Just How Random Are Mutations?

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In the nineteenth century, biologists recognized that animals and plants possess traits that can be beneficial (e.g., increase strength) or detrimental (e.g., slower growth). Those with a beneficial trait may be more likely to survive, and those with detrimental traits may be less likely to survive. The essence of this paradigm has become known as natural selection.

Charles Darwin understood that sometimes the traits of various organisms can change. However, since his studies predated the field of genetics, there was yet no understanding of how these changes occurred. Instead, he attributed such changes to the effects of natural selection, as if natural selection somehow magically could cause traits to appear.

Not bound by any laws of genetics, Darwin made a lot of assumptions.

In fact, not bound by any laws of genetics, Darwin made a lot of assumptions. One key assumption was that there was “no reason to limit” how much organisms could change their traits.1 With no limits, he further assumed that such changes can dramatically transform fish into amphibians or reptiles into mammals. His presumptions provided the basic outlines of universal common descent—the idea that all life forms have arisen from a common ancestry.


While Darwin was writing about his ideas of evolution and natural selection, an Austrian Monk was conducting experiments with pea plants. From these experiments, Gregor Mendel observed that peas contain something he called “factors,” which caused the plants to grow tall or short and the pea pod to be yellow or green. These factors were also passed onto subsequent generations, affecting their growth and color as well.

Unfortunately, few biologists at that time understood Mendel’s research. In fact, it would be decades before the importance of his work would become recognized. What Mendel had unknowingly discovered was the inheritance patterns of chromosomal DNA. Mendel’s “factors” were actually different alleles (different versions of genes) on each pair of chromosomes.

We now understand that chromosomal DNA is composed of four different types of nucleotides (generally abbreviated A, T, C, G; see figure 1). Changes to the sequence of these nucleotides (e.g., mutations) can alter the genetic information of the organism, which, in turn can alter the organism’s physical features. Thus, some mutations may provide a beneficial trait, but most are either neutral or negative in their effect.

Some mutations may provide a beneficial trait, but most are either neutral or negative in their effect.

During the same time period that Mendel’s work languished in obscurity, Darwin’s work would gain wider and wider acceptance. But this acceptance came without an adequate understanding of the genetic mechanisms for evolutionary change. This is not coincidental; rather, Darwinism profited from this huge void.

Modern Synthesis

It was not until the mid-twentieth century that evolutionists finally attempted to incorporate the basics of Mendel’s ideas into Darwinian teachings. This “updating” became known as the “modern synthesis” of Darwinism. Sometimes also referred to as neo-Darwinism, this paradigm assumes random mutations can achieve the physical changes necessary for dramatic transformations; e.g., amphibians evolving legs, birds evolving wings, and mammals evolving hair.

Yet this new anthology still fell far short of providing a truly accurate mechanism for Darwinism. Much information about genetic activity and the molecular nature of mutations was not understood for several more decades. For example, we now know that mutations rarely, if ever, provide the genetic changes necessary for extensive Darwinian transformations.2 Despite Darwin’s assumption of unlimited change, very distinct genetic barriers are continually encountered.3

Not Entirely Random

What is more, since Darwinism cannot have a specific goal or plan, it has generally been assumed that mutations must be random. At least they must be random in their usefulness if not in their DNA location. Mutations would not occur because the organism needs them. Rather, they can have no intended purpose or deliberate advantage. Mutations will randomly alter the organism’s traits, and natural selection determines if the altered trait is useful to the organism. This is classic neo-Darwinism.

Randomness was also a necessary tenet to separate neo-Darwinism from Lamarckian evolution, which predicted that organisms can develop traits based upon environmental factors—and these traits can be inherited by subsequent generations. Furthermore, randomness was considered necessary to exclude any suggestion of Divine guidance or intelligent programming. However, this was more a philosophical than scientific paradigm, as there has always been an absence of direct evidence that all mutations are fully random.4

Recent studies have found distinct patterns in the location of mutations on the DNA, rather than a random scattering.

Recent studies have found distinct patterns in the location of mutations on the DNA, rather than a random scattering.5 Far fewer mutations occur in areas of high gene expression, the opposite of what would be predicted since Darwinism requires dramatic changes to gene expression.6 It has long been recognized that DNA contains “hotspots”—locations where mutations are more likely to occur.7 However, the precise and predictable locations of many mutations indicate involvement of more than just “hotspots.”

Also, since the DNA location of many mutations is not random, this challenges an assumption frequently made by evolutionary biologists. When two organisms share nearly identical mutations, biologists often assume this is evidence of shared evolutionary history. The identical mutations must have been inherited from a common ancestor. The shared mutational pattern presumably shows a Darwinian lineage.

However, this reasoning assumes mutations are randomly scattered throughout the DNA. Thus, the only way two organisms can share identical mutations is through shared ancestry. Yet because many mutations are not randomly located, shared mutations could result from shared mutational hotspots rather than shared evolutionary history. Thus, identical mutations do not verify Darwinian descent.

