Maquiziliducks

The Language of Evolution

Sean D. Pitman M.D.

© June 2003
© October 2007

Table of Contents
• An Explosion in a Junkyard
• Functionally Different
• Irreducible Complexity
• More Bad than Good
• Neutral Mutations
• Antibiotic Resistance
• Humpty Dumpty Sat on a Wall . . .
• Single Protein Enzymes - not so simple
• The Language of DNA
• Cats Turning into Dogs
• A Million Monkeys Typing . . .
• Methinks it is Like a Weasel
 • Common Examples of Evolution in Action
• Crystals, Fractals, Chaos and Complexity
• So Confusing!

Home

An Explosion in a Junkyard

A common argument put forward against the theory of evolution is that evolution is

statistically impossible, like an explosion in a junkyard creating a Boeing 747.

Evolutionists ridicule this argument and hold it up as proof of the ignorance of those who

use such “strawman” arguments. Of course strawman arguments are those that

attempt to attack a particular position or idea by presenting a false idea as the real

thing. In other words, the opposing position is misrepresented by a weaker and easily

defeated strawman argument. So, what is the “real man” of evolution?

It is undeniable that the simplest

living system far outshines the

complexity of a Boeing 747. Even

the "simplest" living cell easily does

the job. So, here we have our

biological Boeing 747. How did it get here from the surrounding pile of non-functional

biological “junk”? The odds of such complexity suddenly assembling itself from the

biochemical junkyard are truly more remote than a Boeing 747 being created by an

explosion in the city dump. Of course evolutionists see no problem here since they

understand just how easily this problem is solved. Obviously such complexity is not

created suddenly, but gradually. The energy of the explosion is not random and

suddenly spent, but is directed over long periods of time through a selection process

called natural selection. In this way, increasing complexity is formed gradually, in a

stepwise fashion.

So, to represent the theory of evolution as requiring the sudden formation of

complexity is simply the building of a strawman that does not really exist. The true man

of evolution is built upon the concept of gradual change. These changes are made

possible because each tiny step is recognized as something functionally new and

beneficial by nature. If the change is seen as reproductively advantageous by nature,

this new step will be maintained. Conversely, all detrimental steps will be eliminated by

nature. In this way natural selection guides the random changes in a non-random way.

So, when challenged to explain how randomness can create complexity, evolutionists

just smile a knowing smile and proceed to explain just how simple it all is. Evolutionists

see this truth so clearly that it is really quite amusing for them to hear the confusion of

creationists and design theorists who try to question the validity of such a simple and

obvious fact of nature with arguments that reveal only ignorance as to the very process

of evolution.
 BioVisions at Harvard University

Cellular Visions: The Inner Life of a Cell

(Link)

Functionally Different

However, there is just one little problem. Did you notice it? The catch for the theory

of evolution is the word “functional.” In order for changes to be selected for or against

by nature, in a positive non-random way, they must be functionally different from the

other previous functions. Many genetic changes are in fact "detrimental" or "neutral"

changes with regard to reproductive advantage. There are also portions of genetic
elements that have no known function at all. Changes to these genetic sequences are

also functionally neutral because they have the same non-function as they had before.

In order for nature to be able to "select" between two difference sequences, they must

be functionally different from each other; not just sequentially different. The reason for

this is because nature does not analyze sequences. Nature only analyzes function.

Once there are functional differences between two sequences, nature selects for the

one that has more beneficial function, with regard to reproductive advantage, over the

other. So, not only do changes have to be functionally different in some way to enter

the selection process, but, to avoid discard, the changes must be beneficial as well.

So, can something that is at least as complex as a Boeing 747 be made in a

stepwise fashion with each step being functionally beneficial? Before we answer this

question, we must first check with the evolutionists to see if they agree that evolution

must work this way. Do evolutionists agree that each step of evolution must be

functionally beneficial?

Irreducible Complexity

In order to answer this question one needs only look at how ardently evolutionists

oppose the idea of “irreducible complexity.” This idea was proposed in 1996 by the

biochemist Michael Behe in his book, Darwin’s Black Box.1 His book ignited a fair bit of

controversy and discussion, even in the scientific community. The concept of irreducible

complexity is basically the idea that some types of function or systems of function will
not work at all, in their original capacity, if any one part is removed. In other words, a

minimum number of parts is required for a particular function to work. The obvious

assumption is that the existence of such a system cannot be explained by any

gradualistic mechanism of assembly such as the one proposed by the theory of

evolution. Behe proposed several examples of irreducibly complex systems to include a

bacterial flagellum and a common mousetrap.

