Intelligent Design and the Origin of Biological Information: A Response to Dennis Venema
[Editor’s Note: This article is adapted from a series of articles originally posted on Evolution News and Views. The originals may be seen here: Part 1, Part 2, Part 3, Part 4, Part 5, Part 6, Part 7, Part 8.]
Section 1: Executive Summary
In this section, we:
- Define ID, seeing that it’s a positive argument that doesn’t deny natural selection can do some things
- Summarize the problems with Venema’s critiques: he mis-defines ID and fails to acknowledge responses from ID proponents to the evidence he raises
- Emphasize that this is simply a substantive response and I have no reason to doubt that Dr. Venema is a nice guy and highly competent scientist
What does intelligent design (ID) say about the origin of biological information? Simply put, ID claims that we can find in nature the type of information that, in our experience, comes from intelligence.
To make this positive scientific inference to design, ID begins with observations about the types of information that are generated by intelligent agents. ID theorists observe that in our experience, high levels of complex and specified information come from intelligence. As Stephen C. Meyer writes:
[W]e have repeated experience of rational and conscious agents — in particular ourselves — generating or causing increases in complex specified information, both in the form of sequence-specific lines of code and in the form of hierarchically arranged systems of parts. … Our experience-based knowledge of information-flow confirms that systems with large amounts of specified complexity (especially codes and languages) invariably originate from an intelligent source from a mind or personal agent.
(Stephen C. Meyer, “The origin of biological information and the higher taxonomic categories,” Proceedings of the Biological Society of Washington, Vol. 117(2):213-239 (2004).)
Thus, the form of information that reliably indicates design is high levels of “specified complexity” or “complex and specified information.” So what exactly is the technical-term “complex specified information” or “CSI”? Something is complex if it is unlikely, and it is specified if it matches a pre-existing pattern.
It’s important to note that ID is thus not a purely negative argument against Darwinian evolution. Again, it’s a positive argument based upon finding nature the type of information which in our experience comes from intelligence.
In that regard, ID doesn’t say that neo-Darwinian evolution cannot do anything. ID doesn’t claim that neo-Darwinism mechanisms cannot cause small-scale changes in organisms that might represent small changes in specified complexity.
But the observation that neo-Darwinism can do some things does not imply that neo-Darwinism can do all things. Thus, the leading pro-ID biochemist Michael Behe argues that there is an “edge” to evolution — i.e., there are limits to what Darwinian mechanisms can accomplish.
As a result, the proper way to test neo-Darwinism against intelligent design is not to say “intelligent design says that neo-Darwinism can do nothing, so if neo-Darwinism can do anything then ID is refuted.” Rather, we should say: “Let’s study the causes of neo-Darwinism and intelligent design and seek to understand their respective information-generative powers. If some biological structures are within the ‘edge of evolution,’ let’s not then assume that all biological structures are within the edge of evolution. Rather, let’s test natural objects to determine which explanation is warranted in each case.”
In this article, I will be discussing how we test intelligent design while responding to a recent series of articles on the BioLogos website, “Evolution and the Origin of Biological Information,” by theistic Darwinian evolutionist biologist Dennis Venema. Unfortunately, in his series, Venema makes some common mistakes in defining ID, and dramatically misstates the nature of intelligent design.
Before getting into that, let me first say that I’ve had some private correspondence with Dr. Venema and I’ve found him to be nothing but cordial. This is in no way an attack on Dr. Venema personally but simply a respectful reply to his scientific critiques of intelligent design. Academic debate allows for this — in fact it encourages the respectful exchange of views.
Misunderstanding Meyer’s Argument
Venema framed his series as a response to Stephen Meyer’s arguments in Signature in the Cell, as well as those of the entire “Intelligent Design Movement,” which Venema calls the “IDM.” According to Venema: “The obvious problem for Meyer’s case is that biologists are well aware of a natural mechanism that does add functional, specified information to DNA sequences (and in some cases, creates new genes de novo): natural selection acting on genetic variation produced through random mutation.” While discussing intelligent design and the origin of new biological information, I will analyze Dr. Venema’s arguments, showing that he:
- Misstates Stephen Meyer’s thesis as being a “denial of random mutation and natural selection” which “ignores the possibility of natural mechanisms that allow ‘information’ to accumulate in an additive fashion.” Since Meyer’s thesis pertains to the origin of information in the first life, before natural selection could have operated, Venema’s discussion of random mutation and natural selection does not respond to Meyer’s basic thesis.
- Misstates ID’s scientific arguments, implying ID denies natural selection can do anything, and then sets up a straw man test of ID which effectively says that if natural selection can do anything, then ID is falsified.
- Misunderstands ID as a purely negative argument against evolution where he mistakenly believes “The main ID view is that some features of life are too complex to be the result of evolution, thus indicating that they were ‘designed.'”
- Misunderstands ID’s theological implications, setting up a false dichotomy by wrongly implying that ID denies God can use material “natural” processes.
- Offers two long-rebutted empirical examples which purportedly back his claim that natural selection can produce high levels of complex and specified information (CSI). In both cases, ID proponents have extensively discussed and rebutted these specific examples for years. Though Venema does not mention these rebuttals, ID proponents have observed the examples Venema raises likely entail “loss of function” changes, and do not show an increase in complex and specified information. To be more specific:
- Venema’s first example of how natural selection can allegedly increase biological information cites Richard Lenski’s Long Term Evolution Experiments (“LTEE”) with E. coli. According to Venema, “One of the defining features of E. Coli is that it is unable to use citrate as a food source,” but after a series of mutations in the LTEE, “bacteria that use citrate dominate the population.” Venema claims these experiments show “Complex, specified information can indeed arise through natural mechanisms.” But Venema fails to recognize that ID’s leading biochemist, Michael Behe, has published an extensive critique regarding this experiment, including lengthy commentary in a peer-reviewed paper Behe published in Quarterly Review of Biology (QRB) in 2010, as well as critiques in 2008 when the citrate claims were first published. As Behe explains in both rebuttals, normal E. coli have the machinery to uptake and metabolize citrate, and thus Venema’s unqualified claims that they evolved the ability to “use citrate as a food source” are overstated. Moreover, in his QRB article, Behe points out that the ability of E. coli to uptake citrate under oxic conditions in the LTEE was not a new finding, and likely resulted from loss-of-function mutations that did not increase CSI. Oddly, Venema focuses on attacking Stephen Meyer’s arguments which are not even rebutted by the findings of the LTEE, making no mention of Behe’s extensive responses or these important qualifications to his claims about this experiment.
- Venema also cites the research of University of Oregon biochemist Joe Thornton, claiming it shows natural selection and random mutation can produce “CSI on steroids.” Again, Venema fails to note that when Thornton’s research was first published in 2006, multiple leading ID proponents (including Michael Behe, Paul Nelson, and Stephen Meyer) wrote responses, pointing out that the research merely showed that a couple mutations could cause an allegedly ancestral protein to lose function. In this case too, Venema ignores Michael Behe’s extensive responses to his evidence — responses that stated: “The bottom line of the study is this: the authors started with a protein which already had the ability to strongly interact with three kinds of steroid hormones (aldosterone, cortisol, and ‘DOC’ [11-deoxycorticosterone]). After introducing several simple mutations the protein interacted much more weakly with all of those steroids. In other words, a pre-existing ability was decreased. That’s it! The fact that this extremely modest and substantially irrelevant study is ballyhooed with press releases, a commentary in Science by Christoph Adami, and forthcoming stories in the mainstream media, demonstrates the great anxiety some folks feel about intelligent design.”
- Venema’s latter posts in the series discuss evidence that could count as weak, or circumstantial, evidence for common descent — evidence such as high levels of human / ape genetic similarities. At most, however, this evidence shows circumstantial evidence for common ancestry. It says nothing about the information-generative abilities of random mutation and natural selection. Venema would have done well to heed Behe’s advice in The Edge of Evolution that “modern Darwinists point to evidence of common descent and erroneously assume it to be evidence of the power of random mutation.” In fact, if we factor into the analysis the possibility of common design of functional genetic programs, Venema’s evidence doesn’t even strongly point to common descent. But Venema ignores the possibility of common design.
- In sum, Venema’s series, “Evolution and the Origin of Biological Information,” badly misstates the nature of the theory of intelligent design, and the arguments of specific ID proponents, and fails to note the many rebuttals which ID proponents have written to his primary examples purporting to show how Darwinian evolution can increase CSI.
Again, I want to reiterate that my purpose here is to help bring clarity to how we test intelligent design and to show what ID proponents have said about these examples which Venema claims show Darwinian causes increasing biological information. And let me again say that although Venema makes some mistakes, I have no intent to attack him personally during this series. I have no reason whatsoever to believe that Venema is anything but a highly competent and intelligent professional biologist. But Dr. Venema’s mistakes and misunderstandings are common ones among ID critics. I hope this series of responses will help readers — including critics — better understand what intelligent design claims.
Section 2: Why Did One Theistic Evolutionist Part Ways with BioLogos?
In this section, we:
- Explain why natural selection was irrelevant to Stephen Meyer’s discussions of the origin of life
- Explain that neither Meyer nor ID deny that natural selection operates
- See that when testing whether unguided mechanisms can produce new genetic information, it’s important to understand which causes could have been at work
A couple months ago, self-described theistic evolutionist Jon Garvey became disillusioned with BioLogos’s tone and approach. Specifically, the British physician and blogger was concerned about cited BioLogos’s treatment of Stephen Meyer and his award–winning book Signature in the Cell. In explaining his reasons for leaving the BioLogos camp, Dr. Garvey wrote:
What struck me in all this was that every single contribution contained at least some degree of ad hominem attack, and most included dire warnings about the damage the book threatened to science, religion, society or all three. That, combined with the protests of many that the BioLogos articles were misrepresenting Meyer’s arguments, made a good case for assessing it carefully, my reading informed by 18 months of confutation rather than vice versa.
Biologist Dennis Venema was one of the authors who responded to Signature in the Cell on the BioLogos website. In his series on “Evolution and the Origin of Biological Information,” Dr. Venema quotes a passage from Signature in the Cell that refers to information and the “origin of DNA.” Meyer is clearly talking about the birth of information at the origin of life, not during the subsequent diversification of life by Darwinian or other processes. Yet Venema’s entire series deals with how Darwinian processes can purportedly create new information. Framed as a response to Meyer, it really isn’t that at all. The former BioLogos supporter critiqued Venema’s response as follows:
A later response was Dennis Venema’s five-part series, “Evolution and the Origin of Biological Information.” Not only the title, but the introduction, made it clear that this was a response to Meyer. But as several posters pointed out, whatever its merits the first article was about claimed examples of information-gain in current evolution. It was pointed out that SITC is actually about the Origin of Life, and hopes were expressed that Venema would cover this later in the series. He never did, basing his whole critique on an appendix about predictions that ID might make in the future. In this appendix Meyer not only stresses that his book is only concerned with OoL, but that many ID supporters believe that normal evolutionary processes can account for all subsequent increases in information, though he personally doubts this. In his own comments, Venema cannot resist the temptation to describe what he calls his “Behe moment,” in which he realised that Meyer lacks even an elementary grasp of basic biology (a neat way of dismissing two writers in one go by ad hominem attacks).