Adaptive Mutations

Another key question is whether some mutations occur because the organism needs them. Is there an intent or purpose behind the formation of specific mutations? This question was raised following the discovery that certain mutations appear in bacteria only when needed.8 The issue is further illustrated with a study that found rare yet beneficial mutations occurring sequentially within the same bacterium.9 Some researchers attempt to explain these mutations within a classic neo-Darwinian framework,10 but even their own calculations reveal it is highly unlikely these mutations occurred as just part of a random mutational background.11 Instead, neither of these examples can readily be explained by randomly occurring mutations.

This phenomenon, originally called directed mutations, is now more commonly known as adaptive mutations (presumably to lessen the implication of mutations occurring for a directed purpose). Understandably, the concept has been highly controversial. If some mutations arise due to the need of an organism, rather than just happening randomly, this indicates a directing program—the very opposite of classic neo-Darwinism.

There is a growing body of evidence that many mutations are not random in their formation.

Yet there is a growing body of evidence that many mutations are not random in their formation.12 In fact, many mutations and other genetic alterations seem to be specifically programmed. This programming occurs at precise phases of cellular activity or in response to specific cues from the environment.

Recent studies have found that adaptive responses in bacteria can involve the same mutation independently arising in different populations.13 Also, short template switches (inversion of short segments of DNA) can generate complex mutation patterns in human chromosomes.14 In addition, we now know that certain immune cells use a highly directed mutational pathway to generate unique antibodies.15 Cells can change their chromosome state and DNA methylation patterns in response to environmental cues.16 And, at least one group of enzymes has been implicated in controlling both the occurrence and location of mutations in humans.17


Molecular biologist James Shapiro argues that randomly occurring mutations can no longer be viewed as a viable mechanism for evolution. There must be a program directing their occurrence.18 The origin of this directing program has been called the evolution of evolution (EVOEVO). Early in life’s history, Darwinian change was driven by a process of random, undirected mutations. Gradually, directing programs were written into the genetic code. EVOEVO suggests that the very process of evolutionary change has “evolved” from a random mutating process to a directing program.19 Thus, EVOEVO assumes these programs were an inevitable product of primordial blind and random processes. This assumption is as significant a problem for evolution to accomplish as the genetic activity these programs are intended to explain.

Information engineer Perry Marshall attempts to give Darwinism a reboot, agreeing that life possesses directing programs that respond to certain environmental cues.20 He proposes that the directing programs are part of an alternate version of evolution, which he labels as evolution 2.0. Marshall describes the mechanism of version 2.0 as the action of “modular systems programmed to make sudden dramatic changes.”21 These modular systems are similar to systems a biblical creation model also employs (e.g., hybridization, gene transfer, and epigenetics). Marshall readily attributes the origin of this programming to a creator. However, he still seeks to incorporate the unnecessary and genetically untenable baggage of universal common descent.

As more is understood about genetic activities in cells, the original neo-Darwinian idea of undirected mutation becomes less tenable.

Interestingly, as more is understood about genetic activities in cells, the original neo-Darwinian idea of undirected mutation becomes less tenable. Instead, as Marshall acknowledges, organisms function with intent. This sometimes includes intentional alteration of physical traits.

Biblical Model

Such programming contradicts neo-Darwinian teaching, but fits within a biblical creation framework. Organisms were created with programs that can intentionally alter their genetic activity. This programming gives plants and animals the needed flexibility to adapt to differing environments and constantly changing conditions. Plants, animals, and humans were engineered to fulfill God’s directive of multiplying and filling the earth (Genesis 1:28).


