Defining Evolution

And its Boundaries

Sean D. Pitman M.D.
© September 2006

Table of Contents
• Introduction
• Charles Darwin
• Gregor Mendel
• Breeding by Human Selection
• Random Mutations
• Functional vs. Neutral Mutations
• Antibiotic Resistance
• Enzyme Evolution
• Limited Evolutionary Potential
• Growing Neutral Gaps
• The Ladder of Functional Complexity
• An Illiterate Construction Forman
• Adding a Stereo to a Car

Home Page
 The theory of evolution is based on a very simple and elegant idea. The idea is that

all living things have a common ancestor. The differences between living things that

exist today are thought to be the result of "common decent with modification" or slight

changes over time that have simply added up over many millions of generations to

produce the remarkable variety that we see today. These modifications are the result of

mindless non-directed random genetic mutations combined with natural selection.

Natural selection is able to select between these randomly produced genetic sequences

in such a way that those sequences with the greatest attached beneficial function

provide their host the the greatest reproductive advantage. In this way, natural

selection, while still mindless or non-intentional, is the non-random part of

evolution. 3,4,5,6

If the amazing diversity of life forms on this planet arose from the evolutionary

potential of a common ancestor life form, the assumption can be made that all or nearly

all life forms living today have the same potential for future diversity. If true, this

mindless force is a very creative force. But, how does this mindless force work?

Most will agree that if living things change over time, they change because their

D.N.A. (deoxyribonucleic acid) changed. The information contained in the DNA is called

the “genotype.” The expression of this information in the physical form of the creature is

called the “phenotype.” 1, 2 DNA is very much like the paper that the blueprint for a

house is written down on. This blueprint is equivalent to the genotype. The actual

house, once it is built, is equivalent to the phenotype. The phenotype changes only if

the blueprint changes.

 The theory of evolution proposes that all the

various blueprints of living things are descendents of

a single common ancestor blueprint. The diversity

of blueprints that exist today is simply the result of

variations on a single theme. If true, the power of

the mindless evolutionary force of nature is truly

astounding. The sheer creativity and magnificent

diversity of nature is enough to make even the most

cynical stand in silent awe. If humankind could harness this power and speed it up with

the aid of our intelligent minds, the implications for advancement seem unlimited.

How then does this mindless evolution work? How does the equivalent of a

blueprint for a house change over time to code for phenotypic structures as diverse as

an automobile, a battleship, a skyscraper, or a screwdriver? Obviously, at least this

degree of diversity is seen in living things in the forms of creatures like bacteria, oak

trees, and elephants. In considering this question perhaps we should begin with Darwin

and what he saw. (Back to Top)

Charles Darwin

Charles Darwin (1809-1882) came up with his famous version of the theory of

evolution after observing some very interesting differences, such as the variation in the

size and shape of finch beaks on the Galapagos Islands. Many other similar changes
have also been observed and carefully documented. Certainly these are “changes” and

as changes many would call them evolutionary changes. If the theory of evolution is

defined as any and every phenotypic change that occurs from parents to offspring, then

it might be perfectly fine to say that finches are demonstrating evolution in real time.

But, are they demonstrating genotypic evolution? Has the blueprint changed in an

informationally unique way? Is it possible to have change in phenotype without a

change in genotype? In other words, do the phenotypic changes in the finches that

Darwin observed require new meaningful genetic information that the ancestor finches

never had? (Back to Top)

Gregor Mendel

Darwin was unable to

answer this question

although the answer was in

fact available in his own day.

Gregor Mendel (1822-1884),

the father of genetics, came

up with the idea of “alleles”

or unchanging “traits” after

studying pea plants. 3,7

What he discovered is that certain phenotypic traits, such a pea color, texture, shape,

and a number of other traits, are passed on by unchanging genotypic alleles. Different

combinations of these alleles result in different allelic expressions in the phenotype.

For example, lets say that a house needs colored carpet. Colored carpet is a “trait”

or characteristic of the house listed in the blueprint. The blueprint of this particular

house is interesting however in that it is a double blueprint. There are two pieces of

paper that code for every aspect of the house. The two blueprints are identical as far as

the traits that they code for (ie: colored carpet), but they are different as far as the trait

variations are concerned (ie: red, yellow, green, blue or white carpet). If one blueprint

coded for green carpet and the other coded for white carpet, what color would the

carpet be? It will be the “dominant” color.