What exactly did Venema say that so badly misrepresented Meyer’s thesis? Well, here’s one example from Venema’s first post in his series. He writes:
When I reviewed Signature for the American Scientific Affiliation journal Perspectives on Science and Christian Faith (PSCF) what struck me, repeatedly, was that Meyer made no mention of the evidence for natural selection as a mechanism to increase biological information.
Venema further states: “Meyer ignores the possibility of natural mechanisms that allow ‘information’ to accumulate in an additive fashion … Natural selection acting on a population of imperfectly replicating variants is exactly this sort of mechanism.”
Stephen Meyer has a compelling rebuttal to Dr. Venema that will be published shortly in a forthcoming issue of PSCF. Until it is published, however, let’s begin with some analysis and evaluation of Venema’s claims: Did Meyer really “ignore the possibility” of natural selection and make “no mention” of it?
No, not at all.
Rather, Meyer observes that since the subject of Signature in the Cell is how information arose in the first life, natural selection is not relevant to his discussion. Natural selection presupposes replication, but prior to the first life there was no replication, and thus natural selection could not have been at work.
Nonetheless, it’s not the case that Meyer makes “no mention” of natural selection. In fact, there are over 45 pages in the index of Signature in the Cell which discuss natural selection. In one of those passages, Meyer explains why natural selection can’t explain how information arose in the first life:
[M]any scientists recognized that Oparin’s concept of prebiotic natural selection begged the question. Natural selection occurs only in organisms capable of reproducing or replicating themselves. Yet, in all extant cells, self-replication depends on functional and, therefore, sequence-specific DNA and protein molecules. As theoretical biologist Howard Pattee explains, “There is no evidence that hereditary evolution [natural selection] occurs except in cells which already have … the DNA, the replicating and translating enzymes, and all the control systems and structures necessary to reproduce themselves.” But this fact of molecular biology posed an obvious difficulty for Oparin’s theory of prebiotic natural selection. In order to explain the origin of specified information in DNA, Oparin invoked a process that depends on preexisting sequence-specific (i.e. information-rich) DNA molecules. Yet the origin of these molecules is precisely what his theory needed to explain. As Christian de Duve explains, theories of prebiotic natural selection necessarily fail because they “need information which implies they have to presuppose what is to be explained in the first place.”
(Stephen C. Meyer, Signature in the Cell: DNA and the Evidence for Intelligent Design, pp. 274-275 (HarperOne, 2009) (emphasis in original).)
So notwithstanding Venema’s claim, Meyer indeed makes “mention” of the evidence regarding natural selection. As is evident in the passage above, Meyer’s primary point is that whatever evidence there may (or may not) be that natural selection can produce information is not relevant to the origin of information in the first life.
Venema again misstates Meyer’s thesis when he accuses Meyer of “denial of random mutation and natural selection as an information generator.” But as we’ve seen, there is no “denial” of natural selection. Rather, Meyer cites leading experts who explain why natural selection is not relevant to the question explored in Meyer’s book.
Thus, a general point we can take away from this consideration of Venema’s critique is that when testing whether unguided mechanisms can produce new genetic information, it’s important to understand which causes could be at work. Venema’s arguments focus on the origin of information via Darwinian processes — after the origin of life. The arguments he makes, while missing the point of Meyer’s book, are relevant to many other ID claims. They are, for that reason, worth investigating.
Section 3: What Is a Proper Test of Intelligent Design?
In this section, we:
- Explain why ID is not a negative argument or “anti-evolution”; ID does not deny that random mutation and natural selection occur—it simply claims that there is a limit to what they can accomplish
- Discuss research conducted by ID proponents to determine the information generative abilities of ID vs. Darwinian mechanisms
- Understand why finding that some structures are within the ‘edge of evolution’ doesn’t mean that all are
- Distinguish between the wrong questions (e.g. “Can Darwinian evolution do anything?”) and the right questions (e.g. “Can Darwinian evolution do virtually everything, as proponents of naturalism often claim?”)
The very first line of Dennis Venema’s first post in his “Evolution and the Origin of Biological Information” series states: “One prominent antievolutionary argument put forward by the Intelligent Design Movement (IDM) is that significant amounts of biological information cannot be created through evolutionary mechanisms — processes such as random mutation and natural selection.” (emphasis added)
While Dr. Venema accurately described this common intelligent design (ID) argument, it’s noteworthy that he chooses to use the label “antievolutionary” to describe ID. That is, of course, a pejorative term favored by the Darwin lobby and its semi-official headquarters, the National Center for Science Education.
In another recent venue, Venema misdefines ID as a purely negative argument against “evolution,” stating: “The main ID view is that some features of life are too complex to be the result of evolution, thus indicating that they were ‘designed.'”
Here, Venema’s definition of ID is wrong on two counts: First, ID is not merely a negative argument against “evolution,” and second, ID does not necessarily challenge “evolution,” depending on how one defines evolution.
If we define evolution as “change over time,” “small-scale change,” or “common descent,” then ID certainly does not challenge evolution and is not “antievolution.”
But we already knew Venema has a misguided view of ID. In the previous section, we saw how Venema misstated Stephen Meyer’s basic thesis in Signature in the Cell as being a “denial of random mutation and natural selection” as a mechanism that can change the information in DNA.
Unfortunately, these misunderstandings lead Venema to set up an inaccurate method of testing of ID:
The issue is that Meyer’s case is open to refutation by counterexample, and even one counterexample would suffice. If any natural mechanism can be shown to produce “functional, information-rich genes and proteins,” then intelligent design is no longer the best explanation for the origin of information we observe in DNA, by Meyer’s own stated criteria. His entire (500+ page) argument would simply unravel.
The basic problem with Venema’s test is this: Intelligent design is not “antievolution” and has never stated that neo-Darwinian processes cannot do anything. That neo-Darwinian processes or other natural mechanisms can do some things is a true but trivial assertion as far as ID is concerned. In fact, in his book The Edge of Evolution, Michael Behe readily agrees that neo-Darwinian evolution can effect some changes in populations of organisms. ID does not deny that random mutation and natural selection are at work—it simply claims, as Michael Behe argues, that there is a limit to what they can accomplish.
Behe has further written elsewhere: “if only one mutation is needed to confer some ability, then Darwinian evolution has little problem finding it.” The question is not “Can Darwinian evolution do anything?” but rather “Can Darwinian evolution do virtually everything, as proponents of naturalism often claim?” ID proponents want to avoid presupposing answers, and instead want to follow the evidence wherever it leads. Thus, ID might frame the question like this: “What can neo-Darwinian processes accomplish, and what is best explained by intelligent causes?”***
Darwin himself correctly defined the outer boundary of the causal abilities of natural selection. He wrote that structures must evolve by “numerous, successive slight modifications.” In The Edge of Evolution, Behe postulates a “two mutation rule” where features that require two or more mutations before providing some functional advantage are unlikely to arise by random mutation and natural selection. Research is confirming Behe’s thesis.
In their 2004 peer-reviewed paper in the journal Protein Science, Behe and physicist David Snoke simulated the Darwinian evolution of protein-protein interactions that required multiple amino acids. They found that for eukaryotic organisms, evolving a simple protein-protein interaction involving two or more mutations might require more probabilistic resources (i.e., population sizes and numbers of generations) than would be generally available. 
In 2008, Behe and Snoke’s would-be critics tried to refute them in the journal Genetics, but found that to obtain only two specific mutations via Darwinian evolution “for humans with a much smaller effective population size, this type of change would take > 100 million years.” The critics admitted this was “very unlikely to occur on a reasonable timescale.” 
In 2010, Doug Axe published another peer-reviewed research paper which seemed to confirm Behe and Snoke’s results. He presented calculations modeling the Darwinian evolution of bacteria including a structure which required multiple mutations to yield any benefit. Axe’s model made exceedingly generous assumptions in favor of the Darwinian model. He assumed the existence of a huge population of asexually reproducing bacteria that could replicate quickly — perhaps nearly 3 times per day — over the course of billions of years. Despite the fact that bacteria have some of the highest known mutation rates, even here molecular adaptations requiring more than six mutations to function would not arise in the history of the earth. 
In 2010, research published by molecular biologist Ann Gauger of the Biologic Institute, Ralph Seelke at the University of Wisconsin-Superior, and two other biologists provided empirical backing to the claims of Axe and Behe. Their team started by breaking a gene in the bacterium E. coli required for synthesizing the amino acid tryptophan. When the bacteria’s genome was broken in just one place, random mutations were capable of “fixing” the gene. But when two mutations were required to restore function, Darwinian evolution could not do the job. 
These results suggest that on a reasonable timescale, there is too much complex and specified information in many proteins and enzymes to be generated by Darwinian processes. The reason, as Axe’s 2000 and 2004 papers in Journal of Molecular Biology suggest, is that functional amino acid sequences are very rare. 
Drs. Axe, Gauger, and Seelke are by no means the only scientists to observe the rarity of functional amino acid sequences. A leading college-level biology textbook states that “even a slight change in primary structure can affect a protein’s conformation and ability to function.”  Likewise, evolutionary biologist David S. Goodsell writes:
[O]nly a small fraction of the possible combinations of amino acids will fold spontaneously into a stable structure. If you make a protein with a random sequence of amino acids, chances are that it will only form a gooey tangle when placed in water. 
Goodsell goes on to assert that “cells have perfected the sequences of amino acids over many years of evolutionary selection.” But if functional protein sequences are rare, then natural selection will be unable to take proteins from one functional sequence to the next without getting stuck at some maladaptive or non-beneficial stage.
So when we test a particular protein to assess its origin, a very important question is: Is there a step-wise Darwinian pathway by which new genes and proteins can evolve? This mirrors Darwin’s observation that, under his model, evolution requires that structures evolve by “numerous successive slight modifications.”
Venema’s hope that perhaps we can observe one gene or protein evolving by a stepwise Darwinian pathway does not imply that all genes or proteins are amenable to stepwise Darwinian evolution via numerous successive slight modifications. Some genes and proteins might be within what Behe calls the “edge of evolution,” but some might be beyond it.
Venema seeks to refute ID wholesale and prove neo-Darwinian evolution through what he calls “one counterexample.” But this reflects a fundamental misunderstanding of ID. Research from pro-ID scientists is beginning to understand and elaborate exactly where the “edge of evolution” lies, and the observation that one gene or protein might be within the “edge” does not imply that all are.
In the next section, we’ll assess whether the empirical examples cited by Venema are actually within the “edge of evolution” and if they shows, as he suggests, that natural selection and random mutation can produce “functional, information-rich genes and proteins.”
