Archive for the ‘The Edge of Evolution’ category

The omphalosity of Behe/ID

December 18, 2008

As is well known, Philip Henry Gosse argued that the world had to be created with the “appearance of age,” which is purportedly why the religiously-asserted “young earth” looks like it is much older than it “really is.”  This is now known as the “Omphalos hypothesis.”

Of course it always seemed like so much special pleading, particularly since one can hardly understand why the earth “appears to have” extremely ancient sediments and river beds which do not at all seem necessary for a “young earth” to function.  That it is a way of trying to prevent the “young earth hypothesis” from being properly tested by observation is more than a little apparent as well.

The “new” (!) science of ID has managed to come just that far.  Paley tried to honestly provide evidence for the kind of design that an artificer or architect would produce.  ID–Behe being prominent in it–proclaims that not only must “design” look like it comes through a very long process (which has never been seen with design), it also must appear like “Darwinian” evolution predicts that it will look.  To be sure, Behe wouldn’t state matters just like I did in the foregoing, but how does that differ from the following passage from The Edge of Evolution?

Evolution from a common ancestor, via changes in DNA, is very well supported.  It may or may not be random.  EoE, 12

Of course Behe shows his dullness with the second sentence there, as evolution is hardly random, it occurs according to natural selection.  That its raw materials (mutations) are effectively random may be shown by the lack of any “common authorship” after a line has truly diverged from another one (without significant lateral transfer of genes).

And we have this previously used quote from Darwin’s Black Box:

Another problem with the argument from imperfection is that it critically depends on a psychoanalysis of the unidentified designer.  Yet the reasons that a designer would or would not do anything are virtually impossible to know unless the designer tells you specifically what those reasons are.  One only has to go into a modern art gallery to come across designed objects for which the purposes are completely obscure (to me at least).  Features that strike us as odd in a design might have been placed there by the designer for a reason–for artistic reasons, for variety, to show off, for some as-yet-undetected practical purpose, or for some unguessable reason–or they might not.  DBB, 223

Except, of course, what we see in organisms have the aspects predicted by evolution, and have none of the effects of “artistic reason” or of other design affects–let alone the evident rationality found in the frame of the artist’s picture.  No, Behe is content to say that evolution is very well supported while utterly ignoring the fact that it can only be supported by matching up cause and effect, and the only causes of evolution of which we know are the familiar mutation, natural selection, founder effects, etc., of non-teleological evolution.  Implicit in his acceptance of the evidence of evolution is the fact that life was not (detectably, at least) designed, and yet he claims that life is just too complex to have evolved without intelligent help.

How can that be anything but a degraded form of the “Omphalos hypothesis,” one that stupidly asserts that life was designed to appear evolved, but for no reason whatsoever? 

And of course we’re still waiting to find out how “design” could add anything to knowledge, when “design” is supposed to produce exactly what evolution predicts.  Wouldn’t it be simpler just to adopt non-teleological evolution to understand life?  The designer doesn’t differ at all from that pattern, hence there is no knowledge added by tacking on a “designer.”

Of course I’ve ignored any number of his claims in this short post, like the idea that “random mutation” and “common descent” are unrelated, when of course we rely on the assumed (and tested so far as is practicable) lack of tampering by unknown forces in order to determine common descent both in paternity cases and in evolutionary relationships.  One cannot at once tackle every claim divorced from reality that Behe makes, as nearly all of them are separate from reality to some extent. 

The fact is that, like all creationism, Behe and the IDists end up claiming that God just had to make things as predicted by non-teleological forces, namely because they can’t find evidence of teleological forces acting in our world (other than those by animals such as ourselves).  It’s Omphalos all over again, just with a rather unimaginative twist.

This is part of a series of posts that I am combining into one long post, which may be found at The Edge of Evolution


What is ID’s efficient cause?

October 29, 2008

IDists are keen to return Aristotle’s “final cause” to the sciences, or at least to biology (see Dembski, for example).  Which is rather sad, because they can give us no evidence for the purpose of organisms, instead they wish to insist that life “had to be designed” and thus has purpose.  One has to wonder what good that would be to know, since we would still need to be able to discover purpose for it to impact us, and ID has never been able to demonstrate any purpose (to be sure, nearly all IDists have sacred writings in mind to provide specific purpose, but will not admit it in their supposed science).

