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What’s in your genetic future?

Is humanity evolving – up? Or de-volving – down? What about the rest of Earth’s creatures, from microbes to clams to petunias to whales? Is our future reflected in the Star Trek vision of man growing ever smarter, ever wiser, exploring the universe, with life spans increasing, with riches and glory without limits? More personally, what about your children, grandchildren . . . great-great-great grandchildren? Will your descendants be healthier, stronger, happier, perhaps immortal some day?

John C. Sanford

John C. Sanford

This isn’t, actually, an open question. The answers are clear, explained by Genetic Entropy, the biological reality that in any population of organisms, including man, deleterious mutations accumulate from generation to generation, producing an inevitable decline of fitness . . . leading to extinction. Some mutations arise from copying errors in DNA replication in the germ cells; despite a variety of fabulous error-correcting systems to try to replicate our 3-billion nucleotide DNA chain perfectly, errors creep in. Additionally, our daily lives intersect radiation, nasty chemicals, and infectious viruses that add mutations. Some errors get into the germ cells and pass on to the kids, and a multitude of errors degrade the rest of our bodies’ cells, aging us, eventually killing us if we live long enough.

Genetic Entropy is also the title of a book by John C. Sanford, a Cornell University professor and geneticist. The book’s latest edition (2014) includes reports of discoveries made since his first edition (2005), that serve to strengthen his thesis: the same mutations that result in aging and the death of individuals also insure that all populations must eventually go extinct. This world is fallen, the ship is going down, and the question is whether you can find the lifeboat.

Sanford defines the Primary Axiom of biological evolution: “Life is life because random mutations at the molecular level are filtered through a reproductive sieve acting on the level of the whole organism.” The Primary Axiom is the foundation of neo-Darwinism.


(A mini-tutorial: Darwinism, per se, is the idea that natural selection, typically acting via environmental pressures, helps some creatures to survive and to reproduce more prolifically than others, and the population changes over time, taken over by those lucky enough to have some little variation in their body that offers advantage. Charles Darwin knew nothing of genetics, nothing of DNA. 20th century evolutionists came to realize that the only hope for Darwinism’s raw materials, the random variations that might produce advantage, is mutation in the replication of DNA. The supposed teamwork of DNA-based mutations and natural selection is termed <em>neo-Darwinism</em>.)

Sanford, having worked as a frontline researcher in this area for decades, concludes that the Primary Axiom “is essentially indefensible. Its apparent invincibility derives largely from bluster, smoke, and mirrors.” It’s held tightly, though, as a mystical faith by those who control academia, whose worldview is atheism. They have no other recourse.

Genetic Entropy is written for popular consumption, and so you should consider adding it to your shelf. You don’t have to be a biologist to appreciate the arguments. (I’m only a simple physicist, yet I can handle it.) The author begins his case by describing a bit of the complexity of the human genome – the 3 billion nucleotide letters (Adenine, Guanine, Cytosine, Thymine) that make up your genetic code. Most people tend to think of DNA as a linear code of ‘letters’ (A, G, C, T), divided neatly into distinct segments called genes, each of which codes for a protein, with a lot of junk DNA in between the genes.

This picture is wrong. The human genome has about 20,000 genes which code for about 100,000 different proteins. How is that possible? The DNA code has overlapping programs, in which genes can be read forwards or backwards, and different proteins are coded from different segments of a given gene. The portion of DNA code that corresponds to an average protein may be about 3,000 nucleotides long. But the gene containing that section may encompass 50,000 nucleotides. Different ‘subroutines’ called within that one gene’s program can account for several different proteins and a variety of RNA-based control machinery.


About half of transcribed DNA is doubly functional, transcribed in both directions. (Think of that! No software geek can do machine code like that!) The 97% of the DNA that does not specifically translate into protein is not ‘junk’ at all – an evolutionary presumption over the last few decades, now disproven – but contains genes that regulate genes . . . that regulate still more genes. Most of this DNA is transcribed into RNA which serves the many regulatory functions. The genome is an incredibly sophisticated computer program, full of loops and branches, self-interacting, self-regulating, responsive to the cellular environment and ultimately, the organism’s environment. There are large sections of DNA between what counts as ‘genes’ long supposed to be junk, but research continues to uncover regulatory functions. Many top scientists in the field expect that 100% of the genome will turn out to be brilliantly functional. This is no shock to creationists who have long held this position. The evolutionary idea of ‘junk DNA’ has held back science for many years.

