Darwin’s Black Box

If a theory claims to be able to explain some phenomenon but does not generate even an attempt at an explanation, then it should be banished. Michael J. Behe, DBB p.186

Note: This is an ongoing post made over many days. The dates that matter are the ones found below. Newest posts are at the bottom, to maintain proper reading order.

Entries to this post are below the table of contents.

Table of Contents for this post (click on titles)

1. Behe is incoherent on what design and evolution are (8.12)
2. “Design” for Behe is merely an attempt to redefine biochemistry as designed (8.13)
3. In criticizing Dawkins, Behe conflates Paley’s “design” with his own (8.14)
4. Behe brings up physical precursors, then fails to acknowledge their ubiquity in organisms (8.18`)
5. What are the odds that designed entities would be composed only of “physical precursors”? (8.19)
6. Behe is misleading about textbooks (8.20)
7. Design in life is easy to detect–look for breaks in evolution (8.21)
8. Large questions are fine–if it’s the Big Bang (8.26)
9. Blood clotting’s dependency on Vitamin K leaves us vulnerable (8.27)
10. With causes of evolution of clotting given, Behe declares otherwise (8.28)
11. The primary issue at stake is the foundation of knowledge (9.2)
12. Endosymbiosis shows how some cell transport evolved (9.3)
13. Science is about evidence of occurrence, not mere possibility (9.9)
14. Evidence for the complex evolution of oxygenic photosynthesis is strong(9.11)
15. Photosynthesis facilitated the “Cambrian explosion” (9.15)
16. So, why were Ediacaran fauna, and Hallucigenia, designed? (9.17)
17. So why were the Ediacaran fauna designed, then annihilated? (9.18)
18. Evolution of the eukaryote flagellum (9.22)
19. Eukaryotic flagella are derived from intracellular transport systems (9.23)
20. Common descent is demonstrable only when causes are known (9.24)
21. The cilium evolved into part of the “irreducibly complex” chordate eye (9.27)
22. Behe denies all avenues to understanding the evolution of pathways (9.29)
23. Behe and language origination (9.30)
24. If evolution is true, why can’t gazelles run 433 mph? (10.2)
25. Evolution of adaptive immunity I–Phylogeny (10.6)
26. Evolution of Adaptive Immunity II–Building on Innate Immunity (10.8)
27. Evolution of Adaptive Immunity III–It Has the Marks of Irreducible Randomness (10.11)

1. Behe is incoherent on what design and evolution are

Behe tends to define terms as he desires, and then to redefine them again, with no consistency, reason, or scientific justification for doing so. For instance, he apparently just makes up his own definition of “macroevolution”:

Roughly speaking, microevolution describes changes that can be made in one or a few small jumps, whereas macroevolution describes changes that appear to require large jumps. DBB 14.

That simply isn’t true. Roughly speaking, microevolution involves changes within species, macroevolution occurs when species evolve. There is no difference in size of “jumps” inherent in the definitions at all. Here Behe seems (if witting–which is by no means certain) to be trying to change the discussion by shifting terms from what they mean.

Parenthetically, I suggested above that Behe might be unaware of his redefinition of microevolution and macroevolution (which remains a good possibility), and yet in his preface he would seem to suggest that “Darwinism” explains only microevolution, as it is known to science. There he writes:

Darwin was ignorant of the reasons for variation within a species (one of the requirements of his theory), but biochemistry has identified the molecular basis for it. DBB x.

He does not write that Darwin only explains variation within species, I would emphasize. Yet the context involves his continuous claims about how complex life is and how this complexity is not explained by Darwin. Your average creationist might be comforted by the quote above–which is in the preface, I repeat–for it seems to suggest that evolution might be very limited indeed.

Nevertheless, Behe rather quickly allows that larger scale evolution might happen by Darwinian means. On page four of DBB he writes that “Darwin’s idea might explain horse hoofs, but can it explain life’s foundation?”

Much of the rest of Behe’s argumentation seems to suggest that only complex metabolic pathways are really a problem for evolution. Paley had argued that the eye is so well-made (with “relational” parts) that it must be designed, while Behe’s argument against the evolution of the eye moves directly to the “black box” of the biochemistry of the eye (DBB, 18 and on).

Biochemical pathways are what require “large jumps” in his view, so he focuses on these. Nevertheless, he returns to granting very little to evolution by stating that Darwinism “explains microevolution very nicely” (DBB, 22). To most evolutionists and creationists, that allows very little evolution, in fact. And even if we were to accept his “definition” of microevolution, what does it even mean? What is a “large jump”?

At one point he even states that, “The behavior of hemoglobin can be achieved by a rather simple modification of the behavior of myoglobin…” and he states that therefore the case for design (he considers doubt regarding evolution to be evidence of design) of hemoglobin is weak (DBB, 207). And since hemoglobin apparently evolved prior to our split from lampreys, that would suggest that an enormous amount of evolution could occur. Mostly his “unevolvable” systems in DBB date back to the Cambrian or earlier.

As I have previously stated, I have not yet read Edge of Evolution. Nevertheless, reviews of the book give evidence that, as implied in DBB‘s preface, he may not allow for much unassisted evolution. Here is a quote from Edge of Evolution:

“If two mutations have to occur before there is a net beneficial effect – if an intermediate state is harmful, or less fit than the starting state – then there is already a big evolutionary problem.” (Edge of Evolution, p.106, as quoted at

Of course various evidences are against that conclusion (many disadvantageous mutations persist in populations), including the fairly recent report of the evolution of citrate transport in E. coli in extremely small populations (compared to the world, that is) and in a fairly short time. That’s not the point I wish to make with today’s entry, however. Currently I wish to demonstrate what extremely variable and mostly useless “criteria” he uses in these discussions, at least prior to Edge of Evolution. How anyone is to make sense of his incoherent usage of terminology and concepts, I do not know.

His use of the word “design” is equally reprehensible in intellectual terms, but I will leave discussion of that for tomorrow’s entry. These discussions of terms are not especially interesting, in my view, but they are essential to start off the discussion of the remainder of the issues in Behe’s writings. For, it is difficult to make sense of Behe, and one might end up criticizing what he wrote in one area, when he does not make the same error in another area.

Because Behe really has little or no idea of what is possible in evolution (the complexity that does make particular evolution more difficult in isolation also increases the material with which evolutionary processes may proceed, a fact that he does not adequately consider), and even less idea of what meaningful criteria for design are, he shifts the meaning of terms with little regard for scientific precision and accuracy. Yet it seems likely that anyone who thinks “anything might have been designed” (DBB, 205) is essentially uninterested in what terms and concepts mean–especially the most central word in his “explanation”, the word “design.”

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Glen Davidson

2. “Design” for Behe is merely an attempt to redefine biochemistry as designed

Ought it then to be said, that, though we have little notion of an internal mold, we have not much more of a designing mind? The very contrary of this assertion is the truth. When we speak of an artificer or an architect, we talk of what is comprehensible to our understanding, and familiar to our experience. William Paley Natural Theology chapter 23.

Prior to the quote above, Paley was criticizing metaphysical ideas of “internal molds,” which according to some were responsible for the forms of organisms, as being vacuous. In that quote, he fends off any notion that his “designer” would be meaningless, or something much different from what we understand about human artificers and architects. We don’t know what a designing mind is? Perish the thought, is Paley’s response.

Contrast this comparatively scientific viewpoint (to which Paley only partly adheres) with biochemist Behe’s decidedly unscientific claims about design. He writes:

What is “design”? Design is simply the purposeful arrangement of parts. With such a broad definition we can see that anything might have been designed. DBB 193

To support the last sentence of that quote he points out that an accident might be staged, apparent chance meetings might have been arranged, art may be made to look “random”.

Could anybody come up with a less useful notion of “design” than that one? Importantly, he has nothing that shows design in the manner that Paley suggests is reasonable, so he claims that anything could be designed. Of course that is as meaningful as saying that any and every scientific measurement might be faked, that it is designed to produce desired conclusions, rather than to actually measure a given phenomenon.

What may be even more important is that there he essentially concedes that his oft-repeated definition of design as the “purposeful arrangement of parts” has no rigor, and basically no meaning. And of course it does not. In the first place, a “purposeful anything” indicates design in the broader meaning of “design,” so adding “arrangement of parts” does nothing other than to attempt to deflect questions of how to discover “purpose” and to prejudice people into supposing that arrangments of parts indicates design.

Even he knows that evolution produces “arrangements of parts.” So does the wind. And if one recognizes that he has absolutely no means of discovering purpose at all (though he often conflates purpose and function), clearly he’s trying to redefine “arrangement of parts” as design.

Of course he’s doing more than just that in DBB. He’s trying to demonstrate that some aspects of life cannot have evolved. Yet cleric Paley even had the sense to recognize that merely showing that the other ideas don’t work isn’t good enough, that the word “design” has to refer to something limited and meaningful, and that life has to yield up evidence that is “comprehensible to our understanding, and familiar to our experience,” if life is to be rightly identified as being the result of design. One cannot criticize another’s ideas for being vacuous, if one’s own idea has no limits, nor criteria for adducing positive evidence in favor of one’s claims.

Paley the cleric was trying (if not succeeding) to do what Behe the biochemist does not attempt, or even seem to understand to be part of science: To come up with actual evidence of design that is claimed to be evident.

In order to be more specific and meaningful than Paley himself was, I would note that an “artificer or an architect”–in other words, a designer–is rational, purposeful, able to take an idea from one context and to put it into another one, and (one hopes) is capable of novelty. These aspects are basically missing from life, although one might excuse Paley for thinking that these attributes exist in biology.

“Design” will be revisited in many future entries. I wanted to make a more general criticism of Behe’s (non) concept of “design” near the beginning, because his lack of a meaningful design concept undermines everything that he states regarding design, and evolution.

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3. In criticizing Dawkins, Behe conflates Paley’s “design” with his own

About a year and a half ago, I heard two lectures by Behe, and went to a question and answer session, at a religious college. Behe said at one point that ID was not, in fact, a dead end, for if one found some designed machines on a planet somewhere with none of their creators in sight, one would still be interested in trying to figure out why the machines were made, and who the designers were. This begs a good many questions, like how he can compare the alien designs that we could hope to understand, with his supernatural “design” that he insists cannot be understood regarding purpose and means of designing. However, the question I wanted to ask him was, how does he even distinguish between machines and life, considering that his lectures suggested that he saw life as a collection of machines which are quite analogous with our own designed machines.

I didn’t get to ask that, though, because the college students were allowed first dibs on asking questions, and one ignorant loudmouthed “social work” student ranted on for a considerable period about how dishonest scientists were to deny design when, as Behe had claimed, all scientists admit that aspects of life appear to be designed. Unsurprisingly, not all scientists do so:

However, where a creationist sees a design or plan, a scientist sees merely order, or regular arrangement.… The fact is, order in nature is no evidence of design.

Douglas Futuyma. Science on Trial. New York: Pantheon Books, 1983. p. 114

How many scientists do or do not agree that aspects of life appear designed I wouldn’t presume to even guess, but a lot of Behe’s “argument” for design rested on the “fact” that all agree with that claim. Hence a single example (of a well-known evolutionary biologist) suffices to demonstrate that Behe confuses the universal with the specific, as well as relying on Dawkins’s authority (a fallacy onf Behe’s part) to make his generalization. It is, indeed, true, as one reads in Darwin’s Black Box, that Dawkins does understand life to have the appearance of design. Here is one of Dawkins’s strongest statements on the issue:

Biology is the study of complicated things that give the appearance of having been designed for a purpose. p. 1 Dawkins The Blind Watchmaker New York: Norton, 1987

In light of the quote above, I would have to ask Dawkins, along with Behe, for what purpose do liver flukes appear to have been designed? Aristotle, thanks to his philosophical viewpoint, could believe that the organism is the end or telos of the parts of which it is made, but it makes no sense in the philosophy of science nor in Christian philosophy to make the same assumption of “purpose” of parts when the whole organism (or ecology) has no discernable purpose. Paley waffled on this issue, sometimes suggesting that “design of the parts” was sufficient evidence of design, yet always looking for a purpose beyond mere metabolism and reproduction.

With that caveat out of the way for now, here is what Behe makes of Dawkins’s various statement about the “appearance of design”:

A crucial, often-overlooked point is that the overwhelming appearance of design strongly affects the burden of proof: In the presence of manifest design, the onus of proof is on the one who denies the plain evidence of his eyes. DBB (copyright 2006) p. 265

Of course Dawkins is not saying that design is manifest, particularly with close study. What really makes Behe appear hypocritical, however, is that Dawkins’s various statements regarding the “appearance of design” are largely focused on Paley’s macro-scale “case for design” (“The analogy between telescope and eye, between watch and living organism, is false. All appearances to the contrary…” The Blind Watchmaker, p.5) and Behe himself warns against assuming design on the macro-scale:

So those who labor in the fields of paleontology, comparative anatomy, population genetics, and biogeography should not invoke design until the molecular sciences show that design has an effect at those levels. DBB 230

Behe himself is saying there that Paley’s examples, to which Dawkins is referring in the main, should not be accepted as having been designed, unless molecular science indicates that it was (by confusing function and purpose, in Behe’s scenario). Behe himself is stating that Dawkins is wrong to infer design in Paley’s examples, and yet in the earlier quote he was placing the burden of evidence on Dawkins (the context for the quote from page 265) to show that Paley’s examples are not designed. Talk about double-speak!

I am not claiming that Dawkins does not also accept that the appearance of design exists at the molecular level, for evidently he does. My only point on this specific matter is that Behe hypocritically chides Dawkins for denying that the “appearance of design” indicates design, when Dawkins is mostly discussing examples in which Behe himself denies that the “appearance of design” actually indicates design–until it is “shown” to exist on the molecular level.

I will not speculate on whether Behe deliberately confuses the “appearance of design” that Dawkins discusses, with his own “proof of design,” or if he is simply that bad at arguing evolution and ID. It suffices to say that he is wrong on this, as he is on most issues (at least regarding some aspect or another of an issue). He has no business trying to make a big deal about Dawkins’s claim that life “appears designed,” since he himself denies that most of the examples of “appearance of design” to which Dawkins refers actually do (by themselves) indicate design.

Again, I make this post not only because this issue matters in Behe’s case, but also because it indicates how sloppy (at best) he really is in his argumentation. There is little point in moving on to more specific problems of DBB before demonstrating how contradictory, incoherent, and just plain wrong his argumentation is in general.

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4. Behe brings up physical precursors, then fails to acknowledge their ubiquity in organisms

“…Can we evolve a bicycle into a motorcycle? …A motorcycle depends on a source of fuel, and a bicycle has nothing that can be slightly modified to become a gasoline tank. And what part of the bicycle could be duplicated to begin building a motor?” DBB, 44

“A bicycle thus may be a conceptual precursor to a motorcycle, but it is not a physical one. Darwinian evolution requires physical precursors.” DBB, 45

The fact is that in DBB Behe hits on a very important phenomenon in determining whether or not evolution occurs, which is that evolution requires, and predicts, that any complex organ or system needs physical precursors. A designed object, like a motorcycle, does not. He carefully avoids generalizing what he says in the quote, and, as predictably, he avoids testing evolution on the availability of “physical precursors of systems and organs. Yet it is there, he does tell us that a motorcycle cannot evolve because it does not have the beginnings of components that are necessary for an evolution.

And what does he do in the rest of the book? He assiduously ignores or minimizes the importance of the fact that life is made up of modified parts, which he recognizes in the quote above is not the case in designed entities like motorcycles. Right there is a crucial difference between designed and evolved objects, and even though he is willing to bring up the difference in yet another of his ill-suited analogies, he will not mention the importance of the fact that most of his “irreducibly complex” systems are made up of components that, totally unlike a gas tank for a motorcycle, are known to have uses in other systems and pathways (he does point out a few biochemicals that do not have related molecules in other systems–though biomolecules lacking known relatives would not be unexpected in evolved organisms).

For instance, does Behe bring up the fact that the complement cascade is shared by both the adaptive and the innate immune systems, and that there is evidence that these molecules evolved first for the innate system? Certainly not, he writes as though adaptive immunity arose with no antecedents. Does he discuss the fact that adaptive immunity may have arisen to spare symbionts? No. And although I do not know if that hypothesis was well known when DBB was written, his lack of imagination is no argument against evolution. He does in fact bring up “an alternative pathway,” the innate immunity, on p. 134 of DBB, which he notes can active the “membrane-attack complex.” Yet he does not admit that adaptive immunity would therefore indeed have the innate immune system upon which to piggyback the evolution of adaptive immunity (such evolution still has a great many gaps, as might be expected of such an old system, but Behe’s clearly not stating the matter fairly).

I intend to discuss the points in the above paragraph in more detail in a later entry.

Getting back to his pathetic bike to motorcycle “analogy” with evolution, clearly adaptive immunity did have a “gas tank” or “an engine” from which it could evolve step by step. No matter what problems remain, this completely undermines this particular analogy, which is really quite a misleading bit of rhetoric. Notably, there is no meaningful analogy between the designed objects that humans make, which very frequently have components which are taken from an entirely different sort of “conceptual evolution,” and biological evolution, which in many lineages is almost totally incapable of using anything but “physical precursors” coming from direct ancestors.

Other examples are much the same, like the clotting cascade. When I heard him speak, he did admit that many of the molecules involved in clotting do indeed have relatives acting in other pathways, but in DBB this fact is generally smothered over. For, if he were to honestly face up to his own proclamation that “Darwinian evolution” requires physical precursors, while design evolution can make do with conceptual precursors, he would be stuck admitting that Darwinian evolution typically has evidence of such precursors in biochemical (and morphological) relatives–and to the degree that it does not, there are reasonable explanations for this (like the extinction of biochemical relatives–extinction being a prediction of any real evolutionary scenario).

There is little question that Behe slit his own throat by bringing up in DBB the necessity of “physical precursors” in organisms (aside from lateral transfers of genes, that is) under the “Darwinian” scenario, while designed objects like bicycles can make do with “conceptual precursors”. Had he properly analyzed the biochemical pathways in his book according to that crucial distinction, he’d have done nothing but to show, first, that they were not designed, and second, that they in fact evolved. Instead, he ignores, or smothers the importance of, the large number of cases where physical precursors do indeed exist for exactly the kind of evolution that he denies happened, and instead he tries to shift the test for evolution away from his very own criterion on page 45 of DBB, instead insisting that we explain the details of an evolution which happened very long ago and without leaving much evidence regarding its pathways. Making up stuff is the very means of “ID science,” as most of us already know, but it is not the way that real science operates.

There is much more to be said regarding these issues. At this point, it is sufficient to demonstrate that Behe is completely and utterly oblivious (unless he is wittingly dishonest) to the manner in which his very own distinction between “conceptual precursors” and “physical precursors” destroys his design claims, and bolsters “Darwinian” evolutionary theory. Said distinction is probably the single best scientific test for “Darwinian” evolution, and the cumulative evidence is thus very much in favor of life having evolved sans design. So the truth is that Behe and ID are not completely without an understanding of science–they just know enough in order to refrain from applying such tests whenever and wherever they recognize that ID will fail such tests.

