Summary
Many people, including Christians, embrace evolution, and the main reason is that they have been led to believe that evolution is a scientific fact. Yet, population genetics, the very field of science that serves as the foundation for the neo-Darwinian theory, has powerfully undermined its primary axiom. The mutation/selection process cannot build the genome, let alone stop the relentless process of genetic entropy caused by mutation accumulation. This article discusses why genetic entropy is the lethal blow to the theory of evolution and why natural selection is hopeless to prevent "mutational meltdown."
Article written by Dr. Christopher Rupe
December 01, 2025
For 7 years, I was given the humbling opportunity to conduct research alongside Dr. John Sanford, a former atheist and geneticist of Cornell University. Dr. Sanford and I have devoted much time to the study of population genetics, which serves as the theoretical bedrock of the modern theory of evolution (also called the neo-Darwinian theory).
Our research focused on what Dr. Sanford refers to it in his book Genetic Entropy as the “primary axiom” of the neo-Darwinian theory. An axiom can be defined as a core assumption—a foundational premise upon which a theory’s major claims rely. Thus, if a primary axiom is flawed, a theory that it is built upon must be flawed by extension.
In the case of the neo-Darwinian theory, the primary axiom is the “mutation/selection process”. According to the theory of evolution, populations evolve through copying errors in the DNA called mutations (heritable variations), coupled with the reproductive filter of natural selection. It is believed that on very rare occasions, beneficial mutations resulting in adaptations (or useful variations) will arise in populations and that those traits will increase in frequency due to their selective advantage. In other words, individuals with more “fit” genotypes are more likely to survive and produce offspring carrying the same traits. For evolutionary progress, those novel traits must eventually become established in a population through a process population geneticists refer to as genetic fixation, where every individual in a (diploid) population has two copies of the allele, such that the new mutation represents the only variant of that particular gene in the entire population.
According to evolutionary scientists, this mutation/selection process is believed to be responsible for transforming a so-called primitive bacterium into all the magnificently diverse lifeforms that inhabit our planet. We’re told that the mutation/selection process is capable of large-scale, aka “macroevolutionary” changes, such as the transmutation of apes into humans, wolf-like creatures into whales, dinosaurs into penguins, and microbes into microbiologists.
Understand that none of those large-scale transformations is directly observable. Aware of this, famous evolutionists like Richard Dawkins admit that macroevolutionary changes occur far too slowly to be directly observed. Hence, to support their claim, evolutionists look to the fossil record in search of transitional forms, such as Archeopteryx, Tiktaalik, Lucy, etc.—all of which are hotly contested, even amongst evolutionary paleontologists (click here for articles on so-called “missing link” fossils, such as the whale evolution series).
At the time Darwin published his book, the molecule of heredity (DNA) had not yet been discovered; Mendel’s laws of inheritance were obscure to him, and he did not understand the nature of mutations. Despite not knowing even the most basic concepts that are now understood to be foundational to population genetics, Darwin boldly claimed that all living (and extinct) creatures descended from a single common ancestor, known as the Last Universal Common Ancestor (LUCA)—a hypothetical single-celled bacterium, which allegedly spontaneously arose from non-living matter in what Darwin referred to as “some warm little pond.”
Realize that none of what was just described is scientifically verifiable. Such events, including large-scale, macroevolutionary transformations (e.g., wolf-to-whale, ape-to-man, fish-to-tetrapod, etc.), are nothing more than speculative stories about the past.
Yet, because scientists can clearly see that the mutation/selection process is capable of small-scale changes (so-called “microevolution”)—such as allele frequency changes in traits affecting beak sizes in Darwin’s finches—this gives them confidence that small-scale changes, which we can directly observe today, will eventually lead to the large-scale changes (macroevolution) that cannot be directly observed.
On that basis, textbooks and evolutionary scientists argue that macroevolution is simply microevolution writ large; and so, evolution is therefore both inevitable and scientifically verifiable. This has led to the popular claim that “Given enough time, the small-scale changes (microevolution) will eventually add up to large-scale changes (macroevolution).” And the mechanism by which those large-scale changes eventually come about, or so we’re told, is through the mutation/selection process. This is why the “primary axiom” of the neo-Darwinian theory is so important to address. It’s the crux of the debate.
If what creationists claim is true, that the mutation/selection process is unable to generate the new DNA information that is required for large-scale evolutionary changes, such as transforming a wolf-like creature into whales equipped with baleen filters and fluke tails, then the theory of evolution collapses.
So, what is the main issue with the primary axiom as far as creationists are concerned? In simple language, mutations happen; selection happens—but fitness is going in the wrong direction for genome-building evolution. What scientists are actually observing is evolution in reverse, called devolution. Let me explain, starting with the origin of mutations from a biblical perspective.
According to the early chapters in Genesis, mutations did not exist at the time Adam was created. Before Adam sinned, there was no death or disease—there were no mutations. Sadly, many who embrace evolution find it hard to believe Adam and Eve were real people from whom all people descended. Instead, they think the fossil record has shown that humans evolved from so-called “ape-men” like Lucy’s species that supposedly had an ape skull and a human-like body, similar to the big foot myth (see ch. 7 in Contested Bones). In scene 4 of our full-length feature film, Dismantled, geneticists Dr. Sanford and Dr. Rob Carter discuss the remarkable evidence that scientists have uncovered through genome sequencing, which shows that all humans are descended from a single mother and a single father of us all.
Evolutionary geneticists refer to these two historical ancestors as “Mitochondrial Eve” and “Y-Chromosome Adam”. Of course, evolutionists are emphatic in letting everyone know that they are in no way referring to the biblical Adam and Eve; they are simply nicknames proposed as tongue-in-cheek to describe what superficially happens to resemble a biblical scenario—the serendipitous outcome of extraordinary circumstances that left humanity with a single surviving male and female lineage that happens to trace back to just two people. In Dismantled, Dr. Sanford shows why this evolutionary scenario (based on a theory called coalescence) is not merely a statistical coincidence, but rather, a powerful confirmation of biblical history recorded in Genesis.
