July 5, 2022 | Jerry Bergman

Do Mutations Provide New Genetic Information?

The source of new genetic information is still
a large thorn in the side of evolutionary theory.
Has it been finally settled?


by Jerry Bergman, PhD

The three main pillars of evolution are the origin of life from non-life, natural selection and mutations. Destroy any one of these three pillars, and evolution theory fails.[1]

The origin of life has been researched for over a century and, although theories abound, all are problematic. A common response to this impasse by evolution advocates is that evolution only covers the first cell onward to humans.[2]

The second pillar, natural selection, requires genetic variation to function. Evolution’s difficulty is thus not the survival of the fittest, but the arrival of the fittest. The most common explanation for the arrival of the fittest is mutations, the accidental changes in the genomic code caused by radiation, mutagens (such as cancer-causing chemicals), or simply DNA copying mistakes. Mutations are summarized as follows in the textbook Biology For Majors by Lumen Learning:

Mutation, a change in DNA, is the ultimate source of new alleles, or new genetic variation in any population. The genetic changes caused by mutation can have one of three outcomes on the phenotype. A mutation affects the phenotype of the organism in a way that gives it reduced fitness—lower likelihood of survival or fewer offspring. A mutation may produce a phenotype with a beneficial effect on fitness. And, many mutations will also have no effect on the fitness of the phenotype; these are called neutral mutations.[3]

The idea of mutations as a source of genetic variety has its detractors. In June 2022, New Scientist reporter Michael LePage attempted to determine current thinking about mutations and whether they can be considered the central source for the “arrival of the fittest.” His headline asserted that “debate about the source of evolution’s diversity may have been settled” by the long-term evolutionary experiment (LTEE) conducted since 1988 at Michigan State University under the direction of Richard Lenski. LePage says that the LTEE attempted to solve the “long-standing debate in biology about the relative importance of existing variation versus new mutations in evolution.”[4]

Background: Darwin and Lamarck

A major concern in evolutionary theory from Darwin’s day to today is the source of new genetic variation. Darwin assumed for most of his life that the source was existing variation, also called standing variation. Darwin could not even hypothesize another source of genetic variety. He actually moved toward the Lamarckian theory of the origin of genetic information, as was shown in the sixth edition of the Origin of Species.[5] Yongsheng Liu, of the Faculty of Medicine at the University of Alberta, Edmonton, wrote that the Lamarckian theory of

inheritance of acquired characters was also the driving force of Darwin’s theory of evolution. It is a historical fact that, in genetics, Darwin was a Lamarckist. He accepted the inheritance of acquired characters as subsidiary aids in the development of species, and as a possible source of new variation upon which natural selection acted.[6]

Lamarckism had been proposed by French naturalist Jean-Baptiste Lamarck in 1809. His evolution theory was based on the belief that physical changes organisms acquired during their lifetimes could be transmitted to their offspring. His classic example of “inheritance of acquired characteristics” concerns how the giraffe got its long neck.  According to Lamarckian view, the giraffe’s ancestors stretched their necks to eat leaves that were just out of reach. Through “use and disuse” the stretched-neck trait was passed on to its offspring. Over many generations, the neck evolved to its current length.

Lamarck’s theory influenced evolutionary thought throughout most of the nineteenth century. It was largely rejected after 1930.[7] One of the most well-known experiments disproving it was conducted by German biologist August Weismann in 1889. He showed that chopping off rat’s tails for generations did not lead to the birth of tailless rats. Brian Hayes echoed the consensus view in 1999 in American Scientist:

Experimental protocols have gotten more sophisticated since then, but the verdict is the same: There’s no sign of Lamarckian inheritance anywhere in the kingdoms of life.[8]


Although only a relatively small percent of all mutations are detrimental enough to cause disease, the total number occurring in each generation is enormous. It was once believed that the vast majority of all mutations were neutral because most do not code for protein. For this reason, most of the genome was believed to be “junk.” However, now that it has been experimentally shown that the vast number of genes are functional, it is recognized that most mutations are near-neutral. While near- neutral mutations are only a problem when they accumulate to a certain level, it is the “near- neutral” mutations that cause mutational meltdown and death.

Overtly harmful mutations, by contrast, are often effectively eliminated from the gene pool. Consequently, depending on the specific set of mutations, it is the near-neutral mutations that are collectively lethal over the long term. The accumulation of mutations is a major problem for Darwinism because the large number of near-neutral mutations that are not readily selected out of the gene pool accumulate in each generation, eventually causing extinction. Mutations, rather than being the engine that drives evolution, lead to genetic entropy.[9] This background is basic to understanding claims about the LTEE.

The Izutsu and Lenski Research

 The mutation theory has been put to the test for decades now. Some 75,000 generations of bacteria have been grown during the LTEE since 1988. LePage says in the New Scientist article,

Mutations in the genomes of organisms provide the variation on which natural selection can act – that is something biologists agree on. What they have long argued about is whether evolution acts mainly on past mutations or has to hang around waiting for new mutations, and to what extent evolution can be shaped by chance mutations.

In one experiment derived from the LTEE, Lenski’s colleague Minako Izutsu isolated four groups of 18 populations of Escherichia coli bacteria ranging from genetically identical to genetically highly-diverse. The bacteria that had formerly been fed glucose were now fed D-serine instead to determine if they could adapt to a new nutritional environment. Izutsu and Lenski determined that the original genetic variation mattered only early in the experiment. After 500 generations, the beginning variations no longer were important and mutations became more important.[10] They concluded that the ability to use another food was due to a mutational alteration in the bacterium’s genome.