Furthermore, DNA folds into 2-D and 3-D structures, embodying structural information that determines how and when genes are turned on and off. Altogether, the information content of the multidimensional, multi-overlapping genetic code has not been fully counted, but even evolutionists understand that human life is far more complex than all human technologies combined. Where did this info come from and how can it be indefinitely maintained?


Sanford poses an analogy of the evolution of vehicles, starting with a little red wagon, built from a manual with detailed assembly instructions. Each wagon exiting the manufacturing plant has its own manual taped to the bottom, a manual generated by a myopic scribe who copied the previous version. But the scribe makes mistakes. If the quality control inspector (natural selection) finds the wagon functional, he authorizes another wagon, built from the slightly erroneous manual attached. The myopic scribe makes another copy of the manual, adding a few more typos, to attach to the new wagon. Over time, and many generations of wagons built by increasingly erroneous manuals, what do you expect?

The errors – mutations – are random and cannot be fixed individually. The inspector selects only at the wagon (organism) level. Will the process produce better wagons? Some biological mutations are not just nucleotide substitutions (point mutations). Mutations can include duplication of DNA segments or even whole genes, analogous to lines of text or whole pages in the wagon’s manual. Does a duplicate page imply more information?

Sanford argues that the overwhelmingly likely outcome is dysfunctional little red wagons. Misspellings, substitutions, and duplications – typographical errors – will not turn wagons into automobiles, planes, Space Shuttles, or Star Ships. Analogously, the complexity difference between wagon and Star Ship is far, far less than between microbe and man. And from raw materials to that first microbe – there is no analogy because even a microbe’s biotechnology far surpasses that of any supercomputer or any construct of man.

F-22 Raptor -- designed by typos?

F-22 Raptor — designed by typos?

Sanford: “Random mutations consistently destroy information.” Examples abound, including birth defects and cancer. We’re all mutants. Cancer is the result of accumulating mutations within our somatic (body) cells. The same goes for aging and inevitable death. What about so-called ‘beneficial mutations’? Every case that has been cited by evolutionists as beneficial involves loss of information. For example, antibiotic resistance in bacteria typically derives from a mutated, defective structure in the microbe that is not vulnerable to a drug designed to target a normally healthy metabolic or reproductive structure. The mutants survive in the presence of the drug, but in the wild do not compete well with the non-mutant ‘wild’ strain.

If you’re worried about burglars in your neighborhood, a ‘beneficial’ modification to your house you might consider would be to weld your doors shut to prevent home invasion. You may successfully foil the burglar, but your house has lost some resale value, hasn’t it? And your daily routine might be a tad more awkward.

Vast effort over the last century has been put into trying to use mutations to generate useful plant varieties. Radiation and chemical mutagens have been used to clobber countless plants in attempts to generate better crops. Mostly, you get small sick, deformed, and otherwise aberrant plants. Generally, these projects have been complete failures. Modest success is rare, as in the case of low phytate corn, which can be a useful animal feed. The mutant low phytate corn arises from damaged genetic machinery which produces less phytic acid . . . a net loss of information.


Successful plant and animal breeding experiments have made use of the pre-existing natural variation within animal species or genera. All this makes sense if the existing variation arose by design, by creation. Sanford cites Jerry Bergman who reported (in 2004) a simple biological literature search, finding 453,732 “mutation” hits – only 186 of them mentioned the word “beneficial.” Reviewing those 186 references revealed a consistent loss of function in producing some narrow “benefit.”

Yet for evolution to occur, information-creating mutations must occur. Evolutionary geneticists, in designing computer models and working to support the Primary Axiom, invariably assume lots of beneficial mutations that magically produce information that can code for new structures . . . somehow. The problem is that most mutations, by far, must be deleterious. Think of the little red wagon construction manual. It’s hard to even think of a typo that might improve the wagon – perhaps a typo that generates 5 coats of paint instead of 4? But even so, that comes with a cost. A typo that results in 5 wheels instead of 4, though, how does that work? Alternatively, a 3-wheeled wagon is not on the path toward a functional tricycle. (It’s not a better wagon at all and will be rejected by the inspector.)

