Methinks it is Like a Weasel

                                                                                                                        Sean D. Pitman M.D.

                                                                                                                             © June 2003







The observation that things in nature change has been considered and theories proposed as explanations throughout recorded history. Plato, Socrates, Aristotle, etc. all proposed theories to explain the “flowing” or “liquid” quality of a changing nature.1 Naturalistic and evolutionary ideas appeared early on in recorded human history. However, not until Charles Darwin (1809-1882) published his On the Origin of Species in 1859 did a purely naturalistic process become generally accepted by scientists and even society. For the first time, a logical, apparently rational, evidence-based theory had been proposed that seemed to clearly explain most, if not all, of the observed changes in the natural world.

Obviously Darwin was correct in his observations that living creatures do in fact change over time. He then proposed a theory to explain these changes. He theorized that the small changes he observed in nature could add up over generations to produce larger, and still larger changes to the point of evolution between species. He in fact proposed that all living things, including humans, evolved from a single common ancestor and that all life continues to evolve. The proposed process of evolution suggested that very slight random changes in some creatures give them an advantage in a particular environment. This very slight advantage translates into better survival for that particular creature. Increased survival in turn translates into an increased ability to pass on this trait to more offspring, who in turn survive better. More and more traits are added (or subtracted) in each generation until, over the course of millions of years, the incredible diversity of living things that we see today is the result.

This is a great theory. It sounds reasonable. It does in fact explain some interesting observations and it makes some predictions that can be tested. Darwin did in fact observe small changes, such as changes in the size and shape of finch beaks etc. However, Darwin never did see a finch turn into an iguana or visa versa (or any other such major change). The small changes are testable, but the larger changes are not because they are theorized to take many thousands or even millions of years to occur. This is far too long to be observed or tested for, even in many lifetimes. Can it then be said that large-scale evolution is not observable or directly testable and therefore not a true science? Well, no… not at this point.  We first have to see if small-scale evolution really does happen just as Darwin observed. 

Darwin did observe very clear changes in creatures, no doubt. These changes are so impressive as to make evolution appear quite reasonable if not downright obvious to the candid mind. In fact, it seems like the only reason that it was not accepted without any qualms whatsoever is because it clashed with the prevailing understanding of origins in the religious communities of the day. However, just because truth might be distasteful, does not change the fact that it is true. Those with strong religious convictions seemed unable to explain the obvious evidence in existence before their own eyes. The reaction of many a religious person was not calm and considered, but explosive, defensive, and authoritative. This is a common human reaction in the face of an unanswerable challenge to a cherished idea. However, just because no effective challenge could be given during Darwin’s day does not mean that a theory should not continue to be tested and questioned. Only by testing and retesting do theories grow and improve. We are now in the age of genetics where these small changes noted by Darwin can be analyzed on the sub-cellular/molecular level.

Gregor Mendel (1822-1884) is the father of modern genetics. He was an Austrian monk who lived during the time of Darwin, although Darwin was never made aware of Mendel's work. During Darwin’s time, no one knew about DNA or genes or exactly how traits were passed on from parents to offspring. It was generally known that certain traits could be selected for since this was commonly done with the breeding of animals such as dogs, cats, cows and horses etc. But, until Mendel, no good explanation for the process of inheritance had been proposed. Mendel observed predictable changes in specific characteristics of various plants in his garden as he bred them in specific ways. He observed that certain “traits” were predictably “dominant” in expression over other less expressed or “recessive” traits. So what does this prove? Mendel’s experiments proved that not all observed changes are random, but are based on predictable rules of inheritance. A certain degree of variation is programmed into the “genetic pools” of many creatures giving them a variety of available “options” or characteristics to pass on to their offspring.2