All that to say, mutations were never part of God’s original “very good” creation (Genesis 1:31). God created Adam and Eve, and they were real people—not allegorical archetypes. They were created with a perfect genome, and before they sinned, they had no “copying errors” in their DNA. They had a “mutation-free” genome during the time that they lived in an uncorrupted state in the garden that God prepared for them. Thus, mutations did not enter creation until after Adam’s sin.
With Adam’s sin and The Fall in mind, we are better prepared to understand why mutations are overwhelmingly harmful in terms of their effect on fitness. Mutations were a direct consequence of Adam’s sin, which God instituted as part of His judgment on humanity, which is death. God warned Adam about the consequences of his sin if he chose to disobey His command, saying, “Of every tree of the garden you may freely eat; but of the tree of knowledge of good and evil you shall not eat, for in the day that you eat of it you shall surely die.” (Genesis 2:16-17)
In light of this biblical view of history described in Genesis, it should be of no surprise to learn that mutations and their related effects on the body are the underlying cause of aging and death at the individual level—it’s why our hair turns gray, and our skin becomes saggy and wrinkly.
Sadly, not only are we dying at the individual level due to mutation accumulation in our body cells, but our genomes are also deteriorating at the population level due to mutations that are passed on via our sex cells during reproduction. Those new mutations that are passed on to our children are likewise, overwhelmingly harmful or destructive—the technical term is “deleterious.”
This is not something that is debated. Evolutionary population geneticists are the first to acknowledge that the vast majority of mutations that enter a population are deleterious. Think about the impact on fitness of so many mutations arising in the population every generation; how could that result in evolution? Wouldn’t that mean populations must devolve rather than evolve? The obvious answer is “Yes, absolutely!” It’s the inevitable result of mutation accumulation over time. Yet, evolutionists will typically respond by saying something along the lines of:
“No, we won’t devolve due to the accumulation of harmful mutations over time because they will be eliminated from the population by natural selection. Those individuals with harmful alleles are less likely to survive and reproduce, and so those harmful mutations will decrease in frequency and be removed from the population by negative (purifying) selection.”
On the surface, this scenario sounds credible, yet to the informed population geneticist, this claim represents a gross oversimplification of the mutation/selection process since it assumes that all or most harmful mutations can be removed from the population through death of the unfit (negative selection). The problem with this thinking is that most harmful mutations are too subtle to be “seen” by purifying natural selection. Let me explain.
While it is true that the most destructive/disease-causing mutations can be easily noticed and removed from the population, such mutations represent only a tiny fraction of the total number of harmful mutations that arise. Most harmful mutations fall into the category of what population geneticists refer to as “very slightly deleterious” or “nearly neutral”. Given what we know about the genome, this must logically be true. The information content of our genome is incredibly vast, such that the typical mutation is far more likely to produce very slightly deleterious effects in terms of overall fitness.
The logic behind this thinking can be understood in simpler terms using the analogy of a very large book. A single typo in a given passage is not going to affect the overall readability of that book to any significant degree. And that’s because a single letter contributes very little to the overall information content of a very large book. In the same way, a single mutation in a very large genome, such as in humans with 3.2 billion DNA letters, in most cases, is likely to cause only the slightest impact on overall fitness or total functionality.
High-impact mutations that are considered strongly deleterious, on the other hand, are far less common. Although they may seem common to us, that’s only because those are the ones that we notice since they cause abnormalities and diseases that are outwardly manifest in an organism’s physicality or “phenotype.” Nevertheless, they are not the most prevalent class of mutation—very slightly harmful mutations or nearly neutral mutations are the most prevalent class. There is no such thing as perfectly neutral mutations; even synonymous mutations are more accurately defined as nearly neutral or very slightly harmful. This is consistent with continuous probability distributions that population geneticists use to model the fitness effects of new mutations.
Population geneticists understand that most mutations are very slightly deleterious, or nearly neutral, which means nearly zero effect on fitness. Their effect on fitness is so subtle, they do not affect reproductive success. Not affecting reproductive success, they are called "effectively neutral" (they are subject to genetic drift, not natural selection). Consequently, these very slightly deleterious mutations will be “overlooked” by negative selection. This may be challenging to grasp… in simple language, what does it mean to be “overlooked” by natural selection?
In Genetic Entropy, Dr. Sanford provides a simplifying illustration of The Princess and the Pea fairy tale. The princess writhes in discomfort because she can somehow feel a tiny pea beneath a large stack of multiple bed mattresses. Of course, only a true princess can feel a tiny pea under so many layers of cushion. Dr. Sanford likens the absurdity of this story to emphasize the inefficiency of natural selection. Evolutionary scientists would have us believe that nearly all harmful mutations can be eliminated from the population due to negative selection. Yet, how can selection “see” the most minute (“pea-sized”) mutations in a large genome of 3.2 billion DNA “letters” in humans, for example?
The answer is, selection cannot see them, meaning they will not be selectively removed from the population. Hence, a significant portion of very slightly deleterious mutations (those that escape random loss due to genetic drift) will persist in all subsequent generations, resulting in the genetic fixation of an ever-increasing load of mutations. This, of course, is devastating to the neo-Darwinian theory. How then can a population evolve, let alone stop degeneration? Genetic degeneration is the opposite of evolution—it is devolution.