So OK, they want final causes (aside from those of animals such as humans), and perhaps formal and material causes as well, but where is their “efficient cause”?  That is the closest that Aristotle’s “causes” (aitia, which probably would translate better as “reasons” than “causes”) come to fitting with scientific causation in the classical realm, they do not deny the importance of efficient causes, and yet they have none whatsoever.

It should be noted that Aristotle was not one who simply called “intelligence” or “design” the cause or the reason (not of a manufactured item, that is), the aition, because intelligence is just a faculty, and design is merely a category of actions or “causes”.  Thought using intelligence might be a cause, and design may be part of a specific process, but simply invoking intelligence, thought, or design would explain nothing by themselves.  There is an apparent exception to Aristotle’s “efficient cause” as a specific cause or set of causes, which is God the unmoved mover–a very indefinite “cause”–but even IDists don’t appeal to such ancient fictions, partly because it would too readily reveal the religious motivation behind ID.

Aristotle has these things to say of the “efficient cause”:

Again (3) the primary source of the change or coming to rest; e.g. the man who gave advice is a cause, the father is cause of the child, and generally what makes of what is made and what causes change of what is changed.

e.g. both the art of the sculptor and the bronze are causes of the statue. These are causes of the statue qua statue, not in virtue of anything else that it may be-only not in the same way, the one being the material cause, the other the cause whence the motion comes.

All causes, both proper and incidental, may be spoken of either as potential or as actual; e.g. the cause of a house being built is either ‘house-builder’ or ‘house-builder building’.

In investigating the cause of each thing it is always necessary to seek what is most precise (as also in other things): thus man builds because he is a builder, and a builder builds in virtue of his art of building. This last cause then is prior: and so generally.

Further, generic effects should be assigned to generic causes, particular effects to particular causes, e.g. statue to sculptor, this statue to this sculptor; and powers are relative to possible effects, actually operating causes to things which are actually being effected.  Aristotle’s Physics

In a scientific sense, this is all rather imprecise.  But even Aristotle’s generic causes, such as “the art of building,” is far more precise and meaningful than anything we have gotten out of ID as an efficient cause.  Dembski even makes “efficient cause” more precise than Aristotle does:

The efficient cause is the immediate activity that produced the statue–Michelangelo’s actual chipping away at a marble slab with hammer and chisel.  Dembski

Dembski’s example of an efficient cause moves us closer to scientific causation, and is a typical example used by those who are explaining Aristotle’s “four causes”.  Despite the fact that he waffles on mechanism in that article–and attacks the strawman of design being “barred from the content of science” (has any archaeologist tried to explain pottery without intelligent agents involved somehow?)–he is still hardly consistent when he makes statements such as this one:

You’re asking me to play a game: “Provide as much detail in terms of possible causal mechanisms for your ID position as I do for my Darwinian position.” ID is not a mechanistic theory, and it’s not ID’s task to match your pathetic level of detail in telling mechanistic stories. Notorious Dembski comment

Ah yes, Dembski has neither evidence for a final cause, nor for an efficient cause.  Likewise with Behe, who pretends to take a more scientific approach than Dembski, he will not even commit to the specificity that an ancient thinker like Aristotle would:

Another problem with the argument from imperfection is that it critically depends on a psychoanalysis of the unidentified designer.  Yet the reasons that a designer would or would not do anything are virtually impossible to know unless the designer tells you specifically what those reasons are.  One only has to go into a modern art gallery to come across designed objects for which the purposes are completely obscure (to me at least).  Features that strike us as odd in a design might have been placed there by the designer for a reason–for artistic reasons, for variety, to show off, for some as-yet-undetected practical purpose, or for some unguessable reason–or they might not.  DBB, 223

What, people refuse to call something like that science?  Notice how desperate he is to claim no distinguishing marks of design (since he knows that these are lacking from life that we have not engineered) that he goes to deliberately obscure art as his “example.” 