Similarly, selection must take place at the organism level. If a gene accumulates several bad mutations and one beneficial one, the only issue is whether the entire organism survives and reproduces more liberally, and the pattern continues until the beneficial mutation takes over the entire population, outcompeting all organisms that don’t have that mutation. (Note that wimpy individuals within a population can have a lot of kids, too. And the strong ones don’t always have kids.) All the while, though, generation after generation, more bad mutations are accumulating.

To work through these issues in detail requires serious computer simulations. These have been done, some realistically and others not so much. Rare beneficial mutations, even if they exist, will get swamped by a multitude of bad mutations. In a realistic simulation, you must take into account that bad mutations and (allegedly) good mutations are tied together into the same genes and chromosomes. They can’t be separated.

Since the 1950s geneticists have been worried about the buildup of mutations in the human population . . . the ever-increasing mutational load. There has been a long held consensus that if the mutation rate approached one harmful mutation per person per generation, then the human race would be doomed to eventual extinction. From an evolutionary view, selection would have to eliminate mutations as fast as they occur. Yet it’s clear that most mutations are only slightly deleterious – they degrade the software a little, but the individual survives; ie., the wagon still works, but one of the wheels is a little lopsided.

Lots of slightly deleterious mutations accumulate, yet people still grow up and reproduce, but genetic diseases increase in frequency. Eventually, the errors accumulate until the wagon simply breaks. Any slightly ‘beneficial’ errors are lost in the sea of slightly harmful mistakes.

J. B. S. Haldane

J. B. S. Haldane

So, what is humanity’s actual reproductive mutation rate? Is it approaching one per person per generation? No . . . it’s far worse!! Research indicates that it’s in the range of 75 – 175. Sanford (and others) note that this has profound implications, not just for the human race but for the fable of evolution’s Primary Axiom. “There is no realistic method to halt genomic degeneration.” Sanford observes that the 75 – 175 range represents only single nucleotide substitutions. Other mutation types include tandem repeats, deletions, insertions, duplications, translocations, inversions, conversions, and mitochondrial mutations. Sanford’s analysis indicates that when all mutation types are factored in, the average mutation rate might easily be 1,000 per person per generation.

Even if you take 100 as a conservative estimate, it’s clear that humanity is being flooded by mutations, more than at any time in history. With 7 billion people, our generation has added 700 billion new mutations, more than 200 mutations for every nucleotide position within the genome. (The human genome has ‘only’ 3 billion nucleotides.) Sanford: “We are on a downward slide that cannot be stopped.”

This genetic scenario is termed “error catastrophe.” Extinction is inevitable, and begins to show up with indications such as declining fertility, greater susceptibility to infectious disease, and increasing incidence of genetic diseases. The latter stages are described by the cheerful term, “mutational meltdown.”

As genetic information is lost (typos never add info), a population declines in “fitness,” a measure of the likelihood of individuals to grow up and reproduce successfully. Current estimates for the decline in human fitness due to mutations is in the range 1-2% per generation. Some think the number is closer to 5% at this point in history. Yes, medical technology tends to preserve and extend life, but it’s a losing battle.

By the way, have you heard anything about this in the news? Is it in the kids’ textbooks? Doesn’t it count as a national – no, international crisis? Nope, we’re headed for a cliff and nobody seems to notice . . . or care. The political ramifications of widespread knowledge of this subject would be unimaginable, and so no one with a public platform is likely to speak up. Death is just so gloomy.

Sanford discusses in detail how natural selection cannot save the day. Selection occurs only at the organism level, culling the man or woman before they can reproduce. But between a nucleotide and the organism are many different levels of organization. Sanford’s example: “A single nucleotide may affect a specific gene’s transcription, which may then affect mRNA processing, which may then affect the abundance of a given enzyme, which may then affect a given metabolic pathway, which may then affect the division of a cell, which may then affect a certain tissue, which may then affect the whole organism, which may then affect the chance for that specific mutation to get passed on to the next generation.”

