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Natural Selection

Sean D. Pitman M.D.


© July 2003

According to evolutionary theory,

natural selection is the driving force behind

the process of evolution. The mindless

processes of nature are thought by most

modern scientists to be the creative forces

the mold and govern everything that we

see in and around us - to include all life forms. Truly then, Nature is the Creator. Nature

is a mindless god of sorts. But, by what power does this god create all the fantastic

variety and creativity that we see around us? - especially when we look at the workings

of living things?

As far as the variety of life forms are concerned, the theory of evolution proposes

that the nature created and is still creating the huge variety of living creatures via

random genetic mutations that can be selected as advantageous or disadvantageous in

particular competitive environments over vast spans of time. Nature is said to do this by
preferentially selecting those life forms that survive and pass on their genes to their

offspring the best. This "natural selection" uses competition for survival. The

production of slightly different offspring provides the opportunity of sorting out

advantageous traits from the less advantageous ones. More and more traits are added

or subtracted in this way until a creature's offspring are fine tuned to the particular

environmental niche that they occupy. The whole process is often referred to as, "The

Survival of the Fittest." This is rather a neat idea, but exactly how does it work? Does

natural selection tend toward genetic diversity or stability?

A famous example of natural

selection is England's peppered moth

(Biston betularia). Despite the current

debate on the actual methods of the

original study it is still a good example to

illustrate natural selection. In the original

study by H.B. Kettlewell, he was wondering why the peppered moth was more

commonly dark than specimens that had been collected and saved from earlier times in

England’s history. The peppered moth had been generally much whiter in color, but

now it was much blacker. Why this change? It was suggested that when the industrial

revolution arrived in England, the pollution had turned the bark of the trees a much

darker color. Since light colored moths are much easier for birds to see on a dark

background, they were preferentially eaten. However, the few darker moths survived

better to pass on their darker coloring to their offspring. Pretty soon, there were lots of

dark moths and very few light colored moths - or so the story went. In reality, England's
peppered moths do not generally rest on tree trunks (despite what some of the staged

pictures produced by Kettlewell seem to suggest). However, subsequent studies

seemed to confirm Kettlewell's main hypothesis that England's peppered moths were in

fact getting darker over time. Still, this is still not necessarily an example of evolution

in action.

Gregor Johann Mendel (1822-1884), an Austrian monk and a

contemporary of Darwin, is generally recognized as the father of

modern genetics and the study of genetic inheritance. Mendel showed

conclusively that the genes (alleles) of creatures contained built-in

abilities for inherited variation that are not dependent upon mutational

changes but upon the built-in variety potential of a given gene pool of allelic options. He

found that some allelic traits were "dominant" while others were "recessive." Each trait

was coded for by two separate allelic codes on equivalent positions on two separate but

matching chromosomes. As long as one of the codes was the dominant code, it would

block out the other code. So, an individual with two different codes for the same allelic

positions would express the dominant trait. For example, if one parent had two

dominant color codes and the other parent had two recessive color codes at the allelic

position coding for hair color, then the offspring would all be the dominant color (i.e.,

brown vs. blond). However, if each parent had one dominant and one recessive color

code then, according to the calculated odds of inheritance, three-quarters of the

offspring would be dominant in color and one-quarter recessive (The offspring with both

dominant and recessive codes would express the dominant color. Only those offspring
with both recessive codes would express the recessive color). If both parents had both

recessive color codes then all the offspring would have the recessive color.

So you see, such a method of option swapping at set locations on chromosomes

allows for a huge variety of expressed morphologies or phenotypes. However, since the

codes only swap with each other at set locations, the body parts themselves maintain

their usual orientation with each other. In other words, genetic recombination will not

cause an eye to grown on a baby's foot or an ear to grow inside its stomach. The

swapping of options is random, but limited as to exactly where the swapping can and

cannot take place. For example, it works much like interchangeable parts on a car. If I

don't like the hubcaps on my car, I can swap them out for new ones that still fit in the

same location, but they may look very different. I can also swap out the steering wheel

for a very different looking one, but it still fits in exactly the same place on the car and it

does pretty much the same job.

