If it's not natural selection, then it must be...

The folks at the Discovery Institute (DI) are engaged in an extensive attempt to rebut my friend Dennis Venema's critiques of Stephen Meyer's surprisingly lame ID manifesto, Signature in the Cell. There are several aspects of this conversation that I hope to address in the coming days and weeks, but one jumped out at me today: the consistent confusion about natural selection in depictions of evolutionary theory by design advocates.

Consider this excerpt from a recent blog post by a writer at the Discovery Institute:

...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.

A few sentences later, the same claim is repeated:

Indeed, given that natural selection favors only functionally advantageous variations, ...

Those claims were first made in a piece written by unnamed DI "fellows" mocking the work and conclusions of Joe Thornton, an evolutionary biologist at the University of Oregon and the University of Chicago. And the claims are badly misleading.

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Design and falsifiability

Last month I had an interesting conversation with Casey Luskin of the Discovery Institute (DI), at Evolution News and Views (ENV), a DI blog/site that recently opened some articles to comments. The topic of the original post was common ancestry in humans and other primates, but Casey and I discussed various aspects of design thought.

One subject that came up was the falsifiability of design. I maintain that design arguments, whenever they also postulate the existence of an omnipotent deity (or any super-powerful being, for that matter), are inherently unfalsifiable. And I want some feedback on my argument.

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Alu need to know about parasitic DNA: telling the whole story about Alu elements and "design"

So, Alu elements are mobile DNA modules that can exert diverse influences on genomes and the organisms harboring them. They can affect genome function in constructive ways, by altering gene expression or supporting chromosome structure. And they can be damaging, even deadly. There are more than a million of them in the human genome, and we don't know what each one does. But, as I explained in the first post in this series, we do know that they can play both helpful and harmful roles, in the same way that other kinds of parasites can be good, bad, or indifferent.

Alu elements and other genome-wide repeats are a big problem for intelligent design (ID) theorists of some stripes. Any ID proponent who claims that genomes are carefully-designed, well-optimized systems must deal with the reality of the enormous numbers of mobile elements in (for example) the human genome. Now, I can think of various ways such an ID theorist might discuss Alu elements. She could propose that all of their characteristics (including their mobility) are part of their design, such that they can bring new design features quickly into being; she could propose that their mobility is a "bug" rather than a "feature," and perhaps speculate on how things went wrong; she could postulate that the damage caused by their expression and their mobility is being misattributed to the genome when it is instead caused by some other external process. (Or she could say, "We're still working on that one.")

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Exploring the protein universe: a response to Doug Axe

One of the goals of the intelligent design (ID) movement is to show that evolution cannot be random and/or unguided, and one way to demonstrate this is to show that an evolutionary transition is impossibly unlikely without guidance or intervention. Michael Behe has attempted to do this, without success. And Doug Axe, the director of Biologic Institute, is working on a similar problem. Axe's work (most recently with a colleague, Ann Gauger) aims (in part, at least) to show that evolutionary transitions at the level of protein structure and function are so fantastically improbable that they could not have occurred "randomly."

Recently, Axe has been writing on this issue. First, he and Gauger just published some experimental results in the ID journal BIO-Complexity. Second, Axe wrote a blog post at the Biologic site in which he defends his approach against critics like Art Hunt and me. Here are some comments on both.

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Introns. Let's think about this, people. Part IV.

So why is it that I and many other biologists hypothesize that introns are mostly non-functional?

(I'll assume that you've read the previous posts, and that you understand what it is that I mean when I challenge claims that introns are functional elements in an information-rich genome. And to avoid confusion, I'll speak only for myself, although I surmise that a tiny minority of biologists would agree with creationist characterizations of the human genome.)

Here are the basic data that lead me to conclude that intron sequences are mostly dispensable for biological function. I've provided links to key references, and we can go into more detail in further posts or in the comments.

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Bread and circus: Signature in the Cell at Biola (Part III)

Here I'm continuing my discussion of the Signature in the Cell book-signing event at Biola University on 14 May. You'll want to read Parts I and II before reading on.

My second question to Steve Meyer was the one question I most wanted to ask him, both out of personal curiosity and because I thought the answer would help demystify many of his claims. The exchange that resulted was memorable – on that, everyone seems to agree. But the nature of my comments has been profoundly misrepresented by Meyer's hired guns. I hope that this will be crystal clear when I'm done here.

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Signature in the Cell: Chapter 8

It's been a month and a half since my last post in this series, and recently a friend asked me why I stopped. I can think of two reasons: first, I spent the month of March teaching a graduate course for the first time; second, I'm worried about how this is going to go. I'm worried because I can see that the book is poor scholarship – Meyer is either underinformed or overcommitted to his cause – and I can see that my critique will be considered within a religious milieu that hinders straightforward criticism and analysis. Ergo, I think this might not be very pretty. It would be a lot more fun to blog about any of 15 different papers from the last two issues of Nature.

But we need to finish, partly because I'll be on a panel of critics at an event with Stephen Meyer himself in Los Angeles next month. (Not just critics: "a powerful group of credentialed critics." More later.)

Chapter 8 is called "Chance Elimination and Pattern Recognition." It deals first with the notion of chance and then with subjects that are at the very heart of design thought – the dual consideration of improbable events and the genesis of phenomena that exhibit "patterns." The chapter is pretty good, but seems to contain seeds of significant future confusion.

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Introns and design

Mike Gene has posted an interesting series on introns that's worthy of a few comments. His thesis is that "introns facilitated the evolution of multicellular life."

A. The idea is interesting and rational but not novel. Research on introns and evolution is active and lively, and one prominent scientist in the field, Eugene Koonin, has proposed that introns drove many aspects of the evolution of eukaryotes (i.e., non-bacteria).

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Signature in the Cell: Chapter 7

The chapter is called "Of Clues to Causes" and it's about scientific explanation. That's an interesting and important topic, one that opponents of evolutionary theory rarely understand. Meyer's summary is predictably fluffy but not inaccurate. Those seeking an introduction to philosophical questions pertaining to scientific explanation should look elsewhere, since Meyer says little in the 22-page chapter. His main points:

1. There are indeed legitimately scientific means of understanding and seeking explanation for past events.
2. These approaches validate ID as a "possible scientific explanation for the origin of biological information."

I don't disagree with either assertion. But neither is particularly helpful to ID in its quest for explanatory relevance. (Well, the main quest of the ID movement is to undermine naturalism by any means necessary, but its scientific challenge is to demonstrate that it can provide useful explanation.)

