Expose Expelled

Maybe you know someone who has been suckered in by the numerous distortions, outright lies, and malevolent accusations of the "documentary" Expelled, starring famous bore and Nixon speechwriter Ben Stein. Perhaps even you have been convinced by its "startling" array of important "facts" about the "controversy" between the scientifically useless design conjecture and staggeringly successful evolutionary theory. If so, I urge you to direct your credulous friend (or yourself) to Expelled Exposed, a website devoted to debunking the lies of this appalling propaganda flick. Even if you favor a creationist viewpoint I think you will find it highly disturbing how freely the creators of this film distort the truth to favor their views.

In addition, for general knowledge on debunking the claims of creationists you should check out The Panda's Thumb, TalkOrigins, TalkDesign, TalkReason, and the National Center for Science Education.

Also, New Scientist has an excellent article up featuring 24 misconceptions about evolution. Read it.

Also check out some other articles about the film and its marketing:
Biologist PZ Myers, interviewed in the film, is expelled from a screening of Expelled. But they let Dawkins in.

An animation in Expelled was ripped off from Harvard University and XVIVO. It should be noted that famous cdesign proponentsist William Dembski was for a long time in the habit of stealing this film to display in paid lectures.

Expelled tries to draw a line between belief in evolution and anti-Semitism. Interestingly, one of the creationist scientists they interview is the anti-Semite Maciej Giertych.

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What's that appendix for, anyway?

Well, it keeps coming up, doesn't it? Famous cdesign proponentsist Dembski brought it up again recently in his list of ID "predictions" (click for epic fail). While his point was nicely deconstructed by Afarensis, I think it's worth examining the paper that attributed a function to the appendix. Just what did Bollinger et al. say about its function? On what basis did they draw their conclusions? And, I suppose most exasperatingly, what does the paper mean for evolution? Is the appendix vestigial or not, and if not, does that vindicate ID, evolution, or both?

The paper in question is an elaborately stated hypothesis, premised on the idea that

The occurrence of the appendix sporadically throughout phylogeny might suggest that the structure is evolutionarily derived for a specific function rather than merely a vestige of a once important digestive organ.

The emphasis in the above is mine, and included primarily to demonstrate that regardless of where the paper takes us it cannot be a successful unique prediction of ID, because the rationale behind the search for a function was evolutionary in the first place. But what exactly is it that the authors think the appendix is doing?

Well, they believe that the appendix is a site at which bowel biofilms are created, and a reservoir for commensal bacteria. What does this mean? Well, as we all ought be aware, we share our bodies with a significant number of bacteria who live on what we fail to digest and occasionally assist us by breaking down what we cannot and feeding bits of it to us. In recent years, as we have generally developed a greater appreciation for the role of the extracellular matrix in various aspects of biology, it has been demonstrated that our intestinal flora are to some extent supported by a rich layer of polysaccharides coating our intestinal surfaces. Bollinger et al. premise a role for the appendix in the support of this biofilm on the basis of three main pieces of evidence.

1. The appendix is located at the proximal end of the colon, where the greatest density of biofilm can be found.
2. Bowel biofilm is known to be associated with mucin and IgA, and the lymphoid tissue of the appendix could abundantly produce these molecules.
3. The position of the appendix protects it from the fecal stream.

Given that biofilms benefit the host organism (us), the idea that the appendix promotes the formation of the biofilm and serves as a reservoir of friendly commensal bacteria in the event that the colon was flushed out in response to a pathogenic event (e.g. diarrhea) is an attractive attribution of function.

There are several reasons one might not find this convincing. The first of these is that biofilms are likely to be a ubiquitous feature of mammalian digestive systems. While this does not disprove the idea that the appendix promotes the formation of biofilms, it does suggest that the observed relationship between biofilm presence and the appendix might be coincidental. Similarly, success of bowel biofilms in such organisms would suggest that the abundance of lymphoid tissue in the appendix is not necessary to populate the film with the requisite immune molecules. Given the propensity for the appendix to suffer a blockage (with resulting appendicitis), one might also find proposition 3 to be tenuous, though I would welcome a rebuttal on this point from a professional gastroenterologist or anyone who studies peristalsis rigorously.

In general this hypothesis is difficult to test due to the fact that direct analogues to the human appendix in other organisms are rather rare. However, there are some experiments that can be performed, the most obvious of which is to take some animal that lacks an appendix (a carnivore of some kind?) and examine the distribution of biofilm in its colon. This would likely address whether point (1) represents a causative relationship or coincidence, and an examination of the molecular composition of the biofilms of these animals would give us good information about whether (2) is a valid reason to attribute this function to the appendix. A comparison of biofilm distribution and composition between human subjects who possess an appendix and those who lack one (at least 6% of the population, it would seem) would also indicate whether removal of the appendix deranges biofilm formation. Comparative studies of biofilm regeneration and intestinal recolonization by commensal species following diarrhea in normal and appendix-free individuals would also be of value in assessing the function of the appendix. So there are further experiments to be performed which can speak to this hypothesis.

