September 27, 2021 | Jerry Bergman

Mutations Destroy Evolution

Mutations Are Not the Savior of Evolution but Its Destroyer…
and Now We Know Why


by Jerry Bergman, PhD

New research has determined that even a larger number of  intergenetic connections in humans exist than assumed previously, documenting greater levels of genetic complexity then previously assumed.[1] Specifically, they found that genes related to alcohol use disorder (AUD, aka alcohol dependence syndrome) also affect the risk of Alzheimer’s disease. This implies that drugs currently used for neurodegenerative diseases might help people reduce, or even, stop drinking. Furthermore, if we identify those people more at risk of Alzheimer’s disease, reduction of their drinking may be beneficial in slowing the progression of the disease. As the genome is discovered to be more complex, evolution becomes less tenable.

The lethal problem with Darwinism is not the survival of the fittest but the arrival of the fittest. The only viable source of significant new genetic variation is broken genes in the germ line, a situation called mutation. The vast majority of mutations are either near-neutral, which accumulate over time, leading to genetic meltdown; or, if deleterious, which are often lethal, they end the genetic line.[2] The European Molecular Biology Laboratory summarized mutations this way:

Mutations are the original source of genetic variation. A mutation is a permanent alteration to a DNA sequence. De novo (new) mutations occur when there is an error during DNA replication that is not corrected by DNA repair enzymes. It is only once the error is copied by DNA replication, and fixed in the DNA that it is considered to be a mutation. Mutations may be beneficial to the organism; deleterious (harmful) to the organism; or neutral (have no effect on the fitness of the organism).[3]

Mutations in the somatic cell line cause aging and disease including cancer. We know why most mutations are near-neutral or lethal and extremely few are beneficial. Thousands of genetic mutations occur in cells daily; 99.99 percent of the time the damaged genes are efficiently repaired by our highly effective genetic repair systems.[4]  In the “neo-Darwinian model …. chance plays a central role in the emergence of mutations.”[5]

Figure 1. The percentage of changes of human H1N1 virus nucleotides from 1918 to 2009. (From: Robert Carter. 2014. More evidence for the reality of genetic entropy. Journal of Creation 28(1):16–17.)

The problem for evolution is that the vast majority of mutations are not beneficial, and of those that are, many result from damaging genes allowing other genes to express themselves. In addition, a few rare mutations that cause damage to genes may have a beneficial effect.[6] One classic example is that the gene that causes sickle-cell anemia in humans confers some resistance to malaria.

Another example is a mutation that causes the malarial parasite, Plasmodium falciparum, to develop resistance to certain anti-malarial drugs. Only one mutation is required, which in this case is beneficial to the parasite, not humans; nonetheless, it can be considered a ‘beneficial’ mutation to the microbe. Specifically, the mutation was in the anti-malarial drug’s parasite target, the influx/efflux pumps that affect intraparasitic concentrations of the drug.​ The damage allows the parasite to infect the person, thereby rendering the drug ineffective.[7] Resistance to the anti-malarial drug Chloroquine, however, requires at least two mutations.  Resistance is initially conferred by mutations in a gene encoding a transporter (PfCRT). Only one in 1020 (100 quintillion) P. falciparum parasites have the necessary mutations, and about 1021 of these parasites would be present in about a billion infected people. Thus, resistance to Chloroquine resulted that was again due to mutations beneficial to the parasite.

