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Bill Dembski and the case of the unsupported assertion
By Matt
Inlay
Posted February 19, 2005
While ID 'scientists' vociferously object to being labeled
creationists, they share one notable feature with the creation scientists of
the 80s: their frequent use of discredited sources. In a 1983 PBS special, Duane Gish of the Institute for
Creation Research (ICR), a YEC institution, claimed that certain human proteins
were more similar to bullfrog proteins than chimpanzee homologues, a claim that
would be nearly inexplicable if our current understanding of evolution was
correct. However, despite
countless public and private requests spanning the last 20 years, Gish has
never provided a source for that claim, nor retracted it (see here for more). A few years ago, Bill
Dembski claimed that there was evidence of a biochemical system for which any
slight modification would not only destroy the system's current function, but
any possible function of that system whatsoever. He concluded that such a system could not have evolved
through 'Darwinian' evolution, because of the supposed lack of functional
intermediates between the current system and any hypothetical precursor. However, as I document in this post,
not only is Dembski's claim unsupported by his lone source, Dembski admits
this, and yet he continues to assert that claim, even strengthening it in
recent writings. One of those
writings was even published in the IDists' "peer-reviewed" journal PCID,
despite the editors' knowledge that this claim was unsupported. The intention of this blog entry is to
add yet another example to the list of shoddy scholarship inherent in IDist
writings.
The intelligent design argument basically consists of two
parts. The first is the claim that
evolution cannot explain the origin of certain features of life. The second is that "intelligence"
can, and therefore serves as a better explanation for the origin of
those features. In his 1996 book
Darwin's Black Box, Michael Behe made the first half of the argument
regarding irreducibly complex (IC) biochemical systems, which are supposedly so
complex that they defy evolutionary explanation. Because Behe felt there were no "detailed, testable models"
to explain the origin of IC systems, no such explanations were possible. While detailed, testable models for the
origin of IC systems already existed prior to DBB, and even more have emerged
since its publication, IDists reject those explanations as not being detailed
or testable enough for their satisfaction (see the Talkdesign article
ID demystified
for a more thorough analysis).
Even if we took this argument at face value, it still suffers from a
major oversight. Just because
there's no known natural mechanism for the origin of IC systems now,
doesn't necessarily mean there won't be any in the future. In other words, absence of evidence is
not evidence of absence.
Commonly referred to as the appeal to ignorance, this fallacy is
extremely important to the intelligent design argument because there is no
evidentiary support for intelligent design (like, say, evidence
of a designer). However, it
is very easy for even a beginning biology grad student to propose a
hypothetical model for the origin of an IC system. What IDists needed to keep this
argument from being fallacious was a way to not only eliminate known
natural mechanisms, but also unknown ones as well. In describing his October 2002 article,
"The Logical Underpinnings of ID", Bill Dembski made such a claim:
I also note that there can be cases where all
material mechanisms (known and unknown) can be precluded decisively.
The relevant section is on page 20, where he writes:
But there is now mounting evidence of biological
systems for which any slight modification does not merely destroy the system's
existing function, but also destroys the possibility of any function of the
system whatsoever (Axe, 2000). For such systems, neither direct nor indirect
Darwinian pathways could account for them. In that case we would be dealing with an in-principle
argument showing not merely that no known material mechanism is capable of
accounting for the system but also that any unknown material mechanism is
incapable of accounting for it as well.
Wow, that's a pretty bold claim. This assertion, if true, might be considered pretty damning
evidence against evolution.
However, Dembski offers only a single citation to back this claim, a
2000 Journal of Molecular Biology paper
by Douglas Axe entitled, "Extreme Functional Sensitivity to Conservative Amino
Acid Changes on Enzyme Exteriors".
Does this article really support Dembski's claim? Not even close.
Summary of Axe 2000
In the article, Axe reports the results of a series of
mutagenesis experiments, focusing primarily on the TEM-1 gene, a bacterial
beta-lactamase that confers resistance to the antibiotics penicillin and
ampicillin. Axe made
conservative amino acid substitutions to residues on the exterior of this
protein. Conservative
substitutions are ones that exchange an amino acid for another with the same
basic shape and charge (e.g. leucine to isoleucine, arginine to lysine). Additionally, because those residues
are outside of the active site, they are not considered to have an effect on
the activity of a protein.
