by Chris Cogan
(Copyright 2005)
Feedback,
discussion, comments, questions: Chris Cogan, ccogan@ou.edu
Abstract: Active genetic information is carried by
the sequencing of the DNA nucleotides, so changing that sequence changes the
information, whether creationists want it to or not, and the changed
information is inherently new information: It wasn't there in the parent genes,
and it is there in the offspring genes. The essay is mainly the development or
the explaining of several points pertaining to this idea, such as how
genetically useful new information can be obtained from informational noise by
a sufficiently systematic filtering process.
This essay should really not be needed, but, judging
from the number of creationists and ID-advocates who think Dembski's abuse of
information theory is brilliant, and from recent gross misrepresentations of
observational facts by creationists claiming that mutations are always
"deleterious," I conclude that these people are woefully ignorant (or
worse) in this area.
So, I decided to write up a summary of some ideas that
I've been developing for years (since the early 1990's). It was a remark of
Dawkins about genetic information (in one of his earlier books) that got me
started on developing this general line of thinking in my own case. I would
give some credit to Johnson (for his nonsensical claim that information is a
kind of "stuff") and Dembski (for his gross misrepresentations of
information theory generally, and its application to evolution in particular),
but the fact is, were it not for the fact that both Johnson and Dembski
actually get approving readership among the ignorati, I wouldn't bother, any
more than I would bother trying to refute a flat-earther's claims. There are so
many crackpot theories that one has to restrict one's extended consideration to
those that are popular enough to be or contribute to a social problem (such as
the prospect of removing science from public school science teaching). I have
decided to take on the information-theory issues because I have had an ongoing
interest in the subject since reading Shannon's book while I was still in my
teens (over forty years ago). Despite my interest in information theory and my
love of mathematics, I will not inflict any actual mathematics on you, as
Dembski would (in his attempts at hiding the fundamental wrongness of his
claims, his arguments, and his approach). I won't inflict the actual
mathematics on you, and I have been rather more informal in my use of some of
the ideas than would be ideal, but I hope the main lines of reasoning are clear
enough (one thing I haven't even touched on at this general level is the
definition of information, except insofar as it applies to genetics (a sequence
of genetically active DNA, where it is the sequencing that carries the
information, because a different sequence of the same length would carry different
genetic information).
Mathematics can be used to prove quite a wide array of
things, if it is correct mathematics and if it is applied correctly.
However, while figures may not lie, liars may figure,
as the old saying has it. This is relevant to the issue of whether
(genetically) new information can get into the genotype of the offspring of
another genotype during reproduction.
The really short answer is simply yes.
However, let's consider a slightly longer answer. Note
before continuing that, for now, I will only be considering the simpler case of
non-sexual reproduction.
Let me also note before going on that information is
not some kind of mysterious "stuff" (as professional liar Phillip
Johnson claimed it was). Information is simply the arrangement of parts of
something, or the attributes of it, depending on context. An electron carries
information in the form of charge, "spin," mass, etc. A sequence of
ones and zeros carries information by virtue of that sequencing (not by virtue
of some additional "stuff" other than the ones and zeros).
DNA carries/stores information as a sequence of
nucleotides, and the sequencing is the important part, genetically. If the
nucleotides are in one order, the information content is different from
the information content (in non-genetic terms) of any other order. For
example, deleting ATA from the middle of GATATACCA produces GATCCA.
We can relax this slightly (for the benefit of the
creationist/ID crowd) by saying that two genetic sequences are informationally
different only if they are functionally different in their phenotypical
expression. That is, we can restrict our consideration to genetically active or
effective information, and refer to it as genetic information, or even just
information (as long as context makes it clear that we are using the term in
this sense). This restricts us specifically to genetically functional
information, which is what we are really interested in most of the time. This
way, we can temporarily set aside questions about "junk" DNA.
However, I will note again before going on that, in a technical sense, any
change is still an informational change, even if the information is ignored by
the reproductive or other processes. The pages of an encyclopedia that you
never read still contain information, even if you don't read them; they are
just not informative to you.