Section 4: The False Dichotomy Between Intelligent Design and Natural Causes
In this section, we:
- Explain why ID doesn’t say God can’t use natural causes
- Correct Dr. Venema’s misunderstanding that ID creates a “dichotomy” that disallows God from using natural causes
- Understand why theistic naturalism’s assumption that God must use natural causes hinders inquiry
- Investigate why ID adopts the motto “let’s follow the evidence where it leads”
In Section 2, we saw that a self-described theistic evolutionist had left the BioLogos camp because he was concerned about the way BioLogos writers treat Darwin-critics:
I have got used to the vituperative and often incoherent level of discussion about faith and evolution in the last year or so. Generally speaking, as one would now expect, Gnus attempting to savage anything they can identify as a theist are the greatest offenders. But on BioLogos, a frighteningly similar kind of abuse, if usually expressed with more gentility, is directed not back at non-theists, nor even YECs, but at ID sympathisers….I think I can draw two tentative conclusions about the reasons for this degree of passion, which is clearly far more than an opinion that ID arguments are wrong. In my opinion, although BioLogos is quite a diverse forum, its “ruling spirit” is fundamentally committed to (a) methodological naturalism and (b) theological naturalism.
How does the “theological naturalism” of BioLogos influence its perspective on intelligent design (ID)? Unfortunately, for one, it seems to lead some ID-critics to wrongly think that ID denies that God can use natural causes.
For example, in his series on “Evolution and the Origin of Biological Information,” Dennis Venema sets up a false dichotomy between intelligent design (ID) and natural causes, wrongly claiming ID that creates a “‘natural versus God’ dichotomy” or alternatively claiming that ID tries to “eliminate the possibility of divine action” when “we use science to understand natural cause and effect.” Venema also states:
[D]escribing how specified information can arise through natural means does not in any way imply God’s absence from the process. After all, natural processes are equally a manifestation of God’s activity as what one would call supernatural events. So-called “natural” laws are what Christians understand to be a description of the ongoing, regular and repeatable activity of God. As such, the dichotomy presented in ID writings of “naturalism” versus theism is a false one: is not God the Author of nature, after all?
While defending naturalism, Venema has badly misstated the claims of ID: there is no false dichotomy in intelligent design that says God is never allowed to use natural causes. The only party who’s setting up a false dichotomy here is Dennis Venema, in suggesting that if one accepts ID then God is no longer allowed to use “natural laws
Venema seeks to paint ID as bad theology which somehow denies that God is the author of all nature when God uses secondary material or “natural” causes. ID is a scientific theory and doesn’t make such theological claims. Thus, as a science, ID never claims that if we observe the “ongoing, regular and repeatable activity” of “natural laws” then somehow God is absent from the process.
ID proponents who believe in God never deny that God can use secondary material “natural” causes to achieve his will. In those instances, ID would simply say that material causes are the best explanation. ID does not “eliminate the possibility of divine action” when “we use science to understand natural cause and effect.” To wit: ID proponents have often inferred design from the fine-tuning of the laws that govern the universe and make it friendly for life. Indeed, this is an area where BioLogos supposedly agrees with intelligent design. In any event, Venema’s description of ID is backwards: in contexts of physics and cosmology, the actions of natural laws themselves can trigger a design inference.
Remember, ID is a cautious scientific theory and not a theological doctrine. When ID theorists look for scientifically detectable design at the biological level, they often treat natural causes as background. So the biological design that’s detected normally involves features that (1) go well beyond the capacities of natural causes, and (2) exhibit telltale signs of intelligent agency (such as being the product of foresight). On the other hand, when ID infers a natural cause, pro-ID theists would simply say God used a natural cause, and would not say that God is somehow “absent.”
All theists who support ID affirm that God is behind, in some sense, every event. “Natural cause” never means (for theists anyway) “not caused by God.” I’m not aware of any ID theorist who is also a theist who has ever claimed otherwise.
This leads us to the question, why does ID critique theistic naturalism, and how does ID contrast with theistic evolution?
Theistic naturalism isn’t merely the view that God at times (or even most of the time) works through natural causes. Rather, it is the view that assumes that God must only use natural causes and is never allowed to work in other ways that might break the “ongoing, regular and repeatable activity” of “natural laws.”
ID rejects such assumption-based views. ID is entirely compatible with the view that God at times (or even most of the time) works through natural causes. But ID isn’t precommitted to answers about how God must have acted, and leaves open the possibility that sometimes God doesn’t use “natural” causes. ID simply wants to follow the evidence where it leads.
Thus, theistic naturalism is the wholesale assumption that if God exists, He must always use secondary material causes, and is never allowed to act in nature in a scientifically detectable way. The reason ID proponents critique naturalism is because it tends to presuppose materialistic answers to all questions about how life arose and diversified.
There are thus two potential extreme positions in this debate: (A) Everything is detectably designed and God never uses natural causes, or (B) Nothing is detectably designed and God always uses natural causes.
Ironically, though ID critics (wrongly) accuse ID proponents of adopting extreme position (A), it is ID-critics themselves, including many theistic evolutionist proponents of theistic naturalism, who seem to adopt extreme position (B). This makes for bad science because it presupposes the scientific answers, and bad theology because it tries to dictate to God what He ought to do.
In contrast, ID rejects both extreme positions, and uses this motto: let’s not presuppose answers, but let’s follow the evidence where it leads.
Section 5: Richard Lenski’s Long-Term Evolution Experiments with E. coli and the Origin of New Biological Information
In this section, we:
- Understand why Venema’s citation of Lenski’s “Long Term Evolution Experiments” do not demonstrate that “Complex, specified information can indeed arise through natural mechanisms”
- Review Michael Behe’s 2010 paper in Quarterly Review of Biology which investigated Lenski’s research and found that “mutations were decreasing or eliminating the protein’s function”
- Investigate why Lenski’s E. coli bacteria that evolved the ability to uptake citrate under oxic conditions didn’t evolve anything new and likely experienced loss-of-molecular function
Some critics of intelligent design (ID) misunderstand ID as a denial of natural causes. For example, we have recently seen how theistic evolutionist Dennis Venema wrongly suggests that, in both a scientific and theological sense, ID denies natural causes. Venema imports this misunderstanding into his proposed methods of testing ID, suggesting that if we find natural causes doing anything, then ID is refuted.
Venema writes: “any natural mechanism that can be shown to produce information would render [Stephen Meyer’s] argument that information only arises from intelligent sources null and void.”
Dennis Venema’s argument collapses into this: ‘if Darwinian evolution can do anything, then ID is wrong.’ But this is not how we test ID, for ID readily allows that natural selection and random mutation can effect some changes in populations. The right question is not ‘Can natural selection do anything?’ but rather ‘Can natural selection do everything?’
With this in mind, let’s analyze Dr. Venema’s discussion of Richard Lenski’s Long Term Evolution Experiments (“LTEE”) with E. coli.
Where’s the Behe?
Before discussing the LTEE, it’s important to note that from the beginning of his series for BioLogos on evolution and the origin of information, Venema didn’t just purport to critique Stephen Meyer’s arguments in Signature in the Cell. Rather he referred to rebutting the entire “Intelligent Design Movement” or what he called (following Judge Jones?) the “IDM.”
But if Venema is going to critique the entire “IDM” using Richard Lenski’s “Long Term Evolution Experiments,” then Venema should discuss the most relevant literature of the “IDM” that discusses those experiments. He doesn’t do that.
In Venema’s discussion of the LTEE, there is no mention of a 2010 peer-reviewed scientific paper written by the most prominent biochemist in the “IDM,” published in a prominent biology journal, extensively critiquing Lenski’s LTEE. Venema fails to note and discuss Michael Behe’s December 2010 paper in Quarterly Review of Biology (QRB), which extensively discusses and critiques Lenski’s Long Term Evolution Experiments. Instead, Venema critiques the writings of Stephen Meyer, who hasn’t commented on Lenski’s LTEE because they weren’t relevant to his arguments in Signature in the Cell about the origin of life.
By misrepresenting Meyer’s thesis as being refuted by evidence of the power of natural selection, Venema creates a straw man. Meanwhile he ignores the substantive critiques by leading ID proponents of the very evidence he raises.
Vague Discussions vs. Precise Discussions of Lenski’s LTEE
As an initial salvo regarding Lenski’s LTEE, Venema writes:
[T]here were many possible genetic states of higher fitness available to the original strain, and random mutation and natural selection had explored several paths, all leading to a higher amount of “specified information” — information that specifies increased reproduction and survival in the original environment. All this was by demonstrably natural mechanisms, with a complete history of the relevant mutations, the relative advantages they conferred, and the dynamics of how those variants spread through a population. The LTEE is at once a very simple experiment, and an incredibly detailed window into the inner workings of evolution.
But what exactly was the “specified information” that increased? What new function was gained? Where did natural selection and random mutation produce functional, information-rich genes and proteins? Venema doesn’t say what new functions arose, what changed, or what information was gained. His claim that natural selection produced “specified information” is vague.
By contrast, in critiquing claims that the LTEE has produced something new, Behe’s 2010 Quarterly Review of Biology paper was anything but vague:
By examining the DNA sequence of the E. coli in the neighborhood surrounding the IS [insertion sequence] elements, the investigators saw that several genes involved in central metabolism were knocked out, as well as some cell wall synthesis genes and several others. In subsequent work, Cooper et al. (2001) discovered that twelve of twelve cell lines showed adaptive IS-mediated deletions of their rbs operon, which is involved in making the sugar ribose. Thus, the adaptive mutations that were initially tracked down all involved loss-of-FCT.
Several years later, when the cultures had surpassed their 20,000th generation, Lenski’s group at Michigan State brought more advanced techniques to bear on the problem of identifying the molecular changes underlying the adaptation of the E. coli cultures. Using DNA expression profiles, they were able to reliably track down changes in the expression of 1300 genes of the bacterium, and determined that 59 genes had changed their expression levels from the ancestor, 47 of which were expressed at lower levels (Cooper et al. 2003). The authors stated that “The expression levels of many of these 59 genes are known to be regulated by specific effectors including guanosine tetraphosphate (ppGpp) and cAMP-cAMP receptor protein (CRP)” (Cooper et al. 2003:1074). They also noted that the cellular concentration of ppGpp is controlled by several genes including spoT. After sequencing, they discovered a nonsynonymous point mutation in the spoT gene. When the researchers examined ten other populations that had evolved under the same conditions for 20,000 generations, they found that seven others also had fixed nonsynonymous point mutations in spoT, but with different substitutions than the first one that had been identified, thus suggesting that the mutations were decreasing the protein’s activity.
The group then decided to concentrate on candidate genes suggested by the physiological adaptations that the cells had made over 20,000 generations. One such adaptation was a change in supercoiling density; therefore, genes affecting DNA topology were investigated (Crozat et al. 2005). Two of these genes, topA and fis, had sustained point mutations. In the case of topA, the mutation coded an amino acid substitution, whereas, with fis, a transversion had occurred at the fourth nucleotide before the starting ATG codon. The topA mutation decreased the activity of the enzyme, while the fis mutation decreased the amount of fis gene product produced.
(Michael J. Behe, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” Quarterly Review of Biology, Vol. 85(4) (December, 2010).)