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Signature in the Cell: Chapter 6

The chapter is called "The Origin of Science and the Possibility of Design." It's short, unimportant and uninteresting. Its purposes, along with Chapter 7, are twofold: 1) to counter the claim that ID theory is "not science" and 2) to establish that "historical science" (that which deals with the past) is not all that different from "operations science" (as defined by Charles Thaxton and others), specifically because the theorizing of "historical science" can be considered testable.

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Signature in the Cell: Chapters 4 and 5 - errors and problems

Meyer's basic idea in chapters 4 and 5 is reasonably coherent. But I find further evidence in both chapters that Meyer is careless and underinformed on the subjects he addresses. (I explained before why I think this matters. If you think I'm not being nice enough to Meyer, consider providing me with the Rules of Engagement that apply when criticizing culture warriors who are proposing world-shifting new ideas.)

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Signature in the Cell: Chapters 4 and 5 - major themes

Chapter 4 is called "Signature in the Cell." It's an important chapter for two reasons. First, along with chapter 5 ("The Molecular Labyrinth") it lays out Meyer's central question by pointing to the specific features of cellular information systems in need of explanation. Second, it exemplifies an aspect of ID thought that I want to highlight. I'll discuss these two themes here, then add some further critiques in a second post.

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Signature in the Cell: Chapter 2

The chapter is called "The Evolution of a Mystery and Why It Matters." It's interesting and engaging, and I enjoyed reading it. The "mystery" in question is first described on page 35:

...most philosophers and scientists have long thought that Darwin's theory of evolution by natural selection destroyed the design argument. Yet I also discovered that Darwin himself admitted that his theory did not explain the origin of life itself. [...] His theory assumed rather than explained the origin of the first living thing. Since this limitation of Darwin's theory was widely recognized, it raised a question: Why were nineteenth- and twentieth-century biologists and philosophers so sure that Darwin had undermined the design argument from biology?

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Deep homology and design: why Notch?

The Notch signaling pathway is a golden oldie of genetics in two ways. First, it's a system that was first described at the dawn of modern genetics – named by its founder, Thomas Hunt Morgan – and used to establish some of the most basic principles of "the physical basis of heredity," as Morgan put it. (His book by that title is a founding document of modern genetics, describing in 1919 what we now call chromosomes without any knowledge of their chemical makeup.) Second, it's a system now known to be as ancient as animals themselves.

Why Notch? The name refers to the appearance of some of the first mutant fruit flies described by Morgan and his colleagues in their famous work in the early 20th century. They found flies with notched wings, and found that the trait was dominant.

Figure 1 from T.H. Morgan, "The Theory of the Gene." American Naturalist 51:513-544, 1917.

So aside from its importance in evolution and development, Notch is of historical interest to genetics. Now, Morgan was interested in Notch (the gene name is capitalized because the original trait is dominant, in case you're wondering) because of its mode of inheritance, not specifically because of its biological effects. (I mean, who cares about flies with notched wings?)

But twenty years later, things got more interesting when a different mutation in Notch was found to cause a weird (and lethal) overgrowth of the nervous system. Interesting... then, as geneticists began to probe the genetics of animal development 50 years after Morgan's initial discoveries, using the fruit fly as a model, Notch started turning up again and again. Problems in Notch signaling led to developmental problems all over the place: brain, eyes, gut, wings, bristles.

By the beginning of the 1990's, geneticists had figured out why its activity is so central to proper development: Notch controls a crucial type of cell-to-cell interaction that leads to a change in cell fate. And they had found Notch signaling in animals of every kind, including in humans, mediating the same kinds of inductive developmental interactions. It's not as complicated as it might sound – in such an interaction, two cells interact physically (they have to touch) and after the interaction one or both of the cells changes its developmental fate, choosing to become, say, a nerve cell or a skin cell. That weird brain overgrowth in the flies with no Notch activity results from a failure of cells to communicate in this way, such that all the cells on the outside of the fly's head become brain cells. (Flies, like most animals, prefer to have some skin over their brains, but in these mutants there's very little skin and lots of extra brain. Ick. See Figure 1 of this recent paper in BMC Biology for pictures; the green stain indicates nerve cells and the second animal down has the nasty trait.)

The point is that Notch signaling involves direct cell contact, and typically leads to cells making decisions about what to do when they grow up. So how does it work? Well, we know an awful lot about this particular system, and there are myriad details of mechanism and control that I'm going to skip. The very basic outline is as follows. Some cells make the Notch protein, which is a receptor. Other cells make the Delta protein, which is the signal that activates the receptor. (One useful analogy is that of locks and keys: Notch is the lock, Delta is the key.) Both proteins are displayed on the cell surface. When the two cells come into contact, the Delta protein on one cell activates the Notch protein on the other. When Notch becomes activated, it gets chopped into at least two pieces. One piece leaves the surface of the cell and travels inward to the nucleus of the cell. There, in collaboration with other proteins, it causes changes in gene expression, meaning that some genes are turned on or up and others are turned off or down.

This mode of signaling is unique and extraordinary. What we have is a signaling system that takes cell-to-cell contact and converts it directly into changes in gene expression.

Now, let's think carefully about this. We have a system of receptors and activators, in the form of Notch proteins (there are at least four in humans) and Delta proteins (there are several in humans, in a few different protein families), which serve a critical and unique purpose in cell-to-cell signaling. The function is conserved in all known animals, and that's not surprising – having cells send messages to their immediate neighbors, directing them to adopt particular fates, is key to constructing tissues and organs. I hope you'll agree that we should expect to see these inductive mechanisms in the development of complex organisms. More to the point, one should expect this regardless of one's stance on questions of "intelligent design."

Here's what is surprising. The same Notch proteins are used for this purpose in every known animal. And here's why that's surprising: as far as we know, there's no reason to insist on those particular proteins playing those particular roles. It's easy to envision – and then design and create – a set of locks and keys that bear no resemblance to Notch or Delta but that can accomplish these somewhat basic purposes just as well. There's no need for such a specific solution to a basic challenge. Why does every animal use Notch? Recall the previous post in this series and how we approached this question of common design. Here, again, are our options.

1. These inductive signaling events could only be accomplished by Notch. There is a design constraint, currently unknown, which forces that choice. It may seem that the system could have been effectively constructed using a different lock-and-key combination, but in fact it could not function (or function well) any other way.
2. These inductive signaling events could be mediated in various ways, but the choice of Notch has been forced by common ancestry. The earliest animals settled on this choice, and their descendants have used it ever since.
3. These inductive signaling events could be mediated in various ways, but an intelligent designer has repeatedly chosen Notch for reasons known only to her/him/it.