What is a mutation? It is a change in the DNA
sequencing of nucleotides in a genotype from the parent genotype. That is, a
mutation is a change in information, producing new information.
That information wasn't there in the parent genes (that is, that sequence, in
context, was not present in the parent genes, and it is present in the
offspring genes: It wasn't there, and now it is there.
This applies to duplication (unless it is immediately
"junk" DNA) and to rearrangement (if it has an effect on what
happens) and rearrangements, and insertions, as long as the result is
genetically significant to the offspring. It is also true of the actions of HOX
and other homeobox genes. If one of these genes is modified so that its effect
on other genes is modified, this is new information: It wasn't there, and now
it is there.
Finally, this even applies to deletions (removing the
genes for pigmentation is equivalent to the new instruction to produce an
albino, and removing just a part of a gene may produced a functionally very
different new gene).
If you don't think deletions can change information,
consider two sentences. The second is made from the first by deleting four
letters:
I sent the catalog to Bob
I sent the cat to Bob.
If you don't think the second sentence is new
information, imagine just reading the first sentence, and ask yourself: Does
this tell you that I sent the cat to Bob? No, from reading the first sentence,
even if you actually did think of the question of whether I sent the cat (as
well as the catalog) to Bob, you wouldn't be informed about it from reading the
first sentence.
But the second sentence does tell you this.
It's new information: It wasn't there, and now it is there.
How do we know? Well, how do we know that genes carry
information at all? One way is by seeing the effects. Until recently, this was
the only way we had. If an organism gives birth to offspring that are
phenotypically different from itself (still assuming non-sexual reproduction),
and if that difference is then passed on to the offspring of the offspring, then
the genetic change that produce that phenotypical difference is new
information: It wasn't there in the parent, and it is there in the
offspring.
Further, we can look at the genes themselves, and by
experiment, observation, and testing, determine that there is genetic
information in the offspring that is not present in the parent's genotype.
What is a mutation in informational terms? A mutation
simply is the introduction of new genetic information, and we know this
because of its effects on the organism and its offspring.
That's precisely the problem with mutations. If
they were not new information, mutations would have no phenotypical effects at
all, and there would never be any harm in them. But the fact is that it
is precisely because of their informational content that they become
problematic in a large percentage of cases. The effects on the offspring can
only occur because mutations are new information: It wasn't there in the
parent, and it is there in the offspring.
Creationists who admit that mutations affect the
offspring but deny that there is any new genetic information in them contradict
themselves. When they admit that phenotypically effective mutations do occur,
the admit that there is in fact new genetic information, but when they then
deny that there is new genetic information, they are denying, by implication,
that genetically effective mutations occur.
Now, let's consider genetic recombination. In order to
avoid having to insert qualifiers too frequently, I'm assuming that we are
talking only about active genetic material, not "junk" DNA.
Recombination nearly always produces new information
except in extremely bizarre cases where the genes of the offspring are an exact
functional duplicate of the genes of one of the parents, and in those cases
where what is different as a result of recombination is truly "junk"
DNA. All other recombinations that have an effect on the carrier's phenotype
produce new information. ALL, without exception, since that simply is
what new information is, in physical terms. That is, if two people give birth
to child whose effective or active genes do not exactly duplicate all of the
genes of just one of the parents, there is new information: That
combination of "words" (or whatever) wasn't in either of the
parents, and it is there in the offspring.
We know it's new, even in functional terms, because it
produces offspring that are phenotypically different in ways not due to
environmental effects on development. For example, a child may be said to have
its mother's eyes and its father's hair, producing a combination that is a new
combination (it wasn't in either of the parents, but it is there
in the offspring). The same genetic considerations apply to all (or virtually
all) sexually reproducing species (I think it even applies to Cheetahs and
other animals that have gone through a genetic "bottleneck" that
reduced their genetic variation to nearly zero (all alleles the same except for
gender-specific ones). Why do I say this? Because even Cheetahs are not perfectly
genetically identical (as far as I know). Also, some lab mice are specially
bred to be as nearly identical as possible, so they might count as a true
exception (but, of course, even their genes are subject to mutation).