Since Mendel, the human understanding of genetics has grown at an astounding rate. We now know that all traits in all living cells are written in a coded language and stored in a molecular book called D.N.A. (Deoxyribonucleic Acid). We know that this language is written using an alphabet of four chemical letters labeled A, T, G and C (Adenine, Thymine, Guanine, and Cytosine). The language of DNA has also been decoded. We know that this language only recognizes three letter words or “codons.” A three-letter codon in turn is “transcribed and translated” into one of twenty different amino acids. Amino acids are also letters in another code-like language of proteins. Specific orders and lengths of the twenty different amino acids make different proteins with specific functions much like different letter sequences make words with different functions. Not every series of amino acids is recognized by an individual cell, but only those that have a recognized function within that particular cell (Just as not every series of letters in the alphabet is recognized by an English speaking person as having meaning). Proteins are in fact the functional units of the cell. So, in order to have function a cell must make proteins. In order to make proteins, a cell must have DNA that tells it exactly how (and when) to make each protein as well as how to use each protein. DNA is the “blueprint” for the cell/creature. DNA contains all the instructions for the building and function of every part of the creature. If there is any change in structure or function, it will be as a result of change in DNA. Therefore, if evolution occurs, it will be occurring in DNA since the creature is just an expression of the instructions of DNA.

So, in the study of genetic inheritance, what happens to the DNA? Why are some traits “dominant” while others are “recessive?” The dominance and recessiveness of genes is made possible because of sex. Creatures that have the ability to reproduce sexually have some pretty interesting DNA. Half of that creature’s DNA came from its mother and half from its father. This creature is able to make specialized cells called “gametes.” As this cell develops during a very complex process called “meiosis,” the DNA that came from one parent mixes with the DNA that came from the other parent in a very specific and yet random way called “genetic recombination.” If all goes according to plan, by the time a gamete is fully developed, it is uniquely different from every other gamete produced by that creature and yet none of them have any gene that their “parent” did not have. Genetic recombination does not involve any mutational changes in the genes, and yet it allows for a huge variety in expression of these genes. A gamete that is produced by the “mother” is then joined with a gamete that is produced by the “father” and they fuse into a single cell and combine their DNA. During its life, the creature expresses only those traits that it received from its parents via their combined DNA. Because of genetic recombination, the expression of traits is always unique and yet predictable. The likelihood of having two identical offspring from the same set of parents at different times is, for all practical purposes, zero.3, 13 For example, I have light skin, light brown hair and blue-green eyes. My brother by the same parents has very dark skin, dark brown hair, and dark green eyes. We do have similarities, but we do not look exactly like each other, or even our parents. These differences are not the result of any evolutionary changes, but are simply the result of genetic recombination of pre-existing options in our “gene pool.”

Selective breeding has been going on throughout recorded history. However, it is impossible to breed beyond certain limits. For example, in dog breeding there is a limit to the maximum or minimum size that can be bred for. No matter how much selection pressure is applied, a Great Dane is about as big as a dog can get, and a Chihuahua is probably at the limit of doggy smallness. There is definitely a very wide range for size, color, temperament et cetera that can be bred for, but there are limits to the expression of each of these traits. This applies to all creatures that multiply using sexual reproduction. Likewise, the variation in groups of finch beaks that Darwin noted is easily explained using genetic recombination. The same can be said for the famous color changes in England’s peppered moth. The major variations between the different human races are also easily explained using genetic recombination. These are not examples of evolution at all. 

Dr. Walter Veith, zoologist and senior professor at the University of the Western Cape, says, “By selecting from the built-in natural variation of the gene pool, various breeds of dogs and domestic cattle were produced. Great changes in physiology and morphology are involved, and evolution is here certainly excluded.”4 Darwin had no idea since he was not capable of understanding the genetics involved, so he can be excused for assuming some sort of evolutionary process here. However, for us in this modern age of increased enlightenment we can no longer use Darwin’s finch beaks or other minor variations within a “kind” as examples of evolution in action. Why? Because in none of these examples has anything that is actually genetically new or unique evolved!

The Theory of Evolution claims not only that life has evolved in the past, but that it continues to evolve. Its claim to the past is one thing, but its claim to the present and to the future is quite another. If this claim to the present and the future is to be born up scientifically, then this theory is going to have to be subjected to tests that give evidence to this present evolutionary activity. To do this, not only do changes that are informationally unique have to be demonstrated, but the extent to which these changes can add up must be tested.  For example, by appealing to genetic recombination alone, it is impossible to turn a dog into a cat or a monkey into a man regardless of the selection pressure applied. Different gene pools are involved and some similar genes work together in different ways in different pools. Some other process outside of genetic recombination is needed to explain the “missing links” between unique, functionally different genes and gene combinations.