Evolutionists generally responded by denying that any irreducibly complex system

exists in the natural world. They claimed that all functional systems can be broken

down into smaller and yet smaller functional systems. By their adamant opposition to

the idea of irreducibly complex systems, evolutionists seem to be admitting that each

evolutionary step must be functionally beneficial. In fact they attempt to show how

mousetraps and bacterial flagella can be formed gradually where each mutation is

functionally beneficial. Obviously therefore, the maintenance of function and the

generation of improved function, each step along the evolutionary pathway, is of key

importance to the theory of evolution.

What many fail to realize is that all systems of function are irreducibly complex.

Take Behe's mousetrap illustration for example. There are those who claim that all of

the parts can be removed in various ways and the resulting mousetraps will still catch

mice. Certainly there are a great many different ways to catch mice, but each way is

irreducibly complex. Removing or changing this part or that part may still catch mice,

but not in the same way. Each different way is uniquely functional as well as irreducibly

complex. Even if the changes still catch mice, the unique function of the original

mousetrap has still been lost. Of course, if a series of mousetraps could be built with
each and every small change resulting is a better mousetrap, a very complex

mousetrap could be evolved, one step at a time. However, the resulting complexity of

the most complex mousetrap is still irreducible. There are still a minimum number of

parts required for it to catch mice in that particular way.

Really then, an irreducibly complex system is not impossible to evolve. It happens

all the time in real life. For example, single protein enzymes, like lactase and nylonase,

have been shown to have evolved in real time in various bacteria. These enzymes are

actually very complex. They are formed from even smaller subunits called amino

acids. Long strings of these amino acids must be assembled in the proper sequence or

the particular enzymatic function in question will not be realized. Certainly, to produce a

function like the lactase function, there must be a minimum number of parts in the right

order. The lactase function is therefore, "irreducibly complex". Of course, there are

many different recognized as well as potential lactase enzymes out there in the

vastness of sequence/structure space. Yet, all of them are irreducibly complex. They all

require a minimum number of parts (amino acids) all working together at the same time

to produce a specific type of potentially beneficial function - like the lactase function.

The question is, do these "irreducible" sequence and structural requirements prevent

such systems from evolving? Surprisingly for some, the answer is no. On occasion,

such single-protein enzymes have been shown to evolve de novo in certain bacteria.

Really then, the fact that a function is irreducibly complex does not mean that it is

beyond the reach of mindless evolutionary processes.

So, where is the problem? If irreducible systems of function can be evolved, and

they clearly can be evolved, the case is closed is it not? Well . . . not quite.
 More Bad than Good

It is interesting to note that the vast majority of the inheritable changes in biological

systems are neutral or even harmful. As previously discussed, neutral changes cannot

be selected for or against by nature and harmful changes (defined by being

reproductively disadvantageous) are selected against. We must consider then only

those very few mutations that actually result in some detectable, beneficial, phenotypic

change.

To understand a little of the rarity of such "beneficial" mutations, consider that the

overall mutation rate for an average living cell is on the order of one mutation per gene

per 100,000 generations.9,10,11 Estimates for the average human genomic mutation rate

run between 100 and 300 mutations per generation.13,14 In other words, a human child

will have from 100 to 300 mutational differences from his or her parents. Of these

mutations, only around 2% will be "functional" mutations. Of all functional mutations,

most estimates use a ratio for beneficial vs. detrimental mutations of 1:1000.15,16 That

means that it would take around 500 generations (about 10,000 years) to get just one

beneficial mutation in a single family line.

So, from the perspective of a single human gene, it would take around 50 million

generations (a billion years) to realize a single beneficial mutation in a single family

line. During this time each gene in the family genome would have also been hit by

around 1,000 detrimental mutations. No one seems to have a satisfactory explanation

as to how all these detrimental mutations are eliminated fast enough in order for the

very rare beneficial mutations to keep up. Unless beneficial mutations can keep up with

the much higher detrimental mutation rate, extinction will occur in relatively short order.

In fact, estimates show that in order to keep up with such a low ratio of beneficial vs.

detrimental mutations, the average human woman would have to give birth to more than

20 children in each generation. Some authors suggest that a more realistic number is a

reproductive rate of 148 children per woman per generation (link to discussion).

