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12 September 2009
A Scientific Critique Of Evolution
Dr. Lee Spetner
in an exchange with Dr. Edward E. Max
2000 L.M. Spetner. All Rights Reserved.
r. Edward E. Max posted an essay entitled The Evolution of Improved Fitness by Random
Mutation Plus Selection on http://www.talkorigins.org/faqs/fitness.html. He asked me for
my comments and, as a result, I wrote a critique of his essay (of his version updated 12 July
1999) and sent it to him on 2 August 2000. He promised me he would have it posted on the
talkorigins website with a link from his essay. He responded to my critique on 22 August and I
replied to his response on 29 August. I received a reply from him on 25 September that he was
looking forward to responding, but was busy at the time. At the time of this writing (27
November 2000) I have not received any further substantive reply from him, and my comments
have so far not appeared on the above website. I have therefore decided to post here a unified
version of the present status of our debate. I have merged my original critique, his response, and
my reply to his response to present our debate in an understandable flow. In my original critique I
refer to Dr. Max in the third person. In my reply to his response, I address him in the second
person.
I recommend you first read his original essay posted at the above-mentioned URL, and then read
the following. I have interspersed Maxs comments into my critique where they are applicable,
followed by my response to them.
At the outset, I shall establish an important and necessary guideline in this discussion of
evolution. The word evolution is generally used in at least two different senses, and the
distinction between them is important. On the one hand, the word evolution is used to denote the
descent of all life from a putative single primitive source. It is the grand sweep of evolution that is
supposed to have led from a simple beginning, something perhaps simpler than a bacterium, to all
organisms living today, including humans. This descent is supposed to have occurred through
purely natural means. Neo-Darwinian theory (NDT), which is the prevailing theory of evolution,
teaches that this development occurred through random heritable variations in the organisms
followed by natural selection. I shall denote the word evolution used in this sense as Evolution A.
When evolution is discussed for popular consumption, it is most often Evolution A.
The second sense in which the word evolution is used is to denote any kind of change of a
population. The change can sometimes occur in response to environmental pressure (artificial or
natural selection), and sometimes it can just be random (genetic drift). I shall denote the word
used in this second sense as Evolution B. Evolution B has been observed. Evolution A is an
inference, but is not observable. The distinction between these two meanings of evolution
parallels the distinction between macroevolution and microevolution, but the two pairs of terms
are not identical. Evolution A is certainly what is called macroevolution, but what is called
macroevolution is not identical with Evolution A. In any case, I prefer to use the A and B to avoid
having to carry whatever baggage might go with the macro/micro distinction.
The distinction between these two meanings of evolution is often ignored by the defenders of Neo-
Darwinian evolution. But the distinction is critical. The claim is made for Evolution A, but the
proof offered is often limited to Evolution B. The implication is that the observation of Evolution
B is a substantiation of Evolution A. But this is not so. Since Evolution A is not an observable, it
can only be substantiated by circumstantial evidence. This circumstantial evidence is principally
the fossil record, amino-acid-sequence comparisons, and comparative anatomy. Circumstantial
evidence must be accompanied by a theory of how it relates to what is to be proved. NDT is
generally accepted to be that theory. The strength of the circumstantial evidence for Evolution A
can therefore be no better than the strength of NDT.
The important claim of Neo-Darwinism is that it can account for Evolution A. The public
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perceives this claim as the core of the controversy over evolution. This claim is also the source of
the contention by evolutionists that life is the result of purely natural processes, which ensue from
well-known natural laws. I have examined this claim in my book Not By Chance!, and have
found it to be empty.
Evolution A is the principle message of evolution, namely that all life descended with
modification from a putative single primitive source. The mechanism offered for the process of
modification is basically the Darwinian one of a long series of steps of random variation, each
followed by natural selection. The variation is generally understood today to be random
mutations in the DNA. That primitive source of life is assumed to be sufficiently simple that it
could have arisen from nonliving material by chance. There is no theory today that can account
for such an event, but I shall refrain from addressing that issue here. That is for another place and
another time. What is relevant to this discussion is that the requirement that life arose
spontaneously sets, at the very least, a stringent upper limit on the complexity and information
content of the putative first organism that could reproduce itself, and thus serve as a vehicle from
which to launch Darwinian evolution. The issue I address here is the alleged development of all
life by the Neo-Darwinian process of random mutation and natural selection, starting from a
sufficiently simple beginning.
Despite the insistence of evolutionists that evolution is a fact, it is really no more than an
improbable story. No one has ever shown that the mechanism of NDT can result in Evolution A.
Most evolutionists assume that long sequences of microevolutionary events can produce
Evolution A, but no one has ever shown it to be so. (Those few evolutionists who hold that
macroevolution is really different from microevolution have changed their story several times
since they first came out with it, and their mechanism is so fuzzy that I have a hard time telling
what it is.)
For Evolution A to work, long series of beneficial mutations must be possible, each building on
the previous one and conferring a selective advantage on the organism. The process must be able
to lead not only from one species to another, but to the entire advance of life from a simple
beginning to the full complexity of present-day life. There must be a long series of possible
mutations, each conferring a selective advantage on the organism so that natural selection can
enable it to take over the population. Moreover, there must be not just one, but a great many
such, series.
The chain must be continuous in that at each stage a change of a single base pair somewhere in
the genome can lead to a more adaptive organism in some environmental context. The concept of
the adaptive landscape is useful here. This concept was first introduced by Sewall Wright
[1]
, but
now nucleotide sequences of the mean population genome have taken the place of Wrights gene
combinations. There are a great many adaptive hills of various heights spread over the genomic
landscape. NDT then says that it should be possible to continue to climb an adaptive hill to a
large global maximum (or near-maximum), one base change at a time, without getting hung up on
a small local maximum. No one has ever shown this to be possible.
Evolutionists often claim that if the evolutionary process were hung up on a small local adaptive
maximum, a large genetic change like a recombination, or other genetic rearrangement, could
bring it to another hill that has a higher peak, and place it higher up on that hill than it was before.
Large adaptive changes are, however, highly improbable. They are orders of magnitude less
probable than getting an adaptive change with a single nucleotide substitution, which is itself
improbable. No one has shown this to be possible either.
Moreover, as I have noted in my book, the large mutations such as recombinations and
transpositions are mediated by special enzymes and are executed with precisionnot the sort of
doings one would expect of events that were supposed to be the products of chance. Evolutionists
chose the mechanism of randomness, by the way, because no one can think of any other way that
beneficial mutations might occur in the absence of a law requiring them to occur. Genetic
rearrangements may not be really random at all. They do not seem to qualify as the random
mutations Neo-Darwinists can invoke whenever needed for a population to escape from a local
small adaptive maximum.
Evolutionists can argue, and rightly so, that we have no way of observing long series of
mutations, since our observation time is limited to a relatively short interval. Our genetic
observations over the past 100 years is thought to be more like a snapshot of evolution rather than
a representative interval in which we can search for the required long series of changes. But our
inability to observe such series cannot be used as a justification for the assumption that the series
Darwinian theory requires indeed exist.
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Max: An equally reasonable conclusion, in my view, would be that our inability
to observe such series cannot be used as a justification for the assumption that
such a series of mutations did NOT occur.
Spetner: Thank you for acknowledging that what I said was reasonable. But the two statements,
yours and mine, are not symmetrical. I dont have to assume the series did not occur to make a
case for the inadequacy of NDT. Those who base a theory of evolution on the occurrence of such
a series are required to show that it exists, or at least that it is likely to exist. They are obliged to
demonstrate an existence. I am not obliged to prove a non-existence. NDT has the convenient
characteristic that the very events that would prove the theory valid are inherently not observable.
Pleading that one should be excused from bringing such proofs because they are not observable
does not help the evolutionists case. If you want to prove the theory, you had better find
something observable.
Continuing my original critique, I pointed out that the argument against evolution is considerably
stronger than merely noting that the evolutionists have not proved their case. It turns out that
there is evidence that the series of mutations NDT requires do not, in fact, exist. The theory
requires there be a vast number of possible point mutations which, coupled with natural selection,
can generate the evolutionary advances that could produce Evolution A. If there really are a large
number of potentially qualifying mutations, at least a few of them should have been observed in
some of the many genetics laboratories around the world. All the mutations in these long series
must not only confer selective advantage on the organism but they must, on the average, also
contribute to the information, or complexity, increase that surely distinguishes present-day life
from the putative primitive organism.