Mendel found that allelic traits could be either dominant or recessive (We now know

that they can also be co-dominant, incompletely dominant, additive, multiplicative etc.)

This is made possible because of the fact that many traits have at least two alleles, or

two separate codes on two blueprint copies, that code for the same trait. If both alleles

are the same, then the expressed phenotype will match both alleles. If the two alleles

are different, then the phenotypic expression will match the dominant allele. Each allele

is inherited unchanged, one from each parent. During the process of sexual

reproduction, the alleles coding for the same trait trade places with each other randomly

(from one blueprint copy to the same place on the other blueprint copy) so that the next

generation will be uniquely different from the current generation in their phenotypic

expression of the same alleles. This is why siblings from the same parents never look

exactly alike unless they are twins arising from the same fertilized egg. Siblings can in
fact look very different from each other and even their parents. One may have a big

nose and the other a small nose. Similarly, a finch may have a bigger or smaller beak

than its siblings. Such phenotypic changes do indeed occur, but they need not be

based in any change of the common "gene pool" of options. 2 (Back to Top)

Breeding via Human Selection

The variation in allelic expression

can be quite dramatic. It is

responsible for the majority of

changes seen in animal breeding.

For example, the main differences

between a Chihuahua and a Great

Dane are primarily the result of trait

selection where desired traits

contained by a common gene pool

were gathered together over a few generations into one animal. Most of traits

themselves already existed, fully formed, in the common ancestral gene pool of dogs.

Thus, neither of these breeds has “evolved” much of anything that their common

ancestors did not already have in their common gene pool of options.

The ability for great phenotypic variation is obvious, but there are clear limits to this

variation. Using genetic recombination alone, a dog cannot be anything but a dog. A
dog can never be changed, via genetic recombination alone, into a cat or a chicken or

anything else. Why? Because cats, dogs, and chickens are made from different

blueprints that code for different trait types and trait options that are not contained by

the gene pools of the others. Also, traits that may be similar may not necessarily be

located at the same relative positions on their respective genetic blueprints.

Again, using the house blueprint analogy as an example, one house might have a

blueprint that codes for carpet at the bottom right-hand corner of the page. Another

house might have a blueprint that codes for an electric garage door opener at this

location and has no code for carpet at all. Also, the first house might not have a code

for a garage much less an electric garage door opener. Neither one of the blueprints for

one house will match with the options or order of options for the other house.

So, what does this mean? It means that the blueprints for the different houses in

this case cannot talk to each other, mix and match, or "recombine" their collective

information in any functional way. They cannot "interbreed" so to speak to produce

viable "offspring". Only blueprints that have the same setup and "trait" types can

exchange equivalent information with each other. It is impossible then for blueprints

that do not have a position for a garage code to trade equivalent information that results

in the formation of a garage. The same is true for different animals such as dogs,

chickens and cats. They cannot breed with each other, nor can they be bred to look like

each other, using genetic recombination alone.

Although genetic recombination can and does result in some very dramatic

phenotypic changes for these creatures, this process is limited by the edges of a large

but finite pool of options. Such a gene pool remains fixed while various creatures within
the gene pool give phenotypic expression to various aspects of this genotypic pool of

options. The pool provides the means for huge phenotypic variation or “change” but the

genotypic pool itself may not change from one generation to the next. 8 The changing

phenotypic creature is nothing more than a partial reflection of a non-changing or

"static" genotypic pool. Thus, it is the genotypic pool and not the phenotypic creature

that "real" evolution must act on.

But, if Darwin’s finch beaks are not examples of gene pool evolution is there

anything that is? Is there any creature that has unique traits that its ancestors did not

have in their gene pool? (Back to Top)

Random Mutations

This is where mutations come into play. Genetic mutations are relatively rare

random changes that occur in a creature's genotypic blueprint that were not in the

blueprints of that creature’s parents. There are many different types of mutations.