The Theory of Evolution is in serious crisis because of this very problem despite much effort by many great minds to explain it away.  One valiant attempt was made by the famous British evolutionary biologist Richard Dawkins. In his 1986 book called “The Blind Watchmaker” Dawkins described an experiment of his that showed how evolution is supposed to work. He programmed a computer to generate random sequences of letters to see if the computer would, over time, generate the line from Hamlet, “METHINKS IT IS LIKE A WEASEL.” This line has 28 characters (including spaces), so the computer was programmed to make 28 selections using the 26 letters of the alphabet plus a space to make 27 possible characters to pick from. A typical output was “MWR SWTNUZMLDCLEUBXTQHNZVJQF.” With this information, a calculation of the probability of picking the “correct” sequence can be made, as well as how long it would take, on average, to find this correct sequence. Dawkins figured that it would take his computer a million million million million million million years (or a trillion trillion trillion years… 1 x 1036 years), on average. Well, this is clearly way too long for the current theory. So, how could evolution possibly take place? Dawkins now put some “natural selection” into the computer program to simulate “real life” more closely. The computer made multiple copies of “MWR SWTNUZMLDCLEUBXTQHNZVJQF” (Offspring) while introducing random “errors” (mutations) into the copies. The computer then examined all the mutated “offspring” and selected the one that had the closest match to, “METHINKS IT IS LIKE A WEASEL.” This selection by the computer (nature) was now used to make new copies and random mutations (in a “new generation”), from which the best copy was selected again… and so on. By ten “generations” the sequence had “evolved” to read something like, “MDLDMNLS ITJISWHRQEZ MECS P.” By the thirtieth generation it read something like, “METHINGS IT ISWLIKE B WECSEL.” Instead of taking many trillions and zillions of years this time, the computer came up with the “fittest” phrase in about 40 generations.5      Of course Dawkins made a disclaimer that this experiment was not intended to show how real evolution works, but that it does illustrate the advantages gained by a selection mechanism in an evolutionary process.

Certainly this is a fine illustration except for one subtle flaw.  Dawkins's computer did not make its selection based on phrase function, but on phrase sequence comparisons to an "ideal" phrase.  Why is this a problem?  After all, its just an illustration.  Perhaps it is an illustration, but it is not illustrating anything even close to what natural selection is capable of.  The theory of evolution is based on natural selection and natural selection selects based only on sequence function.   If two genetic sequences are both non-functional or if they both have the same function, then natural selection cannot select between them.  In other words, nature is blind to their genetic differences if they both have the same function.  If Dawkins had wished to mirror the type of selection proposed by the theory of evolution, he would have based his computer model on functional phrase selection.  The problem here is that "MDLDMNLS ITJISWHRQEZ MECS P" doesn't mean anything.  This phrase has no language function.  A selection mechanism that only recognized changes in function would look at this phrase and compare its function to the function of the phrase, "SDLDMNLS ITJISWHRQEZ MECS P" where an M was mutated into an S.  Of course, both phrases have the same non-functional function.  A selection mechanism that is based on function will not be able to tell the difference between them.  Therefore, one will not be selected over the other for "survival" in the next generation.  Therefore, there will be no "directed" evolutionary change toward some sort of improvement or new function.  

Another problem with Dawkins's illustration is that the computer already had the "ideal" phrase programmed into it by an intelligent designer (Dawkins) to begin with.  The evolution of something that is already there is not the evolution of anything new at all. If nature already has what it wants or needs, then it does not need to “evolve" it.   

Dawkins uses a selection mechanism that does seem to work, but mindless natural processes do not have access to such a selection mechanism.  Dawkins uses a selection mechanism that is capable of comparing non-functional sequences with an ideal sequence.  A mindless nature only recognizes functional differences, not sequence differences since mindless nature has no ideal sequence to compare other sequences with.

Mindless nature does not “see” the actual letters of words (in DNA or Protein). All that a mindless nature can see is what function results. Since function is arbitrarily attached to words by an outside source of information, such as a system of function or definition, a gradual change in the letters of the words themselves is not necessarily going to result in a gradual evolution of their meaning or function. A gradual change in a recognized word or phrase will most likely destroy its original meaning well before any new word or phrase is recognized as having meaning.  Without function the entire way, natural selection is blind and even Richard Dawkins will admit that without natural selection to guide evolution, evolution is statistically impossible.