Why living things with relatively long generation times, like humans and apes, have

not yet gone extinct over the course of millions of years remains a mystery. Consider

an excerpt from a fairly recent Scientific American article entitled, "The Degeneration of

Man" :

According to standard population genetics theory, the figure of three harmful

mutations per person per generation implies that three people would have to die

prematurely in each generation (or fail to reproduce) for each person who reproduced in

order to eliminate the now absent deleterious mutations [75% death rate]. Humans do

not reproduce fast enough to support such a huge death toll. As James F. Crow of the

University of Wisconsin asked rhetorically, in a commentary in ‘Nature’ on Eyre-Walker

and Keightley's analysis: “Why aren't we extinct?"

Crow's answer is that sex, which shuffles genes around, allows detrimental

mutations to be eliminated in bunches. The new findings thus support the idea that sex

evolved because individuals who (thanks to sex) inherited several bad mutations rid the

gene pool of all of them at once, by failing to survive or reproduce.

 Yet natural selection has weakened in human populations with the advent of modern

medicine, Crow notes. So he theorizes that harmful mutations may now be starting to

accumulate at an even higher rate, with possibly worrisome consequences for health.

Keightley is skeptical: he thinks that many mildly deleterious mutations have already

become widespread in human populations through random events in evolution and that

various adaptations, notably intelligence, have more than compensated. “I doubt that

we'll have to pay a penalty as Crow seems to think,” he remarks. “We've managed

perfectly well up until now." 17

Even though I do not agree with much of Crow's thinking, I do agree with him when

he says that harmful mutations are accumulating in the human gene pool far faster than

they are leaving it. However, on what basis does he suggest that harmful mutations

spontaneously cluster themselves into “bunches” for batch elimination from the gene

pool of a given population? Crow does not suggest a mechanism nor does it seem

remotely intuitive as to how this even might occur via naturalistic means. Calculations

show that at best the advantage provided by sexual reproduction reduces the

detrimental effect of detrimental mutations by half. This reduction is not significant

enough to solve the enormity of the problem (see further discussion).

Also, Keightley is far too optimistic in my view. He assumes that because evolution

has happened in the past, that somehow evolution will solve the problem. He fails to

even consider the notion that perhaps humans, apes, and other species with

comparably long breeding times have been gradually degenerating all along. Perhaps
evolution only proceeds downhill (devolution)? Perhaps mutations do not improve

functions over time so much as they remove functions over time in species with slow

generation times?

Then again, even if the degenerative effects of mutations were somehow solved in

populations with slow reproduction times, the addition of new information to the gene

pool that goes beyond very low level functional systems involves the crossing of huge

oceans of neutral or even detrimental sequence gaps that would take, for all practical

purposes, forever to cross. It seems as though mutations, averaged over an extended

period of time, tend toward loss and extinction rather than toward any sort of

improvement or gain.

Neutral Mutations

Of course, there are some who argue that functional mutations are not the only

mutations that contribute toward phenotypic evolution. Many claim that even neutral

mutations have a contribution. Motoo Kimura's work, "The Neutral Theory of Molecular

Evolution", published in 1983, is often quoted in support of this assertion. However,

Kimura's basic idea was that many genetic changes are in fact neutral and that these

changes are beyond the detection of natural selection. He writes, "Of course, Darwinian

change is necessary to explain change at the phenotypic level - fish becoming man -

but in terms of molecules, the vast majority of them are not like that." 4 Kimura basically

considered random genetic drifts in populations and did not primarily concern himself
with phenotypic or functional genetic changes. Kimura's work was the first to seriously

challenge the notion that all or even most mutational changes can be guided by natural

selection.

Certainly then, it is an error to say that Kimura’s work with neutral evolution

explains any sort of phenotypic evolution. Of course, Darwinian evolution is all about

phenotypic or functional evolution. Kimura himself said that neutral evolution could not

explain Darwinian evolution. Therefore, the neutral theory of evolution does not get

Darwinian evolutionists out of the task of explaining how functionally different

phenotypes evolve gradually.

Many continue to argue though that neutral mutations are not significant since they

really do not interpose themselves between the various functions of living things to any

significant degree. It is suggested that a series of mousetraps can be built from the

most simple to the most complex with each tiny change being functionally beneficial the

entire way. There really are no significant neutral or detrimental gaps to hinder this

process. Therefore, no significant random drift is or was required to cross the distance

between each beneficial change.