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5. What are the odds that designed entities would be composed only of “physical precursors”?

Behe does a great job of changing the subject to problems of evolution, and exaggerating them. What he never does at all well is to explain why things look as they do, why even his precious little “irreducibly complex” biochemical pathways are largely composed of demonstrable “physical precursors”, and are never demonstrably composed of any merely “conceptual precursors”. He produces good PR when he tries to suggest that evolution has questionable odds, but he never touches the odds against life being composed exclusively of physical precursors when it is supposedly designed–and for a very good reason, since that is far less likely than the odds against any evolutionary pathway whose details remain obscure.

Casey Luskin even gave us an ID “prediction” that is testable and falsifiable, and of course, it has been both tested and falsified:

(3) Intelligent agents ‘re-use’ functional components that work over and over in different systems (e.g., wheels for cars and airplanes):

“An intelligent cause may reuse or redeploy the same module in different systems, without there necessarily being any material or physical connection between those systems. Even more simply, intelligent causes can generate identical patterns independently.”

Mostly bogus “predictions” of ID, plus a falsified one

Why yes, C. Luskin and M. Behe, intelligent agents can re-use parts independently of heredity and lateral transfers. So if ID is responsible for life, why don’t we see bat wings on pterosaurs, bird wings on bats, or octopus eyes in vertebrates?

Luskin made a very big mistake there, just as Behe did in noting that designed motorcycles are not dependent upon inherited (or laterally transferred) genetic materials. There is absolutely no evidence of independent agents producing similar systems in organisms without there “being any material or physical connection between those systems,” unless you consider what humans genetically engineering organisms (although Luskin obviously doesn’t recognize that intelligent agents are a part of the “material or physical connection” between such systems).

So come on, Behe, tell us what the odds are that life would have all of the patterns expected of undirected evolution, including a continual reliance upon and limitation to “physical precursors,” if in fact life was designed? Astronomically against, is it not? And one can’t simply resort to the typical expedient that “we don’t know what the designer wants.” Clearly the only explanatory or scientific reason to ever bring in a “designer” would be to explain why life has evidence of design, such as organs or systems having some merely conceptual precursors. Both Luskin and Behe fail to come up with a single clear instance of such evidence, hence they owe us an explanation for why design does not immediately fail the test for “conceptual precursors,” which ought to exist in designed objects.

I will state more definitely now what is at stake here: Luskin and Behe need to supply the evidence that conceptual precursors (even if these are first principles) exist in organisms, as both of them have indicated that this would be expected from intelligent agents. This is a strong test for their ID claims. And, they need to tell us what the odds are of designed entities having purely physical precursors, as well as these existing in the patterns expected from undirected evolution. This is a strong test (actually, several tests summed up as one) of evolutionary theory.

Unless they can demonstrate that conceptual precursors (or re-used modules without “material or physical connections,” using Luskin’s botched phrase) exist in organisms, ID fails. And unless they can produce a “designer” that oddly “designs” only by using physical precursors, evolution wins–at least until something else comes along that can explain what evolution does, plus being able to explain even more. That is how science works. ID ends up being falsified using its own predictions, and nevertheless it continues claiming to be a “legitimate science” that is “persecuted” by being treated like every other hypothesis that the evidence has failed to support.

Too many replies to Behe are focused on responding to the framing (that’s about all that we get from Behe) that Behe builds in order to avoid the colossal lack of explanatory value, along with avoiding the glaring falsification of genuine prediction, of his own “ID program”. There is, in fact, nothing wrong with responding to his questions, for many of these do in fact touch on important remaining questions in evolutionary biology.

However, both Luskin and Behe should have their feet held to the fire over the enormous lacuna that ID is. ID is not something that has gaps, it simply is a gap, one that would like to replace what we do know with the bleat “God did it,” or in another version, “the Designer did it.”

One can make predictions with an “intelligent design” hypothesis. Both Behe and Luskin have done so (though Behe did so more implicitly than Luskin’s explicit prediction), and their predictions have been falsified. Were they actually interested in doing science, they would acknowledge this fact, and drop ID altogether.

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6. Behe is misleading about textbooks

From pages 180 to 183 of Darwin’s Black Box, Behe discusses, of all things, biochemistry textbooks with respect to the numbers and types of mentions of evolution in the indexes of these texts. Not molecular biology textbooks, cell biology textbooks, or genetics textbooks, apparently the standard is biochemistry textbooks. Is that perchance a result of his being a biochemist? Possibly?

His point is, of course, that evolution is not discussed much in biochemistry texts, and he disparages many that are there.

There are several rebuttals to make. One is that biochemistry is mostly about unchanging chemical processes, and fairly well conserved biochemistry. Another is that there are many mentions of evolution in at least my old biochemistry text which do not appear in the index. Furthermore, my biochem text uses evolution to justify its discussions of “model organisms”. And the last point is that non-biochemistry biology texts of the time did mention evolution a good deal more than his biochemistry textbooks.

Behe makes a sloppy case in just about everything he discusses (with relation to ID, anyway). It is impossible to know how much of this is due to ignorance, and how much is due to lack of concern for the facts. However, I can show how meaningless his little table of numbers of mentions of evolution in biochemistry textbooks is, by listing a considerable number of mentions in my biochemistry textbook. Behe has a table of 30 biochemistry textbooks (many are different editions of single textbooks) on page 182 of DBB, many of which have zero mentions of evolution in their indexes, and none of which has more than 22. The textbook I used in my biochemistry course is in the median, at 12 index entries. This textbook is titled Biochemistry, written by Moran, et al., 2nd edition, published by Neil Patterson, and copyrighted in 1994 by Prentice Hall.

In the first place, even the count of 12 entries is misleading, since there are 16 places in the text indexed, since some entries have multiple text references. That’s still not a lot, however.

When we consider mentions that are not in the index, however, the number doubles, just using the ones that I found by scanning. I couldn’t have found all of the times evolution was brought up, but here are the ones I found fairly quickly which are not in the index, with representative text (so you know it’s really about evolution):

1. 2-2 “The basic plan of the ancestor cell has been elaborated upon with spectacular inventiveness by billions of years of evolution.”

2. 2-4 “Yet evolution has produced tremendous diversity…”

3. 27-4 “The distribution of antigenic determinants in the B components of DNA-dependent RNA polymerases of archaebacteria, eubacteria, and eukaryotes suggests the primeval character of the extremely thermophilic archaebacteria.” [the accompanying figure compares RNA polymerases across the three domains of life]

4. 27-23 “The deduced amino acid sequences show considerable similarity in spite of their distant evolutionary relationships”

5. 29-7 “In plant mitochondria and in chloroplasts, the standard genetic code is used. But in mitochondria of all other organisms, there are some deviations from the standard code (…). …And it has been suggested that the altered genetic code allows translation to proceed efficiently…”

6. 29-12 “Conservation of the nucleotide sequence in the D arm is more pronounced among eukaryotes than between prokaryotes and eukaryotes.”

7. 32-8 “These parallels suggest that bacterial transposons and retroviruses might be distantly related. As we will see in the next section, eukaryotic transposons and retroviruses are even more intimately related.”

8. 32-17 “Most mammals appear to be descended from a common ancestor that lived approximately 100 million years ago, indicating that the organization of genes can be preserved for a considerable time.”

9. 32-19 “Closely related species, such as mouse and rat, which diverged only 30 million years ago, can differ significantly in the amount of repetitive DNA.”

10. 32-20 “These pseudogenes share a common ancestor with a corresponding intact gene.”

11. 32-22 “This is probably because the various genes that make up each family were generated by localized gene duplications that occurred relatively recently.”

12. 32-33 “Any theory concerning the evolutionary origin of introns must satisfactorily explain why the vast majority of prokaryotic genes do not contain introns.”

13. 32-25 “As is the case in bacteria, there has likely been selection for a small genome in this organism.”

14. 32-27 “We have seen that the organization of the genome can change as a result of evolution, but large-scale reorganizations are only evident after millions of years.”

15. 32-33 “The available evidence suggests that introns in protein-encoding genes arose late in evolution.”

The best mention of evolution not in the index explains why model organisms are useful in general:

16. 2-31, 2-32 “How do we use knowledge gained from biological systems as evolutionarily remote from us as E. coli? As we probe deeper into the chemistry of life, we find that at the molecular level diversity gives way to unity, and themes emerge that pertain to all life. Knowledge gained from studies on an accommodating organism like E. coli can be applied to more recalcitrant model systems, such as the rat. With educated intuition developed from studies of simpler systems, researchers can devise experiments that coax more complex systems to reveal their own intricate mechanisms.

A proper appreciation of the balance between unity and diversity is essential when assessing results of biochemical studies. It is highly unlikely that glycolysis in E. coli will be regulated in exactly the same way as glycolysis in rat liver cells. Yet with experience, patterns of regulation are detectable.”

Granted, these do not bring the total up to anything enormous. Yet the authors recognize the importance of the relatedness of all life in the study of biochemistry, since evolution is responsible for relatedness, and for divergence. Note #9, evolution is mentioned when it has to be, such as where closely related organisms diverge in the amount of repetitive DNA.

Of course, evolution is a theory of biology, and biochemistry is, in the main, about chemistry. The explanation for why evolution is not dealt with greatly in a biochemistry text like mine is given in the first chapter of the same text:

One might at first assume that biochemistry is merely a combination of two major sciences, chemistry and biology. However, the defining feature of biochemistry is that it uses principles and language of one science–chemistry–to explain the other science–biology–at the molecular level (chapter one, page one, of Moran et al.)

Of course biochemistry texts aren’t especially heavy on evolution, as in many ways it’s an extension or application of organic chemistry to life. Even so, a text like the one I own does invoke evolution not infrequently, since design is hardly responsible for either the unity or divergence found in life. At the beginning of chapter 32, this is written:

Until now, we have assumed that a gene is unchanging, static over time. We have implied that a gene exists at a fixed locus in a chromosome and that its structure and function are not affected by rearrangement or recombination….

This gradual change in genetic information is the basis of evolution. (Chap. 32 p. 1 of Moran et al.–this, by the way, is found under “evolution” in the index).

Why would they ever treat the gene as if it were static? The answer is quite obvious to anyone who understands the issues, biochemistry is dealing with the chemistry of what is found, not being particularly interested in evolution as such. The basics are being taught, and then these basics can be applied to dynamic systems.

So as usual, Behe is misleading in DBB. While this is not an especially important matter, it goes to show that once again Behe has distorted the issues, particularly for the many naive people who are likely to read his book.

Although I have shown that at least my textbook finds evolution to be important despite its emphasis on applying chemistry to biology, I also took a look at my old cell biology book from around the same time period. It is Molecular Biology of the Cell, 3rd edition, by Bruce Alberts, et al., New York, Garland Publishing, 1994. I counted 81 entries for evolution in the index, many of which have multiple page listings. There are three more entries under “Evolutionary Relationships.” I didn’t bother even looking for mentions not found in the index.

Molecular biology is a lot more like what biochemistry is not, a combination of chemistry and biology. Is it at all surprising that it deals much more heavily in the biological theory of evolution?

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7. Design in life is easy to detect–look for breaks in evolution

Since Dawkins agrees that biochemical systems can be designed, and that people who did not see or hear about the designing can nonetheless detect it, then the question of whether a given biochemical system was designed boils down to simply adducing evidence to support design. DBB, 203

Behe gets that much right. But how do you adduce evidence to support design? Well, a rationally thought out system would indicate design, and so would some actual purpose in living organisms, to bring up two important criteria. Less precisely, “conceptual precursors” instead of “physical precursors,” would fit the bill, as Behe pointed out, and as I discussed previously. Or another way of putting that fairly inchoate (but usable) conception–and extending it somewhat–would be that we would look for arrangements that do not fit evolutionary patterns.

In other words, probably one of the best ways of looking for design candidates would be to find something that does not fit with evolutionary predictions. After all, what would be a better potential marker for intelligent design than something that wouldn’t occur via natural processes (now using the definition “natural” which means “not caused by humans”)? One would probably still have to check to see if rational thought was used, and if the putative “design” serves a likely purpose, but merely breaking the mold of evolutionary expectations would tend to suggest that something has intervened in the natural processes of evolution.

Behe himself brings up the subject, writing, “…The work does show that an intelligent agent can design a system exhibiting biochemical-like properties without using the biochemicals known to occur in living systems.” DBB 202.

Yes, finding something like that would indeed be a pretty good first indication of design. For instance, find an malaria strain that has a completely new protein, which also has novel amino acids in it. But we wouldn’t have to be that exacting in our demands, a completely new protein would certainly flag researchers that this strain of P. falciparum likely was engineered.

By the way, I used Plasmodium falciparum for an example quite on purpose, since it does not normally share genes with other organisms (not so far as I know, anyway), like anthrax does. Since sharing genes is “natural” for anthrax, and not for malaria, a new protein in the latter would break the evolutionary expectations rather better than a new (or unknown) protein in anthrax would.

There are less clear examples of design, those which simply take a gene from one organism and insert it into a very distantly related organism. Interestingly, these also are relatively easy to find, at least so long as we have their genetically unmodified relatives around. I really do not think that aliens that came to earth would have any difficulty discovering that many of our food crops have been genetically modified by injecting the Bt gene (which produces an insect-killing protein) into these crops, even though the Bt gene has evolved naturally.

Aliens could discover design of Bt crops because, of course, Bt in corn breaks the evolutionary patterns of inheritance and change. Corn, like P. falciparum, does not typically receive genes from other species, while intelligent humans know how to insert Bt genes into the corn genome. To be sure, there are other tell-tale marks of genetic engineering, although many of these are also taken from nature and placed in “unnatural” contexts (like viral promoters are). Nevertheless, even if the genes were entirely “natural,” the fact that evolution would not be expected to produce corn plants with Bt toxin (and liverworts are not) would tend to give the game away. The other “unnatural” components only enhance the notion that Bt genes and other deliberately introduced genes were “designed” to at least a degree.

So why doesn’t Behe drive home the point that he delicately prompts, namely the easy manner in which human designs in nature could be detected (though generally they are detected by looking for known specific patterns of “engineered” genes), by recognizing their breaks from the evolutionary patterns? There is only one reason, this being the fact that he can produce nothing that does not fit the expected evolutionary patterns (aside from our own interventions). He wants to suggest in DBB that there is really no problem with deciding that life was designed because we can do it, while he pointedly ignores the fact that our interventions do not follow the (evolutionarily-produced) taxonomic patterns of nature, and also need not rely upon physical precursors (although we often do–yet we produce unnatural patterns even then).

The fact is that, in both of Behe’s books, he avoids integrating knowledge. That is unsurprising, since said lack would be expected in a creationist. He’ll happily bring up human modification of life as an analogy, but he will not discuss the fact that quite obviously our designs purposefully break the evolutionary patterns, unlike what we see in wild-type organisms. He insists that design can be detected in life (which almost all of us have agreed was possible from the beginning), but he avoids the fact that design would not follow evolutionary patterns, nor would it rely upon physical precursors, as empirically-known evolution does.

The one thing that we would expect almost any kind of biological design to do–step in where evolutionary limits prevent a desired capability–is absent from biology. And even more absurdly, Behe insists that evolution cannot produce complex biology–which conforms to evolutionary limitations–but he insists that design nudged evolution along without producing any of the evidence of genetic modification that even humans have done with their decidedly limited late 20th and early 21st century capabilities. Intelligent intervention is supposed to have occurred, and yet that intelligence didn’t dare to break the rules of evolution, or to deviate from evolutionary patterns.

Instead of breaking the evolutionary patterns, as we would expect of design, Behe insists that design is responsible for complex evolutionary patterns. Has any other crank scientist ever worked so hard to avoid the meaningful tests of his claims as Behe has with his “intelligent design”?

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8. Large questions are fine–if it’s the Big Bang

Behe finds fault with scientists who do not accept the evidence when large questions remain:

It is impossible to deny that the Big Bang has been an enormously fruitful physical model of the universe and, even though large questions remain (as they inevitably do in basic science), that model was justified by the observational data. Scientists such as Einstein, Eddington, and Hoyle fudged and twisted in their efforts to resist a scientific theory that flowed naturally from the data because they thought they would be forced to accept unpleasant philosophical or theological conclusions. DBB, 45.

It’s now well over a decade since that statement was first made, and still no sign of self-awareness from Behe. In it, he mischaracterizes Einstein’s role in the matter as well.

Basic science is not the only type that has many questions left, of course, and it is generally accepted that historical sciences will be increasingly patchy in the details the further back one looks. Not for Behe, though, who blithely demands all of the details. Or rather, he demands all of the details for evolution, but not for geology, for ancient plate tectonics, for the crash of Theia into earth creating the moon, or for the Big Bang. And he certainly does not demand any details regarding his so-called “design,” nor even any identifiable causes–instead he resists everything that would be expected from the concept “design,” from purpose, to meaning, to rationality, and on to any specific role of intelligence in his supposed “design.”

He does thereby implicitly admit, however, that science should be able to come up with answers although ID has absolutely none. There is no way that he can do science with ID to supply any answers, but he can do what every pseudoscientist does to divert attention from the fact that their favorite crank idea has hordes of large questions and no answers, which is to demand that real science supply answers to every question, while completely disregarding the ravages of time on the available evidence:

…Kenneth Miller argued in response [to Behe’s “challenge” in DBB] that the two-hundred component cilium is not really irreducibly complex, he offered no Darwinian explanation for the step-by-step origin of the cilium. Edge of Evolution 95

The rank hypocrisy of this is evident by comparing the first and second Behe quotes, above. Behe faults scientists for not accepting the evidence that the Big Bang happened, despite the fact that rather fundamental questions remain about the Big Bang, especially with respect to inflation (without inflation the Big Bang has many unexplained gaps). While the cilium has known precursors homologous with other cellular machinery, is made of the physical precursors that Behe himself states is demanded by evolutionary theory (and is missing the conceptual precursors so common in known design), and is made by genes which have basically the expected relationships and homologies coming from early in eukaryotic evolution.

I will soon deal some with what is known about the evolution of the fundamental biochemistry of biology, not because it is at all fair to judge evolution by its ability to answer the details of long-past evolution for which so little evidence remains as Behe wishes people to believe is a “fair test,” but because these are interesting questions which do have rather more answers than Behe admits or addresses. They are interesting in their own right, is what I am saying, and Behe’s treatment of them is abysmal. The sound tests of evolution involve the tests of relatedness, not only of organisms, but of the parts (“physical presursors,” as Behe notes).