In response to this, a keen evolutionist might argue, “If most new mutations that enter a population are 'very slightly deleterious' such that they do not affect reproductive success, how then can they pose a problem for the theory of evolution?” On an individual basis, the evolutionist is correct: a slightly harmful mutation, by itself, is as unnoticeable as a pea under a thousand mattresses; it won’t affect the organism’s reproductive fitness in any noticeable way. Yet, the combined effect of the accumulation (and fixation) of many peas over deep time is how they pose a very serious threat to the neo-Darwinian theory.
Consider once again our analogy of typos in a very large book. Individual typos are most often inconsequential to overall readability and comprehension. Yet, now consider new typos being introduced every time a book is duplicated over many thousands of copying iterations (generations). What do you think will happen to that book after, say, a million years? Eventually, a certain threshold number of typos will accumulate, whereby the information content of the book will become so thoroughly garbled that it becomes incomprehensible, unreadable.
Evolutionary population geneticists have referred to the analogous process of mutation accumulation in living populations as “mutational meltdown” or “error catastrophe”. As mutations accumulate over many generations (spanning millions of years of evolutionary time), eventually a species will be driven to extinction due to an unbearably heavy load of mutations. Over time, more and more mutations arise and become fixed until a certain threshold is reached when the amount of information-bearing “letters” (nucleotides) in the DNA can no longer encode life’s basic functions—i.e., the genome becomes incomprehensible, too garbled if you will. At that point, the functional genome size of the population will have shrunk to the point where the population size crashes, and extinction is inevitable and sudden (this is precisely what happened to the 1918 H1N1 influenza virus, see paper here). That is what is meant by “mutational meltdown.” Population geneticists have compared this to a ticking “time bomb” that runs down as very slightly harmful mutations become fixed in a population over time until suddenly, the bomb goes off! (Technical note: very slightly deleterious mutations that are below the selection threshold fix at a rate equal to the effectively neutral mutation rate per generation).
As discussed, selection cannot come to the rescue by removing these slightly harmful mutations because they fly under selection’s radar, so to speak. Every generation, the average couple passes on about 100 new mutations to their offspring, resulting in the de-evolution of the human population. Thus, every generation we are becoming increasingly mutant—my children inherited 100 more mutations than I inherited, 200 more mutations than my father inherited, 300 more mutations than my grandfather inherited, and so on. Extrapolate this process over evolutionary timescales, and you are left with a hopeless situation.
If selection is too ineffective to stop the accumulation of very slightly harmful mutations, how can populations survive, let alone evolve, over geologic timescales? It is for this reason that famous population geneticist, Dr. Alexy Kondrashov, wrote as the title of his famous paper, “Contamination of the genome by very slightly deleterious mutations—why have we not died 100 times over.” He argues that after just 20 million years, all vertebrate lineages should have gone extinct. And yet, here we are. Kondrashov refers to this mystery as the "mutational load paradox". Of course, this isn’t a paradox for the biblical view of origins, which provides a dramatically shorter timespan of biological history.
For several decades, many other leading evolutionary population geneticists have attempted to resolve the mutation load paradox. Their findings have been reported in the mainstream peer-reviewed scientific literature and are carefully documented in the appendix of Genetic Entropy. Thus, the concept of genetic entropy is not a new one; the phrase was coined by Dr. John Sanford in the early 2000s, whereas the population genetic literature refers to the same problem as the “mutation load paradox,” “genomic decay paradox,” “Muller’s Ratchet,” "genetic load," etc. Dr. Sanford, with contributions from Dr. Rob Carter and me, has documented the reality of genetic entropy in real-world populations of bacteria, viruses (H1N1), and mammals—including the sequenced genomes of fossil hominins like Neanderthals (see ch. 14 in Contested Bones). Some of Dr. Sanford's findings supporting the reality of genetic entropy have been published in secular peer-reviewed journals (see list of papers referenced below).
For this article, we have one loose end to tie up. So far, we have only discussed the role of harmful mutations, but what then do we make of beneficial mutations? Surely there are rare beneficial mutations that can improve fitness. Therefore, can’t we simply extrapolate over deep time a process of evolution through a long series of beneficial mutations? This is a common objection; however, it overlooks an important finding in genetics.
It turns out, beneficial mutations, just like we observe in harmful mutations, are caused by loss-of-function or loss-of-regulation changes in gene expression or gene function. This includes all studied examples of bacterial resistance to antibiotics (for example, see the article here and Dismantled scene 2, here). Ironically, this means that even beneficial mutations further contribute to the problem of genetic entropy. This is true even though beneficial mutations can be adaptive to a certain set of narrow conditions (see article on Lenski’s long-term E. coli experiment, here). In the scientific literature, it is described as “reductive evolution”, whereby adaptation occurs through loss-of-function beneficial mutations. In our article examining beneficial mutations in E. coli populations, Dr. Sanford and I describe the phenomenon similarly as “adaptive degeneration.”
The bottom line is, genetic entropy is not merely a theoretical problem; it is supported by empirical data, from real genomes, in real populations. It is a legitimate scientific problem, one that directly undermines the primary axiom of neo-Darwinian Theory. I would argue, it is the lethal blow to the modern theory of evolution—microbes-to-man evolution is simply not possible via the mutation/selection process.
Conclusions
Many people, including Christians, embrace evolution, and the main reason is that they have been led to believe that evolution is a scientific fact. Yet, population genetics, the very field of science that serves as the foundation for the neo-Darwinian theory, has powerfully undermined its primary axiom. The mutation/selection process cannot build the genome, let alone stop the relentless process of genetic entropy caused by mutation accumulation.