Is the new information from recombinations and
mutations ever beneficial?
The short answer, again, is yes.
(Note that, even though there is no special objective
reason, at this level, to separate out mutations from recombination, I do so
for the moment to humor creationists, since they claim there is some
fundamental difference between them.)
Recombinations obviously occasionally produce
beneficial results: The offspring of people fairly frequently have traits that
are clearly beneficial, clearly genetically based, and that are the result of
combining genes from each of their parents.
Is this sufficient for evolution? Only up to a point,
because recombination (as normally conceived) does not include genetic changes
that encompass less than a gene (such as a single base-pair substitution from
one parent into a gene that is otherwise entirely from the other parent; I
think this would always be considered a mutation rather than a recombination),
and most especially after complex genomes are established, when lots of genes
may contribute to more or less "single" phenotypical differences.
Mutations are defined, for the moment, as any change
in the genes other than those that are purely recombinations. For example, if
the genotype of the offspring is longer or shorter than that of its parents,
there has been a mutation of some sort. As we know, most mutations are either
junk or harmful, so the question is whether there are any that are
beneficial to the organism.
Yes there are. One example: Experiments with yeast in
labs has shown that yeast living in a sugar-scares environment can develop additional
genes for more-efficient sugar-scavenging, and we know that bacteria introduce
new genetic information that's beneficial (to them, not us) as a
response to antibiotics. Another, and more commonly noted, example: Bacterial
adaptation to antibiotics.
It is sometimes irrelevantly claimed that these
changes always result in some other effect that is negative, such as less
efficient protein construction. First, I don't think this was true in the case
of the additional gene in yeast, but, in any case, it's irrelevant because the
definition of "beneficial to the organism" has nothing inherently to
do with efficiency in the production of protein (or efficiency in any other
process, for that matter). The claim that it does is creationist
misrepresentation of both biology and the theory of evolution. What counts as
beneficial in evolutionary terms is ongoing reproductive success, not
any particular level of protein-making efficiency. Even the fact that these
bacteria do not do well in competition with non-resistant bacteria when they
are put into an environment without antibiotics is irrelevant because that's
not the environment the adaptations were for. Humans would not do well in
competition with birds as flying organisms, but that doesn't mean we are not
well adapted to the environment we live in and to the resources we have access
to.
The creationist argument in this case is like saying
that the adaptation of most birds to flight is deleterious because it means
they can't live well as burrowing animals. Whether or not an adaptation is
deleterious or not depends on the environment that the organism is living in,
not the environment their ancestors lived in.
The dishonesty of the creationist's claim in this
respect is shown in the way they characterize such changes as
"deterioration" even though it clearly benefits the bacteria (reproductively)
to have this "deterioration," as long as they remain in their
environment. Creationists further characterize the non-antibiotic environment
as the "normal" one, even though the fact that the bacteria had to
evolve to deal with the antibiotics means that that environment is
normal for them.
The implication of the creationist claims is that
there is some sort of Platonic Idea of what is "normal" that is to be
applied regardless of the changes in the environment and in the
organisms themselves. For them, "normal" is simply arbitrarily taken
to be: Whatever the environment was like before the evolutionary process
occurred. This is arbitrary, like saying that normal for humans is living
without antibiotics merely because there were (presumably) no antibiotics in
the Garden of Eden (pretending for the moment that Eden ever existed). At least
as far as biology and science generally are concerned, normal is determined by
facts, not by some floating abstractions about what constitutes normal or about
what normal was at some irrelevant past time.
Further, if there are negative side effects of
beneficial mutations (and there are negative side effects of many genes anyway,
possibly even of the "normal" genes that code for efficient
protein production in bacteria), further evolution may remove at least some of
them. Evolution works in particular directions by a process of refinements as
well as by introducing new alleles. Thus, a bacterium that has adapted to
become resistant to antibiotics may later also adapt to regain the efficiency
of protein production that was lost in the first round of mutations. Obviously,
this is not always possible, because the side effects may be inherent in the
modifications (if, for example, it was somehow the very inefficiency of protein
production that was responsible for the resistance to antibiotics), but, it is typically
the case that an organism that has adapted to some environmental change can
also recover any needed functionality that was lost in the initial adaptation.