Option #1 is, in my view, unreasonable. The system is not complicated in its basic design. There are no clear constraints on the choice of lock and key. A designer who is crafting an organism from the ground up need not select that particular lock/key combination, and someone who intends to argue otherwise needs to demonstrate how that particular combination is superior.

Option #3 is, I think, perfectly reasonable. The only problem is that one must know quite a lot about the designer to begin to surmise her/his/its goals and proclivities. Without that knowledge, it is no more reasonable to assume a preference than it is to assume a constraint.

The point is not that we can ever rule out preferences or other characteristics of a creator or designer. The point is that we can rarely make explanatory use of them. Consider that while we may assert that the Creator/Intelligent Designer prefers that pine trees have needles, we would not advance that as a useful explanation for why pine trees have needles. Specifically, we would never advance that as an alternative explanation in place of one that notes that today's pine trees have the same needles that last century's pine trees had, by virtue of biological ancestry.

Notch signaling represents one of the classic examples of deep homology. It seems to me that design theorists need to deal with deep homology before they can ever be taken seriously as scientific thinkers. Deep homology is crying out for explanation, and those who believe that the biosphere cries "design" are remiss in not offering a serious design-based explanation for the fact that every animal on the planet uses the same lock-and-key mechanism to achieve basic cell-to-cell inductive communication.

Next, we'll look at a recent and very interesting example of new findings that illustrate the striking conservation of Notch-mediated developmental events – an example of deep homology that could arise from the very root of animal ancestry.

Deep homology and design: common design and its implications

Consider these not-so-random samples from the animal world: a cockroach, a zebrafish, a mouse. What do these creatures have in common?

Left to right: American cockroach (Periplaneta americana), zebrafish (Danio rerio), house mouse (Mus musculus). Cockroach image from Wikimedia Commons, zebrafish and mouse from Wellcome Images.

Well, they're all animals and that means they're all eukaryotes, for example. They all have DNA-based genomes. They all like water to some extent. They all have muscles that cause them to move. And so on.

But let's think of them in a different way. Let's think of them as things that exhibit design. (Not Design. Just design.) We see similarities like the ones we just listed, and we see some dramatic differences. Insect, exoskeleton, open circulatory system. Fish, gills, egg-laying. Mammal, milk, hair, live birth, temperature control. We can see elements of common design (limbs and joints, eyes, nerves) and elements of specialized design (lungs, fins, antennae).

Now let's forget everything we know about common descent and adopt an Intelligent Design perspective. This isn't hard to do: just think of each animal as a machine that was designed to be the way it is. The machines have some common design elements and some specialized design elements. Now this is important: let's assume that each machine was designed separately, such that design decisions were made on a case-by-case basis (for each type of machine, not for each individual machine). In other words, let's think of the cockroach as designed from the ground up to be a cockroach, and the fish and the mouse likewise. Simple, right? I think so.

Now, let's look under the hood of each machine and ask detailed questions about how it's built, again with the assumption that it was designed. Not just its overall structure, but also the procedures used for its assembly. Let's look, in other words, at its molecular machinery – machinery for signaling between cells and tissues, machinery for signaling within individual cells, machinery for directing gene function during development and normal function. And let's focus specifically on the signaling systems in these creatures and in their developmental stages. What would we expect to see? Well, let's consider some basic scenarios.

1. Maybe the signaling systems will be roughly the same – or even largely the same – in all three animals. This would imply that such systems are hard to assemble and perhaps even harder to tune and maintain, and therefore we would conclude that there are very few ways to make a working system. The only other explanation would refer to preferences on the part of the designer, who was unconstrained by design limitations but nevertheless insisted on doing things a certain way.

2. Maybe the signaling systems will differ between the three animals, to such an extent that it is clear that the choice of a system is somewhat arbitrary, arbitrary in the sense that the choice of a particular system is largely independent of the context or the function that is specified. The implication is that there are plenty of ways in which cells and molecules can communicate, and no strong constraints on the designer's choices.

Now of course we may find examples of both scenarios in our analysis. Perhaps some signaling systems will appear to be highly constrained while others will be largely different among the three species. The point, though, is this: when examining machines that were separately designed, common design implies either design constraint or designer preference. Divergent design implies a lack of design constraint. There are no further options: either the designer was constrained, or she wasn't; if unconstrained, she could nevertheless choose a favorite scheme and leave the impression that she was somehow constrained.

Designer constraint could arise in various ways. It could be that a particular signaling system is uniquely suited to a particular purpose. It could be that a particular signaling system is highly robust to damage or other challenges. It could be that there are only a handful of different possibilities due to limitations in the raw materials. One variation of that last possibility would look a lot like how evolution is known to work: the designer tweaks the system a little at a time, working with the materials supplied by each generation and therefore constrained by common descent.

Design proponents can be stunningly cavalier about all this. "Common elements in animal biology? Well of course! Common design!" But wait: common design implies either design constraint (that was the best way to do it – or the only way to do it) or designer preference (she just happens to like it that way), and those are dramatically different from an explanatory standpoint.

It turns out that signaling systems in animal development are so universally conserved that they require an extraordinary explanation. The commonality of the elements is so striking that it took most biologists by surprise when it first became evident, and remains one of the most remarkable facts of developmental biology today. We'll look at some recent advances in this area of evo-devo in posts to come.

But one last thing: I'd like to try a thought experiment to illustrate how we might approach questions of signaling in animal cells and embryos. Consider a group of 50 people who have agreed to help with your experiment. You divide them into pairs and tell each pair to send one person out of the room. Then you tell the remaining people to greet their partners upon their return, using a single word of their choosing that is certain to convey the greeting. You observe that all of the people employ either "hello" or "hi" for this purpose.

Question: would you conclude that "hello" and "hi" are uniquely suited for the task, and that no other word could possibly have worked? I hope you would seek another explanation and perhaps consider trying the experiment in, say, Shanghai or Guadalajara. You would conclude, I wager, that the word itself is of little explanatory value. In other words, the choice of a word was constrained, but not by anything specific to the word itself. In Shanghai, it's "ni hao." Maybe somewhere it's "duuuuuuude." And in a matter of minutes, you could change it to "ahoy" or "blorp" or anything you want.

And if you really wanted to probe the notion of constraint in human conversation, you would ask your 25 pairs of subjects to come up with an identifying word or phrase that they could call out to find each other in the dark. You would find, of course, that the choice of that word or phrase would be almost completely unconstrained.

