Let's put the intelligent design (ID) argument to rest now, by a simple appeal to the evidence. This essay deals with ID by first explaining what it is - at least as proposed by Behe - and then by using facts to demonstrate the shortsightedness, and folly, of using it as an argument against evolution.

Let me inject here that I myself hope (believe?) that there was some first Cause - God. I do not think that evolution destroys God. Indeed, if there is a God, an understanding of evolution honestly sheds a brilliant light on one part of His universe.

To Behe, intelligent design is found in the fact that cells contain irreducibly complex systems. An irreducibly complex system is a system "composed of several well matched, interacting parts that contribute to the basic function, wherein the removal of any one of the parts causes the system to effectively cease functioning."(1) In other words, if all the parts are absolutely needed for a system to work, then the system is irreducibly complex.

There is no dispute as to the fact that there are many biological systems that are irreducibly complex. The problem is Behe claims evolution could not produce such systems. According to Behe, "an irreducibly complex system cannot be produced directly by numerous, successive, slight modifications of a precursor system, because any precursor to an irreducibly complex system that is missing a part is, by definition, nonfunctional."(2) In other words, natural selection cannot create an irreducibly complex system because all the parts have to be there from the beginning, and natural selection works by choosing the better of systems that are already working. Thus, for evolution to create an irreducibly complex system one has to imagine a full system arising in one multi-gigantic mutational swoop. Even biologists agree this is statistically impossible.

A Typical Problem According to Behe

Here is an example of what Behe considers the problem. Assume a channel that allows a certain ion through the cell membrane is made of 15 working parts, the absence of any one making the channel ineffective. Where did the channel come from? Of course, evolution is the answer. A simple opening that allowed the ion through came about by mutation. It was selected because it did something beneficial for the cell. It didn't work great, but something is better than nothing. Over time new mutations allowed for a part here or there to join the channel, making it a little more effective - until eventually the channel reached the point of complexity at which it now stands. Behe balks at this point.

Behe sees a problem. He argues that since the channel is irreducibly complex (requires all the parts to work at all), there is no way it could have evolved by natural selection. The current channel requires all 15 parts. A partially assembled channel doesn't work at all. Hence, according to Behe, the only way evolution could account for the channel would be by assembling 15 very lucky mutations at once to produce the instantly functioning channel. Even biologists must agree that the odds of this are well beyond reasonable expectations. Behe sees irreducibly complex structures everywhere in the cell. Indeed they are everywhere....Darwin, we have a problem! The cell looks "designed."

There is no problem at all. Behe, smart as he is, doesn't appear to understand how natural selection works. He comes across as somewhat shortsighted. I'll give a thought example first, and follow it up with several actual examples that demonstrate the folly of the ID argument.

Countering Behe's Arguments

Assume a mutation allows a certain peptide (A) to bind to a chemical toxin until both A and the toxin are removed to the bloodstream. Assume A doesn't bind to the toxin real well - but it still confers some benefit. Later, a mutation causes another peptide (B) to bind to a spot on A, which makes A bind a little better to the toxin. The system works better now. Next assume that A mutates in a way that makes it bind better to B which enhances A's ability to bind the toxin even more. However, this most recent mutation to A causes it to be unable to bind the toxin at all without the presence of B. Now we have an irreducibly complex system. A will not work at all without B. But, the system didn't start off that way. (Note - Some of you may be wondering how A could have come about in the first place, since it derived from a mutation. Wouldn't its original job be lost? What good is this new job if the cell loses its original function? The answer is the well documented phenomena of gene duplication. Often genes get accidentally duplicated in the process of cell division. This means the genome now has extra copies of genes hanging around - indeed, we see this in all eukaryotic species genomes. One copy of the gene is still able to perform the original function while the duplicated copy is free to undergo mutation without ill effect to the species. This allows for the increase in genetic information over time.)

The point is thus; there is no guarantee that improvements will remain merely improvements. Later changes build on previous ones, thus earlier improvements may, in the future, become indispensable parts of the system.

This simple example should suffice to demonstrate that natural selection can, and often does, create irreducibly complex structures. It does so at the molecular level and the tissue/organ level. Behe is simply wrong when he says the parts of an irreducibly complex system have to be in place from the beginning.

Exaptation and New Functions

I've already discussed gene duplication above. I want to mention exaptation now. Exaptation is the idea that evolution often works by scavenging existing genes (and their products) and putting them together for a new function. This is possible because of gene duplication. Once a gene has been duplicated, the original gene can produce the original protein and the duplicated gene is free to undergo mutation without harm to the species. These extra genes often end up, after several mutations, creating a slightly different (and new) protein that gets paired up with others and selected by nature because the combination happens to perform a beneficial task, or make an already existing cellular machine or pathway more efficient.