But I thought that, once again, the ground rules have to be in place prior to any such discussions. One of the ground rules is that unanswered questions in science are no show-stopper, and Behe knows this to be the case. He only fully admits it in the latter part of his book when he is criticizing others, though, and not when he is leveling his own illegitimate and almost completely unargued criticisms (he points to complexity, ignores the evidence problems, and points out that questions remain–hardly argumentation in any intellectual sense of the word). I do not doubt that the opening quote appears in the latter part of the book because many people would remember this admission as he tried to make as much as he can of the fact that considerable questions remain from the distant past.

I mean to address some of his questions, not as he demands, but as the available evidence (particularly evolutionary evidence involving various sequencings) actually indicates evolution. Questions remain, but they are not at all as difficult questions as those that continue to vex the Big Bang, or even the collision that is believed to have produced earth’s moon. Behe only demands that the hardest evolutionary questions be answered because he has nothing else to throw at it–certainly no evidence in favor of design–and not at all because of any principle of his that science actually requires that the hard questions have to be answered before good explanations are accepted.

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9. Blood clotting’s dependency on Vitamin K leaves us vulnerable

Bleeding disorders also accompany deficiencies in FSF, vitamin K, or α2-antiplasmin, which are not involved directly in clotting. DBB 89

As Behe stresses, the clotting cascade is rather complex, and is vulnerable to a number of disruptions. He wants to make this into an argument against evolution, and yet the dependency of the crucial function of blood clotting on not entirely dependable sources of vitamin K is clearly what would be more expected from the contingencies existing in “Darwinian” evolution, and not of some highly intelligent designer dealing with the issues of complexity and of vulnerability. While vitamin K deficiency is not typically a major threat to human life, in pre-industrial societies vitamin K deficiency is not uncommon precisely when humans are otherwise quite vulnerable, just after birth:

Newborns are especially prone to vitamin K deficiency. A nursing-mother’s milk is low in the vitamin; breast milk can supply only about 20% of the infant’s requirement. Infants are born with low levels of vitamin K in their body; they do not have any vitamin K-producing bacteria in their intestines. Their digestive tracts are sterile. As a result, a form of vitamin K deficiency, called hemorrhagic disease of the newborn, may develop. This disease involves spontaneous bleeding beneath the skin or elsewhere in the infant’s body, and occurs in about 1% of all infants. In rare cases, it causes death due to spontaneous bleeding in the brain.

Source on Vitamin K deficiency

What Behe deliberately tries to do is to blur the differences between evolution and design, mainly because all of the evidence is in favor of evolution. If he really wanted to make a scientific case for design, he’d sharpen the distinctions between the two, pointing out what evolution explains and what design could explain.

Since he dares not discuss the differences, I would like to point out that evolution is what is expected to co-opt already existing pieces into its complexity, so that the result is “good enough.” Sure, babies are vulnerable to insufficient blood clotting due to vitamin K deficiency, but most make it without medical intervention. Best of all, vitamin K was available to assist one step of the clotting cascade (p. 84 of DBB). Evolution is often constrained by a lack of needed components to its complexity. Evolution makes do with vitamin K, then, despite the fact that newborns lack crucial sources of vitamin K, and adults can run into deficiencies as well. The point is that already-available vitamin K works much better during evolution than having to evolve something anew from something lacking vitamin K’s abilities.

Design, on the other hand, looks ahead to difficulties and tries to make complexity robust against disruptions in nutrition. A designer actually might be quite happy to use vitamin K, then, but would give to mammals the ability to synthesize vitamin K, or otherwise prevent the vulnerabilities that dietary and bacterial supplies of vitamin K pose for us.

Behe fails to bring up these matters, because they would clearly underline the fact that the constraints on evolution that Behe likes to point to have indeed shaped what we are. The designer is concerned about constraints of operation, while evolution is “concerned about” (constrained by, in the more proper non-anthropomorphic terms) its severe restrictions of biochemicals and adaptive abilities to supply function. Thus evolution often fails to provide the kinds of functions that design could provide (although over time, and with reasonably good adaptive pathways to follow, highly efficient systems often do appear), but it does find its way to function in many cases (although many functions, like radio communications, are essentially precluded from biological adaptation).

Vitamin K was adopted during the course of evolution not because it would ensure the kind of clotting function that vertebrates need throughout their entire lives, but because it was already provided by diet and/or bacterial symbionts. It is a “good enough” solution, certainly, yet it is exactly the sort of “solution” that would be expected from undirected evolution, and not from a designer.

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10. With causes of evolution of clotting given, Behe declares otherwise

Prothrombin appears in an ancient guise with EGF domain(s) attached, the result of a … protease gene duplication and … shuffling. DBB 92 (quoting Russell Doolittle)

The above is only one example of a host of instances of duplications and gene shuffling that Doolittle mentions on pp. 92-93 as causes in the evolution of the clotting cascade. And yet Behe has either the stupidity or the dishonesty to write this:

Now let’s take a little time to give Professor Doolittle’s scenario a critical look. The first thing to notice is that no causative factors are cited. DBB 93

Except that the causative factors were right there in front of his face. He does actually cite them again in the same paragraph, apparently being too dull to recognize a causal factor even when he is writing about it: Doolittle appears to have in mind a step-by-step Darwinian scenario involving the undirected, random duplication and recombination of gene pieces. (Ibid.) Now it’s probably true that Behe does not credit those factors as being adequate causes (and note also that he essentially ignores the role of natural selection), and he could argue against them as such. But it’s nothing less than dishonest (or the kind of stupidity that precludes honest discussion) to say that causative factors (ones that are clearly documented in the genome) are not mentioned by Doolittle.

There is little reason to try to meet Behe’s demands for all of the desired details from a half billions years or more back. The real point is that the evidence does indicate evolution, as even Behe essentially admits in the clotting chapter, “Rube Goldberg in the Blood.” And his various writings become painfully contrary to each other as he continually tries to evade the evidence of unguided evolution. In The Edge of Evolution he writes:

Yet genome duplication…and…time seem not to have given baker’s yeast any advantage it wouldn’t have otherwise have had. EoE 74

Yes, there needs to be selective pressure for duplications to be of any value. More to the point, in the clotting cascade, as well as in many other cases (plants are particularly known to be “evolvable” due to their frequent genetic duplications), the opportunity to evolve advantage does appear to have come partly from gene duplications.

The more I read Behe, the more I recognize these obvious lacunae. He will generalize from a single example, as with the yeast, while completely ignoring the fact that duplications are not expected to always have a dramatic effect and that sometimes they apparently have allowed for dramatic evolution. Plus, one has to wonder how competent he is at any science when he can list the causes that Doolittle adduced for the evolution of the clotting cascade, then to blithely state that no causative factors were cited.

Furthermore, he is clearly treating similar evidence in completely different ways between duplications involved in the origin of the clotting cascade and duplications in yeast. Since he insists that the clotting cascade did not evolve, the duplications behind the clotting cascade are magical, intelligently caused duplications (the “designer” is revealed as supplier of mutations in EoE), and duplications in yeast are merely accidental. How does he know that? Easy, he had already decided that the clotting cascade did not evolve as it appears to have done.

A real scientist looks at the evidence for common descent and apparently random mutations, plus selection, and asks how the clotting cascade evolved by those causes (among others), since one must match up cause and effect in science. Behe is quite the opposite, because he had already decided that life was designed. He simply looks at the sort of evidence he accepts in the evolution of yeast and tries to come up with a “designer” whose causation does not leave effects different from those of unguided evolution (aside from providing a more efficient supply of beneficial mutations, that is), which is easy to do when one’s “designer” was always one that could simply “do anything” at all. Proving only that those who won’t give up “design” will shift their concept of “the designer” until it can no longer be distinguished from mindless processes.

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11. The primary issue at stake is the foundation of knowledge

In this cause, therefore, we ought to rest; in this cause the common sense of mankind has, in fact, rested, because it agrees with that which in all cases is the foundation of knowledge,–the undeviating course of their experience. The reasoning is the same as that by which we conclude any ancient appearances to have been the effects of volcanoes or inundations, namely, because they resemble the effects which fire and water produce before our eyes; and because we have never known these effects to result from any other operation. William Paley Natural Theology Chap. 23 (pp. 232-233 in the link)

Paley actually understood the epistemology of science fairly well. As he mentions there, we have to use our experience, our observations of causes, in order to understand the causes behind anciently produced phenomena. We watch what “fire” and water produce today, and if we see what seems to be the results of these particular “forces” in phenomena from the past, we ascribe “fire” and water as the causes of said phenomena.

To be sure, the context of the above quote makes it clear that he believed that design could be properly inferred to be behind the structure and function of animals in the same manner, something that even in Paley’s time strained the meaning of experience, considering how different animals are from our own designs. Nevertheless, the principle he called upon for the foundation of knowledge is sound, and not a few considered design to be a legitimate inference prior to the development of evolutionary theory. Dawkins still writes as if it would be a sound inference without Darwin’s insights and subsequent developments of theory, although I myself do not think that inferring from human design to a very different sort of “design” in life was ever as clearcut as either Paley or Dawkins consider it to be in the early nineteenth century (many ancients did not see animals mechanistically, so it appears that the industrial revolution was partly responsible for such reductionism). Let us allow that it was reasonable enough for Paley to make his arguments at that time, however.

I bring up Paley’s sound epistemology (whatever we think of his application of it) as a sort of follow-up to recent posts about Darwin’s Black Box, and equally, as a prelude to further evidences of evolution in basic biochemical pathways (whether or not Behe touches upon these). For it is one thing to claim that we do not have exact knowledge of the evolution of even something as evidently evolved as the clotting cascade, while it is quite another thing to ignore the clear evidence that it did evolve as the result of selection and also of contingency and of “accident”. Paley did not supply the exact mechanisms of design, although he typically suggests that it is quite like those of “artificers” and of “architects” (following his belief that we make proper inferences from experience). Behe not only does not provide any exact mechanisms, he seems to deliberately avoid any suggestion that the foundation of knowledge is experience, for we certainly do not experience design producing anything like the constrained and partly accidental constructions of Archaeopteryx, the clotting cascade, the systems of photosynthesis, nor an adaptive immune system built upon the innate immune system. Behe demands near-total knowledge of pathways that evolved long ago, without ever having accepted the burden to provide even a tiny level of explanation via his claims regarding “design”.

Evolutionary theory (the non-woo variety) rests upon our experience that certain physical characteristics allow animals to succeed, ultimately in the reproduction stakes, and that these physical characteristics vary from animal to animal within species, and likewise across species. More exactly in today’s understanding, evolution is recognized as being founded considerably upon the natural selection of random mutations–with both what is selected and what is “merely accidental” revealing the accidental nature of these mutations. Experience only provides us with knowledge of random mutation in nature, and of natural selection, outside of a bit of human meddling, and whatever intelligence enters into the mating strategies of the smarter animals.

So if we follow “Paley’s principle” (in reality, these could be considered to be principles of “natural philosophy” going back to Newton, and continuing through Hume, and Kant) of using experience as our guide, we can hardly suppose that the apparent duplications of genes found in the clotting cascade were caused by anything but random processes of duplication and of natural selection. What else have we ever seen producing duplication, and fixing it into genomes? Nothing, that is all.

But what of Behe’s analogies with design? Might we have we sufficient reason to suppose that cilia and the clotting cascade were in fact be designed, and thereby have at least a competing hypothesis? Hardly. Paley was quite careful to use for his examples what he understood to actually be like what human artificers and architects would produce. Behe avoids exactly such examples, because he happens to know that the most humanly design-like structures in organisms are actually quite well explained by Darwinian selection from random mutations. So from whence does he even have analogy, let alone the kind of knowledge that is firmly founded upon experience and observation?

He has none, for there is no precedent for design making the clotting cascade. And more importantly, the evidence of origination only points to causes which we know by experience are those of natural selection and random mutation. Vitamin K is crucial to the clotting cascade only because of the accident of its already existing in the organism evolving a clotting mechanism. The various proteins involved were simply co-opted and adapted because of the accident that these particular proteins already existed in the organism, apparently were duplicated (or genes were shuffled, or some other process occurred–depending on the particular protein being considered), and either had some of the needed function immediately, or did soon after a few changes occurred.

Behe actually has no evidence of design whatsoever, only his unwarranted and never substantiated belief that if evolution is not sufficient for complex articulated processes that design is responsible. Paley actually tried to make a positive case for design (he knew that it would be hypocritical to criticize the evolutionary ideas of his day for lacking proper evidence if he did not provide some for his claim), while Behe does not even make an argument in favor of design. If he and the other IDists cannot make a case for design, as they have definitely failed to do thus far, the only recourse that any real scientist has is to follow Paley’s dictum about using experience to match up known causes to known effects, and to conclude that accident and selection produced the clotting cascade that has all of the marks of random mutation, common descent, and of selection.

This is why ID is such a potential menace to science and to science education. While Paley and other proponents of natural theology prior to the development of scientific evolutionary theory were quite content to be scientific and thus to argue from cause to effect–from experience and observation to the apparently similar phenomena that happened in the past–today’s IDists pointedly bypass any rigorous match-up between the mechanisms of life and their claims of “intelligent design”. Indeed, it is in the “accidental” (in a broader sense than as used above) characters that one discerns cause, and the accidental characteristics all point to random mutation, common inheritance, and natural selection. We do not know exactly how the clotting cascade arose, but we know that we should be looking at evolution to provide the answer to that question (insofar as the question can be answered), for the only evidence of origination that we have for it points toward evolutionary. Behe’s shift to “the design provides the mutations” is as lacking in evidence (and experience) as all of his other claims, and it avoids addressing all of the random characteristics that pervade the cases which he claims could not have evolved without assistance.

The question is whether or not science is going to continue to be rigorous, and thus to apply Paley’s principle that we must use our experience as our foundation of knowledge. We say yes. The IDists say no. It does not appear as though there is any room for discussion between the “two positions,” rather the IDists would simply deny the principle by which we must gain any knowledge about the world.

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12. Endosymbiosis shows how some cell transport evolved

My main goal in responding to Behe’s books is not to try to answer everything. My primary aims are to show how inadequate his simplistic criticisms of evolution are, how he does not address the evidence that demonstrates evolution which does not betray the slightest bit of design nor deviance from the usual mechanisms of evolution, and of course, evidence of the evolution of complex pathways. In line with the last bit, while I am neither knowledgeable enough to discuss the intricacies of cellular transport, nor aware of the evolutionary evidence behind most of it, I can point to the obvious example that endosymbiosis did occur, and it co-opted bacterial export mechanisms for at least some cellular transport.

This post is in response to Chapter 5, “From here to there” (pp. 98-116), of Darwin’s Black Box. But this is not a direct response to his “challenge,” since of course he merely caricatures the problems, and fails to recognize that intracellular transport would likely evolve gradually as membrane-bounded cellular compartments themselves gained and lost functions. Moreover, his response to the evidence for bacterial export systems evolving into intracellular transport would be to demand that we explain the bacterial export systems, ignoring the complexity of the system into which the latter had evolved (as well as how it almost certainly gradually evolved the “irreducibly complex” steps after endosymbiosis took place). Always demand explanation of the hardest problems, and you have your excuse to deny evolution. Never mind that, the point is what the evidence shows, not Behe’s endless attempts to deny the direction the evidence points.

Endosymbiosis itself is very interesting evolutionarily, because it not only supports the notion that evolution of biochemical pathways was not easy, it demonstrates that evolution had to deal with that fact. Eukaryotes are complex organisms which do not seem to easily evolve new biochemical pathways (probably due in part to their specific complexity), and are generally (with some exceptions) not good at exchanging DNA with unrelated species. While many biochemical pathways almost certainly were horizontally exchanged between all of the early organisms–the archaea, bacteria, and the precursors of the eukarya–when it came to aerobic respiration and photosynthesis, neither ability would be passed to eukaryotes via horizontal gene transfer. Only endosymbiosis gave us and our nucleated relatives aerobic respiration, as bacteria(the α-subgroup of proteobacteria)-derived mitochondria, and photosynthesis came endosymbiotically to plants as cyanobacteria-derived chloroplasts.

Indeed, it appears that neither of those pathways do evolve readily, nor did design make up for the difficulty in eukaryotes. Physical precursors, not conceptual precursors, are demanded from Darwinian evolution, as Behe pointed out (DBB 44-45), and of course that is exactly what we find. With design not operating in the origin of biochemical pathways as we generally would expect it to act, evolution of photosynthesis and of aerobic respiration instead had to come another way, via endosymbiosis.

But of course there were no transport mechanisms to deal with the now-intracellular output of chloroplasts once these were engulfed by a proto-eukaryotic (or a “eukaryotic”) cell, nor for the proteins needed by chloroplasts as genes were moved out of the chloroplasts and into the nucleus. It is unlikely that early chloroplasts really needed specific intracellular transport mechanisms for the symbiotic relationship to be mutually beneficial, however there would not be much coordination of the needs and abilities of both the eukaryotic host and the endosymbiotic cyanobacterium/chloroplast. So intracellular transport and communication would almost certainly be selected-for at once, with much more transport capability evolving as genes moved from the chloroplast genome to the nucleus of the eukaryotic cell.

I will not exhaustively discuss the transport system that evolved, for it has been done by more qualified individuals in a Nature article which happily is available without a fee. Mostly that article is only detailing the transport mechanisms and processes, but it also addresses evolutionary issues to some degree. One window in particular addresses the evolution of intracellular transport with chloroplasts:

Endosymbiosis was accompanied by massive gene transfer from the endosymbiont to the host nucleus. However, before genes could be eliminated from the endosymbiont genome, a system to import the now nuclear-encoded gene products into the new organelle had to be established. Although the endosymbiotic bacterium had several systems to export (or secrete) proteins across the membranes, the organelle now had to import proteins (see figure).

Most striking is the homology of the translocon of the outer-chloroplast-envelope subunit TOC75 to bacterial outer-membrane proteins that are involved in the transport of polypeptides across the outer membrane of Gram-negative bacteria. This conserved β-barrel ion channel has, in most cases, no strong preference for the direction of ion permeation and therefore represents an ideal starting point to build a translocon. Subunits that convey the specificity and directionality of transport are eukaryotic additions, for example, the TOC34 receptor and the TOC159 motor.

But, what formed the translocon of the inner chloroplast envelope (TIC)? There is no detectable homologue for the putative TIC110 channel, and the putative second channel subunit TIC20 shows only a low homology to bacterial proteins. Maybe the early endosymbiont continued to use bacterial export systems in reverse, such as the secretory pathway (SEC), the twin-arginine translocon (TAT) system or the albino3 (ALB3) homologue YIDC. Therefore, the TIC translocon — including the adaptation of chaperones in the stroma to provide the driving force for import — could have been an invention of the endosymbiont. Gram-negative bacteria, including cyanobacteria, use the Sec or the Tat system, YidC and an SRP (signal-recognition particle)-dependent pathway to translocate proteins into and across the plasma membrane and the thylakoid membranes. All these systems are still operational in chloroplasts today and are essential for thylakoid biogenesis.