Yet in the first and second Dembski links (to the same source), it is argued, against a strawman, that design is readily detectable.  To be sure, he misunderstands his own sci-fi analogy as the search for “complex specified information,” when in fact it was rationality behind the signal that indicated intelligence.  Dembski explaining what was detected in the movie Contact:

In this sequence of 1126 bits, 1’s correspond to beats and 0’s to pauses. This sequence represents the prime numbers from 2 to 101, where a given prime number is represented by the corresponding number of beats (i.e., 1’s), and the individual prime numbers are separated by pauses i.e., 0’s).  Dembski

Yes, that’s right, it isn’t complexity that is discovered (Dembski calls unlikely simplicity by the name “complexity,” a distortion even of the meaning of the term), it is rationality.  Even Behe gets it slightly, and ludicrously brings up rational agents:

Rational agents can coordinate pieces into a larger system (like the ship) to accomplish a purpose.  Edge of Evolution, 168

Yes, and the context from which that comes has any number of rationally-devised artifacts being discovered.  Nevertheless, note how carefully he words it, to avoid the implication that life ought to appear rationally designed if it was intelligently designed.  He’s still relying on evident “purpose,” which he deliberately tried to avoid as a test of “design” in the previous quote.  There, too, he wrote of “reasons” for design, as he denied their visibility, suggesting that he knew very well that he was denying that purpose is evident in life, while in this later quote he is trying to suggest that rationality is found exactly through evident purpose (as he had also done in DBB, prior to denying it in order to avoid predicting evident purpose in life–in response to those who noted exactly the lack of purpose in so many aspects of life).

The fact of the matter is that both Dembski and Behe do not wish “design” to be tested by evidence of purpose, for they know that, for instance, malaria pathogens do not seem to fit any kind of evident purpose.  They bring up purpose in order to ignore efficient causation and the rationality typically evident behind such causation (even if some art is hard to figure out, the rationality of the frames betrays intelligence via rational efficient causation).  Likewise, they totally avoid efficient causation, for as I previously argued, they have no causes at all, only unconstrained accident (or whim).

Evolution is also fraught with accident (see link above), but these are “lawful accidents,” of the kind that are permitted and even (probabilistically) predicted.  We have “efficient causation,” or more exactly, scientific causation.  And what is interesting to note is that while Dembski and Behe contradict themselves and each other with their “arguments,” primarily because they can show no “intelligent design” causation whatsoever, earlier ID really did mean to find the marks of intelligence and rationality in life:

…We allege, that the same principle of intelligence, design, and mechanical contrivance, was exerted in the formation of natural bodies, as we employ in making of the various instruments by which our purposes are served […]. William Paley

Paley was looking for efficient cause (see also pp. 8 & 233 of the above link for his criticisms of explanations lacking in efficient causes), and for observable purpose.  Behe and Dembski contradict themselves on these matters, while generally trying to smuggle “purpose” in via “complexity.” 

Paley’s ID was tolerably close to a scientific hypothesis–which Darwin took seriously.  By avoiding all causes (even the ones they bring up, like “purpose”–Aristotle’s “final cause”), the current crop of IDists cannot even match Paley’s now-failed “science,” nor even keep from contradicting themselves as they both claim that purpose and rationality are evident, and that they are not.

This is part of a series of posts that I am combining into one long post, which may be found at Darwin’s Black Box.

Evolutionary history of tuberculosis deciphered

October 28, 2008

Or more exactly, the evolutionary history of Mycobacterium tuberculosis complex has been deciphered, indicating that there are two clades:

ScienceDaily (Oct. 22, 2008) — The evolutionary timing and spread of the Mycobacterium tuberculosis complex (MTBC), one of the most successful groups of bacterial pathogens, remains largely unknown. Here, using mycobacterial tandem repeat sequences as genetic markers, we show that the MTBC consists of two independent clades, one composed exclusively of M. tuberculosis lineages from humans and the other composed of both animal and human isolates.

The latter also likely derived from a human pathogenic lineage, supporting the hypothesis of an original human host. Using Bayesian statistics and experimental data on the variability of the mycobacterial markers in infected patients, we estimated the age of the MTBC at 40,000 years, coinciding with the expansion of “modern” human populations out of Africa. Moreover, the diversification of the oldest EAI and LAM populations took place during plant and animal domestication. Science Daily

It’s a somewhat interesting story, particularly due to its relevance to understanding tuberculosis as a disease.