Why Most Mutations Damage Genes

Genes consist of DNA, an abbreviation for deoxyribonucleic acid. Water, oxygen, and radiation constantly damage our DNA:

DNA can get overly twisted and literally snap in half. DNA copying enzymes constantly make mistakes. The cell uses all sorts of sophisticated DNA repair systems to continually scan and fix the errors that constantly pop up in this very sensitive of molecules. Yet, these systems are imperfect. Mutations are mistakes. Despite all the effort at fixing them, mutations still slip through.[8]

Another fact explains why some mutations are far more likely than others to cause deterioration of the genome. The human H1N1 virus is a useful example which illustrates this fact. The four chemical bases in the DNA are adenine (A), cytosine (C), guanine (G), and thymine (T). In the viral RNA genome are adenine (A), cytosine (C), guanine (G), and uracil (U). A study analyzing 70 years of data indicated that, as shown in Figure 1 above, the number of adenine and uracil consistently increased and the number of guanine and cytosine consistently decreased.[4] As a result, the genome deteriorates over time. Imagine if in an originally well-written paragraph some letters such as C and G spontaneously convert into U and C. The paragraph would rapidly become nonsensical. A word such as including would become inuludina, which is not a word.

Figure 2. A diagram showing the spontaneous deamination of cytosine (left) by water, converting it to uracil (right). Note the NH2 is replaced with oxygen, a double bond results and the nitrogen is replaced with HN. In essence, water is added and ammonia (NH3) is lost. The 6-sided structure is made out of 6 carbon atoms. The single lines are single bonds and the double lines represent double bonds (i.e., two pairs of shared electrons).

One of the most common chemical changes in DNA and RNA occurs when water reacts with cytosine; a loss of an amine (–NH2) results. The result changes cytosine in RNA to uracil (Figure 2). For the same reason, in DNA, cytosine-to-thymine mutations dominate. Less than one in 1,000 accidental base changes in DNA result in a permanent mutation. The “rest are eliminated with remarkable efficiency by DNA repair” systems.[9]


This is one more example of the increasingly clear fact that the laws of physics and chemistry render Darwinian evolution untenable. Yet one may wonder, as the evidence against molecules-to-man piles up, why has academia ignored the implications of the science? The reason is that belief in evolution, and rejection of an intelligent creator, is so strong that adherents cling to the belief that science will eventually figure out how evolution occurs in spite of the overwhelming evidence against it. Clearly, though, the more we learn about the complexity of the human body and all life, the less credible the molecules-to-man worldview becomes and the more difficult it is to ignore the scientific evidence.


[1] Yasinski, Emma. 2021. Genes for alcohol use disorder and Alzheimer’s risk overlap: Study. The Scientist, August 24.

[2] Institute of Cancer Research. 2020. Mapping how evolutionary forces affect cancer growth could help doctors choose biopsies. PHYS.ORG, May 15.

[3] European Molecular Biology Laboratory. 2021. What is genetic variation. Origins of genetic variation.

[4] Bergman, Jerry. 2005. The mutational repair system: A major problem for macroevolution. CRSQ 41(4):265-273, March.

[5] Catania, Francesco, et al. 2021. Bridging tumorigenesis and therapy resistance with a non-Darwinian and non-Lamarckian mechanism of adaptive evolution. Frontiers in Oncology, September 10.

[6] Behe, Michael. 2007. The Edge of Evolution: The Search for the Limits of Darwinism. Free Press, New York, NY.

[7] White, Nicholas. 2004. Antimalarial drug resistance. Journal of  Clinical Investigation, 113(8):1084–1092, April 15.

[8] Carter, Robert. 2021. Is Covid-19 evolving? No, but it is changing rapidly., August 24.

[9] Alberts, Bruce, et al. 2002. Molecular Biology of the Cell, 4th edition. Garland Science, New York, NY.

Dr. Jerry Bergman has taught biology, genetics, chemistry, biochemistry, anthropology, geology, and microbiology for over 40 years at several colleges and universities including Bowling Green State University, Medical College of Ohio where he was a research associate in experimental pathology, and The University of Toledo. He is a graduate of the Medical College of Ohio, Wayne State University in Detroit, the University of Toledo, and Bowling Green State University. He has over 1,300 publications in 12 languages and 40 books and monographs. His books and textbooks that include chapters that he authored are in over 1,500 college libraries in 27 countries. So far over 80,000 copies of the 40 books and monographs that he has authored or co-authored are in print. For more articles by Dr Bergman, see his Author Profile.

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