What does all this have to do with signaling systems and design? That's for next time. Till then, blorp.

Deep homology and design: a new series

Recently I was reading a superb review article [doi] on the subject of a famous and important cellular signaling pathway called the Notch pathway. The author, Mark Fortini of Thomas Jefferson University, quoted James Puckle (an 18th-century English inventor and writer) on the "wonderful frame of the human body" in which "so many strings and springs" which all must "be in their right frame and order" for life and concluding that "it is next to a miracle we survived the day we were born." (If you must know, it's maxim #914 in The Club, in a section called "Death.")

This reminded me of some personal tragedy in our own family, after which Puckle's conclusion was repeated almost verbatim. It also reminded me of my need to write about the amazing homology of developmental signaling mechanisms in animals. For many months, I've listed an article on "deep homology" as the subject of my next Journal Club. But this topic won't fit into one article review, so I've decided to turn it into a little series.

Here's what Fortini writes in his introduction, after quoting Mr. Puckle:

Surprisingly, research over the past few decades has revealed that the orderly differentiation and arrangement of these many physiological ‘‘strings and springs’’ are controlled by a relatively small number of developmental signaling pathways. These pathways, including the Notch, Ras/MAPK, Hedgehog, Wnt, TGFβ, and JAK/STAT pathways, among others, are widely conserved throughout the animal kingdom and they cooperate throughout development to pattern a diverse array of tissues in different animal species.

The lingo might seem strange, but I hope the point is clear. The vast diversity of animal life, with "endless forms most beautiful," is assembled through the action of a small set of signaling systems. And, remarkably, the systems are used in the same ways in animals that couldn't be more different in behavior or structure.

This fact raises interesting questions about design and evolution. Why so few systems? Why are they used again and again, for the very same purpose? Are these choices forced by design constraints of some kind, or is there another explanation? Could it have been otherwise? Can it be otherwise? I'll tackle those questions while discussing some recent experiments in evolutionary developmental biology, or evo-devo.

And what of this phrase "deep homology"? It was coined by some of the founding minds of evo-devo – Neil Shubin, Cliff Tabin and Sean Carroll – as they considered the fact that animal limbs of every kind are "organized by a similar genetic regulatory system that may have been established in a common ancestor." And we mean limbs of every kind: whale flippers, fish fins, bat wings, human arms, and, amazingly, insect limbs. Such disparate structures may not be evolutionarily homologous (meaning that they were modified from a common ancestor) but the signaling systems that create them are homologous.

This, then, is deep homology: the sharing of signaling mechanisms that are used to create diverse (though often functionally similar) animal structures. So please join me, and maybe we'll lure interesting commenters into the discussion.

Critiquing Nature's Destiny by Michael Denton, Part I

I've mentioned before that we've had an intelligent design proponent (code named Timaeus) as an official guest on the ASA email list. The discussion has been mostly useful. One thing that became clear early on was the fact that Timaeus is not a scientist and has not read much science outside of the works of ID defenders. His repeated and enthusiastic citation of Michael Denton led some to request commentary on Denton's work, by knowledgeable scientists. This is my contribution.

Timaeus has made frequent mention of the work of Michael Denton, who has written two books that are popular among ID sympathizers. The first, Evolution: A Theory in Crisis, was published in 1985 and is regarded as a major influence on the early ID movement. The second, Nature's Destiny, was published in 1998 and seems to be far less influential. I recently read Nature's Destiny, and offer here a review in two posts. In this post, I present an overview of the book and its arguments, with a general critique and comments on the portrayal of the book by Timaeus. The second post (if I find time to collate it) will contain more detailed comments on technical aspects of Denton's claims in areas of my expertise. In separate posts, I will comment on Evolution: A Theory in Crisis (henceforth abbreviated as ETC).

Overview

Reading Timaeus' characterizations, one might reasonably suppose that Michael Denton has written books that demolish "Darwinian evolution," in ways not seen before and not answered (or answerable) by evolutionary biologists. Timaeus asserts, for example, that Denton "rips the Darwinian mechanism to shreds, armed with thousands of references to the latest knowledge in biochemistry, genetics, embryology, physiology, comparative anatomy, etc." And that quote clearly refers to Nature's Destiny.

This is a very serious mischaracterization of Denton's work. Denton did attempt, in ETC, to undermine "Darwinian evolution" – unsuccessfully, as I will explain elsewhere. In Nature's Destiny, his project is wholly different. Nature's Destiny seeks to defend a law-based, teleological view of cosmic history in which the development of humanity is the ultimate goal. The view is non-Darwinian for sure, in the sense that such strong teleological conceptions are non-Darwinian by definition. But any claim that Nature's Destiny does damage to modern evolutionary biology is a significant distortion. In fact, I would be most interested in a conversation with Michael Denton, both because I find his work intriguing and because I would be quite curious to hear his response to Timaeus' triumphalistic pronouncements regarding his ideas. Specifically, I wonder if Denton believes that he has "shredded" the "Darwinian mechanism," and whether he would acknowledge that many of the challenges he raised in his first book have failed completely in the face of vast amounts of data arising from completely new biological subdisciplines. (More on this in a future post on ETC.) My point is not that I think Denton is a fool, but that on the contrary I'm pretty sure he'd be embarrassed by the propagandistic ends toward which his ideas are being employed. (Perhaps there is a clue here regarding his divestiture from the Discovery Institute.)

I found Nature's Destiny to be mostly interesting, occasionally informative, occasionally exasperating, and ultimately unpersuasive. Ominously, I found that the chapters I judged to be the weakest were the chapters on topics I know the best. I suspect that cosmologists, physicists, biophysicists and perhaps chemists would feel the same way. In any case, I hasten to add that I have not concluded that Denton is wrong or that his failure to assemble a convincing case is somehow evidence to the contrary. His book is far stronger than Behe's Edge of Evolution, and unlike that unacceptably misleading and inaccurate work of folk science, Denton does not invite speculation that he is willing to abuse science in the course of metaphysical argumentation. Nevertheless, there are times when he's clearly trying too hard, and this is one of my main criticisms of the work.


Nature's Destiny does not attempt to destroy "Darwinism." It attempts to defend a "teleological religious concept of the cosmos as a specifically designed whole, with life and mankind as its primary goal and purpose." (p. xi) As Denton describes in his autobiographical account in Uncommon Dissent and in the prologue, the book can be viewed as an updating and expanding of a classic work by Lawrence Henderson (The Fitness of the Environment, 1913) that describes the ways in which the cosmos (specifically its chemistry) is remarkably fit for life. As Denton puts it in Uncommon Dissent (p. 168), Henderson demonstrated that

there is clear evidence that some adaptive fitness is given from within. This is adaptation "for free" arising out of the intrinsic properties of matter...