There are point mutations where just one letter is changed in the wording of the genetic

blueprint. There are translocation mutations where a section of the blueprint is cut out

and pasted in another place on the blueprint. There are inversion mutations where a

section of the blueprint is cut out and turned upside down and pasted back in the same

place. There are duplication mutations where a section of the blueprint is copied and

then pasted in another place. The list goes on and on, but basically the mutated
blueprint has genes/alleles or genetic sequences that were not in the blueprints of either

one of the parent blueprints. 1,2,4 (Back to Top)

Functional vs. Neutral Mutations

As would seem intuitive, most functional mutations are harmful and may even be

lethal. Fortunately though, most mutations are not functional. Most mutations are silent

or "neutral" and result in no detectable phenotypic change. Very rarely, some mutations

are “beneficial.” The ratio of beneficial vs. detrimental mutations is on the order of 1 in

1,000 for certain types of functions (discussed in more detail below). Common

examples of beneficial mutations are those that give bacteria antibiotic resistance or

those that cause sickle cell anemia in people who live where malaria is prevalent. But

how, exactly, do beneficial mutations achieve their benefits? (Back to Top)

Antibiotic Resistance

In the case of bacterial antibiotic resistance, certain mutations actually do result in

the fairly sudden creation of new as well as beneficial functions that the "parent"

bacteria did not have in their collective gene pool of options.

Now, it should be noted that bacteria are not like dogs, cats, and chickens, or

anything else that uses sex or genetic recombination as a means of reproduction.

Bacteria reproduce themselves by a relatively simple method of cell division. In other

words, all of the offspring of a given bacterium will be identical with itself as well as with

each other. They are basically clones of each other. Because of this, there are no trait

options to choose from. There is only one copy of the blueprint instead of the two copies

used in sexual recombination. So, there is only one option for each bacterial "trait."

There is no gene "pool" of options for each trait - so to speak. Of course, many types of

bacteria can in fact laterally exchange genetic information via plasmids and the like.

But, as a general rule of thumb, bacteria do not undergo genetic recombination. So, for

all practical purposes, all bacteria within a given isolated population are identical except

if a mutational change occurs. Such mutations, when they do occur, are passed on to

all subsequent offspring.

So, back to the notion of beneficial mutations. They do happen in bacterial

populations all the time. For example, penicillin resistance is not always gained by the

production of the famous ß-lactamase enzyme "penicillinase." There are several other

ways that bacteria become resistant to penicillin. A notable example occurs in

Streptococcus pneumoniae bacteria. ß-lactamase have never been identified in S.

pneumoniae and yet they are capable of penicillin antibiotic resistance due to

modification of their penicillin binding proteins (PBPs). Since PBPs are the natural

target of penicillin, many different point mutations within this target are capable of

interfering with the target-antibiotic interaction. It is this interference that results in

penicillin resistance. And, importantly, this resistance, combined with what are called

"compensatory mutations", can be achieved without any significant loss of any other

functional system within the bacterium. So, the argument that all mutations end up
producing at least some detectably harmful effect to gain a beneficial effect simply isn't

true.

Other antibiotics require a specialized transport protein to bring them into the

bacterium. Again, many different point mutations can interfere with the ability of the

transport protein to interact properly with the antibiotic. This interference results in

resistance to this particular antibiotic. Again, this interference gained be gained without

any significant functional loss of the mutant bacteria relative to their peers.

Other bacteria already make more complex antibiotic enzymes, such as the

penicillinase enzyme. Such enzymes do not evolve in previously susceptible bacterial

populations. There is not a single documented case where the penicillinase enzyme

code has been observed to evolve in a population where it wasn't already there. The

coded sequence or "gene" needed to produce the penicillinase enzyme was already

there or it was gained via lateral transfer from other bacteria who already had this code

(often via plasmids). The problem is that this coded sequence is usually regulated so

that the penicillinase enzyme is not produce in sufficient enough quantities to protect the

bacterium from high levels of the penicillin antibiotic. Several different mutations are

capable of blocking or interfering with the suppression of penicillinase production so that

much greater quantities can be made, which results in enhanced penicillin resistance.

Similarly, Mycobacterium tuberculosis, the cause of the tuberculosis disease,

produces an enzyme that (as well as its other useful functions) changes the non-harmful

antibiotic "isoniazid" into its active and lethal form. The now active isoniazid proceeds to

kill the Mycobacterium. Several different mutations are capable of interfering with the
isoniazid-enzyme interaction. And again, this interference results in Mycobacterial

resistance to isoniazid.

To give another example, the 4-quinolone antibiotics attack the enzyme “DNA

gyrase” inside various bacteria. Again, several different point mutations are capable of

interfering with the gyrase-antibiotic interaction.9

Perhaps the most famous and oft quoted example of a beneficial mutation is the

point mutation of the hemoglobin molecule that is seen in people affected by a condition

known as sickle cell anemia. This single point mutation decreases the effective oxygen

carrying capacity of the hemoglobin molecule. It still carries oxygen, just not as well.