But, let us assume for Mr. Dembski's sake that all of these experiments have taken place and yielded results which cast the best possible light on this hypothesis. Would it establish that the appendix was not vestigial? Well, no, not if you genuinely understand what vestigial means. Again, Afarensis makes some good points here, and there is also an interesting discussion of vestigiality on the appendix page at TalkOrigins. The fundamental point that you must appreciate is that vestigial does not mean useless. The word "vestigial" describes a particular kind of evolutionary history of a feature, specifically that a given physiological construct has lost the purpose it possessed in ancestral species. Vestigiality implies nothing about present function. Thus, even if it has a function in humans, the appendix would still be vestigial unless we could use it to ferment all those cellulose-laden tree leaves we eat. So it simply isn't true that the discovery of a function for the appendix means it's not vestigial—indeed, the presence or absence of a modern function doesn't speak to the vestigiality of the appendix at all.

Supposing that the hypothesis proves to be valid, it doesn't pose a real problem for evolution. Remember that the reason Bollinger et al. claim to have developed this hypothesis is to find an evolutionary rationale for the preservation of the appendix. If it turns out to provide a benefit, even in the form of a marginal improvement in biofilm robustness, then this might provide an explanation why the organ has not been lost completely. On the other hand, such an explanation is not strictly necessary; our anatomists may just be catching the appendix on the way out.

And actually, given the ubiquity of biofilms, validation of this hypothesis would represent a(nother) philosophical disaster for the intelligent design conjecture. If the appendix truly provides a significant benefit to biofilm formation, then it seems logical to ask why the designer included it in so few mammals, of such disparate kinds. Why not put it in all of them? If it's not important for that, then why put it in any? The apparently random distribution (and dissimilarity) of appendices in mammals is consistent neither with a purposeful insertion of elements known to be of benefit, nor with a purposeful trimming of elements known to be useless. Evolution, on the other hand, is perfectly at home with this kind of convergent funny business. In this sense, it doesn't matter whether a function is ever found for the appendix or not. Vestigiality aside, the existence of the appendix cannot be explained by the design conjecture if it is useless, nor can it be explained by design conjecture if it possesses a function, as this hypothesis suggests, that would be of benefit to all animals, including those that lack one.

Bollinger, R.R., Barbas, A., Bush, E., Lin, S., Parker, W. (2007). Biofilms in the large bowel suggest an apparent function of the human vermiform appendix. Journal of Theoretical Biology, 249(4), 826-831. DOI: 10.1016/j.jtbi.2007.08.032

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What was Leslie Orgel saying?

Well, my first impression on reading Leslie Orgel's recent (posthumous) essay in PLoS Biology was that it was just the sort of rich quote-ore that creationists and cdesign proponentsists cannot resist mining. Indeed, it was not long before famous cdesign proponentsist Casey Luskin began distorting the article in a way that served his personal beliefs. Others have dissected the failures of Mr. Luskin's analysis, and of course volumes were written about his putative misuse of the Research Blogging icon. In all the clamor condemning Mr. Luskin, Orgel's actual paper seems to have gotten lost. I thought I might write about it.

Orgel's article itself doesn't contain any new research, and those who are keeping track might notice similarities to a previous essay on the same topic from 2000. The issue at hand is the origin of life, which owing to our inability to travel back in time is one of the most difficult subjects in biochemical research. It is almost impossible to know exactly what chemicals were present in the prebiotic milieu, what minerals and surfaces were available to perform catalysis, and which of the many possible environments was the one in which life actually arose. As such, the field is highly speculative. Orgel's essay is something of a reaction to this.

It is popular to speak of an "RNA world" of primitive organisms in which most or all of the functions currently performed by proteins were instead performed by RNA. This model has the advantage that RNA can have both informational content and catalytic activity, but it demands the question of where the RNA came from. Some elements of nucleic acids can form nonenzymatically from simple chemicals likely to be present in the prebiotic milieu, but the transition from adenine and ribose to a diverse oligosaccharide with a phosphate backbone is not trivial. If, however, enormous autocatalytic cycles existed on the prebiotic Earth, that would resolve many of these objections.

In his essay, Orgel seemingly meant to quell enthusiasm (I use the term in its pejorative sense) for this idea, not because he believes it is intrinsically false, but because it doesn't really make things easier for us. He takes as an example the reverse citric acid cycle, pointing out that although it is extremely useful, and moreover is autocatalytic, it requires numerous and diverse chemical activities, many of which could go awry if the wrong substrate were used for a step. The assertion that this cycle underpins the existence of life requires appropriate colocal catalysts acting with sufficient efficiency to keep the cycle running. Moreover, it requires that unproductive (or toxic) side-reactions not drain away the reactants at any step. That is, the catalysts present must discriminate between different possible reactants, so as not to break down components inappropriately before they advance in the cycle. It is not immediately apparent that this is possible (certainly it does not appear to be probable), and Orgel was not convinced by several of the attempts to justify prebiotic catalytic cycles. This article summarized his reasons for skepticism.