Massive amounts of uncertainty and dilution are added at each organizational level, resulting in a massive increase in ‘noise,’ and loss of resolution. There must be a vanishingly small correlation between any given nucleotide (a single molecule), and a whole organism’s probability of reproductive success . . . Human genes never exist in ‘pools.’ They exist in massive integrated assemblies within real people. Each nucleotide is intimately associated with all the other nucleotides within a given person, and they are only selected or rejected as a set of 6 billion.” (2 strands of DNA at 3 billion nucleotides each gives 6 billion total.)

And so an allegedly beneficial mutation gets lost in the noise, not only of the surrounding crowd of somewhat harmful mutations, but also due to all the levels between the molecule and whether the man survives to have children. Sanford uses the analogy of the Princess and the Pea fable. The levels represent many thick mattresses. Also – importantly – additional external sources of ‘noise’ should typically dominate, including ‘selection’ by war, crime, infectious disease, accident, and culture. (As if the Princess is getting poked and prodded and annoyed by others trying to keep her from noticing the pea under the stack of mattresses.)

In brief, there is simply no opportunity for beneficial mutations to accumulate and overcome the harmful errors . . . not to mention building the information necessary for new tissues and organs; yet harmful mutations must eventually build up to destroy a population. (Accumulating typos never helps. You can gloss over a few and get by, but when typos get too numerous, the message is lost.)

The science of this subject is ignored by evolutionary zealots – even professional geneticists – who fantasize that the Primary Axiom works because a ‘good letter’ is independently selected for (or against), and ‘beneficials’ somehow arise as frequently as ‘harmfuls’ and that ‘beneficials’ somehow build new information content. They choose to ignore the reality that chromosomes (big bundles of genes) are inherited in toto by offspring; there is no magic genie to weed out the harmful mutations and select for the beneficials.

Yet this was the approach of the famous evolutionary geneticists of the 20th century, including J.B. S. Haldane, Ronald Fisher, and Sewall Wright, who established the field of population genetics. But to their chagrin, even with incredibly favorable and unrealistic assumptions, we’re faced with “Haldane’s Dilemma.” Haldane calculated that (on average) it would take 300 generations (6,000 years) to “fix” a single new mutation – for it to take over a population. Therefore you could only fix about 1,000 beneficial mutations in the 6 million years it allegedly took for humans to evolve from a chimp-like ancestor. But the difference between chimp and human genomes is about 150 million nucleotides – in the 1-D code – not counting the substantive differences in the 2-D and 3-D configurations. Evolutionists are sunk without a trace even when they defy reality!

When realistic simulations are performed, as Sanford and his colleagues have done, then it’s clear that genes and populations deteriorate. Haldane’s alleged 1,000 good mutations would be swamped by millions of bad mutations. Sanford: “This would not just make us inferior to our chimp-like ancestors; in 6 million years it would obviously have killed us!”

Cloning provides an interesting case study. You would clone a human by taking a somatic (body) cell from a mature individual and use that cell to produce copies of of him. Animal cloning experiments have been plagued by the appearance of pre-aging in the more successful clones. (There are lots of dead-on-arrival clones, too.) Somatic cells have undergone many cell divisions since the embryonic stage and mutations accumulate with each division. So the clone starts with far more mutations than a child would, which would have developed from the germ line of the parent. As you grow and age, every cell in your body becomes more mutant and more unique – not in a good way. Your clone would be genetically equivalent – in deterioration – to a descendant of yours many generations into the future. Another way to look at this: your descendants will be in as much genetic trouble as your defective clone.

Where does genetic information come from in the first place? Books don’t come from an explosion of ink in a paper factory. Information must come from the mind of the Creator. Once you have a functional genome and a healthy creature (Adam and Eve, for example), mutations degrade. There are no mutational paths from one type of creature to another, no path from chemicals to the first microbe, no path from microbes to jellyfish to eels to fish to amphibians. At each step along the path you have to have a newly functional and competitively winning – by the measure of differential reproductive success – organism. Just as there is no typo-path from wagons to Star Ships. By the way, the fossil record confirms the ‘separateness’ of the kinds. For a brief review, click on the two pdfs below, which discuss the ‘fossil tree’ for mammals. (I give away thousands of copies of this tract.)



Important note: Since there are no mutational paths, this puts the lie to any scheme of theistic evolution. God simply did not create mutational pathways to develop Earth’s ecosystem. The paths are not there. The vast genetic differences between kinds of creatures must be created in whole. You can design a little red wagon or a jet fighter, but you can’t get from wagon to fighter via typos, with functional vehicles at every step in between, even if you brilliantly select the typos yourself.