Genetic entropy is a sad consequence of Adam’s sin and The Fall. Our decaying bodies and the declining fitness in populations should remind us of how fragile and transient life is. The Bible reminds, “For, ‘All flesh is like grass, and all its glory like the flower of the field. The grass withers and the flower falls, but the word of the Lord endures forever.’” (1 Peter 1:24). In addition, genetic entropy should remind us of our need for a Savior as we long for our incorruptible resurrection bodies, which repentant sinners will receive once we are united with Christ in the New Heavens and New Earth, just as Revelation chapter 20-21 teaches.
The reason Back2Genesis exists is to share the Good News of the Gospel. Romans 6:23 says, “The wages of sin is death but the free gift of God is eternal life in Christ Jesus our Lord.” Sadly, when Adam sinned, God’s punishment was not merely physical death due to mutations—it was also spiritual death as a consequence of our sins, which severed our right relationship with God, causing us to be separated from Him for all eternity. Yet, by God’s grace, He did not intend to leave us in an unredeemable condition. God had a plan. He sent His one and only son, Jesus Christ, who was God in the flesh, come down from heaven, as a descendant of Adam and Eve, to live a perfect, sinless life that none of us could do, so that he could become the perfect sacrifice for our sins. As it is written, "Therefore, just as sin entered the world through one man, and death through sin, and in this way death came to all people, because all sinned.” (Romans 5:12) And, “For as by one man’s disobedience many were made sinners, so also by one Man’s obedience many will be made righteous.” (Romans 5:19)
This is why Jesus is referred to as the Last Adam. The first Adam introduced death into the world and separation from God through his sin, and the second Adam, Jesus Christ, removed the sting of death by dying as our substitute on the cross, so that we could be forgiven of our sins and reconciled to God through His victory over death.
Through the shedding of Christ's blood, we can receive complete forgiveness for our sins and receive the free gift of eternal life: “For God so loved the world, that He gave His only begotten Son, that whosoever believeth in Him should not perish, but have everlasting life.” (John 3:16). This is the Good News of the Gospel! Will you put your full trust in Jesus today? What is stopping you from committing your life to the lover of your soul?
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Technical Papers by Dr. John Sanford and
Colleagues Relating to Genetic Entropy
1) Biological Information – What is It?
2) Multiple Overlapping Genetic Codes Profoundly Reduce the Probability of Beneficial Mutation
3) Can Purifying Natural Selection Preserve Biological Information?
4) Selection Threshold Severely Constrains Capture of Beneficial Mutations
5) Using Numerical Simulation to Test the “Mutation-Count” Hypothesis
6) Can Synergistic Epistasis Halt Mutation Accumulation? Results from Numerical Simulation
7) Computational Evolution Experiments Reveal a Net Loss of Genetic Information Despite Selection
8) Information Loss: Potential for Accelerating Natural Genetic Attenuation of RNA Viruses
10) The Fundamental Theorem of Natural Selection with Mutations
11) The Waiting Time Problem in a Model Hominin Population
13) Mendel's Accountant: A Biologically Realistic Forward-Time Population Genetics Program
14) Mendel’s Accountant: A New Population Genetics Simulation Tool for Studying Mutation and Natural Selection
15) Using Computer simulation to Understand Mutation Accumulation Dynamics and Genetic Load
16) The effects of low-impact mutations in digital organisms
17) The Next Step in Understanding Population Dynamics: Comprehensive Numerical Simulation
18) Nylonase Genes and Proteins–Distribution, Conservation, and Possible Origins
19) The Most Famous Evolution Experiment of All Time Shows that Evolution Goes the Wrong Way
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Responding to Critics of Genetic Entropy
Entry Date: 01-07-26
The following objections were raised by an atheist who commonly engages with creationists on YouTube. The comment was posted on my companion video to this article on January 05, 2026, available here. His objections are pasted below in red, followed by my responses. Please don't attack this person, but rather pray for him in love, including any skeptics who watch this video or read this response, in the hope that their eyes might be opened to the truth of the Gospel and the love and kindness of our Savior.
Never understood the egotism of creationists attacking well understood sciences.
Hi, thanks for your comments. I appreciate it! I tried to keep my response as brief as possible, but I failed miserably. Sorry about that. Normally, I don’t spend so much time on comments, but for the sake of my audience, I felt I needed to. Your objections had a number of serious flaws and revealed a fundamental misunderstanding of population genetics. Although it is easy for me to spot the blunders, I am concerned that many others may not be so keen to identify them, so I took the time to thoroughly address them.
The first thing I want to point out is that I am not “attacking” the field of population genetics. I think that comes across pretty clearly in the video. I actually agree with its basic principles and have studied them as part of my past research with Dr. John Sanford. It is ironic that although population genetics was founded by a small group of deeply committed evolutionists, its basic principles powerfully demonstrate why the mutation/selection process fails as a workable mechanism for large-scale macroevolutionary changes, such as the evolution of humans from a hypothetical "chimp-like" last common ancestor, or the evolution of Pakicetids into cetaceans (whales, dolphins, and porpoises). When utilized properly, population genetic principles place biologically realistic constraints on what can feasibly be accomplished via the mutation/selection process.
Let's first wreck this presentation and ask, why the creationists need logical fallacies, lies, and misrepresentations to assert nonsense. Logical Fallacies Straw Man Argument: The narrator defines the "Primary Axiom" of evolution as the belief that mutation/selection can turn a bacterium into a human [01:51]. By defining it as a singular "axiom" rather than a complex framework of multiple mechanisms (genetic drift, gene flow, endosymbiosis, etc.), he makes it easier to "refute" by attacking only one component.