If you weren’t following all the technical language, here’s what’s going on: For the first 20,000 generations of Lenski’s LTEE, very little happened. There were a few molecular adaptations observed, yet whenever we understood their molecular basis, they involved the knocking out of genes, or decreasing protein activity — in essence, a decrease in specificity. Behe summarizes:
The fact that multiple point mutations in each gene could serve an adaptive role — and that disruption by IS insertion was beneficial — suggests that the point mutations were decreasing or eliminating the protein’s function.
(Michael J. Behe, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” Quarterly Review of Biology, Vol. 85(4) (December, 2010) (emphasis added).)
Unlike Venema’s discussion, Behe’s is precise, giving multiple examples and detailed descriptions of the types of changes observed in Lenski’s LTEE. And Behe found that the types of changes taking place in the E. coli tended to decrease or eliminate protein function.
Before getting into a discussion of the citrate-using strain of E. coli, Behe closes with another specific example that involved decreasing gene activity in Lenski’s LTEE:
In an investigation of global protein profiles of the evolved E. coli, Lenski’s group discovered that the MalT protein of the maltose operon had suffered mutations in 8 out of 12 strains (Pelosi et al. 2006). Several mutations were small deletions while others were point mutations, thus suggesting that decreasing the activity of the MalT protein was adaptive in minimal glucose media.
Looking at Table 3 of Behe’s QRB paper, not a single example of an adaptive mutation in Lenski’s LTEE entailed a gain of a new molecular function. In fact, over the course of his entire paper, Behe goes further and explains that most of our known examples of molecular adaptations in bacteria entail “loss-of-function” mutations. Somehow, Venema doesn’t discuss any of these findings.
E coli. Could Uptake and Metabolize Citrate Before Lenski’s LTEE
Later, when referring to a different stage of the LTEE, Venema claims that a new function did arise in Lenski’s E. coli bacteria during the experiments: the ability of E. coli to metabolize citrate. Venema claims that “One of the defining features of E. Coli is that it is unable to use citrate as a food source,” but after a series of mutations “bacteria that use citrate dominate the population.” According to Venema, these experiments show “Complex, specified information can indeed arise through natural mechanisms.”
Yet Venema leaves out important details, creating an inaccurate impression. As we’ll discuss below, normal E. coli already have machinery to uptake and metabolize citrate, so the general fact that Lenski’s bacteria showed this ability is really quite unremarkable.
Unfortunately, Venema’s readers on the BioLogos will never hear that. They also won’t learn that Michael Behe has written extensively about Lenski’s research, showing that the machinery for E. coli to uptake and metabolize citrate already existed in these bacteria. This isn’t an entirely new biochemical pathway. Venema fails to note that normal E. coli already have the ability to uptake and metabolize citrate. They just can’t normally uptake it under oxic conditions; Lenski’s bacteria evolved the ability to uptake it under oxic conditions used in the experiment. Then the E. coli used their normal metabolic pathways to use citrate as a food source. Behe made this point while commenting on these claims soon after they were first published in 2008:
Now, wild E. coli already has a number of enzymes that normally use citrate and can digest it (it’s not some exotic chemical the bacterium has never seen before). However, the wild bacterium lacks an enzyme called a “citrate permease” which can transport citrate from outside the cell through the cell’s membrane into its interior. So all the bacterium needed to do to use citrate was to find a way to get it into the cell. The rest of the machinery for its metabolism was already there. As Lenski put it, “The only known barrier to aerobic growth on citrate is its inability to transport citrate under oxic conditions.”
(Michael Behe, Amazon Blog, “Multiple Mutations Needed for E. Coli” (June 6, 2008).)
Likewise, Behe’s recent 2010 paper in Quarterly Review of Biology provided an extensive critique of claims that Lenski’s LTEE showed the evolution of a new pathway that could metabolize citrate. Venema doesn’t cite or mention Behe’s QRB paper, but it too explains that E. coli already had the ability to metabolize citrate. Behe explains:
Recently, Lenski’s group reported the isolation of a mutant E. coli that had evolved a Cit+ phenotype. That is, the strain could grow under aerobic conditions in a culture of citrate (Blount et al. 2008). Wild E. coli cannot grow under such conditions, as it lacks a citrate permease to import the metabolite under oxic conditions. (It should be noted that, once inside the cell, however, E. coli has the enzymatic capacity to metabolize citrate.) The phenotype, whose underlying molecular changes have not yet been reported, conferred an enormous growth advantage because the culture media contained excess citrate but only limited glucose, which the ancestral bacteria metabolized.
(Michael J. Behe, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” Quarterly Review of Biology, Vol. 85(4) (December, 2010).)
Thus, Behe explains that the precise genetic mechanisms that allowed E. coli to uptake citrate under oxic conditions are not known. But Behe goes further and points out that the citrate-metabolizing E. coli strains really aren’t anything new, and that previous investigations suggest that the ability of the E. coli to uptake citrate under oxic conditions might result from molecular loss-of-function:
As Blount et al. (2008) discussed, several other laboratories had, in the past, also identified mutant E. coli strains with such a phenotype. In one such case, the underlying mutation was not identified (Hall 1982); however, in another case, high-level constitutive expression on a multicopy plasmid of a citrate transporter gene, citT, which normally transports citrate in the absence of oxygen, was responsible for eliciting the phenotype (Pos et al. 1998). If the phenotype of the Lenski Cit+ strain is caused by the loss of the activity of a normal genetic regulatory element, such as a repressor binding site or other FCT, it will, of course, be a loss-of-FCT mutation, despite its highly adaptive effects in the presence of citrate. If the phenotype is due to one or more mutations that result in, for example, the addition of a novel genetic regulatory element, gene-duplication with sequence divergence, or the gain of a new binding site, then it will be a noteworthy gain-of-FCT mutation.
(Michael J. Behe, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” Quarterly Review of Biology, Vol. 85(4) (December, 2010).)
Thus, previous research suggests that the adaptation which allowed these E. coli to uptake citrate under oxic conditions might be caused “by the loss of the activity of a normal genetic regulatory element.” Here’s what is likely going on here:
- Under normal conditions, E. coli can metabolize citrate; after all metabolizing citrate is an important step in the Krebs cycle, a pathway used by virtually all living organisms when creating energy.
- But under oxic conditions, E. coli lack the ability to transport citrate through the cell membrane into the cell. E. coli can do this under reducing conditions, but under oxic conditions E. coli can’t normally uptake citrate.
- If Lenski’s citrate-using E. coli are like previous E. coli which were discovered uptaking citrate under oxic conditions, then it seems likely that the bacteria underwent a mutation that knocked out the regulation mechanism of a citrate-transport gene, causing over-expression, allowing the E. coli to uptake citrate under oxic conditions.
In other words, the machinery for both transporting and metabolizing citrate was already present in these bacteria. But a series of knockout mutations broke the regulation of pre-existing citrate transport mechanisms, causing over-expression of a citrate transport gene, allowing citrate to be transported under both oxic and anaerobic conditions. If this is the case, then clearly this example of Darwinian “evolution” entails the loss of a molecular function, not the gain of a new one. And there was no wholesale acquisition of the ability to metabolize or, as Venema put it, “use” citrate.
In fact, as Behe notes, we don’t really yet understand the precise molecular mechanisms that caused these E. coli to be able to uptake citrate under oxic conditions. So as far as we can tell, these changes entailed the origin of no new functional genes or proteins but might have resulted from a broken regulatory mechanism. We have not seen that natural selection and random mutation can produce functional, information-rich genes and proteins, and Venema is wrong to suggest otherwise.
Contra Venema, this example hardly shows the Darwinian evolution of a “new function,” especially since E. coli already had the ability to uptake and metabolize citrate. Venema claims that CSI has arisen, but if we don’t even know what mechanisms were involved in this change, how does he know that it is new CSI?
What do Lenski’s LTEE Really Tell Us?
In his QRB paper, Behe goes on to explain that to date, the known adaptations that have occurred in Lenski’s LTEE are either modification-of-function or loss-of-function changes:
The results of future work aside, so far, during the course of the longest, most open-ended, and most extensive laboratory investigation of bacterial evolution, a number of adaptive mutations have been identified that endow the bacterial strain with greater fitness compared to that of the ancestral strain in the particular growth medium. The goal of Lenski’s research was not to analyze adaptive mutations in terms of gain or loss of function, as is the focus here, but rather to address other longstanding evolutionary questions. Nonetheless, all of the mutations identified to date can readily be classified as either modification-of-function or loss-of-FCT.
(Michael J. Behe, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” Quarterly Review of Biology, Vol. 85(4) (December, 2010).)
Behe’s paper further suggests that when there are several kinds of potential adaptive mutations that might occur, loss or modification of function adaptations will be far more common than gain-of-function adaptations. He concludes:
Even if there were several possible pathways by which to construct a gain-of-FCT mutation, or several possible kinds of adaptive gain-of-FCT features, the rate of appearance of an adaptive mutation that would arise from the diminishment or elimination of the activity of a protein is expected to be 100-1000 times the rate of appearance of an adaptive mutation that requires specific changes to a gene.
(Michael J. Behe, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” Quarterly Review of Biology, Vol. 85(4) (December, 2010).)
The sort of loss-of-function examples seen in the LTEE will never show that natural selection can increase high CSI. To understand why, imagine the following hypothetical situation.
Consider an imaginary order of insects, the Evolutionoptera. Let’s say there are 1 million species of Evolutionoptera, but ecologists find that the extinction rate among Evolutionoptera is 1000 species per millennium. The speciation rate (the rate at which new species arise) during the same period is 1 new species per 1000 years. At these rates, every thousand years 1000 species of Evolutionoptera will die off, while one new species will develop—a net loss of 999 species. If these processes continue, in 1,000,001 years there will be no species of Evolutionoptera left on earth.
If Behe is correct, then Darwinian evolution at the molecular level faces a similar problem. If, all other things being equal, a loss or modification of function adaptation is generally 100-1000 times more likely than gain of function adaptations, then eventually an evolving population might run out of molecular functions to lose or modify. Neo-Darwinian evolution cannot forever rely on examples of loss or modification-of-function mutations to explain molecular evolution. At some point, there must be a gain of function.
Vaguely Appealing to Vast Probablistic Resources Won’t Work
Venema closes his post on the LTEE by saying: “what the IDM claims is impossible, these ‘tiny and lowly’ organisms have simply been doing — and it only took 15 years in a single lab in Michigan. Imagine what could happen over 3,500,000,000 years over millions of square miles of the earth’s surface.”
But vague appeals to vast eons of time and huge population sizes are unconvincing. You just have to do the math. As David Abel reminds us:
Mere possibility is not an adequate basis for asserting scientific plausibility. A precisely defined universal bound is needed beyond which the assertion of plausibility, particularly in life-origin models, can be considered operationally falsified. But can something so seemingly relative and subjective as plausibility ever be quantified? Amazingly, the answer is, “Yes.” … One chance in 10200 is theoretically possible, but given maximum cosmic probabilistic resources, such a possibility is hardly plausible. With funding resources rapidly drying up, science needs a foundational principle by which to falsify a myriad of theoretical possibilities that are not worthy of serious scientific consideration and modeling.