David Stern (Howard Hughes Medical Institute) deduced from the LTEE data that the results “provide pretty compelling evidence that standing variation contributed to very early stages of evolution in these bacteria, but that long-term adaptation appears to require new mutations.”[11] Original standing variation gave an advantage at first, they believe, but it was mutational change that conferred a long-term advantage. The Izutsu and Lenski report ignored the well-documented fact that mutations lead to genetic deterioration, so how do we explain their results which seem to contradict the research cited above?

Problems with the Research

One of many problems with the study is that the research was on aerobic bacteria whose genome, compared to a mammal’s genome, is fairly simple. Attempts to generalize conclusion are therefore problematic. Mammals have many different organs, and with them very complex nutritional needs. They correspondingly have a highly complex genome. Bacteria require only a source of water, oxygen, and sugar, plus a few minerals. The mutations only allowed them to convert the use of glucose (C₆H₁₂O₆) as the main food source to the amino acid D-serine (C3H7NO3).

Bacteria are enormously adaptive. They have built-in systems that may have made the nutrient switch common – a possibility that the authors did not mention. As they admit, the adaptation could be due to a “preadapted” genotype among the founding population of bacteria that were used in the experiments.[12] If caused by a mutation it could be the result of a “back mutation.” Back mutations reverse a previous mutation to bring the genome back to the original pre-mutational state. If the amino acid D-serine (C3H7NO3) was fed to the untrained bacteria, would they eventually switch back to using glucose (C₆H₁₂O₆), reversing the results of the previous experiment? The adaptation to the food source could have been due to a small change in the enzyme that breaks down glucose to enable the bacteria to use D-serine. Without knowing the mutational change, it could have been as small as a single “letter” in the code.

No one denies that, although very rare, beneficial mutations exist. To determine whether this result was due to a beneficial mutation would require gene sequencing. If this was done, it was not reported in the Izutsu and Lenski paper.[13]  The original paper was not very helpful and did not specify the mutation, which required sequencing both the pre-mutant genome and comparing it with the mutated form.[14] All of these options should have been attempted before sweeping conclusions were drawn. A comparable example would be for an anthropologist to interview one member of an African tribe and then apply his findings to the entire tribe of 4,264 persons. LePage quotes Stern again with doubts about the findings:

What is less clear is whether this also applies to sexually reproducing organisms. Stern thinks long-term evolution in animals and plants is also dominated by new mutations, but says he has long arguments with colleagues who think standing variation dominates.

“We simply don’t have the right kind of data at the moment to settle this question,” he says.


The results and unreported problems with the Izutsu and Lenski research do not even come close to supporting the headlines. This is an important question because genetic variation is at the heart of evolution; variation is required before natural selection can hypothetically operate. The debate about the source of evolution’s diversity was hardly settled by the Izutsu and Lenski research in spite of the headlines. LePage claimed that “Debate about the source of evolution’s diversity may have been settled,” but then he had to qualify the claim with, “in E. coli, at least.”[15] The report by Izutsu and Lenski simply did not give enough information to settle this and many other questions.[16] They have utterly failed to solve the problem of the source of new genetic information. At best Izutsu and Lenski found evidence for a very slight variation of existing genetic information. And it is likely they did not even find this much.

Bergman, Jerry. 2022. The Three Pillars of Evolution Demolished. Westbow Press: Bloomington, IN (a division of Thomas Nelson & Zondervan).


[1] Bergman, Jerry. The Three Pillars of Evolution Demolished. Westbow Press: Bloomington, IN (a Division of Thomas Nelson & Zondervan), 2022.

[2] https://www.quora.com/Is-it-true-that-evolution-only-explains-things-once-there-was-a-first-living-cell-but-evolution-does-not-explain-how-that-first-living-cell-got-there, 2022.

[3] Lumen Learning. “Darwin and the Theory of Evolution.” Biology For Majors; https://courses.lumenlearning.com/wm-biology1/chapter/reading-darwin-and-the-theory-of-evolution/, 2022.

[4] Le Page, Michael. Debate about the source of evolution’s diversity may have been settled. New Scientist 254(3391):10; https://doi.org/10.1016/S0262-4079(22)01040-5, June 2022.

[5] Liu, Yongsheng. Darwinian evolution includes Lamarckian inheritance of acquired characters. International Journal of Epidemiology 45(6):2206-2297; https://doi.org/10.1093/ije/dyw182, December 2016.

[6] Liu, 2016.

[7] Rafferty, John. New Thinking About Evolution. Britannica Educational Publishing: Chicago, IL, p. 38, 2010.

[8] Hayes, Brian. Computing Science: Experimental Lamarckism. American Scientist 87(6):494-498; https://www.americanscientist.org/article/experimental-lamarckism, November-December 1999.

[9] Chapter 5 in Bergman, Jerry. The Three Pillars of Evolution Demolished. Westbow Press: Bloomington, IN (a division of Thomas Nelson & Zondervan), 2022.

[10] Izutsu, Minako, and Richard E. Lenski. Experimental Test of the Contributions of Initial Variation and New Mutations to Adaptive Evolution in a Novel Environment. bioRxiv. doi: https://doi.org/10.1101/2022.05.31.494207;

https://www.biorxiv.org/content/10.1101/2022.05.31.494207v2, posted 1 June 2022.

[11] Le Page, Michael. 2022.

[12] Izutsu and Lenski, 2022.

[13] Izutsu and Lenski, 2022.

[14] Izutsu and Lenski, 2022.

[15] Yirka, Bob. Debate about the source of evolution’s diversity may have been settled. PhysOrghttps://phys.org/news/2022-06-debate-evolutionin-coli.html, 17 June 2022.

[16] Quoted in Le Page. 2022; see Ref. 4.

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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