Thank you for stating your case. I am well aware that there are other mechanisms, such as genetic drift, genetic fixation, selective mating, gene flow, etc. In fact, right at the beginning of the video, when I describe the mechanism of evolutionary change, I explain the process of genetic fixation. I also discuss the influence of genetic drift and how it relates to the mutational load problem. In addition, I make a critical distinction between effectively neutral and strictly neutral mutations. I went deeper still to establish the neutral substitution rate, which is a core concept of Kimura’s Neutral Theory of Molecular Evolution. That’s a pretty substantial dose of population genetic principles and mechanisms for a relatively short video, which was intended to be an introduction to the topic of genetic entropy. What other mechanisms and principles was I supposed to discuss to make you happy? Was I supposed to include gene flows and selective matings as well? The point of the video was not to discuss every possible genetic mechanism that occurs in populations (that’s what textbooks are for), but only the most crucial.
More to your point, the mutation/selection is indeed the primary axiom of the Neo-Darwinian theory. In standard evolutionary theory, without mutations as a source of new variation and without natural selection as a nonrandom mechanism, there is no way to form novel sets of genetic specifications to encode complex organs or systems. That doesn’t mean mutation and selection are the only mechanisms, nor did I say that. My point was, mutation/selection is the indispensable core process. Let me explain. Mutations without selection are insufficient because there would be no positive selection to amplify beneficial mutations and no purifying selection to eliminate deleterious alleles from the population. Selection without mutations is insufficient because there would be no source of variation for selection to act upon. Genetic drift, apart from any selection, is likewise insufficient because, without the nonrandom mechanism of differential reproduction, the formation of novel, innovative features, such as baleen filters, sonar systems, fluke tails, or any other complex organ would not be possible. Evolutionary biologist, Jerry Coyne, affirms this, stating: “As a purely random process, genetic drift can’t cause the evolution of adaptations. It could never build a wing or an eye. That takes nonrandom natural selection.” Thus, mutation/selection truly is the indispensable core process of evolutionary change, hence why Dr. Sanford refers to it as the primary axiom.
False Dilemma (Bifurcation): The video presents a choice between "Biblical Genesis" (6,000-year timescale) and "Evolutionary Meltdown" (20 million years) [16:14]. It ignores other scientific explanations for why genomes don't collapse, such as synergistic epistasis and recombination.
I deliberately chose not to discuss synergistic epistasis because this is the first video on the topic that I’ve made, and it was intended to serve as an introduction to the topic of genetic entropy. A professor teaching Physics 101 will do the same thing and focus only on the basic concepts before diving into higher-level concepts such as quantum field theory. Synergistic epistasis is conceptually simple, but mathematically and biologically, it is highly complex. If I got into the weeds, I probably would lose 90% of my audience, and my audience is already very small, so why would I do that? Nevertheless, at the end of the companion article I wrote on this topic, I provided a link to a published technical paper discussing why there is no empirical evidence for strong, genome-wide synergistic epistasis at the level required to resolve the mutational load paradox. It therefore fails as a rescue mechanism. Most people are not interested in the technical deep dives, but here is the link to the scientific article if you’re interested.
Dr. Sanford discusses synergistic epistasis in simpler language in his book Genetic Entropy. He also discusses recombination. Although recombination reduces linkage interference (a form of selection interference) and slows “Muller’s Ratchet”, it cannot prevent the fixation of effectively neutral, very slightly deleterious mutations. Recombination reshuffles existing variants, but it does not alter the mutation rate or fundamentally change the proportion of mutations that are invisible to purifying selection, so it cannot resolve the mutational load problem. Moreover, it’s worth emphasizing a related limitation of genetic recombination: the genome contains large persistent linkage blocks that undergo little or no recombination; consequently, they are subject to Muller’s Ratchet. As Sanford comments, “in genomic regions where there is no sexual recombination, the good and bad mutations are inseparably linked and cannot be teased apart. In such genomes (or in such chromosomal regions), the predominant bad mutations cannot be separated from the rare good mutations – resulting in a downward ratchet mechanism that guarantees net genetic degeneration.” For further clarification on these topics, you can use the index and look up the terms: “recombination”, “linkage”, and “Muller’s Ratchet.”
Equivocation: The video uses the term "Information" loosely [04:26]. In biology, "information" is often measured by functional complexity or Kolmogorov complexity, but the video treats it like a language in a book [13:31] where any change is a "typo," ignoring that many mutations are actually synonymous or create new functional pathways.
In the video, I explicitly mention synonymous mutations, so it is not true to say that I ignore them. And it is no longer defensible to argue that synonymous mutations do not affect fitness. They are now widely considered to be nearly neutral or weakly deleterious as opposed to strictly neutral. And your claim that mutations “create new functional pathways” is asserted, but not demonstrated.
Regarding my use of the term “information”, I think it is entirely appropriate in this context. “Information” does not have a single agreed-upon definition in biology, and there is no consensus that biological information is adequately captured by any single conceptual framework, such as Kolmogorov complexity, functional complexity, or Shannon information. Instead, the term “information” is used by biologists in different ways, depending on what is being studied or described.
For example, one way that it is commonly used is to describe the specific ordering of nucleotides (DNA “letters”) that encode biological functions. This is why the analogy of a book is so fitting and so commonly used by scientists, including evolutionary biologists, genetics textbooks, and scholarly sources such as Nature. Using an analogy of human language, as in a book of text, is a pedagogical metaphor, which is simply a teaching tool used to explain an abstract concept in more familiar terms for a general audience; I’m not claiming it is literally equivalent to human-written text. That would be silly. My definition of biological information falls more in line with information theorist, Dr. Werner Gitt's analysis, provided here.