This is because further mutations will occur, and
those that tend to refine the organism's functioning so as to retain the new
features while recovering the missing ones will be favored. The proto-giraffe
that evolves a somewhat longer neck may pick up genes for a bigger heart from
another proto-giraffe and thus get rid of one of the main side effects of the
longer neck (greater strain on the heart, and possibly insufficient blood flow
to the head, etc.). A further mutation that increases the strength of the blood
vessels going to and from the head may overcome any tendency to bursting caused
by the increased blood pressure.
[Note: Significantly, despite the claims of supporters
of "Haldane's Dilemma," if there is a population of many organisms,
they need not establish each beneficial mutation before the next one comes,
because one member of the population can have a longer neck while another
member has a larger heart and yet another has sturdier blood vessels. Because
they recombine genes, there is a chance that the ones with the longer necks
will breed with the ones that have the larger hearts, and so on. Since these
combinations will typically be beneficial (in the case where each trait
separately is beneficial), they can easily be favored by reproductive success
for transmission to future generations, thus eventually becoming
"fixated" in the population.]
But the basic fact is that not all mutations have
negative side effects, especially if the main function of a mutation is to
correct a side effect of an earlier mutation. Such additional mutations will
typically be smaller than the initial one because they only need to introduce
enough of a modification to overcome or partially overcome the side effect.
Thus, if resistance to antibiotics brings reduced protein-making efficiency, it
may well be the case that this protein-making efficiency can be recovered by a
mutation (or a series of mutations) smaller than the one that produces the
antibiotic resistance. This will not always be the case, of course, but, unless
the reduced protein-making efficiency and the resistance to antibiotics are
exactly the same at some physiological level (if, for example, the antibiotics
are tuned to efficient protein-making as such and somehow take advantage of it
to kill the bacterium -- by making it overproduce some proteins, I suppose),
then there is no reason that further mutations can't fix the problem, given
enough time. Since we tend to switch antibiotics when one becomes less useful
due to resistance, we rarely keep a consistent evolutionary
"pressure" on the bacteria to evolve both resistance and
efficient protein making.
But, suppose we continued using an antibiotic at the
same rate even after bacteria were almost completely immune to its effects.
Then what? I predict that, if there is any significant advantage to the
more-efficient protein-making processes, there will be evolution to recover
this efficiency despite the side effects of the antibiotic resistance (again,
unless the protein-making inefficiency and the resistance are really the same
thing physically and genetically).
It would be possible to do such an experiment with
animals and a selected bacteria species that has already developed resistance.
Basically we would keep the animals frequently dosed with this antibiotic so
that it became a constant in the environment of the bacteria, and thus
providing plenty of opportunity for beneficial mutations to occur to that would
eliminate or reduce any negative side effects of the antibiotic resistance.
Would anyone like to bet that this will never happen (I can always use a
few extra bucks)?
These mutations can include mutations to the same
genes that introduced the benefit to begin with. Suppose that there is
something about the antibiotic resistance gene that causes the reduced
protein-making efficiency, but that that aspect of the gene is not really
essential to its antibiotic resistance, because it is merely a holdover from
some previous function of the gene from which this new gene evolved (by
duplication, perhaps). Now, suppose that this antibiotic resistance gene itself
is modified over time so that it retains the antibiotic resistance effect but
simply loses its negative effect on protein making.
Although I say "suppose" a lot in the
preceding paragraph, it's because I'm only giving a hypothetical example. Such
modifications upon modifications do in fact occur, both in nature and in
the lab. This is an observational fact, not a theoretical one.
Because all of this talk about mutations modifying the
effects of previous mutations is actually information-theory talk in disguise.
