Friday, 17 December 2010

Behe in Britain, Miller's mousetrap, and the origins of malaria

(A version of this article is appearing in The Beacon, house organ of the [New Mexico] Coalition For excellence in Science and Mathematics Education)


Prof Behe (yes, him again) has been touring United Kingdom, as the guest of a new obscurantist organisation calling itself the Centre for Intelligent Design (C4ID). The Centre's president, Prof Norman Nevin, believes that Genesis 1 through 11 (garden, talking snake, Noah's Ark, the lot) is literally and historically true, and the Centre's list of friends is a rollcall of religiously motivated UK creationists. And three of Prof Behe’s lectures were delivered in churches, one in a biblical literalist church in Belfast, one in London’s Notting Hill (preceded by hymn singing), [1] and one in Westminster. According to the published itinerary, the last of these was held “in association with Premier Christian Radio.” However, C4ID, like Prof Behe himself, assures us that Intelligent Design concerns itself with science, not religion, and has nothing to do with creationism. At the lectures, the Discovery Institute's fake [2] textbook Explore Evolution was on sale, alongside copies of Ben Stein’s thoroughly discredited [3] movie, Expelled; no Intelligence Allowed. The Centre nonetheless assures us that it is completely independent of the Discovery Institute, which has merely supplied its ideas, its materials, its inaugural speaker and, one fears, its standards of intellectual integrity.

Reports are in of the actual content of Prof Behe's lecture, [4] and I feel as if I have travelled backwards in time. He spoke about the “irreducible complexity” of a mousetrap, an argument that first appeared in Darwin's Black Box, way back in 1996. Ken Miller's hilarious deconstruction (of the mousetrap, as well as the argument) is available online, [5] as is Prof Behe’s lame attempt [6] to put it back together. His next exhibit, believe it or not, was the bacterial flagellum. But what about all the evidence linking it to its simpler precursors, he was asked. Irrelevant, because until it became a complete flagellum, it was not functioning as such, so it is indeed irreducible. A rather unconvincing semantic trick, worked by changing the meaning [7] of “irreducible” in mid-argument. We also got the claim that since mutations are the result of copying errors, they must involve degradation, or loss of function, so they couldn't explain the elaboration of function anyway. The flood of counterexamples that immediately come to mind merely serve to illustrate the effects of Intelligent Design. When asked about Kitzmiller v Dover School Board, he explained that the judge was not in a position to give an informed opinion, since he was not a scientist, and was taking his opinions from the scientific establishment. The same scientific establishment that, he said, stops him from publishing his views in the peer-reviewed literature. ID, it seems, comes with its own conspiracy theory. Prof Behe, I conclude, is completely sincere, unsinkable, and factproof.

Very recently, [8] Prof Behe has published a paper in Quarterly Reviews of Biology in which he aims, rather unsuccessfully, to minimise the constructive role of mutation combined with selection. He does this by confining attention to prokaryotes grown in isolation, by introducing his own asymmetric criteria as to what would count as constructive, and by admitting for consideration only those relatively few cases where the mutation and its operation are understood at the molecular level. Limiting the playing field, tilting the playing field, and moving the goalposts closer together. Even so, he has to admit some cases of gain of function, any one of which would suffice to destroy the argument for design. By a delightful coincidence, if such it be, the same issue of the journal contains a detailed philosophical analysis [9] of the logical errors and rhetorical devices used by Prof Behe and his associates, some of which I have mentioned here.

Malaria, unlike the mousetrap, does not merit an index entry in Darwin's Black Box, but featured in his UK lecture, and plays a major role in his 2007 book, The Edge of Evolution. Here he explains at some length [10] why he does not consider the emergence of chloroquine resistance in the malaria parasite to be a Darwinian process. This book, too, has been mercilessly dissected by reviewers far more qualified than I am, [11] as has the specific claim regarding chloroquine resistance. [12] So I'll content myself at this stage with the observation that if chloroquine resistance really is the result of intelligent design, that tells us something rather disconcerting about the Designer.

Malaria itself is a parasitic disease involving two separate species, a vertebrate host and an insect vector. The full life-cycle involves a number of separate phases depending on the exact species, [13] with infection of the host by an insect bite, migration to the liver and thence to red blood cells, asexual reproduction within the red blood cells, and formation of male and female gametes. When the insect takes a blood meal from a host, the gametes recombine within its stomach, giving rise to a new generation and a new cycle. The parasite is a magnificent (if that is the correct word) example of adaptive evolution in action. Like any infectious agent, it needs to evade the host's immune system. It does this, first by hiding in the liver, and later by hiding within the red blood cells. It prolongs the bodily residence time of the infected blood cells by increasing their stickiness, causing them to cling to the walls of blood vessels, rather than making their way to the spleen, which would remove them. This, incidentally, is among the ways in which it induces weakness in the hosts, making them less capable of defending themselves against the insect carriers. Since the parasites cannot remain fully hidden as they migrate, hosts (including humans) do tend to build up immunity over time. The parasite counters this by the position of the sexual phase in its life cycle. The function of sex, as always, is to juggle information (sex, after all, is not necessary for reproduction), so that each new infection will bring parasites with rearranged genomes, coated with proteins that the host has not seen before.