Although we can both agree the genome is not equivalent to human-written text, that doesn’t mean we can downplay the reality of biological information. Renowned evolutionary population geneticist, Dr. John Maynard Smith, has pointed out that DNA sequence order is indeed real information, and not merely a metaphor. This makes sense, complex organs such as the human eye require highly specific nucleotide sequences, reflecting an astounding degree of functional specification; it is indeed highly specified information. This type of high-level information has never been shown to arise by itself in matter, and certainly not via a Darwinian trial and error process (refer to the article by Dr. Gitt referenced above). The CEO of Microsoft has noted, “DNA is like a computer program but far, far more advanced than any software ever created.” National Medal of Science recipient, Norbert Wiener, once said, “Information is information, neither matter nor energy.” Indeed, this type of high-level information has only been shown to come from an intelligent source (a mind). A book of typed information indicates there must have been an author; a computer program indicates there must have been a programmer; in the same way, our genome indicates there must have been an Author of Life. I happen to know Him personally; His name is Jesus! It is my prayer that you would come to know the love and goodness of God that was put on full display through Christ’s death on the cross for our sins. He loves you that much.
Appeal to Authority: The video repeatedly cites Dr. John Sanford's credentials at Cornell to lend credibility to the claims [00:14]. While he was a researcher there, his specific "Genetic Entropy" work is considered "fringe" and has not gained acceptance in the broader scientific community.
My argument does not depend on Sanford’s credentials. I simply mention his relevant scientific background because oftentimes skeptics of creation claim we cannot be real scientists and have no credibility to make our claims. Citing John’s scientific credentials undercuts that and shows that he can speak authoritatively on this topic based on his many years of study.
In the appendix of Genetic Entropy, Dr. Sanford cites numerous papers published by respected evolutionary population geneticists who have attempted to resolve the mutational load paradox. It is indeed a very real problem, one that has been wrestled with for several decades by some of the most renowned evolutionary population geneticists. I encourage you to take a look at the appendix and go through the relevant published papers that are cited therein. If you think the problem does not exist, then why have so many population geneticists spent so much of their time publishing papers and devising all kinds of theoretical rescue devices, including synergistic epistasis, mutation count mechanism, weak stabilizing selection, and more—all in an attempt to resolve the problem? That is why Dr. Sanford published his book Genetic Entropy, as well as several technical papers addressing those rescue attempts. A list of his papers addressing those rescue mechanisms can be found on this webpage; scroll to the end of the article.
Lies and Misrepresentations Misrepresentation of "Mitochondrial Eve" and "Y-Chromosomal Adam": The narrator claims genome sequencing shows we descend from a "single mother and father" [05:36]. The Fact: These are the most recent common ancestors (MRCAs) of all living humans for specific genetic lineages, not the only humans alive at the time. They lived tens of thousands of years apart (Adam ~200k-300k years ago; Eve ~150k-200k years ago) and were part of a larger breeding population.
I am not lying. As a former skeptic turned born-again Christian, I sincerely believe the Bible is true and that the evidence from real science supports the biblical view of human history. I am simply offering a viable, alternative scientific model. You state that your claims above are facts; however, they are more accurately an interpretation of the genomic data based on evolutionary assumptions and models. Different models can explain the same data; that is the nature of any model. The question is, which model explains the data best? I would argue the biblical “Out of Middle East” model, beginning with a literal Adam and Eve, offers a more parsimonious interpretation of the genetic data than the “Out of Africa” theory, which has become increasingly convoluted over the years. In scene 4 of Dismantled, Dr. John Sanford and geneticist Dr. Rob Carter explain why the larger population size hypothesized in the Out of Africa model is merely an inference (it is not a scientific fact). In addition, they discuss the differences between the phylogenetic and the pedigree-based methods of estimating mutation rates, which are used to calculate the timeframe. Interestingly, there is a discrepancy between these two methods. It turns out, the pedigree-based method, which does not assume we share a common ancestor with chimps (a less biased approach), tends to yield dates for genetic Adam and Eve that fall much closer, or neatly within a biblical timescale, according to some evolutionary studies. This is quite remarkable since they are not creationists, yet they cannot explain why it supports a biblical timeline. To learn more, feel free to check out scene 4 of our film, Dismantled, here.
Mischaracterization of Neutral Mutations: The video claims "effectively neutral" mutations are always slightly deleterious and "fly under the radar" of natural selection [15:07]. The Fact: Neutral theory (Kimura) posits that many mutations have zero effect on fitness.
To clarify, I did not say that effectively neutral mutations must “always” be slightly deleterious. What I explained was that based on modern DFE, the dominant class of new mutations is very slightly deleterious with very small fitness effects such that they are effectively neutral (invisible to purifying selection).
Your next objection was that Kimura posited that “many” mutations have zero effect on fitness. This is not true. Your claim reflects a common misunderstanding of Kimura’s Neutral Theory of Molecular Evolution. In the Fundamentals of Molecular Evolution, Dr. Dan Gruar and Wen-Hsiung Li clarify that, “Neutrality, in the sense of the theory [Kimura, 1968] does not imply strict equality in fitness for all alleles. It only means that the fate of alleles is determined largely by genetic drift.” Thus, Kimura’s definition of neutrality has to do with |s| relative to 1/Ne, and not by whether s = 0. Put simply, neutral is defined in relation to whether genetic drift dominates over selection. The work of Kimura’s colleague and protégé, Tomoko Ohta, took this a step further with her refinement of his Neutral Theory, and proposed the Nearly Neutral Theory of Molecular Evolution. Ohta explicitly emphasized that most mutations are not strictly neutral (S = 0), but rather are very slightly deleterious or nearly neutral. Even synonymous mutations are now recognized to have non-zero, slightly deleterious effects on fitness. This claim is supported by a number of studies in the peer-reviewed scientific literature. The bottom line is, the consensus view among evolutionary population geneticists is that the majority of new mutations fall in the category of nearly neutral, very slightly deleterious, or mildly deleterious. This is consistent with empirically inferred DFEs modeled by population geneticists, which indicate a continuous distribution of fitness effects, rather than a single large spike (point mass) directly over strictly neutrals (S = 0).
