GENETIC MUTATIONS CHALLENGE DARWINS EVOLUTION THEORY

The death of Darwin’s evolution theory continues due to the evidence found in genome deterioration, sickle cell anemia mortality, beneficial mutations elusiveness, disease proliferation, and recent genetic mutations.

 
Analysis of DNA/RNA mutations reveals that these genetic transformations cannot offer meaningful new information in significant quantities. Rather, these mutations will generate information degradation in the genome. This scientific observation is against the neo-Darwinian origins predictions and evolution model. The genome degradation is neutralized by natural selection that assists in maintaining the animal population’s status quo.

 

Degradation results for many reasons, two of which are reviewed here. First, there is a tendency for mutations to produce a highly disproportionate number of certain nucleotide bases such as thymine and second many mutations occur in only a relatively few places within the “hot spots genes” and rarely occur in others, such as “cold spots genes.” An exhaustive examination of science literature fails to reveal a single clear example of any beneficial information-gaining mutation. On the other hand, many deleterious mutations exist, supporting the hypothesis that very few mutations are beneficial. These findings support the intelligent design theory and creation model, according to Dr. Jerry Bergman.

 
Beneficial mutations are extremely rare. The few mutations that are considered “beneficial” always involve the loss of genetic information and they generally result in the deterioration of the animal’s health. For example, while sickle-cell anemia is considered a beneficial mutation because it protects many Africans against malaria, sickle-cell anemia is simply a very unhealthy disease, according to the National Heart Lung Blood Institute and the New England Journal of Medicine.

 
Sickle cell anemia is a genetic disorder where the red blood cells have a sickle-like shape rather than the round donut shape of a healthy red blood cell. While this deformity prevents the body from carrying malaria, protecting people in high-malaria areas from dying from the disease, the sickle cell anemia is itself dangerous because sickle cell blood cells transport less oxygen than normal cells. These misshapen cells tend to clump up and get stuck in blood vessels, contributing to organ damage and infection, according to the National Heart Lung Blood Institute. Sickle-shaped cells often die within 10 to 20 days, while healthy red blood cells live on for 120 days before dying. The life expectancy for many suffering with sickle-cell anemia is less than 45 years, according to the New England Journal of Medicine. If sickle cell anemia is the best beneficial mutation out there, our hopes for evolving through mutations are empty and doomed to disappointment. The fact is, examples of truly beneficial mutations are massively lacking.

 
Geneticists Thomas Morgan and Herman Muller conducted a prolonged study of fruit flies (drosophila) looking for traces of evolution. But generation after generation, the uncooperative flies refused to evolve. Eventually they solved the problem, or at least they thought they had. They subjected a pure strain of fruit flies to chemical and radiation treatments. The result was mutilated flies. Flies developed yellow, brown, or purple eyes; or bulging, flat, or dented eyes. Some flies had no eyes. However, despite all the mutated flies that resulted from the experiment no new genetic information evolved and no beneficial mutations occurred and the flies always remained flies. The most important lesson to learn from the fruit fly experiment is the remarkable stability of this species, according to Dr. Jason Richard Boon.

 
Researchers on the 2000 Human Genome Project used genetic data from 179 individuals and found that all had between 40 and 110 potentially disease-causing mutations in their DNA. The individuals had 281-515 actual substitutions each, but the trouble only really started when both parents had passed on a mutation in the same gene. The researchers, estimated, “approximately 400 damaging variants and roughly 2 bona fide disease mutations per individual,” according to the American Journal of Human Genetics.

 
Damaging mutation do not always shows up immediately. Mutations sometimes increase a person’s chances for heart disease. Another might simply weaken the kidneys or slow the production of insulin. The body is also good at covering for an improperly functioning gene, using backup systems or compensating in some way when a gene is not doing its job right. However, when everything fails, mutations tend to cause disease, according to the American Journal of Human Genetics.

 
Science researchers have been working to develop a complete Human Gene Mutation Database with the more dangerous genetic defects, giving doctors a tool in diagnosing inherited diseases. It is distinctly noticeable that while some mutations are not as destructive as others, the researchers are not developing a database of all the improvements made by random changes in the genetic code, according to American Journal of Human Genetics.

 
Many human genetic mutations in human DNA are only 5,000 to 10,000 years old, according to a study by the Exome Sequencing Project at the National Institutes of Health. Nucleotides are biological molecules that form the building blocks of nucleic acids (DNA and RNA) and serve to carry packets of energy within the cell (ATP), according to the journal Nature reports. Many of the remaining mutations of this nature may have no effect on people, and a few might be beneficial, according to project researchers. While each specific mutation is rare, the findings suggest that the human population acquired an abundance of these single-nucleotide genetic variants in a relatively short time, according to the Exome Sequencing Project at the National Institutes of Health.

 
ANALYSIS

 
Genetic mutations show that macro-evolution cannot and never did happen during life’s history on planet Earth. For evolution to work on a grand scale, where nature transforms a family of animals into a new family of animals, beneficial mutations must appear to add new information to the genetic code. Without mutations, there cannot be any major evolutionary steps. While the weight of scientific evidence demonstrates clearly that the genetic information already existing within a species can contribute variation within animal populations due to natural selection, this process always strains out information and it never adds new genetic information, or previously non-existent coding to the genome. However, while many Darwinists claim that rare, beneficial mutations do exist, the math shows that random mutations result in the net removal of functional programming from the genetic code rather than adding new information to it.

 
Beneficial mutations are extremely rare. The few mutations that are considered “beneficial” always involve the loss of genetic information and they generally result in the deterioration of the animal’s health. We learn in biology class that our genetic code is made up of DNA, the long strands of the nucleotide bases Adenine, Guanine, Thymine, and Cytocine, which are A, G, T, and C for short. These four bases provide the digital code for our system, resembling the way 0s and 1s make up binary code for computers. Within the cell, during the process of translation, these nucleotides are read in groups of three, referred to as codons. Every codon is similar to a small transport vehicle of three letters that code for an amino acid, which go on to make up proteins.

 
Finally, if neo-Darwinian evolutionary model of origins were history, we should expect to discover a number of beneficial mutations that were the result of added genetic information. However, the weight of scientific evidence demonstrates clearly that we all inherited a damaged, deteriorating version of a once perfectly designed and fully functioning genetic code.

This article, GENETIC MUTATIONS CHALLENGE DARWINS EVOLUTION THEORY, first appeared on Christian Apologetics Study.