These mutations must have whatever characteristics are necessary for them to serve as elements
of Evolution A. Thus, for a mutation to qualify as a representative member of the required
multitude of the long series that are supposed to produce evolution, it must bring new information
not just to the genome of the organism, but the information must be new to the entire biocosm.
[2]

The horizontal transfer of a gene from one species to another does not inject new information into
the biocosm. To show evolution in action, one must at least demonstrate examples of a mutation
that can serve as a prototype of those required by the theory. Such a mutation must be one that
could be a contributing member of a series of mutations that could lead to the vast increase in
information required by the theory. Thus, for example, a mutation that yields an enzyme new to
the biocosm, or one that makes an enzyme more specific than anything in the biocosm, would be
adding information. On the other hand, a mutation that disables a repressor gene causing a
constitutive synthesis of an enzyme might be advantageous to an organism under special
circumstances, but the disabling of a gene is not the kind of mutation the theory requires. Once in
a while, such a mutation might make an adaptive contribution, but it cannot be typical of the
mutations required by the theory.
Max devoted a good portion of his essay to challenging what he calls the creationist arguments
against evolution. The arguments he challenged include false statements such as: (1) all
mutations are harmful; (2) random mutations cannot increase the information content of a system;
(3) the proteins had to arise by random trials without the benefit of natural selection. If he found
creationists that said such things, then I suppose its part of the job he has assumed upon himself
to refute them. His challenges, however, are hardly a telling argument for evolution. (1)
Mutations have indeed been observed that confer an adaptive advantage, but that alone does not
qualify them to serve as components of a series of Neo-Darwinian steps. (2) Some special cases
of mutations may add information to the genome, but here again, that alone does not qualify them
to serve as components of an evolutionary series. (3) Although the creation of proteins by
random trials is not the thesis of NDT, no one has shown that they can be generated by random
mutations and natural selection in the context of evolution. His challenges are valid, but they are
far from sufficient to establish NDT. I shall address these points in what follows.
The following is additional criticism of Maxs original essay that was not included in my original
response.
Max challenged point (1) by indicating that beneficial mutations indeed occur. The intention of
his essay was to argue for Evolution A. Had he limited himself to Evolution B, I would have no
quarrel with him. He claimed that a rare beneficial mutation can confer a survival, or
reproductive, advantage to the individuals that carry it, thereby leadingover several
generationsto the spread of the mutation throughout a population.
His description is of what is often called a step in the evolutionary process. Max stated
categorically that such a step can occur. Moreover, to support Evolution A, the kind of step he
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described must have happened over and over again, millions upon millions of times. He
presented no evidence that it has ever happened, but simply tacitly assumed that it could. Can it
indeed? I address that question.
One must understand that at the heart of NDT lies chance and randomness. Mutations are random
events. The occurrence of a beneficial mutation at any given time in any given population is
governed by chance. Even natural selection, which carries the burden of being the directive force
of evolution, is subject to the laws of chance. Selection coefficients are average values. What
happens in any particular instance is a random event. A mutation, even one that confers adaptive
benefit on the organism, is likely to be wiped out by chance events (see Chapter 3 of my book).
There is a good chance that it will disappear before it can take over the population. The question
is not if it can happen, but, with what probability will it happen?
NDT is a theory that is supposed to account for the natural development of all life from a simple
beginning. I dont know why we need such a theory, because the development of life from a
simple beginning is not an observable. The theory is gratuitous; it comes to account for
something that was never observed.
Actually, evolutionary thinking goes like this.
1. One observes present life.
2. One then assumes that it arose in a natural way.
3. One then concocts a theory (e.g., the NDT) to account for the observation, given the
assumption.
I suppose that if the theory were really a good one, and could really explain well how life could
have developed in a natural way, it would lend some credence to the assumption that life did
indeed develop in a natural way. But it is not a good theory, and it does not account for what it is
supposed to. Evolutionists, realizing this, have lately been reduced to arguing that if no one has a
better theory that can account for the natural origin of life, then one must accept NDT. As you
will see from some of Maxs comments below, he also adopts this approach. I dont know why
NDT merits the pedestal on which evolutionists have put it.
Now lets get back to the probability of occurrence of one of those evolutionary steps of Maxs.
Since they are chance events, we cannot say with any certainty that they will happen. The best we
can do is to say with what probability such an event will occur. So, evolutionists have offered us
a theory (NDT) that postulates a long string of random events to account for the existence of life,
assuming it developed in a natural way. If the probability of those events were to turn out to be
close to 1, then one could say that the theory accounts for the observation. On the other hand, if,
according to the theory, the probability of those events were very low, one would have to say that
the theory does not account for the observation. If a theory predicts observed events to be highly
improbable, then one cannot justifiably say that the theory accounts for those events.
You would think that, since the issue of the probabilities of the evolutionary events is so crucial to
the validity of the theory, the advocates of evolution would have calculated the necessary
probabilities to make their case. But they havent. Since they have not made these calculations,
Max is not entitled to assume that evolutionary steps can occur.
There is some difficulty in calculating these probabilities because the values of the relevant
parameters are not all known. In my book, I addressed the problem of the probability of getting
enough successful evolutionary steps to account for the evolution of the horse. In spite of the
difficulties I just mentioned, I was able to calculate an important result. I found that either the
probability of the horse evolving was impossibly low, or else convergent evolution cannot occur.
This result refutes NDT, and with it Evolution A. Not only is Maxs point here not substantiated,
it stands refuted.
Antibiotic Resistance as an Example of Evolution
Continuing his effort to show the evolutionary efficacy of beneficial mutations, Max presented in
his essay the acquisition of antibiotic resistance by microorganisms as an example of evolution.
He said one can demonstrate a beneficial mutation with laboratory organisms that multiply
rapidly, and indeed such experiments have shown that rare beneficial mutations can occur. For
instance, from a single bacterium one can grow a population in the presence of an antibiotic, and
demonstrate that organisms surviving this culture have mutations in genes that confer antibiotic
resistance. Such an experiment shows that de novo beneficial mutations can arise.
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My response to this is that I have shown in my book that mutations leading to antibiotic resistance
fail the test of representing the mutations necessary for evolution. I summarize that argument
here.
All antibiotics are derived from microorganisms. Recall the story of the serendipitous discovery
of penicillin by Alexander Fleming in 1928, when he noticed that his plate of Staphylococcus
bacteria was clear in the vicinity of a bread-mold contaminant. The mold was found to produce
something that could lyse and kill the bacteria. That something was a molecule later named
penicillin. Afterwards, other antibiotics were found to be produced by other microorganisms,
such as soil bacteria. Soil has long been recognized in folk medicine as a cure for infections.
The antibiotics produced by these microorganisms serve them as a defense against attack by other
microorganisms. Some microorganisms are endowed with genes that grant resistance to these
antibiotics. This resistance can take the form of degrading the antibiotic molecule or of ejecting it
from the cell. Unfortunately for human health care, the organisms having these genes can transfer
them to other bacteria making them resistant as well. Although the resistance mechanisms are
specific to a particular antibiotic, most pathogenic bacteria have, to our misfortune, succeeded in
accumulating several sets of genes granting them resistance to a variety of antibiotics.
The acquisition of antibiotic resistance in this manner qualifies as evolution only in the sense that
it is an adaptive hereditary change. It is an example only of Evolution B. It is not the type of
evolution that can make a baboon out of a bacterium. The genetic change is not the kind that can
serve as a prototype for the mutations needed to account for Evolution A. The genetic changes
that could illustrate the theory must not only add information to the bacteriums genome, they
must add new information to the biocosm. The horizontal transfer of genes only spreads around
genes that are already in some species.
