UD Subscriber Magnan pinches his nose closed long enough to fisk Mark Chu-Carrol’s vitriolic spittle strewn imbecilic
diatribe “review” of Michael Behe’s new book The Edge of Evolution: The Search for the Limits of Darwinism in a comment here. I reproduce it in its entirety. Now that someone has responded to it point by point I hope those who have been losing sleep over it can get some rest.
I read Chu-CarrollÃ¢â‚¬â„¢s hatchet job against BeheÃ¢â‚¬â„¢s book The Edge of Evolution and against Behe personally. This Ã¢â‚¬Å“reviewÃ¢â‚¬Â is in his blog and hardly deserves to be so called, but it apparently has been cited in other Darwinist websites, so it interested me to see if there is any substance under all the insulting vituperation. Though not a biologist I found it interesting to try to evaluate some of his arguments. After all, he isnÃ¢â‚¬â„¢t a biologist either but that doesnÃ¢â‚¬â„¢t seem to have held him back. As distasteful as it is to examine such angry ravings in detail. I perused the sections of The Edge of Evolution most relevant to ChuÃ¢â‚¬â„¢s tirade, in advance of thoroughly reading the book. This seems OK since Chu obviously hasnÃ¢â‚¬â„¢t read much of it either.
I found mostly prejudiced misinterpretations and invalid arguments, more than I can completely recount here. The Edge of Evolution is quite evidently directed at nonscientist readers and is simplified accordingly, unfortunately glossing over the fine points. So Chu pounces on every relatively simplified description of evolutionary theory as an indication of BeheÃ¢â‚¬â„¢s supposed ignorance and stupidity. For instance, he claims that Behe says that mutations are always single point changes. This is absolutely ridiculous and of course deliberately insulting. Chu, look at Chapter 3 page 62 first paragraph. Another example: Ã¢â‚¬Å“Ã¢â‚¬Â¦his (BeheÃ¢â‚¬â„¢s) ignorance of any source of genetic diversity other than mutation.Ã¢â‚¬Â Of course Behe is aware of other sources of variation. Recombination is supposed to be the major source other than mutation. Behe doesnÃ¢â‚¬â„¢t mention recombination because mutation is still the major source of change to the genome, as admitted in many orthodox MET sources. Recombination mainly reshuffles alleles (different mutated versions of genes) during reproduction of sex cells in eukaryotic organisms.
BeheÃ¢â‚¬â„¢s prime statistical example of the limits of Darwinian evolution with only random variation is the malaria parasite, and this is a protozoan eukaryote (plasmodium) in which meiotic recombination continually occurs. This example gives every advantage to random variations from all types of mutations and recombinational events in a huge population over millions of generations, but the limitations still applied.
Chu goes into a long diatribe over BeheÃ¢â‚¬â„¢s use of the Ã¢â‚¬Å“fitness landscapeÃ¢â‚¬Â concept in his argument. It seems to me these criticisms are obfuscations and irrelevant to BeheÃ¢â‚¬â„¢s thesis. However many dimensions of different interacting fitness functions, and however this Ã¢â‚¬Å“landscapeÃ¢â‚¬Â changes with time for a species, for any particular reproductive fitness function the species can still be trapped at a local maximum, unable to get across the Ã¢â‚¬Å“valleyÃ¢â‚¬Â to the next, higher peak without an extremely improbable giant leap. The reason for this is that the physical genetic loci coding for different fitness functions or factors are generally uncorrelated with each other. Usually they are not even in the same gene. No matter how many other varied genetic changes affect the phenotype in varied ways, certain specific mutational or other genetic changes are needed to make the jump from phenotype structure A to elaborated structure B in time T as evidenced by the fossil record. The probability of this occurring by accumulation of small random changes or by one giant (random) leap is a function of the total complexity of that particular genetic change, the likely presence of steps that are too deleterious to reproductive fitness to spread and fix in the population, and the number of generations. This is regardless of abstract models like the Ã¢â‚¬Å“fitness landscapeÃ¢â‚¬Â.
The malaria parasite drug resistance example (in addition to others) demonstrates these limitations in the living world, regardless of abstract models.
Chu then sets up a straw man and demolishes it by implying Behe doesnÃ¢â‚¬â„¢t even account for the trillion or so malaria protozoa in each human individual with the disease, in estimating the total number of reproducing parasites subject to Darwinian evolution in the human population. Of course this is ridiculous – Behe clearly accounts for this in his calculations, as shown in numerous places in chapter 3.
After this travesty, Chu continues to use rhetoric rather than specific arguments and counterexamples, to somehow through any means destroy BeheÃ¢â‚¬â„¢s malaria test case. He grudgingly admits some validity to BeheÃ¢â‚¬â„¢s statistical estimates for the malaria parasite acquisition of chloroquine resistance, but claims the malaria example is still an Ã¢â‚¬Å“artificially inflated probability number based on the biochemistry of one specific organismÃ¢â‚¬Â. He vaguely asserts without substantiation that for an organism like malaria these numbers just arenÃ¢â‚¬â„¢t Ã¢â‚¬Å“compellingÃ¢â‚¬Â. I guess we are supposed to take this on faith in his wisdom. He has plenty of rant and bluster, but doesnÃ¢â‚¬â„¢t show any specific valid way these numbers were inflated, and he doesnÃ¢â‚¬â„¢t show specifically why BeheÃ¢â‚¬â„¢s application of these results to human population genetics is invalid. This did, however, make me wonder if this extrapolation was perhaps simplistic. The only factor I could identify that might be questionable in relating the basic population genetics of the two organisms in this way was genome mutation rate per individual per generation. This is fairly low for unicellular organisms with very short lifespans and generation times, but higher animals (metazoans) accumulate mutations in their germ (sex) cells over a much longer time for each individual, so their mutation rate per generation is much higher. To try to correct for this I found some published mutation rate estimates, which indicated that the ratio is a factor of about 10,000. I tried correcting for this and BeheÃ¢â‚¬â„¢s numerical argument was not significantly affected. ItÃ¢â‚¬â„¢s in the noise compared to the other factors. Behe didnÃ¢â‚¬â„¢t mention this aspect probably because it is beyond the detail level of the presentation.
Chu doesnÃ¢â‚¬â„¢t even try to address the other related points made in the book, such as in chapter 7 on the failure of the malaria parasite over human history to have evolved any new cellular protein-protein interactions (binding sites).
Chu also makes the usual hand-waving general claim that the chances of producing any particular biological change is admittedly extremely small, but that the chances of producing at least something or anything adaptive is very high. As if this really explains anything. So if it looks like you were chosen by design it really is only the end of a long chance winnowing process. This is just a rhetorical ploy and carefully avoids trying to apply it to explain any particular evolutionary development sequence.