While one might prefer recognizable homologies throughout, rather than a seemingly new TIC translocon, there is nothing implausible about the scenario given in the quote above. Furthermore, homology indicates that TOC75 did evolve from gram-negative outer membrane transport protein.

The fact is, then, that a highly specific intracellular transport system arose after endosymbiosis took place. Behe simply complains in DBB that because gated transport requires “a minimum of three separate components to function, it is irreducibly complex”:

And for this reason the putative gradual, Darwinian evolution of gated transport in the cell faces massive problems. If proteins contained no signal for transport, they would not be recognized. If there were no receptor to recognize a signal or no channel to pass through, again transport would not take place. And if the channel were open for all proteins, then the enclosed compartment would not be any different from the rest of the cell. DBB 113

All of that is hardly the case for the endosymbiotic cyanobacterium/chloroplast at the first, for signals could evolve as genes transferred into the nucleus (most certainly not all cyanobacteria proteins would already be recognized for export from the cyanobacterium). And what I primarily wished to point out here is that a complex transport system (subsystem) can arise from endosymbiosis.

Also important, however, to the general case is that Behe gets things wrong once again in the case of non-endosymbiotic compartments. If, as is likely, many membranes of eukaryotic compartments evolved from eukaryotic cell membranes (either primarily or secondarily), they would already be selective in ways which could be useful in a compartment, just as the cyanobacterium’s membrane was already selective in the endosymbiotic example. No doubt adaptation would change transport across those membranes, much as the transport across the membranes of chloroplasts adapted to changing relationships between it and the nucleus.

Anyway, that’s it for the “irreducible complexity” of intracellular transport. I did not touch upon many specifics in the chapter, like the fact that Behe seemed to anticipate the fact that such transport could evolve, and seemingly for that reason chose to bring in the “problem” of evolving transport across cell membranes, in a rather confusing manner. But that’s a sideshow to the fact that intracellular transport can evolve gradually, as both the homological evidence demonstrates in the case of chloroplasts, and because of the reasons I brought up for both the specific case and in the general case.

The particular phenomenon of chloroplast evolution from the cyanobacterium points to an inconvenient fact that Behe would all too gladly ignore. This being the fact that–almost certainly especially so in the later complex and more precisely controlled reproduction of later organisms, such as eukaryotes–biochemical pathways do not readily evolve, thus (there being no design evident in life) the basic pathways have had to be horizontally transferred either by sharing genes or through endosymbiotic means. This is why chloroplast transport processes had to evolve later on, or rather, it had to evolve for that reason and because no designer steps in to recreate pathways in organisms which had been lacking these.

The fact is that oxygenic photosynthesis only evolved once, which is likely also the case for photosynthesis itself. Yet it is perhaps even more interesting that oxygenic photosynthesis evolved only once, because it has all of the earmarks of duplication of photosystem I, plus rather significant changes once that occurred (which almost certainly is the truly constraining part of the evolution of oxygenic photosynthesis), showing that it did evolve. Nevertheless, this evolution was so difficult that it happened only once, and then it had to be endosymbiosed and extensively adapted to supply eukaryotes with solar energy.

More on that story in a later post.

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13. Science is about evidence of occurrence, not mere possibility

Behe’s lack of scientific acumen is most glaring when he demands evidence of “possibility” of an evolution for which its actuality has hordes of evidence, and also when he treats “design” as the default because presumably just about anything could be designed–especially if it were designed to appear undesigned by some intelligence far beyond our own. The trouble is that in science we have to produce evidence that something happened, not simply that it could have happened, for it really is the case that most phenomena could occur according to several different causal pathways–notably, by design, if one adopts Behe’s “design can do anything” nonsense.

Crucially, even though Behe makes stringent demands upon evolution to show that this or that biochemical pathway could evolve, actually showing that it could evolve would do nothing to show that it actually did evolve. The actual evidence that a particular pathway evolved is dismissed by Behe, based on his hackneyed understandings of the issues of evidence, evolution, and what science is about. Here is an example of his position, taken from an interview:

I claim, for example, that the bacterial flagellum could not be produced by natural selection; it needed to be deliberately intelligently designed. Well, all a scientist has to do to prove me wrong is to take a bacterium without a flagellum, or knock out the genes for the flagellum in a bacterium, go into his lab and grow that bug for a long time and see if it produces anything resembling a flagellum. If that happened, intelligent design, as I understand it, would be knocked out of the water. I certainly don’t expect it to happen, but it’s easily falsified by a series of such experiments.

Now let’s turn that around and ask, How do we falsify the contention that natural selection produced the bacterial flagellum? If that same scientist went into the lab and knocked out the bacterial flagellum genes, grew the bacterium for a long time, and nothing much happened, well, he’d say maybe we didn’t start with the right bacterium, maybe we didn’t wait long enough, maybe we need a bigger population, and it would be very much more difficult to falsify the Darwinian hypothesis.

More Behe on falsification

First off, on the relatively trivial matter of what would “falsify the Darwinian hypothesis,” sufficient evidence of rational design in non-engineered life would. Apparently he doesn’t even think to turn his false dichotomy of “either evolution or design” around, because he has no conception of what actual evidence for design would entail. Then, a lack of nested hierarchies–measured morphologically, via DNA, and through proteins (each is a fairly independent set evidence in certain aspects)–in the taxa which do not readily exchange genetic material is another possibility for falsification. Many models can accommodate nested hierarchies, while only unguided evolutionary processes in our context actually predict the nested hierarchies we see. Another test of “Darwinian evolution” which does not involve design is if life utilizes “physical precursors” and is devoid of “conceptual precursors,” a test for evolution that Behe himself brought up in DBB (and then fails to apply, for the obvious reason–it passes that test, along with the others).

Another fairly trivial issue that Behe gets laughably wrong is that any of this would constitute a test of design. There are three reasons, one being that he knows very well that bacterial flagella are not in the least considered to easily evolve at all–and it is in fact possible that it is essentially impossible today due to bacterial specialization, when it was not impossible to do in the past. He chose his “test” in order prevent any real testing, and perhaps to mislead the gullible. A second, philosophical, problem is that this “test” would not show that the bacterial flagellum evolved at all, merely that it could evolve, as previously mentioned. The third reason, another philosophical problem, is that it relies upon the false dilemma that if it did not evolve it was designed.

The more important matter is that falsification simply is not everything, regardless of what Popper said. Suppose that a man is charged with shooting another man. The judge is not going to be impressed with evidence that it is possible for men to shoot men. Nor will the judge care that evolution cannot shoot men. What is more, the court is going to demand evidence that the man actually was shot, and also that the accused was the one who shot him.

Let us suppose that the projectile that killed the victim turns out to be a piece of meteoric iron. Behe, as the prosecuting attorney, will drone on and on about how it is possible for humans to hurl meteoric at lethal speeds, whether with compressed gases or, conceivably, with an electromagnetic impulse. Another line he uses is that “anything might have been designed,” (DBB 193) including this death. It really does not take very long for the judge to tell him to either deal with some actual evidence, or to sit down and be quiet. Why? Because saying that anything could be design, or that it is possible for a human to launch meteoric iron at great speeds, means nothing to the claim that anyone, let alone a particular person, actually was responsible. Behe would have to demonstrate design behind the meteorite which struck the man even to “prove” that a murder was committed at all.

The truth is that the justice system demands essentially the same kind of evidence that science does, only the courts often are intent upon “proof” that an individual was responsible (science often plays a part in this endeavor, however, as in forensic science) and science often is not focused on individual actions. Falsifiability only matters with “entailed predictions,” that is to say, evolutionary theory is falsifiable because evolutionary processes actually must produce cladistic branchings such as we see, if it is true. Finding those cladistic branches not only means that evolutionary theory was not falsified, it means that such evidence supports evolutionary theory. Essentially the same obtains in the courtroom, where the interventions of gods, demons, and miracles cannot be ruled out entirely, but which are not taken seriously for the lack of evidence of these occurring within our sphere of existence.

Behe’s conception of “design” is completely unfalsifiable (I consider falsification a rule of thumb for scientific propositions, not an absolute rule), and not just because even demonstrating the evolution of the flagellum is possible would not actually indicate that the flagellum had evolved. It is because for Behe (unlike for archaeologists and SETI researchers) “design” has no identifiable characteristics, and even if we found out that a god exists that knows everything and can do everything (so far as we can discern), that would be no indication that life was designed. Crucially, life appears far too constrained by heredity and the possibilities for mutation to believe that any mind that can deal with life’s complexity would opt for designing within those constraints.

The important evidence is that which indicates what occurred. Even Behe’s examples which supposedly cannot evolve frequently have such evidences, and the endosymbiotic events have such evidences in abundance. The duplications, mutations, apparently slow adaptations of endosymbiotic and duplicated information, all point to the clotting cascade and P. falciparum’s plastid as having evolved over some time. This is the evidence required by science, evidence of occurrence, not some proof of a mere possibility such as Behe mistakes as being a scientific test.

To be fair to the actual argument, it is worth noting that if we did have actual evidence that evolution is not and was never up to the task of producing the forms of life attributed to it, that would be important evidence. But of course neither Behe nor anyone else is close to being able to show that evolution could not produce the complexities of life, any more than our ignorance of the causes of some of the dynamics on the sun can demonstrate that physics is unable to explain such dynamics, at least in theory. Indeed, what we see in life bears all of the marks of the difficulty in evolving complexity, especially in a short time.

So it is that, just as with unexplained complexities of magnetohydrodynamics on the sun, we take our bearings from the evidence that we have of the origination of observed phenomena, and we follow that evidence to try to discover what remains unknown. This is why the evidence of occurrence is so very important, because just as it would be a waste of resources to try to understand the origination of evidently rationally designed machines (like UFOs) according to evolution, it is equally useless to try to explain life according to rational design, when it turns out that there are no marks of rational design in non-GMO organisms.

Nobody’s liberty is directly at stake in this matter, unlike in the hypothetical court case, however, the fate of human knowledge does depend upon properly interpreting the evidence of what actually happened, instead of chasing after the mere possibilities upon which Behe’s “case for design” relies. Rather than bypassing the evidence that points directly to what happened, as Behe does, science relies upon that evidence in order to find out what was not only possible but truly did happen, through the course of evolution. For it turns out that the possibilities which correlate with the data are the ones that matter, both in science and in prosecuting a case in court.

I decided to write this post on which evidence matters, and how it does, because I have recently written several posts about the evidence of what happened to make certain systems found in life, and I intend to write some more, regarding photosynthesis and at least on one or two more about Behe’s “examples” of what “cannot evolve.” In his books he discusses “what is possible,” while ignoring all of the evidence for what actually did occur. Empirically, that is almost completely backward, and is another in a long string of indictments against ID for being effectively opposed to science and its methods.

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14. Evidence for the complex evolution of oxygenic photosynthesis is strong

Other examples of irreducible complexity abound, including…photosynthesis…. DBB. 160

I wrote a post discussing the importance of evidence for actual occurrence vs. mere possibility here, in part to lead into the evidence for the evolution of oxygenic (oxygen-releasing) photosynthesis. There is firm evidence for only one case of evolution of oxygenic photosynthesis, which uses both photosystem I (PSI) and photosystem II (PSII), and all of the evidence points to simple duplication of the photosynthetic genes of one photosystem (PSI-type, most think now) leading to the evolution of another photosystem (PSII-type), which was later coupled to produce oxygenic photosynthesis. At some point after that, algae and plants took in cyanobacteria in primary, secondary, or perhaps even tertiary and above, endosymbioses, to evolve plastids in which their own photosynthesis occurs.

I won’t bother trying to explain how the two photosystems interact in plants, algae, and cyanobacteria, since the process is rather involved and is explained in many places. For anyone wanting those basics, here is a diagram of the electron flow between the two photosystems, and here is a site that tells more about photosynthesis than most people wish to know. I am interested in the powerful evidence that oxygenic evolution evolved in part by the duplications that Behe continually claims are inadequate (and of course they are, by themselves) for evolution, and also in some of the details that Behe likes to demand–though I am rather less interested in the latter because these are not nearly so important to the question of whether or not oxygenic photosynthesis did evolve.

First off, it is interesting that the distribution of the PSI-type and PSII-type photosystems do not seem to follow any consistent “tree” in the various bacterial lines. Some modern bacteria utilize PSI-type photosynthesis, others the PSII-type, and, aside from the cyanobacteria, their photosynthesis is anoxygenic. But of course it is not very surprising if their photosynthetic systems do not produce a “tree of bacterial life” pattern, since bacteria rarely do have marks of consistent “vertical transmission” patterns, such as we mostly observe in eukaryotes, because the bacteria exchange a great deal of genetic material with species not closely related to themselves (Allen, John F., & Martin, William (2007).Out of thin air.” Nature, 445, 610-612).

That the two photosystems are related (paralogous, in this instance) is clear from the evidence, however, and gene duplication is responsible:

Another striking example of gene duplication is found with the gene for the PSI-like RC core polypeptide. H. mobilis and C. limicola use a single RC core polypeptide (PshA and PscA, respectively) to form a homodimeric PSI-type RC complex. In contrast, oxygenic species synthesize a heterodimeric PSI RC with two highly related polypeptides, PsaA and PsaB. A composite phylogenetic tree (3E) of the PSI RC core polypeptides from a broad representation of oxygenic lineages with PscA of C. limicola as root indicates that PsaA and PsaB are divided into two distinct clades and are derived from an ancient gene duplication from a PscA/PshA-like common ancestor. Thus, the RC gene duplication seems to have occurred well before diversification of all oxygenic lineages. Interestingly, PSI RC polypeptides also share significant similarity to CP47 (PsbB) and CP43 (2), both of which are core antenna polypeptides of PSII. Our phylogenetic analysis (3E) indicates that these genes have undergone gene duplication from a pshA-like common ancestor that preceded the divergence of all oxygenic lineages.

Tracking molecular evolution of photosynthesis…

In other words, oxygenic photosynthesis (in cyanobacteria, etc.) uses polypeptides in both its PSI and its PSII systems which phylogenetic analysis (see the references, to which I linked, or just use this to see the results of their phylogenetic analysis) indicates came from genetic duplication events.

I do not include these technical details because I think people here should pay close attention to them, but so that it is clear that peer-reviewed analysis is behind the assertions that gene duplications produced PSII from PSI.

Another source using somewhat different evidence states:

The arrangement of these helices [in photosystem II] is remarkably similar to that of the helices in the reaction centres of purple bacteria and of plant photosystem I, indicating a common evolutionary origin for these assemblies. “Three-dimensional structure of the plant photosystem II reaction centre at 8 Å resolution”

And a more recent source states:

Like others, they suggest that photosystem I was the ancestral prototype, from which an evolutionary precursor of photosystem II arose. The reaction-centre cores of the photosystems are similar in stucture, and their divergence probably began with a simple duplication of the associated gene cluster. Allen, John F., & Martin, William (2007).Out of thin air.” Nature, 445, 610-612

There seems to be little reason to belabor this particular point further. If we simply pay attention to the evidence of what actually happened, normal observable processes gave bacteria the two photosystems, namely, gene duplications caused two photosystems to appear where there had been one. As appears to have often been the case, almost certainly many or all of the genes for the PSI-type system would have been duplicated in one generation, producing a second copy.

Behe demands the details of this 2.3 billion year old event–which left only bits and pieces of information behind–because he knows that the firm details are in many cases impossible to obtain. Well, that hardly matters, yet the details are of interest to scientists, so speculation and plausible scenarios are discussed. A good source for possible pathways of subsequent evolution of photosynthesis is the one used in the last quote, “Out of thin air.”

One supposes that the duplicate photosystem might have supplied redundancy to the bacterium for a while, perhaps also boosting peak photosynthetic capacity of the cell. Later, however, one would likely change to fit certain situations better than other environmental conditions. Eventually it would become like the authors of “Out of thin air” state, the bacterium would switch between photosystems to fit the conditions. Modern bacteria do this to some extent, as related here. According to some researchers, this putative bacterium which evolved to have two photosystems was in a now-extinct group, which laterally transferred photosynthesis genes to other groups, many of which ended up with only one system, while cyanobacteria obtained both photosystems. (Ibid.)

What is interesting in the article is how relatively smoothly the evolution of the highly coordinated oxygenic system might have evolved in an organism containing both systems. There is reason to believe that, in an environment enriched in manganese, ultraviolet light may well have jammed proto-photosystem II with electrons, meaning that it would have to shut down. Photosystem I (which paradoxically is second in line to photosystem II in the electron chain) would then have to be switched on, and when that happened it would be able (after a bit of evolutionary tinkering, at least) to take the electrons from photosystem II, relieving the jam. If the electron-jamming were too frequent, pressure for both photosystems to work concurrently, rather than successively, would exist, and then both photosystems would be linked and would readily evolve further adaptations to coordinate electron transfer properly (Ibid.).

Those are reasonable possibilities, unlike the mere supposition that a pluripotent, yet oddly constrained (very oddly, because the constraints appear similar to those of unguided evolution), “designer” steps in to “help evolution along.” No doubt Behe would not give much credit to such speculation, for the little that is worth. What is important to science having any kind of integrity, however, is that it builds upon the evidence of what actually occurred, and that is exactly what speculative hypotheses like the one sketched out above does. For we know that duplications set off the evolution of the two photosystems needed to split water (splitting water takes too much energy for any single photosystem that we find in life, but, fortunately, other molecules like hydrogen sulfide can be and are split by a single photosystem), and the question is simply how well we can narrow down the possible ways in which these evolutionary events may have happened.

I do not know for sure whether Behe would deny that oxygenic photosynthesis could evolve from anoxygenic photosynthesis in his DBB days. It would seem so, though, especially since he failed even to credit duplications as “causes” for the clotting cascade, as I discussed here. The fact is that this goes along well with discussions of the evolution of transport and of gene transfers with respect to chloroplasts and P. falciparum‘s apicoplast, for the documented evolution of photosynthesis (and of non-photosynthetic plastids descending from chloroplasts) from a single photosystem involves a great deal of complexity. Behe did well to ignore these biochemical pathways, for the evidence that these indeed evolved would be hard to ignore. I am sure that he would have ignored most or all of that evidence, however. The fact is that I will not be constrained to discuss only the pathways he prefers, since evolution is a whole, with none of the expected breaks coming from “designed interventions” being even slightly visible.

Furthermore, photosynthesis almost certainly has some role in the “Cambrian explosion,” which event Behe, like other creationists, likes to throw out there as a “problem,” without bothering to discuss the details of the selective pressures that might be behind it–like a dramatic rise in oxygen levels. I intend to get into that issue relatively soon.

