The modern evolutionist is called a neo-Darwinian. He still accepts Darwin’s ideas about natural selection, but something new (neo-) has been added. The modern evolutionist believes that new traits come about by chance, by random changes in genes called “mutations,” and not by use and disuse.

Almost everyone has heard about mutations—from Saturday morning cartoons or horror movies, if nowhere else. In those flicks, some atomic disaster produces people with gnarled skin, one big bulging eye, and other “new traits.” In the real world, mutations are responsible for a number of genetic defects, including hemophilia (bleeders’ disease), loss of protective color in the skin and eyes (albinism), and certain kinds of cancer and brain malfunction.

We have abundant evidence that various kinds of radiations, errors in DNA replication, and certain chemicals can indeed produce mutations, and mutations in reproductive cells can be passed on to future generations. Fig. 16 shows some of the changes that have been brought about in fruit-fly wings because of mutations: shorter wings, very short wings, curled wings, spread-apart wings, miniature wings, wings without cross veins. Students in my genetics classes work with these fruit flies each year, crossing different ones and working out inheritance patterns.

Figure 16

Figure 16. Mutations are random changes in genes (DNA), often caused by radiation. The mutations in the wings above were produced by X-raying fruit flies. According to the modern, neo-Darwinian view, mutations are the source of new traits for evolution, and selection culls out the fittest combinations (or eliminates the “unfittest”) that are first produced just by chance. Mutations certainly occur, but are there limits to extrapolating from mutational changes to evolutionary changes (e.g., “fish to philosopher”)?

Then there’s the flu virus. Why haven’t we yet been able to solve the flu problem? Part of the problem is that this year’s vaccine and your own antibodies are only good against last year’s flu. (They don’t usually tell you that when you get the shot, but it’s already out of date.) The smallpox virus has the common decency to stay the same year in and year out, so once you’re vaccinated or build up an immunity, that’s it. But the flu virus mutates quite easily, so each year its proteins are slightly different from last year’s. They are still flu viruses, but they don’t quite fit our antibodies, so we have to build up our immunity all over again. When it recombines with animal viruses (on the average of once every ten years), the problem is even worse.

Mutations are certainly real. They have profound effects on our lives. And, according to the neo-Darwinian evolutionists, mutations are the raw material for evolution.

But is that possible? Can mutations produce real evolutionary changes? Don’t make any mistakes here. Mutations are real; they’re something we observe; they do make changes in traits. But the question remains: do they produce evolutionary changes? Do they really produce new traits? Do they really help to explain that postulated change from molecules to man, or fish to philosopher?

The answer seems to be: “Mutations, yes. Evolution, no.” In the last analysis, mutations really don’t help evolutionary theory at all. There are three major problems or limits (and many minor ones) that prevent scientific extrapolation from mutational change to evolutionary change.

(1) Mathematical challenges. Problem number one is the mathematical. I won’t dwell on this one, because it’s written up in many books and widely acknowledged by evolutionists themselves as a serious problem for their theory.

Fortunately, mutations are very rare. They occur on an average of perhaps once in every ten million duplications of a DNA molecule (107, a one followed by seven zeroes). That’s fairly rare. On the other hand, it’s not that rare. Our bodies contain nearly 100 trillion cells (1014). So the odds are quite good that we have a couple of cells with a mutated form of almost any gene. A test tube can hold millions of bacteria, so, again, the odds are quite good that there will be mutant forms among them.

The mathematical problem for evolution comes when you want a series of related mutations. The odds of getting two mutations that are related to one another is the product of the separate probabilities: one in 107 x 107, or 1014. That’s a one followed by 14 zeroes, a hundred trillion! Any two mutations might produce no more than a fly with a wavy edge on a bent wing. That’s a long way from producing a truly new structure, and certainly a long way from changing a fly into some new kind of organism. You need more mutations for that. So, what are the odds of getting three mutations in a row? That’s one in a billion trillion (1021). Suddenly, the ocean isn’t big enough to hold enough bacteria to make it likely for you to find a bacterium with three simultaneous or sequential related mutations.

What about trying for four related mutations? One in 1028. Suddenly, the earth isn’t big enough to hold enough organisms to make that very likely. And we’re talking about only four mutations. It would take many more than that to change a fish into a philosopher, or even a fish into a frog. Four mutations don’t even make a start toward any real evolution. But already at this point some evolutionists have given up the classic idea of evolution, because it just plainly doesn’t work.