It turns out, however, that a microorganism can sometimes acquire resistance to an antibiotic
through a random substitution of a single nucleotide, and this is the kind of example Max
presented. Streptomycin, which was discovered by Selman Waksman and Albert Schatz and first
reported in 1944, is an antibiotic against which bacteria can acquire resistance in this way. But
although the mutation they undergo in the process is beneficial to the microorganism in the
presence of streptomycin, it cannot serve as a prototype for the kind of mutations needed by
NDT. The type of mutation that grants resistance to streptomycin is manifest in the ribosome and
degrades its molecular match with the antibiotic molecule. This change in the surface of the
microorganisms ribosome prevents the streptomycin molecule from attaching and carrying out its
antibiotic function. It turns out that this degradation is a loss of specificity and therefore a loss of
information. The main point is that Evolution A cannot be achieved by mutations of this sort, no
matter how many of them there are. Evolution cannot be built by accumulating mutations that
only degrade specificity.
In the final paragraph of my original critique, I said the following:
The mutations needed for macroevolution have never been observed. No random mutations that
could represent the mutations required by NDT that have been examined on the molecular level
have added any information. The question I address is: Are the mutations that have been
observed the kind the theory needs for support? The answer turns out to be NO! Many have lost
information. To support NDT one would have to show many examples of random mutations that
add information.Unless the aggregate results of the genetic experiments performed until now is a
grossly biased sample, we can safely dismiss Neo-Darwinian theory as an explanation of how life
developed from a single simple source.
Max: I think that the sample of genetic mutations you cite is in fact biased,
incorrectly interpreted, and much too small and non-systematic to draw such a
sweeping conclusion. I will try to explain why I believe this.
Some streptomycin resistance mutations do, as you point out, reflect mutations
of the ribosomal protein S12 which cause loss of binding of this antibiotic, which
you interpret as loss of information. However, you ignore other mutations of
this protein that do not lead to loss of antibiotic binding (e.g. Timms et al., Mol
Gen Genet 232:89, 1992). According to your formulation, these mutations
would not represent a loss of information, yet they are represent natural
mutations that are adaptive under conditions of exposure to streptomycin.
Would you accept that this kind of mutation is a good model for an adaptive
evolutionary change consistent with Neo-Darwinian Theory?
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Using your own example of streptomycin resistance, I have pointed out that
some mutations of the S12 ribosomal protein do not represent a loss of
information even by your own questionable criteria.
Spetner: First of all, I would recommend that you not refer to my criteria of information loss as
questionable until you understand them. See below, where I explain your misunderstanding.
You let your own tacit assumptions get in the way of understanding my thesis.
Furthermore, you misunderstood the paper by Timms et al., which you cited. All of the adaptive
mutations reported in that paper show reduced binding of the streptomycin molecule. The 12
adaptive mutations reported in the S12 protein fall into two categories. There was no example of
what you claimed I ignored. Five of those mutants are designated as streptomycin resistant (Smr),
and seven are designated as streptomycin dependent (Smd). All 12 of them, in the words of the
authors reduce the affinity of the ribosome for streptomycin. Perhaps you would like to point
out to me where in that paper they mention mutations in S12 do not lead to reduced binding, and
which you claim I have ignored.
Max: how about the single amino acid substitution in a blowfly
carboxylesterase that converts this enzyme into an organophosphorus hydrolase
under selection by organophosphate insecticides [Newcomb et al., PNAS 94:464,
1997]?
Spetner: In the Newcomb et al. paper that you cited, the experimenters started with 15 existing
strains of blowflies, some of which were resistant to organophosphorus (OP) insecticide and some
were not. No mutations were imposed or observed. The amino-acid differences between the two
groups were only assumed to have arisen by mutation.
The esterase enzyme E3 plays an important role in the operation of the flys nervous system. OP
insecticides kill the insects by interfering with this activity. Newcomb et al. found that the
resistant allele of the gene encoding the enzyme E3 and the corresponding susceptible allele differ
from each other in 19 nucleotides. These differences translate into 5 amino-acid differences
between the enzymes. The authors concluded from their study that one of those 5, namely
Gly
137
Asp, could account for both a loss of esterase activity and an acquisition of OP hydrolase
activity.
Although it is not certain that the difference in the activities of this enzyme arose through a
random mutation, let us even suppose it did. If it did, then this mutation is not likely to have
occurred recently, because much time would be needed to have accumulated all the 19 nucleotide
differences between these two phenotypes. Both phenotypes have likely been in the populations
of blowflies long before OP insecticides entered the environment. The resistant allele must
therefore have adaptive advantages in addition to OP insecticide resistance.
One can say with a large measure of confidence that the resistant strain did not arise through a
single random mutation and proliferate through natural selection in the presence of OP. This is
evident from a close examination of Fig. 2 of the above-cited paper. From what the authors have
shown, if there were such a mutation it would have been the substitution Gly
137
Asp. The
authors created two chimeric alleles of the E3 enzyme.One of these (lets call it the susceptible
chimera) had Gly
137
, corresponding to the allele susceptible to diazinon insecticide, but had the
other 4 of the 5 discordant amino acids identical with the wild-type allele resistant to diazinon.
The other chimera (well call it the resistant chimera) had the opposite; it had Asp
137
, and the
other 4 of the 5 discordant amino acids identical with the susceptible allele. The authors
measured the OP hydrolase activity in the wild-type susceptible allele, the susceptible chimera,
the wild-type resistant allele, and the resistant chimera. They presented the results of their
measurements in Fig. 2 of their paper, which shows the following:
1. There is negligible OP hydrolase activity in the wild-type susceptible allele of E3 and in the
susceptible chimera.
2. There is marked OP hydrolase activity in the wild-type resistant allele of E3 and in the
resistant chimera. It is this activity that the authors understand to be responsible for the
resistance to OP insecticide.
3. The OP hydrolase activity of the resistant chimera is about two and a half times that of the
wild-type resistant allele.
Accepting the authors premise that the OP hydrolase activity is responsible for the resistance, we
can say that a strain of blow fly whose E3 enzyme is identical with that of the wild-type
susceptible, except for the single substitution Asp
137
, should be even more resistant than the wild-
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type resistant strain. Therefore, if a mutation occurred in the susceptible strain achieving the
substitution Gly
137
Asp, it should be more adaptive than the wild-type susceptible strain in the
presence of diazinon insecticide. That being the case, the resistant population of blow flies should
have an E3 enzyme with only Asp
137
differing from that of the wild-type susceptible strain. Since
that is not the case, one can conclude that the other 4 of the discordant amino acids must have
some overriding adaptive value that trumps the greater OP hydrolase activity of the resistant
chimera, even though we dont know what that adaptive value is.In light of these data, one can
conclude that the substitution Gly
137
Asp did not arise by random mutation from the susceptible
strain.
Moreover, to tell if the substitution, Gly
137
Asp, even if it did arise by a random mutation,
represents an addition or a loss of information, we must know more about how the mutation
affects the enzymes hydrolase activity on more than just the one substrate. As in the example I
showed in my book (and described briefly below), what looked like an enhancement of activity on
one substrate, coupled with a degradation of activity on another, turned out to be nothing more
than a simple reduction of specificity of the enzyme over wider a set of substrates. As I wrote in
my original comments (see below) on your posting, one must be careful about jumping to
conclusions about what constitutes an information increase. This is not a weasel statement. One
can know when one has enough data to make a judgment. If the activity profile of the mutant
enzyme over several different substrates sharpens by increasing the activity on one substrate and
concomitantly decreasing the activity on other substrates, there is an increase in selectivity and
hence an increase in information. If, on the other hand, the activity profile of the mutant enzyme
over a set of substrates is flatter than that that of the wild type, then information has been lost.
One just needs enough data to be able to see an activity profile over several substrates for both the
mutant and the wild type.
Max: Certainly you are not correct when you say all known examples of these
mutations lose information rather than gain it.
Spetner: Since you have not shown any valid counterexamples, my statement still stands, and
your statement falls. None of the examples you gave qualifies as a random mutation in the germ
line that could be typical of those required for Evolution A. The context in which I made the
above statement was that of random mutations in the germ line that, according to NDT, are
capable of producing Evolution A.
