Natural Selection

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.²This 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, 3^rd 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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