I had the guts to make several comments on Professor Larry Moran’s blog, Sandwalk; he has responded to one of these comments with two blog posts (here and here). And now, I have the chutzpah to respond to Professor Larry Moran (to get the gist of what’s going on see my comments on Sandwalk) on BioTalk.
The comment to which Prof. Moran responded to was pretty straightforward. Namely, I argued that “intelligent design proponents need only demonstrate that the odds of a particular biochemical system evolving are 10^-40 or less in order for intelligent design to be a more adequate explanation for the origin of such a biochemical system. This is because there have been no more than 10^39 bacterial cells in the history of life on earth.”
Prof. Moran contends that the above argument cannot possibly hold much water, and he attempts to substantiate that assertion by bringing up the following argument:
That the odds of a specified sperm uniting with an egg is deplorably low, and as a result, through various calculations he does, he concludes that the probability of his four great-grandparents being born is lower than 10^-64 – a probability significantly lower than my stated 10^-40.
Unfortunately by arguing thusly our dear professor is opening a can of worms for the entire common descent framework in that he is tacitly “refuting” the evidence for common descent. One of the oft-cited evidences for common descent are the shared insertion sites of endogenous retroviruses between humans and chimpanzees. However, if we are to accept Prof. Moran’s dictum that something having a probability of occurring of 10^-64 is in fact perfectly plausible, then we must accept that it is perfectly plausible that the shared ERV insertion sites between humans and chimpanzees may be the result of mere coincidence. Prof. Moran is trying to have it both ways but that is a of course a blatant contradiction.
Moreover, I would like to ask Prof. Moran to please explain to me in terms of probability, why precisely polyvalent antimalarial treatments are more effective than standard treatments? It seems as if Prof. Moran is wishing to go against the peer-reviewed literature, where we see that White (2004) says,
"If two drugs are used with different modes of action, and therefore different resistance mechanisms, then the per-parasite probability of developing resistance to both drugs is the product of their individual per-parasite probabilities. This is particularly powerful in malaria, because there are only about 1017 malaria parasites in the entire world. For example, if the per-parasite probabilities of developing resistance to drug A and drug B are both 1 in 1012, then a simultaneously resistant mutant will arise spontaneously every 1 in 1024 parasites. As there is a cumulative total of less than 1020 malaria parasites in existence in one year, such a simultaneously resistant parasite would arise spontaneously roughly once every 10,000 years — provided the drugs always confronted the parasites in combination. Thus the lower the de novo per-parasite probability of developing resistance, the greater the delay in the emergence of resistance.”
Now, to support my assertion that it is implausible to expect Darwinian processes to produce a biochemical system having a probability of origin less than 10^40, we must merely use a little logic.
If the per-E.coli probability of evolving biochemical system A is 10^40, then a mutant E. coli with this biochemical system will arise every 1 in 10^40 cells. As there is a cumulative total of about 10^30 bacterial cells in existence in one year [Whitman et al. 1998], such a mutant E. coli would arise roughly once every 3.55 billion years.
Sound familiar? I’m using the exact same math that White 2004 is using, yet amusingly I don’t see Prof. Moran talking about how the referee(s) of White’s paper messed up in their review of his paper; nor for that matter do I see him criticizing N.J. White’s work; nor for that matter have I seen a letter from Prof. Moran to the Journal of Clinical Investigation correcting White’s work. I wonder why that could be? Oh right, I forgot, I’m advocating intelligent design so only I can be wrong when I use the same reasoning a peer-reviewed paper uses. Neat, isn’t it?
References:
1. White, Nicholas J. Antimalarial drug resistance. J. Clin. Invest, 113(8):1084–1092 (2004).
2. Whitman W.B, Coleman D.C, Wiebe W.J. Prokaryotes: the unseen majority Proc. Natl Acad. Sci. 95(12): 6578-6583 (1998).
Addendum: I said that,
"If the per-E.coli probability of evolving biochemical system A is 10^40, then a mutant E. coli with this biochemical system will arise every 1 in 10^40 cells. As there is a cumulative total of about 10^30 bacterial cells in existence in one year [Whitman et al. 1998], such a mutant E. coli would arise roughly once every 3.55 billion years."
I might add that " thus the lower the per-E.coli probability of developing biochemical system A the greater the delay in the emergence of biochemical system A", a statement consistent with White's paper.
Addendum: I said that,
"If the per-E.coli probability of evolving biochemical system A is 10^40, then a mutant E. coli with this biochemical system will arise every 1 in 10^40 cells. As there is a cumulative total of about 10^30 bacterial cells in existence in one year [Whitman et al. 1998], such a mutant E. coli would arise roughly once every 3.55 billion years."
I might add that " thus the lower the per-E.coli probability of developing biochemical system A the greater the delay in the emergence of biochemical system A", a statement consistent with White's paper.