You must admit that the most widely used examples by evolutionists to show evolution in action
do in fact lose information. You have used such an example yourself in your posted essaythe
evolution of antibiotic resistance in microorganisms. These so-called best examples are poor
and do not demonstrate, nor even indicate a typical contribution to, Evolution A.
You failed in your attempt to rebut my statement that all known examples of random mutations
that could play a role in Evolution A lose information rather than gain it.
Evolution and the Increase of Information
In my critique, I included for pedagogical purposes the following short explanation of the
information in enzymatic activity and its measurement:
I shall emphasize again: There is no theorem requiring mutations to lose information. I can
easily imagine mutations that gain information. The simplest example is what is known as a back
mutation. A back mutation undoes the effect of a previous mutation. If the change of a single
base pair in the genome were to change to another and lose information, then a subsequent
mutation back to the previous condition would regain the lost information. Since these mutations
are known to occur, they form a counterexample to any conjecture that random mutations must
lose information. An important point I make in my book, and which I emphasize here, is that, as
far as I know, no mutations observed so far qualify as examples of the kind of mutations required
for Evolution A.
In discussing mutations in my book I noted in each case in which the molecular change was
known, that it could not serve as a prototype for the mutations required by NDT. In all the cases I
discussed, it was the loss of information that prevented the mutation from serving as a prototype
of those required by NDT. The back mutation likewise cannot serve as a prototype of the NDT-
required mutations. Here, the reason is not that it loses informationit actually gains
information. But the information it gains is already in the biocosm and the mutation contributes
nothing new. Evolution is not accounted for if the only information gain was by back mutations.
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In my book, I did not quantify the information gain or loss in a mutation. I left it out mainly
because I was reluctant to introduce equations and scare off the average reader. And anyway, I
thought it rather obvious that a mutation that destroys the functionality of a gene (such as a
repressor gene) is a loss of information. I also thought it rather obvious that a mutation that
reduces the specificity of an enzyme is also a loss of information. But I shall take this opportunity
to quantify the information difference before and after mutation in an important special case,
which I described in my book.
The information content of the genome is difficult to evaluate with any precision. Fortunately, for
my purposes, I need only consider the change in the information in an enzyme caused by a
mutation. The information content of an enzyme is the sum of many parts, among which are:
Level of catalytic activity
Specificity with respect to the substrate
Strength of binding to cell structure
Specificity of binding to cell structure
Specificity of the amino-acid sequence devoted to specifying the enzyme for degradation
These are all difficult to evaluate, but the easiest to get a handle on is the information in the
substrate specificity.
To estimate the information in an enzyme I shall assume that the information content of the
enzyme itself is at least the maximum information gained in transforming the substrate
distribution into the product distribution. (I think this assumption is reasonable, but to be rigorous
it should really be proved.)
We can think of the substrate specificity of the enzyme as a kind of filter. The entropy of the
ensemble of substances separated after filtration is less than the entropy of the original ensemble
of the mixture. We can therefore say that the filtration process results in an information gain
equal to the decrease in entropy. Lets imagine a uniform distribution of substrates presented to
many copies of an enzyme. I choose a uniform distribution of substrates because that will permit
the enzyme to express its maximum information gain. The substrates considered here are
restricted to a set of similar molecules on which the enzyme has the same metabolic effect. This
restriction not only simplifies our exercise but it applies to the case I discussed in my book.
The products of a substrate on which the enzyme has a higher activity will be more numerous
than those of a substrate on which the enzyme has a lower activity. Because of the filtering, the
distribution of concentrations of products will have a lower entropy than that of substrates. Note
that we are neglecting whatever entropy change stems from the chemical changes of the substrates
into products, and we are focusing on the entropy change reflected in the distributions of the
products of the substrates acted upon by the enzyme.
The entropy of an ensemble of n elements with fractional concentrations f
1
,,f
n
is given by
and if the base of the logarithm is 2, the units of entropy are bits.
As a first illustration of this formula let us take the extreme case where there are n possible
substrates, and the enzyme has a nonzero activity on only one of them. This is perfect filtering.
The input entropy for a uniform distribution of n elements is, from (1), given by
since the fis are each 1/n. The entropy of the output is zero,
because all the concentrations except one are zero, and the concentration of that one is 1. Then
the decrease in entropy brought about by the selectivity of the enzyme is then the difference
between (2) and (3), or
Another example is the other extreme case in which the enzyme does not discriminate at all
among the n substrates. In this case the input and output entropies are the same, namely
Therefore, the information gain, which is the difference between H
O
and H
I
, in this case is zero,
We normalize the activities of the enzyme on the various substrates and these normalized
activities will then be the fractional concentrations of the products. This normalization will
(1)
(2)
(3)

(4)
(5)
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eliminate from our consideration the effect of the absolute activity level on the information
content, leaving us with only the effect of the selectivity.
Although these simplifications prevent us from calculating the total entropy decrease achieved by
action of the enzyme, we are able to calculate the entropy change due to enzyme specificity alone.
The Dangers of Conclusion Jumping
As a final example let me take part of a series of experiments I discussed in my book, which
demonstrate the dangers of conclusion jumping. This subject bears emphasis because
evolutionists from Darwin on have been guilty of jumping to unwarranted conclusions from
inadequate data. I shall here take only a portion of the discussion in my book, namely, what I
took from a paper by Burleigh et al.
[3]
to illustrate my point.
Ribitol is a naturally occurring sugar that some soil
bacteria can normally metabolize, and ribitol
dehydrogenase is the enzyme that catalyzes the first step
in its metabolism. Xylitol is a sugar very similar in
structure to ribitol, but does not occur in nature. Bacteria
cannot normally live on xylitol, but when a large
population of them were cultured on only xylitol,
mutants appeared that were able to metabolize it. The
wild-type enzyme was found to have a small activity on
xylitol, but not large enough for the bacteria to live on
xylitol alone. The mutant enzyme had an activity large
enough to permit the bacterium to live on xylitol alone.
Fig. 1 shows the activity of the wild-type enzyme and
the mutant enzyme on both ribitol and xylitol. Note that
the mutant enzyme has a lower activity on ribitol and a
higher activity on xylitol than does the wild-type enzyme. An evolutionist would be tempted to
see here the beginning of a trend. He might be inclined to jump to the conclusion that with a
series of many mutations of this kind, one after another, evolution could produce an enzyme that
would have a high activity on xylitol and a low, or zero, activity on ribitol. Now wouldnt that be
a useful thing for a bacterium that had only xylitol available and no ribitol? Such a series would
produce the kind of evolutionary change NDT calls for. It would be an example of the kind of
series that would support NDT. The series would have to consist of mutations that would, step by
step, lower the activity of the enzyme on the first substrate while increasing it on the second.
But Fig. 1 is misleading in this regard because
it provides only a restricted view of the story.
Burleigh and his colleagues also measured the
activities of the two enzymes on another
similar sugar, L-arabitol, and the results of
these measurements are shown in Fig. 2.
With the additional data on L-arabitol, a
different picture emerges. No longer do we
see the mutation just swinging the activity
away from ribitol and toward xylitol. We see
instead a general lowering of the selectivity of
the enzyme over the set of substrates. The
activity profiles in Fig. 2 show that the wild-
type enzyme is more selective than is the
mutant enzyme.
In Fig. 1 alone, there appears to be a trend
evolving an enzyme with a high activity on
xylitol and a low activity on ribitol. But Fig. 2 shows that such an extrapolation is unwarranted.
It shows instead a much different trend. An extrapolation of the trend that appears in Fig. 2 would
indicate that a series of such mutations could result in an enzyme that had no selectivity at all, but
exhibited the same low activity on a wide set of substrates.
The point to be made from this example is that conclusion jumping from the observation of an
apparent trend is a risky business. From a little data, the mutation appears to add information to
the enzyme. From a little more data, the mutation appears to be degrading the enzymes
specificity and losing information.
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Just as we calculated information in the two special cases above, we can calculate the information
in the enzyme acting on a uniform mixture of the three substrates for both the wild type and the
mutant enzyme. Using the measured activity values reported by Burleigh et al. we find the
information in the specificities of the two enzymes to be 0.74 and 0.38 bits respectively. The
information in the wild-type enzyme then turns out to be about twice that of the mutant.