It was at this level (just four related mutations) that microbiologists gave up on the idea that mutations could explain why some bacteria are resistant to four different antibiotics at the same time. The odds against the mutation explanation were simply too great, so they began to look for another mechanism—and they found it. First of all, using cultures that are routinely kept for long periods of time, they found out that bacteria were resistant to antibiotics, even before commercial antibiotics were “invented.” Genetic variability was “built right into” the bacteria. Did the nonresistant varieties get resistant by mutation? No. Resistant forms were already present. Furthermore, certain bacteria have little rings of DNA, called plasmids, that they trade around among themselves, and they passed on their resistance to antibiotics in that way. It wasn’t mutation and asexual reproduction at all, just ordinary recombination and variation within kind.

Bacteria can be made antibiotic resistant by mutation, but biologist Novick9 calls such forms “evolutionary cripples.” The mutation typically damages a growth factor, so that the mutationally crippled bacteria can scarcely survive outside the lab. The antibiotic resistance carried by plasmids results from enzymes produced to break down the antibiotic. Such bacteria do not have their growth crippled by mutation. Their resistance is by design.

But why, you might well ask, would God create antibiotic resistance? It’s possible God designed antibiotic resistance in bacteria, and antibiotic production by fungi, to balance the growth of these prolific organisms in the soil. Only after the corruption of creation did some bacteria become disease causers, making antibiotic resistance “inadvertently” a medical problem.

Contrary to popular opinion, drug resistance in bacteria does not demonstrate evolution. It doesn’t even demonstrate the production of favorable mutations. It does demonstrate natural selection (or a sort of artificial selection, in this case), but only selection among already existing variations within a kind. It also demonstrates that when the odds that a particular process will produce a given effect get too low, good scientists normally look for a better explanation, such as the plasmid explanation for resistance to multiple antibiotics.

At this point, evolutionists often say that “Time is the hero of the plot.” That’s what I used to say to my students. “Sure, the odds are low, but there’s all that time, nearly 5 billion years!” But 5 billion years is only about 1017 seconds, and the whole universe contains fewer than 1080 atoms. So even by the wildest “guesstimates,” the universe isn’t old enough or big enough to reach odds like the 1 in 103,000,000 that Huxley, an evolutionist, estimated as the odds against the evolution of the horse.

Way back in 1967, a prestigious group of internationally known biologists and mathematicians gathered at the Wistar Institute to consider Mathematical Challenges to the Neo-Darwinian Interpretation of Evolution.10 All present were evolutionists, and they agreed, as the preface clearly states, that no one would be questioning evolution itself. The only question was, could mutations serve as the basis—with natural selection—as a mechanism for evolutionary change? The answer of the mathematicians: no. Just plain no!

Emotions ran high. After a particularly telling paper by Marcel Schutzenberger of the University of Paris, the chairman of the gathering, C. H. Waddington, said, “Your argument is simply that life must have come about by special creation!” The stenographer records, “Schutzenberger: No! Voices: No!” Anything but creation; it wasn’t even fair (in spite of the evidence!) to bring up the word.

Dr. Waddington later called himself, impressively, a “post-neo-Darwinist,” someone who believes in evolution, but who also believes that mutation-selection cannot explain how evolution can occur. Many research evolutionists (but not many textbook writers or teachers) recognize the need for a new generation of evolutionists to forge the “post-neo-Darwinian synthesis.”

In his chapter “Beyond the Reach of Chance,” Denton11 discusses attempts to simulate evolutionary processes on computers. He concludes with these strong words:

If complex computer programs cannot be changed by random mechanisms, then surely the same must apply to the genetic programs of living organisms. The fact that systems in every way analogous to living organisms cannot undergo evolution by pure trial and error [i.e., by mutation and selection] and that their functional distribution invariably conforms to an improbable discontinuum comes, in my opinion, very close to a formal disproof of the whole Darwinian paradigm of nature. By what strange capacity do living organisms defy the laws of chance which are apparently obeyed by all analogous complex systems? (Emphasis added).

Most gratifyingly, Denton seems to look beyond the merely negative insufficiency of chance to glimpse a solution to “The Puzzle of Perfection,” as he calls it, in the “design hypothesis”:

It is the sheer universality of perfection, the fact that everywhere we look, we find an elegance and ingenuity of an absolutely transcending quality, which so mitigates against the idea of chance. … In practically every field of fundamental biological research ever-increasing levels of design and complexity are being revealed at an ever-accelerating rate. The credibility of natural selection is weakened, therefore, not only by the perfection we have already glimpsed but by the expectation of further as yet undreampt [sic] of depths of ingenuity and complexity (p. 342).

Unfortunately, we also have evidence that the transcendent ingenuity and design Denton sees has been marred and scarred. In that sense, mathematics isn’t even the most serious challenge to using mutations as the basis for evolution.