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15.  Photosynthesis facilitated the “Cambrian explosion”

With the discovery of the biological Big Bang [Cambrian radiation], however, the window of time for life to go from simple to complex has shrunk to much less than nineteenth-century estimates of the earth’s age. DBB 28

First, one should note that in the quote above that Behe does not use the already hyperbolic “Cambrian explosion” to designate the rapid radiation occurring at the start of the Cambrian, he uses an even more hyperventilating term for what is in fact a considerable period for evolution (rather more than the time in which humans evolved from walking apes), “the biological Big Bang.”

Secondly, of course, he’d need to show that the animals that gave rise to “complex life” were not themselves complex, if not large. This is quite unlikely, because there seems to have been no vast genetic change at the start of the Cambrian. Indeed, the preceding Ediacaran fauna were evidently quite complex, though probably were less so than the Cambrian fauna.

And third, while the causes of the radiation of the Cambrian fauna remains controversial, the previously-discussed complex evolution of photosynthesis almost certainly played a role in it, by releasing oxygen to the atmosphere. As one highly credible source states:

Geochemical and physical evidence suggests that a stepwise increase in oxygen occurred around 1.1 to 0.54 billion years ago (Ga) and was a necessary precondition to support the physiological needs of large metazoans. Martin Kennedy, et al. “Late Precambrian Oxygenation; Inception of the Clay Mineral Factory.” 10 March 2006 Science 311:1446-1449

Would it be at all suprising if, in the low oxygen conditions of the later Precambrian, the ability to produce complex body types for the sake of advantage in predation would occur? And then, when oxygen levels rose, the very ability to develop larger bodies becomes possible for the first time, and a predatory arms race leads to an “explosive” evolution of body types, armor, and the like. This seems to be virtually certain, given the extreme conservatism in development across the phyla, so that virtually the same Hox genes pattern insect bodies as pattern human bodies.

This does not in the least mean that rising oxygen levels were the “trigger” for the “Cambrian explosion.” Some have argued that the Ediacaran fauna were large, hence, oxygen levels apparently were not holding those animals back evolutionarily. However, that does not seem persuasive, for it seems that Edicaran fauna were relatively flat in shape (presenting a relatively large surface area to the water), and may have had relatively low metabolic rates in any case. More important than that, though, is that Ediacaran fauna were only slightly earlier (on the geological scale), and there is recent evidence that the extinction of the Ediacaran fauna may have led to the rise of the Cambrian fauna. The same paper which provides evidence of a likely extinction event also credits the rise of Ediacaran fauna to oxygenation (due to photosynthesis):

Increasing oxygenation of the upper ocean and atmosphere following the Marinoan glaciation is thought to have triggered the development o fthe Ediacaran fauna, and to have caused destabilization of the oceanic chemocline. As a consequence, upwelling euxinic bottom water is likely to have rapidly poisoned the Edicaran fauna. Martin Wille, et al. “Hyrogen sulphide release to surface waters at the Precambrian/Cambrian boundary.” 5 June 2008 Nature 453:767-769.

The upshot being that increased oxygen levels appear to have allowed Ediacaran fauna to evolve, while hydrogen sulfide upwellings to the surface waters ended up killing them off, at least according their interpretation of the molybdenum isotope record discussed in the aforementioned paper. Then the photosynthetically-caused oxygen levels were able to support the evolution of Cambrian fauna, after the Ediacaran extinction.

The fact is that the entire scenario of the evolution of photosynthesis is what happens to explain (in part) the “explosive” evolutions of both the Ediacaran and the Cambrian fauna, insofar as we have any kind of explanation worthy of the name. We have the DNA evidence of gene doublings being causal in the evolution of oxygenic photosynthesis, which led to the endosymbiosis and some rather complex evolution of eukaryotic photosynthesis, which led in time to rising oxygen levels which then supported not one, but two, evolutions of metazoan organisms.

Above all, perhaps, we have the use of human intelligence where we are pursuing identifiable causes. Not that obscuring and ignoring science, in the manner that Behe does, is completely devoid of intelligence, yet it is not a very impressive kind of intelligence used in that endeavor. Evolution setting the stage for further evolutionary development is the fascinating story of deep time, far more interesting and useful than any “poof” tale that Behe can conjure up.

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16. So, why were Ediacaran fauna, and Hallucigenia, designed?

Darwinian evolution cannot pursue a future goal. The Edge of Evolution 112

One cannot write about life, present or past, as if it had ever been the result of “future goals,” except by ignoring the many constraints that “Darwinian evolution” has imposed upon humans and the other organisms. The most glaring lack of future goals is probably seen in the exceedingly great number of extinctions that have occurred–the many “designs” that evolution has tried out, and that then were callously killed off without thought or regret.

Perhaps it is not then surprising that, even in its early days, ID had trouble identifying purpose. Paley went so far as to state the following:

For although more of this apparent chance may perhaps upon other principles, be accounted for, than is generally supposed, yet a future state alone rectifies all disorders; (emphasis added). Natural theology    chap. 26

The context makes the issue out to be more complex in Paley’s thinking, suffice it to say that he retains a belief in identifiable purposes which is absent in today’s ID. One of these “purposes” seems to hark back to creation for the sake of diversity, a kind of sense of an abounding goodness that theologians like St. Augustine believed that were behind God’s creation. But, of course, what would be the point of creating diversity only for it to be lost to extinction? So we get this statement from Paley:

The result is, that out of the many thousands of different plants which cover the earth, not a single species, perhaps, has been lost since the creation. Natural theology    chap. 20

Paley is always useful to juxtapose against the appallingly meaningless sense of “design” that the IDists insist upon today–the latter being a misrepresentation of all meanings of “design” meant to avoid any honest test for design that could possibly be devised. None of the early proponents–of the concept of life having been designed–imagined calling the high level of waste and extinction documented in the fossil record a case of “design,” rather they imagined that life was designed to survive (with little or no extinction), and even to lead to a relatively beneficial state in sentient organisms.

This is why I chose to linger a bit longer on the issue of Ediacaran and Cambrian fauna, after posting about the matter here. There are two crucial follow-up issues that ought to be mentioned. One is the fact that evolutionary theory predicts (unlike modern ID, which can predict nothing at all in an entailed way) that more and more of the organisms we see as we move back in time will be members of extinct lines. We see this in both the Cambrian and in the Precambrian, as none of the Ediacaran fauna can be definitely said to belong to any extant lines, and many of the Cambrian fauna also have died out. That is not the issue to which I have been leading and wish to discuss presently, however, this being the fact that, unlike any intellectually honest design expectations, the carnage of evolution has been very great indeed, with no evident purpose behind the “design” of Ediacaran fauna at all–not even the imagined purposes that Paley and other theologians used in their discussions.

The Ediacaran fauna are a strange mix of soft and strange animals, some of whose impressions may be seen here. As I mentioned in my previous DBB post, it appears as though they all died out, after a radiation not very dissimilar from that of the Cambrian radiation. While it remains possible that there are close affinities between some Cambrian fauna and at least some of the Ediacaran fauna, the latter assemblage of animals largely died out prior to the Cambrian radiation.

The closest that Behe comes to defining “design” is as a “purposeful arrangement of parts.” Not only does he avoid telling us how malaria pathogens fit into any kind of “purposeful arrangement of parts,” he certainly doesn’t bother telling us the purpose of “designing” all of the hapless Ediacaran animals, only for them to be wiped out by some cause or other, quite possibly the upwelling of euxinic waters previously mentioned. Here is a diagram using long lines for living phyla, and short lines for extinct phyla, showing that many groups died out soon after they appeared. I note also that phyla are generally considered to have arisen in the Cambrian.

Hallucigenia is one of the bizarre organisms which arose in the Cambrian, only to go extinct relatively soon thereafter.

Apparently the designer has nothing much to do except to design exquisitely complex organisms, only to cause, or at least allow, them to go extinct. The Ediacaran fauna are possibly the best example of the carelessness of life that “Darwinian evolution” is expected to have, but the Cambrian period’s animals have largely become extinct as well, albeit with many lines producing living descendents. Yet most of the lines of even the living phyla end at extinction, with only a relatively few lines producing the “crown groups” that exist today in all of their diversity. The non-avian dinosaurs are only one of many groups that have gone extinct, as some “dominant groups” that existed prior to them also went extinct.

Closer to ourselves, we find a host of upright apes and Homo species existing and then going extinct. If the IDists cannot inform us about any purpose or reason for Hallucigenia or the dinosaurs existing, can they at least not tell us why australopithecines, Homo erectus, and Homo neanderthalis existed, only to end up on the scrapheap of history? No?

Well then surely we have essentially no reason to turn to “design” to explain the patterns of life that we see.

What is sort of amazing is that Behe seems quite willing to bring up the aspects of life that tell decidedly against design, and which usually militate in favor of evolution. Malaria is wholly unproblematic within unguided evolution, and extremely problematic for claims of design–whether because of its lack any rational design existing behind it, or due to the lack of demonstrable purpose for its existence. And why should Behe bring up the lack of “future goals” in evolution, when all of the extinctions, evolutionarily-constrained “poor designs” existing in today’s animals, and parasitical relationships, exhibit no future goals existing behind them?

Above all, why would Behe wish to bring up the fact that design typically uses “conceptual precursors” (although one wonders why God would), and evolution is constrained to use “physical precursors” (DBB 45)? The only reason evolutionary theory is able to accurately predict that complex metazoan life will appear less and less familiar the further back we go is precisely because it cannot use “conceptual precursors.” For the same reason, an honest model of design could not predict that at all. And that is even before we note that his “irreducibly complex” biochemical pathways always betray the use of the physical precursors.

Unsurprisingly, many of these questions have been asked of the IDists repeatedly, with silence being almost the only response. The very rare times when a fellow of the Discovery Institute have engaged any of us on the various forums have always demonstrated that they are nothing but disingenuous propagandists, with no interest in actually coming up with any answers to relevant biological questions. All that they ever want to do is to insist that evolution “is impossible,” and that a “design” lacking answers to any of the scientific questions should replace it by default. Behe is likely their best, but he, too, manages to avoid practically all of the questions we moderns ask, and even practically all of the issues that Paley at least attempted to address in his day.

Nothing speaks worse of ID than the fact that it has rather fewer (zero, to be exact) relatively causal hypotheses to answer the questions of biology than existed two centuries ago.

9.17.08                                          To top

17. So why were the Ediacaran fauna designed, then annihilated?

Darwinian evolution cannot pursue a future goal. The Edge of Evolution, 112

I recently wrote several posts regarding the evolution of photosynthesis, which released the oxygen that allowed the Ediacaran radiation. My last post (not counting yesterday’s post that I thought was lost) mainly involved how the extinction of the Ediacaran fauna plus the relatively high levels of oxygen appears to have facilitated the Cambrian radiation. Of course that is all perfectly reasonable under the evolutionary understanding, but what possible sense would there be to designing one radiation, to simply let it all die, and then to design the Cambrian radiation?

The truth is that such a scenario looks a great deal more like the flood story in Genesis than it does either a creation story or whatever “design strategy” is popular this week among the IDists. Even Behe, who tries his very best to make all “ID predictions” empirically indistinguishable from the predictions entailed by evolution, fails to even come up with a myth for why his super-powerful and super-intelligent Designer destroys as readily as it designs, and fails to repeat any of his designs once they have truly died out. Because, of course, it is evolution that predicts that the same organism as such will never rise again (it’s probabilistic, but the probabilities are heavily against), once it has become extinct.

This principle is called in geology “The Law of Fossil Succession,” and it was originally an empirical observation without explanation. The contingencies and accidents of evolution make any exact repetition–such that we could ever see Archaeopteryx evolve again–so unlikely as to be practically impossible. A designer, of course, should be able to make another organism so close to an extinct original as to be indistinguishable from it, if it indeed made the original. Ought we to be amazed that life is unrepeatable, as evolution predicts, and as ID does not? Indeed, one would expect a good extinct design to show up again, more than the poor adaptation of unlikely parts that is typical in transitional organisms.

If the Ediacaran fauna were made by some super-intelligent designer, how come we never observe any of the organisms seen here reappear in the fossil record? It is not certain that none of the Ediacaran animals have descendents or reasonably close relatives in the Cambrian faunal assemblage, of course. What we know most assuredly is that those particular species did not and could not appear again–we know this through the evidence, and our knowledge that they evolved and were not designed.

And it appears that the IDists truly depend upon the Cambrian “explosion” as one of their prime “arguments” against evolution, which surely makes one wonder why they care so little about the Ediacaran “explosion”. Could it be that even they wonder why these animals would be designed, then exterminated, only for the Cambrian “explosion” to repeat none of the exact designs, a non-repetition that only evolution predicts? Why design them in the first place, and why design the considerable number of the Cambrian taxa that also have gone extinct (fortunately, not all of us)? Why are Archaeopteryx and its fellow dinosaurs forever extinct, with only a much more evolved line of birds having descended from relatives of Archaeopteryx?

In fact, it is believed that at least 99% of species which ever evolved have gone extinct. Effectively, this too is a prediction of unguided evolution, for accidents and contingencies, plus the fact that Behe put into words in the opening quote–that Darwinian evolution cannot look ahead–means that organisms will radiate adaptively, only for the environmental conditions to which most species adapted to shift and to cause their extinction. Catastrophes, like meteoroid strikes, are a part of this process, although they differ in important ways from the effects of evolutionary and gradual ecological changes.

With respect to the Ediacaran radiation and extinction (as with the others) we have two predictions of evolutionary theory fulfilled, then–that many organisms will evolve only to go extinct, and that the same organisms will never appear on earth again. Similarly, Ediacaran fauna raise two crucial questions for ID, which is why huge numbers of taxa are “designed” only to go extinct, and why such “designs” never reappear again, unlike the practice of known human designers. I’m sure that we could find any number of fulfilled evolutionary predictions, and unfulfilled design expectations, but these are enough for now.

I simply did not think that I should go on, to where Behe wants to steer us, without asking the questions that he so carefully evades, hence this post.

I should note that I wrote this not realizing that I had not, in fact, lost the post that I wrote yesterday, on the same topic. I am still learning how WordPress works. This one, however, points more directly to evolutionary predictions, hence another post on virtually the same subject may be worthwhile.

9.18.08                                           To top

18. Evolution of the eukaryote flagellum

There is not much truly known about how the eukaryotic flagellum evolved, other than that it did and from what cellular components most of it evolved. That is considerable, of course, and is infinitely more than the facts that ID explains (zero). Yet the one good thing about ID and Behe is that they point out how much is not known, which is often not well discussed in scientific circles–although occasionally journals will have articles discussing what is so little known in many areas, including evolution. So there is some point to agreeing that much remains in question, so long as it noted that it is not as little as Behe claims, nor does the evidence indicate anything that differs from the expectations of unguided processes.

There is an online paper that makes some educated guesses about how the eukaryote’s flagella/cilia evolved, which is worth a look. It is: Speculations on the evolution of 9+2 organelles and the role of central pair microtubules, by David R. Mitchell. It elaborates on the obvious point that cilia are made from part of the framework of the eukaryotic cell and some of the machines that provide intracellular transport.

Soon it gets to the most interesting, and probably the most questionable, speculation, which is that eukaryotes used microtubules radiating from a centrosome in order to partition duplicated chromosomes. Apparently this idea is patterned on the microtubule-based spindle used to separate chromosomes in present-day animal cells. And from the early proto-cilium that was used to separate the chromosomes evolved the cilium, by asymmetrically growing into a bundle (actually, only two at first) of microtubules that extended the cell outward to create gliding motors that acted both to move the cell and to provide sensory activities.

After that the beating cila/flagella would evolve for swimming, and the numbers of microtubules bundled together would increase dramatically, at least in some lines. From that the 9+2 arrangement would evolve because it is fairly good for the sake of controlling the beat of flagella and cilia. A fair bit of the paper is taken up discussing the evolution of the ancestral 9+2 configuration of the cilium and flagellum. Anyhow, I do not intend to try to re-write what is written in that short paper, particularly not the 9+2 configuration, which seems least relevant to the evolvability of the eukarote flagellum.

What is important is that there does exist at least a somewhat reasonable path toward evolution of the flagellum in the literature, and there seems to be nothing to preclude our cilia and spermatic flagella from evolving in that manner. Surely it could happen.

I have to wonder about the step in which the cilium evolves from microtubules involved in mitosis, however, which is credited to earlier authors by Mitchell. One problem is that in present-day mitosis the spindle only operates during mitosis, and is dissassembled rather quickly afterward. Why would an early eukaryote keep its spindle-equivalent around, when it would just get in the way? Furthermore, the operation and set-up of microtubules during mitosis have relatively little to do with the operation of a cilium. Combining mitotic processes with even the processes occurring in a gliding cilium (gliding cilia, by the way, are found in a few modern eukaryotes) does not appear to be a successful evolutionary “strategy”.

Evidently part of the reason various authors want to understand the cilium as coming from microtubules involved in mitosis is that it provides an explanation for how eukaryotic cells become polar. Yet that, too, seems to be insufficient to combine mitotic and ciliary microtubules, because the cells only need to use the polarity provided by mitosis to place a flagellum at one pole. It seems far more likely to me that intracellular transport mechanisms might evolve into gliding motors (for movement, chemosensation, or both), which evolved to be more efficient by protruding from one pole of the cell. This could be somewhat similar to the movements that amoebae have evolved, it’s just that in this case the movement became compartmentalized and specialized to a far greater degree.

Like I implied above, this is all just speculation without a great deal of constraint. Take it or leave it, whether it is Mitchell’s paper, or my criticisms of the hypothetical mitosis-flagellum link. They are included because, once again, these are examples of how caring about observable causes can lead to thought, as poof “explanations” cannot. What really matters is all of the evidence that the eukaryotic flagellum did evolve, and the hope that this might eventually help us to tease apart the mystery of how our cilia/flagella evolved–though it is not certain that all distant evolutionary processes will be knowable, including this one.

The evidence that it evolved will soon be the subject of another post. The fact is that we have enough reason to believe that the evolution of the eukaryotic flagellum is possible, but more importantly, we have good evidence that it did. Real science proceeds from the evidence that, say, language evolution, or biological evolution, happened to the actual causes behind it. And of course “actual causes” means “observable causes” (at least in principle), if we take epistemology at all seriously.

9.22.08                                                                                                                       To top

19. Eukaryotic flagella are derived from intracellular transport systems

One of the problems in discovering how cilia/flagella arose in eukaryotic cells is that such a large proportion of the “parts” are used for non-ciliary purposes. As one paper discussing the evolutionary and functional aspects of cila notes, regarding the research that went into it:

Ciliary genes that serve multiple cellular functions were not selected in this screen, mainly because they are still present in organisms that have lost ciliated structures. For example, dyneins are critical components of the ciliary motility apparatus, yet many were filtered out in our screens because they are also involved in intracellular transport in nonciliated organisms. Indeed, we suggest that the reason so few candidate genes were recovered in the “all ciliated organisms” subgroup is because proteins common to all cilia, like those involved in axoneme assembly, are also required in basic cellular processes and therefore conserved in nonciliated organisms (e.g. α-tubulin, β-tubulin, γ-tubulin, centrin, pericentrin, etc.). (Avidor-Reiss, T., et al., 2004. Decoding cilia function: Defining specialized genes required for compartmentalized cilia biogenesis. Cell 117, 527-539)

However many times I have mentioned this, it remains important that even Behe notes that “In Darwinian evolution, only physical precursors count” (DBB, 118). And yes, they exist in great abundance, while the “conceptual precursors” likely in design do not have any credible evidence for existing in life at all (if we exclude our limited meddling). In eukaryotic flagella, we don’t just have a great many homologous components, we have a great many components that are simply shared between flagella/cilia and the structures and machines that transport intracellular materials.

