Mutations Battle Living Fossils

Attempts to harmonize
living fossil research with
mutation research fail

 

by Jerry Bergman, PhD

Living fossils are organisms, such as horseshoe crabs or ginkgo trees, that from what can be determined from morphology, have remained unchanged since their evolutionarily hypothesized origins in ancient geologic times. The concept was introduced by Charles Darwin in 1859. Darwin coined the term “living fossils” to describe living organisms that display very little species diversity or physical differences from their ancestors found in the fossil record.[1]

A new analysis of genetic comparisons of an ancient group of ray-finned fishes, the alligator gar and longnose gar has challenged the core assumption of living fossils. Evolutionists assumed these gars shared a common ancestor at least 100 million years ago. Their genetic similarity, though, was proved from the fact that modern examples produce viable and fertile hybrids.[2] The genetic analysis using two gar-fish examples that fit the living fossil definition were found to have the slowest rate of molecular changes (mutations) among all jawed vertebrates.

The dataset analyzed was a sample of the DNA coding regions, specially 1,105 exons from a sample of 471 jawed vertebrate species.[3] The researchers concluded that gars’ DNA consistently evolved up to three orders of magnitude slower than any other major group of vertebrates. Similar very slow rates were also determined for two other examples of living fossils, the sturgeon and the paddlefish. Consequently, their genomes also would be expected to change more slowly than that of other animals.

The reason for the slower change of DNA in gar fish was, the

researchers speculate, that gars have an unusually strong DNA repair apparatus, allowing them to correct somatic and germline mutations — alterations to DNA that occur before and after conception — more efficiently than most other vertebrates.[4]

In other words, one can assume that natural selection would select against mutations that interfere with the effectiveness of the repair mechanism as, in this case at least, it slows down evolution. This assumption is problematic because if this repair system was damaged, more genetic mutations would result because fewer mutations would be repaired. This situation, according to orthodox evolution theory, would allow evolution that improved its adaptation and fitness to its environmental niche. The basis of evolution is genetic variety which is selected by natural selection. Consequently, less genetic variety works against evolutionary progress.

Mutation-Causing Radiation Surrounds Us

A major problem that the Brownstein et al. research reviewed in this paper has shown, is that ‘living fossils’ are organisms which evolutionists have determined have not changed morphologically in at least 100 million years. Yet background radiation causing mutations is present in the natural environment that is all around us all of the time. On average, it accounts for over half of our yearly radiation exposure. Before industrialization, the main source of ionizing radiation was from radionuclides present in the Earth’s crust that eventually end up in the soil, water, and air.

The other major source of  radionuclides was those created by cosmic rays striking atoms in Earth’s atmosphere. Our sun, and the other stars in our galaxy, emit a steady stream of cosmic radiation which regularly strikes the Earth. When cosmic rays collide with atoms they become radioactive. These radioactive atoms are called cosmogenic radionuclides. Some of these radionuclides reach Earth’s surface and mix with the soil and water.[5] This ionizing radiation affects the gonad’s germ cells, causing damage to their genetic material, thereby resulting in mutations. Genetically induced changes arise from radiation exposure and are also due to other environmental factors. In addition, some mutations occur spontaneously. Radiation has been proven to be mutagenic in all of the organisms studied so far.  These mutations contribute to disease.

The ‘living fossil’ research evaluating mutational changes that cause evolution assumed that in living fossils far fewer mutations occurred. This conclusion accounted for the finding that close to no evolutionary was change found in the Brownstein et al. research findings. Given the 100-million-year-old date, a large number of mutations would have accumulated during these long eons of time. Even if only a few mutations occurred during each decade, the gar fish would have become extinct long ago.

Living Fossils Surround Us

Another problem is, from 1860 to the present, over 800 plants and animals were identified as living fossils across all kingdoms and in the biological hierarchy of organisms from the simplest to the most complex.[6] Consequently, if a large number of organisms manifested very little change in 100 million years, it would have to be due to an enormously effective mutation repair system even in the lowest life forms known that is far more effective than all currently known mutation repair systems. Professors Meisenberg and Simmons note that DNA analysis evidence exists for a large number of mutations occurring in all life which is so large that the mutational load must be

kept in check by natural selection. In most traditional societies, almost half of all children used to die before they had a chance to reproduce. Investigators can only guess that those who died had, on average, more “mildly detrimental” mutations than those who survived.[7]

Mutations are widely recognized as being so common that they are a major cause of many diseases, including cancer and heart disease. An estimated 99.9% of all mutations are, in the long run, harmful. In a review of the mechanisms that drive genetic degeneration, Charlesworth and Charlesworth conclude that “most mutations with observable phenotypic effects are deleterious.”[8] Estimates vary greatly, but generally around one new mutation occurs in “each round of cell division, even in cells with unimpaired DNA repair and in the absence of external mutagens.”[9]

As a result, for germ-line mutations, “every child is born with an estimated 100 to 200 new mutations that were not present in the parents.”[10] Former Cornell University Professor John Sanford puts the number of new point mutations at about 200, and for all new mutation types the number is closer to 1,000 in each generation.[11]

Of these, “an estimated one or two new mutations are ‘mildly detrimental,’” meaning they do not cause disease, but can impair physiological functions that contribute to multifactorial disease.[12]  The result is that, on average, every child has “new mutations on top of those inherited from their parents” causing an accumulation of mutations that increase the mutational load in each generation, eventually causing genetic meltdown and in some cases species extinction.[13] Somatic mutations cause aging, cancer and other diseases and, eventually, death.