Antibiotic Resistance

Is it true? Is the argument that no significant neutral or detrimental gaps exist that

must be crossed without the help of natural selection actually true?

 Well, this argument is certainly true when it comes to the de novo evolution of

antibiotic resistance in many different types of bacteria. It is quite interesting to note

how bacteria evolve antibiotic resistance. All of them do it pretty much the same way.

The method is really quite simple. It is based on the fact that antibiotics have very

specific interactions with particular targets within bacteria. Many different point

mutations to a particular target sequence will interfere with its interaction with the

antibiotic. This interference results in bacterial resistance to that antibiotic. Such

resistance develops very rapidly because a very large ratio of mutations to the target

sequence have the potential to significantly interfere with antibiotic's interaction with the

target. Because it is so likely to get at least one out of many potentially interfering

mutations to occur in at least one member of a large population of several billion

bacteria, the average time needed to evolve antibiotic resistance, regardless of the type

of bacteria or antibiotic used, is usually measurable in days to weeks (under sublethal

levels of antibiotic exposure).

Other bacteria have pre-formed genetic codes for certain enzymes that attack a

particular antibiotic directly (i.e., penicillinase). Such enzymes are fairly complex and

have not been shown to evolve directly in real observable time. However, those

bacteria that have access to the pre-formed codes/genes for these enzymes usually

regulate the production of these genes so that limited quantities are produced. When

exposed to large quantities of the antibiotic, there simply isn't enough enzyme to deal

with such large quantities of antibiotic and the bacterium dies. However, many different

point mutations are capable of disabling the control of enzyme production so that

massive quantities of the enzyme are produced. So, when very high levels of the
antibiotic come around again, these bacteria are able to survive and pass on their

poorly controlled enzyme gene to their offspring.

Humpty Dumpty Sat on a Wall . . .

Of course, in both of the above described methods of antibiotic resistance, the

lucky bacteria gained the antibiotic resistance function through mutations that interfered

with various interactions or previously functional systems. They did not make a new

function from scratch, but only interfered with an existing function (i.e., the antibiotic-

target interaction). This sort of disruption of a previous function or interaction is

analogous to the famous children's story of Humpty Dumpty who fell off the wall.

Remember that it was much easier to break Humpty Dumpty than it was to put him back

together again. Every child knows this law of nature. It is far easier to destroy than it is

to create.

Why is this? Why is it easier to destroy than it is to create from scratch? The

reason is that there are a lot more ways to destroy than there are to create. There are a

zillion more ways to break a glass vase than there are to fix or re-create that glass vase

from the resulting shards of glass. The same thing holds true for the various functions

in living things. They are like glass vases.

The evolution of antibiotic resistance was easy because it involved the breaking of

an established function. However, many more functions exist in living things that cannot

be created by breaking some pre-established function. The relatively simple functions

of single protein enzymes are good example of this. There is certainly no way to get a

function like the penicillinase enzyme to evolve by disrupting some other interaction.

The same is true for the lactase and nylonase enzymes. The functions of these

enzymes cannot be realized by interfering with other pre-established functions. The

experiments of Barry Hall point this problem out quite clearly.

Single Protein Enzymes - Not So Simple

Barry Hall did a very interesting experiment with E. coli bacteria. E. coli bacteria

naturally produce a lactase enzyme that hydrolyses the sugar lactose into the sugars

glucose and galactose, which it can break down further to produce usable energy.

What Hall did was to delete this lacZ gene so that these particular E. coli bacteria could

no longer make the lactase enzyme. He then grew these bacteria on a lactose-enriched

media. In a very short time (one generation), these bacteria evolved the ability to use

lactose again. Upon further investigation, Hall found that a single point mutation to

another very different gene resulted in the production of a lactase enzyme. Hall named

this new gene the "evolved beta-galactosidase" gene (ebgA). What Hall did next is very

interesting. He deleted both the lacZ and ebgA genes in the E. coli and then grew them

on the same lactose-rich media. They never again evolved the ability to make a lactase

enzyme despite thousands of generations of time, a high mutation rate, huge population

numbers, and a selective lactose media that would have benefited them if they ever did

evolve the lactase function again. Hall was mystified. He determined that these double
mutant bacteria had "limited evolutionary potential."4 There are also many other types of

bacteria that have never evolved the lactase function despite observation and records of

them for over a million generations. Besides certain of Hall's E. coli colonies, these

include certain members of Salmonella, Proteus, and Pseudomonas as well as many

more.