  1. Charles Darwin, The Origin of Species (Reprint. Bantam Books, 1999), 127.
  2. Kevin Anderson, “Citrate Utilizing Mutants of Escherichia Coli,” Creation Research Society Quarterly 52, no. 4 (2016): 310–325; Kevin Anderson, “How Are New Genes Made?,” Answers in Depth 11, (2016): https://answersingenesis.org/genetics/how-are-new-genes-made/; Kevin Anderson and Jean Lightner, “The Challenge of Mount Improbable,” Creation Research Society Quarterly 52, no. 4 (2016): 244–248; and Lee Spetner, Not by Chance, Brooklyn, NY: Judaica Press, 1998.
  3. Anderson and Lightner, “The Challenge of Mount Improbable;” Nathaniel T. Jeanson, “Mitochondrial DNA Clocks Imply Linear Speciation Rates within ‘Kinds’,” Answers Research Journal 8 (2015): 273–304; and Marin Vulić, Francisco Dionisio, François Taddei, and Miroslav Radman, “Molecular Keys to Speciation: DNA Polymorphism and the Control of Genetic Exchange in Enterobacteria,” Proceedings of the National Academy of Sciences 94, no. 18 (September 2, 1997): 9763–9767 http://www.pnas.org/content/94/18/9763.full.
  4. Lars Z. Brundin, “Evolution by Orderly Stepwise Subordination and Largely Nonrandom Mutations,” Systematic Biology 35, no. 4 (1986): 602–607, doi:10.2307/2413119.
  5. Michael R. Garvin and Anthony J. Gharrett, “Evolution: Are the Monkeys’ Typewriters Rigged?,” Royal Society Open Science 1, no. 2 (2014): 140–172, doi:10.1098/rsos.140172; and Iñigo Martincorena, Aswin S. N. Seshasayee, and Nicholas M. Luscombe, “Evidence of Non-random Mutation Rates Suggests an Evolutionary Risk Management Strategy,” Nature 485, no. 7396 (2012): 95–98, doi:10.1038/nature10995.
  6. Martincorena et al., “Evidence of Non-random Mutation.”
  7. Igor B. Rogozin and Youri I. Pavlov, “Theoretical Analysis of Mutation Hotspots and Their DNA Sequence Context Specificity,” Mutation Research/Reviews in Mutation Research 544, no. 1 (2003): 65–85, doi:10.1016/S1383-5742(03)00032-2.
  8. John Cairns, Julie Overbaugh, and Stephan Miller, “The Origin of Mutants,” Nature 335, no. 6186 (1988): 142–145, doi:10.1038/335142a0.
  9. Barry G. Hall, “The EBG System of E. Coli: Origin and Evolution of a Novel β-Galactosidase for the Metabolism of Lactose,” Genetica 118, no. 2 (2003): 143–156; and Barry G. Hall and Daniel L. Hartl, “Regulation of Newly Evolved Enzymes. I. Selection of a Novel Lactase Regulated by Lactose in Escherichia coli,” Genetics 76, no. 3 (1974): 391–400.
  10. John R. Roth, Elisabeth Kugelberg, Andrew B. Reams, Eric Kofoid, and Dan I. Andersson, “Origin of Mutations Under Selection: the Adaptive Mutation Controversy,” Annu. Rev. Microbiol 60 (2006): 477–50, doi:10.1146/annurev.micro.60.080805.142045.
  11. Georgia Purdom and Kevin Anderson, “Analysis of Barry Hall’s Research of the E. coli ebg Operon: Understanding the Implications for Bacterial Adaptation to Adverse Environments,” Proceedings of the Sixth International Conference on Creationism, Pittsburg, PA: Creation Science Fellowship, 2008.
  12. Paulien Hogewoge, “Non-Random Random Mutations: A Signature of Evolution of Evolution (EVOEVO),” Proceedings of the European Conference on Artificial Life (2015): 1, doi:/10.7551/978-0-262-33027-5-ch001 .
  13. Matthew D. Herron and Michael Doebeli, “Parallel Evolutionary Dynamics of Adaptive Diversification in Escherichia coli,” PLoS Biol 11, no. 2 (2013): doi:10.1371/journal.pbio.1001490.
  14. Ari Löytynoja and Nick Goldman, “A Novel Process of Successive Inter-strand Template Switches Explains Complex Mutations and Creates Hair-pins,” bioRxiv (2016): http://biorxiv.org/content/early/2016/02/01/038380.
  15. Darryll D. Dudley, Jayanta Chaudhuri, Craig H. Bassing, and Frederick W. Alt, “Mechanism and Control of V(D)J Recombination versus Class Switch Recombination: Similarities and Differences,” Advances in immunology 86 (2005): 43–112, doi:10.1016/S0065-2776(04)86002-4.
  16. Bernard Angers, Emilie Castonguay, and Rachel Massicotte, “Environmentally Induced Phenotypes and DNA Methylation: How to Deal with Unpredictable Conditions until the Next Generation and After,” Molecular Ecology 19, no. 7 (2010): 1283–1295; and Jiang Zhu, Mazhar Adli, James Y. Zou, Griet Verstappen, Michael Coyne, Xiaolan Zhang, Timothy Durham et al., “Genome-wide Chromatin State Transitions Associated with Developmental and Environmental Cues,” Cell 152, no. 3 (2013): 642–654, doi:10.1016/j.cell.2012.12.033.
  17. Yishay Pinto, Orshay Gabay, Leonardo Arbiza, Aaron J. Sams, Alon Keinan, and Erez Y. Levanon, “Clustered Mutations in Hominid Genome Evolution are Consistent with APOBEC3G Enzymatic Activity,” Genome Research 26, no. 5 (2016): 579–587, doi:10.1101/gr.199240.115.
  18. James Alan Shapiro. Evolution: a View from the 21st Century (Pearson Education, 2011).
  19. Hogewoge, “Non-random Random Mutations.”
  20. Perry Marshall, Evolution 2.0. Breaking the Deadlock between Darwin and Design (Benbella Books, 2015).
  21. Ibid., 224.


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