RE: [asa] FYI: Arrogance, dogma and why science - not faith - is the new enemy of

From: John Walley <>
Date: Thu Aug 23 2007 - 07:43:53 EDT

All in all, Behe's arguments sound poorly founded in data, contradicted by
data and irrelevant to any discussion of the edge of evolution other than by
accepting that 1 in 10^40 may be insurmountable odds but Behe has done
little to show that any evolutionary transition has such odds. To conclude
design in face of these major shortcomings seems to do a disservice to
science and faith alike.

Agreed that Behe should not conclude Design but my takeaway here is that at
best, you can say that malaria and its evolutionary history is not a
relevant gauge of the power of evolution in general. This leads me back to
my original point that most of the reviews of Behe's book took issue with
his numbers and how many mutations may be observed, but none substantively
showed that his basic premise of there existing an edge to evolution was

How do we really know that the current evolutionary theory of compounding
complexity and the continuum of molecules to man is not mostly "fanciful
Darwinian speculations" like Behe suggests? How often do we observe gene
duplication in the lab and how often should we expect to find that in
nature? Why did we not see it in malaria?

I am familiar with Sean Carroll's popular book on the forensic DNA evidence
of evolution and I agree that it is a logical and rational way to explain
the power of evolution but in fairness, a new species of ice cod fish
without hemoglobin and color vision in monkeys is not all that powerful.
This fits easily on this side of Behe's edge of species and classes.

What would disprove this premise of an edge of evolution? What would it take
to show empirically that Behe is wrong and that evolution can do all that
Dawkins suggests? How could we ever settle the Design debate conclusively?

Behe may be guilty of assuming uniformity and extrapolating the evolutionary
history of malaria on to humans when it may not be the same, but Carroll and
others are just as guilty of finding a few forensic single point mutations
and concluding evolution as a fait accompli.

Just to get from chimps to humans we need on the order of millions of just
right sequential mutations but here in this thread Behe's edge of 2
mutations was dismissed due to the evidence of another example of a whopping
5 mutations.

Is it just Behe and I or does the hard evidence for macroevolution beyond
just theories and conjecture seem somewhat faith based?


-----Original Message-----
From: PvM []
Sent: Wednesday, August 22, 2007 12:35 AM
To: John Walley
Cc: AmericanScientificAffiliation
Subject: Re: [asa] FYI: Arrogance, dogma and why science - not faith - is
the new enemy of

So what's the story so far.

Malaria, a deadly parasite, managed to develop chloroquine resistance
in a period of 10-50 years, in 5-8 different instances, perhaps fewer.
In order for malaria to acquire said resistance, the data suggest that
at a minimum a mutation at location K76T is needed and since such a
mutation in the wild type leads to non viable organisms, one or more
compensatory mutations are needed, such as A220S.

So far so good. Now Malaria is caused by an interesting creature which
reproduces both sexually and asexually. Since it gets transported in
mosquitos, the life cycle of the plasmodium is quite complex. I
believe that it only reproduces sexually while in the mosquito. See

<quote>The life cycle of all Plasmodium species is complex. Infection
in humans begins with the bite of an infected female Anopheline
mosquito. Sporozoites released from the salivary glands of the
mosquito enter the bloodstream during feeding quickly invade liver
cells (hepatocytes). Sporozoites are cleared from the circulation
within 30 minutes. During the next 14 days in the case of P.
falciparum, the liver-stage parasites differentiate and undergo
asexual multiplication resulting in tens of thousands of merozoites
which burst from the hepatoctye. Individual merozoites invade red
blood cells (erythrocytes) and undergo an additional round of
multiplication producing 12- 16 merozoites within a schizont. The
length of this erythrocytic stage of the parasite life cycle depends
on the parasite species: 48 hours for P. falciparum, P. vivax, and P.
ovale and 72 hours for P. malariae. The clinical manifestations of
malaria, fever and chills, are associated with the synchronous rupture
of the infected erythrocyte. The released merozoites go on to invade
additional erythrocytes. Not all of the merozoites divide into
schizonts, some differentiate into sexual forms, male and female
gametocytes. These gametocytes are taken up by a female anophylean
mosquito during a blood meal. Within the mosquito midgut, the male
gametocyte undergoes a rapid nuclear division, producing 8 flagellated
microgamtes which fertilize the female macrogamete. The resulting
ookinete traverses the mosquito gut wall and encysts on the exterior
of the gut wall as a oocyst. Soon the oocyst ruptures, releasing
hundreds of sporozoites into the mosquito body cavity where they

So the malaria example used by Behe suffers from some significant
problems but things do get worse.