The evolutionist community, from Darwin to today, has based its major claims on unwarranted
conclusion jumping. Darwin saw that pigeon breeders could achieve a wide variety of forms in
their pigeons by selection, and he assumed that the reach of selection was unlimited.
Evolutionists, who have seen crops and farm animals bred to have many commercially desirable
features, have jumped to the conclusion that natural selection, in the course of millions of years,
could achieve many-fold greater adaptive changes than artificial selection has achieved in only
tens of years. I have shown in my book that such extrapolations are ill founded because breeding
experiments, such as those giving wheat greater protein content or vegetables greater size, result
from mutations that disable repressor genes. The conclusions jumped to were false because they
were based on data that could not be extrapolated to long sequences. One cannot gain
information from a long sequence of steps that all lose information. As I noted in my book, that
would be like the merchant who lost a little money on each sale, but thought he could make it up
on volume.
Max: I want to make it clear that I dont buy your interpretation of certain
specific mutations as reflecting a loss of information. You state that the
information content of an enzyme is the sum of many parts, among which are:
level of catalytic activity, specificity with respect to the substrate, strength [and
specificity] of binding to cell structure, [and] specificity of the amino-acid
sequence devoted to specifying the enzyme for degradation. This formulation is
vague, non-quantitative, not supported by clear logic, not accepted in the
scientific literature (to the best of my knowledge; please educate me if I am
wrong), and in my view not useful.
Spetner: Ed, the level of your argument here is quite low. You have seen this entire section
(above), and you took from the introduction my list of what characteristics can contribute to the
information content of an enzyme and criticized it for being non-quantitative (followed by other
pejorative epithets). Is that supposed to be some sort of debating tactic? In any case, the tactic is
out of place in this discussion. From the context of what I wrote, it should have been clear to you
that this partial list of characteristics that can contribute to the information in an enzyme was an
introduction to my quantitative estimate of one of the characteristics of specificity of an enzyme.
After I showed how one might calculate the information related to a type of specificity, I showed
how a mutation that appeared to enhance activity on a new substrate actually reduced the
information by about 50%.
It is elementary that specificity translates into information and vice versa. Have you ever played
20 questions? With the YES/NO answers to 20 judicious questions, one can discover a
previously-chosen number between 1 and a million. If the questions are well chosen, those
YES/NO answers can be worth one bit of information each, and 20 bits can specify one object out
of a million. Twenty bits of information translates to specificity of one part in a million. Ten
bitsto one part in a thousand.
The Zip codes in the US also demonstrate that specificity and information are two sides of the
same coin and go hand in hand. An address in the United States can be completely specified by
the nine-digit zip code. One digit of information will narrow down the address from being
anywhere in the United States to being in just a few states. Thus if the first digit is a 6, the
address is located somewhere in Illinois, Missouri, Kansas, or Nebraska.
A second digit of information will add specificity by narrowing down the address further. A 3, 4,
or 5 in the second digit puts the address in Missouri. A 3 in the second digit puts it in the eastern
portion of the state. Two digits of information are more specific than one.
A third digit of information is still more specific, narrowing down the address even more, making
it still more specific. If the third digit is a 1, the address is specific to St. Louis and its suburbs.
The next two digits of information pin down the address to within a few blocks. The last 4 digits
of information can locate a specific building. Thus, it is clear that the information contained in
the digits of the zip code translate into specificity.
There is no question about it: SPECIFICITY = INFORMATION.
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Max: there are several other ways of considering how mutations affect
information. In my view, even if all S12 mutations that caused streptomycin
resistance abolished antibiotic binding, a reasonable argument could still be
made that such mutations represent a gain of information rather than a loss. In
the universe of all the possible S12 amino acid sequences that can function in the
ribosome, essentially all S12 proteins found in wild-type bacteria (i.e., those
grown in the absence of streptomycin) bind to this antibiotic. The S12 sequences
that allow bacterial growth in the presence of streptomycin represent a small
subset of the universe of observed functional S12 sequences. Therefore by
growing bacteria in streptomycin we select for a specific and small subset of
possible S12 sequences; thus it might be argued that we have forced a small
increase the information content of the genome by narrowing the choice of S12
sequences.
Spetner: I cannot agree with what you wrote here. The wild-type S12 proteins that bind to the
streptomycin molecule also form a subset of the universe of all possible S12 proteins. The set of
S12 proteins that allow bacterial growth in streptomycin (i.e. that do not bind to the antibiotic)
form a disparate subset of the universe of S12 proteins. My intuition tells me that the set that
binds (the susceptible set) is smaller, and therefore has a smaller entropy, than the set that does
not bind (the resistant set). Mutations that appear in the presence of the antibiotic convert one
subset to the other. A mutation that transfers the enzyme from a low-entropy set to a higher-
entropy set loses information; it does not gain it.
Max: Alternatively, it could just as well be argued that in all cases of single
amino acid replacements there has been no change in information content at all,
in that any given amino acid sequence is equally improbable compared with
any other amino acid sequence of the same length.
Spetner: This is not a useful concept. It is like the pleading of the poker player who had a bust
hand. When it came to the call, his opponent showed four aces. He pleaded that his bust hand
was just as improbable, and therefore worth as much, as the four-aces, and suggested they split
the pot. Hes right about the probabilities of the two hands, but in the context of poker, four aces
win and the bust hand loses. Although in the context of the organisms survival in streptomycin,
the degraded specificity of the S12 protein is beneficial, in the context of evolution, it is a dead
end and it loses.
Max: Certainly you have provided no theoretical justification for using your
arbitrary criteria such as specificity of binding to assess information content;
indeed, you fail to provide any quantitative theory of how all the criteria you list
(level of catalytic activity, specificity with respect to substrate, . . etc) would be
integrated into a quantitative information measure.
Spetner: On the contrary, I have provided substantial theoretical justification for equating
information to specificity. You just chose to ignore what I wrote.
Max: In general, if a protein has evolved under selection for a specific function,
changes in the structure of that protein to meet some new criterion can be
expected to adversely affect the original function. This is true in ribosomal S12
proteins that have become streptomycin resistant (they are less efficient in
proof-reading) and is clear in the example of the carboxylesterase, which loses
this activity essentially completely when mutated to become an
organophosphorus hydrolase. The structure of any proteinlike the product of
engineering designinvolves trade-offs between various opposing optimization
goals. Thus it is likely that intense selection for resistance to a lethal agent
exactly the kind of quick experimental protocol useful for laboratory models of
adaptive evolutionary changewill lead to mutations that involve what might
be construed by you as a loss of information something is always likely to be
lost when a modified, mutated protein becomes prevalent in the face of a new
selective pressure. This fact explains, I believe, why such genetic experiments
may in fact be grossly biased in the way that led you to inappropriately dismiss
Neo-Darwinian theory.
Spetner: You show here that you misunderstand what I mean by a mutation losing information.
If a mutation in an enzyme were to lose its specificity to one substrate and gain specificity to
another substrate, I would credit the mutation with a gain of information and I would not
construe it as a loss. But I will not credit it with a gain if the enzyme increased its activity to
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another substrate merely by becoming less specific, as in the example I gave above with ribitol
and xylitol.
What you have presented is not so much a case for bias as it is a pleading that any modification to
a protein must cause some degradation, and therefore you want to be excused from having to
show a case where information is increased. But you have overplayed your hand. You seem to
be saying in effect that because proteins have evolved so well, any change will degrade them. (If
that were so, it would be a good argument for Creation.)
Suppose a mutation causes a protein to become more adaptive in a particular environment. Then
by your thesis, it is already so well evolved that something is always likely to be lost when a
modified, mutated protein becomes prevalent in the face of a new selective pressure. You imply
that the loss is one of information, because thats the context of this discussion. But then,
according to you, after that modification, it is again well evolved, so the next time it undergoes an
adaptive mutation, it must again lose something. Continuing the process you have described, the
protein will continue to lose something. You have just consigned the evolutionary process to a
dead end!
Max: But consider this: If blowflies happened to have duplicated their
carboxyhydrolase gene before they were exposed to organophosphates, and if
they mutated one of their two copies to organophosphate hydrolase, we would
have a clear example of an increase in genetic information: creation of a new
functional gene without any loss of information since the original sequence
would be intact in the unaltered copy.