This attitude has been misrepresented as meaning that Orgel believed (A) that prebiotic autocatalytic cycles were impossible, and (B) that important life cycles are irreducibly complex. Both propositions are false, and it is also false that Orgel believed them.

Part of the rebuttal to proposition A is referenced in Orgel's paper itself, when he mentions Arthur Weber's recent work in which a reaction of various trioses with ammonia gave autocatalytic products. Although the cycle at work in that instance is not yet understood, Orgel points to it as being particularly promising, in part because it requires no additional catalyst, and in part because it yields high-energy carbon compounds of a kind that might be useful substrates for life.

Granted, the reactions of the Weber experiment may not be directly analogous to anything observed in modern organisms, but I feel that this should not be seen as a problem. After all, why would a primitive organism evolve an activity to perform catalysis already occurring naturally? Rather, one would expect that primitive organisms, whatever their informational and structural characteristics, used the products of autocatalytic cycles as raw material for more exotic activities, which were later repurposed to the production of raw materials as a way to gain a competitive edge or to respond to resource scarcity. If, additionally, very complex abiotic cycles similar to the TCA cycle existed to produce more exotic or useful substrates, it ceases to be quite as problematic if they are not highly efficient or specific. Indeed, these sorts of shortcomings would likely serve as a basis for establishing selective advantage for those organisms that evolved compensating protein catalytic activities.

It is not necessary that abiotic cycles intended to serve as a metabolic origin of life work perfectly, or even that they involve products and intermediates similar to those used by contemporary organisms. They need only be efficient and specific enough for life to get started, with intermediates and products that are useful enough for primitive organisms to benefit from them. Orgel's objection is not that this latter situation is impossible; rather he feels that it is sufficiently implausible that actual evidence is needed, rather than hopefulness and modeling.

The sharp-eyed will (hopefully) note the influence of Orgel's rules in the above, especially the First Rule: "Whenever a spontaneous process is too slow or too inefficient a protein will evolve to speed it up or make it more efficient." The rebuttal to proposition B, of course, comes in the form of Orgel's Second Rule: "Evolution is smarter than you are." The belief that any biological systems are irreducibly complex results merely from a failure to understand the enormous problem-solving potential of selection combined with random mutation and millions upon millions of years of time to work. Certainly Orgel would never have accepted that evolution could not produce these complicated cycles once given a chance, or that these cycles could not be broken down in a useful way for primitive organisms. Orgel's point is not that any of this is impossible, it is that it must be shown to be plausible:

The most serious challenge to proponents of metabolic cycle theories—the problems presented by the lack of specificity of most nonenzymatic catalysts—has, in general, not been appreciated. If it has, it has been ignored. Theories of the origin of life based on metabolic cycles cannot be justified by the inadequacy of competing theories: they must stand on their own.

Orgel's paper does not rule out the possibility of autocatalytic cycles, nor does it assert or even imply that some mystical intervention is necessary to explain how life came about. Orgel's paper is a demand for evidence. It is not enough to say that autocatalytic cycles solve the problem of biogenesis, nor even that they are more plausible than other explanations. Negative arguments do not suffice; a positive argument must be made and backed up by simulations, reconstructions, and experimental evidence. Orgel points favorably to several promising avenues of research in this regard.

Intelligent design is not among those avenues, and it is certain that Orgel would reject it. Having only a (flimsy) negative case in its favor, lacking even the virtue of plausibility, and ignoring his second rule, ID must be seen as weaker than any extant metabolic or genetic theories, which at least are not based on magic. Orgel's overall point is a valuable one. It is disgusting and disgraceful that, with flagrant disregard for his thinking, Orgel's essay should be misrepresented as supporting "if pigs could fly" views of the origin of life.

Primary citation:
Orgel, L.E. (2008). The Implausibility of Metabolic Cycles on the Prebiotic Earth. PLoS Biology, 6(1), e18. DOI: 10.1371/journal.pbio.0060018 OPEN ACCESS

Other peer-reviewed articles referenced:
Orgel, L.E. (2000). Self-organizing biochemical cycles. Proceedings of the National Academy of Sciences, 97(23), 12503-12507. DOI: 10.1073/pnas.220406697 OPEN ACCESS
Roy, D., Najafian, K., von Rague Schleyer, P. (2007). Chemical evolution: The mechanism of the formation of adenine under prebiotic conditions. Proceedings of the National Academy of Sciences, 104(44), 17272-17277. DOI: 10.1073/pnas.0708434104
Weber, A.L. (2007). The Sugar Model: Autocatalytic Activity of the Triose-Ammonia Reaction. Origins of Life and Evolution of Biospheres, 37(2), 105-111. DOI: 10.1007/s11084-006-9059-9

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