Now, it just so happens that the malarial parasite needs a high oxygen concentration to

survive and so cannot survive in blood with the sickle cell mutation.10 Those people who

have only one of their two blueprint DNA copies affected by this mutation do not have

significant anemia, but their blood still doesn't carry oxygen well enough to support the

malarial parasite. So, they are resistant to malaria while at the same time having little

problem with the hemoglobin mutation. However, those unfortunate individuals who end

up with a double mutation, known as a "homozygous" condition, have a severe problem

with their hemoglobin molecules crystallizing under low oxygen tension. This

crystallization effect dramatically distorts the red blood cells and they no longer fit very

well through small vessels in the body. Of course, this means that organs and tissues

supplied by these vessels become starved for oxygen. This causes a very painful and

debilitating condition with significantly reduced life span.

Now, there are several interesting observations to note. Most beneficial mutations

achieve their benefits with just one or rarely two point mutations. Also, it is hard to miss
the fact that all of the functions gained, at least those listed here, were the result of a

mutation that interfered with a previously established function or specific interaction.

And, as we all know from a famous children's story, it is far easier to break than to

create. The reason is that there are so many different ways to break something

compared to the relatively few ways to make something work. Why else couldn't all the

King's men put Humpty Dumpty back together again? (Back to Top)

Enzyme Evolution

But, how did such apparently complex enzymes, such as penicillinase, evolve? A

bacterium is not going to evolve the enzymatic penicillinase function with just one or two

point mutations to some target sequence because the penicillinase function is not based

on the loss or hindrance of a pre-existing function or interaction. So, how could such a

function evolve?

There are many theories as to how the penicillinase enzyme must have evolved.

However, when it comes right down to it, no one has ever demonstrated the evolution of

the penicillinase enzyme in the lab. As previously noted, bacteria that produce the

penicillinase enzyme were always capable of producing this enzyme or they obtained

the code for this enzyme via a plasmid from another bacterium who had this code

already formed.11 Sometimes, a point mutation is required to deregulate the production

of penicillinase so that much greater quantities are produced, rendering the bacterium

(and its subsequence offspring) instantly resistant to greater doses of penicillin. But, this
change really has nothing to do with explaining how the rather complex penicillinase

function evolved.9 So, are there any documented reports of the evolution of a complex

enzymatic function comparable to that of the penicillinase function?

Michael Behe, a professor of biochemistry at Lehigh University, says that,

“Molecular evolution is not based on scientific authority. There is no publication in the

scientific literature in prestigious journals, specialty journals, or books that describe how

molecular evolution of any real, complex, biochemical system either did occur or even

might have occurred. There are assertions that such evolution occurred, but absolutely

none are supported by pertinent experiments or calculations.” 5

Others,

such as the

well known

evolutionary

biologist

Kenneth

Miller,

disagree. In

his 1999

book, Finding

Darwin’s God,

one of Miller’s

challenges of

Behe’s
position includes a 1982 research study by professor Barry Hall, an evolutionary

biologist from the University of Rochester. In this study, Hall deleted a gene (lacZ gene)

in a type of bacteria (E. coli) that makes an enzyme (ß-galactosidase). This enzyme

converts the sugar lactose into the sugars glucose and galactose. The E. coli then use glucose

and galactose for energy.

Without this lactase enzyme one would think that these bacteria and their offspring

would not be able to utilize lactose. However, what Hall found is that after a short time

(just one generation) of exposure to a lactose-enriched environment these bacteria

modified a different gene with just one point mutation so that it gained the ability to

produce a new lactase enzyme.12 Since the original enzyme was composed of a fairly

large tetramer (~1,000 amino acids for each subunit), it seemed like the evolution of the

lactase function might require a fair amount of enzymatic complexity (fairly large number

and specific arrangement of amino acid residues). In other words, it might be rather

difficult to come across very many enzymes with lactase ability out of the vast numbers

of potential arrangments within sequence space. So, the demonstration of such rapid

evolution of a completely different hexametric lactase enzyme was quite a stunning

success for Hall. How did these amazing bacteria evolve a brand new enzyme to do

such an apparently complex task?

As it turns out, these E. coli bacteria had something of a spare tire gene that Hall

called the "evolved ß-galactosidase gene" (ebgA). Just one point mutation was all it

took to give this spare tire gene the ability to produce a protein with the beneficial

lactase activity. Hall was of course disappointed to find out that only one point mutation

was enough to "evolve" this beneficial lactase activity. So, he did a very interesting
thing. He deleted both the original lacZ genes as well as the evolved ebgA gene in

some rather large colonies of E. coli. Interestingly enough, none of these doubly

mutated bacteria nor their offspring never evolved any other gene or DNA sequence into

a functional lactase enzyme despite observation for tens of thousands of generations.