(2) Upward or downward? Even more serious is the fact that mutations are “going the wrong way” as far as evolution is concerned. Almost every mutation we know is identified by the disease or abnormality that it causes. Creationists use mutations to explain the origin of parasites and disease, the origin of hereditary defects, and the loss of traits. In other words, time, chance, and random changes do just what we normally expect: tear things down and make matters worse. Using mutations to explain the breakdown of existing genetic order (creation-corruption) is quite the opposite of using mutations to explain the build up of genetic order (evolution). Clearly, creation-corruption is the most direct inference from the effects of mutations that scientists actually observe.

By producing defects or blocking the normal function of certain genes, mutations have introduced numerous genetic abnormalities into the human population. The hemophilia (bleeders’ disease) that afflicted the royal houses of Europe may have arisen as a mutant of a clotting-factor gene in Queen Victoria, for example; and the dread Tay-Sach’s Disease may have arisen in Czechoslovakia in the 1920’s as a mutation in the gene for producing an enzyme crucial to brain function.

Some people like to call mutations “the means of creation.” But mutations don’t create; they corrupt! Both logically and often observationally, as in the examples above, the ordered state must come before mutations can disorder it. Mutations are real, all right, but they point to a corruption of the created order by time and chance.

As a matter of fact, human beings are now subject to over 3500 mutational disorders. Fortunately, we don’t show as many defects as we carry. The reason they don’t show up is that we each have two sets of genes, one set of genes from our mothers and another set from our fathers. The “bad genes” we inherit from our mothers’ side are usually covered up by our fathers’ genes, and vice versa. We can see what is likely to happen when an animal is born with only one set of genes. Fig. 17, based on a description in a genetics textbook, represents the rare case of a turkey that was hatched from an unfertilized egg, so it had just one set of chromosomes. The poor bird couldn’t hold its head up; instead, it bobbed up and down from a neurological disorder. The feathers were missing in patches, and it finally had to be transferred to a germ-free chamber because its resistance to disease was so low.

Figure 17

Figure 17. Mutations are mostly harmful, and, as time goes on, they impose an increasingly heavy “genetic burden” on a species. The turkey above, lacking a second set of genes to mask its hereditary defects, could scarcely survive. Creationists use mutations to help explain the origin of parasites and disease. Some evolutionists still believe that time, chance, and occasional favorable mutations provide the raw material for “upward-onward” progress, but the “post-neo-Darwinists” are looking for other means to explain evolution.

Now here’s the basis for a good horror story. Picture a mirror at the end of a dark hall. You claw your way through the spider webs to reach the mirror, and then you press a button. The mirror then splits you in two halves, so you can see what you would look like if you had only your mother’s genes or only your father’s genes. In the next scene, you’re writhing there in agony, your hair turning white as you fall over backward and die of fright! Unfortunately, that picture exaggerates only slightly what mutations have done to human beings and to the various kinds of plants and animals as well. If it weren’t for having two sets of genes, few of us would be able to survive.

Evolutionists recognize, of course, the problem of trying to explain “onward and upward” evolution on the basis of mutations that are harmful at least 1000 times more often than they are helpful. No evolutionist believes that standing in front of X-ray machines would eventually improve human beings. No evolutionist argues that destruction of the earth’s ozone layer is good because it increases mutation rates and, therefore, speeds up evolution. Evolutionists know that decrease in the ozone layer will increase mutation rates, but they, like everyone else, recognize that this will lead only to increased skin cancer and to other harmful changes. Perhaps a helpful change might occur, but it would be drowned in the sea of harmful changes.

Because harmful mutations so greatly outnumber any supposed helpful ones, it’s considered unwise nowadays (and illegal in many states) to marry someone too closely related to you. Why? Because you greatly increase the odds that bad genes will show up. By the way, you also increase the odds of bringing out really excellent trait combinations. But did you ever hear anybody say, “Don’t marry your first cousin or you’ll have a genius for a child?” They don’t usually say that, because the odds of something bad happening are far, far, far, far, far greater.

That would not have been a problem, by the way, shortly after creation (no problem for Cain and his wife, for example). Until mutations had a chance to accumulate in the human population, no such risk of bad combinations existed. Mutations are often carried as “hidden genes” (recessives) that are difficult to eliminate by selection, so they tend to build up in populations. The build-up of mutations with time poses a serious problem for plants and animals, as well as for human beings, and time, evolution’s “hero,” only worsens the problem of mutational decay.