So, what was the problem? These very same bacteria that could not evolve the

lactase function over the course of tens of thousands of generations would have quickly

evolved antibiotic resistance to any single antibiotic in just a few generations. Why then

did they have such a problem with a relatively simple single-protein based enzyme

function? The reason is that enzymatic functions are far more complex than the

function of antibiotic resistance. In short, there are different levels of functional

complexity. As it turns out, lower level functions are much easier to evolve Darwinian-

style, exponentially easier, compared to systems of function that have higher minimum

structural threshold requirements.

Consider that a single subunit of the lacZ enzyme is around 1,000 amino acids in

size. The total number of different amino acid sequences of 1,000aa is around

10e1300. That is a huge number. The total number of particles in the entire universe is

estimated to be around 10e80. Out of all these 10e1300 potential amino acid

sequences out there, how many of them would have the lactase function? If there were

a trillion trillion trillion trillion (10e47) lactase enzymes out there of 1,000aa or less, there

would be over 10e1250 non-lactase sequences for every one lactase sequence.

Finding any one of the trillions of functional lactase sequences at random would be like

finding one particular proton in the universes of universes the size of our universe.
Obviously though, the E. coli in Hall's experiment just so happened to evolve a very

different useful lactase sequence in just one generation. Perhaps then the lactase

function is a lot more "simple" or common in the potential of sequence/structure space?

Perhaps the correct ratio would be closer to 1 in 10e23 (trillion trillion) instead of 1 in

10e1250?

This ratio is a lot more reasonable considering that the smallest useful lactase

sequence known is around 380aa in size. One must also consider that the sequence

requirements for a protein of this size are somewhat flexible. For example, if one were

to change a 4 or 5 letters in this paragraph, it's essential meaning or function would

most likely be maintained. However, there is a threshold beyond which too many

changes would completely remove or distort its original meaning/function. The same

thing is true of functional protein-based systems. All such systems have a certain

degree of flexibility. This flexibility translates into an increased number of potentially

beneficial sequences and/or structures in sequence/structure space that could produce

a particular type of functional system - like one with the lactase ability.

In any case, even with a fair degree of sequence flexibility and reduced minimum

size requirements, it is obvious that even the most simple single protein enzymes are

far more complex than most forms of the function of antibiotic resistance. They are

certainly a step up in "functional complexity" or "minimum structural threshold

requirements". With this increased complexity comes a lot more difficulty for the

mindless processes of Darwinian-style evolution to overcome. Antibiotic resistance is

generally quite easy for mindless evolutionary processes to produce because it involves

breaking something. However, these same evolutionary processes have great difficulty
evolving a relatively simple lactase enzyme in thousands upon thousands of

generations in huge populations?

The problems only get worse from here on out. More complex bacterial functions,

such as the motility function, require multiple proteins all working together at the same

time. If just one relatively simple enzyme is hard to evolve, try calculating the time

required for a multi-protein system to evolve. The neutral gaps quickly get

enormous. For example, if one trillion high-level potentially beneficial systems (i.e.,

requiring a minimum of more than 1000 fairly specified amino acid residues) were at

least 30 novel amino acid residue changes away from the currently existing genetic real

estate of a large bacterial colony with a steady state population of one trillion members,

how long would it take for that colony to evolve even one of these potentially beneficial

systems that exist in the potential of sequence/structure space? The gap distance here

is 1e39. If each one of the one trillion bacteria mutated this particular sequence into a

new sequence once every day (without repeating any sequence along the way), it would

take just under 3 trillion years, on average, to cross a gap of just 30 non-selectable

steps.
 Is there

evidence that

such gaps

exist? Well, if

one considers

various

systems with

different

minimum

structural

threshold

requirements,

one starts to

notice a

pattern. The

greater the

minimum

threshold

requirements,

the more

widely

separated

such systems
are in the vastness of sequence space. In short, there is a linear relationship between

the minimum threshold requirements and the number of required amino acid residue

differences between a system and the next closest beneficial system with a novel

function. And, a linear increase in the required residue differences (i.e., the "gap size")

translates into an exponential increase in the amount of time needed for a particular

population size to cross.

Is the problem starting to become clear? If not, perhaps some illustration based on

the way other language systems work may help clarify this issue further.