It may be that some forms of "Darwinism" cannot abide such talk, but those who think that consideration of nature's "eerie perfection" is somehow "anti-Darwinian" should read Simon Conway Morris. In fact, Conway Morris' Life's Solution is the book that every ID proponent should read after reading Nature's Destiny. Conway Morris' project overlaps with Denton's in obvious ways, and Conway Morris cites Denton twice, approvingly. But one never hears an ID propagandist brag that Conway Morris has "shredded the Darwinian mechanism." This, to me, is telling. I urge those who take Denton seriously to read Life's Solution. It simultaneously affirms Denton's basic view (that life is an inevitable result of the "laws" of the cosmos) while putting the lie to any claim that Denton or anyone else has undermined the theoretical foundation of modern evolutionary biology. If there is hope for ID as a serious intellectual movement, it lies in the deep cosmic concepts that unite the work of Simon Conway Morris and Michael Denton. But as long as ID propagandists believe that Denton has wrecked evolutionary explanation, they will purvey ignorance and confusion, and prolong the degeneration that gives us Casey Luskin and the disastrously bad Edge of Evolution.


Critique

1. As the articulation of a certain metaphysical view of the cosmos, Nature's Destiny works fairly well. As a defense of that view, it is wholly unconvincing, and I suspect that Michael Denton would understand my criticism. Nature's Destiny explores the notion of fine tuning and deep direction at every level of organization; it is not primarily a book about biological evolution. It begins with a standard retelling of the physics fine tuning story, then turns to some special examples of proposed fine tuning in chemistry. These chapters are fun to read, and contain very nice historical and scientific summaries on topics such as the properties of water, carbon and other elements, and gases. But even in these better chapters, and frequently in later chapters, careful readers will detect numerous instances of special pleading, and scores of arguments that go like this:

X is a really good thing for life. It is likely that X must be this way to enable biological function.

Or like this:

X is a really good thing for life. It seems there is no other way to do it, but somehow the cosmos found that way.

The key word is "seems." That word occurs over and over and over again, as do "likely" and "appears" and "perhaps" and "it may be," and in one sense it is a credit to Denton that he is careful not to overstate his case. (His admirers often lack this wisdom.) For this reason, it felt somewhat strange to read the book after seeing Timaeus' chest-beating.

The main impression I got from Nature's Destiny was this: Michael Denton is a Platonist who has a strong preference for typology and for teleological conceptions of the universe. To him, the universe seems to exist just for humans. And so everything he looks at is made to conform to this view. Now, this isn't meant to be an insult or a particularly damning criticism. I have some preferences and predilections of my own (I am decidedly not a Platonist, for example), and I would be a fool to claim that my views are unaffected by these precommitments. My point is that those of us who don't share Denton's somewhat odd viewpoint are able to see just how often his arguments and his choices are strongly affected by the momentum of his cause. To Denton, a lot of things "seem" to be extraordinary. Everything, to Denton, appears to be supremely and perfectly optimized, to the point that he must look for perfection (more accurately, fitness) in every aspect of biology and biochemistry. To me and to others, life just doesn't look like this at all.

And so I see much of Nature's Density as weird and extreme, containing speculations that range from reasonable to utterly off-the-wall, forced by a view of cosmic perfection that I don't embrace for various reasons. In chapter 13, "The Principle of Plenitude," the argument reaches a crescendo when Denton embraces the pre-Darwinian notion that all – or nearly all – possible life forms have been actualized on Earth. Phrases like "seems likely" and "difficult to see" appear multiple times on each page. The equivocation does not, to me, mask the odor of special pleading, which is strongest in the sections on biological evolution.

2. When critiquing "Darwinian" evolutionary mechanisms, Nature's Destiny offers nothing more than standard arguments from ignorance. Again, Nature's Destiny is not the demolition of Darwinism of Timaeus' caricature, but it does occasionally touch on the plausibility of Darwinian explanation. Denton offers nothing new or creative here, simply repeating arguments of the "it is difficult to see how" type. His descriptions of "spectacular adaptations" are enjoyable, but the argument is tiresome and weak. It should be unnecessary to make this point: one does not demolish – or even damage – evolutionary explanations by confessing one's personal incredulity.

This would be a good place to address another aspect of Timaeus' claim that Denton's work in Nature's Destiny "rips the Darwinian mechanism to shreds, armed with thousands of references to the latest knowledge in biochemistry, genetics, embryology, physiology, comparative anatomy, etc." The book contains about 600 notes, at least 1/4 of which are ibids. A few notes refer to more than one reference, but scores are to historical sources such as Darwin, Cuvier and Henderson, all of which are cited repeatedly. And more than half of the book is on fine-tuning topics (water, carbon, etc.) that didn't make Timaeus' list and don't concern the "Darwinian mechanism" as he obviously implies. To call Timaeus' statement an exaggeration is to be generous. The truth is that Denton makes relatively little reference to current science, and when he does he creates a mixture of interesting scientific commentary and shameless cherry-picking.

3. Like Behe, Denton peppers his descriptions of nature with effusive metaphors and confessions of wonder and awe. Cherry-picking and inaccuracies aside, these narratives are entertaining, educational and even inspiring. But they cannot take the place of the argument that needs to be made, namely the argument that adaptations, however spectacular or wonderful, are inexplicable outside of the preferred metaphysical framework. Denton overplays his hand in places, creating the impression that he is willing to substitute "shock and awe" for careful argument. Of course biology is cool. Of course it inspires awe. Not even Richard Dawkins would disagree with that.

So in summary, I found the book to be a bemusing and mostly unsuccessful attempt to defend a view of the cosmos built completely on commitments to typology, teleology, and law-based design. Unlike Behe's Edge of Evolution, the book lacks the sinister implication of deliberate duplicity, and contrary to certain propagandistic pronouncements, it neither attempts nor achieves a damaging critique of evolutionary theory. I recommend that Nature's Destiny be read as a metaphysical treatise, written with a distinctly apologetic angle, and that readers understand that it is characterized by special pleading. And I recommend that anyone who reads it follow up by reading Life's Solution by Simon Conway Morris. Both the overlap and the contrast are striking.

