Genetics is an important area in the origins controversy for a number of reasons. Evolutionists love to tout natural selection as a mechanism for evolution. However, natural selection only operates on existing information. This is where genetics comes in. In this article, we will discuss the history of genetics, how it works, and why genetics creates more problems for the evolutionist.
Genetics was a completely unknown phenomena until the mid-1850s when a monk, named Gregor Mendel began his groundbreaking work with pea plants. The monk, born Johann Mendel, did extensive experimentation with the numerous varieties of pea plants found at the monastery, cross-pollinating them in numerous different combinations. He found that the hybrids thus created always followed the same pattern in producing offspring. It was this discovery that allowed him to calculate probabilities of each type of offspring being produced, using something called a Punnett Square.
In order to understand the genius of Mendel, it is helpful to know a few terms. The term geneotype refers to the actual genetic information that produces the outward appearance. The term phenotype refers to the expression of the genetic information in the outward appearance. Thus a geneotype produces a phenotype. The geneotype for many characteristics has two options. These options are called alleles. In some cases there are more than two alleles but for the moment we will stay with just two per trait. In traditional Mendelian genetics, there can be two types of alleles. The first type is the dominant allele, which will always cause the particular trait it represents to show up in the phenotype. The second type of allele is the recessive allele, which only manifests when both alleles are recessive. There are some other combinations that can be made such as codominance and incomplete dominance but those are not tradditional Mendelian genetics and thus will be bypassed for the moment. When using a Punnett Square, each allele is represented with a letter. A dominant allele is represented with a capital letter and a recessive allele is represented with a small letter. Thus a Punnett Square for the height of one of Mendel’s pea plants might look as follows:
In the above diagram, two plants, both tall, are being crossed together. One has two of the same alleles. This is referred to as being homozygous, in this case homozygous dominant since both are capital letters. The second plant has two different alleles, one for tall and one for short. It is still tall since the tall allele is dominant. However, since the alleles are different, this plant is referred to as being heterozygous. In this case, all offspring would share the same phenotype but have different geneotypes. The phenotype would be tall and the geneotypes homozygous tall and heterozygous.
It is possible to perform a Punnett Square calculation for multiple traits at once. Consider the following example: A homozygous recessive short pea plant heterozygous for wrinkled peas and producing white flowers is crossed with a heterozygous tall pea plant hterozygous for red flowers and homozygous for wrinkles peas. The geneotypes might be written as follows: “hhWwrr X HhWWRr” Performing this cross would produce the following Punnett Square:
As you can see, four different phenotypes are produced, each with a probability of 25 %. However, this Punnett Square is actually slightly incorrect. In the pea plant, the alleles for the color of the flower are codominant. Thus every time the allele combination “Rr” appears, the flower produced will be pink, rather than red or white. And this is where genetics begins to get complex.
The complexities of genetics, while very interesting, are beyond the scope of this article. The above was merely a basic crash course in genetics so that you understand the discussion which is to follow. Evolutionists love to insist that mutations could change the genetic alleles, causing them to code for something different. It is this claim that I intended to debunk in the forthcoming discussion.
Noted evolutionary biologist and eugenicist Julian Huxley once said that the odds of getting just one favorable mutation were 1/1000. Let us presume then that these long odds were met once and a favorable mutation could occur, changing one of alleles in a geneotype. If it does not change the dominant allele, the mutation will not show up in the gene pool, unless another organism of the same kind suffers an identical mutation. Going down this path requires changes the odds from 1/1000 to 1/1000000. As if these odds were not long enough, because both alleles are recessive, there is a 1/4 chance that an offspring will actually manifest the mutation. This increases the odds to 1/4000000. This however, is not even enough. This must happen twice, because an organism with two recessive alleles will only pass one to it’s offspring. The other allele must come from the other parent. If only one organism has the mutation, the same problem arises. The recessive allele will dilute into the population and disappear. In order for the recessive allele phenotype to be passed on, their must be a second mutated organism with two recessive alleles. This raises the odds incredibly from 1/4,000000 to 1/16,000,000,000,000. In other words, just to pass a mutation down one generation is a one in sixteen trillion proposition. That is just one mutation and it assumes that the two mutated individuals mate, which is by no means assured.
The odds get a bit better if it is the dominant allele is the one mutated. If an organism is heterozygous and the dominant allele is beneficially mutated, the odds are 1/2 that the beneficial allele will be passed on. However, if the organism is homozygous and only one allele is changed, the odds remain the same. Only if both alleles are are mutated will the mutation be guaranteed to be passed on. This means that the odds of having a favorable mutation, combined with passing it to the offspring for this scenario are 1/2000. Starting out 1/2000 is much better than the 1/1000000 in the previous scenario. If the dominant mutated allele is combined with a recessive standard allele the mutated allele will manifest in the phenotype. However there is still an issue because there is only a 1/2 chance this will happen, raising the odds to 1/4000. However, if it meets with another dominant allele that is not mutated a new issue arises. There is 1/2 chance that this new mutated allele will be manifested, leaving the odds for this path at 1/4000 as well. When offspring are produced, both paths have a 1/2 chance of passing the mutated allele to their offspring, so the odds double again to 1/8000. Not fantastic odds, but much better than the odds of a recessive allele. Remember that the mutation only has a 1/2 chance of mutating the dominant allele, odds that we are ignoring for this comparison.
The best odds evolutionists can muster for passing on just one favorable mutation is 1/8000. This has to be repeated millions of times as each new favorable mutation occurs. The numbers are simply absurd. Throw in the fact that at least some of the alleles mutated will be recessive alleles and the numbers go from absurd to science fiction. Genetics does not support evolutionary theory. The laws of genetics only act on existing information, therefore any mutation to a gene will only change something that already exists, not create something new. And even if something new were created, the odds of passing it down from one generation to the next are incredibly long. Add in the fact that billions of beneficial mutations are needed and you’ll quickly realize it takes far more faith to be an evolutionist than it does to be a creationist.