Geneticists, even evolutionary geneticists, refer to the problem as “genetic load” or “genetic burden” In their textbook on evolution, Dobzhansky et al.12 state clearly that the term is meant to imply a burden that “weighs down” a species and lowers its genetic quality. In an article paradoxically titled “The Mechanisms of Evolution,” Francisco Ayala13 defines a mutation as “an error” in DNA. Then he explains that inbreeding has revealed that mutations in fruit flies have produced “extremely short wings, deformed bristles, blindness, and other serious defects.” Does that sound like “the raw material for evolution?”

It’s not that beneficial mutations are theoretically impossible. Bacteria that lose the ability to digest certain sugars, for example, can regain that ability by mutation. That’s no help to evolution, however, since the bacterium only gets back to where it started, but at least the mutant is helpful.

Actually, only three evolutionists have ever given me an example of a beneficial mutation. It was the same example all three times: sickle-cell anemia. Sickle-cell anemia is a disease of red blood cells. Why would anyone call that a beneficial mutation? Well, in certain parts of Africa, the death rate from malaria is quite high. Malaria is caused by a tiny, one-celled organism that gets inside the red blood cells and eats up the hemoglobin. Now, that particular germ doesn’t like sickle-cell hemoglobin. Carriers of one sickle-cell gene produce about half normal and half sickle-cell hemoglobin, and the malaria germ leaves them alone, too. So, carriers don’t get malaria. But the cost is high: 25% of the children of carriers can die of sickle-cell anemia, and another 25% are subject to malaria. If you want to call that a good mutation, you’re welcome to it! It seems doubtful to me that real improvement of human beings would result from accumulating that kind of “beneficial” mutant, and certainly hemoglobin’s ability to carry oxygen was not improved.

The gene for sickle-cell anemia has built up to high levels in certain African populations, not because it is “beneficial” in some abstract sense, but simply because the death rate from anemia in those areas is less than the death rate from malaria. Natural selection is a “blind” process that automatically accumulates genes for short-term survival, even if it reduces the long-term survival of the species. For that reason, evolutionists recognize that natural selection can occasionally lead to “mischievous results” detrimental to genetic quality. That’s the effect I think we’re seeing with sickle-cell anemia (Fig. 18).

Figure 18

Figure 18. “Sickle-cell anemia” is often given as an example of a favorable mutation, because people carrying sickle-cell hemoglobin in their red blood cells (Ss) are resistant to malaria. But the price for this protection is high: 25% of the children of carriers may die of the anemia (ss), and another 25% (SS) are subject to malaria. The gene will automatically be selected where the death rate from malaria is high, but evolutionists themselves admit that short-term advantages—all that natural selection can ever favor—can produce “mischievous results” detrimental to long-term survival. What do you think? Is sickle-cell anemia a “mischievous result,” or a good example of evolutionary progress? (Drawing after Parker, Reynolds, and Reynolds, Heredity, 2nd ed., Educational Methods, Inc., Chicago, 1977.)

Furthermore, when the frequency of the sickle-cell gene reaches 18%, natural selection for it “stops.” That’s the point at which the death rates from sickle-cell anemia and malaria balance, demonstrating conclusively that sickle-cell anemia is not a suitable model for the continuous genetic expansion that evolutionists seek.

Suppose I told you I had found a way to make cars run uphill without using gasoline. Then, as you watched in eager anticipation, I showed you how applying the brakes would make the car run downhill more slowly. Would you believe I had discovered a means for getting cars to run uphill without fuel? Similarly, natural selection can and does slow the rate of genetic decay produced by accumulating mutations (as it does with sickle-cell hemoglobin), but that hardly proves that mutation-selection produces upward and onward progress!

A better example of favorable mutation might be the one possibly involved in the change from teosinte into corn, as described by Nobel laureate George Beadle.14 But as Beadle points out, the mutation was favorable to people, not to corn.

Corn, he says, is a “biological monstrosity” that could not survive on its own, without man’s special care. There are many other examples of mutations “beneficial” to people: seedless grapes, short-legged sheep, hairless dogs, but these would all be harmful to the organism in its own environment and, hence, harmful in evolutionary perspective.

While taking a graduate course in evolution on his way to a master-of-science degree in biology, one of my graduates asked his professor a simple question during a lecture on mutations as the raw material for evolution: “Would you please give us some examples of beneficial mutations?” After an uncomfortably long pause, the professor finally replied, “I can’t think of any right now, but there must be hundreds of them.” He did not come back to the next class with a list—but, to his credit, he didn’t try to use sickle-cell anemia to illustrate helpful mutations.