Hall was mystified. He described these bacteria as having, "limited evolutionary

potential." 12 The interesting thing is that these same bacteria that were limited in their

ability to evolve the lactase function would easily have evolved resistance to just about

any antibiotic in just a few generations of sublethal exposure. Compared to antibiotic

resistance, the evolution of even a single-protein enzyme is quite a different matter. We

are starting to climb the ladder of increasing functional complexity. (Back to Top)

Limited Evolutionary Potential

Now I ask, what exactly was limiting the evolutionary potential of Hall's bacteria?

Does the theory of evolution explain such limits? If so, how are they explained? The

theory of evolution claims the power to create incredible diversity via mindless

processes if given enough time. Well, how much time, on average, would it take for E.

coli, without lacZ and ebgA, to evolve the lactase function? Can this time be estimated,

even roughly? If so, upon what basis can it be estimated?

According to Hall's own calculations, a function that required just two independent

(neutral) mutations would take around "100,000 years" to achieve in E. coli.12 It seems

as though Hall does not understand the statistics of random walk very well or he would
not have been surprised when he did in fact isolate such a double mutant in just a few

days. The estimated time for fixation is what caused Hall to estimate a time of 100,000

years for the crossing of a gap of just two neutral mutations. What Hall did not realize is

that stepwise fixation of each mutation (spread to all members of a population) is not

required for such a gap to be crossed. With populations the size of Hall's E. coli

colonies, such a double mutation would be realized in at least one bacterium in the

population in just one or two generations using random walk alone. (Back to Top)

Growing Neutral Gaps

So, is the problem solved? Hardly. With each doubling of the neutral gap between

the current genetic real estate and a new potentially beneficial function, the random

walk increases by a factor of two. For example, a gap of 2 amino acid residue

differences has only 400 different options to fill (20 potentially different residues in each

position in a protein sequence). A population of one billion bacteria would quickly

distribute itself among all these 400 options in very short order (given that these 400

options were all functionally neutral with respect to each other). However, doubling the

gap to 4 differences would increase the number of options to 160,000. Doubling the

gap again to 8 differences would increase the number of options to 25.6 billion. A gap

of 16 would yield 655 million trillion (6.5e20). In such a case, each bacterium in the

population of one billion would be surrounded by a sea of 655 billion non-beneficial

options. The time required to traverse this gap, even for a population of one billion
bacteria, would run into the trillions of generations. Why? Because the time required

for a mutation to hit even one of the residues that form the gap runs into the hundreds of

thousands of generations, on average. In other words, each random walk step would

take hundreds of thousands of generations. So, finding one specific spot out of 655

billion options would require 6.55e9 x 1e5 = ~ 1e14 or 100 trillion generations.

This is because natural selection cannot preferentially select for any sequence that

doesn't provide an improved function over what was already there to begin with. The

only forces for change that can sort through such non-beneficial sequences are random

mutations. These random mutations randomly search through sequence space with the

use of either short or long random steps. However, regardless of the size of the

step/mutation, the odds of success are not changed. Such a random walk takes a

whole lot more time than a non-random direct walk would take - exponentially more

time. This simple little problem is what messes things all up for evolution.

For instance, consider that there are many bacterial functions that are far more

complex than the relatively simple single-protein based enzymatic-type functions of

lactase or nylonase. Many single protein enzymes are actually fairly complex, don't get

me wrong. They certainly are far more complex than the function of antibiotic

resistance that arises via an interfering mutation. However, their functions are still

relatively simple when compared to other cellular functions of higher complexity.

For example, there are about 10130 potential protein sequences 100 residues in

length. Of these 10130 potential proteins, how many would have a specific

function? Well, it depends on the function. It depends upon how specific the

arrangement of residues needs to be. So, as an example, lets pick one of the more
specifically arranged functional protein that requires about 100 residues to work - like

cytochrome c. Some scientists, like Yockey, have estimated anywhere between 1050 to

1090 different potential cytochrome c proteins exist in sequence space.15-17 To

understand how big these numbers are, consider that the total number of atoms in the

visible universe is only around 1080. So, one can see that 1090 different cytochrome c

sequences is an absolutely huge number. The problem is, this pile of 1090 cytochrome c

proteins is absolutely miniscule when compared to 10130, which is the total number of

different potential protein sequences 100aa in length. For every one cytochrome c

sequence there would be about 1040 non-cytochrome c sequences in sequence space.