Spetner: I have already shown above that the organophosphorus hydrolase activity did not
necessarily come from a single point mutation. I have also noted that we dont have enough
information to know if the acquisition of this activity is a loss or a gain of information.
Furthermore, you dont have to keep bringing up the necessity of gene duplication. If an enzyme
lost its old activity to gain a new specificity, I would credit it with a gain of information without
regard to the loss of the old activity. I have always assumed that gene duplication is available to
evolution.
Max: Now, gene duplications are rather rare events, and favorable mutations
are also rare; so the combined frequencies of these two events are so rare that
they are not likely to be observable in a laboratory experiment. But if we look at
many gene systems in modern animals we can see how they might have been
caused by duplication followed by mutation to a new, or at least slightly
different, function.
Spetner: As I said above, I grant the possibility of gene duplication, so you neednt throw that in
to make the probability low. If I saw the gain of specificity through a random mutation, I would
credit the mutation with an increase of information without deducting for the loss of the old
activity. A single point mutation (which is all that NDT requires at each step) is not very rare
considering all the genetic experiments that have been performed throughout the world. If there
really are as many adaptive, information-adding mutations as NDT needs, we should expect to
have seen many of them.
Max: As an example of such a system, lets consider a gene locus that I have
studied in my lab: the human immunoglobulin heavy chain (or IgH) locus. In
the human locus one sees evidence of a large DNA duplication that created two
copies that are highly similar in both coding and non-coding flanking regions.
One duplicate includes constant region sequences known as gamma3, gamma1,
pseudo-epsilon and alpha1, while the second copy contains gamma2, gamma4,
epsilon and alpha2. More primitive primates like the New World monkeys
appear to have a single copy of this locus and a single gamma gene. The four
human gamma chain genes are thus thought to have derived from a single
ancestral gamma chain gene in a primate ancestor by a series of duplications
and mutations.In the ancestral primate we had one non-specialized gene
whereas in modern humans we have four specialized genes. This is exactly the
sort of genetic change that would be consistent with Neo-Darwinian evolution
leading to an increase in complexity.
Spetner: Yes, information would have been increased if what you speculate had indeed
happened. The proof would only lie in showing that it has indeed happened through random
mutations and natural selection. Let us not lose sight of the requirement of Neo-Darwinian
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evolution for long series of single-nucleotide substitutions, where each mutation makes the
phenotype sufficiently more adaptive than it was to permit the mutated phenotype to take over the
population through natural selection with a high probability. It is far from clear that the
individual mutations you suggest will each be adaptive and selected at each step. You cannot
show thisyou merely assume it. You are postulating an historical event that cannot possibly be
verified. It seems that all of your arguments are based on postulating events that are inherently
not observable. That should make one a little suspicious of the theory, shouldnt it?
Max: I realize that the above model for the human IgH locus is hypothetical
and assumes that the evolutionary triad of duplication, random mutation and
selection is a reasonable naturalistic explanation for the four human gamma
genes. We cannot verify this explanation since we can never know the
properties of the primordial ancestral gamma immunoglobulin, or know the
series of mutations that occurred in the various duplicate gamma genes during
our evolution from that primordial ancestor. What I am asking is: is there
anything so implausible in this model to justify your suggestion that we should
dismiss Neo-Darwinian theory as an explanation for this example?
Spetner: Yes, it is implausible because you are postulating a series of events of a type for which
there is evidence that they have not occurred. If they had occurred to produce Evolution A, there
should have been a vast number of them, and there arent. Had there been the required large
number of them, we should have seen some of them in all the genetic experiments performed in
all the laboratories of the world. And we havent, to my knowledge, seen a single one.
Max: Or more to the point, exactly what alternative explanation for the origin
of the four human gamma genes do you propose that is more plausible than the
one I offered?
Spetner: How does Creation grab you? You probably are reluctant to admit that possibility, but
you can think of it as a default position. It cannot be demonstrated scientifically, not because of
any philosophical defect in the proposition, but because of the limitations of Science. Because
Science is incapable of dealing with it does not mean it hasnt happened. There are, after all,
some truths in the physical world that cannot be reached by Science, just as there are
mathematical truths that cannot be reached by mathematical proof.
[4]
If we dont have a
scientifically viable theory to account for the origin of the four human gamma genes, or for the
origin of life itself, we neednt despair. Not every mystery necessarily has a scientific solution. I
do not mean to say that one should not look for a scientific solution. One should. But not having
such a solution is not a license to make up stories and pass them off to a gullible public as
Science. Because I dont have a (scientifically) plausible explanation of the origin of life, does
not mean that your improbable stories are correct and should be foisted on the public under the
guise of scientific truth.
Max: This is important, because considering the weaknesses I have pointed out
in your arguments, you are far from having definitively ruled out the Neo-
Darwinian evolutionary triad as the correct explanation for what you call the
grand sweep of evolution[I am now calling this Evolution A (LMS)].
Spetner: As you can see from my above remarks, you have not succeeded in pointing out any
weakness in my arguments. What you call the Darwinian evolutionary triad is no more than a
big bluff. It has great theoretical and empirical difficulties, which neither you nor anyone else has
succeeded in overcoming.
Mutations in the Immune System
Maxs field of expertise is the immune system. This is the field in which he does research and in
which he has published. In his original posting, his pice de rsistance was the presentation of
somatic mutations in B lymphocytes (B cells) of the vertebrate immune system as examples of
random mutations that add information. He implied that Evolution A could follow this method to
achieve baboons from bacteria. I agree with him that these mutations add information to the B-
cell genome. I also agree that they are random. They are random, however, only in the base
changes they make; they are not random in where in the genome they can occur. More important,
I do not agree that the Evolution A could be achieved through such mutations, and I shall show
why.
Although the somatic mutations to which Max referred are point mutations that do indeed add
information to the genome of the B cells, they cannot be applied to Darwinian evolution. These
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are not the kind of mutations that can operate as the random mutations required by NDT, which
allegedly can, through chance errors, build information one base change at a time.
For one thing, the rate of the somatic mutations in the immune system is extremely highmore
than a million times normal germ-line mutation rates. For this reason they are called
hypermutations. If an organism had a germline mutation rate that was even a small fraction of
this rate it could not survive. For a second thing, the hypermutations in the B cells are restricted
to a specific tiny portion of the genome, where they can do no harm but only good. The entire
genome of the B cell could not mutate at this rate; the hypermutation must be restricted only to
the region encoding selected portions of the variable part of the antibody.
The mutation rate of the hypermutating part of the B cells genome is usually about 10
-3
per base
pair per replication
[5]
, and it can be as high as 10
-2
per base pair per replication
[6]
. These rates
cannot produce Darwinian evolution. If a genome were to mutate at this rate, there would be, on
the average, several mutations in every gene, with a high probability that many of them would be
fatal for the organism. Darwinian evolution could not occur with such rates.
These high rates are essential for the working of the immune system. In each replication of a B
cell, about 30 of the 300 or so gene regions encoding the CDRs (complementarity-determining
regions) will have a mutation. A lower mutation rate would make for a less efficient immune
system. The high mutation rates, so necessary for the immune system, if applied to an entire
organism for evolutionary purposes, would be fatal many times over.
Note that these hypermutations are limited to a restricted portion of the genome. Moreover, the
hypermutations are mediated by special enzymes. Although the hypermutations are random in the
changes they make in the bases of the genome, they are not random in the positions in which they
occur. They occur only in the small region in which they are needed, and occur there through
enzymes that apparently play only that role. Furthermore, they occur only when they are
switched on by the controlling mechanism of B-cell maturation. Thus, it is clear that the
hypermutations in B cells cannot serve as a prototype for the random mutations required for NDT.
Max: You declare that the B cell example is a poor model for what happens
in Darwinian evolution, and you cite two reasons: (1) the mutation rate in this
model is much higher than what is seen in non-immunoglobulin genes and in
non-B-cells; and (2) these hypermutations are mediated by special enzymes.