Why I'm not a Behe fan: conclusion and a challenge

About 2 months ago, I finished a series on Michael Behe's latest book, The Edge of Evolution. I concluded that it was a terrible book, displaying significant errors of both fact and judgment. The book's main argument is a population genetics argument, and Behe seems to have little knowledge or understanding of that difficult subject. The book is a joke, and I believe it will someday be seen as one of the more disastrous mistakes made by the ID movement. But I think it's important to distinguish between Behe's errors (which reflect on his scientific credibility and on his decision-making habits) and his thesis. His book is full of mistakes, but that doesn't mean that his proposal is known to be false. So I'd like to make it clear what my verdict on his book actually is, then present an outline of one way to actually test Behe's hypothesis.

1. In The Edge of Evolution, Behe correctly identified a biological process – the generation of genetic variants that lead to evolutionary change – as a likely focus of deliberate design. Having concluded that common descent is true, he reasoned that the trajectory of change through the tree of life might be expected to show evidence of non-random direction. Design, as he and others in the ID movement conceive it, might be manifested in the pattern by which the tree of life came to be. (Some might go as far as to say that it must be manifested in such a way, but I don't think Behe suggests this.) My point is that there is nothing stupid, irrational, or unscientific about Behe's reasoning. So, Behe conceived a hypothesis, which I will restate as follows:

• Based on the consideration of life's complexity, specifically on the consideration of the integrated complexity that characterizes the molecular machinery of the cell, it is proposed that random mutation and subsequent selection cannot fully account for the evolutionary development of biological systems.
• Consequently, it is proposed that the process of mutation is non-random.

Again, I find nothing outrageous or stupid about the hypothesis, or even its rationale. Molecular machines are astoundingly complex and integrated, and I do think it's reasonable to wonder how such things can come about without the aid of a superintelligence. In other words, Behe's proposal is not inherently incoherent or otherwise easily dismissed. Might the machinery of life have emerged through non-random processes? Sure. EoE is a joke, but not because the proposal is a joke.

EoE is a joke because Behe seems not to have even attempted to establish the strength of the hypothesis. Very little of the book is devoted to this central concern, and those sections that take up the task are so laughably wrong that they have led me to question Behe's scientific integrity. (Sorry, no apologies: the errors are too basic, and the proposal too world-altering, to give someone who is vying for scientific immortality a pass on standards of scientific conduct.)

But this is important: Behe's failure to even attempt an honest defense of his proposal does not imply that the proposal has been falsified. It hasn't. It remains possible that the development of biological machines – especially in the early days of the tree of life – was characterized by a non-random, directed trajectory. (I happen to doubt this, but that's not relevant here.) Behe's book is a failure, but his hypothesis stands.

So here we are: an interesting and potentially revolutionary hypothesis has been advanced. It has a certain explanatory appeal, and it has unquestioned relevance for believers of many kinds. It is empirical and rational. And, I maintain, it is testable, at least in principle. And so I'm offering to collaborate on a real effort to test it.

2. Behe's proposal leads to certain types of testable predictions. He claims that the genetic changes that underlie certain levels of evolutionary change occurred non-randomly. In other words, he claims that there is a dramatic mismatch between rates of genetic mutation and rates of evolutionary change. His efforts in EoE were ridiculously inadequate. Here is an outline of an approach that could succeed.

• One major mistake that Behe made was to devote most of his attention to a "case study" in which significant genetic change did not occur. His case study was poorly suited to his purpose, but even if it had been better conceived it would be worthless. We can't learn about how evolution works by analyzing examples in which it didn't occur. (Well, of course it did occur in Behe's case study, but the changes that he claims are non-random are different by his own definition.)
• So, any approach to the detection of non-random influences on evolutionary change needs to focus on case studies that actually involve the relevant level of evolutionary change. Examples should be easy to find, by considering the tree of life and the branching levels at which one would hypothesize non-random change.
• The evolutionary lineage(s) selected for analysis should be fairly well-documented, so that the nature of the relevant common ancestors can be reasonably inferred. This probably means that much deeper lineages (such as eukaryotes or even multicellular eukaryotes) would not make good subjects of analysis. Since Behe is pretty sure that design characterizes differences at the level of class (and deeper), this concern is not a barrier to addressing his hypothesis, at least at those levels of divergence. The tetrapod lineage could serve well, but there are any number of evolutionary trajectories that could be considered.
• Within the selected lineage(s), one or more evolutionary changes would be selected for genetic analysis. Changes could be simple (such as the molecular evolution of a particular protein of interest) or more complex (such as the development of a particular attribute like teeth or feathers or lungs), and could even include the sum total of the genetic changes in a lineage, but must be amenable to genetic description. Most importantly, the evolutionary changes that are analyzed must be associated with the specific design postulate. The goal is to examine the genetic changes underlying an evolutionary transition that Behe would identify as designed.
• Once the genetic changes of interest have been identified, analysis can proceed the way Behe pretended to proceed in EoE: inferred mutational trajectories can be considered in the light of estimated mutation rates and estimated generation numbers. If non-random mutation is clearly necessary for the evolutionary changes in question, it should be apparent that even the simplest mutational paths leading to change are well beyond the explanation of random mutation.

My description makes the undertaking sound straightforward, and in principle it is, but of course such examination of even a relatively simple evolutionary change is a significant and demanding project. Inferring the genetic makeup of the common ancestor is a project all by itself, and constructing postulated mutational pathways is the kind of work that occupies many professional biologists full-time. (Consider the work of Joe Thornton and his group, considered among the best analyses of this kind.) Estimates of generation number will span huge ranges even after the most careful consideration of the variables.

But this is the work that any real scientist and scholar would know has to be done. Behe's hypothesis is completely untested, and only the kind of study that I have outlined can change that. I invite any scholar with interest in undertaking this project to contact me. I would be interested in joining a collaborative effort to test the non-random mutation hypothesis, and I have some significant resources that could be brought to bear on the problem. This is a serious offer, and I would encourage readers to forward it to anyone who might be interested in discussing the details.

And we're back!

Okay, wow, that was a long hiatus. I can explain, really I can. Here's a report on my activities in the last six weeks.

1. I wandered into Telic Thoughts in search of intelligent intelligent design advocates. It went okay -- there was real discussion (because TT actually wants dialogue) but it was painfully difficult to get through some major misconceptions (created by Michael Behe). The painful part was in the thread called Behe's Test, Take 2, in which some of us tried to explain the relevance of some recent work on bacterial antibiotic resistance to "Darwinian" evolution. I'll repost one of my contributions here soon.