Yes, blind evolution might result in change to the spelling of genetic sequences, but the changes would not necessarily be functional changes. Changing one nonfunctional word into another nonfunctional word is a "change", but it is not a functional change since both words remain, well, nonfunctional.  Two nonfunctional words both have the same nonfunctional function.  You see, although natural selection is a real force of nature, it acts as a “stabilizing effect, but it does not promote speciation. It is not a creative force as many people have suggested.”16

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.”6

Many might say that bacterial antibiotic resistance or diseases such as sickle-cell anemia (SCA) are examples of evolution in action.  To a certain extent I would agree, but these changes and the unique functions that result have their limits.  Often such changes are the result of a loss of a gene.  Such changes might make a creature look different (maybe even survive better in certain environments, such as flightless birds on windy islands or cavefish without eyes).  Certainly such changes are the result of genetic modifications where genes that where once functional are no longer functional.  However, it is very easy to mutate a sequence so that it looses function.  The reason for this is that each functional sequence is surrounded by a vast ocean of nonfunctional sequences.  A very few mutations are all that are needed to evolve a functional sequence into a nonfunctional sequence.  A huge number of evolutionary paths lead from function to nonfunction.  Any one of these paths will do.  So, this type of evolution is simple and happens all the time.   Remember, it was much easier to break Humpty Dumpty than it was to put him back together again.  Why?  Because there are a lot more ways for Humpty Dumpty to be broken than there are ways for him to be fixed.  But, there are actually some ways to make new Humpty Dumptys . . . right?

Well, yes there are.  The actual gain of new gene functions have in fact been demonstrated with experiments that include the evolution of the lactase enzyme in E. coli bacteria demonstrated by Professor Barry Hall,23 and the evolution of the nylonase enzyme demonstrated by Kinoshita, et. al., 24,25 to name just two of many such examples.  However, all such examples of the evolution of novel functions occur as the result of one or two point mutations.  No gaps of neutral or nonfunction wider than two mutations have, to my knowledge, ever been crossed.  Statistically speaking, large populations could cross neutral gaps in function a bit larger than this (20 or 30 base pairs), but as the size of the gaps increase, the time required to cross these gaps increases exponentially to the point were increasing the population size simply cannot keep up.  Pretty soon trillions upon trillions upon zillions of years are required to cross apparently small gaps in neutral genetic function.

 If it could be demonstrated that no gaps of neutral function wider than a very few point mutations exist between some widely separated sequences in cellular or multicellular system functions, then the theory of evolution and of common descent would be much more believable.  And yet, very significant gaps do seem to exist between various cellular functions of living things and these gaps only increase in size as functional complexity increases.

To understand this problem a little more, lets take a closer look at proteins and how they work.  In a living cell, proteins work like locks and keys called enzymes and substrates. Like other locks and keys, proteins are very specific molecules. All proteins have certain  amino acids or protein “letters” in their makeup that cannot change without a loss of protein function. These amino acids are called “invariant” and are generally the foundation of the functional three-dimensional shape of the protein. There are other locations, besides these, that can change only between certain types of amino acids (twelve polar (including two acidic and three basic ones) vs. eight nonpolar amino acids). For example, the hemoglobin protein consists of four amino acid chains (of two different types) adding up to a total of 574 amino acids. Richard Dawkins claims that 190 (33%) of these are “invariant.”5 Much more of the molecule is “nonpolar” and can only change within a group of nonpolar amino acids (partially variant).7  

Cytochrome C, part of the electron transport chain of proteins responsible for making usable energy for the cell, also seems to have a fair percentage of "invariant" amino acids in its structure.  Out of the usual 104 amino acids that make up cytochrome c humans differ from bread mold by only 44 amino acids.  Even with these differences, the various cytochrome c sequences are basically the same, having essentially the "same 3D topology."  Furthermore, in vitro studies have shown that the cytochrome c sequences from any species can integrate themselves correctly with the other elements of the oxidation processes of all other creatures using cytochrome c.  In other words, all the varieties are interchangeable because they are basically identical in 3D structure and function.  In order to maintain this specificity, other studies that compared sequences of 40 species have shown that at least "35 of the 104 amino acids are invariant."  "Furthermore, at another 40 sites, only 2 or 3 amino acids occur, and at each of those sites, the pairs of triplets are always very similar in chemical character-i.e., they are either hydrophilic, hydrophobic, or neutral with respect to water.  At only a very few sites can radically different amino acids occur.  Why might this be?  Presumably, mutations occur at all sites.  However, changes at some sites presumably destroy the function of the molecule, whereas at other sites, some change is tolerable, and at a few sites, major changes don't seem to be of much consequence.  Subsequent detailed studies of molecular structure confirmed these premises.  Many of the invariant sites are critical in causing the molecule to fold itself properly--changes at these sites would completely disrupt the molecule's function." 27 