One just has to wonder, in addition, how IDists propose to decide that this branch indicates normal processes of evolution (as at least most self-identified “IDists” would), while another branching happens to be due to design, despite the fact that it reveals no substantially different patterns.  Of course I have brought this up several times already, however it’s worth bringing up yet again, because it is important to understanding diseases like malaria (how adaptable are pathogens?), and because this aspect puts IDists squarely in the camp of creationists and their inability to tell “design” apart from “Darwinism.”

To put it more starkly than I have previously–the methods used for determining clades do not differ substantially across the taxa.  Some of the details change, of course, but the principles, the standards, are the same going back to the Cambrian and beforehand.  Furthermore, they do not differ meaningfully for “suddenly evolving” immunity genes like TCR and BCR (at least parts of which exist in the agnathans–hagfish and lampreys, but are much more diversified and important to jawed vertebrates–the gnathostomes–which use them in their adaptive immune systems, unlike agnathans with their adaptive immune systems), or the apparently far more sedately-changing Toll and Toll-like receptor genes.

Surely it is (in any “design” sense) a mystery of how malaria, tuberculosis, and humans, along with their ancestors, can be phylogenetically analyzed in essentially the same manner no matter whether we study their “designed” parts or their “evolved” parts.  Meaning that there is no obvious difference in causation of evolution across the taxonomic groups (and there is no definite way to assign the taxonomic categories, other than species, although the cladistic branches are not at all arbitrary), and no reason at all to think that design makes any difference to understanding the relationships of pathogens and hosts.  This is important to recognize when analyzing disease and our immune system, as well as when we recognize that Plasmodium spp. are vulnerable to certain drugs precisely because of their very different “lawfully accidental” evolutionary history–which means that drugs targeting the Plasmodium apicoplast have a good chance of being non-toxic to humans.

Then again, in a sense it’s somewhat silly to be discussing the IDist inability to distinguish “design” from “normal evolution” when they have no ability even to show that resistance to chloroquine (which Behe goes on about) actually evolved, rather than be the result of a miracle, or a series of miracles.  The fact is that the IDists attempt to empty science of any and all of the meaning that science gains by matching up cause and effect, and by understanding that similar effects have similar causes (unless, of course, another identifiable cause producing similar effects has been found–IDists only claim that it has, by refusing to differentiate the effects of “design” from those of evolution).

So it’s fail all the way, actually.  Of course they can’t say how “designed clades” differ from “evolved clades,” because they can’t ever rule out “design” with their (lack of) standards.

Malaria has evolved cold tolerance

October 25, 2008

To put matters in perspective, consider a related problem that has stumped malaria.  Although malaria is a ferocious parasite, quite willing to eat anything that gets in its path, P. falciparum needs a warm climate to reproduce.  If the temperature falls below about 65°F, the parasite slows down.  When the temperature gets to 61°F, it can’t reproduce  It’s stymied.  If a mutant parasite appeared that was tolerant to somewhat lower temperatures–not to freezing conditions, just to cool temperatures–it would be able to invade regions that are now closed to it.  Edge of Evolution, 82

Behe seems to think that P. falciparum is the only malarial parasite that infects humans.  P. falciparum is restricted to quite warm regions, but P. vivax has indeed invaded much cooler regions, including London in past centuries.  P. vivax tolerates temperatures of five degrees Celsius cooler, which amounts to nine degrees Fahrenheit cooler:

Compared with the more virulent Plasmodium falciparum, P. vivax tolerates a wide range of temperature environments (minimum: 16°C vs. 21°C for P. falciparum), which may explain its broader distribution. Host Switch Leads to Emergence of Plasmodium vivax Malaria in Humans

Then too, since Behe has no idea of what temperatures P. falciparum endured in the past, he does not know that it has not evolved to tolerate lower temperatures than it could initially.  Regardless of that, it is unsurprising that a Plasmodium species can live in cooler regions than can P. falciparum.

And when one species can survive in a region in which a related species cannot, competition often prevents evolution to fit the competitor’s adaptation.  After all, it may require several changes to endure cooler temperatures, and they may initially come with costs which make the species less fit.  When one species already can endure cooler temperatures it is not particularly likely that another species will, and especially not in the rather short time period in which P. falciparum has been infecting humans.  Nevertheless, P. vivax suggests that it could happen in other species, particularly if somehow P. vivax went extinct.