We see simple evidence of this in the lens crystallines of eyes. The genes for lactate dehydrogenase, aldehyde dehydrogenase, and enolase have all been duplicated and the nature has modified them into lens crystallines. The evidence is found not only in the remarkable similarity of the base pairs of the genes and their crystalline counterparts, but in the fact that the original proteins can be used as lens crystallines in the same form as they carry out their normal functions.(3) We also see the result of several gene duplications throughout time in the various forms hemoglobin and myoglobins now present in vertebrates. For instance the hemoglobin of lampreys, a primitive jawless fish, consist of a single protein chain. In later evolved vertebrates, like amphibians and reptiles, hemoglobin consist of four protein chains - each protein being very similar. This four chain molecule has a much greater oxygen binding capacity than the one chain hemoglobin of lampreys. In mammals, there are even more genes for hemoglobin, each differing only slightly and resulting in the gamma and epsilon chains that characterize the different hemoglobins in human fetuses and adults. So, we can see over time a succession of gene duplications giving rise to the "irreducibly complex" system of respiratory proteins in vertebrates.(4) Each system is irreducibly complex in its own right, but evolution has modified them to create the increased complexity over time.

Evolved Irreducible Complexity

One of the examples of irreducible complexity Behe uses is the cilium - a structure used most often for movement by small cells. Cilia are composed of long chains of microtubules bundled together to make a whip-like structure. I remember studying the cilium in my biochemistry class in college. It is very complex. But to be honest, I don't remember all the details. So, I'll borrow a lot here from Kenneth Miller who is a cellular biologist.(5) Dr. Miller was actually amused at Behe's suggestion that the complexity of the cilium is irreducible (remember, even if it was irreducible it could have evolved). Since the cilium is a complex structure and the 9+2 microtubule structure is found everywhere in nature from algae to human sperm cells, it may easily be assumed that this is the only pattern that worked - hence irreducible complexity. But an appeal to any biologist with a knowledge of cilia would have informed Behe that such is not the case. Sperm from the caddis fly have a 9+7 microtubule arrangement. Some mosquito species have a 9+9+1 arrangement. Eel sperm have a 9+0 arrangement (lacking a central microtubule chain altogether). Finally, the protozoan Diplauxis hatti has a 3+0 arrangement in which many of the supposedly indispensable parts of the 9+2 structure are missing. Some of these cilia work better than others. All the species make do. But it is obvious the 9+2 arrangement isn't irreducibly complex. And the existence of so many simpler versions of cilia demonstrates that Behe's central thesis - that the cilium couldn't have "functional precursors" - is flat wrong.

Here is another actual example that destroys the irreducible complexity argument. In 1997, a group of scientists decided to watch the evolution of human growth hormone (a protein) HGH in the lab. (6) HGH binds to cells by means of precisely shaped receptor molecules on cell surfaces that fit the shape of a portion of HGH - kind of like a key fits into a lock. If you alter the shape of the HGH, or one of the receptor molecules on the cell surface, the binding will not occur - like your car key will not open your house door.

The researchers genetically engineered the genes to produce a receptor that had a detrimental amino acid deletion. This changed the shape of the receptor and the HGH no longer "fit," so the bonding could not occur.

The scientists then randomly mutated the coding regions of the HGH gene, generating millions of different mutant combinations. The bacteria with the mutations that caused the new HGH to bind to the modified receptor were selected. Now get this, the random mutations generated a new version of HGH that bonded to the modified receptor one hundred times tighter than the original nonmutant version. This is now an irreducibly complex system - but it evolved. The parts of the system evolved together, right in the lab.

Bigger, More Complex Systems

How about the "Lac" genes in bacteria. Lactose is a double-sugar that bacteria can use as food. But to do so the bacteria have to produce an enzyme that can cut lactose up into its two constituent sugars, glucose and galactose. The enzyme that does this is called galactosidase. Bacteria are pretty smart, because they do not produce galactosidase when there is no lactose on their environment. The galactosidase genes automatically shut off when no lactose is present.

The bacteria are able to keep the galactosidase genes turned off by means of a control gene that only allows the genes to be expressed in the presence of lactose. A group of scientists deleted the gene for galactosidase in a culture of bacteria.(7) They then grew the culture in a medium of lactose. Of course, because they lacked the ability to produce galactosidase, the altered bacteria and their offspring could not use lactose for food - at first. But before long, mutant strains appeared that could digest and use the lactose almost as well as the original strains.

What happened? How could mutations randomly reproduce the galactosidase gene so quickly? They didn't! The mutant bacteria did not make new galactosidase . Nature simply tinkered with another gene. A new mutation in an existing gene made its protein capable of breaking apart the lactose sugar. But the bacteria didn't stop there. The researchers looked at the control genes for the new gene that cleaved the lactose. They had become modified too, and some of them responded directly to lactose, switching the gene on and off as needed.