The Language of DNA

Living biological systems are built using information that is written in the coded order

of four chemical "letters" labeled A, T, C, and G (Adenine, Thymine, Cytosine, and

Guanine). Strings of these letters are called, "DNA" (DeoxyriboNucleic Acid). The

cellular structure (phenotype) is but a reflection of the information written like a book in

the coded language of its DNA. As with other languages, the genetic code is arbitrary.

It codes for letters in another arbitrary language code of proteins. Proteins are also built

using chemical letters that are often assigned meaning or function by the cell or system

of cells that make and use them. There is even a third language of sugars called

glycans that is extremely complex. All of these languages work very much like any

human language-system works.2

 Now, what is the value of an arbitrary symbol in a language? What inherent

meaning do the letters of the alphabet carry? By themselves, do they have any inherent

meaning or function? Obviously not. Their meaning only comes after the meaning or

function is arbitrarily assigned to the symbols by a language system or code. Before

this, the symbols or letters were just like so many random scraps all jumbled together in

an alphabet junkyard, like "maquiziliducks."

What does the sequence of letters, “maquiziliducks” mean? Maquiziliducks is not a

word. The letters are all jumbled up and mean nothing. But why? Why does this

particular series of letters have no meaning? There are some other words such as

"xylophone" that look just a strange and yet xylophone means something in English.

Obviously the reason is that maquiziliducks has no meaning is because it is not part of

the English language system. It gets no points in a game of Scrabble. Of course

maquiziliducks might mean something to an alien from the planet Quaziduck, but what

good it that to an Englishman in an English speaking environment?

So what’s the point? The point is that living biological systems are language

systems just like the English language system or computer language systems. Like all

other language systems, biological language systems use chemical letters and words

that are defined by a limited cellular system and its interaction with its limited

environment. Nothing functions by itself just as no letter or series of letters has inherent

meaning.

Cats Turning Into Dogs

 I have often heard that genetic evolution of new genes with new traits is easy. A

common example used to demonstrate this sort of evolution is the series of words, "cat

to hat to bat to bad to bid to big to dig to dog." This word evolution obviously shows a

dramatic evolutionary sequence that changes meaning with each and every letter

change. There are no "neutral" changes in this evolutionary sequence. It seems pretty

convincing until we remember that there are is a lot higher ratio of three-letter words

when compared to six-letter words. Three-letter words are relatively "simple" in

structure and function. However, just as we discovered above, the neutral gaps get

exponentially wider as we move up the ladder of functional complexity. Moving from the

evolution of antibiotic functions to the evolution of simple enzymes is like going from the

evolution of three-letter words to the evolution of ten-letter words.

A Million Monkeys . . .

Some try to explain this problem by saying that, "A million monkeys typing away will

eventually create all the works of Shakespeare... if given enough time." However, some

quick calculations will show that forming just a small phrase of Shakespeare such as,

"Methinks it is like a weasel.", would take a million monkeys each randomly typing 100

five-letter words a minute, around one trillion trillion trillion years on average. Clearly

then, random chance is powerless to explain the existence of complex language

systems or the evolution of one system into another. There must be something that

helps random chance along. But what is it?

Methinks it is Like a Weasel

Maybe it is not quite fair to compare the English language to the workings of DNA

and proteins. Some evolutionists might balk at this, but many actually do accept the

validity of such a correlation. This acceptance indicates that evolutionists do generally

recognize the coded nature of genetic information systems. In fact, Richard Dawkins,

perhaps the most famous living evolutionary biologist, also explains how evolution might

work by appealing to examples of English-phrase evolution. His “Methinks it is like a

weasel” phrase evolution is really quite famous.3 It has convinced many very intelligent

people that the theory of evolution easily explains the formation of complex biological

language systems. So, let's look a bit into exactly what Dawkins did.

What Dawkins did was to evolve his chosen target phrase with a computer algorithm

that began with a random computer generated series of letters such as “MWR

SWTNUZMLDCLEUBXTQHNZVJQF.” Dawkins begins with a non-functional

meaningless phrase and then evolves “Methinks it is like a weasel” in very short order

by having the computer select for those copies that are "closest" in sequencing to,

"Methinks it is like a weasel." It seems almost miraculous to watch this evolution

happen before one's very eyes on similar algorithms until one realizes that the computer

is selecting based on genotypic similarity to an ideal genotypic sequence - - not on

phenotypic changes in function. None of the intermediate steps in this example of

sequence evolution have any phenotypic (English language) function whatsoever. The

intermediate phrases are meaningless, much less beneficial. These intermediate

phrases represent links in an evolutionary chain of function and yet none of the links

make any sense in the English language.

