The Edge of Evolution

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. The Delimitations of Design (8.21)
2. Only if it is found can the edge of evolution be calculated (8.25)
3. Malaria’s diminished chloroplast is on purpose? Really? (9.4)
4. Photosynthetic “missing link” to malaria pathogen found (9.8)
5. Science is about evidence of occurrence, not mere possibility (9.9)
6. Common descent is demonstrable only when causes are known (9.24)
7. ID has problems with keeping its dogma straight (9.25)
8. If evolution is true, why can’t gazelles run 433 mph? (10.2)
9. Evolution of Adaptive Immunity III–It Has the Marks of Irreducible Randomness (10.11)

1. The Delimitations of Design

Behe has been kind enough to show us the edge of evolution, so I thought I would return the favor with respect to design. Of course this isn’t just any design, this is supernatural design, so you can’t expect the kind of competence that a good engineer would produce. And because we can hardly look to known design in order to understand supernatural design, we’d best make a tentative list of the limits of Behe’s supernatural design. It is tentative, since we don’t know what the designer does after hours in heaven, yet we can at least list what appear to be the limits that the designer follows in our world. Understand that when “design” is written below, it refers to the special design capabilities that would fail engineering school, yet made extremely complex biological systems (you know, complexity more like genetic algorithms produce, than does human thought):

1. Design can’t make a controlled world. Instead we have this world, which has disastrous shifts in weather and climate, nearly killing off all vertebrate life in the Permian extinction event.

2. Design can’t make a decent photosynthetic protein. In bright sunlight, the D1 protein has to be replaced about every half hour.

3. Design can’t make a functional human being in less than around three and a half billion years. Oddly, that’s about how long it would take evolution, in most estimates.

4. Design can’t look ahead. If it could, it would have given a better Rubisco protein to plants (like the one in red algae), or would have provided C4 compensation at the beginning (instead of it having to evolve independently again and again).

5. Design has no purpose. Otherwise, why would malarial parasites and human immune systems be evenly matched to do no more than carry on trench warfare, a massive killing fest? Or was that the purpose?

6. Design has essentially the same limitations as evolution does. Apparently it can’t produce a primate bipedal skeleton other than by morphing and tweaking a quadrupedal skeleton to lift its forelimbs off of the ground.

7. Design is incapable of producing radio transmission and reception. Sort of the Gilligan’s Island syndrome (though there transmission was the problem, not reception). Surely any number of organisms would benefit from radio communication, but only the inferior minds of humans could produce radio communication. The designer never had the proper courses, it would seem.

8. Design can’t make really strong materials, like graphene, carbon nanotubes, or Kevlar. Indeed, we know the designer is a stone age god, because it can’t even smelt copper and iron, hence no organism (save humans who learned how to smelt) can take advantage of the great properties of metals.

9. Design can only imitate and tweak. Also, it was into ancestor worship when it made almost all eukaryotes, since few eukaryotes can accept genes from distantly related organisms, so that eukaryotes must use and tweak genes from direct ancestors.

10. Design must follow the evolutionary patterns expected from their respective lineages. Therefore, prokaryotes have to fit taxonomic patterns expected of clonal lines that have considerable lateral gene flow. Eukaryotes must have other evolutionary patterns, namely as though they had evolved according to their reproductive capabilities, sexually and with little or no gene flow (there are some exceptions to the latter).

11. Design doesn’t know front from back. This is why the vertebrate retina has blood vessels in front of it. Of course this wasn’t a good way to make an eye, so that primate foveas, and the pectens of birds, had to be designed to get around it. But this design simply doesn’t know spatial directions, so it has to work around its inability to ask for directions (old joke–the designer is therefore male).

12. Design cannot produce anything superb the first time around. This is why archaeopteryx is rather less well-designed than are modern birds, and why the Cambrian (explosion, you know, only an explosion of far less sophisticated and complex forms than exist today) had much less evolved chordates than we see around us. In fact, design can’t produce anything good until hundreds of thousands of tries have been made, as evidenced in genomes and in the fossil record.

13. Design is absolutely blind to solutions in separate lineages, when those lineages lack the ability to swap genes with distantly related species. So the blood of crustaceans is unlike vertebrate blood, and not nearly as good at carrying oxygen. Granting that the purposeless design that throws malaria and humans into protracted trench warfare might have liked to give inferior blood to crustaceans, why not simply a much worse version of hemoglobin? Because it’s a blind watchmaker (you know, couldn’t see which way the light was coming when making the “basic plan” of the vertebrate eye).