And yet, this ratio gets exponentially worse as the complexity of function increases.

For example, the function of bacterial motility involves the interactions of many different

proteins all working together at the same time - over 20 different structural protein parts

in specific arrangement totaling well over 10,000aa that must be specifically coded for in

correct sequence. The question is, how many different arrangements of these amino

acid residues would produce a motility system (or how many arrangements of 10,000

letters would produce a meaningful, much less beneficial, essay in English)? For

argument's sake, lets say that 102000 different motility systems could be made with such

a stretch of amino acids. Despite this apparently astronomical number of different

motility systems, 102000 is still a tiny fraction of 1013,010 - the minimum potential protein

sequence space at this level of complexity (10,000aa level). Each sequence with a

motility function would be surrounded by at least 1011,000 sequences without the motility

function. In fact, the beneficial sequence density at this level of complexity seems to be

so miniscule that evolution is powerless to evolve any function at such a level of

complexity. There simply are no observable examples of any such function evolving in

real time - not one example (i.e., a function that requires more than a few thousand

fairly specifically arranged residues).

Now, there are a whole lot of stories about how such functions must have evolved.

These stories are exclusively based on the notion that sequence similarities of portions

of such systems to portions of sequences in other systems of function must mean that

they share a common evolutionary ancestor. Certainly the similarities do seem to

indicate a common origin of some kind. However, as Behe has repeatedly pointed out,

nobody has provided any detailed explanation as to how evolutionary mechanisms of

random mutation and function-based selection could give rise to the functional

differences at higher levels of minimum functional complexity. The functional

differences are what are important here - not so much the similarities. How are these

differences explained by any non-deliberate process? Both deliberate and non-

deliberate processes can explain the similarities, but how well can non-deliberate

evolutionary forces explain the differences?

The problem is that there is always more potential junk than non-junk at any given

level of complexity. The real problem though is that this junk pile grows exponentially,

relative to the pile of potentially beneficial sequences, with each step up the ladder of

functional complexity. (Back to Top)

The Junk Pile and The Ladder of Functional Complexity

 The ladder of complexity limits the ability of evolution to evolve beyond its lowest

rungs where the most simple functions, such as antibiotic resistance, can be found. The

target mutations required to achieve antibiotic resistance are extremely simple to get

"right" because there are so many "right" options. However, the evolution of specific

enzymatic functions, like the lactase function, are a lot harder to get "right" because far

fewer options are "right." Then again, even these functions are relatively easy to get

"right" compared to more complex multipart functions, such as bacterial motility

systems, where all the protein parts work together at the same time in a specific 3-D

orientation with each other. So, as one moves up the ladder of functional complexity,

the difficulty of finding any sequence that does anything beneficial at such a level of

complexity becomes exponentially harder and harder to do until not even trillions upon

trillions of years are enough. (Back to Top)

A Construction Foreman Who

Cannot Read

It is all very much like a construction

foreman who never learned how to read

a blueprint, but who intuitively knows

what works when he sees it in action.

His workers are the ones that know how to read blueprints and follow directions exactly.

The workers also copy parent blueprints to use as templates for each new house that is
to be built. However, although they are extremely careful copyists, the workers make

little mistakes every now an then. These little mistakes may not result in any phenotypic

change whatsoever, but sometimes they translate into slight or even major variations

among the actual houses built (the phenotype). The foreman then comes to inspect the

completed houses and picks the one that is the “best” given the particular needs of that

house for that location and housing market. The choice of the foreman is based only

on current function.5,6 He knows only what works right now. He has no imagination,

memory, or vision for the future. If there is a part of a house that he does not recognize

as having current beneficial overall function, he will not select to keep that house and

the offending part will be lost from future blueprint options. The foreman goes around

saying, “Keeping do-dads around that don’t work is expensive!” He will not maintain

what he does not recognize as beneficial right now in hopes that sometime in the future,

with some potential change in the housing market/environment, it may develop into

something beneficial. Once the selection for the best overall house is made by the

foreman, the workers find the blueprint for this house and use it as a template for the

next building project.

But what happens if the housing market changes the next year? What if certain

changes would benefit the house in this new environment? For example, what if there

were a prolonged drought and wild fires became a threat making houses with tile

shingles more resistant to fire than houses with wooden or asphalt shingles? Would the

foreman be able to make these beneficial changes?