Therefore, evolutionary theory would predict that those residues could
switch to other similar amino acids via neutral evolution. Axe tested this prediction by making an
increasing number of conservative substitutions to see how many the protein
could tolerate while still retaining function. He made four groups of substitutions (blaM, blaY, blaG, and
blaB), with 10 substitutions in each group. Here are the results, in his own words:
The single-group substitutions in blaM, blaY, and
blaG affect function only mildly, yet these substitutions result in >99%
inactivation when combined.
Only the combination of all four groups resulted in the
complete inactivation of the protein's activity. Based on these experiments, Axe
concluded that the exterior residues of a protein are more sensitive to
conservative substitutions than previously thought.
Let's compare this to Dembski's interpretation:
any slight modification does not merely destroy the
system's existing function, but also destroys the possibility of any function
of the system whatsoever.
On at least four levels Dembski's conclusion regarding the
Axe paper is completely and utterly wrong.
1.
Any slight modification destroys the function of the
system.
(note that I'm paraphrasing Dembski)
All of the single-group substitutions retained their
beta-lactamase activity. Only when
they were combined into triple and quadruple group mutations was activity
abolished. So clearly there were
modifications that did not destroy the function of the system.
2. Any
slight modification destroys the function of the system.
As previously mentioned, at least 30 substitutions were
required to reduce activity greater than 99%, and 40 mutations to completely
abolish it. This amounts to about
20% of the exterior residues, or 10% of the total protein. This can hardly be considered "slight",
by any definition of the word.
One substitution would be considered slight, not 30 to 40. This is not just a semantic quibble, as
the changes that occur during the course of gradual, 'Darwinian' evolution
occur one substitution at a time (except in cases of recombination and exon
shuffling).
3. Any
slight modification does not merely destroy the system's existing function, but
also destroys the possibility of any function of the system
whatsoever.
I don't know how Dembski can claim that the mutations
destroyed other functions of the system, since Axe never tested for other
functions. This is basically an
appeal to ignorance. However, as
it turns out, another group
analyzed mutations in the active site of the exact same gene (TEM-1) and
found that certain "slight modifications" drastically reduced the original
function of the system (penicillin and ampicillin resistance), but
increased a separate, distinct function (cephalosporin resistance). In their words:
When purified, mutant enzymes had increased activity
against cephalosporin antibiotics but lost both thermodynamic stability and
kinetic activity against their ancestral targets, penicillins.
(It should be noted that these researchers studied mutations
within the active site, whereas Axe made mutations on the exterior of the
protein.) So contrary to Dembski's
claim, mutations that result in the loss of the original function do not
necessarily cause the loss of any possible function. This is significant because a major
contention of Dembski's is that protein sequences that contain a function are
completely isolated from one another, such that random mutation cannot create
one functional protein from another without passing through a non-functional
state. However, recent research
has shown that oftentimes mutations can increase the activity of a new function
of a protein without seriously hindering the protein's original
function, a concept known as promiscuity.
Steve Reuland has blogged this topic here.
4. Any
slight modification does not merely destroy the system's existing function, but
also destroys the possibility of any function of the system
whatsoever.
This point is a little confusing, but if you read Dembski's
claim as a whole, you can infer what I think Dembski is really trying to get
at. There are some mutations that
can completely destroy a protein's function. Nonsense mutations, whereby a codon is mutated into a stop
codon, creating a truncated protein, is one example. However, many truncated proteins still retain some
function. Frameshift mutations,
where a nucleotide is either inserted or deleted from the gene, altering its
reading frame, more often than not leads to a nonfunctional protein (for
example, trying shifting your hand one key to the right and typing a
sentence). However, I think what
Dembski is trying to claim is a third possibility, that certain single amino
acid substitutions can drastically affect the stability of the protein. If, at a key residue, a charged amino
acid is substituted for a nonpolar one, or vice versa, this could lead to the
inability of the protein to fold properly and rendering it useless. In this case, you could say the
mutation destroyed all possibility of function. However, this is a rare event (I can't
think of an example), and certainly not demonstrated in the Axe paper. For Dembski's claim to be accurate, he
would need to find a protein for which all mutations catastrophically
disrupt the stability of the protein.