Missing links in the fossil record are not the real problem for evolution. The really

significant missing links are found in genetics. Where are these missing genetic links?

Without them, all we have are huge neutral/non-beneficial gaps. Really, what real time

examples are there to adequately support the theory of common descent via mindless

Darwinian evolution beyond very low levels of functional complexity?

Common Examples of Evolution in Action

Common examples of

evolution, to include the

differences among the

finches of the Galapagos

islands that Darwin noted,

are really nothing more than

variations within a common

unchanging or "static" gene

pool. As early as 1865

Gregor Mendel, the father of genetics, described such variations as the result of the

mixing and matching of constant traits or alleles. He described the variations of pea

plants by stating that, “Pea hybrids form germinal and pollen cells that in their

composition correspond in equal numbers to all the constant forms resulting from the

combination of traits united through fertilization.”12 In other words, all the various forms

that exist in the pea plant were contained within a common gene pool of trait options.

Mendel found that the phenotypic expression of individual plants was merely the

reflection of a small portion of a large but finite pool of options within a common gene

pool.

Therefore, although such changes

can be very dramatic, they need not be

dependent upon mutation or the

acquisition of new genes or traits that

were not already available. The same

can be said for other famous examples

such as the shift in the color of England's peppered moth - - not to mention the fact that

there have arisen a few questions as to the methods used by Kettlewell in his original

analysis of peppered moth pigment "evolution".6,7,8 But, even if his methods were

completely flawless, such changes are only examples of phenotypic variance within the

same gene pool. In other words, the moths did not evolve a color or pattern that was

not already being expressed by moths within the same gene pool. This type of

phenotypic variation, although directed by natural selection, is not an example of

Darwinian-style genetic evolution since no new genes, systems or traits with novel

functions were added to the pool.

Other famous examples of evolution in action, such as flightless birds on windy

islands, cave fish without eyes, and sickle cell anemia, among many others that are

based on destruction or interference with existing genes and traits rather than on the

evolution of new traits/functions from scratch. All of these examples involve either the

loss of a gene or its regulation. Of course a change in the degree of function or the

complete loss of a gene is far different from the evolution of a new and unique genetic

function (remember Humpty Dumpty). Such genetic losses of and interference with

established functions do have phenotypic effects that can be detected and selected for

or against by nature, but nothing really new or unique is made that was not already

there. Of course, there are in fact many examples detailing the evolution of unique

genes producing uniquely functional products, but such examples of real evolution in

action are clearly limited to the lowest rungs of the ladder of increasing functional

complexity (i.e., The "limited evolutionary potential" of Hall's E. coli bacteria).

Crystals, Fractals, Chaos, and Complexity

Some might say that crystal formation is an example of the spontaneous formation of

self-replicating complexity. However, crystal formation is not an example of a language

system where the collective function of the parts is greater than the sum of all the parts.

The information needed for the order of a crystalline structure is entirely contained by
each molecule within that structure. This is not the case with the information contained

in a molecule of human DNA. The information for the specific order of this molecule is

not contained by any of the individual molecules that make up this strand of DNA. The

information content is more complex than the molecules themselves. The information

carried by DNA is greater than the sum of its parts. The same thing is true of the

English language system. The letters in this sentence that you are reading do not know

how to self-assemble themselves to form this sentence in a meaningful way. Clearly

then, the information in a crystalline structure does not even come close to the most

simple language system, much less the information content of DNA or living systems of

function.

Of course, many crystalline structures appear to be very "complex", but they this

complexity is based on the relatively low "information" content needed to form fractals.