Malaria type parasites have been identified in the abdominal cavity of a biting midge trapped in early Cretaceous amber. The midge seems to be adapted to feeding on cold-blooded animals, and indeed it has been suggested that malaria was among the many diseases afflicting the dinosaurs. [14] Molecular evidence [15] suggests an even older origin for the disease, around 130 million years ago, with malaria both in mammals and in birds having originated from a form parasitic on reptiles. The vectors for human malaria are several species of Anopheles mosquitoes, and the parasites that they carry are closely related to those causing similar diseases in the other great apes. It was long believed that the protozoan Plasmodiaum falciparum that is responsible for the most virulent form of human malaria came from chimpanzees, but the most recent studies [16] show that its closest relative is one that infects gorillas. Either way, malaria, like HIV, is among the human diseases that have found their way to us from our close relatives. P. falciparum is most prevalent in hot, damp climates, and appears (from molecular studies) to have started spreading widely among humans around 6000 years ago, perhaps as a result of the higher population densities and irrigation practices associated with agriculture. [17]

Like all parasites, Plasmodium must at some stage have evolved from free living organisms. It seems plausible that these were aquatic, and acquired the ability to recognise, feed on, and finally live within insect larvae. Every parasite has the problem of moving from one individual host animal to another, and for this genus, the problem is solved by transfer of fluids when the vector insect is feeding. A necessary cost of the parasitic lifestyle is exposure to extreme changes of environment, which parasites deal with by adopting different phases at different stages in their life cycle. This is an option open to protozoans and to multicellular parasites, which have large enough genomes to include the instructions for all the necessary quick change acts, and which respond to environmental clues that determine which set is activated.

The evolution of chloroquine resistance in P. falciparum is a matter of enormous practical importance, since malaria kills something like 1 million people a year. The precise genetic mechanism, involving a sequence of changes to one particular protein, is under active investigation, as is the intriguing fact that a parasite lineage that has acquired resistant to one drug can have increased sensitivity to others. [18] Such are the fruits of the “materialistic explanations” that Behe and his colleagues wish to replace [19] with “theistic understanding”.

Addendum: shortly after Behe's review appeared, an extensive study of the evolutionary history of 3,983 gene families across the three domains of life (Archaea, Eubacteria, Eukaryotes) was published in Nature.[20] To quote the MIT press release,[21] “The work suggests that the collective genome of all life underwent an expansion between 3.3 and 2.8 billion years ago, during which time 27 percent of all presently existing gene families came into being.” As Figure 1 (publicly available; see Footnote 20) clearly shows, the generation of new function outstrips and precedes the loss of older function. This is a massive refutation of Behe's line of argument, and of the use that the Creationists and their allies would wish to make of it.

“Intelligent design” or effective science? There is not room for both.

Paul Braterman
Professor Emeritus, University of North Texas
Honorary Sr. Research Fellow in Chemistry,
University of Glasgow



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7 More exactly, the referent; it is the flagellicity, not the complexity, that on Behe's terms really is irreducible
8 The Quarterly Review of Biology, December 2010, Vol. 85, No. 4, 419-445.
9 Ibid., 473-482
10 The usual statistical sleight-of-hand, pretending that sequential changes in a highly variable protein have to happen simultaneously.
11 For a particularly scathing and detailed analysis by Jerry Coyne, see http://www.talkreason.org/articles/Mutator.cfm 
12 Matzke NJ, The edge of creationism, Trends in ecology and Evolution 22, 566, 2007, and references therein
14 Poinar G, jr and Telford, SR Parasitology 131, 79, 2005; What Bugged the Dinosaurs?, Poinar, G., jr and Poinar, R., Princeton University Press, 2008.
15 From analysis of cytochrome B: Yotoko, KSC and Elisei, C. Malaria parasites and their relationships with their hosts.. Journal of Zoological Systematics and Evolutionary Research 44, 265, 2006
16 Liu W et al. Origin of the human malaria parasite Plasmodium falciparum in western gorillas. Nature 467, 420, 2010.
17 Hume JCC, Lyons EJ and Day KP, Malaria in antiquity: a genetics perspective, World Archaeology 35, 180, 2003
18 See e.g. Johnson DJ et al., Evidence for a Central Role for PfCRT in Conferring Plasmodium falciparum Resistance to Diverse Antimalarial Agents, Molecular Cell, 15, 867, 2004,
19 www.antievolution.org/features/wedge.pdf, p4, “Governing Goals”


20 Nature 469, 93-96 (19 December 2010); Abstract, and figure referred to, publicly available at http://www.nature.com/nature/journal/v469/n7328/full/nature09649.html

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