But once again, let me say that it’s not that good mutations are theoretically impossible. Rather, the price is too high. To explain evolution by the gradual selection of beneficial mutations, one must also put up with the millions of harmful mutations that would have to occur along the way. Even though he has been one of the “old guard” defenders of classic neo-Darwinian evolution, Ayala15 faces the problem squarely in his article in the Scientific American book Evolution. He is talking about variation within species (not kind, but species, the smallest possible unit). He says that variation within species is much greater than Darwin postulated. He speaks of such variation as “enormous” and “staggering.” Yet when he gets to the actual figures, the variation is less than I, as a creationist, would have expected. (Ayala did say his figures underestimated the real variation.)

For creationists, all this variation poses no problem at all. If living things were created to multiply and fill the earth, then great variation within kind is simply good design. There would be no price to pay for created variability, since it would result from creation, not from time, chance, and mutation. (Mutations have introduced further variability since creation was corrupted, but it’s the kind of variability a bull introduces into a china shop!)

What problem did Ayala, as an evolutionist, see with all this staggering variability? Just this: for each beneficial mutant a species accumulated, the price would be a thousand or more harmful mutations. When genetic burden gets too great, offspring are so likely to have serious hereditary defects that the ability of the species to survive is threatened.

Time only makes this evolutionary problem worse. Thanks to our accumulated genetic burden, serious hereditary defects are present in perhaps 5% of all human births, and that percentage greatly increases among the children of closely related parents. All of us have some genetic shortcomings, and it’s really only by common consent that most of us agree to call each other “normal.”

Natural selection cannot save us from this awful situation either. Selection can and does eliminate or reduce the worst mutations—but only when these mutants come to visible (phenotypic) expression. Most mutations “hide” as recessives, “invisible” to selection, and continue to build up in secret at multiple loci, somewhat like a “genetic cancer” slowly but steadily eating away at genetic quality.

If early evolutionists had known what we know now about mutations, it’s most unlikely that mutations would ever have been proposed as the pathway to evolutionary progress.

Figure 19

Figure 19. The most logical inference from our scientific observations of mutation, selection, and genetic recombination would seem to be variation within created kinds. There’s no “genetic burden” to bear if variety is produced by creation instead of time, chance, and mutation. But could there be enough variation in each created kind to produce all the diversity we see today? Creationists now have some promising answers to that question. (Drawing after Bliss, Origins Two Models, 2nd ed., Master Books, Colorado Springs, 1978.)

(3) Mutations point back to creation. Mathematics and genetic load are huge problems for evolution, but the biggest reason mutations cannot lead to evolution is an extremely simple one. It’s so simple, I’m almost afraid to say it. But really, mutations presuppose creation. After all, mutations are only changes in genes that already exist.

Most mutations are caused by radiation or replication errors. But what do you have to have before you can have a mutation? Obviously, the gene has to be there first, before the radiation can hit it or before it can make a copying mistake. In one sense, it’s as simple as that: the gene has to be there before it can mutate. All you get as a result of mutation is just a varied form of an already-existing gene, i.e., variation within kind. (Fig. 19.)

Genes of the same kind, like those for straight and curly hair or those for yellow and green seeds, arc called alleles. There are over 300 alleles of the hemoglobin gene. That’s a lot of variation, but all those alleles produce hemoglobin, a protein for carrying oxygen in red blood cells (none better than the normal allele). By concept and definition, alleles are just variants of a given gene, producing variation in a given trait. Mutations produce only alleles, which means they can produce only variation within kind (creation), not change from one kind to others (evolution).

To make evolution happen—or even to make evolution a scientific theory—evolutionists need some kind of “genetic script writer” to increase the quantity and quality of genetic information. Mutations are just “typographic errors” that occur as genetic script is copied. Mutations have no ability to compose genetic sentences, and thus no ability to make evolution happen at all.

References

  1. Novick, Richard, Plasmids, Scientific American, December 1980. Return to text.
  2. Moorehead, Paul A., and Martin M. Kaplan, Mathematical Challenges to the Neo-Darwinian Interpretation of Evolution, Wistar Symposium No. 5, Wistar Institute Press,Philadelphia, 1967. Return to text.
  3. Denton, Michael, Evolution: A Theory in Crisis, Burnett Books, London, 1985. Return to text.
  4. Dobzhansky, Theodosius, F. Ayala, L. Stebbins, and J. Valentine, Evolution, W. H. Freeman and Co., San Francisco, 1977. Return to text.
  5. Ayala, Francisco, The Mechanisms of Evolution, Scientific American (and Scientific American book Evolution), September 1978. Return to text.
  6. Beadle, George W., The Ancestry of Corn, Scientific American, January 1980. Return to text.
  7. Ayala, Francisco, The Mechanisms of Evolution, Scientific American (and Scientific American book Evolution), September 1978. Return to text.

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