2. Some months ago, after hearing Richard Colling give a talk at Calvin (on his ideas set forth in his book Random Designer) my colleague and friend Randy Pruim (of the mathematics and statistics department) and I decided we should get some people together to get serious about this whole question of randomness and God's action. We got a grant from the Calvin Center for Christian Scholarship to fund a yearlong reading group. We've met once already, and it was a blast. I'll separately post on our activities and ideas and my thoughts. Randy, by the way, is also the director of our new HHMI-funded Integrated Science Research Institute (ISRI), and he's devoted a page to our reading group, affectionately known as Random Readers.

3. My blogging buddy over at Clashing Culture, Mike Haubrich, had me as a guest on his cool radio show (Atheists Talk) in the Twin Cities. The subject was "Defending Theistic Evolution," broadcast October 5. It was fun, and I even took an email question from PZ Myers. (Well, it was more like the abstract of a dissertation than a radio show question, but maybe Mike will have me back and we can talk longer.) Some of the questions we discussed:

• How do you separate your science from your belief?
• What is your take on theistic evolution?
• Were humans the goal of creation?
• "All of the facets that shape evolution involve lots of cruelty and pain only partially tempered by the joy of sex. I have trouble reconciling a loving God with what we know about evolution. How do you defend this view of evolution?"

You can listen to the interview at the Atheists Talk page.

4. I'm not the only one who was dumb enough to think that Uncommon Descent is a place where people might be able to intelligently discuss evolution, design and faith; Ted Davis made the same mistake (and I do think we were mistaken to go there in the first place). Last month, Ted engaged in an interesting discussion there, for a time, with two other commenters, going by the names of Jack Krebs and Timaeus. They were soon all banned, because Uncommon Descent is not, and does not pretend to be, a place where thoughtful adults hold discussions. But Ted persuaded Timaeus to come to the ASA email list instead, for the purpose of examining and addressing the perceived animus held by "theistic evolutionists" toward ID proponents. (Note: if you follow any of the links to read Timaeus' posts, you'll see a lot of odd characters, which result from the unwise use of Microsoft Word (!) to compose email.)

The conversation began about 3 weeks ago, and peaked about a week and a half later. It's not over, but everyone seems to be taking a breather. I would say that it's going better now than it did at first, though it still seems that Timaeus (a defender of ID) is not able to understand the reasons why Christians like me can see no good reason to suppose that Darwin's theory is inherently or necessarily atheistic or a-teleological. Timaeus is (by his own admission) a non-scientist, and it shows when he mentions evolutionary theory or quotes the usual ID suspects. (He repeats the "Darwinists never studied non-coding DNA" myth, and is unjustifiably impressed by Denton, Behe and even Egnor.) He has a penchant for propagandistic rhetoric, exacerbated by his shallow understanding of the science that is misused by ID apologists. At first, I thought it was pretty clear that he had come to the ASA to argue for ID, and not to listen to the responses of people who have thought about all of this before. And it's still not apparent that Timaeus understands or respects the evolutionary creation position, or that he finds any significant value in listening to what knowledgeable scientists say about ID proposals. But the last few exchanges have been quite a bit better. When the subject is just plain design, and not science or religion, actual dialogue seems to happen, and we're currently discussing Del Ratzsch's work on the nature of design and the marks it might leave.

Talking to ID apologists about design itself is hard enough without all the pollution of anti-science propaganda and theological incompetence. But maybe there can be some progress, at least toward peaceful coexistence of Christians who do and don't prefer certain types of explanation. So watch for updates on the Random Readers, and I'll post any further discussion with Timaeus here.

Why I'm not a Behe fan, Part IIB: abusing genetics

In a previous post, I started to explain a fact that some people (who don't know me) seem to find surprising or noteworthy. Michael Behe is a Christian who accepts common ancestry and an ancient cosmos, so you'd think I would be excited about the work of a fellow "theistic evolutionist." But I'm not. Two overall problems come to mind. (Basically, I find his conduct as a scientist to be unacceptable, and I find his proposals to be laughable failures.) I'm addressing the second one here. The discussion is quite long, so I divided it into two sections, Part A and this post, Part B, which will have to be split up. I'm sorry about the length; it would really take a whole book to carefully explain how Behe has misused genetics and probability.

1. Behe's fans say that he's a nice guy, and that the evolutionists are "crucifying" him. Both claims seem to be true, but they can't hide some serious problems with his conduct as a scientist.

Those issues are the subject of the first post.

2. Some of Behe's defenders think that he has effectively answered his critics. He has not, nor has he understood or acknowledged the most important criticisms of his crude claims.

Behe's recent book The Edge of Evolution (henceforth EoE) is the focus of this series, and as I exlained in Part A:

EoE makes exactly one specific scientific claim, accompanied by simplistic genetic assumptions and supported by a "case study." The scientific claim is that the mutations that drive large-scale evolution, and that are thought to underlie all evolutionary change (past and present), are non-random. And the "case study" is a long-winded account of the adaptation of the malaria parasite in the face of drugs intended for its destruction.

Part A dealt with the laughable case study. But the heart of EoE is the claim that random mutation rates are insufficient – spectacularly insufficient – to support step-by-step evolution of complex features. The implication, then, is that the mutations that underlie major evolutionary change did not occur randomly.

First, some important points of clarification:

• Behe is not denying that common descent is true, or that evolutionary change results from mutation. He acknowledges both. He is saying that the most important mutations – those that led to, say, new cell types – could not have been random.
• Behe is not saying that the combination of random mutation and natural selection (the "darwinian" mechanism) is not a driving force in evolutionary change. He acknowledges the efficacy of the process in explaining "a number of important details of life," such as drug resistance in bacteria or pesticide resistance in insects, and is willing to attribute the differences between widely divergent organisms to the workings of "randomness." Specifically, he writes that "explicit design appears to reach into biology to a certain level, to the level of the vertebrate class, but not necessarily further." (p. 220) This means that Behe claims to be certain that the major distinctions between goldfish and bats are non-random, but that the major distinctions between bats and people could be accounted for by random mechanisms. (He asserts the "edge of evolution" to lie somewhere between the species level and the class level. [p. 201])
  
• Behe does not commit himself to a particular mode of divine intervention whereby the supposedly non-random mutations came about, and in fact he seems to favor a front-loading scenario in which God "was able to specify from the start not only laws, but much more." (p. 231)

These clarifications are important, because much of the criticism of EoE has been botched significantly. The book is bad, really bad, but it can't be honestly characterized as an anti-evolution argument. Ultimately, Behe seeks to prove that evolution had to be guided. That's the way to understand EoE, and as Joan Roughgarden wisely noted in her review, there are some "constructive" aspects of the book, including the abandonment of opposition to – or even ambivalence about – common descent.