Behe could always ask why P. vivax can’t endure 6°C, or -6°C, or cryogenic temperatures.  And who knows, maybe he will.   But as I have previously argued, it is not for us who accept the constraints of science and evolution to explain why evolution is not all-powerful, it is for him to try to explain why his omnipotent god fails to reveal omnipotence in “his designs.” 

Evolving to live at lower temperatures has not “stumped malaria,” as he claims.  In fact, with P. vivax living at lower temperatures, P. falciparum‘s lack of evolution to tolerate lower temperatures is in line with evolutionary expectations, considering the relatively short time in which it has has to evolve.  So there you are, malaria seems to fit evolutionary expectations quite well, and Behe fails in this detail as well.

This is part of a series of posts that I am combining into one long post, which may be found at The Edge of Evolution

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

October 11, 2008

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 other 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.

This is part of a series of posts that I am combining into one long post, which may be found at Darwin’s Black Box.

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

October 2, 2008

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-γ (IFN-γ) and T helper type 1 (TH1) 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.

This is part of a series of posts that I am combining into one long post, which may be found at Darwin’s Black Box.

ID has problems with keeping its dogma straight

September 25, 2008

But in fact, DNA isn’t exactly like a blueprint.  Only a fraction of its sections are directly involved in creating proteins and building life.  Most of it seems to be excess DNA, where mutations can occur harmlessly.  Edge of Evolution, p. 66

The above is a rather unexceptional statement by Behe, a reasonable inference from past data, if possibly it is being superseded by later research results. 

But one of the more persistent, if typically bizarre (particularly in light of how IDists typically deny that “design” has any expectations, other than irreducible complexity and the like), claims of IDists is that ID predicts that most “junk DNA” has uses.  Somehow, one of their “leading lights” failed to recognize this “prediction,” quite possibly because it cannot be derived from the vague claims of “ID theory.”

Of course evolution doesn’t really make predictions either way about “junk DNA,” other than that nothing in evolution precludes junk DNA from existing in genomes (very little apparent junk DNA exists in most prokaryotic organisms, while tandem repeats, duplications, and transposons almost certainly produce some true junk DNA in eukaryotes).  This hasn’t prevented IDists from claiming that “neo-Darwinism” insists that much of our genomes has to be junk.  Here’s a recent example from the ignorant Casey Luskin:

Study Challenges Two Icons of Evolution: Functional Junk DNA Shows “Surprising” Genetic Differences Between Humans and Apes

These sources promoting the classic “junk DNA” icon of neo-Darwinism need updating, as a Yale University news release from earlier this month recalls the fact that “[i]n the last several years, scientists have discovered that non-coding regions of the genome, far from being junk, contain thousands of regulatory elements that act as genetic ‘switches’ to turn genes on or off.” In this case, the junk triggered genes that control human thumb and foot development.

Most studies that have claimed that humans and apes have nearly identical genomes have primarily looked at the gene-coding portions of the genome, not the non-coding DNA (formerly claimed to be “junk”). Perhaps as biologists study the non-coding regions of our genome, they will find evidence that challenges two icons of evolution: Not only does “junk” DNA have function, but humans aren’t as genetically similar to apes as was once thought.  [bolding added] Casey Luskin lying for the DI

I guess if you have nothing honest to say, just pick your favorite lie and call it an “icon of evolution,” never bothering to consider why it is that Behe repeats “the classic “junk DNA” icon of neo-Darwinism,” being oblivious both to its “neo-Darwinian” status and to any “prediction” of ID that “most junk DNA” will be found to have a purpose.

The only apparent reason for the constant drumbeat about how “junk DNA” really does have function, and that ID is supposed to predict that it does while “neo-Darwinism” is supposed to predict otherwise, is that IDists are desperate to come up with any kind of evidence for their claims.  That they have none is adequately shown by the fact that one of ID’s “leading theorists,” Behe, fails to recognize either assertion in his most recent book, in spite of his own eagerness to fault “neo-Darwinism” at every turn.

You’d think that people who just make up things as they go along would have the sense to get together to get their stories straight.  ID fails even to design its own propaganda intelligently.

This is part of a series of posts that I am combining into one long post, which may be found at Darwin’s Black Box.