14. For the same reason, design can’t produce high-temperature spermatogenesis in mammals, although it did in birds. This is why most mammal testes are prone to injury, why males are vulnerable to hernias, and why there are undescended testicles. What’s especially odd from a human design perspective is why testes still have to be developed in a roughly ancestral position (inside the abdomen) and then weaken the abdominal walls as they descend into the scrotum. See #10, it somehow pleases the designer to make things appear to have evolved. We must please the god, or gods, by developing in a problem-causing manner.

15. Design lacks rationality. Contrary to what some say, the mousetrap does not look like something that could evolve. Why? Because it is shot through with rational thought, from the use of metal, to straight lines where useful, and on to the lack of any evolutionary limitations. On a molecular level, some facsimile of it probably could evolve by using biological materials (if selection pressures for it existed, that is), because it is so simple. However, nothing in biology really shows the kind of planning and thought that rational design exhibits, even though there is some overlap between rational thought and organs and systems that have evolved for a very long time (see Paley, who at least had a point at that stage of knowledge).

Usually we can tell Behe’s “designed organisms” from machines very easily, partly due to the rational “jumps” possible in human design, and impossible in Behe’s supernatural design. If it is true that archaeologists can detect design (and it is), why don’t they confuse life with human design? Mainly because it is so different, for many reasons, including materials (constrained by the designer’s evolutionary thought), reproduction, lack of rational design, and indeed, having complexity and capabilities unlike we have seen in any human design. But then it also lacks far simpler capabilities that we can manage, too, like radio, like nuclear power, like semiconductors and superconductors, to name just a few.

16. Last, design is unable to give the basics of knowledge to any organism, quite unlike how we supply information to computers. We had no formal capabilities in painting, writing, or mathematics, and had to develop all such capabilities in their formal splendor. Likewise, there was no science as we now know it until around the time of Newton (I would place the beginning of modern science with Newton, no matter how many giants came beforehand). We routinely place this sort of information into computers, but apparently design in Behe’s sense is unable to do so.

There it is, an incomplete list of the delimitations of design, in Behe’s sense. It’s strange, I really don’t envy the designer, for it apparently has no integrated knowledge whatsoever. Note the fact that Behe is God’s man on this earth, which probably explains why he betrays no integrated conception of the world either.

Glen Davidson
8.21.08                                                                                                                       To top

2. Only if it is found can the edge of evolution be calculated

No person–Darwinist, design proponent, or other–who wants to make a rational argument can seriously entertain an idea that pulls the rug out from under reason. Edge of Evolution, 226

No matter that Behe pulled the rug out from under reason at the beginning of the book.

There is a plethora of problems with Edge of Evolution, many of which I hope to address in the future. But the really big problem is something I want to address now, before I resume posting about DBB. The impossible problem for Behe is that he never once was able to show that evolution is responsible for some organic change, and that design is responsible for other organic change. Crucially, this is true for P. falciparum’s evolution of chloroquine resistance. Since under his own assumptions he cannot show that Plasmodium falciparum was not designed, either in the past (front-loading of the universe or of the genome) or in an ongoing intervention by the Creator, to develop resistance–and he merely assumes that such resistance evolved–from the very beginning his calculations have absolutely no basis at all.

Don’t suppose for a second that there aren’t many other problems with his calculations, which include the fact that he has no understanding of or regard for the population dynamics of malaria, knowledge of the selectional pressures for and against the mutations that give P. falciparum its resistance to chloroquine, nor even how many mutations are needed to confer positive selection. My present point is that from the very beginning he has no criterion for deciding what is designed and what is not, but he comes up with calculations based upon his mere belief that malaria evolved chloroquine resistance, rather than that resistance being designed.

The trouble is that the instant he decided that the supernatural designs organisms via evolution, and without any of the normally-recognized design characteristics being involved (like rationality, evident purpose), finding out what was caused by evolution and what was caused by “design” became completely and utterly impossible. Apparently the “designer” simply adds in mutations which cannot be expected to occur by chance, and (apparently) natural selection does the rest. And there is no qualitatively or quantitatively noticeable break between this “design process” and evolution. So how can this doofus ever presume to find out what evolved and what had to be designed, when he has nothing by which to decide what was designed and what was not?

