Re: [asa] Atheist finds God thru Behe's books....

From: Rich Blinne <>
Date: Tue Oct 13 2009 - 22:59:22 EDT

On Mon, Oct 12, 2009 at 11:45 AM, Cameron Wybrow <>wrote:

> It does not seem to me obvious what the right answer is, nor do some of
> the greatest philosophers of science (who have wrestled quite seriously with
> teleological explanation) think it is obvious what the right answer is; TE
> people, on the other hand, just take for granted that consistency of method
> trumps adequacy of explanation every time.
The reason why scientists insist on rigor is that it produces adequate
explanations while those whom try to "expand" the scientific method to get
around the rigorous requirements -- in part to explain why they don't end up
in peer-reviewed journals -- in the end produce less adequate explanations.
So called adequacy is a way to get the camel's nose in the tent. For
example, ID proponents want to use abduction rather than induction, cf.
Chapter 7 Signature in the Cell. The reason why induction is superior for
scientific study is that through the process of falsification errors in the
original "adequate" explanations can be removed or "inadequate" explanations
can be reconsidered. In general, MN is used because it's easier to produce
falsifiable propositions but as I will show MN is not necessary in order to
be in bounds of tightly-demarcated science. ID fails demarcation not because
it considers the natural effects of the supernatural but because it isn't
empirical and inductive.

Take the drug resistance of the malaria parasite in EoE. Behe claimed that
the "odds" of producing a drug-resistant strain was in essence impossible.
First off, let's assume for the sake of discussion the God of Scripture. He
created the Universe, sustains it, and is a God of order (cf. 1 Cor. 14). We
know for a fact that currently Plasmodium is resisting previously successful
drug therapies -- and this next point is very significant -- after a delay
where the therapies were very successful. We also know that the genetic
difference between the old and new strains is something that wouldn't easily
be achieved by a single mutation. Behe concedes both common descent and
natural selection. He does not concede that abilility of so-called random
mutation to generate parasites to select from. This leaves us with three

1. The drug-resistant parasites are the mutated descendants of the
non-drug-resistent ones. This Behe claims is impossible.

2. The drug-resistant strains already existed and were merely selected once
the drugs were introduced. This appears to be what Behe prefers. But there's
a problem. The delay. If the drug resistant parasites are available to be
selected population genetics tells us that they start taking over quickly.
More on this later.

3. The drug-resistant strains were created *de novo* by God after the drugs
were introduced. This possibility is not testable by science but is the only
option if 1 and 2 are eliminated. To use ID speak this is the most
"adequate" explanation. The theological implications of this are immense.
Behe claims that he is not out to prove the Christian God and this shows
that this is true. Behe has just proven an evil, pagan god. Tell all the
Christian doctors to pack it up because there is no way to know whether your
therapy will be directly thwarted by God.

Fortunately this inevitable conclusion that no Christian including Michael
Behe would want is solved by plain ole mainstream science. See this paper by
Rich Lenski as part of the LTEE (long term evolution experiment). They have
taken several lines of E Coli bacteria for decades and gave it an
environment rich in citrate which E Coli does not normally metabolize. For
many many generations the E Coli did nothing with it and then after 20 years
(33,127 generations) E Coli that metabolized citrate appeared and started to

The role of historical contingency in evolution has been much debated, but
> rarely tested. Twelve initially identical populations of *Escherichia coli
> * were founded in 1988 to investigate this issue. They have since evolved
> in a glucose-limited medium that also contains citrate, which *E. coli*cannot use as a carbon source under oxic conditions. No population evolved
> the capacity to exploit citrate for >30,000 generations, although each
> population tested billions of mutations. A citrate-using (Cit+) variant
> finally evolved in one population by 31,500 generations, causing an increase
> in population size and diversity. The long-delayed and unique evolution of
> this function might indicate the involvement of some extremely rare
> mutation. Alternately, it may involve an ordinary mutation, but one whose
> physical occurrence or phenotypic expression is contingent on prior
> mutations in that population. We tested these hypotheses in experiments that
> “replayed” evolution from different points in that population's history. *We
> observed no Cit+ mutants among 8.4 × 1012 ancestral cells, nor among 9 ×
> 1012+, indicating that some potentiating mutation arose by 20,000
> generations. This potentiating change increased the mutation rate to Cit+but did not cause generalized hypermutability. Thus, the evolution of this
> phenotype was contingent on the particular history of that population. More
> generally, we suggest that historical contingency is especially important
> when it facilitates the evolution of key innovations that are not easily
> evolved by gradual, cumulative selection.*

The relevance to Behe's example is he assumed that a single probability of a
giant mutation was applicable. In short, Behe assumes the mutations are
statistically independent. Rather, what Rich Lenski showed was a
potentiating mutation which made the rare jump easier (cf. Figures 1 and 3
of the paper) and the mutations are thus not statistically independent.

Viewed another way a prediction that something is impossible is falsified by
the existence of the impossible event. Unless you want to admit God created
a parasite deliberately to thwart drug therapy then the fact that Plasmodium
did mutate falsified Behe's "prediction". We see from Lenski et al the
prediction failed because Behe's view of mutation was flawed and
oversimplified. At least that's the way science normally operates but ID
wants it to be different so that normal falsification rules don't apply.

Rich Blinne
Member ASA

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Received on Tue Oct 13 23:00:05 2009

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