In 2005, Michael Behe published an op-ed in the New York Times entitled “Design for Living. Paul Gross has now reviewed Michael Behe’s book The Edge of Evolution in The New Criterion, using exactly the same title as Behe’s 2005 New York Times op-ed, accusing Behe of making so many mistakes that “it would need a book longer than The Edge to restate the model together with its already noticed (in print and online) errors and omissions.” Yet as I will recount in this four-part response, Dr. Gross’s review has many mistakes, and many of his key criticisms of Behe are misplaced.
Gross’s first error was claiming that Behe presumes that the mutations that allow malaria to evolve resistance to the antibiotic drug chloroquine must all occur simultaneously. Gross thus writes, “[T]he calculated probabilities, upon which the main argument of the book depends, come from a single report in the literature on the frequency of spontaneous resistance to a drug in the malaria parasite (Plasmodium). That frequency was in the first place a mere guess by its author, and it does not anyway measure the likelihood of what Behe thinks it measures. … Behe assumes simultaneous mutations at two sites in the relevant gene, but there is no such necessity and plenty of evidence that cumulativeness, rather than simultaneity, is the rule.” (Emphasis added.)
Gross is repeating the same misplaced argument that both Ken Miller and Jerry Coyne made earlier. Behe has responded to this argument repeatedly on his Amazon.com blog:
The number of one in 1020 is not a probability calculation. Rather, it is statistical data. It is perhaps not too surprising that both Miller and Coyne make that mistake, because in general Darwinists are not used to constraining their speculations with quantitative data. The fundamental message of The Edge of Evolution, however, is that such data are now available. Instead of imagining what the power of random mutation and selection might do, we can look at examples of what it has done. And when we do look at the best, clearest examples, the results are, to say the least, quite modest. Time and again we see that random mutations are incoherent and much more likely to degrade a genome than to add to it — and these are the positively-selected, “beneficial” random mutations.
Behe’s point is that, rather than he being the one who presumes that malaria resistance to chloroquine requires two mutations, it is Gross who, in his standard mode of Darwinian thinking, presumes that it can be selected cumulatively. In fact, Behe’s argument is much sounder than Gross’s argument. Behe’s point is that the degree to which the mutations confer a cumulative advantage is relatively unimportant, because, as he wrote on his Amazon blog, the 1020 statistic is an empirically derived fact that is valid regardless of the mutational pathway taken:
Miller asserts that I have ruled out cumulative selection and required Plasmodium falciparum to achieve a predetermined result. I’m flattered that he thinks I have such powers. However, the malaria parasite does not take orders from me or anyone else. I had no ability to rule out or require anything. The parasite was free in the wild to come up with any solution that might help it, by any mutational pathway that was available. I simply reported the results of what the parasite achieved. … Certainly, there may be several routes, maybe permutations of pathways, too. But whether or not there are several routes, the bottom line is that resistance arises only once for every 1020 parasites.
Similarly, Behe says in response to Jerry Coyne:
The number I cite, one parasite in every 1020 for de novo chloroquine resistance, is not a probability calculation. Rather, it is a statistic, a result, a data point. (Furthermore, it is not my number, but that of the eminent malariologist Nicholas White.) I do not assume that “adaptation cannot occur one mutation at a time”; I assume nothing at all. I am simply looking at the results. The malaria parasite was free to do whatever it could in nature; to evolve resistance, or outcompete its fellow parasites, by whatever evolutionary pathway was available in the wild. Neither I nor anyone else were manipulating the results. What we see when we look at chloroquine-resistant malaria is pristine data — it is the best that random mutation plus selection was able to accomplish in the wild in 1020 tries.
It seems indisputable that the claim of one instance of spontaneous resistance per 1020 cells was based upon statistical data, and is not dependent upon an assumption that all mutations must occur simultaneously to acquire resistance. If anything, Behe makes no assumptions, but rather the rarity of this resistance could imply that multiple mutations are required to confer such a resistance advantage.
Calculating the “Mere Guess”
Gross asserts that the statistic was, “a mere guess by its author.” Is Gross correct? In fact Gross has blatantly misrepresented the methodology behind the statistic Behe cites: it is a calculation, not “a mere guess.”
Behe cites his source that spontaneous resistance to chloroquine occurs in one in every 1020 malaria cells. It’s from a review article published in the prestigious Journal of Clinical Investigation entitled, “Antimalarial drug resistance” (Vol. 113(8) (April 2004)). The author, Nicholas J. White, holds two doctorates and is an esteemed researcher in his field. As White’s bio states:
Professor White has contributed to over 500 peer reviewed scientific publications and has written over 30 book chapters. He is a full Professor at Mahidol University and also Oxford University. He is a member of several WHO advisory panels, and is on the International Editorial Advisory boards of several international journals including The Lancet and the Journal of Infectious Diseases.
White’s article states precisely what Behe claims it does: “the per-parasite probability of developing resistance de novo is on the order of 1 in 1020 parasite multiplications.” Suffice to say, this kind of author wouldn’t print such a statement in this type of article in this journal if it were a “mere guess.” Behe roughly outlines how White performs this calculation as follows:
Nicholas White of Mahidol University in Thailand points out that if you multiply the number of parasites in a person who is very ill with malaria times the number of people who get malaria per year times the number of years since the introduction of chloroquine, then you can estimate the odds of a parasite developing resistance to chloroquine is roughly one in a hundred billion billion. In shorthand scientific notation, that’s one in 1020.
(Behe, Edge of Evolution, pg. 57.)
To re-produce the calculation:
- Instances of chloroquine resistance in the past 50 years: Less than 10 (White, 2004). To be generous, we’ll say 10 per 50 years, or 1 instance of chloroquine resistance per 5 years.
- Total malaria cells that exist each year: approximately 1020 cells per year. (White, 2004; White & Pongtavornpinyo, 2003).
- = 1 instance of chloroquine resistance per 5 x 1020 malaria cells, or roughly speaking, 1 instance of chloroquine resistance per 1020 malaria cells
Even science writing that has been simplified for public consumption in The New Criterion cannot fairly characterize the 1 in 1020 statistic as “a mere guess.” It’s the result of real-world studies of malaria behavior in response to chloroquine and reproducible calculations, as reported in review articles by leaders in the field in one of the world’s top medical journals. It was anything but “a mere guess.”