Consider the thought that languages and thus blueprints are arbitrary in that they

use arbitrary symbols to represent ideas. A change or evolution of a symbol does not
necessarily correlate to an equivalent change in the attached idea. If a symbol

changes, even a little bit, the attached idea may simply disappear, leaving the “new”

symbol without any recognized function. The symbol is now meaningless. For

example, what if the blueprint for our house in question called for “wooden shingles.”

Each of the words, “wooden” and “shingles” is an arbitrary group of symbols that

represents an idea to an English speaking person. If the blueprint could be changed to

read “tile shingles”, the understood change in meaning and the resultant change in

house building would be a clear advantage in our fire-hazard environment. If no pre-

established alleles for “tile shingles” are available in the blueprint pool of trait options, is

there any way to create the “tile allele” from anything that already exists in the gene

pool?

The problem for gradual change is that each letter change must make sense. If

“wood” is changed to “hood”, the actual word “hood” has meaning. However, is the

meaning for “hood” any closer to the meaning for “tile”? Even though hood has

meaning, does it have beneficial meaning in this case? What does “hood shingles”

mean?

So, not only does each word of the blueprint have to make sense to the workers, but

the combination or location of the words on the blueprint has to make sense as well or

else the workers cannot make anything, much less something beneficial. Order is

important at all levels of complexity. Amino acid residue order is important for the

proper function of a single protein. Also, the order of multiple proteins is important for

the formation of a multiprotein system. Again, if the workers build something that the
foreman cannot recognize as beneficial right now, it will be rejected. It is as simple as

that.

In order to better visualize the problem, put yourself in place of the foreman. You

can only select based on functions that work “right now.” With this in mind, consider the

phrase, “Methinks it is like a weasel.” 6 Now, add, subtract, or change one letter at a

time from the phrase in any position or order that you want. There are just two more

little rules to this game. Each change that you make must make sense in English and

each change must be beneficial in a particular situation/environment. See how far you

can go and how much change in meaning you can get. Changing the meaning very far

is a lot more difficult than one might think even if the beneficial nature of the change is

not a concern.

Nature runs into this same little problem. Changing genetic sequences too much

destroys all phenotypic function before any new function can be reached. Maintaining a

functional phenotypic trait along the path towards any uniquely functional trait requires

multiple changes (maybe even hundreds or thousands at higher levels of functional

complexity) that do not change the original function and do not achieve new function,

until all the changes are in place.5,12 This is because many functional genetic elements

are isolated from each other like islands on a large ocean of neutral function or even

detrimental function.

Consider the fact that most character sequences of a given length have no meaning

to an English speaking person. The same is true for sequences of DNA. The vast

majority of potential genes of a given length mean nothing to a given cell. Any gene that

happens to get mutated into one of these unrecognized or neutral genes becomes
suddenly lost in the ocean of neutrality where no guidance is available. Without

guidance, evolution drowns in this ocean. (Back to Top)

Adding a Stereo System to a Car

Some say that evolution need not work like this but that the mindless processes of

nature evolve new traits and gene pools by simply adding on previously defined genetic

elements to an established system of function... like the addition of a stereo system to a

car. The addition of these units enhances the function of the established system, even

to the point of giving it new functions that it never had before. In this way, a simple

system of function can be enhanced in complexity step by tiny step.

Let's try a thought experiment to illustrate this point. Consider the sentence in a

large book of sentences that reads, "I am." Now add any other word onto this

sentence. The only rule is that whatever word you choose must make sense in the

context of the other sentences and the book as a whole. For example, I could add the

pre-formed word, "pleased" and make the new sentence read, "I am pleased." This

makes sense in English and it adds meaning to the sentence (whether or not it makes

sense to the rest of the paragraph is another story). The new word, "pleased" could

have been the result of a duplication mutation of a gene somewhere else that just

happened to get inserted into our sentence. But, if the mutation had read, "I am very",

this phrase does not necessarily make sense in most situations/environments. The

addition of the word "very" probably destroyed the previous function of our sentence
without creating a new function. However, if the phrase "I am pleased" was first to

evolve, the phrase, "I am very pleased" could evolve next and make sense.