Axe never found a single catastrophic mutation in TEM-1, but
plenty of non-catastrophic ones.
Each of these errors by themselves is enough to derail
Dembski's conclusion. Furthermore,
each of the four points is absolutely necessary for Dembski to make the
conclusion "not merely that no known material mechanism is capable of
accounting for the system but also that any unknown material mechanism is
incapable of accounting for it as well".
Taken together, these errors demonstrate that either Dembski really
doesn't understand the evidence, or that he is willfully misinterpreting
it. While Dembski is not a
biologist, and frequently makes claims regarding biology that display a
fundamental lack of understanding of the field (see this thread
for an example), I'm more inclined toward the latter. In fairness to Axe, his research wasn't even about Darwinian
evolution or the origin of new protein functions. Rather, he focused on the amount of "drift" a protein's
exterior can endure while still retaining function, which is an issue of
neutral evolution. In fact, Axe,
when asked directly whether his work supports Dembski's conclusions, remained
neutral on the topic, despite the fact that his research was supported in part
by funding from the DI, and he was a senior fellow of the DI. Here are his own words, as said in
Forrest and Gross' Creationism's Trojan Horse [1]:
These three statements summarize my position:
- I
remain open-minded with respect to the possibility that a sound argument can be
made for intelligent design in biology.
- I
have not attempted to make such an argument in any publications.
- Since
I understand that Bill Dembski has referred to my work in making such an
argument, I shall remain open to the possibility that my published findings may
support such an inference until I have had a chance to see his
argument.
See Trojan Horse if you want to read more about Axe's
association with the DI.
Calling Dembski's bluff
When Dembski first announced his "Logical Underpinnings of
ID" article on the ISCID forum in November
2002, ID critics immediately pounced on him for making such an unsupported
claim. After repeatedly hounding
him, Dembski finally conceded:
I met with Douglas Axe at the recent RAPID conference
and I've had a preview of where his research is going for some time (at least
since the summer of 2000), so in reading his JMB paper, I'm anticipating
where's he's going. I agree that the JMB paper does not resolve the issues
we are debating. That's why I put it in terms of "preliminary
indications."
(boldface added for emphasis)
So essentially Dembski agreed that his claim was unsupported
by the Axe paper. Is it ethical to
make an assertion using a reference that you know does not support it?
Ironically, one ISCID forum participant, "charlie_d"
commented,
Hopefully, this very basic mistake will now cease to
find its way into ID literature.
Unfortunately, he was very much mistaken.
Nearly a year later, in September 2003, Dembski again
mentions the Axe paper, this time in an FAQ
entitled, "Three Frequently Asked Questions About Intelligent Design", as an
example of research supporting intelligent design in the peer-reviewed
literature.
This work shows that certain enzymes are extremely
sensitive to perturbation. Perturbation in this case does not simply diminish
existing function or alter function, but removes all possibility of function.
This implies that neo-Darwinian theory has no purchase on these
systems.
Not only does Dembski not soften his interpretation of the
paper, he no longer bothers to qualify it as a "preliminary indication". He did remove the "any slight
modification" phrase, replacing it with the more nebulous "perturbation". However, I don't think readers will
assume that perturbation means "30 to 40 amino acid substitutions", especially
considering that "neo-Darwinian theory" does not propose that proteins evolve
30 to 40 mutations at a time.
In January 2004, Dembski submitted another
article
for publication on ISCID's online journal PCID. This article, titled "Irreducible Complexity Revisted",
purported to clarify the IC argument with greater scientific detail. Notice this passage, from page 34.
Moreover, recent work on the extreme functional
sensitivity of proteins provides strong evidence that certain classes of
proteins are in principle unevolvable by gradual means (and thus a fortiori by
the Darwinian mechanism) because small perturbations of these proteins destroy
all conceivable biological function (and not merely existing biological
function).31
Yes, reference 31 is Axe 2000. Rather than tone the comment down, Dembski apparently
decided to bump his claim up a notch or two. Now "preliminary indications" has evolved into "strong
evidence", and "perturbations" into "small perturbations". Again Dembski implies that 30 amino
acid substitutions is "gradual".
