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Message from discussion Finally lost faith in I.D.
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Wade Hines  
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 More options Jan 19 2002, 3:46 pm
Newsgroups: talk.origins
From: Wade Hines <wade.hi...@rcn.com>
Date: 19 Jan 2002 15:43:12 -0500
Local: Sat, Jan 19 2002 3:43 pm
Subject: Re: Finally lost faith in I.D.
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Richard Alexander wrote:

> Wade Hines <wade.hi...@rcn.com> wrote in message <news:3C47AFD0.6D2506E5@rcn.com>...
> > Richard Alexander wrote:

> > > Bob Casanova <nos...@buzz.off> wrote in message <news:7rje4usq1o67ofc9r7n6foqs5sdb6b3agt@4ax.com>...

> > > > IIRC what has been
> > > > shown is that there is no such thing as an irreducibly
> > > > complex biological structure anywhere in nature. Behe's
> > > > definition of IC as "remove any part and it doesn't work" is
> > > > a strawman; the correct definition of IC from the standpoint
> > > > of descent with modification would be "a structure which
> > > > *could not* have been produced by descent with
> > > > modification"; such structures have never been observed. Or
> > > > am I incorrect?

> > > AFAIK, the only way to produce an irreducibly complex structure is
> > > through the use of a scaffolding or support mechanism. The trouble the
> > > support mechanism would have to take into account the needs of the
> > > structure being built, in addition to its own structural needs; thus,
> > > it would seem the scaffolding would need to be more complex than the
> > > structure being built. Another problem is in wondering why the support
> > > mechanism would exist, then disappear?

> > Hemoglobin is IC.

> I don't know why you think so. Behe makes the case in DBB that
> hemoglobin is *not* IC, due to it being a minor variation of
> myoglobin.

No he doesn't. Please read what you have quoted again. He does
argue that we can't infer design from hemoglobin. He does not
argue it isn't IC.

I will add more about Behe's attempt to minimize the functional
difference between hemoglobin and myoglobin.

> One of the conditions for being IC is that the system
> cannot be produced by simply re-arranging the component parts. Behe
> makes discusses hemoglobin on Page 207.

> "There is also another protein, called myoglobin, that is very similar
> to
> hemoglobin except that it has only one protein chain, not four, and
> therefore binds only one oxygen. The binding of oxygen to myoglobin is
> not cooperative. The question is, if we assume that we already have an
> oxygen-binding protein like myoglobin, can we infer intelligent design
> from the function of hemoglobin? The case for design is weak. The
> starting point, myoglobin, already can bind oxygen. The behavior of
> hemoglobin can be achieved by a rather simple modification of the
> behavior of myoglobin, and the individual proteins of hemoglobin
> strongly resemble myoglobin. So although hemoglobin can be thought of
> as a system with interacting parts, the interaction does nothing much
> that
> is clearly beyond the individual components of the system. Given the
> starting point of myoglobin, I would say that hemoglobin shows the
> same evidence for design as does the man in the moon: intriguing, but
> far from convincing."

Again, Behe did not make a case that hemoglobin is not IC, rather he
says it makes a poor case for design. It would be more honest of him
to say it is a well studied case that is fully explainable by the
well studied mechanisms of evolution.

Behe mentions cooperativity but does not say what it is or why it is
essential to the function of hemoglobin in mammals. This seems unfair
given his take on blood clotting where he demands full functionality
as in his criticisms of Doolittles counter examples of clotting as
IC. Cooperativity is required for efficient loading and unloading
of oxygen by the blood. Further, hemoglobin must be sensitive to
other allosteric effectors to further modulate O2 binding sensitive
to tissue type and stress levels. By the standards Behe employes
respective to blood clotting, these are essential aspects of the
function of hemoglobin.

There are however, many observable intermediates between organisms
that only have simple O2 binding proteins like myoglobin and more
complex systems like avian and mammalian hemoglobin. The evolutionary
route between them is well understood.

> Behe cites the case of hemoglobin in his sub-section, "Making
> Distinctions," in which he states,

> "Just because we can infer that some biochemical systems were designed
> does not mean that all subcellular systems were explicitly
> designed.... let's take a brief look at a couple of systems where
> design is hard to see."

Again, Behe is distancing himself from an inference of design, not from
the systems being IC. IC is not the same as design as Behe is sometimes
careful to point out. The point seems to be lost in some readers, perhaps
because Behe isn't clear enough. Hemoglobin is IC by the definition and
standards that Behe employs. It is not only true that "the case for design
is weak": rather the case for evolution of hemoglobin is very very strong.

> > The Krebs cycle is IC.
> Again, I don't know why you think so, but maybe that is due to my
> ignorance of the system? Behe makes the point that the AMP cycle is
> IC, because AMP is required to make AMP in all known organisms. I
> never studied the citric acid cycle, so I don't know why you consider
> the Krebs cycle to be IC.

Refer to Behe's definition of IC. Remove one of the enzymes of the
Krebs cycle and the cycle is broken. This means it stops cycling:
it would cease to function.

There are alternative cycles. You may consider those as "scaffolding"
in your usage, I don't know. The same enzymes used in the Krebs cycle
are used in other cycles. The point here is that it is relatively
trivial to produce one specific cycle from enzymes that were allocated
to other "systems".

If you apply some critical thinking, you'll quickly see that "systems"
and "function" are rather capricious criteria. The depend on perspective
and there isn't any OneTrue perspective. Even Behe's perspective that
hemoglobin isn't that big a deal given myoglobin is a valid perspective
but please recognize it is akin to the perspective that the blood clotting
cascade isn't a big deal given zymogen proteases active against
fibrinogen.

> > The evolution of these systems do not require scaffolding.
> Well, apparently they aren't IC, either, so that they require no
> scaffolding is no wonder.