Every mutation that has any effect at all introduces new information, so there
is no reason to think that beneficial mutations will just magically stop
altogether if one has already occurred. If a beneficial mutation for antibiotic
resistance can occur, then so can one for improved protein-making efficiency,
and one for any side-effects of that mutation, and so on, to the limits
of their benefit to the bacterium's reproductive success.
The claim that beneficial mutations are always
deleterious in some other way is simply false, except by reference to
irrelevant ideas of what is beneficial and what is not. In objective terms, a
mutation that removes a side effect may be purely beneficial, because
all it may do is remove the code that is producing the negative side effect.
The claim that mutations can only have negative
side effects, or worse, that they are always, deleterious is simply delusional
wishful thinking on the part of creationists. It's wishful for obvious reasons,
and delusional because, in order to maintain this bizarre anti-science in their
own minds, they have to deny or corrupt all of the key concepts and facts.
-- Along with mathematics. Many mutations are either
duplications of existing genetic material or modifications of existing genetic
material. For sufficiently small mutations, it is mathematically absurd
to claim that none of them can be beneficial overall to the organism, even if
we grant the silly premise that the environment before antibiotics (for
example) is the "normal" to be used as the standard (etc.). It's like
claiming that no one can ever win an (honest) lottery. If there
is any physical possibility of a win occurring at all, then, given enough
lottery cycles, someone will win. It's also like saying that no random
changes to a book can ever make for an improved book, even if all it
does is add a needed word or letter, or delete a typo.
The only way this creationist claim could be true
would be if there were simply no genetic change that can be beneficial in
principle even if we tried to construct it nucleotide by nucleotide, a
claim that is simply empirically false in the real world. Creationists would
very much like it to be true that mutations are never beneficial
information, but they are simply factually wrong. They would like it to be true
because it fits their theory, not the facts of the real world.
This is why they have to use incorrect definitions of
terms like "normal" and "beneficial." Without this
"stopper" claim, the door is open for evolution to continue
making small beneficial changes, until, viola! (and voila!, too, of course),
the ever-dreaded monster of "macroevolution" would occur, and their
case would be exposed as the pitiful excuse for a theory that it has always
been (since long before Wallace and Darwin). If they didn't make up their own
biologically nonsensical definitions of such concepts as "normal" and
"beneficial," they would lose an entire major category of unsound
arguments.
What makes it seem plausible to them at all, aside
from their desire to have it be so for propaganda purposes (or is it
plausible to them at all?)?
I think it's this: Since most mutations are not
beneficial but are either neutral or harmful, it's almost (in their
minds) the same as all mutations being either neutral or harmful, as if
we could simply ignore anything that doesn't occur with an extremely high
relative frequency (relative to the population).
But, this is precisely what makes their math such bad
math: We can't do this in biology, diseases, fire control, and computer-virus
control. If ninety-nine out of a hundred bonks on the head are quite definitely
harmful (or, at best, neutral), we can pretty much ignore the one bonk that
might be beneficial (because we don't want to pay for it with, on average, 99
harmful bonks). But, if we are trying to prevent fires, the fact that most
campers in the forest don't start forest fires is, at any particular time,
unimportant if one camper does start a forest fire, no matter how
small, because that initially tiny blaze may grow and burn down the entire
forest. Similarly, if you eat food that is not in good condition but which has
no bacteria dangerous to you in it, you may do just fine. But, if you eat food
that has even just a few deadly (to you) bacteria in it (even if the food is otherwise
in perfect condition), they may kill you, even though there are just a few of
them (initially).
Why? Because, like forest fires, bacteria reproduce.
Fires "reproduce" by spreading to new fuel. Bacteria do it by
cell-division and growth of the resulting cells.
In reproductive biology, even one mutation that
is genuinely beneficial cannot rationally be ignored, because the fact
that it is beneficial gives it a better chance (on average) than other
mutations or even existing gene alleles at the same locus. Given time, it can
spread to become universal in the population of the species, even if it started
out as just an insignificant statistical "fluke" in the eyes of
creationists.
Why can this happen? Why does it happen?