Mutations and natural selection “cannot create a single gene ever . . . This constitutes what is essentially a logical proof that the Primary Axiom is false.” The only reason that some cling to theistic evolution is to beg for some respect from atheistic academia, trusting that they’ve got the science right. They don’t. And God-haters are going to disrespect you anyway.

Sanford expands on this point in a discussion of the nature of DNA, in that it is both poly-functional and poly-constrained. We already discussed the poly-functional character in that a given gene can be read in a variety of different ways, choosing alternative segments to transcribe, in order to generate alternative proteins and / or RNA machines. Since a given nucleotide may find itself in multiple codes, corresponding to a variety of machines, a random change in that position will be far more destructive than if you had a simple 1-D code . . . 1 machine for 1 gene. This property constrains the genome drastically. You don’t want to mess with it, because the accumulation of errors will ultimately impact multiple systems. It’s somewhat equivalent to data compression, but far more sophisticated. Sanford: “Changing anything seems to potentially change everything.”

Some mutations can be recessive. In sexual reproduction, the healthier chromosome from the other partner may be inherited by the child. But as mutations accumulate in a population, recessives eventually run into each other. Don’t marry your first cousin. You each may have the same recessive mutation. Unfortunately, though, we’re all cousins to some degree. When too many have the same mutations, meltdown will eventually occur. Sanford: “Inbreeding is like a sneak-preview of where we are going genetically as a species. The reduced life expectancy of inbred children reflects the overall aging of the genome.”

Human lifespans are long and our cells have genetic repair mechanisms that keep the damage down to what it is. Sanford cites an interesting case study of organisms that are small, reproduce rapidly, and have relatively high mutation rates. He publishes graphs illustrating the accumulation of mutations in the human influenza virus, including the H1N1 strain that produced the 1918 pandemic, along with two other 20th century pandemics, caused by H2N2 and H3N2. In all three cases the pandemics ‘burned out’ due to accumulated mutations. Evolutionists would see them as ‘evolving,’ but the data show that they de-volved to extinction. Life can’t build itself up from scratch via typos!

lifeboat-rescueIs there a way out, a lifeboat for humanity . . . for you? Sanford concludes his book with a personal testimony: “When I was young, I accepted the fact that I was going to die, and that all of the people I Ioved were going to die. I accepted it, but it robbed me of joy, to say the least. I was taught that there was still one hope: that the world was getting better. Science was advancing . . . Even mankind was getting better . . . Through evolution, we could evolve into something better. Through progress, we might eventually defeat death itself.”

He came to realize these hopes were false. Why is the universe and life itself falling apart, wearing out? You can read all about it in Genesis chapters 1 to 3. We’re still under that curse, but there will be a day when it is lifted. (See Revelation 22:3) This world, this universe, belongs to its Creator, the Lord Jesus Christ. The world isn’t getting better (have you noticed?), you’re not going to live forever, and medical science won’t save you or the rest of humanity. Since mutations occur at the molecular level, in every cell in your body, a ‘medical cure’ would necessitate continual screening of your body at the molecular level – and insert molecular replacements as needed. Anyone who can do that might have a claim on Godhood.

In the meantime, you will need your genome rebuilt. Wouldn’t you like the assured hope of a resurrection to a new genome, a new body, one that won’t wear out? The Author of Life has already demonstrated, through His resurrection, that He has the technology to help you. He can rejuvenate your body – every molecule.

Your part? Humble yourself. Repent from the specific sins in your life and trust Him. He will give you eternal life – spiritually for now, but eventually in a revitalized body. Jump into the lifeboat. The ship is going down and it’s the only one available.


In an appendix, Sanford reports that he has sent copies of his book and related scientific papers to geneticists in his field, asking for comments and criticism. They have refused to respond. Sanford finds this hard to understand, because science can progress only with honest and healthy communication . . . and criticism. He asked a good friend, a geneticist and committed evolutionist, “Why don’t they engage my arguments?” His answer: “They do not have answers.” Sanford notes that many of the problems he addresses in the book have been more ‘quietly acknowledged’ in the research papers of his evolutionary peers. But they would never dare to admit the implications for the fable of evolution.


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