With these thoughts in mind, lets do a few calculations and see if we cannot make the situation a little more clear.  Let's take a protein sequences of 100 amino acids.  How many different 100aa protein sequences are possible?  There are just over 10e129 different possible amino acid arrangements in a 100aa protein.  That is a huge number.  Scientists estimate that there are only 10e80 particles of matter (electrons, proteins, neutrons) in the entire universe.  The question is, of these 10e129 different sequences, how many of them would have the cytochrome c function?  If we say that 35aa of the 100aa are invariant and that another 40aa can only change between two amino acids, and perhaps another 20aa can change between 5 or so amino acids and the five that are left over can change between all 20 amino acids . . . how many variations will still have the cytochrome c function?  These numbers add up to around 10e40.  Of course, 10e40 is the tiniest of tiniest tidbits when compared to a number like 10e129.  However, there are some who suggest that there are actually several more "variant" amino acids in cytochrome c and that even certain amino acids that are "invariant" between many different groups of animals can in fact be changed without a complete loss of cytochrome c function.  They suggest that a more reasonable number of amino acid sequences with potential cytochrome c function would be on the order of 10e60.  Certainly 10e60 is a great deal larger than 10e40, but this is still nothing compared with a number like 10e129.  In comparison, each one of the functional 10e40 sequences would be surrounded by 10e89 sequences that would have absolutely no cytochrome c function.  This is an absolutely huge sea of protein sequences that would not have even a small bit of cytochrome c function.  Finding even one of the 10e60 functional cytochrome c sequences out of 10e129 possibilities would be like finding a particular proton out of all the subatomic particles in the universe. 

In this light, starting with a random 100aa sequence, the odds are very good that it would be quite a long ways away from the nearest functional cytochrome c sequence, and this is a relatively simple function based on just one relatively short amino acid sequence.  It is like trying to evolve one sentence into another sentence one letter at a time with each change making beneficial sense in English.  Try it sometime and see how far you can go.  Start with a sentence 100 characters in length and then, by changing one letter at a time, see how many different functional sentences you can get with each change making some sort of beneficial sense in a certain hypothetical situation.  It is a lot more difficult than you might initially realize.

When one understands the specific nature of most proteins, it becomes that much harder to understand how protein evolution can occur if at least some functional proteins or systems of proteins are separated from each other in sequencing and three-dimensional shape by anything that involves more than a very minor change.  The reason for this problem is that the statistical time involved to cross gaps of neutral function is simply enormous.  Functionally neutral/nonfunctional genes and proteins are not subject to the evolutionary pressure of natural selection.  Because of this, mutational changes are completely random since natural selection cannot determine which neutral or nonfunctional mutations are any better or worse than any other neutral or nonfunctional mutations.  Such neutral changes are therefore left to drift along randomly until they happen upon some new non-neutral function by sheer luck.  Such serendipitously successful voyages are statistically possible, but they average a great deal of time that increases exponentially with each neutral step that must be crossed between various novel functions.  In other words, the more complicated the function, the longer time it will take for random neutral genetic changes to come across it.  Basically, genetic gaps of neutral/nonfunction kill evolution since natural selection is blind to neutral genetic differences.

To help visualize these neutral and/or nonfunctional gaps, consider the word, "armadillo."   This word has a meaning or function in the English language.  However, lets say that the next closest understood word in the English language is "armada."  Obviously no single letter change is going to get us from armadillo to armada.  Before changes to "armadillo" achieve the new function of "armada" all function is going to be lost.  For example, what does "armadallo" mean?  If we are allowed to only select between words that have meaning, we cannot select armadallo over, say, "brmadillo" simply because "armadallo" is closer to our desired goal of "armada."  Why?  Because, as with natural selection, we can only select between functional changes.  Two nonfunctional words are equally nonfunctional or functionally "neutral" when compared with each other.  So, there is no basis for a non-random selection between them.  Without selection ability, it is quite obvious that random chance alone will take a very long time, on average, to cross the functional gap between armadillo and armada.  Remember how long Dawkins said it would take to evolve, "Methinks it it is like a weasel" without the benefits of a selection mechanism. . . zillions of years.  So you see, the gap problem is really a tough one for evolution to explain since the mindless naturalistic theory of evolution must rely on a functionally based selection mechanism.  No intuition, creativity, or intelligence is allowed in the door to help out the process.