Indirect evidence that the mutational genetic load in humans is increasing includes data recorded in the standard list of genetic diseases titled Mendelian Inheritance in Man. The first edition listed 1,487 genetic diseases. The current edition lists over 17,000.[14]  Most genetic mutation-caused diseases involve more than one mutation. For example, there are at least 40 genetic mutations associated with Type 2 diabetes. Many of these genes are involved in pancreatic β cell function, which secretes insulin in response to elevated levels of the three cellular fuel types: sugar, fat, and protein. These well-documented facts argue for dates far less than 100 million years. Actually, they argue for dates closer to less than six thousand years.

Another problem is, according to evolution, hominids first appeared around six million years ago[15] and primates didn’t even exist 100 million years ago. Our ancestors, evolutionists conclude, probably looked something like a rodent 45 to 60 million years ago. One problem with these dates is “The fossil record available to reconstruct the evolution of H. sapiens in Africa is still relatively sparse and poorly dated.” Nonetheless, estimates of the beginning of the Homo sapiens lineage ranges from 550,000 to 750,000 years ago.[16] If in a mere 600,000 years, modern humans evolved from nonhuman pre-humans to modern humans, the claim that almost no evolution of the alligator gar and longnose gar has occurred in 100 million years is irrational. Given this, it is difficult to believe that in 100 million years only a small number of mutations occurred in the alligator gar and longnose gar no matter how effective the repair system is.

Summary

Many major problems exist in the conclusions of the Brownstein et al. research on the genomes of the alligator gar and longnose gar. A major issue is the sparse evidence for the dating which Stringer recognized for human evolution. It appears that all of the other dates given in the literature are also based on relatively sparse evidence. Reducing the date summarized above to a 6,000 year date is one viable solution to the problem elucidated in this paper.

References

[1] Cummings, M. “Study of slowly evolving ‘living fossils’ reveals key genetic insights.” https://news.yale.edu/2024/03/04/study-slowly-evolving-living-fossils-reveals-key-genetic-insights, 2024.

[2] Brownstein, C., et al. “The genomic signatures of evolutionary stasis” Evolution; https://academic.oup.com/evolut/advance-article/doi/10.1093/evolut/qpae028/7615529.

[3] Brownstein, et al., 2024.

[4] Cummings, 2024.

[5] U.S. Environmental Protection Agency. “Background Radiation.” https://www.epa.gov/radtown/background-radiation, 2024.

[6] Lidgard, S., and E. Kitchen. “Revealing the rise of a living fossil menagerie.” Frontiers in Ecology and Evolution. Section on Paleontology. Volume 11. https://doi.org/10.3389/fevo.2023.1112764, 21 April 2023.

[7] Meisenberg, G., and W.H. Simmons. Principles of Medical Biochemistry,  2nd edition.  Mosby/Elsevier, Linn, MO, 2006.

[8] Charlesworth, Brian and Deborah Charlesworth. Some evolutionary consequences of deleterious mutations.”  Genetica, 102/103:3-19.1998, p. 3.

[9] Meisenberg and Simmons, 2006, p. 153.

[10] Meisenberg and Simmons, 2006, p. 153.

[11]Sanford, J. Genetic Entropy and the Mystery of the Genome,3^rd edition. Waterloo, NY: FMS Publications, 2008.

[12] Meisenberg and Simmons, 2006, p. 153.

[13] Meisenberg and Simmons, 2006, p. 153.

[14]  McKusick, Victor (Editor) 1966. Mendelian Inheritance in Man: A Catalog of Human Genes and Genetic Disorders. Baltimore, MD: Johns Hopkins University Press; 1998. Mendelian Inheritance in Man: A Catalog of Human Genes and Genetic Disorders. Baltimore, MD: Johns Hopkins University Press.

[15] Hall, D.H. “The Age of Humans: Evolutionary Perspectives on the Anthropocene.” Smithsonian https://humanorigins.si.edu/research/age-humans-evolutionary-perspectives-anthropocene, 2024.

[16] Stringer, C. “The Origin and Evolution of Homo sapiens.” Philosophical Transactions of the Royal . Society B371: 20150237, 2016.

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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 1,900 publications in 14 languages and 40 books and monographs. His books and textbooks that include chapters that he authored are in over 1,800 college libraries in 27 countries. So far over 80,000 copies of the 60 books and monographs that he has authored or co-authored are in print. For more articles by Dr Bergman, see his Author Profile.