What real science does is to understand cause and effect relationships first, and then to show reliably how one cause produces discernable effects, and to distinguish these effects from those caused by other processes, as best as can be done (and it is not possible to always distinguish effects). You already know what is design and what is not.

Behe’s way of determining what is designed and what is completely circular, save his initial assumption that what is happening today is not caused by non-human design. Because he simply believes that what is happening today is evolution and not design, he takes the mutations in humans and in P. falciparum to have evolved, and then makes illegitimate extrapolations from the already bogus figures that he got from that. Only if he already knew how to distinguish between design and evolution based on cause-and-effect criteria would he be able to show that chloroquine resistance is not the result of design, however, and he has no criteria which indicate that chloroquine resistance is not designed by his shadowy supernatural designer (or a designer indistinguishable from a supernatural one).

So he “found the edge of evolution” by merely assuming the edge of evolution–through his fully unsupported belief that design is not responsible for what is happening today. Even if he had begun this quest in all intellectual honesty (there is little indication of intellectual honesty in Behe’s writings), he would, as he himself noted, have to reevaluate what might have been designed in light of his “conclusion” that life was designed (see EoE 168), and would have to question his previous assumption that malaria has simply evolved. He does not do so, and if he had he would have had to face up to the fact that, lacking anything that distinguishes “design in life” from what has evolved, he simply cannot distinguish between the “two processes” at all.

He has pulled the rug out from any ability to reason in the empirical sciences, mainly because he’s strained so hard to claim that what evidently evolved was designed. By asserting that “looks designed” and “looks evolved” mean the same things, he has no basis whatsoever to come up with qualitative or quantitative criteria for determining design. This is another place where I made similar points.

The man seems to have no self-awareness, nor any capacity for thinking through his “scientific claims”. It appears that he is a hedgehog, plodding along with his one idea, and oblivious to the fact that he undermines his own claims during the course of his “argumentation.

8.25.08                                                                                                                       To top

3. Malaria’s diminished chloroplast is on purpose? Really?

This post is a kind of follow-up to this post.

Behe seems to have learned that taking the offensive is often the best strategy (especially since he has no hope in playing by the rules of science discussion). Rather than answering our questions about what parasites were designed to do, and what purpose they serve, he uses Plasmodium falciparum, the organism which causes malaria, as his test case for what evolution can do, while he assigns everything that evolution supposedly cannot do to “design”. In fact, he doesn’t in the slightest try to show that life is not the result of inheritance and accident, plus selection, rather he wants to claim that this is not so because life is just “too complex” to have evolved, and so, in his usual resort to false dichotomy, he resorts to “design”.

But we have no reason to follow the channel of “thought” that he attempts to impose because he lacks any kind of evidence for design. As I have demonstrated repeatedly, life’s characteristics are often due to accident (either accident of inheritance, or of various kinds mutations, duplications, etc.), and many of the “irreducibly complex” characteristics such as the chloroplast and its integration into the cells of many eukaryotes have very clear indications of being due to accident plus a considerable amount of complex evolution–notably the evolution of transport mechanisms after engulfment by a (proto?)eukaryotic cell, with respect to the chloroplast. As noted above, I wrote a post regarding this previously.

Remarkably, P. falciparum contains the remains of a chloroplast, which is called an “apicoplast.” What is currently believed to be the case is that an ancestor of the malaria parasite engulfed, not a cyanobacterium, rather a green alga which had cyanobacterium-derived chloroplasts within it. All that remains today is the apicoplast, which has only a very small genome (32 kb), and evidently no genes for photosynthesis. Oddly enough, relatively few of the proteins targeted to this apicoplast actually derive from the chloroplast from which it evolved. Nature article used as a source for this paragraph

The details are in sources like the on in the link just above. What I want to mention are the many accidents involved in the origination of this “irreducibly complex” and essential organelle used by P. falciparum to parasitize humanity.

First, rather than design providing photosynthesis to eukaryotes, a eukaryotic cell had to engulf a cyanobacterium without digesting it, in order to provide a very crude photosynthetic symbiosis. Subsequently, transport mechanisms evolved (though Behe denies the possibility), genes were transferred to the nuclei of the algae (some of these algae evolved into plants) containing what became these chloroplasts, and regulatory functions of the chloroplasts evolved as well. If any design or identifiable purpose can be found in any of these changes, no one has adequately shown their existence.