Very little information is needed to form such fractal-type structures, even though the

final structure might appear to be very complicated indeed. But, this "complexity" isn't

really "informational complexity", but is better termed "chaos" or "randomness". Fractals

and other such structures are not more informationally complex than the information

contained by the least common denominator. This is not like DNA and other symbol-

based language systems where the information carried by the order of the parts is much

greater than the total sum of the information carried inherently within the parts

themselves.18

So Confusing!
 It all seems quite confusing. The theory of evolution is not so easy to understand as

many have led us to believe. Even those who have been trained as evolutionists and

who are experts in the field of genetics, such as Michael Behe and others like Nobel

Laureates Richard Smalley and Charles Hard Townes, astronomer Sir Frederick Hoyle,

mathematician Chandra Wickramasinghe, and many others seemed confused (Power

Point Link). If evolution is so simple to understand, then how can some of the most

educated, intelligent, rational scientists who have had the best and most rigorous

training that evolutionary thought and science has to offer... still not get it? If anyone

should be clear on how evolution works these scientists should be. And yet some of

these scientists challenging the very existence of genetic evolution? Is the idea of

irreducible complexity all that really crazy? And yet, the truth of evolution is just so

obvious to so many that those who are skeptical of it must either be "stupid, ignorant, or

insane"19; or all of the above. But what about all those maquiziliducks?

1. Behe, Michael J. Darwin’s Black Box, The Free Press, 1996.

2. Stryer, Lubert. Biochemistry, 3rd ed., 1988, pp. 153, 744.
3. Dawkins, Richard. The Blind Watchmaker, 1987.
4. B.G. Hall, Evolution on a Petri Dish. The Evolved B-Galactosidase System as a
Model for Studying Acquisitive Evolution in the Laboratory, Evolutionary
Biology, 15(1982): 85-150.
5. Kimura, Motoo. The neurtral theory of molecular evolution, New Scientist, 1985,
pp41-46.
6. D.R. Lees & E.R. Creed, ‘Industrial melanism in Biston betularia: the role of
selective predation’, Journal of Animal Ecology 44:67–83, 1975.
7. J.A. Coyne, Nature 396(6706):35–36.
8. The Washington Times, January 17, 1999, p. D8.
 9. Dugaiczyk, Achilles. Lecture Notes, Biochemistry 110-A, University California
Riverside, Fall 1999.
10. Ayala, Francisco J. Teleological Explanations in Evolutionary Biology, Philosophy
of Science, March, 1970, p. 3.
11. Lewin, Benjamin. Genes V, Oxford University Press, 1994.
12. Mendel, Gregor. Experiments in Plant Hybridization. 1865.
13. Ninth International Conference on Microbial Genomes, October 28th-November
1st, 2001. Gatlinburg, TN (
http://cgb.utmem.edu/meeting_reports/redwards_11_06_01.htm )
14. http://genetics.hannam.ac.kr/lecture/Mgen02/Mutation%20Rates.htm
15. http://www.cs.unc.edu/~plaisted/ce/genetics.html
16. http://socrates.barry.edu/snhs-jmontague/courses/BIO%20440%20-
%20Evolution/440%20ppt%20lectures/440%20web%20lec%2005%202002.ppt
17. Beardsley, Tim, The Degeneration of Man, Scientific American, April, 1999, p32
18. Baranger, Michel, Chaos, Complexity, and Entropy, A physics talk for non-physicists, Center for
Theoretical Physics, Laboratory for Nuclear Science and Department of Physics Massachusetts
Institute of Technology, Cambridge, MA 02139, USA and New England Complex Systems
Institute, Cambridge, MA 02138, USAMIT-CTP-3112 ( http://necsi.org/projects/baranger/cce.pdf )
19. Richard Dawkins, "Put Your Money on Evolution", Review of Johanson D. & Edey
M.A., "Blueprints: Solving the Mystery of Evolution", in the New York Times, April
9, 1989, sec. 7, p. 34

. Home Page . Truth, the Scientific

Method, and Evolution

. Methinks it is Like a Weasel . The Cat and the Hat -

The Evolution of Code

. Maquiziliducks - The Language of Evolution . Defining Evolution

. The God of the Gaps . Rube Goldberg

Machines
. Evolving the Irreducible . Gregor Mendel

. Natural Selection . Computer Evolution

. The Chicken or the Egg . Antibiotic

Resistance

. The Immune System . Pseudogenes

. Genetic Phylogeny . Fossils and DNA

. DNA Mutation Rates . Donkeys, Horses,

Mules and Evolution

. The Fossil Record . The Geologic

Column

. Early Man . The Human Eye

. Carbon 14 and Tree Ring Dating . Radiometric Dating

. Amino Acid Racemization Dating . The Steppingstone

Problem
. Quotes from Scientists . Ancient Ice

. Meaningful Information . The Flagellum

. Harlen Bretz . Milankovitch Cycles

. Kenneth Miller's Best Arguments

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