This same thing happens during genetic recombination. One particular position on a

chromosome might code for eye color. Many different interchangeable parts or codes

for eye color have the potential to occupy and "work" in this spot. But, codes for eye

color would not work so well if they were placed where the code for nose size is

supposed to go. This would be like trying to put a hubcap where the carburetor is

supposed to go. Some parts are simply not interchangeable, and the process of genetic

recombination knows this. So, during the process of genetic recombination, the genes

or allelic options themselves have not been changed, just their expression (i.e., The

hubcaps, steering wheels, carburetors, and all other part options are still the same. It is
just that some parts are used to make some car "expressions" while other part types are

used to make other car "expressions").

There are many different variations and complications, but this is the basic idea that

Mendel discovered. In other words, great diversity can be had through a selection

process that picks between previously established traits or allelic part options. This is

why breeding has been such a thriving occupation for centuries. Selective breeding

based on the potential of genetic recombination alone (for the most part) is responsible

for the great varieties of cats, dogs, horses, and even humans, as well as a host of

other breeds - to include Darwin’s famous finches. Mendelian genetics and other types

of genetic recombination are the primary reason why children do not look exactly like

their parents or each other (unless they

happen to be twins). Children from the

same set of parents do have variations in

their appearance and yet these

variations are dependent upon nothing

more than different expressions and

mixes of the same identical gene options

from both parents (the parental gene

pool of options). Note carefully thought

that this process (as it ideally works) has nothing to do with mutation so nothing new as

far as the "gene pool potential" is concerned is created. No unique genetic functions

are evolved during this process (i.e., An exchange of one type of hubcap for another
type of hubcap that already existed in the pool of hubcap options does not make the

pool of options change).

A mutation, on the other hand, is a change in a specific gene that was not originally

inherited. The different white and black colors in the peppered moth are clearly the

result of genetic recombination at work. The peppered moth gene pool already

contained codes for both the light and the dark colors of peppered moths. Nature did in

fact play a role in selecting the most common color from this pre-established pool of

options but it did not create the options in this case (at least not in observable time).

So, such examples of changes do to genetic recombination cannot be used as

examples of evolution in action because clearly, they are not making anything new as

far as the gene pool is concerned. For example, no matter how much selection

pressure is applied to England's peppered moth, a green peppered moth will never

evolve via genetic recombination alone. Why? Because the code for green color is not

in the peppered moth's genetic pool of options (i.e., If there are no green hubcaps at

Wal-Mart, where I do my hubcap shopping, my car will simply have to do without green

hubcaps). The only way to get this option to come into the gene pool of options is for

random mutations or mistakes in the genetic code to create this option de novo.

The problem is that random mutations generally limit

existing genetic functions and so nature almost always

selects against the changes produced by random

mutations. In other words, if an individual sustains a

mutation in one of its genes, this mutation lessens the

function of this gene most of the time. With a less


functional gene, the creature has a higher probability of competing less well than peers.

This mutant creature and its offspring will most likely die off because of this deficiency.

Of course, after the die off occurs, this particular mutation would be removed from the

gene pool of options for this "kind" of creature. In this way, nature in fact limits

mutational change to the genes of most creatures. For many creatures, such as

mammals, mutations are fairly rare to begin with; on the order of one mutation per gene

per 100,000 generations. 1 Understand also that the majority of even this relatively

small number of mutations are detrimental in nature (The ratio of detrimental vs.

beneficial mutations is thought to be around 1000:1 - with the rest being "neutral" as far

as function is concerned). One major problem is one of how to eliminate the detrimental

mutations as fast or faster than the much lower rate of beneficial mutations. For

humans this is turning out to be quite a mysterious problem. In fact, it seems that the

human species may be deteriorating at an alarming rate. 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?” 4

Such problems certainly are a challenge for natural selection to keep up with and get

rid of much less overcome to use in some fantastically beneficial way. Clearly natural

selection is a real force of nature, but it is limited by the genetic options that it can pick

from. New options can only be added through mutation of the original options - and this

seems to be very limited at best.

But what about some famous mutational benefits that have

survived? What about sickle cell anemia for example? Sickle cell

anemia is caused by a single "point" mutation of the hemoglobin

molecule. This molecule is responsible for oxygen transport in red

blood cells. When it has the mutation that causes sickle cell anemia, it does not carry

oxygen as well. It also has a tendency to "sickle" or polymerize into a shape that is

inflexible and unable to pass through very small vessels called capillaries.2 This causes

the individual with sickle cell disease a great deal of pain and eventually an early death.

So, why has nature preserved or "selected" to maintain this mutation in our particular

human gene pool of options? Nature has done this because of another even more

deadly problem called malaria. Malaria is caused by a

microscopic protozoan that lives part of its life cycle as a

parasite in human red blood cells. However, the malaria

parasite needs a specific oxygen concentration to survive.