Problems such as this have caused many well-educated scientists to reevaluate their position on evolution. Two prominent British scientists and outspoken atheistic evolutionists, Sir Frederick Hoyle (Big Bang Theory) and Chandra Wickramsinghe were, in their own words, “driven by logic” to conclude that there must be a creator.  Both of them admitted that this was a tough conclusion for them to admit and that their conclusions were basically forced upon them, "against their will."  Dr. Wickramsinghe went on to say, “From my earliest training as a scientist I was very strongly brainwashed to believe that science cannot be consistent with any kind of deliberate creation. That notion has had to be painfully shed. I am quite uncomfortable in this situation, the state of mind I now find myself in. But there is no logical way out of it. I now find myself driven to this position by logic. There is no other way in which we can understand the precise ordering of the chemicals of life except to invoke the creations on a cosmic scale. . . We were hoping as scientists that there would be a way round our conclusion, but there isn’t.”8 Likewise, in his recent book, “Darwin’s Black Box,” the biochemist Michael Behe promotes the idea of “irreducible complexity” in the natural world as giving evidence of intelligent design.6

There are many more scientists, famous and non-famous, who are leaving the theory of evolution behind, often reluctantly, because of the overwhelming “logical” flaws in the theory. So why does it continue to be so popular with most modern scientists? Perhaps, as Chandra Wickramsinghe suggested, it has to do with the fact that it is an integral part of the public educational system? Evolution is rarely questioned in the public school system, but instead is taught as the gospel truth, as "more than a theory."  Textbooks never question it but instead refer to evolution as an unquestioned fact of nature.  The process of evolution itself may be debated in the public school system, but no one ever challenges the fundamental "truth" that all living things have descended from a common ancestor life form and that this life form arose from the non-living prehistoric ocean chemistry. Perhaps then Dr. Wickramsinghe is correct in describing his educational training in evolution as a “brainwashing”? Maybe it is because of such a bias in training that almost everyone’s understanding of evolution is based on someone else’s authority, even among scientific experts and professors?  No one seems to know exactly how evolution works, but they are sure that others do know.

 Some might have even more personal reasons for their belief in evolution as suggested by the anthropologist Michael Walker when he said, “One is forced to conclude that many scientists and technologists pay lip service to Darwinian theory only because it supposedly excludes a Creator.”9 The idea of a designer/creator or “God” seems to bother a lot of people. For some, God might create meaning in life, and therefore personal responsibility. Many might have a desire to be free from any such personal restraint. Others might have a painful image of God, or associate the idea of God with dogmatic superstition and ignorance. Some might feel like the famous writer and evolutionist Aldous Huxley (grandson of Thomas Huxley) when he stated, “I had motive for not wanting the world to have a meaning; consequently assumed that it had none, and was able without any difficulty to find satisfying reasons for this assumption. The philosopher who finds no meaning in the world is not concerned exclusively with a problem in pure metaphysics, he is also concerned to prove that there is no valid reason why he personally should not do as he wants to do, or why his friends should not seize political power and govern in the way that they find most advantageous to themselves. … For myself, the philosophy of meaninglessness was essentially an instrument of liberation, sexual and political.”10

I find it very interesting that what is supposed to be a completely rational science can be so influenced by personal feelings and philosophy. It seems like even scientists are human. We cannot avoid our personal biases but we can at least be aware of them and how they influence our perception of “truth.” However, if there is a “truth” it will be true regardless of how we might feel about it. An honest seeker for truth will search for it and accept it despite its implications. So, how does one search and sort out truth from error in a non-passionate manner? It seems that the subjective human mind cannot know truth absolutely, but can know error. The scientific method does not prove theories to be absolutely true, but it can prove them to be false. Theories that are beyond the realm of human investigation cannot be proven false and so remain beyond the reach of the scientific method. Such theories are called, “non-falsifiable” or “non-scientific.” The claims of evolutionary theory concerning the past are not directly covered here, but are its claims concerning the present and the future testable? If so, they have yet to be demonstrated or even theorized in a testable way. If this particular part of evolutionary theory is in fact non-testable, then it is not a science. It therefore remains strictly a theory based in historical evidence, however “good” or “bad” that evidence might be. Design Theory is in the same boat. No one has yet been able to demonstrate the “Original Designer of life at work.” However, without the ability for evolutionary theories to demonstrate or even theorize genetic evolution in any meaningful way, the obvious complexity of living things does historically match with the complexity seen in other complex objects/machines, practically all of which were designed outside of any naturalistic process with the use of intelligence in their design. For historical studies, correlation seems to be very important. Design Theory does have the ability to correlate the complexity of living things with the complexity of intelligently designed machines and not with any other known source of complexity or apparent design originating at the present time.