Because such mutations are both beneficial to the organism that has them and
they are informational. Genetic information differs from the configuration of,
say, a long nylon polymer, because it can be (generally) copied, thus
passing the benefit on to further organisms. Once the initial beneficial change
has been "paid for" (by all the other mutations that have to be
accepted in order to find the one beneficial one), the further use of that
benefit is (at least in this respect) "free" (that is, Dembski's
"lunch" has been paid for).
Incidentally, if you doubt any of this, I suggest you
write a computer program to emulate the (actual) principles of evolution on a
population and give it a try. After setting up everything when the program
begins execution, have a beneficial gene introduced into just one member of the
population, but make it such that this single lone beneficial gene provides a
fitness/reproductive advantage to that single lone "organism," so
that it's own chances of dying before reproducing plentifully are lower than
the chances of other otherwise similar organisms for the same reproductive
success. In "fluke" cases, the gene will get wiped out (just
by dumb bad luck). But, in other cases, and over the long haul, such beneficial
genes will often spread through the population, as the members of the species
without this trait are gradually edged out of the reproductive race. At first,
the effect on the larger population will be small simply because the number of
individuals with the new trait is small. But, as they become progressively more
common by virtue of their different attrition rates, the effect will become
more noticeable and will spread faster until "complete" fixation of
the gene occurs.
It will spread through the population faster as time
goes on because there will be, for those organisms that don't already have the
trait, fewer opportunities to breed with others that also don't already
have it. Suppose, for simplicity's sake, that there is an initial population of
a hundred organisms of species S. Suppose just one of them currently has the
beneficial mutation, but that it is not recessive and so has a good chance of
being expressed in this organism's offspring. And suppose it is in fact
expressed in the offspring. And suppose it provides a significant reproductive
fitness advantage as compared to the rest of the population.
At this point, only a few members of the population
have it, and so, most of the time, any randomly-selected organism that doesn't
have this trait will be one that will breed with another organism that also
does not have this trait (simply because of the proportion of those that don't
have it to those that do). However, because this also applies to those few that
do have this trait, they will usually be helping to spread the
trait. When their percentage gets to be higher, the number of organisms that
don't have this trait will be lower (assuming a constant total population), and
so now the chances that an organism that doesn't have this trait will breed
with one that does have it is significantly higher. When the new trait
has spread throughout half the population, there will be about a fifty percent
chance than the breeding partner for an organism that doesn't have the trait
will be one that does have the trait.
This is a big increase from the days when the trait
was only possessed by one lone organism. Thus, the rate of spread will increase
even more now, and even more in the next generation, until, very rapidly, the
new gene has become almost completely universal to the population.
Put another way, the rate at which a beneficial trait
spreads is partly a function of the percentage of the population that already
has it, so the rate itself changes over time, increasing until it reaches the
point where the only members of the species that don't have it are ones that
have a mutation at that locus, or until a point is reached where there is
diminishing returns because of an increase in the value of alternatives due to
the reduction in their frequency (if you have a gene that inclines you to eat a
certain food, the amount of that food available to you may be greater if
other members of your species do not have an inclination to eat that
food, even if their disinclination is due to a gene that is otherwise
beneficial up to its current frequency).
If you write the program suggested above and use
reasonable assumptions, such as that the trait is not one that directly
increases mating attractiveness (then, the effect is even stronger), you can
prove it for yourself. You don't even have to emulate actual evolution by
actually having software or data structures to represent individual organisms.
You only need to represent the mathematics correctly for each generation. This
will be better, in some ways (if you do it right) because it will give you information
about averages directly instead of requiring that you monitor an actual
evolutionary process and keep statistics on it, and do it many times to ensure
that the fluky cases are averaged into the whole.
What is happening in the evolutionary scenario
described above (and which occurs with many variations in the real world)?
Genetically new information enters the genotype and then spreads through a
population via information duplication.
In fact, evolution is the evolution of
information, and it is information which is, in a metaphorical sense,
information "about" how genetic information can survive in its
environment (including the physical medium of DNA). If this information is
sufficiently "correct," the information does survive.