(David L. Abel, “The Universal Plausibility Metric (UPM) & Principle (UPP),” Theoretical Biology and Medical Modelling, Vol. 6:27 (Dec. 3, 2009).)
In the case of E. coli and citrate, the bacteria already had the ability to uptake and metabolize citrate, and simply found a way to transport it under different conditions. It’s likely this occurred by overexpressing pre-existing transport mechanisms. Does this imply that anything and everything “could happen over 3,500,000,000 years over millions of square miles of the earth’s surface”? Well, ID proponents aren’t interested in making vague and ambiguous appeals to vast amounts of probabilistic resources. They want to test these questions, and follow the evidence where it leads.
As discussed here, ID proponents have asked just how long it takes to evolve traits that require multi-mutation features. A multi-mutation feature requires multiple mutations to be present before there is any advantage given to the organism. Doug Axe’s research makes assumptions very generously favoring Darwinian evolution. He assumed the existence of a huge population of asexually reproducing bacteria that could replicate quickly — perhaps nearly 3 times per day — over the course of billions of years. Yet even here, complex adaptations requiring up to six mutations with neutral intermediates can become fixed. Beyond that, things become implausible.
If only slightly maladaptive intermediate mutations are required for a complex adaptation, only a couple (at most two) mutations could be fixed. If highly maladaptive mutations are required, the trait will never appear. Axe discusses the implications of his work:
[T]he most significant implication comes not from how the two cases contrast but rather how they cohere — both showing severe limitations to complex adaptation. To appreciate this, consider the tremendous number of cells needed to achieve adaptations of such limited complexity. As a basis for calculation, we have assumed a bacterial population that maintained an effective size of 109 individuals through 103 generations each year for billions of years. This amounts to well over a billion trillion opportunities (in the form of individuals whose lines were not destined to expire imminently) for evolutionary experimentation. Yet what these enormous resources are expected to have accomplished, in terms of combined base changes, can be counted on the fingers.
(Douglas D. Axe, “The Limits of Complex Adaptation: An Analysis Based on a Simple Model of Structured Bacterial Populations,” BIO-Complexity, Vol. 2010(4):1-10.)
If Axe is correct then we cannot always assume, as Venema seems to do, that sufficient probabilistic resources exist to produce complex features we see in life.
Summarizing Venema’s Argument Regarding the LTEE
In short, Venema’s argument regarding the LTEE collapses into common misconceptions about ID, which go something like this:
- ID holds that Darwinian evolution cannot do anything.
- If Darwinian evolution can do something then it can do anything.
- Lenski’s experiments show Darwinian evolution can allow E. coli bacteria to evolve a “new function” of metabolizing citrate.
- Therefore ID is wrong, and given enough time, Darwinian evolution can do anything we “imagine.”
At each step in his argument, the facts and/or the logic is wrong:
- Regarding (1): In fact, ID does not hold that Darwinian evolution can’t do anything. Rather it claims that natural selection can do some things, but not everything. ID proponents readily acknowledge (as Behe has) that “if only one mutation is needed to confer some ability, then Darwinian evolution has little problem finding it.” The problem comes when multiple mutations are required to produce some new structure—- and as Axe’s research shows, this is where Darwinian evolution typically gets stuck.
- Regarding (2): Darwin-defenders have a long history of over-extrapolating from the data. ID is scientifically cautious and concludes that no one single experiment can show that Darwinian evolution can do everything we ask of it. A single experiment showing the ability of Darwinian evolution to do X simply shows the ability of Darwinian evolution to do X; it doesn’t necessarily show Darwinian evolution can do Y, Z, and A, B, and C, etc. ID says we need to test hypotheses carefully and not over-extrapolate from observed data.
- Regarding (3): In fact Lenski’s experiments did not show the Darwinian evolution of an entirely new function. E. coli bacteria already had the ability to uptake and metabolize citrate, and the experiments simply showed they evolved the ability to uptake it under oxic conditions. This very likely required the loss of a molecular function.
- Regarding (4) ID proponents do not think it is wise or scientifically accurate to vaguely invoke vast eons of time or vast population sizes to document the alleged power of Darwinian evolution. ID cautions that Darwinian evolutionists often assume that there are sufficiently vast probabilistic resources to accomplish any task imaginable, but that assumption might not be valid. Rather than simply assuming, Doug Axe’s research finds that adaptations requiring more than six neutral mutations, or two maladaptive mutations, to provide a functional advantage would not arise in the history of the earth.
Subsequent research by Axe and Ann Gauger suggests that it would not be uncommon for Darwinian evolution to face obstacles that exhaust the probabilistic boundaries as found by Axe’s research. In 2011, they published research in BIO-Complexity that found at least seven mutations (probably many more) would be necessary to convert one protein into a supposedly closely-related protein.
While Darwinians may (or may not) claim that this was a real evolutionary pathway, it’s the type of pathway that is often claimed to have been traversed by natural selection over the course of life’s history. The fact that this simple conversion required more mutations to produce a new function than would be allowed under Axe’s mathematical models shows that there may be real obstacles to the Darwinian evolution of new proteins. Venema’s citation of Lenski’s LTEE certainly does not show otherwise.
Section 6: Another Bogus Claim of “Novel Function Arising Through Mutation and Selection”
In this section, we:
- Understand why Dennis Venema’s citation of Joseph Thornton’s steroid research does do not demonstrate a “fascinating case of a novel function arising through mutation and selection”
- Review the multiple responses to Thornton’s research from leading ID proponents (all ignored by Venema) who found the changes were not information-rich, not necessarily produced by natural selection, entailed diminishment rather than gain of function, and well within the ‘edge of evolution’
- See that Venema undercuts his own claims by admitting, “Steroid hormones are a closely related molecules — it’s not too surprising that slightly different molecules fit into a related group of protein receptors”
In the case of Richard Lenski’s Long Term Evolution Experiments (LTEE) with E. Coli bacteria, we saw that Dennis Venema of BioLogos cited purported examples of natural selection increasing specified and complex information — but intelligent design (ID) proponents had long before critiqued these examples. For example, Lenski’s LTEE had been critiqued by Michael Behe when they first came out in 2008, and then later in Behe’s 2010 paper in Quarterly Review of Biology. Venema, however, discussed none of these critiques.
But Venema has a second empirical example he cites to supposedly show the Darwinian evolution of what he calls “CSI on Steroids.” Citing research co-published by University of Oregon biologist Joe Thornton in 2006, Venema calls this “a second fascinating case of a novel function arising through mutation and selection.” But here too, ID proponents had extensively critiqued the experiment when it was first published. And again, Venema failed to discuss or respond to any of these prior arguments from ID proponents. It’s hard to ignore responses from the ID camp to Thornton’s research since there are so many of them. These responses were all published back in 2006 when Thornton’s research was first published:
- Michael Behe on the Theory of Irreducible Complexity
- How to Explain Irreducible Complexity — A Lab Manual
- Paul Nelson on Debating the Controversy That Doesn’t Exist
- Bruce Chapman on the Science Stories that Fizzled (and the One that Might Have Been)
- CSC Director Stephen C. Meyer Responds to Research on Irreducible Complexity
- Casey Luskin: Science Plays Politics, but Implies Behe and Snoke (2004) Supports Irreducible Complexity and ID After All
Many of these responses will be discussed below.
Venema claims that Thornton’s research shows “a second fascinating case of a novel function arising through mutation and selection.” As we will see, if by “novel function” Venema means “diminishment of function,” then perhaps he is correct. As a brief and cursory summary of problems with the Thornton et al. research, consider the following points:
- The Thornton et al. research cited by Venema merely found that an alleged precursor enzyme could potentially perform two functions, and then supposedly lost the ability to perform one of those functions. At worst it shows loss-of-function through two mutations. At best, this is an example of small-scale change, which the research of ID proponents like Michael Behe readily concedes is possible. Because Thornton et al.‘s research only supported small-scale evolution, which ID proponents don’t question, Behe wrote in response: “This continues the venerable Darwinian tradition of making grandiose claims based on piddling results. There is nothing in the paper that an ID proponent would think was beyond random mutation and natural selection. In other words, it is a straw man.”
- Christoph Adami reviewed Thornton et al.‘s research in Science, claiming it refuted ID. The research was also puffed in the New York Times as addressing intelligent design after the authors issued a press release entitled “Evolution of ‘Irreducible Complexity’ Explained,” purporting to be a direct response to “[a]dvocates of Intelligent Design.” Whether they are right or wrong, this is amusing since we see ID-critics debating over the scientific controversy that they claim does not exist.
- The authors’ press release gave a retroactive confession of ignorance, admitting that “[h]ow natural selection can drive the evolution of tightly integrated molecular systems … has been an unsolved issue in evolutionary biology.” Yet in the New York Times article, Thornton commented that “There’s no scientific controversy over whether this system evolved. The question for scientists is how it evolved.” So before this study they didn’t know how it evolved, yet somehow they knew it did evolve. It sounds like they are assuming the truth of Darwinian theory rather than testing it.
- Before the paper was published, Thornton had stated on his website that his “goal is to illustrate how a complex, tightly integrated molecular system — one which appears to be “irreducibly complex” — evolved by Darwinian processes.” After ID-theorist Paul Nelson pointed out that this implied that Thornton saw irreducible complexity as a legitimate scientific challenge, the words “irreducibly complex” magically disappeared from Thornton’s website. The episode demonstrates that ID raises legitimate scientific challenges of interest to Darwinian evolutionary biologists, even as they sometimes deny that fact for political reasons.
- In sum, this study doesn’t show how Darwinian evolution scales Mount Improbable, as Dawkins has put it. It simply shows that neo-Darwinism can get you the last 10 yards up the mountain after you’ve already spent 10 hours hiking. It’s an exercise in what Behe called “making grandiose claims based on piddling results.”
But there’s much more to say in response to this research. Since much of the work responding to it has already been done, the best thing is simply to quote from some of these responses:
Response 1: Michael Behe’s comments:
The bottom line of the study is this: the authors started with a protein which already had the ability to strongly interact with three kinds of steroid hormones (aldosterone, cortisol, and “DOC” [11-deoxycorticosterone]). After introducing several simple mutations the protein interacted much more weakly with all of those steroids. In other words, a pre-existing ability was decreased.
That’s it! The fact that this extremely modest and substantially irrelevant study is ballyhooed with press releases, a commentary in Science by Christoph Adami, and forthcoming stories in the mainstream media, demonstrates the great anxiety some folks feel about intelligent design.