After all of that evolution happened, the ancestor of P. falciparum secondarily engulfed a green alga, and a symbiotic relationship evolved. While little is actually known specifically about this evolution, no doubt P. falciparum’s ancestor had to evolve essentially the same transport, regulatory, and genetic changes that already occurred in the green alga’s ancestor. It seems that eventually all of the green alga except for the chloroplast (and likely a number of genes from the green alga transferred to the nucleus) disappeared. The chloroplast itself lost most of its functions, including photosynthesis, as what became a parasite quite early in evolution (early in metazoan evolution, at least) no longer needed many of those functions.

This is an extraordinarily convoluted story, one that only makes sense, as famously stated, in the light of evolution. Can anyone actually understand this as a “design strategy”? It most certainly is not, it is a story of accident and of adaptation of various accidents to the evolving needs of a lineage of (eventually) parasitical organisms. And yet Behe would like to credit all of these “irreducibly complex” accidents, and complex adaptations to those accidents, to “design”.

Then again, why not do so from his amoral and nihilistic view of “design”? Only someone grasping without cause or reason would look at the destructive relationship of P. falciparum, Anopheles mosquitoes, and humans, as having been purposely designed instead of itself being an obvious evolutionary accident. Evolution explains such relationships, because it has no inherent moral aim or purpose (or any other kind of aim or purpose), nor any preference for host over parasite or for parasite over host. What we see in the human-mosquito-malaria relationship is at best inexplicable in terms of design and of purpose, and at worst an indictment of the God that Behe blames for malaria.

In addition to the foregoing comments, I would like to bring up a sound principle that I mentioned while discussing DBB, here. William Paley wrote:

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

What does experience, observation, and evidence suggest about the causes of the changes that have occurred to P. falciparum, and especially with respect to its apicoplast? What does experience and observation suggest regarding parasitical relationships? Even Behe admits that experience and observation provide evidence that contingency and selection produce identifiable evolutionary patterns in life. He simply wants everyone to forget that what we see in his “irreducibly complex” examples is the same sort of combination of accident, selection, and inherited contingency that we see in his examples of evolution. But if accident can be identified in “microevolution” due to its evident contingent character, how is not applying the same standard to “macroevolution” to be justified?

All that is evident in the history of life is accident and heredity being worked over by selection. Only by ignoring every principle of design and every principle of evolution can Behe find his way to ignoring the plain evidence that life evolved without guidance, and to instead believe that somehow the highly complex relationship between cyanobacterium, green alga, two eukaryotes engulfing and symbiosing with photosynthesizers, Anopheles, and humanity, is a purposeful arrangement of parts.

Experience and observation tell us that such a relationship is produced by identified and unguided evolutionary processes.

9.4.08                                                                                                                       To top

4. Photosynthetic “missing link” to malaria pathogen found

I recently wrote about how the endosymbiotically-derived apicoplast in P. falciparum fits very well with evolution, and is nonsensical as “design”. What I did not realize when I was writing that post, even though I had read the News and Views version in Nature when the research results were published (it was not very important to me at the time), was that a related organism has recently been found which still uses for photosynthesis a chloroplast which descended from the ancestral chloroplast from which P. falciparum’s apicoplast had also been derived. This is even further evidence which is explained by, and predicted in aspects via, evolution–and never once has such an intricate and step-wise production of a nested hierarchy of “machines” been seen as a design strategy in actions effected by any observable designer.

One of the predictions of evolution is that in nearly all adaptive radiations there will be a variety of adaptations of an organ, organelle, or system which is undergoing selective pressure. Of course there is no guarantee that any of the variations will survive or fossilize, nor that if one variant survives or fossilizes, another variant will. However, not infrequently are variations of a particular evolving system or entity found, thereby confirming the pattern expected of non-teleological evolution. The discovery of the the photosynthetic Chromera velia apparently is one such find which is so closely related to the apicomplexans (and shares a red-alga-derived photosynthetic plastid with some of the more distantly related Dinoflagellates), such as P. falciparum, that it seems unlikely that their respective plastids would not have a common origin.