What this always comes down to is whether or not someone will accept the evidence, since the evidence for the cilium evolving from existing transport structures and machinery is so very clear. Of course one can always claim that a Designer is responsible for a child having half of his genetic material being identical to a certain man’s DNA. It’s always just possible, as far as the merely logical goes. But it makes no sense (and is not worth bringing up in a paternity suit)–it is a stupid inference, let alone being unscientific. The shared material between intracellular transport machinery and the cilium exists because they have a common origin (and not a designer, who would be capable of borrowing from archaea, bacteria, and of completely novel constructions), or you’re just throwing away all of your bases for doing science.

However, as if to clinch the case against the anti-science faction and their delusions about “designed cilia,” researchers were quite capable of finding a set ciliary proteins that are “related to prototypical intracellular transport proteins.” The aforementioned research paper mentions some such homologies in the passage below, involving a specific family of ciliary transport proteins, the OSEGs:

OSEGs are characterized by the presence of two major protein-protein interaction domains, WD and TPR repeats, implicated in the assembly of multiprotein complexes. Significantly, the most closely related proteins outside of the family are α- and β’-coatomer, two cargo-carrying proteins intimiately involved in intracellular trafficking (…). Furthermore, clathrin heavy chains display striking domain similarity to the OSEG family: an N terminus consisting of 7 WD repeats and a C terminus consisting of ~35 TPR-like repeats known as CHCR motifs (…). Interestingly, coatomers and clathrin-mediated transport system use small G proteins of the Arf subfamilies as regulators of the transport process. notably , our screen also identified ARL3 and ARL6, two Arf-like proteins, as components of the ciliary compartement group, with ARL6 expression restricted to mechano- and chemosensory neurons. (Avidor-Reiss, T., et al., 2004. Decoding cilia function: Defining specialized genes required for compartmentalized cilia biogenesis. Cell 117, 527-539)

Or in other words, this is an example of the genes and their products involved in eukaryotic flagella which are homologous with cytoplasmic transporters. Page 533 of the same article has a figure (4) showing some of the homologies. No doubt many more homologies could be found in the literature, but anyway it is the proteins that are exclusive to eukaryotic cilia/flagella that are the exception, while proteins shared with cytoplasmic transport are the rule.

This particular paper comes to the only reasonable conclusion:

Surprisingly, the integration of these proteins into a groups of genes related to the main families of intracellular transport proteins had escaped notice. Our results illustrate a common foundation in the organization of intracellular transport systems, whether mediating internalizations of surface proteins, transferring cargo between organelles, or delivering components from the cell body to distal ciliary compartments. (Ibid.)

Anyone who has read Behe’s books knows, however, what his response would be to this. He would simply agree that common ancestry is shown by the homologous and shared genes and proteins, while “how” it occurred is an entirely separate question in his mind. Of course it is not separate at all, since one had to show a reasonable mechanism for how life could change before it would be accepted that cyanobacteria and humans share a common ancestor (or actually, that far back it might be a shared set of promiscuously conjugating cells not otherwise closely related), for common ancestry alone would suggest that all organisms are of the same species. After all, no one ever simply looked at micro-organisms and humans and immediately leaped to the conclusion that the two were related, rather this had to be worked out in detail.

“Poof” would be no explanation no matter what, hence ID would fail regardless of the evidence for evolution. Yet because Behe’s criticisms of evolution in his books rests upon his specious and appallingly reductive claims that common ancestry, mutations, and natural selection are all separate issues, my next post in the DBB category will be about how they are in fact interconnected.

9.23.08                                                                                                                       To top

20. Common descent is demonstrable only when causes are known

Bear in mind, throughout, that common descent is a distinct concept from the mechanism of natural selection acting on random variation. Edge of Evolution, 64

In the abstract, the quote above is true. It is in reality that Behe’s constant resort to the contingencies of “naturalistic” heredity, while denying “naturalistic” contingencies in adapatation, fails utterly and completely, both on the ground of consistency and because he is unable to differentiate between the causes of various effects. If he is unable to constrain “design,” as he most certainly is not able to do (indeed, he takes pains to try make his claims of design unfalsifiable), then he cannot constrain anything else in the history of life. If “…anything might have been designed” (DBB, 193)–including mutations which are directed (a favorite claim in EoE)–then we have no reason to believe that the evidence of common descent was not also designed, and produced by miracle.

Yet he does believe observable causes are responsible for similarities:

Like the sequence analysts, I believe the evidence strongly supports common descent. DBB, 176

Unsurprisingly, where the actual “naturalistic” causes are unknown, whether in “design models” or in “atheistic models,” such certainties have not been obvious or accepted. A philosopher such as Buffon could propose that life arose to fit “internal molds,” which shaped organisms into set patterns. Paley states that “This similitude, surely, bespeaks the same creation and the same Creator” (Natural Theology, chap. 25).

One might suppose that Behe has more cause to believe in common descent than Paley did, however. Well, yes, that is true, both in the huge amount of evidence which indicates what is expected of common descent, and at least as importantly, because we understand the mechanisms of both conservation and of non-conservation of genetic information in organisms. The processes of preservation and of change are inextricably tied together within biology, never mind the fact that the concepts are different (the processes themselves are occasionally separable, such as during the early part of abiogenesis). That is, we understand how genetic information is preserved both by reproduction and by natural selection, and we know that because we understand the limits of change imposed by (roughly) the neo-Darwinian model of evolution.

Paley credited God for similarity because he could not conceive of how morphology (which is about the only type of evidence that he had) could be preserved as a “general plan,” yet so thoroughly modified. Darwin explained this, which is why he and most modern biologists have understood the evidence of common descent to implicitly support the known causes of organism modification. For, if there is nothing that accounts for the differences between frogs and humans, how are the similarities going to be accounted for via common descent? We have to understand similarities and differences under the same model, and we do so by understanding them all to be due to common descent as modified by mutation plus natural selection (plus other known processes).

Once one believes that an unobservable and unpredictable (in the probabilistic sense of the word) process, or processes, is responsible for the “design” of organisms, how can one possibly determine which aspects of organisms were not poofed into existence? A rat might as easily be descended from, or designed from the template of, an octopus or a petunia, if we are not paying attention to the actual mechanisms of stability and of change. The only apparent reason why Behe accepts the accidents of heredity, and not the evidence of accident in adaptation, is because he wishes his god to be responsible for the latter and not for the former. This goes back to the fact that Behe has absolutely no means of independently observing design in life in an entailed manner, discussed here.

The evidence that life evolved in a process involving natural selection is precisely the evidence of accident and contingency found in life. Two such crucial contingencies are the accidents of heredity and of mutation, and, aside from effects of the filter of natural selection, that is largely what we see in life (I write “largely” because causal regularities exist apart from natural selection and descent). The accidents of heredity are accepted by Behe as causal, even though any accepted meaning of the term “intelligent design” implies that such accidents would not predominate in life as they do–we filter out many undesirable accidents whenever we adapt designs. Then he wants “design” to hide underneath the accidents of mutation, and to be indistinguishable from them, except probabilistically.

Such a position must be called “incoherent,” at least if we are being charitable. The filter of intelligence involves rationality, planning, and the correction of defective accidental characteristics, wherever these occur. We accept that a filter quite different (if with some similarity in output) from intelligence produced life precisely because neither accidents of heredity nor of mutation characterize intelligent activity to any great degree, while they are unquestionably predicated of any unguided natural selectionist evolution involving the sorts of organisms we recognize.

I am writing this now because just one day previously I wrote a post about all of the evidence of evolution in the eukaryote flagellum, one of Behe’s “examples” of “irreducibly complex” systems. I noted there that Behe would accept the evidence of common descent, but would deny that it indicates that it evolved by the mechanisms by which we say it evolved, rather claiming that it had to be designed. That, however, is an absurd notion on his part, for the terms “intelligence,” “design,” and “intelligent design” do not even refer to processes adopting the contingencies of heredity and mutation that we observe in life. “Evolution,” and “evolution by natural selection,” by contrast, do refer to processes including such observed accidents and limitations. We simply match up cause to effect to conclude that eukaryotes’ flagella evolved (with no poofs).

So of course it is true that “common descent” and “natural selection” are separate (at least separable) concepts. In science, though, we do what Behe and other IDists do not, which is to combine the two concepts in order to constrain these concepts as they actually (empirically) do pertain to life.

Because Behe does not follow science at all in the area of origins, we are at a loss to understand how his god of the miracle mutations is in any way preferable to, or more scientific than, the belief that some god simply spoke all of life into existence a few thousand years ago, complete with the evidence predicted for organisms that have evolved without any guidance of intelligence.

9.24.08                                                                                                                       To top

21. The cilium evolved into part of the “irreducibly complex” chordate eye

How do we get theories, and what is their purpose? Is a theory something that we have after every phenomenon encompassed by the theory is completely explained? Why would we even need a theory in biology, if we knew everything that happens in the past and present according to physics, and its theories?

Of course Behe and the other IDists’ understanding of (or at least rhetoric about) theory is as flawed as their understanding of everything else in science. This is not the post for a long discussion about why theories exist, yet it is worth pointing out, yet again, that theories exist to guide research and to organize knowledge, and are not catalogs of everything that has happened, is happening, and will happen. This is why evolutionary theory is a crucial theory, because it acknowledges the constraints that exist in biology and thus explains the limits of biological change. This would even be true if Behe’s mutation-causing God were responsible for some mutations, because in any case this “God” does not transcend the limits of heredity and of mutation, or at best (we have to trust Behe to discuss this claim, since he supplies no evidence for this mutator) only pushes the limits of mutation without doing anything that we understand as design-like (such as giving radio communication to organisms).

The above follows up on my last two posts involving DBB, here, and here, and it introduces the following discussion of how the structures of cilia provided opportunity and constraint in evolution after the cilium first became a fixed eukaryotic structure. No, not everything about the origin of cilia is known, nor is everything about the evolution of cilia into parts of sensory structures understood, but only evolution makes any kind of sense at all of the distributions and modifications of cilia that we find in noses, in eyes, and in the motility of ciliated cells, in addition to its origin.

Sensory reception via cilia appears to be evolutionarily ancient (Mitchell), so the fact that cila comprise parts of the vertebrate eye, olfaction, and of taste buds is not especially surprising. Presumably, cilia have had a sensory role from very early in evolution both because they provide extensions into extracellular media, and because they can set up currents in liquids in order to sense media which would otherwise be beyond the reach of the ancestral free-living cell. Nevertheless, the evolution from what were probably moving cilia to the outer portions of the rods of our eyes is the kind of transformation that we would not suspect, if the evidence of it were not so clear. Here is a photograph (bottom) of a rod cell of the eye, with a cilium clearly visible as part of it.

The transformation of part of the cilium into stacks of lamellae, and the role played by the cilium as a photoreceptor, indicate a rather extensive evolutionary change of this supposedly “irreducibly complex” organelle. Indeed, most (perhaps all) of the “irreducibly complex” visual biochemical pathway that Behe discusses in DBB chapter one (see figue on p. 20) occurs exactly in the region of the rods which are made up substantially of cilia, although these originally evolved for quite different purposes (motility and chemoreception).

My point here is not to go through the complexities of these matters (which can be found on the web quite easily), but rather to show that we have “nested” complexities which reveal successive evolutionary events–not the sudden creation at the Cambrian hinted at by Behe and other IDists–having all of the accidents (hereditary and mutational/selectional) expected in evolution, and highly complex modifications of previously evolved complexities. Importantly, evolution proceeds just as predicted by evolutionary theory, with evolved complexity itself almost certainly providing a major constraint on the evolution of later complexity (of P. falciparum, for instance), so that the complexity of the cilium is utilized by the chordate eye in order to supply the complexity needed for photoreception.

What is perhaps at least as interesting is that the modification of the cilium to function for the eyesight of chordates was not the only solution to the problem of photoreception. We have ciliary photoreceptors, while many animals have rhabdomeric photoreceptors, which apparently evolved from the same cells from which retinal ganglion cells are derived (Evolution of eyes and photoreceptor cell types). Again, the story is of accident, where no design reason can be given for our ciliary photoreceptors, and it is the accidental (initial and subsequent) evolution of cilia that gives us any reason for such an odd switch from rhabdomeric photoreceptors to ciliary photoreceptors in the chordate line. That anyone would try to claim that such obvious accident is the result of “design” strains any notion of design that reasonable people have.

I do not plan to revisit the evolution of the eye after this, since the incorporation of the “irreducibly complex” cilium into the “irreducibly complex” vertebrate eye while all of the hereditary and mutational/selectional constraints of evolution apply, is the only possible, and easily sufficient, evidence that unguided evolution is responsible. Complexity builds upon complexity in the same sorts of evolutionary (cladistic) patterns as exist in microevolutionary processes, and only a fool would fail to match up cause and effect in both microevolution and in macroevolution.

However, since this is probably the only substantial discussion I will have of eye evolution (at least while discussing Behe’s books), I’d like to point to a some more evidence of the evolution of the eye from simple to complex that may be found in the last link/reference. Never mind Behe’s peculiar and unjustified demands for evidence, here is some of the reasoning (from evidence) and conclusion for evolution from simple to complex:

The prevalence of pigment-cup eyes in Bilateria, and their stereotype, simple design, tells us that eyes started off with merely two cell types, photoreceptor cells that associated with pigment cells to detect the direction of light (…). Additional cell types were added during subsequent eye evolution, such as lens cells, various kinds of support cells, muscle cells etc. that also formed part of the eyes. Cell type diversity reached its maximum in the vertebrate and cephalopod camera eye, as well as in the arthropod compound eye. Evolution of eyes and photoreceptor cell types

Opsin homologies go back at least to before the evolution of bilateral animals (“bilaterians”), such as ourselves:

On the molecular level it is long known that all eye photoreceptor cells so far described use a vitamin-A-based light-sensitive photopigment, comprising a chromophore and an apoprotein, opsin. Phylogenetic analysis approves that all opsins trace back to one opsin precursor molecule that predated bilaterians. Evolution of eyes and photoreceptor cell types

Beyond that, the homologies are extensive throughout vertebrate eyes, and yet however common a gene like pax6 may be in animal eye development, it, too, appears to be so due to accidents of heredity, for it is neither exclusive to eye development, nor needed for the development of all animal eyes:

In the vertebrates, pax6 is required for the formation of virtually all retinal cell types…. In Drosophila, the pax6 orthologs eyeless and eye gone are required for the formation of the entire eye disc (…), which gives rise to all ommatidial cell types including the photoreceptor cells. Eyeless and another pax6 ortholog, twin of eyeless are also expressed in precursor cells of the photoreceptive Bolwig organ and ocelli (…), and in the late Bolwig organ (…). In line with a general affiliation with photoreceptor cell specification, pax6 expression also covers the early eye anlagen in cephalopods (…), planarians (…) (…), nemertines (…), and polychaetes (…). However, and even if pax6 started off as an early photoreceptor specification gene in pre-bilaterians, in none of the species investigated is pax6 photoreceptor cell-specific, or even eye-specific (…). This means that the ancestral function of pax6 in cell type specification or differentiation (whatever it was) is not exclusively required in photoreceptor cells. It is also clear that in few cases photoreceptor cells can form in the complete absence of pax6, such as the Hesse eyecups in Branchiostoma (…). Evolution of eyes and photoreceptor cell types

The animal eye is an exquisite adaptation, an organ that is extremely important to the lives of most animals that have eyes, and so eyes are finely-honed instruments. A very crucial point to the use and intellectual sense of the achievement of understanding, however, is how to account for all of the accidents of heredity and apparently of mutation/selection. Thus, we like to know why the chordate eye is a complex of preceding parts, such as cilia, and in turn, why cilia are composed of parts of cytoplasmic transport systems which preceded the cilia.

None of these questions are asked by IDists, for they know that they have no answers via design. Accident is the antithesis of design, despite the fact that Behe tries by analogy to claim that apparent accidents are within the realm of “design” (DBB 193-194). Of course he tries to do so, since he knows that life is shot through with evident accident, including complex accidents (coupled, of course, with natural selection) like ciliary eyes. He does the only thing he can do, however, which is to try to claim that some complexes of accidental characteristics are too complex to be the result of accident, then to claim design without any actual evidence in favor of design.

Actually, though, complexes of accident ought to be accepted as being the result of accident (plus ordering principles, like natural selection) so long as design characteristics (purpose and rationality being the biggest) cannot be demonstrated. For the fact is that when you have the sequential accidents found in life, like oxygenic photosynthesis producing the necessary oxygen for the Ediacaran and the Cambrian “explosions”, or cilia being composed of intracellular transport biochemicals and then cilia hosting crucial photoreceptor biochemical pathways, you really can only honestly conclude that the accidental effects are due to accidents which natural selection filters, not to design.

For, again, design is itself the opposite of accident, if not totally devoid of accident. That is, design filters out most accidents, leaving primarily non-accidental rational organization–at least when it is good design. When it comes right down to it, natural selection only refines accident–it really only filters organic traits out of the accidents of mutation, duplication, deletion, and environmental contingencies–for an incomplete list–and however many accidents are excluded, only accidents remain. Because we see only accident and natural selection behind the integrated complexities of life, we must pick evolution as the cause of life’s configurations.

9.27.08                                                                                                                       To top

22. Behe denies all avenues to understanding the evolution of pathways

This is just a short post, following up recent posts that point to evidence that does indeed give very good hints at how metabolic pathways evolved, such as through the adaptation of cilia for photoreception, gene duplications in general, and duplication of the genes for photosystem I, which allowed for the evolution of photosystem II.

You can see the satisfaction that Behe has in the idea that his claims are beyond the reach of the evidence, in the following DBB quote:

Thus biochemistry offers a Lilliputian chalnge to Darwin. Anatomy is, quite simply, irrelevant to the question of whether evolution could take place on the molecular level. So is the fossil record…. Neither do the patterns of biogeography matter, nor those of population biology, nor the traditional explanations of evolutionary theory for rudimentary organs or species abundance. DBB, 22

Unsurprisingly, he ignores rather crucial issues of falsifiability of unguided evolution, such as whether or not cladistics map out to the expected evolutionary predictions, which, so far as anyone can demonstrate, is indeed the case. He also ignores the fact that if evolutionary thinkers were unable to garner positive evidence in favor of “darwinian evolution” from the various lines of evidence, the exact same fact would exist for ID. But then he fails to understand the need for positive evidence for his claims, unlike the far better scientific thinker, Rev. William Paley (See here).