In the study the authors wished to see if two related modern proteins called the glucocorticoid (GR) receptor and mineralocorticoid receptor (MR) could be derived from a common ancestral protein. Using clever analysis the authors made a protein that they thought represented the ancestral protein. That protein binds several, structurally-similar hormones, as does modern MR. They then introduced two amino acid changes into the protein which are found in modern GR. The two changes caused the ancestral protein to bind the different kinds of hormones anywhere from ten- to a thousand-fold more weakly. That protein bound aldosterone about three-fold more weakly than cortisol. The authors note that modern GR (in tetrapods) also binds aldosterone more weakly than cortisol. So perhaps, the thinking goes, an ancestral gene that could bind both hormones duplicated in the past, one copy accumulated those two mutations to become the modern GR, and the other copy became modern MR.
Here are number of comments in response:
- This continues the venerable Darwinian tradition of making grandiose claims based on piddling results. There is nothing in the paper that an ID proponent would think was beyond random mutation and natural selection. In other words, it is a straw man.
- The authors (including Christoph Adami in his commentary) are conveniently defining “irreducible complexity” way, way down. I certainly would not classify their system as anywhere near IC. The IC systems I discussed in Darwin’s Black Box contain multiple, active protein factors. Their “system”, on the other hand, consists of just a single protein and its ligand. Although in nature the receptor and ligand are part of a larger system that does have a biological function, the piece of that larger system they pick out does not do anything by itself. In other words, the isolated components they work on are not irreducibly complex.
- In the experiment just two amino acid residues were changed! No new components were added, no old components were taken away.
- Nothing new was produced in the experiment; rather, the pre-existing ability of the protein to bind several molecules was simply weakened. The workers begin their experiments with a protein that can strongly bind several, structurally-very-similar steroids, and they end with a protein that at best binds some of the steroids ten-fold more weakly. (Figure 4C)
- Such results are not different from the development of antibiotic resistance, where single amino acid changes can cause the binding of a toxin to a particular protein to decrease (for example, warfarin resistance in rats, and resistance to various AIDS drugs). Intelligent design proponents happily agree that such tiny changes can be accomplished by random mutation and natural selection.
- In the “least promising” intermediate (L111Q) the protein has essentially lost its ability to bind any steroid. In the “most promising” intermediate protein (the one that has just the S106P alteration) the protein has lost about 99% of its ability to bind DOC and cortisol, and lost about 99.9% of its ability to bind aldosterone. (Figure 4C)
- Although the authors imply (and Adami claims directly) that the mutated protein is specific for cortisol, in fact it also binds aldosterone with about half of the affinity. (Compare the red and green curves in the lower right hand graph of Figure 4C.) What’s more, there actually is a much larger difference (about thirty-fold) in binding affinity for aldosterone and cortisol with the beginning, ancestral protein than for the final, mutated protein (about two-fold). So the protein’s ability to discriminate between the two ligands has decreased by ten-fold.
- One would think that the hundred-fold decrease in the ability to bind a steroid would at least initially be a very detrimental change that would be weeded out by natural selection. The authors do not test for that; they simply assume it wouldn’t be a problem, or that the problem could somehow be easily overcome. Nor do they test their speculation that DOC could somehow act as an intermediate ligand. In other words, in typical Darwinian fashion the authors pass over with their imaginations what in reality would very likely be serious biological difficulties.
- The fact that such very modest results are ballyhooed owes more, I strongly suspect, to the antipathy that many scientists feel toward ID than to the intrinsic value of the experiment itself.
- In conclusion, the results (and even the imagined-but-problematic scenario) are well within what an ID proponent already would think Darwinian processes could do, so they won’t affect our evaluation of the science. But it’s nice to know that Science magazine is thinking about us!
Behe’s point (10) is especially noteworthy since Venema writes about Thornton et al.‘s research that “Over and against these lines of evidence, however, the Intelligent Design Movement claims that such novelty is inaccessible to random mutation and natural selection.” But Behe has made it clear that these kinds of modest loss-of-function changes are exactly the type of changes we might expect from Darwinian evolution. So Venema is misrepresenting the claims of the ID movement.
In fact, Venema undercuts his own argument that this research represents significant novel CSI by admitting that: “Steroid hormones are a closely related molecules — it’s not too surprising that slightly different molecules fit into a related group of protein receptors.” This research does not demonstrate that natural selection and random mutation can produce functional, information-rich genes and proteins because what was produced was not information-rich. If anything, function was diminished or lost rather than gained.
Response 2: Stephen Meyer’s Comments:
The Bridgham et al. study published in Science is trivial. ID theorists have long known that a few mutations can slightly alter an existing protein fold. What we question is whether mutation and selection are sufficient to search the enormous combinatorial space of possibilities necessary to finding fundamentally new protein folds and structures. This study does nothing to allay our skepticism on that score.
Contrary to what the authors assume receptor-hormone pairs do not constitute irreducibly complex systems. The receptor-hormone pair is only a small component of a signal transduction circuit that regulates other complex physiological processes. For such pairs to have any selective or functional advantage many other protein components have to be present, including the other components of a signal transduction circuit and the physiological processes that such circuits regulate. If this is the best that Michael Behe’s critics can do after ten years of trying to refute him, then neo-Darwinism is in deep trouble.
The really interesting thing about this paper is not the science it contains—its scientific results are trivial—but the sociological dynamics surrounding the publication of these papers. The AAAS has repeatedly insisted there is no scientific controversy about intelligent design. Now Science, the AAAS flagship journal, publishes two articles taking positions on a controversy that the AAAS says doesn’t exist. Will Science now allow Michael Behe to respond or will it only publish articles about the controversy which claim that ID is wrong?
Response 3: “How to Explain Irreducible Complexity — A Lab Manual“:
Another response to the Thornton et al. research came from various Discovery Institute authors in a fun piece titled How to Explain Irreducible Complexity — A Lab Manual:
What [Bridgham/Thornton et al.] do say, however, is biologically meaningless.
A Tutorial in Evolutionary Theory
To understand why, we need a brief primer in fundamental evolutionary theory. Natural selection preserves randomly arising variations only if those variations cause functional differences affecting reproductive output. Since Bridgham et al. tell their story by invoking natural selection (see below), the system whose origin they claim to explain must have a selectable function for it to qualify as irreducibly complex. Indeed, given that natural selection favors only functionally advantageous variations, Behe has made clear that “function” in a biological context necessarily means a selectable functional advantage, for an obvious reason: a system of well-matched parts that performs a function can’t lose that function unless it possesses one to begin with. Unfortunately, these receptor-ligand pairs do not meet Behe’s definition of irreducible complexity for an equally obvious reason: receptor-ligand pairs do not by themselves confer any selective functional advantage.
Indeed, in Bridgham et al.‘s scenario, the function undergoing natural selection is not simply MR-aldosterone binding, but electrolyte homeostasis, the complex physiological regulation of essential cellular ions such as potassium or calcium. The novel receptor MR evolved, they write, “because it allowed electrolyte homeostasis to be controlled” (p. 100).
Natural selection is acting, therefore, not on MR-aldosterone binding alone. Indeed, it cannot, because unspecified binding confers no functional advantage.
But that is what Bridgham et al. do not seem to understand. They think they are explaining the origin of a single receptor-ligand pair, the mineralocorticoid receptor (MR) protein and the steroid hormone aldosterone. But that is biological nonsense. It is nonsense, moreover, strictly on the grounds of evolutionary theory itself.
Let’s suppose the newly-evolved cellular receptor, MR, interacts with a hormone ligand, aldosterone. This is a novel relationship. Now, will natural selection preserve it?
Who knows? Without more information — that is, without more details about the cellular or organismal effect of that novel binding — the bare function “aldosterone binds to MR” is biologically vacuous.
Compare: Pound a nail, we tell you. Where and why? you ask. Never mind that, we say, just go pound a nail. So you hammer a three-penny nail through the power supply of this blog’s server.
In any case, the receptor-ligand pair by itself is certainly not irreducibly complex. These pairs represent only small components of complex physiological processes such as metabolism, inflammation, immunity, and electrolyte homeostasis. For such pairs to have any selective advantage as part of the regulation of larger physiological processes, many other protein components have to be present. In particular, all the other components of a complete signal transduction circuit have to be present, as well as the component parts of the physiological process that such circuits regulate. (Even the ligand aldosterone itself doesn’t exist apart from a separate enzyme that produces it, and Bridgham et al.‘s gene duplication scenario does not account for the origin of this necessary component either.)
Bridgham et al. appear to grasp the need for more details (albeit in a distressingly loose way) because both early and late in their paper they specify the functional role of MR. The receptor “is activated by aldosterone to control electrolyte homeostasis” (p. 97) they note, and evolved “because it allowed electrolyte homeostasis to be controlled” (p. 100).
Thus, in Bridgham et al.‘s scenario, the actual system undergoing natural selection is electrolyte homeostasis, not simply MR-aldosterone binding. There’s a good reason for that: as noted, the function “aldosterone-MR binding,” considered in isolation, cannot be a target for natural selection. Try it, if you think it can. You’ll quickly find that you are floating in biological limbo. Aldosterone binds to MR…MR interacts with aldosterone…MR and aldosterone…OK, enough of that. Why does MR interact with aldosterone? Hello? Can we get an organism here?
Back to Biological Reality
So — is the physiological system of electrolyte homeostasis, of which both MR and aldosterone are small parts, irreducibly complex? Maybe. Take a look at a physiology textbook, or even any review paper on steroid or receptor biochemistry. Bridgham et al. don’t say much about the complexity of electrolyte homeostasis, however, because they are unaware that they have completely misunderstood the relevant unit of selection in their scenario. They write (p. 98):
It is not obvious how the tight aldosterone-MR partnership could have evolved. If the hormone is not yet present, how can selection drive the receptor’s affinity for it? Conversely, without the receptor, what selection pressure could guide the evolution of the ligand?
By Bridgham et al. ‘s own account, however — although they don’t realize it — natural selection is not acting at this level (the MR-aldosterone relationship alone) at all. To have any selectable function, many more components need to brought into the story. Genuine irreducible complexity re-emerges, and will be quite unexplained by the Bridgham et al. scenario.
Response 4: My Own Comments:
[L]ook at the bottom line of what this research really found: Adami highlights that the lock and key fit of the glucocorticoid enzyme with the cortisol substrate is based upon the specificity of merely two amino acids, where the precursor molecule was also functional (lacking those 2 mutations).
In other words, one enzyme might have evolved into another via 2 mutations. This would appear to be a fairly simple system—and, assuming it did evolve in this fashion, an unimpresive example of evolution. Two meager mutations (something which even Behe and Snoke’s (2004) simulations found could evolve under mutation and selection) is not an impressive evolutionary leap and there seems no reason to assume that many enzyme-substrate interactions might not require the simultaneous substitution of many more amino acid residues in order to function, vastly decreasing the likelihood of their evolution. (In fact, this research would not address the origin of complex molecular machines requiring many interacting parts, like the bacterial flagellum.) Even if we grant that this present system is “reducibly complex” (with regards to at least 2 meager amino acids, that is), why should we assume that all the other enzyme-substrate interactions in biology follow suit?
The last two commentaries combine to make two important points:
First, the fact that one precursor enzyme could potentially perform two functions, and then lost the ability to perform one of those functions, does not imply that all biologically functional enzymes can evolve in this fashion.