So even though Dembski himself admitted over a year ago that this claim
was unsupported by Axe 2000, he felt no obligation to leave it out of future
writings. Why correct when you can
just reassert?
Articles submitted for publication on PCID often have
threads created for them on the ISCID chat forum, to allow readers the
opportunity to comment on the article.
I was so disgusted by this article (sadly, his repeated unsupported
assertion wasn't even its biggest problem, see Mark Perakh's PT
post for more), I
challenged the PCID editors (Micah
Sparacio and John Bracht) to correct it in that ISCID thread.
there is at least one instance here where an
erroneous interpretation, by dembski, of an article he cited that was corrected
by ID critics on this very forum, was repeated again in this article....
i think micah and john need to do some serious
soul-searching and decide if this is the kind of material they want ISCID to be
known for. i realize that ISCID doesn't reject many articles, especially those
submitted by their big-wigs, but if the editors of PCID want to continue to
call their journal "peer-reviewed", then they need to take
responsibility for the material they present.
They certainly saw my challenge, because Micah offered this
in response:
as a note, an article published in the Archive is not
necessarily published in PCID. Dembski's article, featured in this thread, has
not yet been chosen for an issue of PCID.
According to their review
standards, articles are first placed in the archive as a draft, where they are
then subject to review by one or more of the ISCID fellows. Only after they are reviewed are they
eligible for publication in PCID. Also
of note is this requirement: "articles need to meet basic scholarly
standards". Sure enough, the
article was published in the next
issue
of PCID. Was the statement citing
the Axe paper removed? Nope.
Moreover, recent work on the extreme functional
sensitivity of proteins provides strong evidence that certain classes of
proteins are in principle unevolvable by gradual means (and thus a fortiori by the
Darwinian mechanism) because small perturbations of these proteins destroy all
conceivable biological function (and not merely existing biological
function).31
So clearly, correctly supporting statements central to the
primary focus of the article is not considered a "basic scholarly standard" for
PCID.
Accountability
On another
thread,
created solely to discuss Axe's paper, in which PCID editor John Bracht
participated in, "charlie_d" asked John this question:
what do you think about instituting internal
peer-review panels?
While John did not reply, another ISCID heavyweight, Paul
Nelson, said this:
I think it's a good idea. Something more informal
than Charlie's suggestion -- in the way of critical peer review -- is already
going on (e.g., at the recent RAPID meeting), but as the ID research community
matures, it's going to need robust internal quality controls.
So here we have an example of the robust internal quality
controls displayed by the ISCID fellows.
Ironically, I also made this statement when "IC Revisited" was first
made public:
i think it's safe to assume that in the coming
months, this article will be added to the pile of references ID proponents cite
when their ideas are questioned by school boards or the press. the next time
someone brings up a specific critique of IC, some DI rep like dembski will
dismiss their critique as having been answered in this article. we've seen it
before, we'll see it again. the purpose of all of this is to give the
appearance of a controversy.
And in that same issue of PCID:
Irreducible
Complexity Reduced
Dembski shows
that this common refrain [that "Behe's arguments have somehow been refuted"] is
inaccurate at best, and that the intervening period since the publication of
Darwin's Black Box has only underscored the acute lack of any meaningful
explanation for the existence of irreducibly complex systems on the basis of
Darwinian principles.
Is this really the quality of scholarship we can expect from
PCID? I hope that either Dembski
or the PCID editors offer a correction, or at least a defense of Dembski's
continued use of this unsupported assertion. If nothing else, he should at least stop using it, since he
himself admits that the source does not support his claim. While I doubt any of this will happen,
at least we have a documented example of the poor scholarship that IDists
display in their works.
Footnotes:
1. Forrest and
Gross, Creationism's Trojan Horse 2003, pages 40-42
(edited 2/16 to add a trackback to Mark Perakh's
post on IC
revisted)
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