Above all, he wants to pretend that science should not simply use the evidence of origination that fits taxonomy, biogeography, comparative anatomy, and the fossil record, unless actual evidence is found that something else is responsible–or if one found actual evidence that it could not have evolved (he isn’t even close).

But another issue crops up in the book, for note that the quote above came from page 22. Only rather later does he even bring up genetic evidence of molecular evolution, and then denies it without justification or a mention of evidence. The denial is bad enough, and reveals an apparent stupidity on his part, though it could be mendacity instead. Yet, worse, it would seem as though he left this issue alone at the beginning because he actually knew that it could provide such evidence (or if he’s too deeply into denial, he seems to know that others say so). Otherwise, why would he not bring it up on p. 22? On pp. 180-181 can be found his blank, unevidenced denial of this crucial issue (though the same stupid denial is on p. 90, its first appearance I believe):

…Although sequence data can be used to infer relationships, they cannot be used to determine how a complex biochemical structure originated. DBB 180-181

Never mind that he does exactly this time and again, including mitochondria and even to a degree with his “irreducibly complex” examples, for, although he denies that they evolved by “Darwinian” means, he does not deny that genes were adapted from previously existing genes. This is acknowledged more explicitly in Edge of Evolution.

This is not the only time that he brings up crucial issues only when (it appears) he hopes to have already confused people sufficiently that they won’t catch on. I have mentioned this before, but he writes on p. 245 of DBB “…Large questions remain (as they inevitably do in basic science),….” Suppose he had admitted as much at the beginning, rather than well after he had claimed that evolution doesn’t work due to the difficulties we have in the basic historical science of biology? It would have completely undermined his whole case.

Oh, I am quite convinced that he crafted his book to avoid many of the honest questions, at least until after he had already dishonestly misconstrued the science of evolution. Of course even at the end he quite continues to deny the obvious, that genetic sequences give us considerable insight into the evolution of metabolic pathways, no matter that he himself makes many claims based expressly upon genetic sequences.

Could he ever admit that we can indeed find out how genes evolved by observing the evidence of gene splits? Of course he could not, because then he’d have to honestly face (or at least would be pressed to do so) the evidences of duplications behind the evolution of the clotting cascade and in the evolution of oxygenic photosynthesis, as well as having to notice that his “irreducible pathways” in the eye are mainly in an highly modified cilium, which in turn is a highly modified set of pre-existing cellular transport system.

Since he never once was interested in supplying any evidence for design, he doesn’t mind closing off all avenues which provide the evidence that life evolved. The mere fact that he ends up basing his pathetic analogies and “arguments” on exactly what he has denied is not a problem for someone who isn’t concerned about either science or consistency.

9.29.08                                                                                                                       To top

23. Behe and language origination

When Behe was told that both Greek and Latin derive naturally from the ancient Indo-European language, as evidenced by the similarities between the family of languages which includes those two, he said:

Although one may determine relationships of languages by looking at similarities of words and of grammer, how duplications, modifications, and the shuffling of words actually occurred is completely beyond the knowledge of science. One cannot know whether they arose gradually or suddenly, by human selection, or by the intervention of a language designer.

In fact, since no human has ever been able to invent a single language with the complexities of a natural language, as opposed to artificial language, it appears highly unlikely that natural human selection could possibly produce the complexity of Greek and Latin. How could inflections “suddenly appear” in Greek and Latin, if there were no intelligence capable of designing grammar? Furthermore, languages don’t fossilize, so the fossil record will provide no evidence of “naturalistic evolution,” nor will anything else.

Remember, frater might in some way resemble φρατηρ, and Latin verb inflections might resemble Greek verb inflections, but the similarities say nothing about how a language like Latin is produced. The sheer complexity of both Greek and Latin, which has only been understood by humans recently, could hardly have been produced by humans who did not understand the complexities of language.

Well okay, he didn’t really say that, but he wrote something equally unscientific and just plain divorced from reality. What I wrote above is based on the following:

By itself, however, the hypothesis of gene duplication and shuffling says nothing about how any particular protein or protein was first produced–whether slowly or suddenly, or whether by natural selection or some other mechanism. Remember a mousetrap spring might in some way resemble a clock spring, and a crowbar might resemble a mousetrap hammer, but the similarities say nothing about how a mousetrap is produced. In order to claim that a system developed gradually by a Darwinian mechanism a person must show that the function of the system could “have been formed by numerous successive, slight modifications.” DBB 90

Of course I had to change it to fit language evolution, and perversely, I had to shift his analogy to one that actually is roughly analogous with biological evolution, hence it becomes absurd to say that the similarities of an evolved language say nothing about how these originated, although of course the (non-accidental) similarities of his designed object really do give no indication (by themselves) of how they were actually made. When I change his dis-analogous comparison into an analogous comparison, it becomes a senseless claim (think of how differently aliens might make these objects).

I briefly discussed his denial that genetic evidence tells us about evolution yesterday, along with his denial of all of the other evidence. But this particular denial cuts so close to the heart of Behe’s errors and apparent lack of understanding of science that I thought it would be worth discussing further, especially since it tantamount to denying the evidence used to understand language evolution (although the selectional mechanisms are different, which shows up in the details of both evolutions, including their taxonomies). For, nucleotide sequences, coupled with their organization, have many similarities to languages and their structures, even though they also have many dissimilarities.

By contrast, there is no “phenotype evolution” of language comparable to the evolution of phenotypes in biological evolution, and all “language fossils” (texts) are quite recent, certainly more recent than the Indo-European language, which is inferred solely from the vocabulary and grammar of the languages derived from it. We’re stuck comparing evolution of the “languages” of biology and of humans, if we wish for the most honest analogy of the evolutions of both.

And of course one may study languages in context to understand the mechanisms of language evolution. This, by the way, opposes how a science touching upon intelligent cognition actually operates, versus ID which has no mechanism or meaningful causes whatsoever. Indeed, even the rates of language evolution are thought able to be studied, so that one study concluded (as most biologists also conclude regarding organic evolution) that languages typically go through bursts of evolution, as in “punctuated equilibrium.”

Among IDists there seems to be quite an aversion to actually considering evidence. Behe does not look at the gene sequences and ask what they tell him, instead he looks at them and denies that the evidence matters. In addition, he brings in a canard in the above quote, using Darwin as the standard for what sorts of changes are possible in evolution, when in fact many consider that at least some of the changes (like gene duplications) can be quite dramatic and not “slight” changes as such.

If one looks at genes one may observe whether or not gene duplications provided the opportunities for “slight modifications” (at least relatively small changes are thought responsible for modifying most duplicated genes) which in time could produce dramatic changes. In a similar manner, one may detect whether or not there was a single ancestral gene, if one is able to do enough comparison of the appropriate genes, and thus whether or not two or more copies evolved from one or more duplication events (important in the evolution of the adaptive immune system, soon to be discussed here). One may observe ancestral functions of genes by genetic comparisons, and therefore what later genetic capacities have evolved. Above all, one may discover what constraints existed in the evolution of a certain capacity, for instance what sorts of genes were needed for a function like adaptive immunity, and to discover precursor genes that already had some of the needed function. Indeed, that is often enough how the precursor gene itself is found, through the function, and only then it is found to have an ancestral sequence.

Indeed, the constraints of biological evolution are rather more strict–hence cause is more easily matched up with effect–than in language evolution. Yet no one really thinks that we can’t come to reasonable conclusions about many of the mechanisms of the evolution of a given language. Biological evolution is much more precisely understood than is language evolution, and yet the IDists do not complain about the latter, only the former.

I brought up such obvious evidence of origination in the penultimate paragraph in part because I intend to discuss mainly the evidence that adaptive immunity evolved, and not so much the questions about how it “could evolve”–though clues about such possibilities are also to be found in genes, without being resolvable at this time–as has happened often. Someone like Behe (unlike many traditional creationists) does not deny the massive evidence for language evolution merely because no one has ever truly shown that humans are capable of functioning to effect such complex evolution–indeed, one simply uses the evidence of language evolution to understand presently known mechanisms and possibly some remaining unknown ones (on the other hand, Behe would be likely to simply credit “intelligence” as the cause of language evolution, and thus would probably fail once again). Likewise, when we observe genes in agnathans (jawless fish) and gnathostomes (jawed vertebrates) which gave rise to different families of genes for their divergent adaptive immune systems, we understand evolution to occur by sufficient and observable means, crucially via “natural selection,” and seek to understand how these systems evolved by such known means–and possibly by unknown means–if effects of these may be discovered.

The fact is that genomes are coming on-line more and more swiftly–for many reasons–with one of the prominent reasons being in order to discover how genes and pathways evolved. Fortunately for us, several of the “irreducibly complex” pathways not only were reasonably well understood when Darwin’s Black Box was written, but are even better understood today. The evolution of adaptive immunity may be one of the best examples of learning from genetic comparisons how it evolved from innate immunity (primarily), and so, far from being a problem (though questions remain), it is in fact one of the best counterexamples to Behe’s complaint that he doesn’t understand how it evolved, so it must not have done so. And that is what will be discussed soon in the Darwin’s Black Box category.

9.30.08                                                                                                                       To top

24. If evolution is true, why can’t gazelles run 433 mph?

The thrust and parry of human-malaria evolution did not build anything–it only destroyed things. Jettisoning G6PD wrecks, it does not construct. Throwing away band 3 protein does likewise. Sickle hemoglobin itself is not an advancement of the immune system; it’s a regression of the red blood cell. Even the breaking of the normal controls in HPFH doesn’t build a new system; it’s just plugging another hole in the dike. Edge of Evolution 42

Behe has a creationist view of these matters, so that hemoglobin remodeled to confer partial immunity to malaria for those who are heterozygous for sickle cell anemia is “regression.” Scientifically and philosophically, that is nothing other than nonsense. The other mechanisms we have evolved that are mentioned in the above quote have varying degrees of deletion (which science would consider to be a functional regression, if still an improvement to fit current conditions) and/or change. Leaving those aside at the present, let us just note here that the changes that cause sickle cell anemia in homozygotes is definitely an improvement for heterozygotes, and his comparisons to a utopian defense against malaria of the kind a true designer (especially his omniscient “designer”) might produce has no place in understanding evolution.

The larger concern involves something quite different, which are the constraints of evolution. Even Behe mentions the constraints, oblivious to the fact that we accept evolutionary theory precisely because it fits the constraints seen in life. He writes:

Darwinian processes are incoherent and highly constrained. EoE 19

Well, Behe is incoherent, because in other places he claims that evolutionary processes mimic intent (also not true), which is typically not incoherent, even if incoherent statements are the norm in intentional ID arguments). Yet he is correct that evolution is highly constrained. Indeed, why else would the basic elements of our adaptive immune system remain the same for nearly half a billion years (though many of the parts have been significantly modified, added, or deleted)?

Beyond that, well, why can’t gazelles run 433 miles per hour, and cheetahs run somewhat faster, if evolution is constantly selecting both to optimize speed? Said that way, it sounds absurd, as if there are no limits to animal speed, let alone limits to what can evolve. Nevertheless, Behe’s “argument” about malaria and humans not evolving better “strategies” to attack and to defend, respectively, is about as intelligent and apropos as claiming that gazelles ought to run at least 433 mph by now.

What is more, chordates have evolved what is really quite a wonderful immune system, first evolving the innate immune system, and then a supplement to it which uses many of the same components, the adaptive immune system. That he denies that this is the case is hardly of any consequence, for the evolution of the adaptive immune system fits the constraints that he himself brought up, that “Darwinian evolution requires physical precursors.” DBB, 45 If not all such precursors have been found (and it is likely that not all will be, as extinctions of gene lines are not unexpected or uncommon), many have been, and the cladistic patterns map out to evolutionary expectations.

Importantly for our purposes, the complexity of our immune system evolved in stages, and according to the “nested hierarchies” predicted of organisms which are mainly limited to vertical transmission of information. The odds against evolution producing the innate and adaptive immune systems all at once are decisively against, and innate system precursors were needed for the adaptive system to operate and to evolve (not all adaptive system precursors come from the innate system, according to the evidence).

My previous post in this category (Darwin’s Black Box), and this one, are leading up to future posts dealing with the evidence of the evolution of immunity, framing the issue. After all, Behe manipulates the argument by framing everything according to his perspective, which truly does amount to dishonest framing. I am indeed framing (in the way more writers on these matters should do), by restoring the context that Behe stripped away from his own discussions of these things, and I do not doubt that this is quite an honest frame. The immune system is very important in both of his books, so I have an additional point to bring in as introduction, which is that the evidence of the evolution of the immune system goes directly against Behe’s claims of the inadequacy of evolution, in both of his books–but especially in Edge of Evolution (which is why this post is also in the EoE category, and will be put on the EoE cumulative post).

So I want to make clear how Behe’s criticisms of the “inadequacy” of evolution in response to malarial infection in humans fail so badly, since I will be bringing in good evidence that adaptive immunity did evolve. Crucially, we already have evolved an immune system that is both complex and to a considerable degree optimized. This is where the gazelle analogy comes in, for while gazelles run very fast and often leave cheetahs hungry, they can’t just simply keep evolving to run ever faster, due to physical limitations and to evolutionary limitations (indeed, evolution gave birds a better breathing system than it gave mammals, a typical non-design, makes-sense-only-in-the-light-of-evolution, limitation).

It is foolish to ask why evolution has the observed limitations, when the meaningful question is why Behe’s “design” seems to have so many limitations–and notably the same ones that evolution has. Furthermore, Behe still has absolutely no answer to the question of how he can determine what evolved and what has not. This is all the more true in Edge of Evolution, where he brings up the possibility that mutations “look accidental” but are not.

On the science side, I would like to get into a likely problem for evolving the immune system to better resist malaria, which is that Plasmodium falciparum, like many other parasites, actively subverts both the innate and the adaptive immune systems. This is not as important as the above points, in my opinion, but it is likely to play a role in the difficulty of evolutionarily responding to malarial infection.

One way malaria avoids our defenses is that it has an alternative method for taking up iron, that bypasses the body’s sequestration of iron (iron is a crucial element to nearly all life, especially so to growing life which has a high metabolic rate) effected to starve pathogens of iron.

A couple more ways that P. falciparum thwarts the immune system are mentioned in the quotes below:

In vitro studies involving human cells have shown that macrophage functions, including phagocytosis and ROI [reactive oxygen intermediates] generation, are severely impaired after uptake of an insoluble degraded host hemoglobin, called homozoin, generated during blood-stage malarial infection.

From the same source:

One of the more consistent and striking dysfunctions observed in macrophages infected with protozoan parasites [which include P. falciparum] is their inabililty to produce IL-12, which–as the main physiological inducer of interferon-&gamma; (IFN-&gamma;) and T helper type 1 (T<sub><small>H</small></sub> cell differentiation–is an essential cytokine for the development of acquired resistance to most intracellular pathogens. Nature immunology

The same paper details how malarial (and other parasitic protozoa) down-regulate many of the signaling pathways, particularly but not exclusively those involved with IL-12 (interleukin-12), and apparently also prevent maturation of the crucial dendritic cells. Again, I do not think that going into the details is especially instructive, since one can always use the link given, or search engines, to find out about those.

The question pertinent to this subversion of our immune system is: how are the highly evolved protozoan abilities to bypass or suppress our immune response really supposed to be countered by evolution? No doubt evolution has indeed tweaked our immune response to malaria, but our immunity is not an infinite god, it is a limited system whose adaptations are met with even more malarial adaptation. The very complexity of immunity likely inhibits further evolution, and, in any case, no gazelle will be able to evolve to run 433 mph. We have never outrun all parasites in our evolution, and likely we never will.

However, we do manage to fend off pathogens better than most ocean bacteria can, as their death rate is enormous at the hands of viruses. And they can evolve much more quickly than we can. The fact that our adaptive immunity has evolved to allow our line to exist for nearly half a billion years is certainly a testimony to the importance of of that evolution.

The ability of P. falciparum to be able to avoid much of the powerful effects of our immune system is merely one of the many stories of evolution wherein a “stalemate” of sorts has appeared. It is no fault of evolution that gazelles have topped out at around 50 mph, nor that our immune systems are able to handle most infections fairly well, but not the subversive virulence of P. falciparum. That evolution can recruit other changes in parallel with immune system evolution only speaks to the power–and the limitations–predicted of evolution.

Thus it is that the evidence of the evolution of our immune systems is crucial both to demonstrate what evolution can do, and, of course, what it cannot do. While one would like to endlessly ask the IDists how they account for the limitations of organisms, until they either reply to at least one crucial question or learn to keep quiet, the fact is that they will avoid all of the hard questions.

We, on the other hand, can answer a great deal about evolution’s abilities and limitations, so I plan for the next post to begin to lay out the evidence that the adaptive immune system evolved from the innate immune system. Evolution of the innate immune system could also be discussed (and may be in a limited way), but we almost certainly know more about how adaptive immunity evolved, and it is the part of immunity that Behe claimed could not evolve, even as he ignored the evidence that it evolved substantially out of the innate system.

10.02.08                                                                                                                   To top

25. Evolution of adaptive immunity I–Phylogeny

This is posted specifically in response to Chapter Six of Darwin’s Black Box, which claims that our adaptive immune system is irreducibly complex.

Defense against pathogens has a very long evolutionary history, going back at least to bacteria and archea.  Adaptive (or “acquired”) immunity is the tip of the iceberg, very effective, yet built upon and integrated with the earlier “innate immune system.”  Indeed, it should be mentioned at the outset that there is no inherent reason to split up “adaptive immunity” and “innate immunity,” as they are both “parts” of an integrated system.  Evolution and convenience are the reasons for splitting the “two systems” up, for only gnathostomes (jawed vertebrates) and agnathans (jawless vertebrates–now down to only hagfish and lampreys) have full adaptive function added onto the immune system that we share (not without considerable evolved differences, of course) with the rest of multicellular eukaryotic life. It is an interesting and meaningful phenomenon–unless one subscribes to ID/creationism, in which case it is meaningless–that gnathostomes and agnathans have very different, evolutionarily distinct, systems of adaptive immunity.

As I have previously noted, immune functions have emerged in the familiar cladistic patterns, adding complexity to the immune systems as evolution continues–in essentially the way that evolutionary theory predicts. It would be well, though, to lay out some of the details of the evolution of immunity, and not only with respect to adaptive immunity, but as immunity has evolved roughly since before the Cambrian “explosion”.   To start out, phylogeny is very important in demonstrating that (unguided) evolution occurred, and it sets out the framework for understanding the particulars of the evolution of adaptive immunity.