That is not all. The researchers continued to grow the mutant cultures that could utilize lactose. But they grew some on lactulose, a different sugar, and a new mutant strain appeared that could produce allolactose, the same chemical that bacteria normally use to turn on their "Lac" genes. This is significant because now the "Lac" genes could switch on the gene for Lac permease, which is an enzyme that speeds the entry of lactose into the cell. (In the original strain of bacteria the presence of galactosidase turned on this gene for allolactose, but the mutated stains did not produce galactosidase so the Lac gene for Lac permease could not be turned on - until this new mutation.) When the Lac permease gene now gets turned the increased lactose flow into the bacterium causes the control genes for the new lactose cleaving gene to activate. The system is now irreducibly complex.

Look at the complexity of this system. Lactose triggers a sequence that turns on the new lactose-cleaving gene. The enzymes produced by the gene metabolize the lactose. The products of the lactose metabolism then activate the gene for Lac permease, which ensures a steady supply of lactose entering the cell. A completely irreducibly complex system. One part is no good without the other. Each dependent upon the other. But the system evolved in a lab!

The Krebs Cycle -- Complexity Galore

A study of the extremely complex Krebs cycle (also important in terms of energy for the cell) has shown that it was built by modifying smaller existing chemical pathways. The Krebs cycle can be broken up into smaller, intermediate cycles which by themselves function fine - thus they could be favored by natural selection.(8)

Another example of how an irreducibly complex cellular machine evolved by the bringing together of existing molecular machines is the cytochrome c oxidase pump.(9) (Gosh I hate this - we had to draw a diagram of this crap in my biochemistry class - the Krebs cycle too. This is bringing back awful memories.) This pump is important in the cell because it plays a key role in energy transformation. In humans the pump consists of six proteins, each of which is necessary for the functioning of the pump - a perfect example of irreducible complexity. Researchers got to looking around and they found that two of the six proteins are quite similar to a bacterial enzyme known as the cytochrome bo3 complex. This complex works perfectly fine by itself - albeit in a different context. Well what about the rest of the pump? Same thing. Each and every protein of the pump has a closely related protein complex in microorganisms. Thus, we see that the cytochrome c oxidase pump, while appearing to be irreducibly complex, evolved piecemeal in stages that were selected by nature and refined over time.

The evolution of other pathways have been worked out too. I refer you to Kenneth Miller's "Finding Darwin's God" for several more examples with cites. I think I have provided enough here to demonstrate that Behe is incorrect about irreducible complexity. A biological system simply doesn't have to originate in its present form. There isn't even any room for compromise - Behe, and the ID crew, are simply WRONG.

Danger in Behe's Method

Let me end by proposing that Behe's way of doing science is dangerous. He sees a complex system and decides there is no way it could have evolved. Thus, he concludes "design." He invokes a miracle when natural laws suffice. Science cannot not admit defeat this way. That is not the job of science. When a quandary exists, a good scientist looks for the answer - the natural answer. He doesn't throw his hands in the air and lay it on the shoulders of the Big One upstairs.

By so doing, science doesn't negate God. It simply seeks to explain God's universe - down to the minutest detail - using God's laws. God just doesn't appear to be a magician, as many creationists portray Him.

ENDNOTES

1. M. J. Behe, Darwin's Black Box, pg. 39. [Hereinafter: Behe]

2. From a speech by Behe, Evidence for Intelligent Design from Biochemistryat the Discovery Institute's God and Culture Conference, Seattle, August 10, 1996.

3. Missing Links and the Origin of Biochemical Complexity by Barry Palevitz, in The Scientist.

4. Miracles and Molecules by Douglas Futuyma (professor and author) in Boston Review.

5. Kenneth Miller, Finding Darwin's God : A Scientist's Search for Common Ground Between God and Evolution, pp. 140-43. [Hereinafter: Miller]

6. Atwell et al., "Structural Plasticity in a Remodeled Protein-Protein Interface," Science 278 (1997): 1125-1128. Summarized in Miller, pp. 143-44.

7. This experiment, by B.G. Hall, appears in two scientific journals -"Evolutionary Biology" and "Evolution of Genes and Proteins." My summary is taken from Miller, pp. 145-46.

8. E. Melendez-Hevia, Waddell, and Cascante, "The Puzzle of the Krebs Citric Cycle: Assembling the Pieces of Chemically Feasible Reactions, and Opportunism in the Design of Metabolic pathways during Evolution," Journal of Molecular Evolution 43 (1996): 293.

9. Musser and Chan, "Evolution of the Cytochrome C Oxidase Proton Pump," Journal of Molecular Evolution 46 (1998): 508-20. Summarized in Miller, pp. 149-50.