Creation Facts of Life (14 page)

(a.) Pangenesis: Use and Disuse
. Darwin called natural selection "the preservation of favored races," and he recognized that selection alone could not explain origin. When it came to the actual origin of new traits, Darwin wrote that it was "from use and disuse, from the direct and indirect actions of the environment" that new traits arose. About 40 years before Darwin, a famous French evolutionist, Jean Lamarck, argued for this kind of evolution based on the
inheritance of traits acquired by use and disuse.
Most books on the subject hint that we should laugh at Lamarck — but Darwin believed exactly the same thing.

Consider the supposed origin of the giraffe. According to both Darwin and Lamarck, the story begins back on the African prairies a long time ago. Because of prolonged drought, the prairie dried up. But there were green leaves up in the trees, and some of the animals started stretching their necks to reach them. As a result, their necks got a little longer (Figure 15). Now that could be partly true. If you really work at it hard enough and long enough, you could add a little bit to your height. People used to do that to get into the army or some special service where you have to be a certain height. The problem, however, is that the offspring of "stretched" parents start off just as small as all the others. The long neck could not be passed on to the next generation.

Figure 15. For the origin of new traits, Darwin (like Lamarck) resorted to "use and disuse" and the inheritance of acquired characteristics. Giraffes got longer necks, for example, because their ancestors stretched for leaves in trees, then passed on more neck "pangenes" to their offspring. This idea of "progress through effort" contributed to the early popularity of evolution, but has since been disproved.

Like others of his time, Darwin didn't know about the mechanism of heredity. He thought that each organ produced ''pangenes'' that would collect in the blood and flow to the reproductive organs; so, a bigger neck made more neck pangenes. Some people still believe this sort of concept. You've probably run into people who say, for instance, that people will eventually have bigger heads because we think a lot, and no toes because we wear shoes all the time. Darwin even used pangenes to "explain" why (in his opinion) wives grew to resemble their husbands as both got older.

It seems people knew as little about giraffes in Darwin's time as they did about heredity. Because their neck is so long, there's a huge distance between a giraffe's heart and its brain. It needs auxiliary pumps to get blood to the brain so it won't faint when it raises its head up — and it needs pressure reducers so that when it bends its head down to take a drink, it won't blow its brains out! A long neck without these features would be deadly.

Science has since disproved these "flimsy facts" of early evolutionary thought, but back in Darwin's time, pangenes captured people's imagination probably even more than natural selection did. To some, Darwin's original theory of evolution suggested continual progress. How do you make something happen? By use and disuse. If you want to get smarter, use your brain, and both you and your children will be smarter. If you want to be strong, use your muscles, and not only will you get stronger, but so will your children.

Well, almost unfortunately, that's not the modern theory of evolution. The use-disuse theory didn't work and had to be discarded. 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.

(b.) Mutations.
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. Figure 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. 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. 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
.

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. 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?

Mutations, Yes; Evolution, No

The answer seems to be:
"Mutations,
yes
; e
volution,
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
observed
mutational change to
hypothetical
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.
⁵⁰

Fortunately, mutations are very rare — or are they? They occur on an average of perhaps once in every ten million duplications of a DNA molecule (10
⁷
, 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 (10
¹⁴
). 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 their separate probabilities: one in 10
⁷
x 10
⁷
, or 10
¹⁴
. That's a one followed by 14 zeroes, 100 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 (10
²¹
). 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 10
²⁸
. 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. It was at this level (just four related mutations) that microbiologists gave up on the idea that mutations in asexual lines 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." Resistant bacteria were even found in the bodies of explorers frozen more than a century before medical antibiotic use. 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 such forms are "evolutionary cripples." The mutation typically damages a growth factor, so that the mutationally crippled bacteria can scarcely survive outside the lab or hospital. 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 mutations that add information for new categories of protein to the bacterial genome. 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 five billion years!" Five billion years is only about 10
¹⁷
seconds, and the whole universe contains fewer than 10
⁸⁰
atoms. So even by the wildest "guesstimates," the universe isn't old enough or big enough to reach odds like the 1 in 10
^3,000,000
that Huxley, an evolutionist, estimated as the odds against the evolution of the horse. Evolutionists like Huxley do believe in miracles; they just don't believe in the Miracle Worker.