Second, we must keep in mind that the research of Bridgham/Thornton et al. involved intelligently directing mutations in these enzymes. Since they did not identify specific selective advantages, intelligent agents were doing the selection in a goal-directed fashion, hoping to select for future function. This is important when we consider the research of Axe (2010), discussed in Section 3 above. Axe found that when there is no selective advantage to a given mutation, it has a much smaller chance of becoming fixed in a population.  Thus, while a series of intelligently directed mutations might lead back to a functional ancestor, Bridgham/ Thornton et al. have not demonstrated that this pathway is likely to have been followed under natural conditions.
Venema stated that “If any natural mechanism can be shown to produce “functional, information-rich genes and proteins,” then intelligent design is no longer the best explanation for the origin of information we observe in DNA.” But in this example we have seen that:
- The change was not information-rich
- It’s not clear that natural selection produced this change
- Function was diminished or lost rather than gained
In fact, Venema undercuts his own argument that this research represents significant novel CSI by admitting in a comment that: “Steroid hormones are a closely related molecules — it’s not too surprising that slightly different molecules fit into a related group of protein receptors.” ID proponents would say the same thing, which is why this research does not demonstrate that a “natural mechanism can be shown to produce ‘functional, information-rich genes and proteins.'”
Section 7: Confusing Evidence for Common Ancestry with Evidence for Random Mutation and Natural Selection
In this section, we:
- Explain why evidence for common ancestry is not evidence for a Darwinian evolutionary pathway
- Investigate Venema’s citation of a paper that shows genomic similarity across many vertebrates, showing why this is at best evidence for common descent, not natural selection
- Discuss how common design could explain much of this data as well as common descent, if not better
The debate over evolution and intelligent design can be confusing because some keys terms in the discussion are ambiguous. Some people use “evolution” to refer to something as simple as small changes in the sizes of bird beaks. Others use the same word to mean something much more far-reaching. Used one way, “evolution” isn’t controversial at all; used another way, it’s hotly debated.
Dennis Venema’s series for BioLogos on the “Evolution and the Origin of Biological Information” illustrates what happens when a would-be defender of Darwinian theory gets tripped up by such ambiguities. Venema seems to misunderstand exactly which type of “evolution” counts as evidence against intelligent design. He cites evidence for common ancestry, wrongly thinking that it demonstrates Darwinian pathways, and thus refutes ID.
Used equivocally, “evolution” is simply too imprecise a term to be useful in a scientific discussion. In truth, neo-Darwinian evolution is not a single idea. Instead, it is made up of several related ideas, each supported by specific arguments:
- Evolution #1: First, evolution can mean that the life forms we see today are different from the forms that existed in the distant past. Evolution as “change over time” can also refer to minor changes in features of individual species — changes that take place over a short amount of time. Even skeptics of Darwin’s theory agree that this type of “change over time” takes place.
- Evolution #2: Some scientists associate the word “evolution” with the idea that all the organisms we see today are descended from a single common ancestor somewhere in the distant past. The claim became known as the Theory of Universal Common Descent. This theory paints a picture of the history of life on earth as a great branching tree.
- Evolution #3: Finally, some people use the term “evolution” to refer to a cause or mechanism of change, the biological process that Darwin thought was responsible for this branching pattern. Darwin argued that natural selection had the power to produce fundamentally new forms of life. Together, the ideas of Universal Common Descent and natural selection form the core of Darwinian evolutionary theory. “Neo-Darwinian” evolution combines our knowledge of DNA and genetics to claim that mutations in DNA provide the variation upon which natural selection acts.
Intelligent design does not conflict with evolution if by “evolution” one simply means “change over time,” or even that living things are related by common ancestry (Evolution #1 or Evolution #2). However, the dominant theory of evolution today is neo-Darwinism (Evolution #3), which contends that evolution is driven by natural selection acting on random mutations, an unpredictable and purposeless process that “has no discernable direction or goal, including survival of a species.” It is this specific claim made by neo-Darwinism that intelligent design directly challenges.
Venema’s series claimed to demonstrate “a natural mechanism that does add functional, specified information to DNA sequences (and in some cases, creates new genes de novo): natural selection acting on genetic variation produced through random mutation.” He further wrote “If any natural mechanism can be shown to produce ‘functional, information-rich genes and proteins,’ then intelligent design is no longer the best explanation for the origin of information we observe in DNA.” These could potentially be valid ways of testing ID, and I recently responded to Venema’s two primary empirical examples in Sections 5 and 6 above. However, the fifth and sixth posts in Venema’s series both discuss comparative genomics across vertebrate and invertebrate species, claiming that shared functional genetic similarities demonstrate that Darwinian evolution was at work. The two posts share a common theme:
- They confuse evidence for common ancestry with evidence for a Darwinian pathway; and
- They ignore that common design can also generate the shared functional genetic similarities discussed.
For example, in Venema’s fifth post he cites evidence showing that vertebrates tend to have four times as many paralogous genes as urochordates, and notes that “these modern paralogs are still present in four-fold syntenty groups that span about 25% of the human genome.” Venema then claims:
In other words, gene duplication and divergence to produce new CSI [complex and specified information] appears to be commonplace in evolution, including the evolution of our own species. Far from being rare exceptions, multiple lines of genomics evidence point to new structures, functions and information being produced through natural means. If the Intelligent Design Movement wishes to contest that natural mechanisms cannot produce new information, they need to address this widespread and compelling pattern.
But since Venema has cited no evidence for natural selection and random mutation, there is nothing for intelligent design to contest.
What Venema has discussed is shared functional genetic patterns across various classes of vertebrates. None of this evidence says anything about, as he claims his series would show, “a natural mechanism that does add functional, specified information to DNA sequences … natural selection acting on genetic variation produced through random mutation.” At best, these shared functional similarities that Venema has cited provide evidence of common ancestry, which is not incompatible with intelligent design. Michael Behe, for one, reminds us that evidence for common ancestry is not evidence of a Darwinian pathway:
[M]odern Darwinists point to evidence of common descent and erroneously assume it to be evidence of the power of random mutation.
(Michael J. Behe, The Edge of Evolution: The Search for the Limits of Darwinism, p. 95 (Free Press, 2007).)
In Darwin’s Black Box, Behe elaborates on the point:
Although useful for determining lines of descent … comparing sequences cannot show how a complex biochemical system achieved its function — the question that most concerns us in this book. By way of analogy, the instruction manuals for two different models of computer put out by the same company might have many identical words, sentences, and even paragraphs, suggesting a common ancestry (perhaps the same author wrote both manuals), but comparing the sequences of letters in the instruction manuals will never tell us if a computer can be produced step-by-step starting from a typewriter. … Like the sequence analysts, I believe the evidence strongly supports common descent. But the root question remains unanswered: What has caused complex systems to form?
(Michael J. Behe, Darwin’s Black Box: The Biochemical Challenge to Evolution, pp. 175-176 (Free Press, 1996).)
To reiterate, there are two main problems with Venema’s argument in his fifth and sixth posts:
- At most, Venema has cited evidence for common ancestry, not natural selection acting on random mutations.
- Moreover, designers regularly re-use useful functional components in different designs. This is especially seen in software engineering where programmers will re-use programming algorithms repeatedly in different programs because they perform the same function. In the same way, the shared functional genetic components cited by Venema could be evidence for common design just as much as they are evidence for common descent. Thus, Dr. Venema’s examples of synteny for gene locations across various vertebrate groups at most this shows shared functional genetic similarities that could result from common design just as much as common descent. But designers are not always required to re-use parts that work in a pattern that fits a nested hieararchy. This leads us to the third problems with Venema’s case for common descent:
Even in this case, the argument for common descent through a nice, neat nested hierarchy is not entirely clear. According to the paper Venema cited:
The phylogenetic trees for the gene families are not consistently nested, as would be expected in the case of allo-tetraploidy or two widely spaced auto-tetraploidy events. Finally, tree topologies of genes within paralogy blocks are not always congruent, indicating that the process of gene loss and rediploidization spanned the duplication events.
(Paramvir Dehal, Jeffrey L. Boore, “Two Rounds of Whole Genome Duplication in the Ancestral Vertebrate,” PLoS Biology, Vol. 3(10):1700-1708 (October 2005).)
In other words, the phylogenetic trees for the gene families discussed in this paper often don’t fit a nested hierarchy predicted by common descent. To explain away all the data that doesn’t fit with the expectations of common descent, the authors cite gene loss and rediploidization as occurring between and after two widely spaced whole-genome-duplication events across many millions of years. Isn’t that convenient: when the data fits the expected tree, we infer common descent; when it doesn’t, we can invoke gene loss and other factors to explain away the contrary data.
What we’re seeing are shared functional similarities distributed in a pattern that doesn’t always fit a nested hierarchy. Is there a cause that can generate the same pattern in unrelated systems? There is one: common design.
But whether the data does or does not support common ancestry is immaterial to the question of whether Venema has found concrete evidence that all of these genes diverged by natural selection and random mutation. In fact, the authors of the paper he cites make it clear that they don’t even know whether these supposed whole genome duplication provided advantages which natural selection could select:
It remains unclear to what extent such large-scale genomic events have driven macroevolutionary change versus the regular accumulation of small mutations, as is the central tenet of the classical model of evolution.
They further observe that “the vast majority of duplicated genes were subsequently deleted, indicating that relatively few genes may have been responsible for the increased complexity seen in vertebrates.” So it seems that they are not even sure to what extent natural selection was driving the evolution of these supposed new duplicate copies of genes.
The following is the incredibly low level of detail they provide for the alleged Darwinian evolution of vertebrate genetic structure: “We imagine that rapid and extensive evolutionary change could possibly be an emergent property of having all genes duplicated at the same time, allowing this expanded gene repertoire to evolve together.” Such vague assertions of evolutionary processes in no way demonstrate the efficacy of random mutation and natural selection. Instead, without providing any evidence that natural selection and random mutation could produce observed vertebrate diversification, they simply assert that it happened. It’s easy to tell stories when the underlying mechanisms are assumed rather than demonstrated.
Perhaps their imaginations are simply more powerful than those of ID proponents, who find it difficult to “imagine” such “rapid and extensive evolutionary change” across thousands of genes when precise, detailed Darwinian pathways are never given.
In the end, ID is not incompatible with common descent, but Venema has confused evidence for common ancestry with evidence for natural selection and random mutation. This paper doesn’t show a Darwinian pathway; it simply asserts it existed. There’s no evidence against intelligent design here. There isn’t even unequivocal evidence for common ancestry.