With these rules in mind, try and keep adding on words (or subtracting words) and

see how far you can get given a particular situation/environment. Maybe the next

mutation could read, "I am very pleased Tom." Then, "I am pleased Tom." Then, "I am

Tom." We could also go another route and say, "I am very pleased in Tom." Then, "I

am very pleased in seeing Tom." Then "I am very pleased in seeing Tom run." Then, "I

am very pleased in seeing Tom run fast." Then, "I am very pleased in seeing Tom run

real fast." Then, etc. etc. etc. We can evolve quite a few different phrases with quite a

few unique meanings with the simple addition or subtraction of previously defined

words. Could genes in DNA do the same thing? Technically yes, but there are just a

few problems to consider.

Remember that not every defined word that exists in English will make sense when

added to the phrase, "I am." Granted, the odds that one will make sense seem to be

fairly good though. However, the longer our sentence gets, the less words there are

that make sense when they are added to our sentence in the context of a specific

situation/environment. Consider also that the placement of the words within our

sentence is extremely vital to the functionality of the sentence. I might say, "I am

green." This phrase makes sense in English. But what if the word "green" had been

inserted into the wrong place? The sentence could just as easily have "evolved" to

read, "I agreenm." This makes no sense in English and destroys the function of a

previously functional sentence. Consider also that the duplication mutation could have

occurred or been inserted into an area of the book of sentences where it was not
needed. What are the odds that it would land in exactly the right "evolving" sentence in

exactly the right position within that sentence when there are potentially millions of other

locations it could have landed? Then consider that the sentence itself, even if it might

make sense by itself, must make sense as it relates with the other sentences around it

and in the rest of the book. If any of these problems arise, that sentence is lost in the

ocean of non-beneficial function. (Back to Top)

One Last Question

If the theory of evolution runs into such apparently difficult statistical problems, how

is it that this theory can be so earnestly presented as the only "rational" answer to the

question of the origins of living things? (Back to Top)

1. Lewin, Benjamin, Genes V, Oxford University Press, 1994.

2. Gelehrter, Thomas D. et al. Principles of Medical Genetics, 1998.
3. Callender, L. A., Gregor Mendel: An opponent of descent with
modification. History of Science 26: 41-75. 1988.
4. Genetics 131: 245-253, 1992.
5. Behe, Michael J. Darwin’s Black Box, The Free Press, 1996.
6. Dawkins, Richard. The Blind Watchmaker, 1987.
7. Mendel, Gregor. Experiments in Plant Hybridization. 1865.
8. Veith, Walter J. The Genesis Conflict, The Amazing Discoveries
Foundation, 1997, p. 82.
9. Carl Wieland, Antibiotic Resistance in Bacteria, Creation Ex Nihilo
Technical Journal, 8:1 (1994), p. 5.
10. Felix Konotey-Ahulu, The Sickle Cell Disease Patient (New York:
Macmillan, 1991), p. 106-108.
11. R. McQuire, Eerie: human Arctic fossils yield resistant bacteria,
Medical Tribune, 12/29/1988, pp. 1, 23.
 12. 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.
13. Dugaiczyk, Achillies. Lecture Notes, Biochemistry 110-A, University
California Riverside, Fall 1999.
14. Ayala, Francisco J. Teleological Explanations in Evolutionary Biology,
Philosophy of Science, March, 1970, p. 3.
15. Yockey, H.P., J Theor Biol, p. 91, 1981
16. Yockey, H.P., "Information Theory and Molecular Biology", Cambridge
University Press, 1992
17. Sauer, R.T. , James U Bowie, John F.R. Olson, and Wendall A. Lim,
1989, 'Proceedings of the National Academy of Science's USA 86,
2152-2156. and 1990, March 16, Science, 247; and, Olson and R.T.
Sauer, 'Proteins: Structure, Function and Genetics', 7:306 - 316, 1990.

(Back to Top)

. 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

Debates:

Stacking the Deck

God of the Gaps

The Density of Beneficial Functions

All Functions are Irreducibly Complex

Ladder of Complexity

Chaos and Complexity

Confusing Chaos with Complexity

Evolving Bacteria

Irreducible Complexity

Scientific Theory of Intelligent Design

A Circle Within a Circle

Crop Circles

Mindless vs. Mindful

Single Protein Functions

 BCR/ABL Chimeric Protein

Function Flexibility

The Limits of Functional Flexibility

Functions based on Deregulation

Neandertal DNA

Human/Chimp phylogenies

Geology

The Geologic Column

Fish Fossils

Matters of Faith

Evidence of Things Unseen

The Two Impossible Options

Links to Design, Creation, and Evolution Websites

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