So what's so wrong with Behe's argument in EoE? Well, first, here's the argument summarized:

1. Evolutionary changes in the features of organisms require changes in genomes, changes which occur by mutation.
2. Many of the most interesting evolutionary changes require multiple changes in the same genome, often in the same gene.
3. Mutation rates, in terms of number of mutations per generation, are known to be on the order of 1 in 100 million.
4. Based on this mutation rate, the probability of occurrence of an evolutionary change requiring several mutations is vanishingly small, such that the whole of life's history is not nearly long enough for the change to occur via random mutation.

And here are some ways in which Behe's argument is wrong and/or misleading.

I. Behe's assumption of a particular mutation rate is both absurdly oversimplified and inappropriately extrapolated into the entire tree of life.

The basis of all of Behe's calculations is a mutation rate of 1 in 100 million. This is the estimated rate at which misspelling-type mutation occurs in each generation, averaged over the entire genome, in humans. (The number doesn't consider other types of mutation, now known to be more common than previously thought.) Behe uses this number in all of his (flawed) probability calculations. Even if we knew nothing about mutation rates, the notion of extrapolating from an human (or even mammalian) characteristic to the whole of the biosphere (past and present) is ludicrous enough that it would by itself cast doubt on the credibility of the author.

Rates and characteristics of mutation are the focus of active current research, and many important questions remain unanswered. But we know that there is no such thing as "the mutation rate," in the biosphere or even in particular species. In fact, mutation rates can vary significantly, between types of organisms, between organisms in different states of health, in individual subpopulations of organisms, even between regions of the genome of a particular organism.

More importantly, it is ridiculous to assume that "the mutation rate" has always been the same. Consider a flowchart outlining mutation and its effects, taken from a recent review of the evolution of mutation rates:

Image from "Mutation rate variation in multicellular eukaryotes: causes and consequences," by C.F. Baer et al., Nature Reviews Genetics, August 2007. Click to enlarge (opens in new window/tab).

The idea is that mutations are created in at least two ways: 1) damage to DNA from external influences such as radiation; and 2) errors in the replication process. During the evolution of early life, neither of these influences would be expected to be the same as – or even comparable to – similar influences today. And that's just the beginning of the flowchart. There are error-correction systems that erase mutations before they can be passed on to the cell's descendants; again, only a fool would suppose that these systems have been present throughout life's history; indeed, bursts of mutation that occur today are usually caused by deficiencies in DNA repair and the appearance of "mutator lines" is thought to be an accelerating force in adaptation.

My point is not that we know what the genetic landscape was like during the early evolution of life's toolkit, nor am I claiming that we know whether or not certain mutations were "nonrandom." My point is that the extrapolation of estimated mutation rates in modern humans into the deep past is clearly unjustified, a move so foolish that it can only be the product of folk science.

II. Behe's treatment of adaptation always ignores existing genetic variation, and his arguments seem to assume that multiple mutations must occur simultaneously.

I've mentioned these problems before, and they constitute some of Behe's biggest errors. When he envisions the process of adaptation, in which several genetic changes separate one state from another, he automatically assumes that none of the changes exists at the beginning. Yet even Darwin knew that populations of organisms harbor huge amounts of genetic variation, as evidenced by the profound success of domestication (of plants and animals) by human selection. Most of Behe's critics have noted this, and Behe's response was a lame dodge. But perhaps the critics haven't been clear about why superfast evolution under human selection is such a problem for his ideas. Here's why: since organisms are so profoundly diverse genetically, many of the genetic changes that could be exploited by selection already exist. In fact, current theory predicts that rapid evolution, such as that required after significant environmental change, is much more likely in populations with significant standing variation.

With his simplistic view of genetics and variation in mind, Behe then describes how an adaptation that requires two different changes will be extraordinary unlikely, because the probability of each change is one in 100 million, and the probability of each occurring together is one in 100 million times 100 million. His critics argue, correctly, that his calculations assume that the mutations must occur simultaneously, and that is indeed very improbable. (Although maybe not nearly as improbable as we used to think.) In some of the discussions in EoE, he describes sequential acquisition of mutations (e.g., p. 111), but he calculates probabilities according to simultaneous occurrence (e.g., p. 63). Jerry Coyne explains why this is a gigantic error, and Behe seems unable to understand why.

I've written a separate post about Behe's mishandling of probability. It shows that he is not someone to consult when the subject is population genetics.

III. Behe claims that huge population sizes automatically generate more evolutionary opportunity than smaller ones do. This is incorrect.

It seems so obvious. More organisms means more mutations means more beneficial mutations means more and faster evolution. It's the kind of obvious, simplistic, intuitive claim that forms the bedrock of any folk science. But it's wrong.

On the contrary, very large population sizes lead to a so-called "speed limit" on adaptation that results from competition among beneficial mutations. The phenomenon is called clonal interference and it's particularly well understood in asexual organisms such as bacteria. The basic idea has been around for decades, but measurement and modeling of the phenomenon has been increasing in the last ten years. A very recent report, the subject of an upcoming post here, showed that the beneficial mutation rate in bacteria is 1000 times higher than previously thought – and the underestimation is due entirely to clonal interference.

The effect is not limited to asexual organisms; in fact, the problem of clonal interference is thought to constitute one of the major driving forces behind the evolutionary development and maintenance of sexual reproduction. The idea is that the genetic shuffling that accompanies sexual reproduction can bring beneficial mutations together and increase the effectiveness of selection. One of the few studies to examine this experimentally led to the conclusion that clonal interference is a problem for sexual organisms, and that sex reduces the impact of clonal interference and lowers the evolutionary "speed limit." (Interestingly, the malaria parasite is partly asexual, and reproduction inside a human is completely asexual, so clonal interference is probably a very significant "speed limit" on the evolution of P. falciparum – another reason not to use malaria as a benchmark "case study" for the understanding of all of evolutionary genetics.)

In summary, I find Behe's handling of genetics in EoE to be unacceptable. He seems ignorant of basic evolutionary genetics, and is clearly content to create a folk science alternative to modern evolutionary biology. No one has proven that random mutation generated the wonders of biology, to be sure, and so I'm not saying that Behe's conclusion is known to be false. I'm saying that his attempts to establish his conclusion have failed miserably, as have his responses to his critics, and the result is that he cannot be trusted as a careful, thoughtful, knowledgeable critic of evolutionary science. EoE is folk science, nothing more.

My final post in the series will have closing comments and some ideas for how we might go about posing questions about the processes that yield biological design.