Furthermore, selection is a statistical process; even slightly deleterious mutations are often purged in large populations through purifying selection over many generations. Distortion of the "Mutational Load Paradox": The video cites Dr. Alexey Kondrashov’s paper "Why have we not died 100 times over?" as proof of the "Genetic Entropy" problem [15:52]. The Fact: Kondrashov’s paper was identifying a problem to be solved within evolutionary theory (which led to research on sexual recombination and synergistic epistasis as solutions), not a declaration that evolution is impossible. Kondrashov is an evolutionary biologist who supports the theory.
Slightly deleterious mutations are efficiently purged only in large populations when their selection coefficients exceed the selection threshold defined by (|s| ≳ 1/Ne) according to conventional population genetic theory. Thus, the fraction below this threshold represents a substantial fraction of deleterious mutations, especially in effective population sizes of around 10,000, from which humans supposedly evolved. This brings us back to the main point of the video, which is the realization based on modern DFEs that the dominant class of new deleterious mutations has fitness effects that are below the selection threshold, even in large effective population sizes (Ne). This indicates their fate is governed by genetic drift and cannot be systematically purged via negative selection. And when one accounts for sources of biological noise that are evident from real-world populations, the “no selection zone” is greatly expanded. Here is a technical article on that topic.
To your next objection, I never said that Kondrashov is arguing that evolution is impossible. I simply state that he has, along with several other leading population geneticists, wrestled with what he refers to as the “mutation load paradox” for many years—and despite his best attempts to resolve the evolutionary enigma, his proposed rescue devices are model-dependent and debatable. The most serious contention is that these mechanisms lack empirical support in natural populations, especially with respect to synergistic epistasis and truncation selection. Again, strong genome-wide synergistic epistasis has not been robustly demonstrated in natural populations. Sanford et al. (2013) point out in their numerical simulation analysis on synergistic epistasis: “A genetic model in which all mutations interact in a synergistic manner is an artificial model, one that does not represent any real biological population. Moreover, such a model contradicts an extensive body of population genetics literature, which for nearly 90 years has been built on the assumption that most mutational effects combine either additively or multiplicatively (the latter effectively counteracting any generalized SE effect).” This topic is discussed in more detail in Genetic Entropy as well as in the following technical publication, here, which specifically addresses synergistic epistasis.
Claim that Beneficial Mutations are always "Loss of Function": The video asserts that virtually all beneficial mutations result from a loss of information or regulation [17:40]. The Fact: This is factually incorrect. Examples of "gain of function" mutations include gene duplications (which provide new raw material for functions), nylonase-eating bacteria, and the evolution of citrate metabolism in E. coli (the Lenski experiment).
I think you would agree that gene duplications alone are not gain-of-function; they merely copy pre-existing sequences, such as genes that have pre-existing functions. Now, I understand that according to evolutionary theory, once a gene is duplicated, it can be modified via mutations in a process evolutionary scientists refer to as neofunctionalization; however, clear experimental evidence for genuinely novel, complex molecular functions evolving via this mechanism is lacking, at best. Moreover, duplications are overwhelmingly subject to non-functionalization, which is the opposite of neofunctionalization. This is because duplicated genes are typically silenced epigenetically through mechanisms such as DNA methylation, RNA interference, etc. Consequently, the silenced genes are not subject to purifying selection, making them prone to mutation accumulation, which leads to inactivation and degeneration. Here is a helpful article on that subject.
You also mention citrate metabolism in the long-term E. coli experiment headed by Richard Lenski as an example of an “evolutionary innovation”. Yet, the duplications, rearrangements, and mutations responsible for the Cit+ trait resulted in the loss of regulatory control, which allowed the preexisting citrate transporter to be expressed in the presence of free oxygen (normally it is inactivated in aerobic conditions). The citrate operon was inserted in front of an existing aerobically active promoter, which resulted in the constitutive expression of the citrate transporter protein. No new enzymes or metabolic pathways arose, and the citrate transporter already existed. As noted by geneticists, Hofwegen et al. (2016) in a subsequent study of the Cit+ trait in the Journal of Bacteriology, “No new genetic information (novel gene function) evolved.” I discuss Lenski’s experiment in more detail in an article that I co-authored with Dr. Sanford, available on my website here; the results of the long-term experiment are a strong confirmation of genetic entropy in action.
Onto your claim about nylonases. While it is true some bacteria can produce enzymes that can metabolize nylon byproducts, this cannot be considered as a legitimate example of a newly evolved gene, either via duplication (Okada’s hypothesis) or via a hypothetical frameshift mutation (Ohno’s hypothesis), which was never demonstrated experimentally (see paper below). The reason is that those types of enzymes belong to a family of hydrolases that were already in existence and widespread long before nylon was invented in 1935. The bacteria already had enzymes capable of breaking down similar chemical bonds that are found in nature, and those enzymes happen to work on nylon waste, which contains similar chemical bonds. I provide a paper on that topic as well; it is linked at the end of this article here.
Factual Inaccuracies H1N1 "Mutational Meltdown": The narrator claims the 1918 H1N1 virus went extinct due to mutational meltdown [14:46]. The Fact: The 1918 strain didn't "break" due to mutations; it was largely supplanted by more successful, competing strains or evolved into seasonal flu variants. Viruses mutate rapidly as an advantage to evade the immune system, not as a countdown to suicide.
That is precisely the point. The fact that the 1918 H1N1 viral lineage was supplanted by a new H1N1 lineage means the original human H1N1 lineage went extinct as a distinct viral genotype. Lineage replacement is a standard mechanism of extinction. Evolutionists have used similar language when they describe the extinction of Neanderthals. One theory is that they were replaced by more competitive anatomically modern H. sapiens. Now, just because modern humans have some Neanderthal DNA in us through introgression, does that mean Neanderthals as a distinct population did not go extinct? Of course not. Neanderthals are widely regarded to be extinct by evolutionary scientists. I’m not an evolutionist; I’m simply using their own logic to point out the inconsistency in your thinking.