With regard to your first point, I agree that the mutation rate is higher in the B
cell example than in evolution, but I fail to see why that fact weakens the
usefulness of the example as a model for evolution. If adaptive mutations that
increase information in the genome of a B lymphocyte population can occur
over one week given a high mutation rate, what theoretical argument would lead
you to reject the idea that adaptive mutations that increase information in the
genome of a germ cell population could occur over many millions of years given
a much lower mutation rate?
Spetner: The theoretical argument hinges on the fact that the benefit that accrues to the immune
system is a nonlinear function of the mutation rate. Evolution requires a long series of steps each
consisting of an adaptive mutation followed by natural selection. In this series, each mutation
must have a higher selective value than the previous
[7]
. Thus, the evolving population moves
across the adaptive landscape always rising toward higher adaptivity. It is generally accepted that
the adaptive landscape is not just one big smooth hill with a single maximum, but it is many hills
of many different heights. Most likely, the population is on a hill that is one of the many lowest
and not on one of the few highest in the landscape. It will then get stuck on a low local maximum
of adaptivity and will not be able to move from it. That is particularly likely because the steps it
takes are very smallonly one nucleotide change at a time. The problem is compounded by the
lack of freedom of a single nucleotide substitution to cause a change in the encoded amino acid.
A single nucleotide substitution does not have the potential to change an amino acid to any one of
the other 19. In general, its potential for change is limited to only 5 or 6 others. To evolve off the
dead point of adaptivity, a larger step, such as the simultaneous change of more than one
nucleotide, is required
[8]
. Moreover, the probability is close to 1 that a single mutation in a
population, even though it is adaptive, will disappear without taking over the population (see my
book, Chapter 3). Therefore, several adaptive mutations must occur independently and randomly
at each step.
Hypermutation in the B cells does this. It quickly achieves all possible single, double, and triple
mutations for the immune system, which allows them to obtain the information necessary to
match a new antigen. Ordinary mutations, at the normal low rate, cannot add this information
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even over long times. I shall explain why. The effects of mutation rate are nonlinear. Consider a
population of antigen-activated B cells of, say, a billion individuals, which is smaller than the
typical number. In two weeks, there will be about 30 generations. Lets say the population size is
stable, so in two weeks there will be a total of 30 billion replications. With a mutation rate of 1
per 1000 nucleotides per replication, there will be an average of 30 million independent changes
in any particular nucleotide during a two-week period. The probability of getting two particular
nucleotides to change is one per million replications. Thus in two weeks, there will be an average
of 30 thousand changes in any two particular nucleotides. There will be an average of 30 changes
in any three particular nucleotides. If the mutation rate is 1 per 100, these numbers would be
correspondingly larger.
How many generations, and how long, would it take to get a particular multiple-nucleotide change
in a germ cell to have an effect on Neo-Darwinian evolution? Here, the mutation rate is about one
per billion nucleotides per replication. Lets suppose were doing this experiment with a
population of a billion bacteria. Then, in one generation, there will be an average of one change
in any particular base in some one individual. A particular double-base change has a probability
of one per quintillion, or 10
-18
. To get one of these would take a billion generations, or about
100,000 years. To get a triple change would take 10
14
, or a hundred trillion, years. That is why a
long waiting time cannot compensate for a low mutation rate. Ive given numbers here for a
laboratory experiment with bacteria. Many more mutations would be expected world wide. But
the same kind of thing has to happen under NDT with multicelled animals as well. With
vertebrates, for example, the breeding populations seldom exceed a few thousand. Multicelled
animals would have many fewer mutations than those cited above for bacteria.
Max: Your second objection to the somatic mutation model in B-cells, that
special enzymes are involved, is unsupportable. As far as I can tell from my
reading of the literature, the mechanism of somatic hypermutation in B-cells is
not currently known.
Spetner: On the contrary, my objection is well supported in the professional literature. The
somatic hypermutations you cite do indeed require special enzymes, and is not the kind of
mutations held to be responsible for the variation required in NDT. These mutations, unlike
ordinary errors in DNA replication in the germline, are under precise control in the cell. They are
turned on exactly when they are needed, and they are turned off when they have done their job.
They are accurately targeted to the very small regions of the genome where they can provide
variability to the CDRs, which form the antibody-binding site. They do not occur at any other
place in the genome. Although the mechanism of this precisely targeted phenomenon is not yet
known in complete detail, enough is known to say that there has to be a mechanism
hypermutation does not happen by chance. Thus, even 14 years ago, a popular textbook in cell
biology said
[9]
, There must exist mechanisms that direct mutational activity to variable-region
sequences. How this might occur is not known; possibly some sequence in the area of the
variable region directs a special enzyme system to carry out point replacements of nucleotides
independent of template specification. (my emphasis)
Informed current opinion on the subject of somatic hypermutations is overwhelmingly (and
perhaps even unanimously) in favor of the suggestion that they are produced by a special
mechanism requiring special enzymes that are unlike the spontaneous germline mutations
assumed to be responsible for evolution. Experts in this field are very clear on this point. Let me
just bring you a few quotes from a recent paper by Robert Blanden and his colleagues
[10]
, in which
they describe important characteristics of somatic mutations, and note how they differ from
germline mutations [all emphases are mine (LMS)]:
The accumulated findings strongly suggest a complex mechanism [for
hypermutation], which is unlikely to employ simple error-prone DNA repair
processes involving DNA template directed DNA synthesis.
there should logically be a mechanism to ensure that when successful mutation
has taken place, there is no further mutation which may destroy successful V(D)J
sequences.
Let me also bring you a few quotes from another recent paper by David Winter & Patricia
Gearhart (whom you may even know) on the subject of somatic hypermutations
[11]
:
The pattern of somatic mutations in rearranged variable (V) genes differs from the
pattern of meiotic mutations, indicating that a different mechanism generates
hypermutations than generates spontaneous mutation.
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somatic hypermutations may be derived by different mutational processes than
meiotic mutations.
The evidence suggests a model of hypermutation in which the DNA sequence of the
immunoglobulin region directs the rearranged variable gene to a point on the nuclear
matrix where both transcription and hypermutation occur.
B cells that are stimulated by antigen activate an error-prone hypermutation
mechanism to introduce point substitutions throughout the V region.
it has been shown that areas containing transcription promoters and enhancers are
required for [hyper]mutation
It thus seems quite clear that informed opinion in this field supports my contention and rejects
your suggestion that an alternative possibility is that the high rate of accumulation of mutations
simply reflects selective inhibition of normal proof-reading mechanisms. This is your field of
expertise, Ed. Please let me know if you agree or disagree.
Max: The mechanism could perhaps involve special enzymes that create
mutations, but an alternative possibility is that the high rate of accumulation of
mutations simply reflects selective inhibition of normal proof-reading
mechanisms. But again, I fail to see why the source of the random mutations
should influence the general validity of the conclusion that random mutations
and selection can increase genomic information, or why you feel that these
mutations cannot serve as a model for evolutionary adaptations.
Spetner: It should be clear from what I have written above that the hypermutation in B cells
cannot serve as a prototype for the random mutations required by NDT to account for evolution.
There is no known mechanism for mutation in germ cells that is comparable to the hypermutation
in B cells. The example of hypermutation cannot be used to support your contention that random
mutations in germ cells can build up information in the genome to explain Evolution A.
Max: if we accept your argument against extrapolation from B cell
adaptation to species adaptation, should we reject the extrapolation of any
information learned from studying one organism to understand adaptations in a
second organism, unless it is shown that both the rate and mechanism of
mutation are the same in both organisms? In my view this would be like
refusing to use the gravitational constant determined in laboratories on earth to
analyze stellar physics. Such a reluctance to extrapolate would certainly
prevent the use of modern organisms as a basis for understanding evolutionary
events that occurred millions of years ago (which may be precisely your intent).
I sometimes hear arguments like yours from creationists who are demanding
rigorous proof of evolution. These creationists do not seem to understand the
distinction between mathematics, where a rigorous proof is expected, versus
most experimental and observational science, where all we are seeking is the
best theory that explains observed data. Of course, it is possible to extrapolate
unreasonably, but I do not see that you have shown how evolutionary theory (or
my essay) does this.
