Creation Facts of Life (16 page)

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.

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, Ayala 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, struggle, and death (natural selection). (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 mutation 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. Take the Florida panther, for example, which is considered an endangered species. What endangers it? Highway traffic? No. Hunting? No. Habitat destruction? No. It's endangered by too much "evolution," i.e., the accumulation of mutations that have riddled the reproductive and circulatory systems with so much "evolutionary progress" (read that "genetic burden") that the small, inbred population of panthers was unable to produce a cub that could survive and reproduce.

I told my students that Florida officials should import panthers from out West to cross with the Florida panther to dilute the effects of these harmful mutations. To my surprise, that's what happened! The Florida panther is now making a comeback — except that as it becomes a healthier panther, it is less a "Florida" panther (which was never a true species anyway). Unfortunately, there are other cases where "endangered" sickly subspecies with multiple mutational defects are "protected" from good health by preventing their interbreeding with others of their kind.

Time only makes this evolutionary problem worse.
Thanks to our accumulated genetic burden, serious hereditary defects are present in perhaps 5 percent 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.

(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. 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 (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 from Bliss, Origins: Two Models, 2nd edition [Green Forest, AR: Master Books, 1978]).

Uncritical acceptance of evolution has so stunted scientific thinking that people give mutations god-like qualities. They act as if a cosmic ray striking a cell can cause a "mutation" that somehow assembles over 1,500 DNA bases into a brand new gene, regulators and all, that suddenly begins producing a brand new protein responsible for a brand new trait, raising the lucky mutated organism to the next higher rung on the evolutionary ladder! NOTHING remotely like that has ever, or could ever, happen!

Mutations are NOT genetic "script writers"; they are merely "typographic errors" in a genetic script that has already been written. Typically, a mutation changes only one letter in a genetic sentence averaging 1,500 letters long.

To make evolution happen —
or even to make evolution a theory fit for scientific discussion
— evolutionists desperately need some kind of "genetic script writer" to
increase the quantity and quality of genetic
INFORMATION
. Mutations have no ability to compose genetic sentences, no ability to produce genetic information, and, hence, no ability to make evolution happen at all.

That simple, absolutely foundational fact completely stumped Richard Dawkins, the world's leading spokesman for evolution as of this writing. In a video production featuring several evolutionist and creationist leaders and skeptics,
⁵³
Dawkins argued eloquently that millions of years of mutation and natural selection would serve as a "blind watchmaker,"
⁵⁴
producing all appearance of design among living things without any help from some supernatural Designer. Then in a quiet, non-threatening voice, not knowing what the answer would be, the narrator asked Dawkins to give an example of a mutation that
adds information
.

The usually effusive Dawkins gestured, opened his mouth, but stopped before he spoke. With his eyes shifting back and forth as if searching for some answer, he started to speak several times, but always checked himself. Finally, after a long embarrassing silence, the program resumed with Dawkins speaking on a different subject — leaving unanswered the ultimate question, the origin of genetic information.

Yet, molecules-to-man evolution is all about phenomenal expansion of genetic information.
It would take thousands of information-adding mutations to change "simple cells" into invertebrates, vertebrates, and mankind
. If there were any scientific merit at all to mutation-selection as a mechanism for evolution, Dawkins' reply should have been enthusiastic and overwhelming, "My three favorite examples of mutations adding information are…. Excellent examples among plants are …among insects are …among bacteria are…." His answer, instead, was silence, and with no mechanism to add genetic information, the "evolutionary tree" can't grow.

The problem with evolution is not some shortcoming in Dawkins, however. The problem is with the fundamental nature of information itself. The information in a book, for example, cannot be reduced to, nor derived from, the properties of the ink and paper used to write it. Similarly, the information in the genetic code cannot be reduced to, nor derived from, the properties of matter nor the mistakes of mutations; its message and meaning originated instead in the mind of its Maker.

As cogently presented by two of the world's leading information theorists,
⁵⁵
information comes only from pre-existing information
.
⁵⁶
Information systems have the "exherent," created kind of design, which can be logically inferred from our scientific observations as explained earlier (Figure 1). Although mutations may corrupt it and selection may sort variations into different environments, it was not a "blind watchmaker" that composed the genetic script for each kind of organism, but a Creator with a plan and purpose and eyes wide open.

If the evidence and logic is so convincingly clear, why is evolution still so popular? Laying aside personal biases and spiritual concerns, there is a serious semantic problem that could cause honest confusion. After all, evolution is about the continual production of new and different genes, and mutations are continually producing new and different genes — or are they?

Genes of the
same kind,
like those for straight and curly hair or those for yellow and green seeds, are 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).

Genes of the same kind
can be defined objectively as segments of DNA that
occupy corresponding positions
(
loci
; sing.
locus
)
on homologous chromosomes
. Homologous chromosomes are pairs that look alike, but come from two different parents, so their genetic content is similar but not identical. They pair up and then separate in the kind of cell division (meiosis) required for sexual reproduction. Genes that pair up in meiotic cell division
,
therefore, can be identified
as genes of the same kind.
Genes of the same kind are also turned on and off by the same gene regulators. Notice, it is not subjective human opinion that is telling us which genes are the same kind; it is objective, observable cellular processes.

Mutations, random changes in the genetic code, do produce "new genes" not present at creation, but the so-called "new genes" are still found at the same locus, still pair the same way in meiosis, and are still turned on and off by the same regulators, so they are really only
genes of the same kind
as the original, and represent only
variation within kind
(usually harmful variation in the case of mutations).

Notice the terms "new genes" or "different genes" can have two radically different meanings.
As geneticists normally do, we have been calling genes of the same kind
alleles.
The genes for tongue rolling and non-rolling are
"different genes
" in one sense, but only variations of the
same kind
of gene — affecting the same trait, found in corresponding positions (loci) on homologous chromosomes, pairing up in meiosis, and turned on and off by the same regulators. They are NOT different genes in the sense that genes for tongue rolling, and genes for making sickle cell hemoglobin are! Similarly, the sickle cell gene is a "new gene" in the sense that it was not present at creation, but it is only a new (and harmful!)
version of a pre-existing
gene, one that occupies the same chromosomal position, pairs the same way, and is turned on and off by the same regulators as the gene for making normal hemoglobin. In fact, the gene for sickle cell hemoglobin differs in base sequence at only one position out of several hundred in the normal gene for making hemoglobin, again just
variation within kind
or
allelic variation.

We need a new and different term to describe genes that are
truly new and different
— genes with
information
affecting a
different category of trait
— not just information on varieties of shirts, for example, but information on motorcycles! To refer to genes that do NOT occupy corresponding loci on homologs, that do NOT pair in meiosis, and that DO contain information on distinctive categories of traits, we will use the word
genon.
Genes for tongue rolling and non-rolling are different alleles, for example, but genes for tongue rolling and genes for making hemoglobin are different genons, with genes for normal and sickle cell hemoglobin as alleles of the hemoglobin genon.