Indeed, how would anyone even think through the shared plastid features of C. velia and P. falciparum except via evolutionary theory? Why would P. falciparum even have a plastid derived from a cyanobacterium, when the two only share a relatively few pathways at present? Would not a real designer just transfer the design of the pathways (or come up with a new pathway expressly designed for P. falciparum, if the designer is God), either with or without a single or double membrane (it appears P. falciparum has three membranes in its plastid, apparently down from four after its secondary symbiotic origin (double membrane from the cyanobacterium plus a double membrane from the red alga))?

Anyway, those are issues to think about when reading the following excerpts of the article:

[Abstract] Many parasitic Apicomplexa, such as Plasmodium falciparum, contain an unpigmented chloroplast remnant termed the apicoplast, which is a target for malaria treatment. However, no close relative of apicomplexans with with a functional photosynthetic plastid has yet been described. Here we describe a newly cultured organism that has ultrastructural features typical for alveolates, is phylogenetically related to apicomplexans, and contains a photosynthetic plastid. The plastid is surrounded by four membranes, is pigmented by chlorophyll α, and uses the codon UGA to encode tryptophan in the psbA gene. this genetic feature has been found only in coccidian apicoplasts and various mitochondria. The UGA-Trp codon and phylogenies of plastid and nuclear RNA genes indicate that the organism is the closest known photosynthetic relative to apicomplexan parasites and that its plastid shares an origins with the apicoplasts. The discovery of this organism provides a powerful model with which to study the evolution of parasitism in Apicomplexa. p. 959 Moore, et al. “A photosynthetic alveolate closely related to apicomplexan parasites” Nature 21 Feb. 2008 451:959-963

And here is the concluding paragraph:

Phylogenetic analyses support the description of Chromera velia as an alveolate, possessing a photosynthetic plastid that lies in the same secondary endosymbiotic lineage as apicoplasts. The ultrastructure and photosynthetic pigment profile of C. velia are consistent with a chromalveolate-affiliated ancestry. Figure 3 presents a model of the evolutionary history of C. velia, apicomplexans and dinoflagellates based on the phylogeny of the nuclear and plastid lineages and the retention or loss of plastid characteristics. Chromera velia represents the closest known photosynthetic relative of apicomplexan parasites.  Ibid. p. 962

Well, there it is, more evidence that a series of historical accidents lie behind the “irreducibly complex” phenomena of malaria pathogens, along with adaptation of these hereditary and event-produced accidents. Perhaps Behe would be a whole lot more convincing with respect to his design claims if he could elucidate some features of any organism which differed substantially from accident and adaptation, rather than trying to claim, based on nothing but ignorance, that what appears to be the result of accident plus selection must be ruled by some super-intelligent being, but without rationally intelligent responses to needs ever having been made.

9.8.08                                                                                                                       To top

5. 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.

9.9.08                                                                                                                       To top

6. 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

7. ID has problems with keeping its dogma straight

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.

9.25.08                                                                                                                       To top

8. 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-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.

10.02.08                                                                                                                 To top

9. 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.

10.11.08                                                                                                                 To top

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10 Comments on “The Edge of Evolution”

  1. […] weblog « Design in life is easy to detect–look for breaks in evolution The Edge of Evolution […]

  2. […] Behe Fails Weblog Just another weblog « The Edge of Evolution […]

  3. […] is part of a series of posts that I am combining into one long post entitled The Edge of Evolution. I will be posting the latest entries as separate blogposts, but will delete them after one or a […]

  4. […] “missing link” to malaria pathogen found I recently wrote about how the endosymbiotically-derived apicoplast in P. falciparum fits very well with evolution, and is nonsensical as “design”.  What I did not realize […]

  5. […] is part of a series of posts that I am combining into one long post, which may be found at The Edge of Evolution Explore posts in the same categories: […]

  6. […] is part of a series of posts that I am combining into one long post, which may be found at The Edge of Evolution Explore posts in the same categories: The Edge of […]

  7. […] 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. […]

  8. […] 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. […]

  9. […] is part of a series of posts that I am combining into one long post, which may be found at The Edge of Evolution Explore posts in the same categories: The Edge of […]

  10. […] is part of a series of posts that I am combining into one long post, which may be found at The Edge of Evolution Explore posts in the same categories: The Edge of […]

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