Interestingly, there is evidence from the sequenced genomes of Neanderthals that they carried a very heavy genetic load due to mutation accumulation associated with inbreeding, which may have contributed to their loss of competitive edge (at least that’s one possible theory). The same logic applies to H1N1.
In the case of the 1918 H1N1 influenza virus, extinction refers to the loss of the original strain or genotype, not the disappearance of all its descendant lineages. Over 10% of the genome mutated via the linear accumulation of mutations, which coincided with an exponential decline in pathogenicity, a proxy for reduced fitness relative to the ancestral 1918 strain. This evidence is consistent with extinction due to genetic degeneration. To clarify, the H1N1 strain that exists as part of the seasonal flu today is not the same as the 1918 strain—the former originated in part via a reassortment with swine and avian influenza viruses, which the paper explains. The technical paper referenced here was published in the mainstream peer-reviewed literature, not in a creation journal. For your convenience, here is the link to the paper.
Human Mutation Rate: The video claims every generation adds 100 deleterious mutations [15:13]. The Fact: While humans have about 60–100 new mutations per generation, the vast majority occur in non-coding "junk" DNA or are truly neutral. Only a tiny fraction affects fitness, and those that do are subject to selection.
Interestingly, the very concept of “junk DNA” was popularized in the 70s by evolutionary geneticist Susumu Ohno, who argued that our genome must consist mostly of junk. He reasoned that if we had a highly functional genome, we would not be able to survive what he referred to as an “unbearably heavy genetic load” of deleterious mutations due to the high reproductive cost required for purifying selection. Like many other population geneticists, Ohno recognized that the genetic load problem was a serious concern over evolutionary timescales. His solution was to propose that more than 90% of the genome consisted of “junk DNA” to avoid what he thought would be an unsustainable mutational burden, leading to extinction. However, Ohno’s proposal of a predominantly junk genome has not aged well. Over the past several decades since then, numerous studies have consistently indicated that many non-coding regions attributed to so-called “junk” regions exhibit measurable functional constraint, meaning mutations are not accumulating freely in those regions.
The concept of junk DNA was based largely on evolutionary assumptions and concerns about mutational load. In times past, evolutionary biologists recognized that only about 2-5% of the genome encodes for proteins and that the reproductive cost of purifying selection would be too high to maintain a function across the remainder of the genome. And so, the non-coding regions were regarded as non-functional junk. They were often characterized as molecular fossils, the vestigial remains of past evolutionary experiments that failed.
The problem with this thinking is that it strongly biases the interpretations of evolutionists toward assuming non-functionality rather than being open-minded to the possibility that non-coding regions served roles not yet discovered. Many did not have the foresight to recognize that just because non-coding regions don’t encode proteins, it doesn’t mean they don’t perform other functions. Indeed, it is now widely recognized that many non-coding regions play important regulatory and structural roles. Several other studies indicate that mutations arising in non-coding regions are weakly deleterious, as opposed to strictly neutral, which represents the mainstream position amongst evolutionary population geneticists. So, the whole idea that junk DNA can act as a buffer to absorb mutations that would otherwise be deleterious to functional regions does not resolve the mutational load problem, since mutations in those regions have small fitness effects of their own. There’s a lot more I could say about this topic. The bottom line is that scores of published genomic studies are increasingly challenging the junk DNA paradigm.
Regardless, even if we ignore this evidence and assume for the sake of argument that only 10% of the genome is functional, that fraction will still be subject to the continual input and long-term fixation of effectively neutral, very slightly deleterious mutations that are below the selection threshold. As discussed, this process, extended over evolutionary timescales, will inevitably lead to the progressive decline in fitness—a process we describe as genetic degeneration or genetic entropy, which is essentially evolution in reverse—it is devolution.
Population geneticists have historically addressed the mutation load paradox under the working assumption of the “junk DNA” paradigm, indicating that they recognized that a predominantly junk genome does not solve, by itself, the mutation load problem. If they thought it did, they would not have worked so hard to devise several other rescue mechanisms, like the ones discussed above (e.g., synergistic epistatic, truncation, selection, etc.), which were specifically designed to address the mutation load problem.
Finally, you claim that after accounting for mutations arising in so-called junk regions of the genome, "only a tiny fraction" of deleterious mutations affect fitness at all, and the rest are subject to purifying selection. Once again, your assertion is inconsistent with conventional population genetic theory and modern DFEs, which show that very slightly deleterious (nearly neutral) mutations are the dominant class. Because these mutations have very small effects on fitness, a large fraction of these falls below the selection threshold, as defined by |s| ≈ 1 / Ne, in accordance with standard theory. Consequently, they are not efficiently subject to purifying selection but are instead dominated by genetic drift. And as I stated above, a biologically realistic selection threshold would encompass an even larger fraction of slightly deleterious mutations once multiple sources of biological noise characteristic of natural populations are taken into account.
Thus, the problem of genetic entropy cannot be so easily dismissed by invoking purifying selection in the manner that you describe. The bottom line is, the long-term fixation of very slightly deleterious mutations via genetic drift at a rate approximately equal to the effectively neutral mutation rate is an inescapable consequence of standard population genetic theory, and poses as a very serious challenge for explaining how genomic integrity could be maintained over evolutionary timescales. Again, I argue, it is truly the lethal blow to the neo-Darwinian theory.
I apologize for the length. I hope my responses were constructive and clarifying. Thanks again for your comments! I sincerely wish you well.