Should these facts be passed by unacknowledged by the scientific mind? It seems like evolutionary theories have had ample time to prove themselves. “Darwin's theory of natural selection has never had any proof, yet it has been universally accepted.”18 If significant evolution could happen in just a few generations as Dawkins indicates, then why is it not being observed in life forms like bacteria that have very short generation times? Over the past 50+ years, greater than one million generations of E. coli have been observed, radiated, drugged, burned, frozen, dissected, mutated, selected and manipulated in every conceivable manner (talk about selection pressure), yet E. coli are still E. coli. This seems especially strange when one considers that humans supposedly evolved from apes in less than 200,000 generations using a much lower mutation rate (on the order of one mutation per gene per 100,000 generations).19, 20 A similar case can be made for the fruit fly.  Fruit flies are still fruit flies.  Why is this? Dr. Robert Macnab seems to be asking the same question when he states, “…one can only marvel at the intricacy in a simple bacterium, of the total motor and sensory system which has been the subject of this review and remark that our concept of evolution by selective advantage must surely be an oversimplification. What advantage could derive, for example, from a "preflagellum" (meaning a subset of its components), and yet what is the probability of ‘simultaneous’ development of the organelle at a level where it becomes advantageous?”21 Gordon Taylor also observes, “In all the thousands of fly-breeding experiments carried out all over the world for more than fifty years, a distinct new species has never been seen to emerge.”17

 The fact is that scientists are speaking beyond their ability to really know.  They are so cock sure of themselves and the theory of evolution, and yet they really do not have a very good idea about how DNA really works.  They have some idea, but when it really comes down to it, DNA and the information it contains is far more complicated than scientists have even begun to realize.  For example, for many years it was thought that humans had between 60,000 to 100,000 genes.  But, a surprising discovery was made by those working on the human genome project.  When they finished the project in 2001, they estimated a that the actual gene count was somewhere between 35,000 to 40,000 genes.  What is even more surprising is that the estimates for the genes needed to make a mouse were only about 500 or so different from the absolute number needed to make a human. 14  These new estimates were short lived however.  In February of 2002, at the annual meeting of the American Association for the Advancement of Science (publisher of Science), one of the presenters, Victor Velculescu, suggested that the real number of genes in the human genome may actually be closer to 70,000 genes after all.   He and his colleagues, at Johns Hopkins University in Baltimore, Maryland, have gone back to the lab to look for genes that the computer programs may have missed. Their technique, called serial analysis of gene expression (SAGE), works by tracking RNA molecules back to their DNA sources. After isolating RNA from various human tissues, the researchers copy it into DNA, from which they cut out a kind of genetic bar code of 10 to 20 base pairs. The vast majority of these tags are unique to a single gene. The tags can then be compared to the human genome to find out if they match up with genes discovered by the computer algorithms. Velculescu said that only roughly half of the tags match the genes identified earlier.  For him, this is evidence that the human inventory of genes had been underestimated by about half.  The reason for the disparity may be that the standard computer programs were largely developed for the genomes of simple (prokaryotic) organisms, not for the more complex sequences found in the genomes of humans and other eukaryotes. "We're still not very good at predicting genes in eukaryotes," said Claire Fraser of The Institute for Genomic Research in Rockville, Maryland. It's entirely possible that there could be more than 32,000 genes, and SAGE is an important approach to finding them. She adds, "You absolutely have to go back into the lab and get away from the computer terminal." 26

If we still do not really know how many genes we have in our genome, even after having sequenced the entire human genome, how can we be so sure that our genes evolved from lower organisms?  How do we know that we are between 94% and 99% the same as chimps?  And, even if we are, who is to say that our similarities were the result of common descent over some other possibility?  If the differences can be explained by the theory of common descent, well and good.  However, there seem to be differences between various genes and gene functions that cannot be explained as a result of common descent.  The problem is that these “small” differences might turn out to be rather huge. Even a single gene difference can be gigantic depending on how isolated it is in functional sequencing from the available genetic realestate of a given gene pool.