Section 8: Critically Analyzing the Argument from Human/Chimpanzee Genetic Similarity
In this section, we:
- Again discuss why evidence for common ancestry is not evidence for a Darwinian evolutionary pathway
- Falsify Dr. Venema’s reasoning that a 5% DNA difference between humans and chimps tells us anything about whether random mutation and natural selection could produce both species from a common ancestor, or even whether they share a common ancestor
- Show that Dr. Venema is overstating what we currently know about the degree of intraspecies genetic variation within humans
- Suggest that the percent genetic difference between humans and chimps may be much greater than 5%, and might not be accessible by Darwinian evolution
In his series on “Evolution and the Origin of Biological Information,” BioLogos-affiliated scientist Dennis Venema challenges ID to “address” a “widespread and compelling pattern,” which supposedly demonstrates common descent. But as we saw in Section 7, this pattern is not evidence for natural selection and random mutation, so there is nothing here that challenges ID. The problem exists in Venema’s sixth post, which makes the mundane point that humans and chimps share many genetic similarities:
[W]hile the total genetic differences between two species is an overestimation of the genetic changes needed to cause the differences, it is still a useful measure because we know that all of the meaningful changes must be accounted for within it.
Applying this test to humans and our closest (living) evolutionary relative, the chimpanzee, reveals that at a whole-genome level, we are over 95% identical. This value is even an underestimate, since it “counts” mutations that duplicate or delete sections of DNA as if they were separate mutations affecting individual DNA “letters” even though it was created by only one genetic change. Indeed if we use the same criteria to compare the diversity which exists within our own species, we humans are only 98% identical to each other. By whatever measure used, we are but a hand-breadth away from our evolutionary cousins at the DNA level.
Assuming Venema’s numbers are all correct, the short response to his point is So what? None of this bears on the question of whether natural selection acting on random mutations could produce these genetic changes.
As a longer answer, multiple levels of response are possible.
Initially, I must point out that Venema’s post provides no citation for his claim that human intraspecies genetic variation is as much as 2%. I contacted Dr. Venema privately and asked for citations that back this claim, but neither of the two papers he provided proposed an official percentage of human intraspecies genetic variation. One paper suggested that there are about 10 million single nucleotide polymorphisms (SNPs) and about 1.5 million insertion and deletion polymorphisms (INDELs) in the human genome. But the other paper, published in 2011, provided the highest estimates for human intraspecies genetic variation, stating: “Like known SNPs, which affect ~15 Mb of DNA … our INDEL variants affected 11.9 Mb of the human genome.”
Looking at the latter article, if we add those amounts together and round up to about 27 million base pairs, that implies that only about 0.9% of the human genome is known to vary — not 2%. This statistic is corroborated by the National Institutes of Health website which states “Human DNA consists of about 3 billion bases, and more than 99 percent of those bases are the same in all people.”
Perhaps someday Dr. Venema’s claim that “humans are only 98% identical to each other” will turn out to be correct. Perhaps it won’t. The fact of the matter is that we really don’t know at present the exact nature or amount of human intraspecies genetic variation. It thus seems premature for Venema to assert — especially without supporting citations — that humans have 2% intraspecies genetic variation. Presently, we don’t know that to be the case.
This problem of making premature claims that we don’t know are correct plagues Dr. Venema’s discussion of human and chimp genetic variation:
First, Venema claimed his series would show “a natural mechanism that does add functional, specified information to DNA sequences” namely “natural selection acting on genetic variation produced through random mutation.” But shared functional genetic similarity between humans and chimps is (at best) evidence for common descent, not evidence for natural selection and random mutation.
Second, Venema has misstated comparisons of human/ape “whole genome” similarity and human/human DNA similarity. Far from being “but a hand-breadth away from our evolutionary cousins at the DNA level,” the evidence shows that the genetic differences between humans and chimps amount to “35 million base-pair changes, 5 million indels in each species, and 689 extra genes in humans.” Such a level of differences is not known to exist for human/human intraspecies genetic variation. Moreover, as geneticist Richard Buggs has explained, the genetic similarity between humans and chimps may be even lower than 95%:
To compare the two [human and chimpanzee] genomes, the first thing we must do is to line up the parts of each genome that are similar. When we do this alignment, we discover that only 2400 million of the human genome’s 3164.7 million “letters” align with the chimpanzee genome — that is, 76% of the human genome. Some scientists have argued that the 24% of the human genome that does not line up with the chimpanzee genome is useless “junk DNA.” However, it now seems that this DNA could contain over 600 protein-coding genes, and also code for functional RNA molecules.
Looking closely at the chimpanzee-like 76% of the human genome, we find that to make an exact alignment, we often have to introduce artificial gaps in either the human or the chimp genome. These gaps give another 3% difference. So now we have a 73% similarity between the two genomes.
In the neatly aligned sequences we now find another form of difference, where a single “letter” is different between the human and chimp genomes. These provide another 1.23% difference between the two genomes. Thus, the percentage difference is now at around 72%.
We also find places where two pieces of human genome align with only one piece of chimp genome, or two pieces of chimp genome align with one piece of human genome. This “copy number variation” causes another 2.7% difference between the two species. Therefore the total similarity of the genomes could be below 70%.
Third, whatever shared functional genetic similarities do exist between humans and chimps, they might be explained by common design just as well as by common descent. In fact, had the now-refuted statistic that humans and chimps are only 1% genetically different turned out to be correct, why should that demonstrate common ancestry? Why is a 1% genetic difference any better than a 5% genetic difference for demonstrating common ancestry? At what point does the comparison cease to support common ancestry? How about a 10% difference? 25%? Is there an objective metric for falsification here, or are we seeing a fallacious argument for human/chimp common ancestry?
Intelligent design is certainly compatible with human/ape common ancestry, but the truth is that the genetic difference expressed as a percent says nothing about whether humans and chimps share a common ancestor. The genetic similarity between humans and apes does not demonstrate Darwinian evolution, unless one excludes the possibility of intelligent design (and all other non-Darwinian evolutionary scenarios). Just as intelligent agents “re-use” functional components that work over and over in different systems (e.g., wheels for cars and wheels for airplanes), genetic similarities between humans and chimps could also be explained as the result of the re-usage of common genetic programs due to functional requirements of the hominid body plan. Even Francis Collins (who frames the question theologically) admits this is the case:
This evidence alone does not, of course, prove a common ancestor; from a creationist perspective such similarities could simply demonstrate that God used successful design principles over and over again.
(Francis Collins, The Language of God, p. 134 (Free Press, 2006).)
I elaborate further on this point here.
Waiting for Millions of Mutations?
There’s a final problem with Venema’s argument. He suggests that “we are but a hand-breadth away from our evolutionary cousins at the DNA level” and thus evolving humans and chimps from a common ancestor is no problem for random mutation and natural selection:
The differences we see, when examining these two genomes, are consistent with small changes, of the sort easily accessible to evolutionary mechanisms.
This is an incredibly weak argument.
First, as noted, we’re not talking about “small changes” but rather, as the journal Science explained, at the very least these differences entail “35 million base-pair changes, 5 million indels in each species, and 689 extra genes in humans.”
Second, Venema has badly overstated the case for Darwinian evolution, as no one has any idea if these changes are “easily accessible to evolutionary mechanisms.” In fact, we still don’t understand what the vast majority of these differences mean. When speaking of human/chimp genetic differences, David Haussler, a biomolecular engineer at UC Santa Cruz, writes “To sort out the differences that matter from the ones that don’t is really difficult.” And there are good reasons to believe that some (or many) of these differences might encode features not amenable to stepwise Darwinian evolution under known timescales.
In 2008, Michael Behe’s critics Rick Durrett and Deena Schmidt tried to refute him in the journal Genetics with a paper titled “Waiting for Two Mutations: With Applications to Regulatory Sequence Evolution and the Limits of Darwinian Evolution.” But Durrett and Schmidt found that to obtain only two specific mutations via Darwinian evolution “for humans with a much smaller effective population size, this type of change would take > 100 million years.” The critics admitted this was “very unlikely to occur on a reasonable timescale.”
In other words, if any of the 35 million base pair changes between humans and chimps entail adaptive changes that require two or more specific mutations before providing any advantage, then they would be extremely unlikely to evolve by random mutation and natural selection in the mere 6 or 7 million years since we shared our alleged most recent common ancestor with chimps.
Durrett and Schmidt found that it would take too long to wait for two specific mutations to gain an advantage. How does Venema know that there aren’t many differences between humans and chimps that would require two (or perhaps many more—dozens, hundreds, millions?!) mutations before any benefit arises?
Venema’s claim that the genetic differences between humans and chimps are “easily accessible to evolutionary mechanisms” is difficult to accept, because frankly, no one knows that this is true. We should not assume that naturalistic evolutionary explanations are correct; we should test them, and hold on to them only if they are valid.
Additional References Cited:
[1.] Michael J. Behe & David W. Snoke, “Simulating Evolution by Gene Duplication of Protein Features That Require Multiple Amino Acid Residues,” Protein Science, Vol. 13:2651-2664 (2004).
[2.] Rick Durrett and Deena Schmidt, “Waiting for Two Mutations: With Applications to Regulatory Sequence Evolution and the Limits of Darwinian Evolution,” Genetics, Vol. 180: 1501-1509 (November 2008).
[3.] Douglas D. Axe, “The Limits of Complex Adaptation: An Analysis Based on a Simple Model of Structured Bacterial Populations,” BIO-Complexity, Vol. 2010(4):1-10.
[4.] Ann K. Gauger, Stephanie Ebnet, Pamela F. Fahey, and Ralph Seelke, “Reductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness,” BIO-Complexity, Vol. 2010 (2).
[5.] Douglas D. Axe, “Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds,” Journal of Molecular Biology, Vol. 341: 1295-1315 (2004); Douglas D. Axe, “Extreme Functional Sensitivity to Conservative Amino Acid Changes on Enzyme Exteriors,” Journal of Molecular Biology, Vol. 301: 585-595 (2000).
[6.] Neil A. Campbell and Jane B. Reece, Biology, p. 84 (7th ed, 2005).
[7.] David S. Goodsell, The Machinery of Life, pp. 17, 19 (2nd ed, Springer, 2009).
[8.] Ryan E. Mills, Christopher T. Luttig, Christine E. Larkins, Adam Beauchamp, Circe Tsui, W. Stephen Pittard, and Scott E. Devine, “An initial map of insertion and deletion (INDEL) variation in the human genome,” Genome Research, Vol. 16: 1182-1190 (2006).
[9.] Ryan E. Mills, W. Stephen Pittard, Julienne M. Mullaney, Umar Farooq, Todd H. Creasy, Anup A. Mahurkar, David M. Kemeza, Daniel S. Strassler, Chris P. Ponting, Caleb Webber and Scott E. Devine, “Natural genetic variation caused by small insertions and deletions in the human genome,” Genome Research, Vol. 21: 830-839 (2011).
[10.] Jon Cohen, “Relative Differences: The Myth of 1%,” Science, Vol. 316:1836 (June 29, 2007).
*** Regarding properly testing ID, the statement “Thus, ID might frame the question like this: ‘What can neo-Darwinian processes accomplish, and what is best explained by intelligent causes?’,” shows that we must test various causes and determine their causal abilities and compare and contrast the mechanisms. Of course that’s a very general statement, and my purpose here is not to go into great detail about ID’s specific causal abilities. For a discussion of where I’ve done that extensively in the past, please see: A Positive, Testable Case for Intelligent Design.