Scroll past the sequence data below to “part C,” which shows the phylogeny of toll and toll-like receptors, not only of “higher animals,” but of a plant, a nematode, and a sponge.  There, an abbreviation for each organism is used, so here is the key to the abbreviations:  MEDTRU=Barrel medic, a legume plant, CAEL=C. elegans, a nemotode worm, SUBDO=a sponge, DROME=a fruit fly, TRICAS=the red flour beetle, DANIO=zebrafish, HOMO=human, MUS=mouse, GALLUS=chicken.

In the link above, MEDTRU=Barrel medic, a legume plant, CAEL=C. elegans, a nemotode worm, SUBDO=a sponge, DROME=a fruit fly, TRICAS=the red flour beetle, DANIO=zebrafish, HOMO=human, MUS=mouse, GALLUS=chicken.

 Here is the source for the above illustration, and this is the article it illustrates.

While not all of the toll-like receptors (TLRs) give exactly the same relationships, clearly the expected relationships hold in general, with only fairly slight deviations. Mouse and human TLRs are rather closely related, chicken somewhat less, zebrafish is less related, the sponge and the nematode are even less related, and so is the plant. IDists such as Behe like to claim that the Cambrian “explosion” does not fit with “Darwinian evolution” because it appears discontinuous in the fossil record, yet genomes tend to show a reasonably steady progression of divergence of immunity genes, as well as all of the other genes–within our ability to resolve details, of course. That is, on the level of “punctuated equilibrium” evolution may not be especially slow and gradual (based on our resolution of genome sequencing), but immune system evolution across hundreds of millions of years is slow and gradual compared with any design expectations, even if it speeds up and slows down due to “punctuated equilibrium.”

For purposes of discussing Behe’s claims, even more important phylogeny appears right at Behe’s “irreducibly complex” adaptive immunity, for not only do we have excellent evidence that one adaptive immune system evolved, we have excellent evidence that two adaptive immune systems evolved from basically the same “physical precursors” that Behe rightly tells us are predicated of “Darwinian evolution.”  The old familiar accidental character of evolution is thereby evident, for no “design reason” can be adduced (or considered to be at all likely) for two different complex supplemental adaptive systems to be grafted onto the inherited innate immune systems of agnathans (jawless vertebrates) and gnathostomes  (literally “jaw-mouth” vertebrates–the vertebrates other than hagfishes and lampreys), while the inheritance, mutational, and environmental, accidents expected of evolution account quite nicely for the separate agnathan and gnathostome adaptive immune systems.

Here is another phylogenetic tree, this time not going quite so far back, and not based upon toll and toll-like receptors. For copyright reasons I do not think that I should reproduce it here, hence the link.  The main point presently of that linked illustration of phylogeny is the rather striking split of apparently unrelated adaptive immune systems in the two vertebrate groups, the aforementioned agnathans (represented by the lamprey) and gnathostomes.  The fact that molecules other than toll and toll-like receptors produce essentially the same phylogenies is not unimportant, either.

My purpose is never to get too much into the details, although future posts will do so more than this one does.  My objective is to show that biomolecules definitely do reveal a whole lot about evolution, and especially the patterns of splitting and of independent development of systems in organisms lacking in much horizontal (lateral) gene transfer possibilities (all of the organisms mentioned or linked in this post typically transfer genes only “vertically,” and only rarely undergo horizontal gene transfer).  Likewise, by no means do sequences only indicate “relatedness” as Behe wants us to believe, for the relatedness of agnathans and gnathostomes only explains why only certain biomolecules were available for the evolution (not true for design, certainly) of adaptive immunity in their respective cases, and not why a similar set of biomolecules gave rise to very different immune systems.  Only accident explains the latter phenomenon, while design not only provides no answers, it yields no leads to any research possibilities for discovering “design answers” to such questions.

So the phylogenetic tree of the immune system–including both the innate and adaptive parts–indicates the same thing happening through time, the splitting of the “bloodlines” and the fixing of quite different solutions to immune problems independently of whatever “designs” were occurring in genetically separate species.  A seeming paradox (to uninitiates) is that the accidents of evolution, which are predicted by theory and also borne out by the evidence, actually generate the kind of order that anything we can mean by “design” would not create, for only the constraints of evolution will split up agnathans and gnathostomes in the observed precise and unalterable fashion, while design (like horizontal gene transfer among prokaryotes) would mix up the “bloodlines.”

How odd it is for someone like Behe to claim that the evidence for “microevolution” (scare quotes are because he obviously is not using the scientific definition for that term), which is genetically impossible to differentiate from the evidence for “macroevolution,” came from a very different process.  Of course, in real science similar effects are accepted as having similar causes, unless a cause can be shown to cause the same effects, which the IDists know better than to even attempt to do.

Furthermore, it is evolution which produces the tremendous complexity found across life, for only evolution is predicted or expected to very often come up with different solutions to the same problem (convergence also occurs, though its different sources leave their marks).  Not only the level of complexity found in the tree of life, but the sort of complexity found there in which different “bloodlines” produce independent solutions dependent upon accidents of inheritance, environment, and of mutation, is predicted by unguided evolutionary processes alone.

The phylogenetic evidence is unmistakable:  It reeks of accident plus the refinements of natural selection, and it yields no evidence at all of the rationality, purpose, and “conceptual precursors,” which would be expected of design.  Behe has certainly not told us why two very different adaptive immune systems arose “by design” out of a common set of biochemicals in the agnathans and the gnathostomes.  Evolution uses accident to explain the patterns of phylogeny, as both the order and the complexity of life’s branching “bloodlines” can only come by accident,* and not at all by anything (other than a Loki-type god playing a joke on the universe) meant by the word “design.”

*This actually holds fairly well with language evolution as well, although a kind of “design” is able to cause horizontal language “borrowing.”  But essentially, while many of the constraints upon language are at least not wholly accidental (and even intelligence and design can play roles), language is not understandable except as involving a great deal of “inherited” and ongoing accidents.

10.06.08                                                                                                                   To top

26. Evolution of Adaptive Immunity II–Building on Innate Immunity

This is another installment in my response to chapter 6 of Darwin’s Black Box.

The first mouse Toll gene isolated turned out to be defective in two mouse strains that cannot respond to bacterial lipopolysaccharide (LPS), one of the pathogen-associated molecular patterns, or PAMPs, recognized by innate immune system pattern recognition receptors. These mice lack TLR-4 [Toll-like receptor-4] function; in one strain the defect is due to a point mutation in the so-called TIR domain (Toll/IL-1 receptor domain, since it is found in both Toll and IL-1 receptors), while in the other strain it is due to a null mutation that abolishes expression of the gene altogether. These mice are exceptionally susceptible to infection with gram-negative bacteria, which carry LPS on their surface, and cannot mount an adaptive immune response against them. This was, in a sense, the first proof that the loss of innate immunity had a discernible effect on the adaptive immune response, and served as a proof in principle that the adaptive immune response depended on an effective innate immune response, at least in some cases. The question remaining is: How general is this basic principle? Evolution of the innate immune system

And the answer is, the dependency of the “adaptive immune system” upon the “innate immune system” is very general. Just as the eukaryotic flagellum/cilium depends upon previously-existing transport structures which are shared by both the flagellum and cytoplasmic transfer machines, the adaptive immune system is, and apparently was from the beginning, part of and dependent upon the earlier-evolved innate immune system. Of course the “innate immune system” has also evolved in vertebrates, yet it continues to function much as it did in the past, while also priming and signaling the adaptive system to begin defending the body days after the initial response by the innate system.

As typical, my point is not to belabor the details, it is to give a sense of how the “irreducibly complex” adaptive immune system arose from and depends upon the innate system, while details are made available through links. The evolution of molecules is not the focus now, rather it is the fact that adaptive immunity reveals the characteristic and predicted evolutionary expectations of having been built into, and from the parts of, previously existing systems and structures. Some of the specific links to the past will come later, as some parts of adaptive immunity do not seem to have much (if any) role in innate immunity at the present time.

In my last post in this category, I pointed out that Toll and “Toll-like receptors” (TLRs) have evolved in the patterns expected of microevolution, or any other kind. The fact that other molecules of the immune system (adaptive and innate) reveal essentially the same patterns was also pointed out. But the fact is that Toll and the other “innate immune system” proteins are not simply to be found in the “innate” systems of vertebrates as well as in, for instance, fruit flies, they continue to utilize basically the same pathways–and they regulate and inform the adaptive response. All except the last part is borne out in the following quote:

In fruit flies, there is a very strict order of Toll pathway gene products starting with Toll and going on to dMyD88, Pelle, Cactus, and Dif/Relish, all of which are cytoplasmic proteins involved in the transmission of the signal from Toll, a cell-surface receptor, to the nucleus to induce the activation of specific sets of genes. The same order is found in the homologues of the Toll pathway found in the innate immune system in vertebrates(Fig. 1). The plant genes do not seem to be arranged in the same order. However, if one examines the plant genome carefully, there are signs of all these signaling elements. Evolution of the innate immune system

I included both the link to the figure, which shows the striking similarities between fruit fly and human immune systems (not including adaptive immunity, of course, which the fly lacks) and the part about similar parts but different order in plants, because the accidents of heredity have left an indelible mark on even the plants. Significant differences between animal and plant pathways do not seem surprising at all, because we split from plants very early.

However, so far in this post I have written little about adaptive immunity. The figure linked just above shows how close some of the innate signaling is in humans and in fruit flies, this link (picture and caption) shows how the human innate signaling pathway interfaces with adaptive immunity. Notice the TLRs (1-11), which are homologs with fruit fly Toll receptors, and MyD88 which also appeared in the previously linked figure in both humans and in fruit flies. As one may see from the illustration, the TLRs of the innate system signal infection (often via interleukins, ILs, or MyD88) in order to produce T helper cells (Th’s) in the adaptive immune system. The article from which this illustration comes goes into great detail about how the adaptive immune system relies upon the “irreducibly complex” (as Behe would have it) pathways of the innate immune system–which are little changed between humans and flies (which, one should recall, diverged before the “Cambrian explosion” that fills IDist chatter).

This puts the Toll-like receptors into perspective, as evolved molecules which retain something close to (but not identical with) the functions that Toll receptors perform in insects, and even in plants. These proteins are crucial to the function of our adaptive immune system, which surely is not to be ascribed to anything other than accidents of heredity, mutation, and environment (especially to heredity). No design function is served by the evolution of such a conservative complexity–and of course other aspects of our adaptive immune system are not at all conservative, when compared to the divergent and independent evolution of agnathan (lampreys and hagfish) adaptive immunity. And even if we may have shared the agnathan adaptive immunity, or vice-versa, clearly an independent evolution occurred in one line or the other one.

In keeping with my desire not to bog down in details covered well by others (see here for a reasonably good discussion of the immune system, and the basics of its evolvability), I will allow the linked illustrations to carry the argument that adaptive immunity evolved just as evolutionary theory predicts, by co-opting existing pathways and (in Behe’s phrase) “physical precursors.” Yet before closing I would like to note another generally neglected aspect of the “irreducibly complex” adaptive immune system, which is that it did not simply become complex at once and then not evolve (as Behe implies), rather adaptive immunity has evolved greater complexity while conserving its core structure (another commonality of evolution):

While increasing complexity of the adaptive immune system is evident with vertebrate evolution, the same basic construction of the adaptive immune system is conserved throughout the gnathostome [jawed vertebrate] radiations. The Evolution of Adaptive Immune Systems

So it is not as if the adaptive immune system was created in peak complexity, which did not evolve, instead it evolved its basic structure early, and then it evolved further. This should not be the case if such complexity could not evolve in the first place, for how would the irreducibly complex system evolve even more non-trivial complexity? A degenerate complexity might evolve under an ID scenario, but not the adaptive complexity that has evolved in adaptive immunity.

Of course one may tweak one’s “design theory” endlessly to have the unconstrained “designer” do whatever has happened, including the manipulation of mutations and natural selection. The trouble is that one needs constraints and entailed “predictions” if one is to do science at all, and evolution is what is constrained to produce the patterns we see (roughly the same in either microevolution and in macroevolution, at least in the aspects discussed here), while all known design constraints, like rationality and purpose, have the advantage of surpassing the limitations of evolution. The effects of such a transcending intelligence is not seen in life, except where humans have genetically modified organisms.

For instance, there is nothing at all in design that suggests that adaptive immunity should use the same pathways as innate immunity does in both humans and in fruit flies, and the same “physical precursors,” while evolution requires both (or at least modifications of the mentioned pathways–given the developmental constraints imposed prior to our divergence from the ancestors of fruit flies, that is). Evolution predicts the bridges that we see between the prior innate immunity and the later adaptive immunity, while one of the values of using intelligence to design a system is precisely so that one bypasses such constraints.

It is absurd to claim that design was necessary to make all of the rather small (very small by design standards) steps predicted by evolution, when in fact leaps are to be expected of intelligence. Future posts will discuss more of the evidence of small steps, which in fact produced two complex adaptive immune systems, simply because in vertebrate evolution no complex biochemical system can be transferred to a divergent line, while another complex evolution of a needed biochemical system is possible. A quote from one of the above sources well summarizes the matter:

This consistency of function, structure, order, and purpose over such a wide evolutionary range is a most impressive example of the evolution of a biological function, save for essential processes such as DNA and RNA replication and cell division. Evolution of the innate immune system

10.08.08                                                                                                                   To top

27. Evolution of Adaptive Immunity III–It Has the Marks of Irreducible Randomness*

As previously mentioned, adaptive immunity did not appear at the beginning of the Cambrian. Of course, none of the basic biochemical pathways can be pinned down to the Cambrian “explosion,” nor did they appear at the same time as each other, so far as anyone can demonstrate.

Not only does adaptive immunity fail to break any kind of evolutionary patterns, or to come up with anything truly novel, it happened well after the IDists’ favorite “creation event,” the Cambrian “explosion.” Perhaps this does not directly contradict ID or Behe, given how much they refuse to make definite claims, let alone to predict any of the expected effects of design. However, as stated beforehand, the Cambrian “explosion” is one of the events that supposedly could not happen “gradualistically,” thus the IDists imply that some special design event occurred then.

All evidence tends to suggest that most of Behe’s “irreducibly complex” pathways actually appeared well before the Cambrian, from the bacterial flagella and eukaryotic cilia, to photosynthesis, and on to the clotting cascade and the biochemistry of vision. Adaptive immunity is interesting by contrast for appearing around 430 million years ago, about 85 million years after the Cambrian began.

The timing of this, and of the appearance of other biochemical pathways, seems therefore to follow the expectations of evolutionary theory yet again. Obviously, the IDists have no design reason for adaptive immunity appearing when it did, since it likely would have been of use well before the Cambrian period. Combinations of accidents of heredity, environment, and mutation, plus natural selection, are evidently behind two very different forms of adaptive immunity appearing when they did, and evolutionary theory readily accounts for such accidents of timing and of divergence, while “intelligent design” has no accounting for it at all. For, how is design supposed to explain irreducibly random* (in many, but not all, aspects) evolutionary events?

And while evolution is marked by appearances of biochemical pathways according to combinations of fortuity, accident, need, and the ordering principle of selection, it is not as if these causes ended with the appearance of these pathways–especially not in the case of immunity, adaptive or innate. You really would not know that if you read The Edge of Evolution, since Behe there suggests that the immune system does not change (other than for a few point mutations) significantly in response to parasitism. This gets to another of his fundamental misunderstandings, for he operates from a notion that “Darwinian evolution” should specifically adapt the immune system to malarial infection, as if the immune system is a specific defense against malaria, and not a general defense against a huge number of parasites.

Nevertheless, this general defense system has substantially evolved since adaptive immunity itself evolved. One of the reasons for my previous post on adaptive immunity was to show that not only is adaptive immunity “built” as evolution predicts (integrated with what came previously), but that innate and adaptive immunity are not separately acting systems. Toll-like receptors are as important to adaptive immunity as to innate immunity, and the same would go for nearly all of the components of “innate immunity” in organisms having adaptive immunity. In light of that, what is important is that the immune system has evolved enormously in various gnathostomes (jawed vertebrates), which now differ a great deal in the numbers of genes per family, as may be seen in the table below:

Table 1. Comparison of gene family numbers in human, mouse,

opossum, and chicken genomes

Human Mouse Opossum Chicken

Cathelicidin 1 1 12 3

Beta-defensin 39 52 32 13

Alpha-defensin 10 6 1 0

Theta-defensin 1ps 0 0 0

Chemokine 47 45 31 24

KLRA1 (Ly49) 1ps 16 0 0

NKG2D/KLRK1 1 1 1 0

CD69 1 1 1 0

KLRC 4 3 0 0

Ig-like receptor 30 10 45 103

Source: Genome Research

With such a range in the numbers of molecules involved in various aspects of the immune function in different members of the gnathostomes, there is no excuse for writing as if the immune system does not evolve. To be sure, Behe would almost certainly claim that such differences were not random in the aspects I have mentioned (except for heredity, which he seems to think the “designer” could not or would not overcome–clearly an assumption made merely to save his “hypothesis,” and having nothing to do with what we know of design principles), but he has no evidence for that claim, and anyway, the evidence for the evolution of gene families involved in immunity is basically of the same type as what he accepts as evidence that human and P. falciparum responses to each other are due to unguided evolution.

The facts I emphasize in this post are that adaptive immune systems have appeared and evolved as expected in normal evolutionary processes. There is no coordination of evolutionary changes according to design principles, so that while the Cambrian “explosion” appears to have substantially involved an arms and armor race among the evolving phyla (among other likely factors), biochemical pathways appeared independently of that event, and subsequently evolved in accordance with accident, need, and natural selection. Adaptive immunity appeared relatively late, compared with the most basic biochemical pathways, and the two versions of it appear to be as unrelated as, say, bats wings and bird wings are (which is to say, that accidents of heredity are found behind both, but the specific changes to the vertebrate forelimb which made wings in both cases are wholly unrelated). Later evolution has dramatically altered the gene components of divergent jawed vertebrate taxa, quite unlike the stasis that Behe implies in both Darwin’s Black Box and in The Edge of Evolution.

The IDists are correct about one thing, which is that randomness could never produce systems like our immune system. What is at least as certain is that randomness is the only causal factor able to account for the timing, most divergences, uncorrelated adaptations, and the sorts of new information (mutations) appearing through time in the genetic record. By no means is randomness the whole story, yet the whole story includes so much irreducible randomness behind the selective pressures of competition that there is nothing to be concluded than that design was not responsible for life’s biochemical pathways. Only a theory which accounts for the lack of planning, rationality, and purpose, like our evolutionary theory, is able to explain the timing, patterns, and unrelated adaptational radiations of immune systems, as well as the rest of the biochemical pathways of life.

*By “irreducible randomness” and its variations I am using “irreducible” akin to the manner that IDists use “irreducible complexity,” and even more properly, as something that simply does not resolve into something else (especially not design). It has nothing to do with the “irreducible randomness” of quantum mechanics, of course.

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