“...An intelligible communication via radio signal from some distant galaxy would be widely hailed as evidence of an intelligent source. Why then doesn't the message sequence on the DNA molecule also constitute prima facie evidence for an intelligent source? After all, DNA information is not just analogous to a message sequence such as Morse code, it is such a message sequence.”22 Has Design Theory come full circle? Many, even among the most respected of scientific minds, seem to be giving it more than another look.




1. Gaarder, Jostein. Sophie’s World. The Berkley Publishing Corp. 1996.

2. Cotran, Ramzi S., et al., Robins Pathologic Basis of Disease, 6th edition, W.B. Saunders Company, 1999, p. 143.

3. Gelehrter, Thomas D. et al. Principles of Medical Genetics, 1998.

4. Veith, Walter J. The Genesis Conflict, The Amazing Discoveries Foundation, 1997, p. 82.

5. Dawkins, Richard. The Blind Watchmaker, 1987.

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

7. Stryer, Lubert. Biochemistry, 3rd ed., 1988, p. 153, 744.

8. Hoyle, Sir Frederick and Wickramsinghe, Chandra. There Must Be A God, Daily Express, Aug. 14, 1981. & Hoyle On Evolution. Nature, Nov. 12, 1981, 105

9. Walker, Michael. Senior Lecturer — Anthropology, Sydney University. Quadrant, October 1982, p. 44.

10. Huxley, Aldous. Ends and Means, p. 270 ff.

11. Goldschmidt, R. PhD, DSc Prof. Zoology, University of Calif. in Material Basis of Evolution, Yale Univ. Press.

12. Thaxton, Charles B. Walter L Bradley and Robert L Olsen: The Mystery of Life's Origin, Reassessing Current Theories, New York Philosophical Library 1984, p. 211-212.

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

14. Lemonick, M. Gene Mapper, Time, Vol. 156, No. 26, pp110, 2001.

15. Macnab, Robert. Yale University, Bacterial Mobility and Chemotaxis: The Molecular Biology of a Behavioral System, CRC Critical Reviews in Biochemistry, vol. 5, issue 4, Dec., 1978, p. 291-341.

16. Brooks, Daniel. as quoted by Roger Lewin, "A Downward Slope to Greater Diversity," Science, Vol. 217, 24 September 1982, p. 1240.

17. Taylor, Gordon. The Great Evolution Mystery, New York: Harper and Row, 1983, p. 34, 38.

18. Goldschmidt, R. PhD, DSc Prof. Zoology, University of Calif. In Material Basis of Evolution, Yale Univ. Press.

19. Dugaiczyk, Achillies. Lecture Notes, Biochemistry 110-A, University California Riverside, Fall 1999.

20. Ayala, Francisco J. Teleological Explanations in Evolutionary Biology, Philosophy of Science, March, 1970, p. 3.

21. Macnab, Robert. Yale University, Bacterial Mobility and Chemotaxix: The Molecular Biology of a Behavioral System, CRC Critical Reviews in Biochemistry, vol. 5, issue 4, Dec., 1978, p. 291-341.

22. Thaxton, Charles B., Walter L. Bradley and Robert L. Olsen: The Mystery of Life’s Origin, Reassessing Current Theories, New York Philosophical Library, 1984, p. 211-212.

23. 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.

24. Kinoshita, et. al.,"Purification and Characterization of 6-Aminohexanoic-Acid-Oligomer Hydrolase of Flavobacterium sp. K172,"  Eur. J. Biochem. 116, 547-551 (1981), FEBS 1981.

25. Susumu Ohno, "Birth of a unique enzyme from an alternative reading frame of the pre-existed, internally repetitious coding sequence", Proc. Natl. Acad. Sci. USA, Vol. 81, pp. 2421-2425, April 1984.

26.   Shouse, Ben. American Association for the Advancement of Science Annual Meeting:  Human Gene Count on the Rise, Science, 22 Feb. 2002: 1457. (






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