So first back to the double mutation. Behe's calculations are that the
mutations happen simultaneously, although as reported recently by
Randy, Behe suggests that his calculation includes the various
aspects. However, he never presents his own calculation and relies on
a very speculative guess by White. Surely one would expect Behe to do
the hard work to establish the boundary of evolution more carefully
than this?

For instance, assume that 1 in 100,000 parasites has a neutral
mutation at A220S, the probability of chloroquine resistance arising
by chance now is reduced to 10^10*105 or one in 10^15. Since a 2%
infected human carries 10^12 plasmodium parasites, it does not take
much to meet the odds.
In fact, one of the parasites 106/1 found in the Sudan has all the
supplementary mutations found in a chloroquine resistant strain except
for K76T which is essential. Under selective pressures, K76T evolves
quite rapidly as expected. So it depends on the genetic background.
And malaria is well known for its extremely varied genetic background
which enables it to be prepared for anything its host may throw at it.

Now we get to linkage disequilibrium and the Hill-Robertson effect
which is important in clonal interference in sexual species, causing
the actual mutation rate to be much lower than the natural one. All in
all, there are various reasons why Behe's numbers are suspect and he
does not help his case by not presenting his own calculations leading
to the 1 in 10^20, a guestimate which is marked as uncertain and
speculative by the original source.

In the last few days I have learned more about malaria than I ever
hoped to know and I have found the research fascinating as it shows
how science is slowly unraveling the history of malaria and
chloroquine resistance. In addition, research has found how malaria
shows a much longer history of competing with humans in an ever
expanding race between predator and prey.

All in all, Behe's arguments sound poorly founded in data,
contradicted by data and irrelevant to any discussion of the edge of
evolution other than by accepting that 1 in 10^40 may be
insurmountable odds but Behe has done little to show that any
evolutionary transition has such odds. To conclude design in face of
these major shortcomings seems to do a disservice to science and faith

In the next few months we can expect many more reviews of Behe's
thesis and I predict that we will see few if any explanations as to
how ID explains the data, other than by assigning it a label
'designed' rather than admitting the 'we don't know yet but we are
learning more and more' label it really deserves.

This has been a fun learning experience and I hope to be writing up
the lessons learned in a more detailed posting addressing the many
facets of issues surrounding the acquisition of chloroquine and other
drug resistance by the plasmodium parasite.

For instance, there is a documented case of a patient whose blood
showed initially wild type stains, but within 4 hours of the start of
treatment, a resistant strain had outcompeted the original strain.
This is one aspect of malaria which makes it such a hard parasite to
erradicate. Chloroquine, an intelligently designed substance, managed
to withstand the evolutionary pressures for a while but eventually
even intelligent design could not outsmart nature.

Chloroquine (Resochin) (1934, 1946)

Chloroquine was discovered by a German, Hans Andersag, in 1934 at
Bayer I.G. Farbenindustrie A.G. laboratories in Eberfeld, Germany. He
named his compound resochin. Through a series of lapses and confusion
brought about during the war, chloroquine was finally recognized and
established as an effective and safe antimalarial in 1946 by British
and U.S. scientists.

Some late news

This shows a fascinating progression of point mutations amongst 265
plasmodium isolates in India from the wildtype to the strongly
chloroquine resistant CIETS


where the letters stand for the aminoacid at locations 72 74 75 76 and
220 of pfcrt
same for the pfmdr1 gene..

Chloroquine resistance increased from small for CMNKA to intermediate
for SMNTS to strong for CIETS, just as expected.

In Genetic and Biochemical Aspects of Drug Resistance in Malaria
Parasites Hayton and Su show a nicely progressing trend in resistance
amongst 100+ isolates


Fascinating studies which show in further detail how malaria may not
be living up to Behe's expectations and hopes.


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Received on Thu Aug 23 07:44:54 2007

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