Actually, according to Art's own review, it is not evolution in general that
Spetner is critiquing, since he develops his own theory for how evolution
might have worked, but the neo-Darwinian theory of evolution. So Art's
editorial addition at this point is misleading. Ignoring that, however,
let's look at some of the other things Art says about Spetner.
>
> Chapter three concerns the Neodarwinian theory of evolution, asking the
> question: "Can random changes lead to new information?". Citing his own
> published work, much of it from the Journal of Theoretical Biology, he
> contends that even where information increase is possible the rate of
> mutation is far too low in the evolutionary time frame.
>
If Art's characterization is correct here, I find it interesting that Spetner
could find no other researcher who agrees with his conclusions. This does
not mean that Spetner is automatically wrong, but it does suggest that no one
else is impressed with his ideas.
Meanwhile there are other ideas that in fact can explain how neo-Darwinism
can increase information, and well within an evolutionary time frame. The
best in my opinion is the Brooks/Wiley/Collier theory. It links information
and evolutionary diversity with entropy, and demonstrates how increasing
diversity results in both an increase of entropy and an increase in
information. Its simplest demonstration of this is to set
information/entropy proportional to the number of possible microstates in a
systems. If a system consists of a population of animals and a microstate is
a genotype, then as the number of genotypes possessed by that population
increases, so does the entropy of the system, and thus so does the
information of the system. And since new genotypes are known to be made by
mutation, often of duplicated genes, this is a strong case demonstrating how
"random mutation and natural selection" can produce an increase in
information.
Notice also that this method of increasing information does not concern
itself with whether the new genotype represent more, less or about the same
genetic sequence information as previous genotypes. In other words, the new
genotype could be based on a deletion mutation of an existing genotype, thus
representing a loss of information on this scale, but because there is now a
new genotype in the population that did not exist before, at the scale of the
population information has increased. And the existence of a new genotype
far outways the loss of a single nucleotide, so the information increase at
the population level overrides the loss of information that occurred at the
genetic level.
>
> He considers the three types of arguments applied to support evolution.
>
It would have been helpful if Art had provided an example or two. However,
Brooks/Wiley/Collier theory has been used to analyze a number of different
evolutionary events, from population genetics to morphology and ontogeny, to
macroevolutionary change and macroecology, and in each case it has provided
adequate explanations for how evolution would work in those circumstances.
See _Evolution as Entropy_, Second Edition, by Daniel R. Brooks and E. O.
Wiley, for specific examples.
>
> Chapter four deals with the mechanisms for evolution. The tension is
> palpable between a system where errors are catastrophic and great
> effort is exerted to prevent them, and one where errors are required
> as the fuel for evolution. Then there is the question of how frequently
> a new mutation that is beneficial might arise. Using the numbers provided
> by evolutionary scientists, Spetner demonstrates that fixing a mutation
> with a slight advantage in a population is essentially impossible. He
> discusses parallel and convergent evolution, concluding that "·convergent
> evolution is impossible." He states "The average person finds it hard to
> believe that complexity and sophistication of such high order was
> developed by having natural selection organize random events·as we
> have seen·the average person's intuition is correct·"
>
Since Art explains nothing of how Spetner arrived at these conclusions, not
even in general terms, it is hard to evaluate what otherwise appear to be
bald assertions. It is therefore significant to point out that other
theories, such as Brooks/Wiley/Collier theory, come to the exact opposite
conclusions.
>
> Chapter five is the heart of the book. Here Spetner touches the soul of the
> inadequacy of evolutionary theory. Asking the question " Is there any
> evidence that evolution can build up information in living things?," he
then
> proceeds to systematically defrock every claim of increase in information
> in the scientific literature of which I am aware. By assuming the fossil
> record was a record of evolution, evolutionists have then pointed to the
> supposed increase in complexity as evidence for the ability of natural
> selection to increase information in biological systems. Such tautologisms
> do little to help us understand how information content can be increased.
> Spetner wisely avoids committing himself to a thesis that there never
> has been an increase in information. Rather he systematically examines
> each reported case and concludes none of the claims thus far represents
> such an increase. First, Spetner introduces us to the meaning of
information.
> Specificity is crucial. The information necessary to tell a person how to
get
> to Texas is far less than that required to specify a locality such as
Keene,
> Texas.
>
Interestingly enough, this is not strictly true. If I want to specify the
location of Keene, Texas, I can do so with only six numbers -- longitude and
latitude. To tell someone how to get to Keene, Texas, from Denver Colorado,
however, I have to say the following: I-25 south to Raton, New Mexico;
Highway 87 south-east to Dalhart, Texas; Highway 385 south to Vega, Texas;
I-40 east to Amarillo, Texas; I-27 south to Lubbock, Texas; Highway 84
south-east to Roscoe, Texas; I-20 east to Fort Worth, Texas; I-35W south to
Keene, Texas. I can of course greatly simplify this information by using
compass bearings and distance, but I would still need to use more than six
numbers. This of course assumes I will be driving to Keene. If I am flying,
all I need to know theoretically is the bearing and distance -- two numbers
-- but practically I also need to know other information, such as weather
conditions, curvature and rate of rotation of the earth, safe flying
altitudes, and more. The point is, no matter how you look at it, I can
specify the location of Keene, Texas, with less information (often far less
information) than I need to tell how to get there.
Even just telling somehow how to get to Texas -- never mind Keene, Texas --
would still reguire more information than simply six numbers.
>
> Each additional element of specificity requires a higher level of
> information. Thus an enzyme in a bacterial cell that previously
> worked only with substrate A, after undergoing a mutation, will
> accept substrate B as well. This may appear to be an increase in
> information but it is not, since the enzyme is now less specialized
> and has less substrate specificity.