Spetner: Your comparison is fallacious. Extrapolations made in astrophysics and cosmology
may not be entirely valid, but at least they are reasonable based on everything we know. The
extrapolation you propose from B-cell hypermutation to Neo-Darwinian evolution is unreasonable
based on present knowledge, and it is therefore unjustified (as explained above). It is not Science.
I have not asked for a mathematical-like proof for evolution. But for heavens sake, how about
exercising some scientific discipline? Scenarios and just-so stories cannot substitute for proof.
There is no proof of Evolution A that is of a standard that would be acceptable in any other
scientific area.
Max then summarized his arguments against my comments to his posting, which I reproduce
below and to which I have appended my comments.
Max: I have made these opposing points:
(1) Using your own example of streptomycin resistance, I have pointed out that
some mutations of the S12 ribosomal protein do not represent a loss of
information even by your own questionable criteria.
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Spetner: And I have shown above the errors of your argument. Your use of pejorative
adjectives cannot make up for the weakness of your case.
Max: (2) I have argued that your information criteria (for deciding whether
genes gain or lose information after specific mutations) are vague, non-
quantitative, not supported by any logic, not accepted in the scientific literature
and not demonstrably superior to other ways of judging the effects of mutation
on genomic information.
Spetner: Not only have I made it clear above that my criterion for gain/loss of information is
quantitative, and supported by logic and the conventional understanding of these notions in
information theory, I included that section in my first critique of your posting. You chose not to
relate to it at all, and instead you made up the above criticism out of thin air.
Max: (3) I have discussed why examples of adaptive mutations in non-
duplicated genes might appear to show some loss of one type of function (if not
loss of information) as they gain a new function under selection by a novel
environmental stress, and thus exhibit a kind of bias that might have mislead
you into making your rather risky extrapolations about the role of random
mutations in evolution.
(4) I have explained why an example of a gene duplication followed by
differentiation of the two gene copies to enlarge genomic information might be
hard to observe in the laboratory, contributing to the bias mentioned above in
the set of mutations that we do observe in the laboratory.
Spetner: And I have shown above that what you call a possible bias in our observations of
mutations stems from your lack of understanding of my arguments. You have shown no valid
reason why there is any bias in the set of all mutations that have been observed in all the genetic
laboratories in the world.
Max: (5) I have provided an example of duplicated and differentiated
immunoglobulin gamma genes that can plausibly be interpreted by the
evolutionary triad of mechanisms (gene duplication, random mutation and
natural selection) each of which has been demonstrated individually as natural
mechanism in appropriate laboratory experiments; and I have challenged you to
provide an alternative more plausible explanation for the origin of these four
gamma genes.
Spetner: And I have shown above that your laboratory experiments are not applicable to
Evolution A. I have also pointed out that there is no obligation to provide a natural explanation of
origins. There may not be one. But I encourage you to keep looking. But please remember that
the solution to the problem of the origin of proteins, or the origin of life, may not be where you
are looking.
Max: (6) Finally, I have asked you to explain why hypermutation and selection
of immunoglobulin genes in B cells should not serve as an instructive prototype
demonstrating the potential of mutation and selection to improve function of
proteins in evolution; specifically, I have asked why either the faster mutation
rate in the B cell model or the unknown mechanisms of the mutations are
relevant to the question of whether random mutation and natural selection can
lead to increased fitness of proteins in evolution.
Spetner: And I have explained all that above and showed you why the somatic hypermutations
do not qualify as examples that could pertain to the germ-line mutations required for evolution.
Summary
I have shown here, with references to my book, that the examples most often cited by
evolutionists as evidence for evolution occurring now are not evidence at all for the grand sweep
of evolution, which I have called here Evolution A. For an example of evolution happening now
to have any relevance to Evolution A, it must be based on a mutation that could be typical of
those alleged to be in the long series of steps that lead from a bacterium to a baboon. The
mutation must at least be one that when repeated again and again will build up enough
information to turn a bacterium into a baboon. The favorite example cited for evolution is
antibiotic resistance. I have shown that the mutations leading to antibiotic resistance do not add
any information to the biocosm. In some cases, they actually lose information. I have shown an
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example of a mutation that can easily be misconstrued to demonstrate the addition of information
to the genome. Upon the gathering of further data, this example turned out to be a demonstration
of information loss and not gain. Conclusion jumping is always risky, because we seldom have
enough data. Yet, the evolutionist community has persisted in making the shakiest of
extrapolations.
Max has tried to argue that his triad of gene duplication, random mutation, and natural selection,
can add information to the collective genome of the biocosm.
I have exposed his argument as being nothing more that offering possible scenariosit is
argument by just-so-stories. But the argument against NDT does not stop with the failure of its
supporters to show proper theoretical or empirical evidence for it. The telling blow against NDT
is that examples of information addition have never been exhibited. The absence of such
examples is more than just the absence of evidence for evolution. It is actually evidence against
evolution because if NDT were correct, there should be millions of such examples and in all the
genetic experiments performed until now we should have seen many.
Finally, the example of mutations in the B cells of the immune system carries no weight as an
example of a mutation that adds information. Although these mutations do add information to the
B-cell genome, they cannot be applied to evolution for the reasons I laid out above.
Dr. Edward E. Max made a valiant attempt to present a case for evolution in his posting on the
URL cited above. That he failed is not because of any defect in the author. Dr. Max is an
intelligent, competent, and articulate scientist. He has a PhD and an MD, and for many years has
done research and published on the genetics of the immune system, and he has made important
contributions to our knowledge in this field. If he could not make a good case for evolution, there
must be something woefully wrong with evolution.
Dr. Lee M. Spetner
Endnotes
[1] Wright, Sewall, (1932). The roles of mutation, inbreeding, crossbreeding and selection in
evolution, Proceedings 6th Intnational Congress of Genetics, 1: 356-366.[RETURNTOTEXT]
[2] biocosm is a word I have coined to denote the totality of life on our planet.[RETURNTOTEXT]
[3] Burleigh, B. D., P. W. J. Rigby, & B. S. Hartley, (1974). A comparison of wild-type and mutant
ribitol dehydrogenase from Klebsiella aerogenes. Biochem. J., 143: 341-352..[RETURNTOTEXT]
[4] Gdel, Kurt On Formally Undecidable Propositions of Principia Mathematica and Related Systems.
(1962) Translated from the German by B. Meltzer and R. B.Braithwaite. London: Oliver &
Boyd.[RETURNTOTEXT]
[5] Darnell et al. (1986), Molecular Cell Biology, Scientific American Books, p.
1116.[RETURNTOTEXT]
[6] Winter, D. B. & P. J. Gearhart (1998) Dual enigma of somatic hypermutation of immunoglobulin
variable genes: targeting and mechanism. Immunological Reviews 162: 89-96. [RETURNTOTEXT]
[7] For simplicity in explanation I am assuming here that the environment does not change. The same
argument holds when the environment changes, with a slight alteration of the
language.[RETURNTOTEXT]
[8] Evolutionists often glibly argue that a recombination in the chromosomes can provide the large
change to throw the genome off the small adaptive hill it is on and provide the opportunity for it to
land on another adaptive hill. But it is highly improbable that it will land at a higher adaptive
elevation. This argument abandons the Darwinian premise of small, and not unlikely, changes driving
evolution. [RETURNTOTEXT]
[9] Darnell, J., H. Lodish, & D. Baltimore (1986), Molecular Cell Biology, Scientific American
Books, New York: Freeman. p. 1116. [RETURNTOTEXT]
[10] Blanden, R. V., H. S. Rothenfluh, P. Zylstra, G. F. Weiller, & E. J. Steele, (1998). The signature
of somatic hypermutation appears to be written into the germline IgV segment repertoire.
Immunological Reviews 162: 117-132. [RETURNTOTEXT]
Page 18 of 19 A Scientific Defense of a Creationist Position on Evolution
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[11] Winter, D. B. & P. J. Gearhart (1998). Dual enigma of somatic hypermutation of immunoglobulin
variable genes: targeting and mechanism. Immunological Reviews 162: 89-96. [RETURNTOTEXT]
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