Again, reread what you quoted. You seem to be missing what Behe
explicityly says as well as missing his switching standards.

> > To the extent that blood clotting is IC, it does not require scaffolding.
> To form? Why do you say so?
> > So what are you talking about?
> Let's deal with the basics, first, and then maybe the other questions
> will have answers.
> > Consider mammalian hemoglobin with alpha and beta chains. Just
> > mamalian beta won't make a functional hemoglobin and neither
> > will just mammalian alpha.
> I'm guessing from their names that the two are variations of each
> other? Are both required for the production of either? Of course,
> that's moot, because Behe already pointed out that hemoglobin is not
> IC.

Behe says that hemoglobin is a poor case for design. He does not say
it isn't IC. Even if he does say it isn't IC, it fits his definition
of IC because if you remove either alpha or beta hemoglobin, your
blood won't be able to transport enough O2 from your lungs to your
tissues to support a viable existence. This is the standard he uses
for criticisms of his claim that blood clotting is IC. Either you use
the same standards all the time or else you don't have standards
and it's more like something out of Alice in Wonderland.

> > It is likewise currently required
> > that a fetus express variant forms of hemoglobin to extract O2
> > from the placenta.
> I do not see what steps your logic has taken in your argument.

If one looks a O2 transport in humans, one must consider the
case of a mother's lungs being used to supply O2 to a developing
fetus. This requires a hand off of O2 in the placenta. For this
to be effective, the fetus must have hemoglobin with a higher
affinity of O2 than does the mother. This is accomplished by
yet another variant hemoglobin chain beyond alpha and beta.
The seqeunce of delta (fetal) hemoglobin is similar to beta
I believe. It fits a model of gene duplication and divergence.
It represents yet another "system" of O2 transport that is more
complex than lungs --> tissue --> mylogobin and requires three
distinct genes rather than two. As per the definition of IC,
if you remove any of the proteins in question, the system will
fail to function. The evolution of this system requires duplication
and divergence but does not require any "scaffolding". It thus
refutes your contention that scaffolding is required to produce
IC systems.

I agree with Behe that these systems are poor cases for design.
Rather they are clear cases of evolution that have left many
footprints for those trained in reading the tracks of molecular
genetics. Whether or not Behe admits these systems are IC, they
fit his definitions of IC. Thus, not only can IC systems evolve,
there are IC systems that are strongly evidenced as having
evolved as per the example of hemoglobin.

> > How does the evolution of these systems require scaffolding?
> Maybe they don't, because it appears the systems you named aren't IC.

Feel free to show that using the definition of IC. The parts are
alpha and beta hemoglobin. The function if O2 transportation
in mammals. Alternatively, the parts are alpha, beta and delta
hemoglobin and the function is reproduction of viable babies
in humans. Remove any part and the systems ceases to function.
Is that, or is that not the very definition of IC?

> > > There have been several challenges to Behe's suggested examples of
> > > irreducible complexity. Here is a snippet from one of his replies:

> > > "In Darwin's Black Box: The Biochemical Challenge to Evolution I
> > > devoted a chapter to the mechanism of blood clotting, arguing that it
> > > is irreducibly complex and therefore a big problem for Darwinian
> > > evolution. Since my book came out, as far as I am aware there have
> > > been no papers published in the scientific literature giving a
> > > detailed scenario or experiments to show how natural selection could
> > > have built the system. However three scientists publishing outside
> > > science journals have attempted to respond. The first is Russell
> > > Doolittle, a professor of biochemistry at the University of California
> > > at San Diego, member of the National Academy of Sciences, and expert
> > > on blood clotting. Second is Kenneth Miller, a professor of cell
> > > biology at Brown University and author of Finding Darwin's God (Miller
> > > 1999). The third scientist is Keith Robison, who at the time of his
> > > writing was a graduate student at Harvard University.

> > > "I will give their arguments below and my response. Here is a brief
> > > summary.
> >   ...

> > > "3) Keith Robison proposed that a cascade might begin with a single
> > > enzyme with three different properties. Upon duplication of the gene
> > > for the enzyme, the duplicate loses several of the properties,
> > > resulting in a two-component cascade. Repetition of the scenario
> > > builds cascades with more components. Although intriguing, the
> > > scenario starts with a complex, unjustified situation (the enzyme with
> > > multiple abilities) that already has all necessary activities.

> > That's very untrue. Keith made the situation clear enough. There isn't
> > a need for clotting capable of stoping high pressure blood flow at the
> > start. Behe's comments here are quite absurd.

> I don't know very much about this, but I can see that clotting must be
> able to stop high pressure blood flow in humans. Could you present the
> pathway of modification of clotting from low-pressure to high-pressure
> systems without having to invent IC parts?

Others have presented that the precursors of blood clotting are related
molecules that trap pathogens in Invertebrates. It's been discussed
elsewhere in this thread.
http://groups.google.com/groups?selm=3C488ADC.C7C7510A%40rcn.com

The primative systems create a fiberous mesh to trap a pathogen. The
conversion of the precursor of the fiberous proteins are activated
by proteolysis just as in blood coagulation. The sequences of relavant
proteins show similarity and thus imply homology. It isn't suprising
that the evolution of clotting and immunity run in parallel with
similar precursor. Both derive from a response to tissue damage where
the challenge is to stop bad guys from getting in and good stuff
from leaking out.

As to inventing parts, refer to Keith's presentation. The "invention"
of new parts is by the same mechanism of duplication and divergence
that Behe notes respective to myoglobin becoming alpha and beta (and
delta) hemoglobin. There he recognizes the sequence similarity and
acknowledges that the case for design is poor. The same principles
are at work for blood clotting. The sequence similarities are not
as high but they are still hugely significant.


 
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