Those humans with sickle cell anemia cannot maintain the necessary oxygen level

needed for the malaria parasite to survive. So, those with sickle cell anemia, or even

sickle cell "trait" (one sickle cell allele - instead of the two possible sickle cell gene

alleles) survive better in an environment where there is malaria. However, this survival

comes at a high cost. They have a less functional hemoglobin molecule. A loss of

function or a disruption of previous functions or interactions is far easier to achieve via

random mutations than a new function that is not dependent upon the loss of or

interference with any pre-established functions or interactions.

The evolution of new genetic functions that relies on the disruption of pre-

established functions is a quick and easy process that happens all the time. The

evolution of antibiotic resistance to all the various antibiotics that we have developed is

based on this process. The de novo development of the antibiotic function in a colony

of bacteria is dependent upon the fact that all antibiotics are quite specific in their

interactions with particular intra-bacterial target sequences. Any little disruption of the

target sequence will interfere to one degree or another with the antibiotic's interaction

with this sequence. This interference results in equivalent resistance to the antibiotic.

Obviously then, the ratio of interfering mutations involving this target sequence is very

large when compared to the total number of potential mutations that could affect this

sequence. This high ratio of what will "work" compared with what will not "work" creates

a very small gap between what is and what might be more helpful in the current

situation or "environment".

The problem is that there are other cellular functions that are not dependent upon

the disruption of a pre-established functions or interactions. For example, single protein


enzymes act alone, without the need for the loss or interference of any other cellular

function. Several such enzymes have been shown to evolve de novo in living

organisms such as bacteria. However, given the much higher specificity of the average

enzyme (as compared to antibiotic resistant target sequences), it is much harder to

evolve a new beneficial enzyme than it is to evolve the much simpler antibiotic-type

function. Some examples of enzyme evolution include the evolution of the lactase and

nylonase functions in bacteria.3 However, such examples are extremely limited and

highly constrained by both environment as well as the starting genetic real estate of the

population of bacteria. Many if not most types of bacteria simply cannot evolve certain

specific enzymatic function regardless of the size of their population, high mutation

rates, and tens, hundreds, or even millions of generations of time. Of course, the

problems only get worse from here on out. Functions of far greater complexity exist

inside living cells. For example, many functions require the simultaneous action of

multiple proteins interacting in a specified arrangement with each other. If it is difficult to

evolve just one relatively simple enzymatic-type function, imagine how hard it would be

to evolve any function of the level requiring such a specific multi-protein system as is

used in various bacterial systems of motility (i.e., the flagellum - requires 50 or 60

unique proteins all working together at the same time in a specific orientation with each

other). Interestingly enough, no such function that requires multiple proteins working in

specified concert has ever been shown to evolve in real time. It just doesn't happen

even when all the required parts needed to produce some fabulously beneficial function

are already present inside the same cell as parts of other systems of function. The

problem is that the parts themselves, if left to themselves, just don't know how to self-
assemble to form much of anything. They need outside information telling them how to

assemble in specified ways to produce higher and still higher levels of functional

complexity. Without this outside information, in the form of pre-established genetic

codes or the insight of an intelligent mind, the parts are no more creative in their

interactions than a junk pile during an earthquake (even if that earthquake lasts for

millions, billions or even trillions of years - - nothing more complex than a pile of

random parts will be realized).

So, natural selection is a real force of nature. However natural selection is very much limited

to a pre-established gene pool of options. Natural selection generally interacts with Mendelian

laws and other laws of genetic recombination to create diversity. Mutations are almost always

detrimental and are therefore selected against, as a rule, by natural selection. And, even the

mutations that are beneficial are limited to the lowest levels of functional complexity. There

simply are no examples of real evolution producing anything of the level of complex function

that requires multiple proteins working in a specified orientation at the same time. Natural

selection is therefore a force that generally acts against the other natural force of

evolution (random mutations) and even at its best is not much of a help to the popular

theory of evolution.

1. Ayala, Francisco J. Teleological Explanations in Evolutionary Biology, Philosophy of Science,


March, 1970, p. 3.
2. Stryer, Lubert. Biochemistry, 3rd ed., 1988, pp. 153, 744.
3. 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.
4. Beardsley, Tim, The Degeneration of Man, Scientific American, April, 1999, p32
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