preservational regime, or by disappearance of the organisms themselves."

As excited as Schiffbauer is about the new Nevada site with its tubular whatzits, he ends with more stories, more magical anthropomorphic talk, and more promissory notes. His last paragraph even discounts some of his own previous publications.

These tubular and other vermiform (worm-like) organisms have recently been implicated in marginalizing and competitively wedging out the classic Ediacaran forms, owing to such ecological novelties as ecosystem engineering and macropredation (Schiffbauer et al., 2016). However, as shown here in direct context with an isotopic record of environmental perturbation, perhaps the combined ecological and environmental stressors provided an insurmountable double whammy, forcing a coda for the classic Ediacarans. While the terminal Ediacaran of the Deep Spring Formation had been previously examined (e.g., Gevirtzman and Mount, 1986; Signor et al., 1987), Smith et al.'s new work has served to prop the window open for further refinement of the taxonomy of these tubular forms, as well as detailed investigation of their taphonomy and paleoecology. These "wormworld" organisms (Schiffbauer et al., 2016) inhabit an important transition, and their continued investigation may yield clarity into the patterns and mechanisms of biotic turnover at the Ediacaran-Cambrian boundary.

OK, when he finds said clarity, we'll be glad to give him another chance at bat. Till then, we must call it as we see it. Strike three.