>
This is where Spetner's, and Art's, lack of knowledge and experience in
biochemistry cause them to fumble. The situation they describe would be true
only if substrates A and B involve a different form of chemical reaction and
the catalytic site of the enzyme became less specific as far as the chemical
reactions it can catalyze. In point of fact, it is possible for an enzyme to
increase substrate specificity while at the same time increasing the number
of substrates to can handle. The reason for this is because substrate
specificity is not determined by how many substrates an enzyme can handle,
but by how tightly the enzyme binds to substrates and how specific the
enzyme's catalytic site is for a particular chemical reaction. The general
trend is that enzymes that can bind and catalyze a wide variety of substrates
have low substrate specificities, either because they bind substrates loosely
or can catalyze a variety of different reactions, but there are numerous
cases where you can see the opposite occur as well.
For example, if substrates A and B belong to a family of related substrates,
the enzyme in question may only be able to bind A because it binds this
family of substrates so weakly that A is the only one it can hold onto long
enough to catalyze the reaction. A mutation that allowed it to bind B as
well would, under these circumstances, mean an increase in binding efficiency
for that family, thus an increase in substrate specificity. A related
situation would be if the enzyme catalytic mechanism is too weak or too
general to handle substrates with higher energy bonds. Making the mechanism
stronger or more specific would be an increase in substrate specificity, yet
it could also allow the enzyme to handle more than one substrate.
As for specialization, that depends upon the circumstances. If the enzyme
belonged to a family of enzymes, all of which could only bind A, and now this
one enzyme can bind B as well as A, in fact it has become more specialized,
because it can do what no other enzyme in its family can do. Even a loss of
specificity can lead to an increase in specialization. An enzyme that
belongs to a family that can bind A and B, which mutates so that it can only
bind A but now binds it much more strongly, is considered specialized because
it handles A much better than any other enzyme. It should, however, be
pointed out that specialization is not necessarily a good thing when it comes
to enzymes; versatility is often more important. This is where
Brooks/Wiley/Collier theory can help out. If the system in question is a
family of enzymes and the system's microstates consist of substrate
recognition, the more substrates this family can recognize and catalyze the
greater the information possessed by that family. As such, even if the new
substrate recognition comes at the expense of an enzyme molecule with less
information than its previous form before the mutation, the overall increase
in substrate recognition with its increase in family information more than
offsets any loss in individual molecules.
>
> Other examples play out similarly.
>
In more ways than Art imagines. For example, Spetner also discusses
bacterial resistence to antibiotics. He claims that all known examples
involve a loss of information. Unfortunately, the only examples he gives are
of protein structures that are modified so that the antibiotics can no longer
bind to them. Granting for the moment Spetner's claim that this demonstrates
a loss of information (which in fact is not necessarily the case), this is
only one of three major ways that bacteria gain antiobiotic resistence. The
other ways are to create an enzyme that either chemically modifies the
antibiotic (thereby rendering it nonfunctional) or destroys the antibiotic,
or to create a membrane protein that rapidly pumps the antibiotic out of the
bacterium. In the case of the enzymes, some are known to be modifications of
existing enzymes, but others are known to be novel; that is, they did not
already exist in some other form waiting to be modified. In the case of
membrane-bound protein transporters, nearly all are known to novel, ie, not
the result of modification of existing protein transporters. Active
transporters like the kind involved in antibiotic resistence must be specific
for the molecules they transport; if they are too non-specific they let too
much through and the bacterium bleeds to death.
These types of mutations should qualify as increases of information even
using Spetner's restrictions; they certainly do under Brooks/Wiley/Collier
theory.
>
> The author states "Although there are circumstances where point
> mutations are good for the organism, all known point mutations lose
> information" (p.148 para.4), a statement that is well documented in
> the text.
>
And as is well documented by Brooks/Wiley/Collier theory, a minor decrease in
molecular information can still be offset by a major increase in system
information as long as the mutation increases diversity. And the mutation
need not be beneficial to increase diversity.
>
[snip section on Dawkins; no specifics to comment on, just an emtionally
charged tirade]
>
> Chapter seven begins an approach to the question of the origin of
> information that is different than I have encountered elsewhere.
> Citing the well-known and controversial studies of Hall, Cairins and
> others, he develops the paradigm that he calls "the nonrandom
> evolutionary hypothesis." He suggests that a wealth of information
> may be hidden away in the genome, provided with switches that
> can be activated by appropriate environmental cues; a concept
> consonant with Cairins results. He also suggests rather indirectly
> that environment may alter organisms in non-hereditary ways as
> an explanation for some of the differences found in the fossil
> record. Interesting ideas.
Alright, Spetner has an alternative hypothesis based on experimental
evidence; that puts him farther ahead than most anti-Darwinists, especially
those on this listgroup. Now, the question is where is his subsequent
evidence? What experiments has he done to test his hypothesis? Can he
demonstrate the existence of this "wealth of information ... hidden away in
the genome" and of these "switches"? Can he at least predict how this
"hidden information" and these "switches" would affect evolution? Can he
demonstrate even one morphological change such as seen in the fossil record
by using non-hereditary environmental means?
Brooks/Wiley/Collier theory, on the other hand, predicts that biological
information is a closed system; that its properties depend entirely on the
properties intrinsic to the system itself and not on the surroundings or
environment. Brooks and Wiley put it quite succinctly in their book: "To
put it another way, the environment does not 'mold' DNA molecules." As such,
their theory contradicts Spetner's hypothesis. Unlike Spetner's hypothesis,
however, Brooks/Wiley/Collier theory has been extensively tested since it was
first proposed in the mid-Eighties and it has withstood every test. On this
basis alone -- at least until Spetner has had a chance to test his hypothesis
-- Brooks/Wiley/Collier theory appears to be the better model.
Kevin L. O'Brien