If it is not, it is filtered out. Natural selection is
an information filtering process. It takes as input large number of
"messages" represented in a phenotypical form, many of which have
some "noise" in them, and filters out those "messages" that
don't meet the survival requirements of information in that environment. The
organisms are "selected" (or not) directly by the environment, but
the information is already present in the genes, so selecting indirectly
selects genetic information as well. Because of the correlation of phenotypical
traits with genetic information, it is easy to assume that selection is the
selection of phenotypical traits, but the core of selection is the selection of
information.
Noise can become useful information in such a context
because that's the way filtering works on random modifications to a message. It
becomes mathematically almost certain that some instances of such
"noise" will produce useful information if there are a lot of trials,
a lot of messages that may be modified each with its own bit of noise. This is
standard Shannon information theory combined with the fact of many repetitions
of the "messages." For each individual message, the probability is
that noise will not be beneficial to it. But, mathematically, it becomes all
but absolutely certain, over a large enough number of repetitions and
sufficiently nearly random modifications ("noise"), that there will
be some that are beneficial.
To illustrate, consider the "message":
MTAXYBALLY, and suppose this message is in competition with many others of a
similar sort, such that those that have certain combinations of consonants and
vowels will tend to be favored, while the rest will tend to be removed from
further repetitions. Suppose that the environment consists of a set of
statistical rules that happen to be the same as those of English with regard to
combinations of letters, and that these rules are applied blindly, with no
intelligence at all, like laws of physics. Will this system be able to evolve
"MTAXYBALLY" into the word "MATHEMATICALLY"? Yes, even
though, nowhere in the entire system of rules are there any words
(except insofar as they are inherent in the statistics of letter combinations,
as, for example, the word "ion," which is included only because it is
a frequently used three-letter combination at the ends of words (as it is in
the word "combination," for example)). Why can a word like this
evolve in such a clearly "dumb" system (where the rules are
mechanically, unintelligently, applied, and where the rules themselves are mere
probabilities of letter combinations)? It can happen because of the large
number of repetitions, and because each "success" establishes a new "base-line"
from which future changes start. We never have to try to randomly select all
the letters of the final long word all at once, but only by a gradual, evolutionary
process of mechanical trial and error.
[Note, please, that this system does not work because
we have somehow "implanted" our own intelligence into the system
(besides, how many creationsts/ID-ers would settle for a designer no smarter
than the average computer programmer?!). All we have put into it are
probability values for different letter combinations, which involve no
knowledge of English as a language, but only as strings of letters. We have to
have some intelligence to write such a program, but that's different
from having the program itself be intelligent (as many of my own
programs prove). If we were to try to produce evolution by emulating a physical
world, it would take intelligence to create the emulator, but the emulated
physical events themselves would be no more intelligent than the falling of a
rock in the real world.]
Because the signal to noise ratio is high enough,
genetic modifications don't normally destroy the "message" entirely.
Most copies of the information are fairly faithful to the
"original(s)" (but only in a piecemeal way in the case of diploid reproduction).
But there are enough modifications that are make the signal "better"
for the local filtering process that there can be gradual change to a species
(or a subpopulation of a species) over time.
All genetically active mutations are new
information. Information is obtained from "noise" by filtering,
filtering in such a way as to keep changes that constitute improvements.
The direct application of standard Shannon information
theory to evolution shows that, given almost any standard for what constitutes
improvement (as long as it is not some bizarre step function, etc.), and given
a sufficiently nearly randomized introduction of changes in the signal, some
of the changes have to be improvements (by that standard).
It is mathematically improbable in the extreme
that no such changes will ever be beneficial. The environment is an information
filter that works by filtering the organisms themselves and thereby indirectly
filtering their genes, and thereby filtering genetic information,
leaving (mostly) only such bits of "noise" that turn out to be
evolutionarily better information (for survival in that very same
information-filtering environment)
Arbitrary Platonic ideas of what is normal and what is
beneficial are simply not relevant to whether evolution is true or not in the
real world. What is beneficial evolutionarily is whatever promotes reproductive
success.
Feedback, discussion, comments, questions: Chris Cogan, ccogan@ou.edu